introductive course in tropical and humanitarian crisis medicine

INTRODUCTIVE COURSE
IN TROPICAL AND
HUMANITARIAN CRISIS MEDICINE
Manual
ATHENS 2010
Manual
INTRODUCTIVE COURSE IN TROPICAL AND
HUMANITARIAN CRISIS MEDICINE
ATHENS UNIVERSITY | ªEDICAL SCHOOL
MASTER’S COURSE IN:
INTERNATIONAL MEDICINE – HEALTH CRISIS MANAGEMENT
Eleni Kakalou, MD, MSc
Christos Christou, MD, MSc
Manual
Introductive Course
in Tropical
and Humanitarian
Crisis Medicine
compiled by
ELENI KAKALOU, MD, MSc
Internal Medicine specialist
Phone +30 69 71 89 18 40
email: ekakalou@yahoo.gr
CHRISTOS CHRISTOU, MD, MSc
Senior Resident of General Surgery
Phone: +30 69 72 23 79 95
email: christos.christou@athens.msf.org
Editor
THEOFILOS ROSENBERG, MD, PhD
Associate Professor of Surgery
email: rosen@med.uoa.gr
© 2010 – Athens, Medical School, University of Athens, Greece
PAGE EDITING: ∂vangelia Stamatellou
estamatellou@yahoo.gr
Printed by QUICK PRINT CENTER S.A.
qpc@otenet.gr
PHOTOS: Julie Remy
www.julieremy.com
The current text is a partcicipant’s reference guide for the course on
International and Tropical Medicine, taking place in Ifakara, Tanzania since
2008. It is designed to be used as a reference source during the course
taking place in a rural African setting.
The course has been designed as part of the module Tropical Medicine
of the MSc ‘’International Medicine-Health Crises management’’.
The authors had been working in the field on HIV/AIDS care in Zambia
with MSF-OCBA (Medecins Sans Frontieres-Operational Centre BarcelonaAthens) between the years 2003-2005. Prior to undertaking their duties,
they had received training by Mildmay Institute in Kampala Uganda. During
their mission, part of their work had to do with developing curricula and
implementing trainings on HIV/AIDS care for national staff such as clinical
officers, nurses, peer educators and expert patients involved in HIV care and
prevention. Inspired by their own experiences as trainees as well as trainers,
they envisioned an introductive course in Tropical and Humanitarian Crisis
Medicine – the first of its kind to be developed by an academic institution
in Greece. The course aims to be a ‘’hands on’’ experience encompassing
both theoretical learning as well as clinical experience. It aspires to introduce
participants to the epidemiology, socio-economic context, issues of clinical
care and last but not least to the political, financial and research issues
affecting all aspects of the major diseases impacting the lives of poor people
around the world.
The course is not meant to target experts or trainees in Infectious
Diseases seeking specialized training in Tropical or International Medicine.
Further reading and training should be sought in relevance to the
educational and professional needs of each participant.
The development of the material has been based on a collection of
manuals, guides, reports and guidelines produced by WHO, UNICEF and
various medical NGOs such as MSF, Concern, Valid International and others.
Certain parts are a direct adaptation of relevant chapters of the aforementioned documents, while others have been written by the authors
themselves. In any case that the material is a direct adaptation of another
text, this is indicated by a footnote. In the reference part at the end of each
chapter one can find the details of the original documents. Sources of
tables, diagrams or figures are mentioned underneath.
Any comment or errors detected will be greatly appreciated and will
facilitate the revision of the document for next year’s course.
Contents
1. HIV/AIDS and TB .................................................................................................................. 7
2. Diarrhoeal Diseases – Cholera ............................................................................................ 69
3. Management of acute and chronic malnutrition .............................................................. 99
4. Neonatal and Childhood Care .......................................................................................... 183
5. Maternity Health / Care in Normal Birth – Obstetrics .................................................... 205
6. Viral Hemorrhagic fevers (VHF), Onchocerciasis and Leprosy ........................................ 253
7. Malaria care, health policy and research ........................................................................ 291
8. Vaccination programmes and campaigns in emergencies .............................................. 353
9. Sexually Transimitted Infections ...................................................................................... 373
10. Unintentional Injuries .................................................................................................... 415
11. Sexual Violence .............................................................................................................. 425
CONTENTS
12. Neglected Tropical Diseases .......................................................................................... 443
5
chapter 1
∏πV / AIDS and TB
More than 38 million people live with HIV/AIDS in the world and more than 2 million deaths
occur annually. Sub-Saharan Africa carries the main burden of disease. Although important
steps have been taken to increase access to effective treatment, only a fraction of patients
in most countries have access. The natural history, epidemiology and clinical presentation of
HIV disease varies considerably in developing countries. Available diagnostic and treatment
options are limited.
Tuberculosis (TB) is a major cause of illness and death worldwide, especially in Asia and
Africa. Globally, 9.2 million new cases and 1.7 million deaths from TB occurred in 2006, of
which 0.7 million cases and 0.2 million deaths were in HIV-positive people. More than 50% of
AIDS deaths in Sub-Saharan Africa are attributable to TB.
Partcipants will get familiar with epidemiology, the natural history, diagnostic algorithms,
most common Opportunistic Infections and treatment protocols using the expreriences and
evidence based medicine data developed by various programmes adapted to resource limited
context. A syndromic approach to most common problems is used to overcome lack of
diagnostic means. Various issues vital for treatment outcome such as pchycosocial counselling,
adherence issues and support groups will be addressed. A special session on HIV-TB coinfection and on MDR TB and X-MDR TB and its relation to the HIV pandemic is included.
Diagnostic algorithms and treatment options as well as an overall view of TB National
Programmes will be presented using a problem-oriented approach.
HIV/AIDS AND TB
Introduction
7
Epidemiology of HIV/AIDS
HIV/AIDS AND TB
Background 1
8
By the end of 2008 an estimated 33 million people worldwide were living with HIV. That same
year, some 2 million died of AIDS. Globally, less than one person in five at risk of HIV has access
to basic HIV prevention services. Only 42% of people who needed HIV treatment had access
to it by end-2008.
Since the first cases were recorded in 1981, acquired immunodeficiency syndrome (AIDS)
and its causative agent, the human immunodeficiency virus (HIV), have taken an enormous
toll around the world. It is estimated that, at the end of 2005, 38.6 million people were living
with HIV/AIDS. This includes nearly 4.1 million who were infected in 2005 alone. In the last 25
years, more than 25 million people have died of AIDS, including 2.8 million in 2005.
About 95% of people with HIV/AIDS live in developing countries, and nearly two–thirds
of them are in sub-Saharan Africa. In this region, where HIV is mainly spread through
heterosexual sex, prevalence rates exceed 20% in the worst-affected countries, and the
epidemic is disproportionately affecting young women. In the 15-24-year age group, three
young women in sub-Saharan Africa are infected for every young man. Three-quarters of all
women and nearly 90% of children with HIV/AIDS in the world live in this region.
HIV/AIDS epidemics in eastern Europe and east Asia are growing rapidly, notably in the
largest countries –China, India and Russia– where commercial sex and injecting drug use are
the key drivers. The diversity of epidemics between and within regions and countries
highlights the need for a range of responses that can be adapted locally.
Global efforts to address HIV/AIDS have advanced in recent years. Greater international
political commitment has been accompanied by increased financial resources through the
Global Fund to Fight AIDS, TB and Malaria, the United States President’s Emergency Plan For
AIDS Relief (PEPFAR), continued funding through World Bank loan and grant instruments,
increasing investments by bilateral donors and contributions from private foundations. As a
result of the recommendations of the Global Task Team on Improving AIDS Coordination
among Multilateral Institutions and International Donors, more concerted efforts are now
being made to improve coordination and cooperation among United Nations partners, donors
and governments so that the best use is made of these resources in countries.
1. Adapted from: “Towards universal access 2010”, WHO HIV/AIDS programme, 2006.
http://www.who.int/entity/hiv/toronto2006/towardsuniversalaccess.pdf
HIV/AIDS AND TB
Prevention efforts are beginning to bear fruit, with indications of behaviour change and
declines in prevalence rates in a number of high-burden countries. Many countries –supported
by the WHO/Joint United Nations Programme on HIV/AIDS (UNAIDS) ‘3 by 5’ Initiative and the
efforts of many other partners– have also made significant progress in expanding access to
antiretroviral therapy.
Yet much more remains to be done if the goal of universal access is to be achieved. Global
coverage of many of the key health sector interventions against HIV/AIDS remains low, and
growth in the numbers of new infections and people in need of treatment continues to
outpace the capacity of health services to respond. Global financial resources also fall short
of what will be needed to achieve universal access, and the sustained political commitment
needed to tackle AIDS over the long term is still lacking in some countries.
All sectors of society –from political leaders and government agencies to faith-based
organizations (FBOs), community-based organizations (CBOs), businesses, teachers, trade
unions, young people, parents and people living with HIV/AIDS– have contributions to make
in building awareness about HIV/AIDS, helping to prevent the spread of HIV, providing care
and support for those affected and mitigating the disease’s impact. But it is the health sector
that must play the lead role in coordinating the response to the epidemic at national and local
levels, raising resources, administering health systems and delivering many of the most
important interventions for HIV prevention, treatment, care and support through health
services.
In many low- and middle-income countries, the chronically under-resourced health sector
faces severe shortages of financial and human resources, and health systems are struggling
to cope with the impact of the HIV/AIDS epidemic. In some heavily affected countries in subSaharan Africa, people with HIV-related illnesses occupy more than 50% of hospital beds, and
care and support services are overwhelmed by demand. At the same time as demand for
health services increases, more health-care personnel are themselves dying or unable to work
as a result of AIDS. Poor working conditions and low morale have also led many health
workers to leave the sector or to migrate to countries offering better salaries and conditions.
Health infrastructure is also very weak in many countries. Inpatient and outpatient
facilities, laboratory capacity and systems to procure, manage and distribute drugs, diagnostics
and other essential commodities such as disposable gloves and sterile needles and syringes,
must all be strengthened if universal access is to be achieved.
These constraints are contributing to low coverage of many of the major health-sector
interventions against HIV/AIDS in many countries. Furthermore, stigma and discrimination
against people living with HIV and most at-risk groups, including in health-care settings,
continue to prevent people accessing the services they need.
9
Estimated number living with HIV/AIDS
Key challenges
HIV/AIDS AND TB
Scaling up HIV counselling and testing
10
Household surveys in several high-burden countries (Botswana, Burkina Faso, Cameroon,
Ghana, Kenya, Mozambique and Nigeria) have consistently shown that less than 10% of
people living with HIV/AIDS are aware of their HIV status. Because HIV testing and counselling
are the key entry point for individuals and their families to access HIV/AIDS prevention,
treatment and care services, many more people will need to know their HIV status if universal
access is to be achieved. This will require a major scale-up and diversification of HIV testing
and counselling services (using rapid test technology), including both client-initiated and
provider-initiated testing and counselling, as well as expanded coverage of and better tools
for HIV testing in children and infants. Testing and counselling must be closely linked to
prevention, treatment, care and support services. They must also be accompanied by
concerted efforts to increase demand for these services (especially in most-at-risk
communities); protect confidentiality and human rights; reduce stigma and discrimination;
and support disclosure of HIV status.
Preventing sexual transmission
Sexual transmission is a key driver of the HIV/AIDS epidemic, especially in sub-Saharan
Africa. In many Asian countries, sex work is a primary driver of HIV transmission. Sexual
transmission within serodiscordant couples currently accounts for 40-60% of sexual
transmission in some high-burden countries. In Asia, the Caribbean and central Europe, the
proportion of new infections attributable to unprotected sex between men is increasing,
yet globally only 9% of men who have sex with men received any type of HIV prevention
service in 2005.
The health sector needs to play a stronger role in preventing sexual transmission of HIV. It
can do so by incorporating prevention initiatives into HIV/AIDS treatment and care services,
increasing access to good-quality, affordable condoms and supporting 100% condom-use
programmes; expanding services to treat sexually transmitted infections (STIs), and
incorporating HIV/AIDS information and counselling into STI and reproductive health
programmes as well as primary health-care services. The health sector has had limited success
in addressing the needs of the most at-risk groups. It needs to make significant effort to
ensure that services are accessible by and acceptable bycommunities. Strengthening links with
community-based services, is a key factor in sexual transmission prevention efforts.
A major challenge for the health sector is to better address the prevention needs of people
living with HIV/AIDS. Many people diagnosed in voluntary counselling and testing centres are
lost to follow-up and only emerge again when they have advanced HIV disease. Nongovernmental organizations (NGOs) and community-based organizations (CBOs) have focused on
health promotion for people living with HIV/AIDS, but strong links between these types of
services and clinical care are not widespread enough to ensure full coveraged effected
communities.
The health sector has an important role to play in providing a wider range of health
services and evidence-based interventions to assist people with HIV/AIDS maximize their
health; strengthen their immune systems; prevent opportunistic and sexually transmissible
infections; reduce the harms associated with injecting drug use; and avoid passing HIV on
to others. Such services may include information and counselling to prevent transmission to
sexual partners; support for partner notification and beneficial disclosure; HIV testing and
counselling for partners and children, and preventive care such as bed nets for malaria
prevention; co-trimoxazole; safe water and screening; as well as preventive therapy for TB.
This will require additional training and human resources in health services; increased
collaboration with networks of people living with HIV/AIDS and community-based services,
as well as much more attention to issues of stigma and discrimination in health-care settings.
HIV/AIDS AND TB
Prevention for people living with HIV/AIDS
11
Preventing transmission in health-care settings
It is estimated that globally, approximately 5% of new HIV infections annually occur
through unsafe injection practices in health-care settings. Infection prevention guidelines exist
in many countries, but their implementation is variable depending on available resources,
available equipment and trained and motivated staff. Preventing HIV/AIDS transmission in
health-care settings involves primary and secondary prevention measures.
Primary prevention includes standard precautions that benefit both patients and healthcare workers, such as occupational health and safety, safe injections and safe medical
procedures. Secondary prevention measures need to include first aid, counselling and support,
HIV testing and, if necessary, post-exposure prophylaxis or treatment and care. More effort is
needed to guarantee the safety of injections of all types, surgery, obstetrics and dental
procedures, and medical waste disposal.
Measures to prevent tuberculosis (TB) transmission in the health-care setting are also
important. These include rapid evaluation of suspected TB patients in outpatient settings;
separation of infectious TB patients from other inpatients; cough hygiene for patients and
environmental control methods such as good ventilation and ultraviolet light.
Ensuring blood safety
In many countries, people still die due to an inadequate supply of blood and blood
products. Every country has a common need to ensure the availability of adequate supplies
of safe blood and blood products and their accessibility to all patients requiring transfusion
through a nationally coordinated blood transfusion service; collection of blood only from
voluntary unpaid blood donors at low risk of acquiring transfusion-transmissible infections,
with stringent blood donor selection criteria; testing of all donated blood for transfusiontransmissible infections, blood groups and compatibility; and safe and appropriate clinical use
of blood and blood products.
HIV/AIDS AND TB
Reducing vulnerability
12
A longer-term challenge for the health sector involves collaborating with other sectors
to reduce the sexual transmission of HIV through structural interventions, for example, by
promoting laws and policies that are consistent with prevention goals; promoting
interventions to reduce vulnerability, particularly of women and girls, and supporting sex
education for young people. The health sector will also have a central role to play in providing
timely access to and guidance for the appropriate use of new prevention technologies, such
as pre-exposure prophylaxis, microbicides and vaccines, when they become available, and male
circumcision, if the results of one promising study are confirmed by other trials.
Scaling up the prevention of mother-to-child transmission
Services to prevent mother-to-child HIV transmission (PMTCT) are important entry points
for HIV/AIDS prevention, treatment and care services for women, their children and families.
However, it is estimated that only about 1 in 10 pregnant women are offered services to
prevent mother-to-child HIV transmission.
The health sector delivers a range of maternal, newborn and child health services that can
provide a platform for the rapid scale-up of PMTCT programming. Comprehensive PMTCT
programmes must include prevention of primary HIV infection in women of child-bearing age,
prevention of unintended pregnancies among women with HIV/AIDS and HIV transmission
from women with HIV/AIDS to their children, as well as provide care, treatment and support
to women, their children and families. Interventions which need to be available to pregnant
women include HIV testing and counselling in antenatal delivery and other health settings;
couple counselling; promotion of dual protection, including condoms; infant feeding
counselling and support; antiretroviral therapy as prophylaxis for MTCT prevention, and
HIV/AIDS treatment and care.
Stronger linkages between PMTCT services and community-based support, family
planning, STI and general health services are needed to ensure that women receive services
that cover their wide range of health needs. In settings with high TB burden, TB screening,
prevention and treatment also need to be accessible for pregnant women.
Preventing HIV transmission through injecting drug use
An estimated 10% of all new HIV infections globally are related to injecting drug use,
rising to over 30% if sub-Saharan Africa is excluded. Injecting drug use is the major mode
of HIV transmission in eastern Europe and central Asia, where it accounts for over 70% of
all HIV transmission. However, it is estimated that less than 5% of injecting drug users globally
have access to effective HIV prevention, treatment and care services.
The WHO/UNAIDS “3 by 5” Initiative helped to promote a steady increase in access to
antiretroviral therapy in low- and middle-income countries between 2003 and 2005, with the
number of people receiving treatment globally increasing three-fold over that period.
These encouraging global trends continue. By June 2006, an estimated 1 650 000 people
living with HIV/AIDS were receiving treatment in low- and middle-income countries (Table
1), representing around 24% of the estimated 6.8 million people in need of treatment. Trends
in treatment scale-up have been particularly encouraging in the region. Sub-Saharan Africa–
HIV/AIDS AND TB
Scaling up treatment and care
13
HIV/AIDS AND TB
which is now estimated to have more than 1 million people on antiretroviral therapy, with
coverage of 23%, compared to just 100 000 on treatment and 2% coverage at the end of
2003. Sixty-three per cent of all people now receiving antiretroviral treatment in low- and
middle-income countries live in sub-Saharan Africa, compared to 25% in late 2003.
In east, south and south-east Asia, 235,000 people are now on treatment and coverage
is estimated at 16%, up from 70 000 people on treatment at the end of 2003, and
representing a more than three-fold increase. In Latin America and the Caribbean, the number
of people receiving treatment has increased gradually to 345 000 people, up from 210 000
at the end of 2003. In this region, coverage now stands at around 75%, although some
significant disparities in coverage remain between countries. In the low- and middle-income
countries of Europe and central Asia and in north Africa and the Middle East, progress has
been less significant. Some 24 000 people in Europe and central Asia are receiving treatment,
compared to 15 000 at the end of 2003, with coverage now estimated at 13% of those in
need. The region with the lowest estimated coverage (5%), is in north Africa and the Middle
East, where 4 000 people were estimated to be receiving treatment at the end of June 2006,
compared to 70 000 people who are in need.
Estimated coverage in low- and middle-income countries according to region December
00–June 2006:
14
Some numbers do not add up due to rounding
a. For an explanation of the methods used, see Progress on global access to HIV antiretroviral therapy:
a report on “3 by 5” and beyond, WHO and UNAIDS, 2006.
b. Data on children –when available– are included.
HIV/AIDS AND TB
Despite this encouraging progress, approximately three–quarters of those in need of
treatment worldwide still do not have access to it, and although there is presently no reported,
systematic gender bias in access to treatment globally, children and vulnerable populations (such
as injecting drug users) are significantly under-served. The health sector must continue to drive
scale-up towards universal access to treatment through planning, delivering, monitoring and
evaluating HIV treatment, care and support services. Organizing health services and ensuring
equity and quality of programmes is another responsibility. Current priorities include updating
national treatment guidelines to include the most appropriate recommendations for first- and
second-line regimens; developing models of delivery that ensure equity, including reaching those
most at risk; maintaining continuous supplies of drugs and diagnostics developing improved
drug formulations for adults and children. Delivering treatment for displaced persons, refugees
and populations in conflict also remains a major challenge.
Where antiretroviral therapy is widely available, the incidence of opportunistic infections
and associated morbidity and mortality are greatly reduced. However, patients failing
treatment or without access to it need prophylaxis and treatment for a wide range of
opportunistic infections that may be encountered. Access to many of these drugs is still poor.
For example, it is estimated that globally only 4% of adults and 1% of children infected with
HIV have access to co-trimoxazole prophylaxis, an inexpensive and highly effective
intervention for the prevention of pneumocystis jiroveci pneumonia and some bacterial
infections. Drugs for preventing and treating many other common opportunistic infections
remain unaffordable or are not routinely available due to weaknesses in procurement and
supply systems.
Tuberculosis (TB) is one of the leading causes of HIV-related deaths and morbidity. Despite
some progress in recent years, TB continues to fuel the HIV epidemic, especially in Africa, and
the lack of TB diagnostic tests –particularly for sputum smear-negative and extrapulmonary
TB– as well as poor laboratory infrastructure, delay in diagnosis of TB and start of TB
treatment. TB programmes can be important partners in helping to accelerate the
decentralization of HIV treatment and care down to the primary care level. Much more
attention to joint planning, collaboration between TB and HIV programmes and integration
of TB and HIV services are needed in many countries with high rates of coinfection.
Managing the broad range of opportunistic infections and other comorbidities experienced
by people living with HIV/AIDS, requires an integrated and coordinated response from a wide
range of health services. Clinical guidelines need to incorporate the latest recommendations
for prophylaxis and treatment of opportunistic infections. Although most coinfections and
comorbidities can be managed at primary care level, complicated cases may need to be
referred to specialist services addressing such areas as TB, viral hepatitis (which affects up
to 90% of injecting drug users), respiratory medicine, oral health, mental health, drug
dependence, neurology, gastroenterology, oncology and gynaecology. Planning for the
expansion of HIV/AIDS services needs to ensure the capacity of these associated services,
including community-based ones.
15
Other aspects of care also require closer attention. Few HIV/AIDS treatment and care
programmes include nutritional support as a core intervention. Yet adequate nutrition is
essential to maintaining the immune system and ensuring optimal benefits from the use of
antiretroviral therapy and other medicines. Whether antiretroviral therapy is available or not,
there is a need to provide comprehensive palliative and end-of-life care for people living with
HIV/AIDS, including proper management of underlying or associated chronic health conditions
and psychosocial support. Pain management in particular remains a major challenge in most
countries due to poor access to opioid analgesics and negative health worker attitudes
towards prescribing analgesia.
Biology of HIV virus
HIV/AIDS AND TB
The structure of HIV-1
16
HIV-1 is a retrovirus and belongs to the family of lentiviruses. Infections with lentiviruses
typically shows a chronic course of disease, a long period of clinical latency, persistent viral
replication and involvement of the central nervous system. Visna infections in sheep, simian
immunodeficiency virus infections (SIV) in monkeys, or feline immunodeficiency virus
infections (FIV) in cats are typical examples of lentivirus infections. Using electron microscopy,
HIV-1 and HIV-2 resemble each other strikingly. However, they differ with regard to the
molecular weight of their proteins, as well as having differences in their accessory genes. HIV2 is genetically more closely related to the SIV found in sootey mangabeys (SIVsm) rather
than HIV-1 and it is likely that it was introduced into the human population by monkeys.
Both HIV-1 and HIV-2 replicate in CD4+ T-cells and are regarded as pathogenic in infected
persons, although the actual immune deficiency may be less severe in HIV-2 infected
individuals.
A retrovirus, such as HIV, carries genetic material (nine genes) in the form of ribonucleic
acid (RNA) and uses an enzyme, reverse transcriptase, to convert the RNA to deoxyribonucleic
acid (DNA). RNA occurs in a single strand of genetic material and DNA is a double strand of
genetic material. The synthesis of HIV DNA from HIV RNA must occur in the cytoplasm of
the CD4 cell before the virus’ genetic material (DNA) can be inserted into the cell’s DNA. HIV
can infect any cell carrying a CD4 receptor.
The hallmark of sympotomatic HIV infection is the immunodeficiency caused by continuing
viral replication. The virus can infect all cells expressing the CD4 antigen which the virus uses
to attach to the cell. Chemokine receptors such as CCR5 and CXCR4 are essential for virus
entry into the cell. Individuals with CCR5 deletions are resistant to infection and if infected
the disease has a slower progression to AIDS. Once it has entered the cell, HIV can replicate
and cause cell fusion and death. A latent form is established as the virus integrates the HIV
genome into the cell’s genome. The main target for HIV virus is the CD4 helper-inducer
lymphocyte which has a central role in the immune network as it directs other immune cells
in to fighting off infection. As time passes CD4 numbers decrease dramatically and
opportunistic infections occur. However, some of the immunologic defects are explained by
qualitative defects in the CD4 responsiveness and not by the mere decrease in numbers.
Only about 1-2% of lymphocytes are in the circulating blood at any one time. The rest are
in the lymph system/tissue (resting – inactive). Lymphocytes (CD4 T-cells) are infected by HIV
early in the infection phase, probably about the time of the acute HIV infection when the virus
replication bursts forth and “seeds” the cells in the resting stage. Only 3-4% of the virus is
circulating in the blood. The rest of the virus in located in the cells. This pool of infected cells
can persist for years. T-cell lymphocytes are activated via presentation of antigen by
macrophages. Activated T-cells become differentiated into subpopulations in the thymus
gland. All T-cells have CD3 markers, but through a differentiation process, cells express either
CD4 or CD8 receptor sites. The CD4 T-cell is the very cell that is the target of HIV invasion. The
CD4 T-cell is the helper cell (helps other cells), and it functions in helping B cells produce
antibodies, CD8 cells to mature, and assists the cells that activate macrophages. CD8 cells
mature into cytotoxic cells. The normal ratio of CD4 to CD8 is 2:1. The CD8 T-cell blocks
replication of HIV and the decrease in activity of CD8 cells over time may be related to
progression to AIDS in HIV infected individuals.
HIV uses two other enzymes, protease and integrase, to facilitate infection of human CD4
cells. HIV attaches to the CD4 cell by modifying a glycoprotein precursor (gp160). The gp160
is in a non-functional form, and in order for HIV to attach to the CD4 cell, gp160 must be
clipped into two (2) molecules, gp41 and gp120 by the protease enzyme. The gp120 attaches
to the CD4 receptor site and the gp41 harpoons the cell assisting HIV to fuse with the cell.
HIV integrase functions within the CD4 cell nucleus to clip the cell’s DNA so that the HIV DNA
can insert itself into the cell’s genetic code thereby ensuring active replication of virus
whenever the cell becomes active. Recent studies have shown that there is an additional
process that enhances the insertion of HIV DNA into the cell nucleus. After the HIV RNA
synthesizes the HIV DNA in the cytoplasm, and prior to its integration into the cell nucleus,
the HIV DNA stimulates the production of viral proteins. These proteins activate the cell out
of its dormant state enabling the HIV DNA to insert itself more easily into the cell nucleus. The
immune system in HIV infection is activated by an antigen, HIV, which triggers the immune
HIV/AIDS AND TB
Pathogenesis
17
system to respond with vigor. A massive response occurs with the synthesis of antibodies (B
cells) and a cell mediated response (T cells). HIV infected macrophages travel to the germinal
centers in lymph nodes where dendritic cells and CD4 T-cells become infected early. It is
thought that HIV crosses the blood-brain barrier sequestered in macrophages. HIV continues
to replicate in macrophages. Research studies reveal that 10 billion HIV virions are reproduced
(replication takes place in HIV infected activated CD4 cells) and cleared by the immune system
each day in an infected individual. The virus replication is error prone and easily produces viral
mutations. A steady state is maintained between viral production and destruction by the
body’s immune responses for some time, but eventually the immune system is overwhelmed
and the infected individual becomes symptomatic and progresses along the continuum of
disease with increase morbidity, and eventually, dies.
Other immune cells that are infected by HIV include B lymphocytes and macrophages. The
defect in B lymphocyte function is partly due to disordered CD4 functioning. These direct and
indirect defects can lead to hyperglobulinemia and can in turn further depress B cell
responsiveness to antigen challenges. Thus, HIV immunodeficiency is mixed. Both humoral
and cellular immunity are affected, especially in children. Macrophages act as an HIV reservoir,
disseminating the virus to other organ systems, eg the central nervous system.
Apart of the immunologic effects of HIV, the virus can directly cause a variety of neurologic
effects. Neuropathology largely results from the cytokine release and other neurotoxins by
infected macrophages. Pertubations of excitatory neurotransmitters and calcium flux
contribute to neurologic dysfunction. Direct HIV infection of renal tubular cells and
gastrointestinal epithelium may contribute to these organ manifestations of HIV infection.
Transmission of HIV
➠ Blood – exposure can occur through a variety of methods, including used syringes, needle
➠
HIV/AIDS AND TB
➠
18
➠
➠
sticks, transfusions of contaminated blood, mucocutaneous exposure to blood or other
infected body fluids.
Semen – male to female and male to male – HIV has been found in semen even after
treatment with HIV antiretroviral agents.
Vaginal Fluid – vaginal fluid is the least infectious of body fluids because there are fewer
CD4 cells in vaginal fluid. There is still a chance of contracting HIV from vaginal fluids
but the risk is lower then through blood and semen.
Breast Milk – HIV can be transmitted through breast milk. Current recommendation is not
to breast feed if you are HIV infected, or to breast feed only for the first six (6) months
after birth.
Urine, feces, saliva, tears – are NOT infectious unless they contain visible blood. HIV is also
present in other body fluids but represents a very low risk of transmission unless they
contain visible blood.
HIV Clades
As previously mentioned there are two (2) HIVs. HIV-1 and HIV-2. Clade is the term used
to identify the various HIV-1 subtypes. These subtypes or clades (determined by divergence of
nucleotide sequencing) are sufficiently similar to each other to be classified within the larger
category of HIV-1, but dissimilar enough to be designated as a separate subtype (clade). A HIV
infected person may have several strains of HIV in his/her blood, but these strains are
mutations of the person’s original viral infection, not multiple infections with different strains.
Genetically these strains are very similar to each other. Clades (subtypes) have more genetic
diversity than HIV strains. Currently, it is not known what impact clade diversity exactly has
or will have on antiretroviral (ARV) medication efficacy and upon long-term vaccine
development. ARV medications are effective against all clades. The current vaccine research
paradigm reflects that there may be a need to develop vaccines specific to the dominant clade
within a country or region. Different subtypes prevail over diferent world regious:
➠
➠
➠
➠
➠
➠
➠
➠
➠
➠
Clade B in the United States, also found in Asia and South America,
Clade A in central Africa,
Clade C in southern Africa and India,
Clade D found in Africa,
Clade E in Asia and Africa,
Clade F in Africa, Asia, and eastern Europe,
Clade G in Africa and Asia,
Clade H in Africa,
Clade O Africa
Clade C is the primary subtype of new infections, especially in southern Africa.. The
greatest diversity of subtypes is found in west Africa, especially in Cameroon; an area
believed to be the site of where HIV first jumped species from animal primates to
humans.
ñ
ñ
ñ
ñ
ñ
A few of the risk factors are listed below:
unprotected sex – receptive anal/vaginal intercourse without a condom
substance use/abuse – especially sharing injection needles. Use of alcohol may impair
thinking leading to increase in risk behaviors.
other sexually transmitted infections (STIs)
especially STIs that cause genital ulceration that interrupts normal mucosal barriers
poverty – health problems, inadequate access to health care, poor diet, higher incidence
of violence and victimization
HIV/AIDS AND TB
Risk Factors for HIV infection
19
ñ Trauma, abuse – power imbalances between men and women, civil strife, discrimination,
violence.
Pathophysiology
HIV syndromes caused by the infection can be explained through one of three known
mechanisms:
IMMUNODEFICIENCY
Immunodeficiency is the direct effect of HIV virus upon immune cells. A spectrum of
infection is seen as in the case of congenital or acquired immunodeficiency diseases. Listeriosis
and aspergillosis are remarkably low. Where as TB, Lympoma and Kaposi’s sarcoma present
frequently. This latter complication is linked to a herpesvirus (KSHV or HHV-8).
AUTOIMMUNITY
Autoimmunity can result from disordered cellular immune or B cell function. Lymphocytic
infiltration of organs (eg. Lymphocytic interstitial pneumonitis, especially common in infected
children in Africa ) and autoantibody production (eg. Thrombocytopenia) occur. These can
be the only presentation of disease or co-exist with obvious signs of immunodeficiency.
ALLERGIC AND HYPERSENSITIVITY REACTIONS
HIV-infected individuals appear to have higher rates of allergic reactions to unknown
allergens as seen in the case of eosinophilic pustular folliculitis (‘’itchy red bump syndrome’’).
They also have an increased rate of hypersensitivity to medications (for example with
trimethoprim-sulphamethoxazole).
Natural history of disease
The following stages of HIV Progression do not take into account any antiretroviral (ARV)
treatment that can slow disease progression, decrease morbidity, and prolong life.
HIV/AIDS AND TB
ASYMPTOMATIC INFECTION
20
During the initial stage (primary infection) viral replication is rapid and viral load is high.
Seeding of virus into cells of the bone marrow, central nervous system, and lymphoid tissue
occurs rapidly (within 10 days). A person may experience flu-like symptoms especially at the
time of seroconversion (detectable antibodies in the plasma). Second phase of this stage
is the clinical latency, with a significant drop in viral load as the immune system mounts a
massive response. This phase may last for years, but the individual remains infectious to
others if engaging in risky behaviors. During this clinical latency phase HIV infected people
may not have clinical signs and symptoms of clinical disease. However they may be dealing
with emotional issues, such as depression, anxiety, and fear, associated with an HIV
diagnosis.
EARLY SYMPTOMATIC
The rate of viral replication remains relative constant, however the immune system’s
decreasing ability to control the virus results in increase viral load. As the immune system
weakens, the infected individual begins to develop symptoms of opportunistic infections
(O.I.s). Candida (thrush), herpes (shingles), lymphadenopathy (swollen lymph nodes), weight
loss, and fatigue are all – signs of disease progress from mild to moderate and may begin to
interfere with activities of daily living CD4 drop count, may be 200 to 500/ml, and viral load
increases. There may be an increase in the occurance of O.I.s (Opportunistic Infections).
ADVANCED DISEASE
Increase in morbidity. The immune mechanisms continue to fail, resulting in higher viral
loads and a decrease in CD4 count, usually below 200/ml. Clinical manifestations may
include loss of lean body mass and wasting syndrome. An increase in viral infections,
neurological impairment and cancers (lymphomas), eventually leading to death, may be
present.
Natural History of HIV Infection
Chronic
Phase
AIDS
CD4 + Cells
Viral Load
CD4 + Cells
Acute
Phase
Weeks
Years
HIV/AIDS AND TB
Viral Load
21
Diagnosis
Diagmosis in poor resource settings is being done with use of RTDs (Rapid Test Diagnosis
of HIV infection). Although the tests are very sensitive and accurate, there is a “window
period” of several weeks after initial infection with the virus and before the appearance of
detectable antibodies. HIV antibody is primarily used for diagnosis of HIV infection in an
individual, screening of blood and epidemiological surveillance.
Enzyme Linked ImmunoSorbent Assay (ELISA) has in the past been the first test used. If
the results are positive for HIV antibodies, then a Western Blot Assay was done as a
confirmatory test. Confirmatory tests were done because the ELISA, being a very sensitive
test, sometimes yields a false positive finding. Test results were not available immediately, and
in the United States at most of the anonymous testing sites, a person had to wait for two 2
weeks to obtain the results. Many people did not return for their tests results. To use ELISA
tests, WHO states that there are several essential requirements for tests to be performed
accurately:
➠ A constant supply of electricity and routine maintenance of equipment Appropriate
laboratory equipment must be available, including ELISA readers
➠ Skilled technicians
➠ Accurate storage and testing temperatures
➠ Recent advances in testing technology has provided easier and quicker methodologies,
HIV/AIDS AND TB
including an oral test, such as, kits that do not require reagents, equipment,
technicians, or special storage and temperatures. These tests can be done at anytime,
are as accurate as the ELISA test and yield results quickly.
22
Recent advances in testing technology have provided easier and quicker methodologies,
including an oral test, such as, kits that do not require reagents, equipment, technicians, or
special storage and temperatures. These tests can be done at anytime, are as accurate as
the ELISA test and yield results quickly.
Essential part of the diagnostic process is the clinical staging by identifying common
conditions, opportunistic infections, other system disruptions that present with clinical
characteristics defining a certain degree of immunosuppression.
In the west the CDC system is being used (that includes CD4 cell count as criteria), but
in poor-resource settings, the staging system used is that of WHO. In the next page there is
an analytical table with the WHO clinical classification of HIV disease.
23
HIV/AIDS AND TB
WHO Staging System: Laboratory Classification
Benefit of cotrimoxazole prophylaxis
in developing countries 2
This has been proven in several studies. Moreover, the offer of a package of VCT and cotrimoxazole to TB patients was first shown to improve TB treatment outcomes in a district setting
in Malawi. There is also an improvement of anthropometric indicators in HIV-positive adults
who start on cotrimoxazole prophylaxis. The main effect of cotrimoxazole prophylaxis in
developing countries is not on PCP and toxoplasmosis but on other bacterial infections and
on malaria. Even HIV-uninfected family members of HIV patients taking cotrimoxazole
prophylaxis have a decrease in morbidity and mortality.
HIV/AIDS AND TB
Target groups for cotrimoxazole prophylaxis
24
The criteria for starting cotrimoxazole prophylaxis in asymptomatic patients have changed
over time. UNAIDS/WHO guidelines propose CD4 < 500. Some countries used the threshold
of CD4 200 (Thailand) others 350 (Cambodia). It is worth emphasising that HIV-positive
patients with active TB need to be offered cotrimoxazole preventive therapy whatever their
CD4 count, even when there are no other signs of opportunistic infections.
Based on trial data from Zambia, WHO, UNAIDS and UNICEF have revised recommendations
2. Adapted from: Clinical HIV/AIDS care guidelines for resource poor settings, MSF, Brussels, 2006.
for cotrimoxazole prophylaxis in children. Cotrimoxazole is recommended for all HIV exposed
children (whether or not part of a PMTCT programme). PCP prophylaxis is also recommended
for all children identified as HIV-infected with clinical signs or symptoms suggestive of HIV,
regardless of the CD4 count. From the age of 18 months, when a definite serological
diagnosis of HIV infection is made, prophylaxis is also given to asymptomatic children with
CD4<15%.
Discontinuation of cotrimoxazole prophylaxis
Discontinuation of cotrimoxazole for the prevention of PCP and toxoplasmosis is safe in
patients responding to HAART, who have a sustained immune response with CD4>200-250
for more than 3-6 months. Secondary prophylaxis or maintenance therapy was considered a
lifelong necessity before the introduction of HAART.
HIV/AIDS AND TB
When to stop and when to start cotrimoxazole prophylaxis
in adults?
25
Adverse reactions
Adverse reactions are common. Fortunately, the incidence of adverse reactions against
cotrimoxazole seems to be lower in Africa and Asia than in Western countries. The main side
effects of cotrimoxazole are rash, bone marrow suppression and hepatitis. They are more likely
to occur soon after initiation of cotrimoxazole. Minor rashes and itching are common and can
usually be managed with careful observation while continuing cotrimoxazole. More severe
rashes, including Stevens-Johnson syndrome and clinical hepatitis are possible and must lead
to immediate cessation of cotrimoxazole. In fact, cotrimoxazole should be stopped in any
patient well before this stage and at least as soon as there is any mucosal involvement (mouth
or eye lesions).
Side effect management
In cases of non-life-threatening adverse reactions, treatment should be stopped for two
weeks, and the patient should then be re-challenged with cotrimoxazole in a gradually
increasing dose (desensitisation). After desensitisation under surveillance, up to 70% of
patients may again tolerate cotrimoxazole (Dapsone 50-100mg daily, atovaquone 1500
mg/daily with meals, aerolised pentamidine 300mg monthly).
Alternative regimens
If desensitization fails, another regimen needs to be given. Which regimen depends on the
CD4 count, the need to prevent toxoplasmosis and whether cotrimoxazole was being used as
primary or as secondary prophylaxis.
HIV/AIDS AND TB
Isoniazid (INH) prophylaxis
26
HIV infection is the strongest known risk factor for the progression of latent TB infection
to active TB. In countries with high TB prevalence, between 2.4% and 7.5% of HIV-infected
adults may develop active TB each year. In those with a positive PPD test, the rate rises to
between 3.4% and 10% per year with a lifetime risk of 50%.The mechanisms for this include
reactivation of latent infection and/or re-infection with Mycobacterium tuberculosis,
characterised by a rapid progression of primary infection to active disease.
Isoniasid 300 mg/day + pyridoxine 50mg/day peros should be given for 9-12 months to all
HIV-infected patients with positive PPD reactions (>5mm) or STOP TB / Quantiferon (interferon
– Á assays).
Other preventive measures
ANTIFUNGALS
In the industrialised world, most clinicians are reluctant to use azoles for primary
prophylaxis because of the potential promotion of azole-resistant candida species, and the
relatively low incidence of cryptococcal meningitis. In some regions with an unusually high
incidence of cryptococcal meningitis, histoplasmosis or coccidioidomycosis or primary prophylaxis with fluconazole or itraconazole might be considered, given the price reductions in
recent years, and the availability of generic fluconazole. In projects where a generic version is
not available, timely initiation of ART is more cost-effective in preventing OI than primary
prophylaxis with fluconazole. However, in projects where ART is not available or their use is
rationed, fluconazole prophylaxis is justified.
Discontinuation of antifungal prophylaxis: Several studies have shown that it is safe
to interrupt secondary prophylaxis for cryptococcal meningitis in patients who are on HAART
and who have a sustained CD4 > 100 for at least 6 months. No studies were conducted for
primary prophylaxis, but in analogy with other OI it is probably safe to discontinue primary
prophylaxis in patients who have a sustained CD4 > 100 for more than 3 months.
CMV PHOPHYICXIS
Oral ganciclovir 1000 mg x 3 with food, is approved for prophylaxis for patients with <50 cells
/mcL CD4 values. However, as these drugs couse nentropenia, clinicians widely avoid their use.
MARIUM PROPHYLAXIS
Patiens with <75-100 cells/mcL could benefit from clarithromycin 500 mg x 2 and
azithromycin 1200 my/week peros. When CD4 rise above the level of 100 cells/mcL and viral
load is suppressed in response to HAART, prophylaxis should be discontinued.
HIV-infected patients have a sub-optimal antibody response in comparison to healthy
controls, especially when CD4 counts are < 100. There are encouraging data that show that
this response improves again after the administration of HAART. It seems wise, therefore,
to defer vaccination until an increase in CD4 count has occurred. In general, it is best to
vaccinate as soon as possible, while the immune system is still good. In patients who have
very low CD4 counts, it is wise to defer immunisation until ART-induced immune
reconstitution has taken place. The only vaccines that are formally contra-indicated in
symptomatic HIV patients (or patients with CD4<200) is yellow fever vaccine and BCG.
HIV/AIDS AND TB
Vaccination
27
Childhood immunisation
Infant vaccinations should be given according to the regular vaccination scheme. All
asymptomatic children should receive vaccinations as prescribed by the national immunisation
schedule. Except for BCG, all regular vaccinations are recommended in HIV-positive
symptomatic children. It is recommended that HIV-infected children be given an extra dose of
measles vaccine at 6 months, followed by a second dose at 9 months.
23-valent pneumococcal vaccine
The 23-valent-pneumococcal vaccine is immunogenic in HIV-infected people. This vaccine,
while effective in the US, had a negative effect on the incidence of pneumococcal disease in
Kenya, and is therefore not recommended in Africa.
Hepatitis B vaccination
HIV-infected patients have a higher risk of hepatitis B because of common risk factors.
Patients who are HIV-positive are more likely to develop chronic hepatitis. In developing
countries, although some EPI programmes include vaccination against hepatitis B, it is not
routinely recommended in adult HIV patients, because very few countries have funds available
to purchase the vaccine.
Malaria
HIV/AIDS AND TB
A cross-sectional study from Malawi showed that HIV-positive pregnant women are more
likely to have a malaria parasitaemia than HIV (-) women. Preventing malaria during pregnancy
might reduce the MTCT. A monthly dose of sulphadoxine/pyrimethamine during the second
and third trimester of pregnancy seems to be safe and efficacious.
28
Opportunistic infections 3
Common Pulmonary Conditions
in PLWHA (People Living With HIV/AIDS)
Tuberculosis
Clinical presentation:
The presentation of PTB depends on the degree of immunosuppression. At a level of
immunity that is still relatively good, it will present as typical cavitary TB or upper lobe
consolidation (post-primary pattern). Pulmonary TB is a WHO stage 3 condition. With lower
CD4 levels, atypical presentations are more likely: extra-pulmonary TB (pleuritis, pericarditis
and meningitis) and disseminated TB, diffuse pulmonary or miliary infiltrates with usually
negative PPD skin tests. Extra-pulmonary TB and disseminated TB is a WHO stage 4 condition.
Diagnosis of extra-pulmonary TB is more difficult.
TB disease in persons with HIV-1 infection can develop immediately after exposure (i.e.
primary disease) or as a result of progression after establishment of latent TB infection (i.e.
reactivation disease). In up to 35% of HIV co-infected, patients, signs of primary infection
(recent infection) are evident: lower lobe infiltrate, pleural effusion, intra-thoracic adenopathy.
Patients with suspected intra-thoracic tuberculosis frequently have palpable extra-thoracic
lymph nodes (cervical and axillary). The most important symptoms in diagnosis of pulmonary
tuberculosis are cough more than two weeks, weight loss, haemoptysis, chest pain,
breathlessness, fever with night sweats and loss of appetite. Weight loss and fever are more
common in HIV-positive pulmonary TB patients, than in HIV-negative patients. Conversely
productive cough and haemoptysis are less common in HIV-positive patients. This difference
is probably because there are less cavitations, inflammation and endobronchial irritation in
HIV positive patients.
3. Adapted from: Clinical HIV/AIDS care guidelines for resource poor settings, MSF, Brussels, 2006.
HIV/AIDS AND TB
Epidemiology:
TB is one of the most frequent respiratory problems in developing countries. WHO
estimates that TB is the cause of death for 11% of all AIDS patients. In Africa about 1/3 of
deaths in HIV-positive patients are due to disseminated TB and in only 50% of these patients
the diagnosis is made before death. By the end of 2000, about 11.5 million HIV-infected
people worldwide were co-infected with M. tuberculosis.
29
CHARACTERISTICS OF PTB (PULMONARY TB) IN DIFFERENT STAGES OF HIV DISEASE
Microbiological diagnosis:
Sputum examination is the best initial diagnostic test. AFB staining of expectorated
sputum is positive in around 30%-60% of patients with AIDS- related pulmonary TB. When
possible, fluorescence microscopy with auramine staining could be done as its sensitivity is
superior to Ziehl-Neelsen, and it is more cost-effective. Early morning samples (standard three
samples) are best because AFBs concentrate in the respiratory secretions overnight. To reduce
delay and lost to follow-up due to sample collection, WHO recommends 3 sputum samples
over 24 hours: 1 on the spot, second from next early morning brought by patient and the final
sample provided on the spot on that second day. The “on the spot” samples are provided
under supervision. This method seems to be almost as sensitive as the 3 morning samples.
Culture is often not available in resource poor settings. It also takes 6-8 weeks to be
interpretable which limits the usefulness of culture in clinical decision-making. MGIT
(Mycobacteria Growth Incubator Tube) is a more rapid culture technique that allows also for
drug sensitivity testing, but has a relatively high contamination rate and high cost.
Countries affected by both HIV and TB have experienced a disproportionate increase in
smear-negative disease defined as patients with clinical and radiological evidence of
pulmonary TB but repeatedly negative sputum investigations. Smear negative TB has a poorer
prognosis in countries with a high prevalence of HIV infection.
For patients who cannot produce sputum, simple chest physiotherapy may sometimes
help. Otherwise sputum induction by using ultrasonic nebulizers with hypertonic saline can
be used. It enhances diagnostic sensitivity in resource-poor areas, and it is a safe and more
simpler alternative to fiberoptic bronchoscopy with bronchoalveolar lavage.
HIV/AIDS AND TB
Chest X-ray:
Atypical presentations are frequent. However, in HIV patients, a chest X-ray should be
done early in the diagnostic process in order to reduce the delay in the diagnosis of smearnegative PTB. 44-75% of patients with smear-negative TB have an abnormal chest X-ray. It
may also help in making the differential diagnosis from other respiratory conditions.
30
Antibiotic trial:
Most diagnostic algorithms of cough, intending to diagnose or exclude PTB start with
an antibiotic trial, followed by a second trial if no response. The performance of such
algorithms depends on the background prevalence of HIV and other HIV-related conditions
that would not respond to antibiotics (PPV, Positive Predictive Value, PTP Pre-Test Probability).
Antibiotic trials increase the specificity of the diagnosis of smear-negative PTB, but it also
induces an important delay in the start of appropriate anti-tuberculous treatment and loss of
patients who do not return for follow-up assessment.
In patients who have clear symptoms of TB (weight loss, chronic cough, night sweats)
we should use only 1 trial of broad-spectrum antibiotics while waiting for the result of the
sputum. The choice of antibiotics should be guided by the idea to treat the most likely
respiratory pathogens, other than TB. The first choice is amoxycillin which has a slightly
broader spectrum than penicillin because it also covers +/- 50% of H.influenzae strains.
Cotrimoxazole has a broader spectrum, but in patients on cotrimoxazole prophylaxis, the use
of cotrimoxazole to treat bacterial respiratory infections is not indicated. However it remains
a useful antibiotic for patients not yet using that prophylaxis.
Erythromycine would also cover against atypical pneumonia (Mycoplasma or Chlamydia);
however, it is not a first choice in treatment of infection by S.pneumoniae, H.influenzae and
Moraxella cattharalis because there is a high rate of resistance of all those bacteria to
macrolides.
If available amoxy-clavulanic acid or second-generation cephalosporines (cefuroxime,
cefaclor) are a very good alternative because they have very good respiratory coverage and
they are active against S.pneumoniae, Moraxella cattharalis and H.influenzae.
Fluoroquinolones, particularly later-generation agents (levofloxacin, gatifloxacin and
moxifloxacin) shouldn’t be used for an empiric antibiotic trial as they have bactericidal activity
against M.tuberculosis, cause resistance when used in monotherapy, and delay the diagnose
of TB.
Lymph node needle aspiration:
A study carried out in Harare showed the value of fine needle aspiration of extra-thoracic
lymph nodes to confirm the diagnosis of smear-negative pulmonary, pleural or pericardial TB.
In a group of HIV-positive patients with suspected smear-negative PTB, who did not respond
to penicillin and who had no signs of cutaneous or palatal Kaposi’s sarcoma, ZN staining of
fine needle aspirate (18G-19G) of supraclavicular, cervical or axillary lymph nodes, gave the
diagnosis of TB in up to 87% of cases that were later confirmed to have pulmonary, pericardial
or pleural TB!
Differential diagnosis of sputum negative TB:
Differential diagnosis of smear negative PTB can be difficult and include diseases such as
PCP, pulmonary Kaposi’s sarcoma and Nocardiosis. In patients with normal chest X-rays who
present with cough and fever, Gram negative bacteraemias are a possible diagnosis.
HIV/AIDS AND TB
Tuberculin test, PPD:
Reaction to a tuberculin skin test is unreliable in patients with a deficit in cellular immunity.
Also BCG vaccination complicates the interpretation of a positive PPD. Therefore the use of
PPD skin test will not improve the accuracy of the diagnosis of TB in HIV patients. TB-Spot and
Quantiferon interferon-g assays are not available in resource poor setting, although in use
in other settings.
31
HIV/AIDS AND TB
Treatment:
HIV-positive patients respond well to treatment with anti-tuberculous drugs. The highest
priority is the treatment of smear-positive pulmonary TB. Short-course therapy with an initial
intensive phase of 4 drugs (2 months of INH, RIF, PZA and EMB) followed by a 4-month
continuation phase of INH and RIF is superior to the 8-month regimens that use RIF only in
the first 2 months. Therefore this is the preferred regimen, although it means prolonged
observed therapy to avoid rifampicin resistance and difficulties to combine TB treatment with
HAART.
32
HIV/AIDS AND TB
National protocols are to be followed. However, it can be useful to meet the national
authorities and discuss some specific practicalities with them, such as longer duration of
treatment in patients with miliary TB or TB meningitis, the acceptance of higher rates of
smear-negative TB in HIV patients, or the preference to use the 6 months rifampicin
throughout regimen in HIV patients.
Thiacetazone should never be used for people who are known or suspected to be HIVpositive because of the severe hypersensitivity reactions observed (Stevens-Johnson
syndrome). Use of streptomycine is discouraged because of the risk of transmission of HIV
through needle stick injuries. Moreover, these IM injections are painful in wasted HIV-infected
TB patients.
Ethambutol has replaced streptomycin in most national TB program regimens. The
duration of TB therapy for HIV patients remains controversial. The standard 6-month regimen
results in prompt sterilisation of sputum and low rates of treatment failure, similar to those
obtained in HIV-negative persons. Despite this some authorities still recommend longer
treatment in HIV-positive patients. While awaiting for more studies on this, 6 months of
therapy is probably adequate for the majority of cases and 9 months therapy is recommended
(as in HIV-negative) for patients with a delayed clinical or bacteriological response to therapy
(symptomatic or positive culture results at of after 2 months of therapy), respectively.
Intermittent dosing (twice or thrice weekly) facilitates DOT, especially in the 6-month
RIF containing regimens. However, increased rates of rifamycin resistance have been described
in patients who took once or twice weekly INH + RIF. Therefore, especially in patients with
advanced immune deficiency we recommend daily DOT in the first two months, followed
by at least thrice-weekly DOT in the continuation phase.
Resistance to rifampicin M.tuberculosis, mono resistant to rifampicin is more often
described in HIV patients and in patients with a history of TB. It could be due to poor
33
compliance or decreased absorption of rifampicin in HIV patients, however this is controversial.
For those patients, a minimum of 12-18 months of treatment with INH, EMB and a
fluoroquinolone (e.g., levofloxacine) with PZA administered during the first 2 months is
recommended.
Multidrug-resistant TB:
MDR TB is defined as resistant to INH and rifampicin with or without resistance to other
drugs. Cases of MDR TB are highest in areas with the fastest growing HIV epidemic,
particularly the former Soviet republics, China and South Africa. It seems that the spread of
MDR TB is being fuelled by a high prevalence of TB in HIV-positive patients, and also by poor
adherence to TB medication. HIV care settings are likely to see nosocomial outbreaks of MDR
TB. Therefore infection control measures need to receive attention.WHO has published
guidelines for the prevention of TB transmission in care settings, stressing the need to identify
and separate coughing patients from others in waiting rooms.
The emergence of MDR TB as a problem in MSF 4 projects highlights the need for
development of capacity to do drug susceptibility testing and culture. The current readily
available test for MDR TB is manual culture and sensitivity testing using solid LowensteinJensen medium, at a cost of 1.5 USD but the results take 6-9 weeks.
Use of steroids as adjuvant in TB treatment is indicated for CNS tuberculosis with severe
symptoms and for pericarditis (1mg/kg/day during 1 month, slowly tapered over the next 4-6
weeks. A study examining the effect of prednisolone on mortality in HIV-infected patients with
pleural TB failed to show any survival benefit, and it even caused an increased risk for KS.
HIV/AIDS AND TB
Paradoxical reaction:
After initial clinical improvement on TB treatment, paradoxical worsening of disease
develops in up to 36% of patients on HAART, with fever, worsening chest infiltrates on
radiography and peripheral and mediastinal lymphadenopathy.
In contrast, only 7% of patients who received antituberculosis therapy but no ARV therapy
had paradoxical reaction. In patients with clinical findings that are compatible with the
presence of a paradoxical reaction, other diagnosis must be ruled out. Paradoxical reactions
are self-limited and generally last 10 to 40 days. However, some reactions are severe and may
require short treatment with steroids.
34
Response to treatment/ Relapses:
HIV-positive TB patients have a much higher case-fatality rate during and after anti-TB
treatment compared with HIV-negative patients. In sub-Saharan Africa, up to 30% of HIVpositive smear-positive PTB patients die before the end of treatment. HIV-positive smearnegative PTB patients have a worse prognosis than those who have HIV-positive smear4. MSF: Medecins Sans Frontieres (MSF).
positive PTB. Excess death in HIV/TB patients are due to TB and to HIV related problems as
septicaemia, diarrhoea, pneumonia, anaemia, KS and cryptococcal meningitis.
Recurrence rate is higher in HIV-positive than in HIV-negative TB patients. Some studies
suggest to extend the duration of treatment to 12 months or to give post treatment
prophylaxis (for example INH) but further studies are needed before making recommendations
on secondary prophylaxis.
Bacterial pneumonia
Bacterial respiratory infections are more frequent and severe in HIV patients, and the
frequency is related to CD4 count. The most common causes are Streptococcus
pneumoniae, Haemophilus influenzae and Staphylococcus Aureus. Other frequent bacterial
HIV/AIDS AND TB
Integration of TB/HIV programs:
50% of the HIV patients will develop active tuberculosis. Up to 10% of HIV-infected
patients have active TB at first presentation. Every effort should be done to screen HIVinfected patients in developing countries for TB. It is important that they are seen by a medical
doctor or adequately
trained clinical officers
or nurse and that in
case of symptoms a
sputum examination, a
chest X-ray and/or an
abdominal ultrasound is
done to diagnose and
treat TB. Asymptomatic
patients can be started
on INH prophylaxis
TB/HIV co-infected
patients who develop
active TB benefit from
cotrimoxazole
prophylaxis and from
timely initiation of
HAART. Therefore, all
TB patients need to be screened for HIV. Once patients start on HAART, paradoxical reactions
need to be managed correctly. Again an operational link between TB and HIV services is
essential in care for HIV patients.The best results are obtained with fully integrated HIV and
TB clinics.
35
pathogens include Moraxella cattharalis, Klebsiella pneumoniae, P.aeruginosa and Mycoplasma
pneumoniae.
Pneumonia in HIV-positive patients is more frequently associated with bloodstream
infections and they represent a common cause of early death. Risk factors for bacterial
pneumonia are: intravenous drug use, smoking illicit drugs (cocaine, crack, and marijuana),
smoking cigarettes, alcoholism, cirrhosis, asthma, sickle cell disease, low albumin and history
of previous pneumonia. In the new interim guidelines for WHO staging, recurrent bacterial
pneumonia is a stage 4 event.
SYMPTOMATOLOGY
The presentation is similar to that in HIV-negative patients. Most patients have an abrupt
onset of fever, chills, cough with sputum production, dyspnoea, and pleuritic chest pain. An
acute respiratory illness in a patient known to be HIV-positive, accompanied by high fever and
chills, should be treated as an emergency.
CHEST X-RAY
Segmental or lobar consolidations are frequent although diffuse retilunodular infiltrates
and patchy lobar infiltrates may also be seen. Infiltrates that are localised to one lobe,
especially when an air-bronchogram is present, are suggestive of bacterial pneumonia, most
likely S.pneumoniae. More diffuse infiltrates are more likely to be due to H.influenzae. Bilateral
patchy consolidations in a critically ill patient suggest staphylococcal pneumonia. Upper lobe
consolidation with cavitation has been observed in pulmonary nocardiosis, and can mimic
tuberculosis. In nocardiosis there is often evidence of multiple abscesses (brain, lung, skin, etc).
A Gram stain will show Gram-positive thin branching (mycelium-like) filaments.
HIV/AIDS AND TB
LABORATORY FINDINGS
36
The patient usually has a high white blood cell count. Gram stain of sputum and culture
yields the diagnosis in 75% of cases. Gram positive diplococci are suggestive of S.pneumoniae.
Gram negative bacilli are compatible with H.influenzae. Nocardia stains weakly acid-fast on
Ziehl-Neelsen. They are morphologically different however from tubercle bacilli because of
their long branching fine mycelium-like threads. They stain well on Gram stain (see laboratory
section at the end of the chapter). Patients with staphylococcal pneumonia often have other
signs of staphylococcal infection: pyomyositis, abscess. A Gram stain of aspirated pus (Grampositive cocci in clusters) can help in the diagnosis. During an acute pneumonia the CD4 count
is often significantly depressed, and the CD4 count should be repeated after the acute event
in order to assess the immune status of the patient correctly.
TREATMENT
Penicillin has a narrow spectrum and would only cover S.pneumoniae and the anaerobes
of the oral cavity involved in aspiration pneumonia. In some countries, more than 30% of
streptococci are resistant to penicillin. In that case, do not use penicillin for empirical therapy
in lobar pneumonia. The first choice if the condition of the patient is not severe is amoxycillin
or cotrimoxazole. In patients on cotrimoxazole prophylaxis, the use of cotrimoxazole to treat
bacterial respiratory infections is not indicated. However it remains a useful antibiotic for
patients not yet using that prophylaxis.
An alternative is amoxy-clavulanic acid or second-generation cephalosporines (cefuroxime,
cefaclor). Seriously ill patients with a respiratory infection should receive a combination with
chloramphenicol or ceftriaxone (if available) to cover for Gram-negative infections. Treatment
for severe life-threatening pneumonia could be: ceftriaxone + amikacin (Gram-negatives +
Gram-positives, also staphylococcus), or chloramphenicol + cloxacillin (Gram-negatives +
Gram-positives, including staphylococcus, atypical bacteria -chlamydia, mycoplasma).
When a causative agent is identified, treatment is directed against this pathogen.
The antibiotic of choice for staphylococcal infections is (flu)cloxacillin 1-2 g 4 x daily IV
or 500 mg 4 x daily PO. In addition, chloramphenicol, doxycycline and cotrimoxazole are
moderately effective against staphylococci. The recommended treatment for Nocardia is
cotrimoxazole 10/50 mg/kg 2 x daily. This usually corresponds with 2-3 DS tablets 2 x daily.
The duration of the treatment varies from 6 weeks (for localised disease) to 6 months (for
disseminated disease). An alternative treatment for nocardiosis is minocycline 100 mg 2 x daily
combined with amikacin 15-25 mg/kg daily IV, once a day, or ceftriaxone 2 g daily combined
with amikacin. The use of aminoglycosides should be limited to 14 days to avoid adverse
effects.
Pneumonia due to Pneumocystis jiroveci (PCP)
Pneumocystis jiroveci is a ubiquitous organism classified as a fungus but that shares
biologic characteristics with protozoa and causes PCP (Pneumocystis Pneumonia as known
formerly). Initial infection with P. jiroveci occurs in early childhood. PCP is a result either of
reactivation of latent infection or new exposure to the organism. Re-infection may be an
important cause of PCP in the immunocompromised. Human-to-human transmission is
possible, but only responsible for a minority of cases.
The incidence of PCP varies worldwide, ranging from 64% in the US to <5% in reports from
some studies in Africa. PCP occurs frequently in Asia, Central and South-America. PCP is thought
to be rare in Africa and Southeast Asia. However, this may be partly due to under-diagnosis due
to lack of diagnostic facilities or to early death from tuberculosis and bacterial infections before
a sufficient drop in CD4 is reached. Cases of PCP are now also increasing in Africa but whether
this increase results from actual change in PCP incidence or from improved detection techniques
is unclear. In contrast to adults, HIV-infected children in Africa have high rates of PCP. The
probability of developing PCP rises dramatically as the CD4 count drops below 200. With the
HIV/AIDS AND TB
EPIDEMIOLOGY
37
occurrence of HAART and use of prophylaxis, the incidence of PCP has dramatically decreased in
the Western world. PCP is an AIDS defining event (WHO stage 4 condition).
CLINICAL FINDINGS
PCP is characterised by a sub-acute onset of symptoms gradually getting worse in a period
of days to weeks. Patients complain of dyspnoea, fever, and non-productive cough gradually
getting worse. The duration of illness until diagnosis is typically 1 to 2 weeks, although
considerable variation exists. Dyspnoea on exertion is always present.
PHYSICAL EXAMINATION
Physical findings include tachypnoea, tachycardia, and cyanosis. Auscultation of the chest
is generally unremarkable. Some dry crackles can sometimes be found.
CHEST X- RAY
The classic findings on chest X-ray consist of bilateral interstitial shadowing, extending
from the hilar area (ground glass appearance without air-bronchogram, butterfly pattern).
Sometimes there are nodules or cavities, but the X-ray can be (at first presentation)
misleadingly normal (25%). More than 80% of cases of pneumothorax in HIV-infected patients
are due to PCP. Therefore all patients with pneumothorax should be given empirical PCP
treatment. Large plueral effusious are not common in PCP. Their presence suggests an
alternate diagnosis (TB, pleural Kaposi Sarcoma).
BLOOD EXAMINATION
Arterial blood gases demonstrate hypoxaemia, increased alveolar-arterial oxygen gradient
and respiratory alkalosis. If oxygen saturation measurement is possible, it will always show
a decrease in O2 saturation during physical effort in patients with PCP.
Measurement of serum lactate dehydrogenase (LDH) can be helpful. A normal LDH makes
PCP unlikely. A strongly elevated LDH (>2 times the normal value) suggests that PCP is likely.
Rising LDH levels despite treatment heralds a poor prognosis or may be due to another
infection. The mortality rate is also influenced by the CD4 count.
HIV/AIDS AND TB
LABORATORY DIAGNOSIS
38
Whenever practicable, attempts should be made to identify the organism. P. Jiroveci
oocysts are rarely present in sputum. They can be demonstrated in specially prepared induced
sputum smears (sens. 60%) or in bronchoalveolar lavage (BAL: sens. 90%). In patients who
are not taking PCP prophylaxis, the sensitivity of induced sputum may be as high as 90%.
Spontaneously expectorated sputum has low sensitivity and should not be submitted to the
laboratory to diagnose PCP.
DIFFERENTIAL DIAGNOSIS
The most difficult differential diagnosis is with PTB, and many patients may end up with
treatment for both.
DRUG TREATMENT
PROPHYLAXIS
Every HIV-positive patient who has been successfully treated for pneumonia due to
Pneumocystis jiroveci should receive continuous prophylaxis. Various estimates place the 3month relapse rate among patients not receiving prophylaxis following a course of treatment
for PCP at 10%-40%; about one in five of such episodes is fatal. First choice is cotrimoxazole,
followed by dapsone and proguanil-atovaquone, pentadimine.
HIV/AIDS AND TB
Cotrimoxazole IV or PO: cotrimoxazole 20/100 mg/kg daily divided over 4 doses for 1421 days. For mild to moderate disease, oral medication can be used throughout the treatment;
for severe disease, the first 7-10 days treatment is normally administered intravenously, if
possible. Any patient who is hypoxic (pO2<70 mmHg, Sat<90%) should receive prednisone.
Prednisone administered within 72 hours after diagnosis can improve the course of disease
(40 mg for 5 days, then tail-off dosing).
The first few days of antimicrobial treatment are critical since the decomposition of many
dead parasites exacerbates the pre-existing inflammatory process and aggravates hypoxia.
However, the risk of death at this stage can be substantially reduced, especially in patients
whose arterial oxygen tension is less than 70 mmHg, if a corticosteroid is administered.
Corticosteroid treatment should be commenced at the same time as anti-PCP treatment. There
is no benefit from corticosteroid usage in episodes of mild PCP, when there is no hypoxaemia
in rest.
Signs of improvement may not be evident for 4-8 days, and treatment with cotrimoxazole
should be maintained for 3 weeks. In case there is no response after 7-10 days always suspect
a second infection. Patients may have both TB and PCP; and TB seems to account for the most
severe features of disease. CMV, Cryptococcus, Aspergillus, herpes simplex, Candida, M. avium
intracellulare, and bacteria have all been identified in or grown from lung tissues from patients
with PCP. In resource-limited settings, with a high prevalence of TB and where bronchoscopic
evaluation is not feasible, empiric therapy directed against TB and PCP may be reasonable for
patients who are hospitalized with PCP and who are unresponsive to 7-10 days of appropriate
anti-PCP treatment.
When no improvement is evident after 7-10 days, clinicians often resort to switching to
one of the other regimens. The severe toxicity of pentamidine (renal failure, hypotension,
hypoglycaemia) compared to the other regimens has limited its use and it is now used only as
a last resort. If a switch to pentamidine is being considered, there should be an overlap of
2-3 days to allow pentamidine to accumulate in the body (3-4 mg/kg/d for 14-21 days).
39
RESISTANCE TO SULPHONAMIDES
Sulfamethoxazole and dapsone inhibit the enzyme dihydropteroate synthase (DHPS). This
enzyme is doing part of the folate metabolism. Many researchers have reported mutations of
pneumocystis in response to the use of sulphonamides in anti-pneumocystis regimens.
Whether these mutations increase the likelihood of treatment failure is still unclear.
Toxoplasma pneumonitis
This is rare in HIV patients. Sometimes it is difficult to distinguish from PCP pneumonia.
Toxoplasma pneumonitis should be considered in patients who present with fever, cough, and
dyspnoea and where the induced sputum fails to demonstrate PCP.
DIAGNOSIS
Chest X-ray may show diffuse interstitial pattern or reticulonodular infiltrates. The
diagnosis of pulmonary toxoplasmosis can be confirmed by Giemsa staining of BAL.
TREATMENT
A combination of sulfadiazine and pyrimethamine is the regimen of choice. However,
studies with high dose cotrimoxazole for the treatment of Toxoplasma encephalitis have
shown similar efficacy. Cotrimoxazole is a more readily available drug in developing countries.
Pyrimethamine 200 mg po once, then 75 mg/d + sulfadiazine 1.5 mg/6 hour po +
leucovorin (follinic acid) 5-20 mg x 3 weekly, continued for a week after stopping
pyrinethamine (stop the latter one week after “cure”).
Mycobacterium Avium complex (MAC)
MAC rarely gives pulmonary symptoms. It can cause respiratory symptoms in patients
on HAART who develop IRIS.
Clarithromycin 500 mg/12 h + ethambutol 15 mg/kg/d + rifabutin 300 mg/d po.
HIV/AIDS AND TB
Pulmonary Kaposi Sarcoma (KS)
40
Pulmonary KS is rapidly fatal when left untreated. Patients present with dyspnoea without
fever, sometimes with haemoptysis. Visceral involvement is most of the time concomitant with
skin lesions. Generally, lesions are recognised clinically and the diagnosis of KS can be
confirmed by biopsy. A chest X-ray may show reticulo-nodular infiltrates, enlargement of
the mediastinal shadow and sometimes a pleural effusion. Typical red purple lesions can be
seen on bronchoscopy. A patient with pulmonary KS needs a combination of HAART and
chemotherapy.
Clinical management of respiratory problems in HIV patients
Diagnosis of pulmonary disease in HIV-positive patients often requires a multi-step
approach, starting with a thorough history and physical examination and leading up to chest
X-ray and sputum examination. To use resources rationally, it is important to identify those
patients who will benefit from additional tests. E.g. in a smear-positive pulmonary TB patient,
the diagnosis of PTB is confirmed by the positive smear and treatment effect can be evaluated
by examining the smears at certain intervals. A chest X-ray provides no additional benefit.
It is not rare to find more than one pathogen involved. Therefore, in a patient who does
not respond to therapy as expected, do not hesitate to review the history and the physical
examination, to repeat the algorithm and to add a second or even a third treatment if
necessary. Many patients, by the time they present with cough to a health worker, have
already bought over-the-counter antibiotics or have been treated elsewhere. It is important
to take this into account in order not to waste valuable time.
Mycobacterial infections
Africa and Asia have a high TB/HIV co-infection rate (40-50%). Disseminated tuberculosis
has been described in 50% to 72% of patient with AIDS and tuberculosis. Abdominal TB
was the commonest cause of abdominal pain in non white persons with advanced HIV
infection (CD4<200) in South Africa reflecting the high prevalence of TB in these communities.
Abdominal involvement has been found to be universal in HIV-infected persons with
disseminated TB infection.
One autopsy study on 70 HIV patients who died in a department of pulmonary medicine
in a hospital in Ivory Coast showed that pulmonary TB was associated with abdominal TB in
93,5% of cases.
The clinical presentation of TB depends on the degree of immune-suppression. Patients
with moderate immune-suppression (CD4 350-500) demonstrate features similar to non HIV
patients. A big psoas abscess or tuberculous peritonitis can present with abdominal pain in
early stages of HIV disease. However, advanced stage AIDS patients show a high incidence
(60-70%) of disseminated TB.
Symptoms and signs of abdominal TB are non specific. The most common presenting
HIV/AIDS AND TB
Mycobacterium tuberculosis
41
symptoms in abdominal TB in HIV are prolonged high fever and chills (usually >39 ÆC), night
sweats, anorexia, progressive weight loss, abdominal pain, diarrhoea (less common). The most
common physical findings are abdominal tenderness, abdominal swelling and/or mass, and
peripheral lymphadenopathy (>1.5cm in diameter). Unlike in non HIV patients ascites and
jaundice are rarely seen. It can also present as acute abdomen.
The diagnosis of abdominal TB is often missed during life, as shown in an autopsy study
in Ivory Coast. Non-invasive tests often fail to yield a diagnosis and undiagnosed disease
results in significant morbidity and mortality. Common, but non specific, laboratory findings
are anaemia, elevated serum alkaline phosphatase concentration and elevated percentage of
mononuclear cells in peritoneal fluid. Hyponatremia (< 135 mmol/l) was found in 60% of
patients with a diagnosis of generalized TB.
Ultrasound of the abdomen often shows multiple intra-abdominal lymphnodes
(LNs) >1.5 cm or one mass of adherent lymph nodes with central necrosis or multiple
hypoechogenic nodules or abscesses in the spleen and in the liver. The diagnostic yield of
an abdominal ultrasound is so high in abdominal pain in HIV, that all physicians taking care of
HIV patients should develop or have access to skills in ultrasound.
Ascites and omental thickening are rarely found in HIV patients with abdominal TB. Results
from a Ugandese study suggest that in a population with high HIV and TB prevalence, HIVinfected patients with abdominal pain and systemic symptoms suggestive of TB, who have
enlarged peri-aortic or mesenteric lymph nodes should be started on TB medication.
Chest X-rays show evidence of pleuro-pulmonary disease in the majority of patients
(pleural effusion, parenchymal infiltrates, miliary pattern, peri-hilar lymphadenopathies).
A normal chest X-ray does not exclude the diagnosis of abdominal TB, however.
Mycobacteriological diagnosis
HIV/AIDS AND TB
Delayed diagnosis of TB may result in early mortality in AIDS patients. As many patients
with abdominal TB have disseminated TB (93%), an effort should be made to isolate AFB from
one or other site. If AFB on stool culture are identified as Mycobacterium tuberculosis, they
are always considered pathogenic. Blood culture and urine culture are positive in 50-70% of
patients with disseminated disease and a CD4<100.
42
Differential diagnosis
Abdominal tuberculosis has to be differentiated from Mycobacterium avium complex, but
this is a rare pathology in developing countries. The presenting symptoms are similar to TB
infection. One distinguishing feature of TB is that peripheral lymphadenopathy is more
frequently present in TB than in MAC. Lymphoma and Kaposi’s sarcoma can present with
abdominal pain and enlarged lymph nodes.Some of the deep mycoses (cryptococcosis,
histoplasmosis) can present with bulky abdominal lymph nodes causing pain. In patients
presenting with splenic abscesses, visceral leishmaniasis has to be excluded. This disease is a
frequent cause of fever in HIV patients living in Mediterranean countries, the horn of Africa
and India. Nocardiosis can present with multiple abscesses.
Mycobacerium avium complex
The most common non-MTB organisms responsible for pulmonary and disseminated
disease are part of MAC, which includes both M. avium and M. intracellulare. More than 90%
of MAC isolated from AIDS patients is M. avium. It occurs mainly in PLHA with CD4 < 100.
MAC has been isolated from a variety of sources around the world, including soil, natural
water, municipal water system, food, house dust, wild & domestic animal. Disseminated
infection results from recent infection (ingestion or inhalation) rather than reactivation of a
previous infection. MAC infection has not clearly emerged as a problem in the developing
world where Mycobacterium tuberculosis appears to be the predominant pathogen. It is
speculated that acquired immunity against mycobacteria through previous infection with
tuberculosis or through vaccination with BCG provides protection against MAC. Another
possible explanation is the difficulty to diagnose MAC in resource-poor settings, and the short
life expectancy of patients with HIV infection.
Typically MAC presents with prolonged fever, gradual wasting, severe anaemia and
neutropenia. The CD4 count is usually less than 30. MAC infection frequently involves
gastrointestinal tract, liver, abdominal lymph nodes and spleen. More than 70% of patients
have gastrointestinal or hepatobiliary symptoms: diarrhoea, abdominal pain, hepatomegaly,
and raised alkaline phosphatase (more than 2 x ULN) and gamma GT levels (more than 3 x
ULN). When compared with disseminated TB, MAC patients have absence of peripheral
lymphadenopathy, and more severe anaemia and neutropenia.
In patients on HAART, a MAC lymphadenitis can develop and is considered an immune
reconstitution inflammatory syndrome (IRIS). The onset is a few weeks to months after the
start of HAART. MAC IRIS is a localized lymphadenitis; organisms are confined to the infected
LN and surrounding soft tissues. Lymph node inflammation can occur in the neck, in the
axillary region, but also mediastinal and abdominal (mesenteric and retroperitoneal) lymph
nodes. In case of abdominal lymphadenitis the patient presents with a picture of severe
abdominal pain, high fever and leucocytosis.
HIV/AIDS AND TB
Immune Reconstitution Syndrome (IRIS)
43
Diagnosis
The diagnosis of disease caused by MAC requires isolation of the organism and compatible
clinical and pathologic features. Identification of MAC in a single sputum culture does not
mean MAC disease, as colonization can occur in healthy and immunocompromised patients.
Blood cultures are highly sensitive for detection of disseminated MAC in AIDS patients (a
single blood culture has a 90 to 95% sensitivity). However, in rare cases, bone marrow and
liver biopsy may be useful. Stool cultures are often positive, but not helpful to diagnose MAC
disease, as they are also present in 50% of healthy patients.
In a resource-poor setting without possibility to do mycobacterial cultures the diagnosis
is often made by exclusion, in a patient with symptoms compatible with disseminated TB or
MAC, who fails to respond to TB medicines. Absence of peripheral lympadenopathy and
severe anaemia and neutropenia favour the diagnosis of MAC. In AIDS patients with a focal
lymphadenitis syndrome (IRIS), blood cultures are often negative and a LN biopsy is required
for diagnosis. The diseases has to be diferentiated form other atypical mycobacteria, fungal
infections, lympomas or visceral leishmaniasis.
Prognosis and treatment
In a resource-poor setting the diagnosis and treatment of MAC is difficult to realize. MAC
infection occurs in patients with advanced disease, and the median survival without treatment
after the initial diagnosis is around 3 months. However, with HAART the life expectancy has
improved, and in case of sustained immune restoration (more than 6 months CD4 > 100)
the secondary prophylaxis for MAC can be interrupted.
HIV/AIDS AND TB
Bacterial infections
44
In HIV patients the bacterial causes of GI disease are the same as in the general population:
S. Typhi and non S. Typhi, Shigella, Campylobacter, and Clostridium difficile. However, the
incidence of severe disease is higher than in the general population.
Bacterial infections have often a chronic relapsing course and are accompanied with
bacteraemia. In the same way, common bacterial infections that cause abdominal pain (PID,
appendicitis, liver abscess, renal abscess, cholecystitis) can also be found in HIV patients.
Salmonella can lead to peritonitis due to perforation. Secondary bacterial peritonitis may
happen in patients with bowel perforation due to CMV, Kaposi’s sarcoma, tuberculosis and
lymphoma.
Liver and spleen abscesses have multiple infectious causes: staphylococcal, salmonella,
nocardia, mycobacterial, bacillary angiomatosis and visceral leishmaniasis. Bacillary
angiomatosis (Bartonella henselae) causes hemangioproliferative lesions that have to be
distinguished from KS because they respond to erythromycin or doxycycline Disseminated
nocardiosis is mostly localized in skin, brain, lungs and musculoskeletal system. Less-common
sites include spleen and liver.
Most of them present with acute diarrhoea, high fever, and diffuse abdominal pain.
Patients look toxic. In the case of acute bloody diarrhoea and tenesmus, Campylobacter and
Shigella are suspected. When there is a history of previous antibiotic intake and hospitalization Clostridium difficile is possible.
In the case of nocardiosis there is often evidence of multiple abscesses. With bartonellosis,
skin lesions that have to be differentiated from KS, are often present. Diagnosis is based on
blood and stool culture. Treatment depends on the underlying cause. Any peritonitis due
to bowel perforation (free air under diaphragm) should receive surgical attention.
Fungal infections
Although the incidence of oro-esophageal candidiasis in HIV-infection is high,
disseminated candidiasis, involving the liver, spleen and kidney is rare in HIV-infected persons.
If it is diagnosed, severe neutropenia due to medications (chemotherapy) or an indwelling
IV catheter is usually present.
Candida oesophagitis represents 50-70% of dysphagia in AIDS patients, and may cause
in severe cases epigastric pain. In case of odynophagia, the cause is more likely CMV, aphtous
ulcerations or herpes simplex (see chapter dysphagia/odynophagia). The presence (or absence)
of oral thrush has a high positive and negative predictive value for the diagnosis of candida
esophagitis (resp. 90% and 82%), but the absence of oral thrush does not completely exclude
the diagnosis. Especially patients who first have been treated with local lozenges for oral
thrush may present with oesophagitis without oral lesions.
Treatment of candida oesophagitis is with fluconazole 200 mg daily. When disseminated
candidiasis is suspected, prolonged treatment with fluconazole 400 mg daily is preferred. In
patients who are acutely ill, an initial regimen with amphotericin 0.7 mg/kg/day during 1-2
weeks can be given, followed by a course of fluconazole. Therapy should be continued at
least 3 weeks after resolution of lesions in the spleen or the liver, or after negative blood
culture. Secondary prophylaxis with oral fluconazole 200 mg daily is recommended as long
as immune suppression persists, but there is a risk of azole resistance with this long term use.
HIV/AIDS AND TB
Candidiasis
45
Cryptococcosis
Cryptococcus neoformans is the most common life-threatening fungal infection in patients
with AIDS. It is the first cause of meningitis in patients with AIDS in Africa and Asia. When
CD4 < 50, 90% of AIDS patients infected with Cryptococcus neoformans will present with
meningitis.
Extraneural cryptococcal disease, including cryptococcemia, pneumonia, and ulcerative skin
lesions or umbilicated papules mimicking molluscum contagiosum, is present in 25-50% of
cases. Rarely, cryptococcal infection can give rise to bulky abdominal lymphadenopathy, which
may cause abdominal pain. Diagnosis of disseminated cryptococcosis is based on serum
cryptococcal antigen tests, or isolation of the pathogen from biological material such as CSF,
lymph nodes, sputum or ulcerative skin lesion. Treatment of disseminated cryptococcosis is
with amphotericin B and fluconazole Secondary prevention with fluconazole 200 mg/day is
necessary to reduce relapse rates. In countries with a high incidence of cryptococcal disease
it is worthwhile to consider primary prophylaxis with fluconazole.
Penicilliosis
Penicillium marneffei is a common cause of opportunistic infection in HIV-infected patients
in Southeast Asia and Southern China with late-stage disease (CD4 < 100), but rarely causes
abdominal pain.
HIV/AIDS AND TB
Histoplasmosis
46
Histoplasma capsulatum is rarely seen in developing countries, but may be underdiagnosed.
The overall incidence of disseminated histoplasmosis (DH) in HIV-infected persons in these areas
varies from 5% to 27%. Gastrointestinal histoplasmosis differs from other forms of DH in
that pulmonary symptoms and fever may be absent. An oral ulcer is the most common
manifestation, besides splenomegaly, lymphadenopathy (30%) and hepatomegaly (26%).
Diagnosis of DH depends on tests usually not available in resource-poor settings: Antigen
testing in urine and serum (sensitivity of 90% and 70% respectively), blood culture (sens 5070%), bone marrow aspiration or biopsy for fungal stain or culture (positive in 75% of cases).
In developing countries the diagnosis will be clinically and suggested by response to treatment.
Treatment: Amphotericin B 0.5-1 mg/kg daily IV for at least 6 weeks. The recommended
cumulative dose of amphotericin B in histoplasmosis is 10-15 mg/kg. Patients should be
maintained on oral antifungals, itraconazole 200 mg twice daily life-long or as long as immune
suppression is present. Coccidioidomycosis and Aspergillosis are rare in HIV-patients in
developing countries.
Cytomegalovirus infection
Epidemiology
CMV gastrointestinal disease occurs in up to 5% of patients with AIDS, primarily in those
with a CD4 < 50. In the industrialized world the incidence of CMV GI disease has decreased
substantially since HAART became available.
CMV GI disease is characterized histologically by mucosal inflammation and tissue necrosis
with vascular endothelial involvement. Cytomegalovirus enterocolitis may result in deep
ulcers, fistulas, and bowel perforation.
Symptoms depend on the localization. Nearly all patients with gastrointestinal CMV have
fever. CMV oesophagitis presents with odynophagia. CMV gastritis presents with substernal
and/or epigastric burning pain. CMV pancreatitis presents with epigastric pain irradiating
to the back. CMV small bowel disease is manifested clinically by generalized abdominal pain
and sometimes diarrhoea. CMV colitis causes abdominal pain and bloody diarrhoea and
rebound tenderness. CMV of small bowel and colon can cause perforation, leading to
peritonitis. CMV can rarely cause large, painful ulcers of the mouth, pharynx, or anus. CMV
proctitis presents with tenesmus.
The other origin of abdominal pain unique to HIV-positive patients is an AIDS related
sclerosing cholangitis caused by CMV. Disseminated CMV infection can show multifocal
hepatic lesions with increased echogenicity.
Diagnosis and differential diagnosis
In practice in a developing country the diagnosis is suspected in patients with AIDS and
abdominal pain, bloody diarrhoea and/or mucosal ulcers, which do not respond to common
antibacterial and antifungal therapy. A hint towards the diagnosis of CMV gastrointestinal
disease is the presence of CMV retinitis.
HAART with immune restoration is one of the most effective methods to control CMV
disease.
Two antiviral drugs that are recognized for the treatment of CMV are ganciclovir and
foscarnet. Both drugs are very expensive and have serious side effects.
They are not available in developing countries because of their exorbitant cost.
HIV/AIDS AND TB
Treatment
47
Other common conditions in PLWHA
HIV/AIDS AND TB
Drug induced pancreatitis
48
In general acute pancreatitis is much more common in HIV-infected patients than in the
general population. It mostly occurs as a complication of medications taken to combat the
virus or treat opportunistic infections (sulphonamides, didanosine, stavudine, pentamidine).
Drug induced pancreatitis may not develop until after many months of use. Especially the
combination of didanosine and stavudine carries a high risk for pancreatitis. High triglyceride
levels (>1000 mg/dl) can be seen in patients on protease inhibitors, and can cause pancreatitis.
Other causes of pancreatitis in HIV patients include CMV and MAC. Patients with HIV have
less biliary stone induced pancreatitis.
Pancreatitis presents similar as in non HIV patients with acute upper abdominal pain. The
onset is rapid, but not as abrupt as that with a perforated viscus, reaching maximum intensity
in many cases within 10 to 20 minutes. One characteristic of the pain that is present in about
one-half of patients and suggests a pancreatic origin is band-like radiation to the back.
The pain of pancreatitis is classically relieved by sitting up and leaning forward. In contrast
to peritonitis that often causes patients to lie motionless on their backs because any motion
causes pain.
Unlike biliary colic, which lasts a maximum of six to eight hours, the pain of pancreatitis
lasts days.
Hyperamylasemia (more than 3 times the normal value) is frequently seen in pancreatitis.
25 % have an abnormal pancreas on abdominal ultrasound. In the absence of abdominal pain,
routine check of amylase levels is not needed, as it is difficult to interpret the results. In
conditions affecting the salivary glands, amylase (non-pancreatic origin) can be high as well.
This may happen in patients that take drugs which causes dry mouth (didanosine,
amitriptyline).
HIV patients tend to have more fever, hepatomegaly, diarrhoea, anaemia and leukopenia.
The prognosis of drug-induced pancreatitis is generally excellent. Treatment is similar to non
HIV patients: cessation of potential pancreatoxic medications, cessation of enteral feedings,
IV hydration, gastric decompression with nasogastric suction, analgesia). Didanosine should
never be restarted again after a drug-induced pancreatitis. Stavudine must be withdrawn but
can be re-introduced carefully after symptoms and serum amylase have returned to normal.
A reduction of the dose of stavudine from 40 to 30 mg should be considered. Prophylactic
antibiotics (amoxyclavulanic acid, quinolones) are only necessary in case > 30% of the
pancreas seems to affected on U/S.
Drug induced hepatitis
Drug related hepatotoxicity can occur in earlier stage HIV infection (CD4 > 200). Patients may
experience malaise, jaundice, anorexia, nausea, vomiting, abdominal pain, and weight loss.
Drug-induced hepatitis is the most frequent cause of jaundice in HIV patients, most often
related to antituberculous medication and carries a high mortality rate.
INH induced hepatitis
Elevated liver enzymes are observed in 10% of adults taking INH. About 1% of patients
develop INH-induced hepatitis. The onset of INH – induced hepatotoxicity is observed within
the first two months of therapy in approximately 50 percent of patients. Some factors are
related with increased risk: patients >35 years old, those receiving concurrent hepatotoxins
(rifampicin, ketoconazole, pyrazinamide), chronic alcohol use, concurrent liver disease,
African-American and Hispanic women, postpartum women, injection drug users. Patients
who are asymptomatic with AST/ALT elevations less than five times the upper limit of normal
can usually be continued on INH therapy. In many such cases, AST/ALT elevations decline
spontaneously. If transaminases are increased more than 5 times the upper limit, or the
patient has developed jaundiced, INH (and also rifampicin and pyrazinamide) should be
interrupted until the jaundice has disappeared.
In most patients treatment can be restarted with the same regimen without problem.
In case of severe disease, alternative anti-tuberculous treatment is recommended in the
meanwhile (streptomycin, ciprofloxacin and ethambutol).
All antiretroviral drugs are potentially hepatotoxic. Approximately 6-30% of patients
develop an increase in serum liver enzymes when on HAART. Patients with hepatitis B or
hepatitis C co-infection and patients taking nevirapine and ritonavir have a higher risk
(up to 20%) to develop severe hepatotoxicity. In Thailand in the HIV-NAT Trials cohort the
incidence of severe hepatotoxicity was 14% per year in the group of patients taking
nevirapine. Usually hepatitis occurs within the first months after the start of the treatment.
The median duration of treatment before the detection of severe hepatotoxicity was 137
days for nevirapine (IQR 49-305 days) and 100 days (IQR 35-196 days) for efavirenz.
However, occurrence of severe hepatotoxicity is described in > 50% of patients treated with
NNRTI after 12 weeks.Therefore monitoring is needed in all patients on HAART, also after
the 3rd month. The decision to stop ARV in case of raised liver enzymes has to be taken
with caution, because alternative treatment may even be more toxic. Patients with an
HIV/AIDS AND TB
ARV and hepatitis
49
underlying active hepatitis may have abnormal baseline liver function. In case the liver
enzymes are more than 5 times the baseline value the drug should be stopped. In case a
patient had already abnormal liver enzymes before the start of HAART, the cut-off to stop
the offending drug is an increase of enzymes 3.6 x the baseline value.
Even when a patient has experienced severe hepatotoxicity on either EFV or NVP, the
switch to the other compound after normalisation of liver function tests is not accompanied
with an increased risk.
Less frequent is a hypersensitivity syndrome (DRESS = drug rash, eosinophilia, systemic
symptoms: lymph adenopathy, hepatitis, nephritis, myocarditis). This is seen with efavirenz,
nevirapine and abacavir and occurs usually within the first 6 weeks. This is always a reason to
interrupt the treatment, whatever the level of transaminases. Stop the offending drug and
treat with prednisone 1 mg/kg. Do not reintroduce the offending drug. It seems to be a drug
effect and not a class effect, so patients developing hypersensitivity on NVP can be restarted
on EFV and vice versa.
Renal colics, nephrolithiasis
Indinavir and sulfadiazine are eliminated as crystals in the urine. If the patients fail to drink
enough water or do not get sufficient fluid during treatment, they may develop renal stones
and as a consequence present with colicky abdominal pain.
This is more frequent in patients who are on the higher dose of indinavir 800 mg thrice
daily or the boosted indinavir 800 mg twice daily. Other signs of indinavir toxicity are dry skin,
hair loss and paronychia of the toe nail. Also high dose sulfadiazine may cause renal colics.
HIV/AIDS AND TB
Lactic acidosis
50
The NRTI (especially didanosine, stavudine) have a high capacity to inhibit the activity of DNA
Á-polymerase, resulting in mitochondrial dysfunction and subsequently in an overproduction
of lactic acid. All NRTI, except abacavir, have been associated with the syndrome. The onset is
acute or subacute. Asymptomatic hyperlactatemia (not predictive of the development of lactic
acidosis) occurs in 5-25% of the patient treated with HAART. Symptomatic hyperlactatemia is
rare (1 per 1000 patient-years) but life threatening with a mortality rates from 40-77%.
Besides the use of NRTI, expecially ddI and d4T, possible risk factors associated with lactic
acidosis include female sex (conflicting data), obesity, hepatic steatosis, impaired renal
function, severe malnutrition and low nadir CD4 count. The highest risk is in pregnant women
who are treated with ddI and d4T.
Symptoms are non specific and have an insidious onset: fatigue, shortness of breath,
nausea, vomiting, lack of appetite, abdominal pain, weight loss, muscle pain and numbness
or tingling sensations. More severe symptoms are cardiomyopathy, peripheral neuropathy,
ascending neuromuscular weakness, (lower extremity motor weakness that developed over
a period of days or weeks), pancreatitis, bone marrow suppression and lipo-atrophy.
The laboratory tests that confirm the diagnosis of lactic acidosis are an elevated venous
lactate (> 5mmol/L) and an arterial pH less than 7.3. Both tests are usually not available in
resource-poor settings. There is also a low bicarbonate level, a widened anion gap (sodium
– (chloride + bicarbonate) > 13), an elevated LDH, ALT/AST and CPK.
The routine screening of lactate levels is not recommended as asymptomatic
hyperlactatemia is poorly predictive for lactic acidosis. Differential diagnosis has to be made
with other causes of acidosis (sepsis, hypotension, renal failure).
Treatment consists of supportive treatment with correction of the acidosis: IV fluids to
diminish the risk of hypovolemia, oxygen, sodium-bicarbonate (only if arterial pH < 7.1),
and stop of all ARV drugs. Studies have looked at the possible role of thiamine and
riboflavin in the management of severely ill patients. It is advised to give vitamin B
complex as well as coenzyme Q50 and L-carnitine (variable success). In patients who
survive, the venous lactate level returns to normal level 4 to 12 weeks after the stopping
of the NRTI. NRTI should be stopped for at least a month. When restarting HAART, avoid
the use of NRTI, except abacavir and tenofovir. Also 3TC seems to be associated with a
lower risk for lactic acidosis.
Infection with HIV has been associated with an increased risk for cancers, like Kaposi’s sarcoma,
non-Hodgkin lymphoma, cervical cancer. In Africa, the AIDS epidemic has led to Kaposi’s
sarcoma becoming the most frequent cancer in men, and is related to sexually transmitted
HHV8 infection. NHL is rarely diagnosed in Africa, but this may be due to early mortality in HIV
patients from other causes. In a developing country setting the treatment of malignancies is
often limited to palliative care. Kaposi’s sarcoma lesions can subside with HAART; however,
in visceral KS chemotherapy is needed as adjuvant of HAART (see chapter 15, Kaposi’s
sarcoma). Hepatitis B and C have a higher risk for a chronic course in HIV patients. They also
tend to evolve more rapidly to cirrhosis, and therefore hepatocellular carcinoma (HCC)
(although conflicting data). End stage liver disease and HCC are the most frequent causes of
death in hospitalised patients treated with HAART in European cohorts. HCC in the US is
mainly associated with hepatitis C. But in developing countries hepatitis B is more frequent,
and acquired in young age, which leads to more chronic disease. The importance of HCC and
hepatitis B and C patients is not well documented in HIV patients in developing countries.
HIV/AIDS AND TB
Malignancies
51
Clinical management of abdominal pain
The differential diagnosis of disorders that cause abdominal pain in PLHA is very broad. A good
history and physical examination may orient the further investigations. Any common causes
of abdominal discomfort that occur in non-HIV-infected patients also occur in PLHA. The
management of dyspepsia, peptic ulcer disease, PID, biliary and renal colics, appendicitis,
etc. does not differ from the non-immunocompromised host.
Chronic diarrhoea is defined as 3 or more loose stools a day, intermittently or continuously,
for at least one month. It is a very frequent and frustrating problem in PLHA, and is experienced
by at least 50% of them at some time during the evolution of the disease. Chronic diarrhoea
has a significant impact on quality of life. It is often accompanied by nausea, weight loss,
abdominal cramps, fever and dehydration. There is often intermittent watery diarrhoea,
without blood or mucus and in one-third to two-thirds of cases, no cause is identified. In areas
with a high prevalence of HIV infection, chronic diarrhoea is almost invariably due to
symptomatic HIV infection. Whenever possible, the cause of the diarrhoea should be
established and specific treatment provided. Failing this, management is symptomatic. A high
energy and protein intake reduces the degree of muscle wasting. The use of anti-diarrhoeal
agents such as codeine phosphate is justified when symptom relief is a major consideration.
Antiretroviral treatment able to cause immune restoration is very effective in decreasing the
prevalence of diarrhoea (an increase of 50 in CD4 count decreases prevalence by 87%).
Therefore, if appropriate investigation does not lead to the diagnosis of a specific cause
and antiretroviral therapy is available, it may be more efficient to start HAART than to
continue searching for a cause and specific treatment. Prevention consists of: attention to
personal hygiene (hand-washing), drinking boiled water, and eating only thoroughly cooked
meat and cooked or thoroughly washed fruit and vegetables.
HIV/AIDS AND TB
Causes of diarrhoea in AIDS patients
52
An infectious agent can be identified in about 50% of patients with AIDS-associated
diarrhoea.
➠ Protozoal infection: Cryptosporidium parvum, Giardia lamblia, Isospora belli, Entamoeba histolytica, Microsporidium spp (sources vary widely but all indicate that up
to 50% or more are caused by protozoa)
➠ Toxin induced: E. Coli and Clostridium difficile (10-25% USA)
➠ Mycobacterial infection: M. avium complex (25-40%USA), M. tuberculosis
➠ Viral infection: Cytomegalovirus (13-19% USA), Herpes simplex virus
➠ Bacterial infection: Campylobacter, Shigella, and Salmonella spp
➠ Helminthic infection: Strongyloides stercoralis
➠
➠
➠
➠
Fungal infection: Candida spp (seldom a cause of diarrhoea)
Non-infectious disorders: Kaposi’s sarcoma, lymphoma
AIDS enteropathy: direct cytopathic effect of HIV disease
Drugs: antibiotics, antiretrovirals
HIV/AIDS AND TB
Persistent Generalised Lymphadenopathy (PGL)
53
Oral lesions
Many different conditions involving the oral cavity are encountered in patients with AIDS. The
most frequent are oral candidiasis, oral hairy leukoplakia, necrotising ulcerative gingivitis and
recurrent aphthous stomatitis. An examination of the mouth needs to be part of the physical
examination of every patient suspected of HIV infection, even in the absence of complaints.
In practice, people often present with another complaint and it is the presence of oral thrush
that raises the suspicion of HIV infection. Sometimes oral lesions are debilitating because they
interfere with correct nutrition and increase the risk of weight loss. Oral disease significantly
affects quality of life in HIV patients. Some mouth lesions have a prognostic value, and are
helpful to determine the stage of HIV disease, in the absence of viral load and CD4 count.
Since the use of HAART the prevalence of oral lesions has significantly decreased, except for
oral warts. No studies have evaluated the usefulness of oral lesions to predict treatment
success or treatment failure in patients who are treated with HAART in the absence of viral
load and CD4 count.
Candida oesophagitis
HIV/AIDS AND TB
Candida oesophagitis is the most common cause of dysphagia in AIDS patients. In two
prospective studies, candida oesophagitis was detected by endoscopy in up to 64% of
symptomatic patients. The presence of oral thrush has a high positive predictive value for the
diagnosis of candida oesophagitis (90% in the presence of oesophageal symptoms), but the
absence of oral thrush does not completely exclude the diagnosis. Patients complain of
dysphagia and retrosternal pain. Odynophagia is less severe than in CMV oesophagitis.
Barium-meal studies are not sufficient to distinguish candida oesophagitis from malignancy
or viral infection, and should be avoided. Definitive diagnosis of oesophageal candidiasis
requires the demonstration of tissue-invasive mycelia on endoscopic biopsy. However,
presumptive diagnosis and empiric therapy are acceptable, especially when oral thrush is
present, and in sites where there is no access to complex investigations. Treatment consists
of systemic antifungal drugs. Fluconazole is the preferred systemic therapy for oesophageal
candidiasis.
54
Leishmaniasis
Leishmaniasis is a protozoal disease with clinical manifestations which can vary according to
the infecting species (over 20 pathogenic species are known) and the immune response of the
host. The disease is transmitted by the bite of an infected sandfly. Leishmania-HIV co-infection
mostly causes visceral leishmaniasis. Among South European AIDS cases, it is the fourth cause
of opportunistic parasitic disease after toxoplasmosis, pneumocystosis and cryptosporidiosis.
Cutaneous leishmaniasis
Cutaneous leishmaniasis (CL) is common in South Europe, S- western, central and eastern
Asia (India and Pakistan), Africa and Latin America. It can present with ulcers, papules or
nodules of the skin. In HIV patients, CL often presents as a disseminated form with multiple
papules and nodules which can ulcerate. PLHA with CL should be checked carefully to exclude
VL (bone marrow aspirate, buffy coat). In HIV-infected patients cutaneous lesions may be
the first presentation of visceral leishmaniasis. The differential diagnosis has to be made with
Kaposi’s sarcoma, bacillary angiomatosis, herpes zoster, disseminated cryptococcosis.
Incidental finding of leishmania has been described in Kaposi’s sarcoma, herpes zoster lesion,
herpes simplex, cryptococccosis and bacillary angiomatosis.
CL can heal spontaneously after 1 month up to 3 years. Deciding on whether to treat or
not depends on the risk for developing mucocutaneous leishmaniasis and the place of the
lesions (face and joints involvement favours treatment). Pure CL in initial HIV stage responds
to intralesional antimonial treatment: once or twice weekly an infiltration with sodium
stibogluconate (100mg/ml 0.3-3 ml/lesion) or meglumine antimonite (0.2-0.8 ml/lesion) from
all sites, until the lesion has blanched. Per infiltration max 5 ml should be used and a maximum
of 20 mg Sb/kg. Two to fifteen infiltrations are needed to achieve cure.
Mucocutaneous leishmaniasis (MCL) appears in 2 to 3% of all cases of HIV-Leishmania
co-infection. This form occurs rarely outside Latin America, but the mucosal form can occur in
East-Africa. Practically all of the Leishmania species can be responsible for MCL lesions.
Although the nasal septum and the soft palate are usually affected by MCL due to metastasis
from a primary lesion, it can also appear as a primary lesion. Nasal biopsy specimens are
commonly needed to elucidate a definitive diagnosis of MCL.
Sodium stibogluconate or meglumine antimonite 20 mg/kg/day IV during 20-30 days.
Amphotericin B 1mg/kg/day on alternate days for 2 months
HIV/AIDS AND TB
Mucocutaneous leishmaniasis
55
Visceral leishmaniasis
The visceral form (Kala Azar) is spread over Africa, Asia (India, Pakistan, Bangladesh, China,
and Nepal), Southern Europe and Latin America. Usually, cutaneous manifestations are rare
in visceral leishmaniasis, but AIDS is resulting in the development of new forms of cutaneous
involvement.
Two types of skin lesions have been described in visceral leishmaniasis and HIV co-infected
patients: lesions caused by leishmania and lesions in which the finding of leishmania is
incidental. Lesions caused by VL can present in subcutaneous nodules, dermatofibroma-like
lesions Kaposi-like lesions, linear brown lines, or a dermatomyositis-like picture.The presence
of skin lesions in an HIV-positive patient in an area where visceral leishmaniasis is endemic
may disclose a diagnosis of visceral leishmaniasis, since the lesions may provide an accessible
tissue site for diagnosis and treatment response, in contrast with a spleen or bone marrow
aspiration.
Various treatments have been proposed. Amphotericin B dosed as 1 mg/kg/day every
other day for 30 days seems a feasible option in HIV programs, since this drug may be readily
available for treating cryptococcosis and staff is already experienced in its use. The relapse rate
in HIV co-infected patients is high. No treatment can provide a complete sterilization, and HIVpositive patients generally can not develop cellular immunity to Leishmania.
Post Kala-azar dermal leishmaniasis (PKDL)
PKDL is a cutaneous manifestation caused by the same parasite which causes kala-azar
and usually occurs weeks after recovery of kala-azar. The rash is usually macular, papular or
nodular. The lesions can be limited to the face only, but can also cover most of the body,
including mucosa of lips and mouth, with ulcers and crusting. PKDL is not very common in
HIV/AIDS.
HIV/AIDS AND TB
Neurological disorders
56
The reported incidence neurological abnormalities on clinical examination varies greatly, from
16% to 72% among hospitalised AIDS patients. A wide range of neurological manifestations
is reported: cognitive defects, focal deficits such as hemiplegia and acute peripheral facial
palsy, painful feet syndrome, encephalopathy, etc. Some of these manifestations are directly
caused by HIV itself; others are the result of OI caused by different pathogens.
FOCAL SIGNS include seizures, any sort of paralysis, cranial nerve lesions, and visual
disturbance.
VISUAL IMPAIRMENT in PLHA is mostly due to CMV retinitis. This condition can affect both
eyes and lead to progressive loss of vision. Catastrophic vision loss may occur in patients with
cryptococcal and tuberculous meningitis due to severe intracranial hypertension.
MENINGITIS in PLHA can have different causes: early in the course of the a in HIV-infected
people, accounting for 10% f deaths. 347 infection, it is due to HIV itself; later on to
cryptococcal meningitis, TB meningitis, bacterial meningitis (meningococcal and pneumococcal). The most accurate data on the aetiology of neurological disease in Africa come from
autopsy studies in Ivory Coast. Cerebral toxoplasmosis was the hird most common cause of
dethto
CONDITIONS CAUSED BY HIV ITSELF Acute retroviral syndrome. Acute aseptic meningitis is
associated with a high viral load in the CSF. This condition resolves spontaneously. Acute
inflammatory demyelinating polyneuropathy (AIDP) can be seen during acute HIV
seroconversion and resembles Guillain Barré Syndrome (GBS).there is lymphocytic pleocytosis
in CSF in contrast to the non-HIV GBS. Steroids may help.
MONONEUROPATHY AND POLYNEUROPATHY Neuropathy is one of the most common
neurological manifestations in AIDS patients, occurring in as many as 30 % of the patients.
Nearly every patient has one of four readily distinguishable syndromes
Extreme muscle weakness with inability to walk can be due to severe is frequently
encountered in AIDS patients with hypokalemia. Low potassium chronic diarrhoea and during
treatment with amphotericin B.
HIV MYELOPATHY It presents as spastic paresis with bowel and bladder dysfunction, gait
ataxia, incontinence and variable sensory loss. This condition can respond to HAART. DD has
to be made with cord-compression (epidural abscess, tumor), vitamin B12 deficiency or other
viral infections (varicella, CMV, HTLV-1)
dementia. The initial manifestations are loss of memory and strange behaviour. These ill later
be associated with various degrees of incontinence and gait disturbances with ataxia. In very
advanced stages, patients may become demented with associated mutism and even
paraplegia. It is a diagnosis of exclusion, because depression and infectious causes of and
infectious causes of encephalitis may mimic dementia. The CSF is usually normal, although
20% of cases may have a mild mononuclear pleocytosis (<50 WBC/mmÑ) with dding a PI
rather than a NNRTI to the 2 NRTIs. logical involvement in AIDS patients can present in many
different can be treated, early diagnosis is , and is ven indicated for treating intracranial
hypertension in slightly increased protein content (<200 mg/dl). When available, an AZT or
d4T-containing HAART regimen is an effective treatment for HIV-associated dementia.
HIV/AIDS AND TB
HIV ENCEPHALOPATHY / AIDS DEMENTIA Approximately 7-9% of patients with AIDS develop
57
Opportunistic infections involving the brain
The differential diagnosis includes the following pathogens: - Protozoal infection: Toxoplasma
gondii, Trypanosoma Cruzi - Mycobacterial infection: M. tuberculosis, M. Avium (in immune
reconstitution syndrome) - Fungal infection: Cryptococcus neoformans, Histoplasmosis,
Coccidiodomycosis, Candida species (rare) - Viral infection: Cytomegalovirus, Herpes simplex
virus, Varicella zoster virus, JC virus (slow virus causing progressive multifocal leukoencephalopathy - PML). The threshold for performing an LP should therefore be kept very low
in AIDS patients who have headache.
HIV/AIDS AND TB
Cryptococcus neoformans
58
Cryptococcus neoformans is the most common life-threatening fungal infection in patients
with AIDS. It is the first cause of meningitis in patients with AIDS in Africa, Latin America and
Asia. It occurs most often in HIV-positive patients with CD4 <50. In this group of AIDS patients,
90% of those infected with Cryptococcus neoformans will present with meningeal involvement. However, less than 50% have meningeal signs. The onset is insidious, fever nd headache
being often the only symptoms. Neck stiffness can be absent, longed headache and fever,
behavioural changes and confusion. Diagnosis by lumbar puncture: increased opening
pressure, sometimes only slightly elevated WBC count (predominantly lymphocytes).
Because timely diagnosis is very important for treatment outcome several projects have
started to use the cryptococcal Ag test on CSF (CRAg latex agglutination). This test has a
sensitivity of 92%, and is highly specific. Active cryptococcal infection can be present in some
patients with a positive serum CRAg (sCRAg) but negative fungal cultures, which encourages
clinicians to treat HIV patients with a positive sCRAG even in the absence of symptoms. The
serial monitoring of CRAg in serum or CSF has no clinical utility to monitor the response to
therapy. Cryptococcal antigen can remain positive for up to 7 months after cure of the
infection.
We recommend for all MSF missions the combination of amphotericin B and fluconazole.
Amphotericin B (IV) (0.7 mg/kg daily by slow IV injection for 2 weeks) followed by fluconazole
400 mg daily for 8 weeks, followed by fluconazole 200 mg daily s secondary prophylaxis.
In children: Amphotericin B, 0.7-1mg/kg/d IV diluted in 5% glucose infused by slow drip
over 4 hrs, during 2 weeks, followed by maintenance therapy of fluconazole 10-12 mg/kg
during 8 weeks. Secondary prophylaxis: fluconazole 5mg/kg/day lifelong, or until immune
restoration after HAART.
Toxoplasma gondii encephalitis
Toxoplasmosis appears to be infrequently reported (1% to 2%). This can be due either to
the limited diagnostic capacity or to a real low incidence of encephalitis. Hemiparesis,
cognitive disorders, seizures and everal weeks. Fever is resent in about 50% of patients and
headache, which may be very m have seizures. Meningeal irritation is diagnosis SF findings
are non-specific or normal. If a CT scan is available, the on in a patient who has a positive
rophylaxis is very suggestive for toxoplasmosis. A CT scan se of focal brain eurological signs,
and who has treatment by day 7 and 91% by ay 14. The median time to response is 5 days
Response to empirical therapy is currently being considered as a diagnostic criterion. If
possible, Toxoplasma antibody (IgG) can be useful, because the negative predictive value is
high (94-97%).384 In other words, Toxoplasma brain abscess is less likely if the Toxoplasma
serology is negative.
If there is no response to empirical therapy after 2 weeks an alternative diagnosis needs
to be considered. Treatment: sulfadiazine and pyrimethamine and folinic acid for 6-8 weeks.
HAART (Highly active antiretroviral therapy)
HIV/AIDS AND TB
With the wide spread use of HAART the incidence of opportunistic infections (OI) in the
western world has dramatically decreased.The clinical benefit of HAART in reducing the
incidence of OI is especially obvious in patients with CD4 < 200.124 Besides preventing OIs,
HAART also helps to get rid of certain OIs, especially those for which no specific treatment
is available. Nevertheless, in our daily practice, we are still confronted with AIDS-related OIs.
Patients present themselves late with an AIDS defining illness. In the first months after the
initiation of HAART patients may still develop an OI, or a worsening of a pre-existing OI
due to immune reactivation disease (see below). After 6 months of HAART the occurrence
of an OI usually indicates treatment failure, although immune reactivation disease is still
possible. TB remains common, even in the absence of treatment failure, in patients with
CD4 < 350.
59
Possible Sites of Intervention in the Inhibition of HIV Replication
HIV/AIDS AND TB
© Elsevier 2004, Infectious Diseases 2e – www.idreference.com
60
➠
Goals of ART
Maximal and durable suppression of HIV
Restoration and/or preservation of the body’s immune system
Prevention of death and decline in disease burden
Improve quality of life and indirectly improve the life of other family members
There will be no further in depth analysis of the use of ART for the purpose of this manual.
Should someone want to study more in depth about ART principles, resistance issues or side
effects, there are all the relevant references available.
HIV/AIDS AND TB
➠
➠
➠
➠
61
Prevention Mother to Child Transmission 5
The use of antiretroviral therapies to reduce mother-to-child transmission of HIV (MTCT) is an
important advance in preventing HIV infections in children. In well-resourced settings,
treatment has evolved from initial monotherapy with zidovudine (ZDV) to the use of
combination antiretroviral therapy in pregnancy. Although this approach has not been subject
to a randomized trial of efficacy, the reduction of transmission rates to below 2% has made
it the standard of care in these settings. In poorer countries, combination ART is not available
for most people and research has focused on investigating shorter, more feasible and less
expensive antiretroviral regimens. This review includes randomized controlled trials of any
antiretroviral regimen aimed at decreasing the risk of mother-to-child transmission of HIV
infection (MTCT) compared with placebo or no treatment, and randomized controlled trials
comparing two or more antiretroviral regimens aimed at decreasing the risk of MTCT. The
review does not include those trials designed to investigate the interruption of postnatal
transmission through breast milk. Eighteen trials, including more than 14,000 participants
in 16 countries were eligible for inclusion in the review, conducted over the period 1991 to
2006, which met the inclusion criteria. The median trial sample size was 795, ranging from 50
to 1,797 participants. As the design and strategies of these trials vary considerably, the
reviewers divided the trials into several sections.
The first section considered trials of antiretroviral therapy vs. placebo in breastfeeding
populations. Since a significant decrease in the risk of MTCT has been demonstrated in these
trials with antiretroviral use, compared to placebo, it is not necessary or ethical to conduct
further placebo controlled trials. The other twelve studies therefore examine either different
dosing strategies of the same drug, or compare different antiretroviral regimens against each
other.
HIV/AIDS AND TB
Magnitude of the problem
62
An estimated 530,000 children were infected with HIV in 2006, predominantly through
mother-to-child transmission (MTCT). More than 85% of HIV-infected pregnant women are in
sub-Saharan Africa. There has been significant progress in developing and implementing
treatment strategies, but, despite this, UNAIDS estimated that in 2006 less than 8% of all
pregnant women globally, and less than 6% in sub-Saharan Africa, were offered access to HIV
diagnosis and prevention services, and that only 9% of HIV-infected women received an
5. http://apps.who.int/rhl/hiv_aids/jmicom/en/print.html
antiretroviral regimen for PMTCT. In well resourced settings, the dual approach of starting
ongoing combination antiretroviral therapy (ART) in pregnancy for those women who qualify
for it, and using ART through the pregnancy and stopping post-partum for those with higher
CD4 counts, combined with the avoidance of breastfeeding, has become the routine
management in pregnancy. This has resulted in a drop in MTCT rates to below 2%. In most
under-resourced settings, this combination therapy has been unavailable to date, and this
lack of access is reflected in the estimates of transmission: a rate of 26% is estimated in the
thirty-three most affected countries – a ten fold increase over the rates now seen in better
resourced settings.
The prevention of MTCT is a priority for improving child survival in many countries in
Africa and Asia. The review examines the complex array of trials which have attempted to
find effective and feasible short course antiretroviral regimens. These are important for
programme managers and clinicians in under-resourced settings, where the combination
antiretroviral therapies used in richer countries may not be available.
Of these, the “single dose” nevirapine regimen, of a dose of NVP to the mother at the
onset of labour and one dose of NVP syrup to the infant, has become the most widely
implemented strategy, reaching more than a million women and infants since 1999. As the
review demonstrates, this is an effective intervention, but there are more efficacious
antiretroviral combinations. Few low-resourced country programmes have yet been able
to extend beyond single dose NVP, or even to achieve good coverage with this. Estimates
of the proportion of HIV-infected pregnant women receiving antiretroviral prophylaxis
in 2005 varied from under 1% to 54% in sub-Saharan Africa, with overall regional
coverage of 11% (8%- 15%). Coverage in Eastern Europe and Central Asia is estimated at
75% (38%-95%) in Eastern Europe and Central Asia, 24% (13%-46%) in Latin America
and the Caribbean, 5% (3%-10%) in East, South and South-East Asia, and <1% in North
Africa and the Middle East.
The initial focus of PMTCT programmes was solely on the prevention of transmission,
where more complex therapy was not an option for most programmes. The availability of
antiretroviral therapy has changed dramatically since 2002. WHO now estimates that more
than two million people in low and middle income countries were receiving antiretroviral
therapy by December 2006 – approximately 28% of the estimated 7 million in need of ART.
With this increasing access to antiretroviral therapy, the provision of PMTCT services in lowresourced settings needs to be seen more as an integral part of the continuum of care and
treatment for HIV infected women. A new paradigm for PMTCT services is required in these
settings, with a baseline short course treatment regimen for those who do not yet require
ART treatment and access to combination treatment for those who do.This makes it
HIV/AIDS AND TB
Applicability of the results of the Cochrane Review
63
important to identify pregnant women in need of ART and to initiate therapy as soon as
possible in pregnancy, as the use of effective ART in these women will both benefit their own
health and be the best prophylaxis against MTCT.
The 2006 WHO guidelines recommend that women with CD4 counts less than 200/mm3
or Stage 3 or 4 clinical disease start and continue ART. In addition, the guidelines recommend
starting ongoing ART in women with CD4 counts between 200 and 350/mm3 where this is
feasible in the services.
Implementation of the intervention
HIV/AIDS AND TB
In order to implement the use of antiretroviral regimens for the prevention of motherto-child transmission of HIV, antenatal care services must be available and utilized early
enough to identify HIV-positive mothers to start treatment. These services must incorporate
voluntary counselling and testing services for HIV and there must be acceptance of HIV
testing by pregnant women in order to identify those infected. The entry point for access
to PMTCT interventions is HIV testing. In some settings, uptake of testing has been
dramatically improved by offering “routine” testing to pregnant women – rather than
putting the onus on the woman to decide on testing. As an example of this, in Botswana,
this approach in one region increased the proportion of HIV-infected women who knew
their HIV status from 47% to 78% and the percentage receiving PMTCT interventions
increased from 29% to 56%. There have been suggestions that nevirapine is an effective
and inexpensive intervention that could be given to all women in labour in high prevalence
settings. This approach has not been evaluated and many concerns have been raised,
including the rights of women to know their HIV status, development of resistance, effect
on infant feeding practices and the loss of opportunities for HIV prevention education in
the antenatal setting.
In order to fully implement an integrated strategy of providing ART for women with low
CD4 counts or clinical symptoms of AIDS and a “dual therapy” regimen for other HIV-positive
women, the services need to be able to undertake clinical assessment and do a baseline CD4
count. This is not yet available in antenatal services in less-resourced settings. Drug supply
logistics must be in place to provide ART for pregnant women and their children, as does
access to diagnostic HIV testing for exposed children.
64
Research
Research is in progress, and more is required, on the efficacy of antiretroviral therapy in
reducing the risk of transmission of HIV through breastfeeding. While preliminary results
appear encouraging, this remains a priority research area for low-resourced settings where
HIV/AIDS AND TB
replacement feeding may not be feasible or affordable. Additional research is needed on
the impact of PMTCT regimens containing NVP or 3TC on future treatment options for
mothers and children, and the impact of the selection of rug resistant mutations. There are
also some concerns about the use of nevirapine in combination antiretroviral regimens in
women with high CD4 counts (although not about the use of “single dose” nevirapine
regimens), as this has been associated with an increased rate of hepatotoxicity. This may
become more of an issue as antiretrovirals become more available and the use of combination
ART only for PMTCT purposes becomes more common in less-resourced settings. There is also
a need to investigate alternative regimens, particularly the use of tenofovir alone or in
combination as a potential strategy for PMTCT.
65
References
ñ Clinical HIV/AIDS care guidelines for resource poor settings, MSF, Brussels, 2006.
ñ E. Giamarellou et al. Infections and Antimicrobial Therapy. 3rd Volume. Litsas 2005.
ñ Up-to-date, 16.3.
ñ Current diagnosis and treatment of infectious diseases. McGrawHill, 2010.
ñ Hoffmann-Rockstroh-Kamps. HIV Medicine 2007. www.HIVMedicine.com
ñ Palomino-Leao-Ritacco. Tuberculosis 2007: From basic science to patient care.
www.TuberculosisTextbook.com
ñ Mauss-Berg-Rockstroh-Sarrazin-Wdemeyer. Hepatology. A clinical textbook.
www.HepatolgyTextbook.com
ñ David Coetzeea, Katherine Hildebranda, Andrew Boullea et al. Outcomes after two years of providing
antiretroviral treatment in Khayelitsha, South Africa. AIDS 2004, Vol 18 888 No 6, 887-895.
ñ Acquired Immune Deficiency Syndrome: Interim proposal for a WHO Staging System for HIV Infection
and Disease. Weekly Epidemiol Rec 1990, 65:221-224.
ñ Centers for Disease Control and Prevention. Updated guidelines for the use of rifabutin or
rifampin for the treatment and prevention of tuberculosis among HIV-infected patients taking
protease inhibitors or nonnucleoside reverse transcriptase inhibitors. Morb Mortal Wkly Rep 2000,
49:185-189.
ñ Laurent C, Diakhate N, Gueye NF, Toure MA, Sow PS, Faye MA, et al. The Senegalese government’s
highly active antiretroviral therapy initiative: an 18-month follow-up study. AIDS 2002, 16:13631370.
ñ Post FA, Wood R, Maartens G. CD4 and total lymphocyte counts as predictors of HIV disease
progression. Q J Med 1996, 89:505-508.
ñ World Health Organization. Scaling up Antiretroviral Therapy in Resource Limited Settings: Guidelines
for a Public Health Approach. Geneva: WHO; 2002.
HIV/AIDS AND TB
ñ Weidle PJ, Malamba S, Mwebaze R, Sozi C, Rukundo G, Downing R, et al. Assessment of a pilot
66
antiretroviral drug therapy programme in Uganda: patients’ response, survival, and drug resistance.
Lancet 2002, 360:34-40.
ñ Darkoh-Ampem, E, Obita, G, De Korte D, Mazonde P. Scaling up antiretroviral therapy in a resourcepoor setting: Botswana example. International Conference on HIV Therapy. Edinburgh, month? 2002
[abstract Pl4.3].
ñ MSF International AIDS Working Group. A ‘’tool kit’’ for the integration of HIV care and treatment
in MSF programmes. February 2006.
ñ Ministry of Health Zambia. ANTIRETROVIRAL THERAPY FOR CHRONIC HIV INFECTION IN ADULTS AND
ADOLESCENTS. New ART Protocols. May 2007.
ñ World Health Organization. HIV surveillance among TB patients. Geneva 2004.
HIV/AIDS AND TB
ñ World Health Organization. Global Tuberculosis control 2008. Surveillance, Planning, Financing.
67
chapter 2
Diarrhoeal Diseases
– Cholera
General Objective
To provide participants with basic medical knowledge in Diarrhoeal Diseases (DD) and basic
principles for preparedness and response to cholera and epidemic diarrhoeal diseases.
At the end of the session, participants will be familiar with:
➠ Clinical manifestations and diagnosis of DD
➠ Treatment options and prevention of DD
➠ Clinical practice in DD
➠ preparedness and detection of cholera
➠ appropriate response
➠ administration of treatment with the implementation of community
Content
Morbidity and mortality attributable to diarrheal disease in infants and young children can be
reduced by a variety of preventive measures and by improved clinical management of those
episodes that occur. Recent evidence indicates that the incidence of diarrheal disease can be
diminished by decreasing exposure to enteropathogens that frequently are present in foods,
DIARRHOEAL DISEASES – CHOLERA
Specific Objectives
69
and that the severity (purging rate and duration) and frequency of illness can be diminished
by improving the host’s nutritional status.
At the same time about 20% of those who are infected of cholera develop acute, watery
diarrhoea (10-20% of these individuals develop severe watery diarrhoea with vomiting). If
these patients are not promptly and adequately treated, the loss of such large amounts of
fluid and salts can lead to severe dehydration and death within hours. The case-fatality rate
in untreated cases may reach 30-50%.
Treatment is straightforward (basically rehydration) and, if applied appropriately, should
keep case- fatality rate below 1%.
➠ Clinical manifestations and Diagnosis of acute diarrhoea
ñ Clinical evaluation
ñ Laboratory evaluation
ñ Prognostic Factors and differential diagnosis
➠ Treatment Options and Prevention
ñ Rehydration
ñ Supplemental Zinc Therapy, Multivitamins, and Minerals
ñ Diet – Non specific antidiarrheal treatment
ñ Prevention (water, sanitation and hygiene – vaccines)
➠ Clinical Practice in acute diarrhoea (adults, children)
➠ Cholera
ñ New strategies: oral cholera vaccines
ñ Case definition – confirmation
ñ Improved preparedness and treatment (training of health workers, rehydration,
DIARRHOEAL DISEASES – CHOLERA
intravenous therapy, antibiotics, health education, vaccination, trade and travel
restrictions, mass chemoprophylaxis)
ñ Surveillance of patients with severe cholera
70
Methodology
➠ PPt Presentations
➠ Lecture/discussion format
➠ Case study
References
Diarrhoeal Diseases
Clinical Manifestations and Diagnosis
Despite clinical clues, determining the causative agent of diarrhea in an individual patient
on the basis of clinical grounds alone is usually difficult.
Episodes of diarrhea can be classified into three categories:
Diarrhoeal Diseases
Symptoms to the Causes of Acute Diarrhea
CLINICAL EVALUATION
The initial clinical evaluation of the patient (see “Table: Levels of Dehydration in Children
with Acute Diarrhea” below) should focus on:
➠ Assessing the severity of the illness and the need for rehydration
➠ Identifying likely causes on the basis of the history and clinical findings
3
DIARRHOEAL DISEASES – CHOLERA
Table: Linking the Main
71
Table: Evaluation of the Acute Diarrhea Patient
Table: Levels of Dehydration in Children with Acute Diarrhea
DIARRHOEAL DISEASES – CHOLERA
Cautionary note: Being lethargic and sleepy are not the same. A lethargic child is not simply asleep: the child’s
mental state is dull and the child cannot be fully awakened; the child may appear to be drifting into
unconsciousness. In some infants and children, the eyes normally appear somewhat sunken. It is helpful to
ask the mother if the child’s eyes are normal or more sunken than usual. The skin pinch is less useful in
infants or children with marasmus or kwashiorkor, or obese children. Other signs that may be altered in
children with severe malnutrition are described in section 8.1 of the World Health Organization (WHO) 2005
Guideline.
72
Signs of dehydration in adults
➠ Pulse rate >90
➠ Postural hypotension
➠ Supine hypotension and absence of palpable pulse
➠ Dry tongue
➠ Sunken eyeballs
➠ Skin pinch
Laboratory Evaluation
For acute enteritis and colitis, maintaining adequate intravascular volume and correcting
fluid and electrolyte disturbances take priority over the identification of the causing agent.
Stool cultures are usually unnecessary for immunocompetent patients who present within 24
hours after the onset of acute, watery diarrhea. Microbiologic investigation is indicated in
patients who are dehydrated or febrile or have blood or pus in their stool.
Epidemiologic clues to infectious diarrhea can be found by evaluating the incubation period,
history of recent travel, unusual food or eating circumstances, professional risks, recent use
of antimicrobials, institutionalization, and human immunodeficiency virus (HIV) infection risks.
Stool analysis and culture costs can be reduced by improving the selection and testing
of the specimens submitted on the basis of interpreting the case information – such as patient
history, clinical aspects, visual stool inspection, and estimated incubation period.
The identification of a pathogenic bacterium, virus, or parasite in a stool specimen from
a child with diarrhea does not indicate in all cases that it is the cause of illness.
Certain laboratory studies may be important when the underlying diagnosis is unclear
or diagnoses other than acute gastroenteritis are possible.
Measurement of serum electrolytes is only required in children with severe dehydration or
with moderate dehydration and an atypical clinical history or findings. Hypernatremic
dehydration requires specific rehydration methods – irritability and a doughy feel to the skin
are typical manifestations and should be sought specifically.
Prognostic Factors and Differential Diagnosis
DIARRHOEAL DISEASES – CHOLERA
Table: Prognostic Factors in Children
73
Differential diagnosis of acute diarrhea in children
➠ Meningitis
➠ Bacterial sepsis
➠ Pneumonia
➠ Otitis media
➠ Urinary tract infection
5
Treatment Options and Prevention
Rehydration
Oral rehydration therapy (ORT) is the administration of fluid by mouth to prevent or
correct dehydration that is a consequence of diarrhea. ORT is the standard for efficacious and
cost-effective management of acute gastroenteritis, also in developed countries.
Oral rehydration salt (ORS) solution is the fluid specifically developed for ORT. A more
effective, lower-osmolarity ORS (with reduced concentrations of sodium and glucose,
associated with less vomiting, less stool output, and a reduced need for intravenous infusions
in comparison with standard ORS) has been developed for global use (see Table 4 in the
original guideline document). The hypotonic WHO-ORS is also recommended for use in
treating adults and children with cholera. ORT consists of:
DIARRHOEAL DISEASES – CHOLERA
➤ Rehydration – water and electrolytes are administered to replace losses
➤ Maintenance fluid therapy (along with appropriate nutrition) In children who are in
hemodynamic shock or with abdominal ileus, ORT may be contraindicated.
74
For children who are unable to tolerate ORS via the oral route (with persistent vomiting),
nasogastric (NG) feeding can be used to administer ORS.
Global ORS coverage rates are still less than 50%, and efforts must be made to improve
coverage.
Rice-based ORS is superior to standard ORS for adults and children with cholera, and can
be used to treat such patients wherever its preparation is convenient. Rice-based ORS is not
superior to standard ORS in the treatment of children with acute noncholera diarrhea,
especially when food is given shortly after rehydration, as is recommended to prevent
malnutrition.
Supplemental Zinc Therapy, Multivitamins, and Minerals
For all children with diarrhea: 20 mg zinc for 14 days.
Zinc deficiency is widespread among children in developing countries. Micronutrient
supplementation – supplementation treatment with zinc (20 mg per day until the diarrhea
ceases) reduces the duration and severity of diarrheal episodes in children in developing
countries.
Supplementation with zinc sulfate (2 mg per day for 10 to 14 days) reduces the incidence
of diarrhea for 2 to 3 months. It helps reduce mortality rates among children with persistent
diarrheal illness. Administration of zinc sulfate supplements to children suffering from
persistent diarrhea is recommended by the WHO.
All children with persistent diarrhea should receive supplementary multivitamins and
minerals each day for 2 weeks. Locally available commercial preparations are often suitable;
tablets that can be crushed and given with food are least costly. These should provide as broad
a range of vitamins and minerals as possible, including at least two recommended daily
allowances (RDAs) of folate, vitamin A, zinc, magnesium, and copper.
As a guide, one RDA for a child aged 1 year is:
➠ Folate: 50 micrograms
➠ Zinc: 20 micrograms
➠ Vitamin A: 400 micrograms
➠ Copper: 1 mg
➠ Magnesium: 80 mg
6
The practice of withholding food for >4 hours is inappropriate. Food should be started 4
hours after starting ORT or intravenous fluid. The notes below apply to adults and children
unless age is specified.
Give:
➠ An age-appropriate diet – regardless of the fluid used for ORT/maintenance
➠ Infants require more frequent breast feedings or bottle feedings – special formulas or
dilutions unnecessary
➠ Older children should be given appropriately more fluids
➠ Frequent, small meals throughout the day (six meals/day)
➠ Energy and micronutrient-rich foods (grains, meats, fruits, and vegetables)
➠ Increasing energy intake as tolerated following the diarrheal episode
DIARRHOEAL DISEASES – CHOLERA
Diet
75
Avoid:
➠ Canned fruit juices – these are hyperosmolar and can aggravate diarrhea.
➠ Probiotics are specific defined live microorganisms, such as Lactobacillus GG (American
Type Culture Collection [ATCC] 53103), which have demonstrated health effects in
humans.
Nonspecific Antidiarrheal Treatment
None of these drugs addresses the underlying causes of diarrhea. Antidiarrheals have no
practical benefits for children with acute/persistent diarrhea. Antiemetics are usually
unnecessary in acute diarrhea management.
ANTIMOTILITY: Loperamide is the agent of choice for adults (4 to 6 mg/day; 2 to 4 mg/day
for children >8 years).
Should be used mostly for mild to moderate traveler’s diarrhea (without clinical signs of
invasive diarrhea).
Inhibits intestinal peristalsis and has mild antisecretory properties.
Should be avoided in bloody or suspected inflammatory diarrhea (febrile patients).
Significant abdominal pain also suggests inflammatory diarrhea (this is a contraindication
for loperamide use).
Loperamide is not recommended for use in children <2 years.
DIARRHOEAL DISEASES – CHOLERA
Antisecretory agents: Bismuth subsalicylate can alleviate stool output in children or symptoms
of diarrhea, nausea, and abdominal pain in traveler’s diarrhea.
Racecadotril is an enkephalinase inhibitor (nonopiate) with antisecretory activity, and is now
licensed in many countries in the world for use in children. It has been found useful in
children with diarrhea, but not in adults with cholera.
Adsorbents: Kaolin-pectin, activated charcoal, attapulgite. Inadequate proof of efficacy in
acute adult diarrhea
76
Antimicrobials
Antimicrobial therapy is not usually indicated in children. Antimicrobials are reliably helpful
only for children with bloody diarrhea (most likely shigellosis), suspected cholera with severe
dehydration, and serious nonintestinal infections (e.g., pneumonia). Antiprotozoal drugs can
be very effective for diarrhea in children, especially for Giardia, Entamoeba histolytica, and
now Cryptosporidium, with nitazoxanide.
In adults, the clinical benefit should be weighed against the cost, the risk of adverse
reactions, harmful eradication of normal intestinal flora, the induction of Shiga toxin
production, and the increase of antimicrobial resistance.
Antimicrobials are to be considered the drugs of choice for empirical treatment of traveler’s
diarrhea and of community-acquired secretory diarrhea when the pathogen is known (see
Figure 11 in the original guideline document).
Considerations with regard to antimicrobial treatment:
➠ Consider antimicrobial treatment for:
ñ Persistent Shigella, salmonella, campylobacter, or parasitic infections
ñ Infections in the aged, immunocompromised patients, and patients with impaired
resistance, sepsis, or with prostheses
ñ Moderate/severe traveler’s diarrhea or diarrhea with fever and/or with bloody
stools – quinolones (co-trimoxazole second choice)
➠ Nitazoxanide is an antiprotozoal and may be appropriate for Cryptosporidium and
other infections, including some bacteria.
➠ Rifaximin is a broad-spectrum, non-absorbed antimicrobial agent that may be useful.
Note well (N.B.):
➠
➠
➠
➠
➠
➠
➠
the convenience of single dosing. For treating most types of common bacterial infection,
the recommended azithromycin dosage is 250 mg or 500 mg once daily for 3 to 5 days.
Azithromycin dosage for children can range (depending on body weight) from 5 mg to 20
mg per kilogram of body weight per day, once daily for 3 to 5 days.
Quinolone-resistant Campylobacter is present in several areas of South-East Asia (e.g., in
Thailand) and azithromycin is then the appropriate treatment.
Treatment for amoebiasis should, ideally, include diloxanide furoate following the
metronidazole, to get rid of the cysts that may remain after the metronidazole treatment.
All doses shown are for oral administration. If drugs are not available in liquid form for use
in young children, it may be necessary to use tablets and estimate the doses given in this table.
Selection of an antimicrobial should be based on the sensitivity patterns of strains of Vibrio
(V.) cholerae O1 or O139, or Shigella recently isolated in the area.
An antimicrobial is recommended for patients older than 2 years with suspected cholera
and severe dehydration.
Alternative antimicrobials for treating cholera in children are trimethoprim/sulfamethoxazole (TMP-SMX) (5 mg/kg TMP + 25 mg/kg SMX, b.i.d. [twice a day] for 3 days),
furazolidone (1.25 mg/kg, q.i.d. [four times a day ] for 3 days), and norfloxacin. The actual
selection of an antimicrobial will depend on the known resistance/sensitivity pattern of V.
cholerae in the region, which requires the availability of a well-established and consistent
surveillance system.
For adults with acute diarrhea, there is good evidence that an ultrashort course (one or
two doses) of ciprofloxacin or another fluoroquinolone reduces the severity and shortens
the duration of acute traveler’s diarrhea. This area is still controversial; use should be limited
to high- risk individuals or those needing to remain well for short visits to a high-risk area.
DIARRHOEAL DISEASES – CHOLERA
➠ Erythromycin is hardly used for diarrhea today. Azithromycin is widely available and has
77
Prevention
Water, sanitation, and hygiene:
ñ Safe water
ñ Sanitation: houseflies can transfer bacterial pathogens
ñ Hygiene: hand washing
Safe food:
ñ Cooking eliminates most pathogens from foods
ñ Exclusive breastfeeding for infants
ñ Weaning foods are vehicles of enteric infection
Micronutrient supplementation: the effectiveness of this depends on the child’s overall
immunologic and nutritional state; further research is needed.
➠
➠
➠
DIARRHOEAL DISEASES – CHOLERA
➠
78
➠
➠
Vaccines:
Salmonella typhi: Two typhoid vaccines currently are approved for clinical use. No available
vaccine is currently suitable for distribution to children in developing countries.
Shigella organisms: Three vaccines have been shown to be immunogenic and protective
in field trials. Parenteral vaccines may be useful for travelers and the military, but are
impractical for use in developing countries. More promising is a single-dose live-attenuated
vaccine currently under development in several laboratories.
V. cholerae: Oral cholera vaccines are still being investigated, and their use is recommended
only in complex emergencies such as epidemics. Their use in endemic areas remains
controversial. In traveler’s diarrhea, oral cholera vaccine is only recommended for those
working in refugee or relief camps, since the risk of cholera for the usual traveler is very
low.
Enterotoxigenic E. coli (ETEC) vaccines: The most advanced ETEC vaccine candidate
consists of a killed whole cell formulation plus recombinant cholera toxin B subunit. No
vaccines are currently available for protection against Shiga toxin-producing E. coli
infection.
Rotavirus: In 1998, a rotavirus vaccine was licensed in the USA for routine immunization
of infants. In 1999, production was stopped after the vaccine was causally linked to
intussusception in infants. Other rotavirus vaccines are being developed, and preliminary
trials are promising. Currently, two vaccines have been approved: a live oral vaccine
(RotaTeqì) made by Merck for use in children, and GlaxoSmithKline’s Rotarixì.
Measles immunization can substantially reduce the incidence and severity of diarrheal
diseases. Every infant should be immunized against measles at the recommended age.
9
Clinical Practice
Adults
Table: The Approach in Adults with Acute Diarrhea
In 2004, WHO and UNICEF revised their recommendations for the management of
diarrhea, including zinc supplementation as an adjunct therapy to oral rehydration. Since then,
the recommendations have been adopted by more than 40 countries throughout the world.
In countries where both the new ORS and zinc have been introduced, the rate of ORS usage
has dramatically increased.
Table: Principles of Appropriate Treatment for Children with Diarrhea and Dehydration
DIARRHOEAL DISEASES – CHOLERA
Children
79
Treatment for Children Based on the Degree of Dehydration
Table: Minimal or No Dehydration
Table: Mild to Moderate
DIARRHOEAL DISEASES – CHOLERA
Table: Severe Dehydration
80
Cautionary Note: Treating a patient with severe dehydration due to infectious diarrhea with 5% dextrose with
1/4 normal saline is unsafe. Severe dehydration occurs, usually as a result of bacterial infection (cholera, ETEC),
which usually leads to more sodium loss in feces (60 to 110 mmol/L). A 1/4 normal saline solution contains
sodium (Na) 38.5 mmol/L, and this does not balance the sodium losses. Intravenous infusion with 5% dextrose
with 1/4 normal saline will thus lead to severe hyponatremia, convulsion, and loss of consciousness. Five
percent dextrose with 1/2 standard normal saline can only be used when Ringer’s lactate is not available.
The Therapeutic Approach
to Acute Bloody Diarrhea (Dysentery) in Children
The main principles are: treatment of dehydration; stool cultures and microscopy to guide
therapy; and frequent smaller meals with higher protein intakes. (See Figure 15 in the original
guideline document for an algorithm for the therapeutic approach to acute bloody diarrhea
[dysentery] in children.)
With ORS, uncomplicated cases of diarrhea in children can be treated at home, regardless
of the etiologic agent. Caregivers need proper instructions regarding signs of dehydration, when
children appear markedly ill, or do not respond to treatment. Early intervention and
administration of ORS reduces dehydration, malnutrition, and other complications and leads
to fewer clinic visits and potentially fewer hospitalizations and deaths.
Self-medication in otherwise healthy adults is safe. It relieves discomfort and social
dysfunction. There is no evidence that it prolongs the illness.
In adults who can maintain their fluid
intake, ORS does not provide any benefits.
It does not reduce the duration of diarrhea
or the number of stools. In developed
countries, adults with acute watery diarrhea
should be encouraged to drink fluids and
take in salt in soups and salted crackers.
Nutritional support with continued feeding
improves outcomes in children.
Among hundreds of over-the-counter
products promoted as antidiarrheal agents,
only loperamide and bismuth subsalicylate
have sufficient evidence of efficacy and
safety.
Principles of self-medication:
➠ Maintain adequate fluid intake.
➠ Consumption of solid food should be
guided by appetite in adults – small light
meals.
➠ Antidiarrheal medication with loperamide
(flexible dose according to loose bowel movements) may diminish diarrhea and shorten
the duration.
➠ Antimicrobial treatment is reserved for prescription only in residents’ diarrhea or for
inclusion in travel kits (add loperamide). Family knowledge about diarrhea must be
reinforced in areas such as prevention, nutrition, ORT/ORS use, zinc supplementation, and
when and where to seek care (see “Indications for In-Patient Care” above). Where feasible,
families should be encouraged to have ORS ready-to-mix packages and zinc (syrup or
tablet) readily available for use, as needed.
DIARRHOEAL DISEASES – CHOLERA
Home Management of Acute Diarrhea
81
Cascades
A cascade is a hierarchical set of diagnostic or therapeutic techniques for the same disease,
ranked by the resources available.
Cautions:
DIARRHOEAL DISEASES – CHOLERA
➠ If facilities for referral are
82
available, patients with severe
dehydration (at risk of acute
renal failure or death) should be
referred to the nearest facility
with intravenous fluids (levels 5
and 6 cannot replace the need for
referral in case of severe dehydration).
➠ Levels 5 and 6 must be seen as
interim measures and are better
than no treatment if no intravenous facilities are available.
➠ When intravenous facilities are
used, it must be ensured that
needles are sterile and that
needles and drip sets are never
reused, to avoid the risk of hepatitis B and C.
➠ Do not diagnose moderate
dehydration as severe dehydration and thus initiate referral for
intravenous feeding because oral
rehydration is more time-consuming. It is in the mother’s
interest to avoid the unnecessary
complications that may be associated with using intravenous
therapy.
Table: Cascade for Acute Watery Diarrhea –
Cholera-like, with Severe Dehydration
Table: Cascade for Acute Watery Diarrhea, with
Mild/Moderate Dedydration
Table: Acute Bloody Diarrhea, with
Mild/Moderate Dehydration
Notes:
➊ Tetracycline is not recommended in children.
➋ Nasogastric (NG) feeding is not very
feasible for healthy and active older
children, but it is suitable for malnourished,
lethargic children.
➌ NG feeding requires skilled staff.
➍ Often, intravenous fluid treatment is more
easily available than NG tube feeding.
➎ NG feeding (ORS and diet) is especially
helpful in long-term severely malnourished
children (anorexia).
13
Benefits/Harms
of implementing the guidelines recommendatios
Potential Benefits
➠ Appropriate diagnosis, treatment, and management of acute diarrhea in children and
adults
Potential Harms
➤ Antimicrobials: In adults, the clinical benefit of antimicrobials should be weighed against
➤
➤
➤
➤
the cost, the risk of adverse reactions, harmful eradication of normal intestinal flora, the
induction of Shiga toxin production, and the increase of antimicrobial resistance.
Tetracycline is not recommended in children.
Loperamide should be avoided in bloody or suspected inflammatory diarrhea (febrile
patients).
Use of ciprofloxacin or another fluoroquinolone is still controversial; use should be limited
to high-risk individuals or those needing to remain well for short visits to a high-risk area.
Diarrhea vaccine use remains controversial.
DIARRHOEAL DISEASES – CHOLERA
➠ Reduced morbidity and mortality from acute diarrhea
83
DIARRHOEAL DISEASES – CHOLERA
Cholera
84
Cholera is a diarrhoeal disease caused by infection of the intestine with the bacterium Vibrio
cholerae, either type 01 or 0139. Both children and adults can be infected.
About 20% of those who are infected develop acute, watery diarrhoea – 10-20% of these
individuals develop severe watery diarrhoea with vomiting. If these patients are not promptly
and adequately treated, the loss of such large amounts of fluid and salts can lead to severe
dehydration and death within hours.
The case-fatality rate in untreated cases may reach 30-50%.
Treatment is straightforward (basically rehydration) and, if applied appropriately, should
keep case-fatality rate below 1%.
Cholera is usually transmitted through faecally contaminated water or food and remains
an ever- present risk in many countries.
New outbreaks can occur sporadically in any part of the world where water supply,
sanitation, food safety, and hygiene are inadequate. The greatest risk occurs in over-populated
communities and refugee settings characterized by poor sanitation, unsafe drinking-water,
and increased person-to-person transmission. Because the incubation period is very short (2
hours to 5 days), the number of cases can rise extremely quickly.
It is impossible to prevent cholera from being introduced into an area – but spread of
the disease within an area can be prevented through early detection and confirmation of
cases, followed by appropriate response. Because cholera can be an acute public health
problem – with the potential to cause many deaths, to spread quickly and eventually
internationally, and to seriously affect travel and trade – a well coordinated, timely, and
effective response to outbreaks is paramount. Response activities should always be followed
by the planning and implementation of preparedness activities that will allow future cholera
outbreaks to be dealt with more effectively.
A strong cholera preparedness plan and programme is the best preparation for outbreaks
in countries at risk of cholera, whether or not they have yet been affected, or countries in
which seasonal recurrence of the disease may be expected.
New Strategies: Oral Cholera Vaccines
In the long term, improvements in water supply, sanitation, food safety and community
awareness of preventive measures are the best means of preventing cholera, as well as other
diarrhoeal diseases. However, WHO is currently evaluating the use of newer tools to
complement these traditional measures. Oral cholera vaccines of demonstrated safety and
effectiveness have recently become available for use by individuals. Some countries have
already used oral vaccine to immunize populations considered to be at high risk for cholera
outbreaks. Use of these vaccines in both endemic and epidemic situations requires further
assessment.
Work is under way to investigate the role of mass vaccination as a public health strategy
for protecting at-risk populations against cholera. Issues being addressed include logistics,
cost, timing, vaccine production capacity, and criteria for the use of mass vaccination to
contain and prevent outbreaks.
Case Definition
It is most important to ascertain that all patients considered to be cholera cases in fact have
the same disease. According to the WHO case definition, a case of cholera should be suspected
when:
➣ in an area where the disease is not known to be present, a patient aged 5 years or
more develops severe dehydration or dies from acute watery diarrhoea;
➣ in an area where there is a cholera epidemic, a patient aged 5 years or more develops
acute watery diarrhoea, with or without vomiting.
Laboratory Confirmation
The treatment of dehydrated patients should not be delayed until laboratory testing of
samples has been completed. Microbiological confirmation of Vibrio cholerae by direct
observation can be obtained immediately, but it usually takes 2 days to get culture results.
It is important to gather information on:
➣ serogroup of Vibrio (O1 or O139);
➣ antimicrobial sensitivity patterns.
15
DIARRHOEAL DISEASES – CHOLERA
A case of cholera is confirmed when Vibrio cholerae O1 or O139 is isolated from any
patient with diarrhoea.
In children under 5 years of age, a number of pathogens can produce symptoms similar to
those of cholera, such as rice-water diarrhoea. To maintain specificity, therefore, children under
5 are not included in the case definition of cholera.
85
Improved Preparedness and Treatment
Training of health workers is an essential element for preparedness, especially in high-risk
areas. Emergency supply needs should be evaluated in the light of the particular situation:
➠ likely attack rate in refugee camps, with high-risk populations (because of malnutrition),
is 5-8%;
➠ in open settings, an attack rate of 0.2% might be used;
➠ in rural communities of 5000 people or less, the attack rate might reach 2%.
Emergency stocks of basic supplies should be prepared so that they can be mobilized quickly.
Rehydration
DIARRHOEAL DISEASES – CHOLERA
Rehydration with replacement of electrolytes lost is the mainstay of cholera treatment.
According to the dehydration stage (A, B, C), the patient should receive different rehydration
therapy (oral or intravenous fluids). Oral rehydration solution (ORS) should be used during and
after IV therapy. Surveillance of the patient is crucial during the early stage of treatment.
86
Intravenous Therapy for Severe Cases
Ringer’s lactate is the preferred IV fluid. Normal (9%) saline or halfnormal saline with 5%
glucose can also be used, but ORS solution must be given at the same time to replace the
missing electrolytes. Plain glucose solution is not effective in rehydrating cholera patients.
When IV rehydration is not possible and the patient cannot drink, ORS solution can be
given by nasogastric tube. However, nasogastric tubes should not be used for patients who
are unconscious.
16
Antibiotics
They should be given only in severe cases, to reduce the duration of symptoms and
carriage of the pathogen.
Antimicrobial resistance is increasing. In most countries Vibrio cholera is resistant to cotrimoxazole; in some settings it has also developed resistance to tetracycline. The laboratory
should be asked about patterns of resistance of the strain at the beginning of and during the
outbreak: antibiotic sensitivity to antibiotics may return after a certain period.
Mass chemoprophylaxis is not effective in controlling a cholera outbreak.
Selective chemoprophylaxis (one dose of doxycycline) may be useful for members of a
household who share food and shelter with a cholera patient. However, in societies where
intimate social mixing and the exchange of food between households are common, it is
difficult to identify close contacts. Nevertheless, chemoprophylaxis may be useful when a
cholera outbreak occurs in a closed population, such as a prison.
Health Education
The most important messages to prevent the family from being contaminated are:
ENSURE A SAFE SUPPLY OF WATER
Access to safe water is a basic requirement for health, and it is more critical when there
and epidemic dysentery, every effort must be made to provide safe drinking- water, and safe
water for food preparation and for personal hygiene.
Each person should have at least 20 litres of water a day for drinking, cooking and
washing. Health facilities need 40-60 litres per patient a day to maintain adequate levels of
hygiene. Every family should know how to treat water so that it will be safe for drinking.
Piped water, or water that is delivered in trucks or drums, must be adequately chlorinated.
Environmental sanitation workers can test water to be sure that the amount of chlorine is
adequate. Other sources of water are usually contaminated (e.g. rivers, shallow wells), so you
must take measures to reduce the risk of people becoming ill. You may have to close the water
source or provide another source of safe water. If that is not possible, be sure that people
using the water know how to make it safe.
DIARRHOEAL DISEASES – CHOLERA
is an outbreak of diarrhoeal disease. Since contaminated water can be the source of cholera
87
FOOD SAFETY
Cholera and dysentery can be transmitted through contaminated food. Food may be
contaminated before, during or after preparation. Raw or undercooked seafood, and foods
cooked and then kept at room temperature for several hours are especially dangerous. Fruits
and vegetables may be contaminated if they were fertilized with human waste (nightsoil),
irrigated with contaminated water or “freshened” with contaminated water.
HAND WASHING
People can prevent the transmission of cholera and dysentery by washing their hands.
Careful and frequent hand-washing is especially important to stop the transmission of
dysentery. If soap is expensive, or not available, ashes or mud can be used instead. Children,
as well as adults, should wash their hands.
Hand Washing is highly recommended:
➠
➠
➠
➠
➠
after defecation
after any contact with stools (cleaning up after children or patients)
before preparing food
before eating food
before feeding children.
DIARRHOEAL DISEASES – CHOLERA
ENVIRONMENTAL SANITATION
88
In the long term, cholera and dysentery will become rare as environmental hygiene and
water supplies improve. However, in areas where sanitation is poor, you must use temporary
measures to guarantee that stools are disposed of safely when there is an outbreak of
diarrhoeal disease.
The methods to apply are:
➠ not to defecate on the ground or near a water supply
➠ to wash hands with soap or ash after any contact with stools
➠ to dispose of children’s stools in toilets, in latrines, or to bury the stools
➠ to build and use latrines
➠ if there is no latrine, to bury the stools away from water sources, as a temporary
measure.
➠ safe practices at funerals (discourage ritual washing of the dead, hold the funeral soon
after death ensure that people who clean up and prepare the body in the hospital
do not prepare food or serve food etc)
INEFFECTIVE CONTROL MEASURES
The measures described in this section do not stop the spread of epidemics. However,
pressure to use them may come from a frightened public or from uninformed officials. When
ineffective measures are carried out, it gives a false sense of security, and wastes time and
resources that could be used on efforts that are truly effective.
Vaccination: No vaccine currently exists for Shigella dysenteriae type 1. The old parenteral
cholera vaccine is not recommended. Two new oral cholera vaccines offer high-level shortterm protection; they are available for use in travellers in a few countries, but are not
yet recommended for large scale public health use.
Trade and travel restrictions (cordon sanitaire) : It is not possible to detect and isolate all
infected travellers, most of whom have no signs of illness. A cordon sanitaire requires
setting up check- posts and restricting movement. This diverts substantial resources from
more effective control measures. Trade and travel restrictions disrupt the economy of an
area, which may encourage suppressing information about outbreaks.
Mass chemoprophylaxis for cholera: Mass chemoprophylaxis – treating an entire community
with antibiotics – does not limit the spread of cholera. In some places, it contributed to
making the vibrio resistant to antibiotics, which deprives severely ill patients of a valuable
treatment. Selective chemoprophylaxis is usually not recommended. It is justified only if
surveillance shows that the secondary attack rate in the community is high (an average of at
least one household member in five becoming ill after the first case occurs in the household).
If selective chemoprophylaxis is used, it should be given to all close contacts as soon as
possible after the initial case is recognized. The prophylactic dose of antibiotics is the same
as the therapeutic dose. Doxycycline is preferred because only a single dose is needed.
Antibiotic chemoprophylaxis for dysentery: Giving people antibiotics for dysentery before
they become ill does not prevent dysentery and worsens the problem of antibiotic
resistance. It should never be done.
Surveillance of Patients with Severe Cholera
➠
➠
➠
➠
➠
pulse;
dehydration signs;
number and appearance of stools;
respiratory rhythm;
temperature (cholera usually provokes hypothermia – if the temperature is high there
may be associated pathology, e.g. malaria);
➠ urine (present or not);
➠ state of consciousness.
Complications
➠ pulmonary oedema if excessive IV fluid has been given;
➠ renal failure if too little IV fluid is given;
➠ hypoglycaemia and hypokalaemia in children with malnutrition rehydrated with
Ringer lactate only.
DIARRHOEAL DISEASES – CHOLERA
Surveillance and regular reassessment of patients for the following are crucial:
89
References
ñ Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral
rehydration, maintenance, and nutritional therapy . Atlanta, GA: Centers for Disease Control and
Prevention – Federal Government Agency [U.S.]. 2003 Nov 21.
ñ UNICEF/WHO. Clinical management of acute diarrhea: UNICEF/WHO Joint Statement, May 2004
http://www.who.int/child-adolescenthealth/New_Publications/CHILD_HEALTH/ISBN_92_4_159421_7.pdf
ñ World Health Organization. Production of zinc tablets and zinc oral solutions: guidelines for
programme managers and pharmaceutical manufacturers. Geneva: World Health Organization
http://www.who.int/ child-adolescent-health/publications/CHILD_HEALTH/ISBN_92_4_159494_2.htm
ñ World Health Organization. The treatment of diarrhea: a manual for physicians and other senior
health workers, 4th rev. ed. Geneva: World Health Organization, 2005 http://www.who.int/childadolescent- health/New_Publications/CHILD_HEALTH/ISBN_92_4_159318_0.pdf
ñ The treatment of diarrhoea – a manual for physicians and other senior health workers. Geneva, World
Health Organization, 1995 (WHO/CDR/95.3).
ñ WHO recommended strategies for prevention and control of communicable diseases. Geneva, World
Health Organization, 2001 (WHO/CDS/CPE/SMT/2001.13).
ñ Hanquet G. Refugee health – an approach to emergency situations. London, Médecins Sans
Frontières/Macmillan, 1997.
ñ Guidelines for cholera control. Geneva, World Health Organization, 1993.
ñ Guidelines for the collection of clinical specimens during field investigation of outbreaks. Geneva,
World Health Organization, 2000 (WHO/CDS/CSR/EDC/2000.4).
ñ Handbook for emergency field operations. Geneva, World Health Organization, 1999 (EHA/FIELD/-
DIARRHOEAL DISEASES – CHOLERA
99.1).
90
Case Study: Rivas District Outbreak
Read the descriptions and then write brief answers to the questions (write key words instead of complete
sentences). You may look in your modules, if you need help in answering the questions. Notify the
facilitator if you cannot understand a question, and when you have finished. There will be a discussion
afterwards.
Background
Rivas District has a population of 100 000. About half the people live in Rivas Town, and the others
live in scattered villages. The town, which has piped water and sewerage, includes a very crowded
neighbourhood, Bayside, where sanitation is poor and there is no trained health worker. Village A is a
prosperous farming village, with a well-functioning health centre. Most families have latrines and get
water from a borehole. Some people in Village A use shallow wells during the rainy season (October
to March) because the wells are closer than the borehole. Village B (about 5000 people) is further from
the town, on poor roads, and has a health post staffed by a nurse who has not been trained in case
management of diarrhoea in years. The nurse is unhappy at being posted to a rural clinic, and often
escapes to town. Water is from shallow wells and the river, and very few families have latrines.
The district shares a border with the neighbouring country, and there is much traffic across the
border, especially during the yearly festival in Rivas Town. There was an outbreak of cholera in 1991, but
none has been reported since then. The District Medical Officer wants to be sure the district is ready if
another outbreak occurs.
Q1: What are the main things that should be done to prepare for an outbreak?
Q2: If cholera or epidemic dysentery should appear in the district, are there groups or individuals at high
you think they are at risk.
High risk of getting ill:
High risk of dying once ill:
Week of 9-15 January
The District Medical Officer has made an Epidemic Preparedness Plan. On Monday, the District
Medical Officer gets a phone call from the nurse in village A. The nurse is concerned because a 4- yearold boy from the village presented to the clinic with severe dehydration caused by acute watery
diarrhoea, and died while being treated.
Q3: Should the District Medical Officer start the Epidemic Preparedness Plan?
Explain why or why not.
DIARRHOEAL DISEASES – CHOLERA
risk of getting ill? Are there any at high risk of dying, once they are ill? Name them and explain why
91
The nurse from village A calls again on Tuesday. She has treated the sister, the mother and the father
of the boy who died, all for acute watery diarrhoea. She has also treated 6 other people from village A
for acute watery diarrhoea. The District Medical Officer asked the nurse to tell him the age of each
patient, their degree of dehydration and the outcome of their treatment. These were the cases:
Q4: On the list above, put a check next to each patient who meets the casedefinition for
reporting a case of cholera.
Q5: Should the District Medical Officer start the Epidemic Preparedness Plan? Explain why or
why not.
The District Medical Officer decided to call a meeting of the Epidemic Control Committee.
Q6: What four things do you think the Epidemic Control Committee should do first?
DIARRHOEAL DISEASES – CHOLERA
Q7: What are the duties of the Epidemic Control Committee?
92
Week of 16-22 January
There have been more cases of cholera in village A. The nurse and the District Medical
Officer investigated the cases in village A. They found that, about a week before the fouryear-old became ill, he and his family had attended the funeral in village B of a man who died
of diarrhoea. The District Medical Officer checked the records, and found that the nurse
posted to village B had not sent in any reports for two months.
Q8: What should the District Medical Officer do?
Q9: What control measures should NOT be carried out?
Week of 23-29 January
The District Medical Officer receives a laboratory report that confirms cholera.
The Rivas Epidemic Control Committee decides to send a Mobile Control Team to village
B to open a Temporary Treatment Centre.
Q10: What should the team look for when choosing a site for the Temporary Treatment
Centre?
When they arrived in village B, the Mobile Control Team found that cases that met the
cholera case-definition had been occurring there since before the first cases in village A. The
first cases in village A happened in the week of 9-15 January. The team made this table:
Q11: In what week was there the highest number of deaths? In what week did patients with
suspected cholera have the greatest risk of dying?
Q12: How could the deaths have been prevented?
Cholera has arrived in Rivas Town and is spreading in the crowded Bayside neighbourhood.
The town officials urge the District Medical Officer not to say there is an outbreak, because
the town’s yearly festival is only two weeks away, and they fear that people will not come
when there is news of an outbreak.
The epidemic has declined in villages A and B, but continues in the town. Water testing
has shown that the town’s piped water is not sufficiently chlorinated. An environmental
health technician also discovered that people in bayside area had dug holes down to the
water mains and pierced the mains. This created little wells” from which they got water. It
also allowed contamination into the water mains.
Q14: What should be done?
Teams were sent to Bayside to look for patients and to educate the community there on
prevention measures. These are the problems that the team found:
a. the residents could not afford soap
b. the residents could not afford the fuel needed to boil their water
c. men who worked far from home usually carried a home-cooked lunch with them to
work, and ate the lunch 6-8 hours after it had been cooked.
DIARRHOEAL DISEASES – CHOLERA
Q13: What should the District Medical Officer do?
93
Q15: What advice should the team give to solve each problem?
a. (soap)
b. (fuel needed to boil the water)
c. (home-cooked lunch eaten 6-8 hours after it had been cooked).
Week of 6-12 January
The District Medical Officer did send notification of the urban outbreak of cholera, and
began an intensive health education campaign. Many people came to the festival, although
fewer than in the past. Many visitors arrived from the neighbouring country.
Q16: What precautions should be observed to safeguard the health of the people who
attend the festival?
Health officials in the neighbouring country got news of the cholera outbreak the day
before the festival ended. They read about it in the newspaper and immediately ordered
border guards to screen all returning travellers for signs of diarrhoea, and to isolate those who
were ill.
Q17: Will this keep the outbreak from spreading? Explain your answer.
Week of 13-19 January
DIARRHOEAL DISEASES – CHOLERA
The outbreak ended.
Q18: What should the District Medical Officer and the communities involved do now?
94
FIELD EXERCISE
Cholera Theatment Center – Setting up a CTC
General Objective
To provide participants with basic principles of setting up a Cholera Treatment Center (CTC).
Specific objectives
At the end of the exercise, participants will be familiar with:
➠ Screening, admission and observation
➠ Hospitalisation of severely dehydrated patients
➠ Recovery
➠ Neutral area
➠ Mortuary
➠ Water, Hygiene and Sanitation
Case scenario:
A Cholera outbrake occur in a big slum close to your mission area.
Your team has set up a Cholera Treatment Center behind the local hospital.
You are about to screen and treat a few thousands the next weeks. A few of them should
be admitted for parenteral support.
Design an overall map of the CTC and try to find practical ways to make better use of
the space.
Design and architecture of a CTC: the principles
Organisation and design of a CTC are based on simple principles and rules. Patients are
first screened and diagnosed, then sent to specific areas for treatment according to their
status. The CTC is organised in separate areas, following two key principles:
➠ Isolation of the entire facility from other public structures (dispensary, school, market)
➠ Separation of patients (contaminated area) from the “neutral area” (not contaminated)
DIARRHOEAL DISEASES – CHOLERA
Content
95
DIARRHOEAL DISEASES – CHOLERA
Screening, admission and observation
96
Patients are examined by a medical person for screening. If cholera, admit; otherwise send
to normal dispensary.
Patients are admitted with 1 attendant (caregiver). Patients who are admitted are
registered (cholera register). Moderate or mild cases receive oral rehydration therapy in
observation where they stay under medical observation for 6 hours. Patients stay under tents
or shelters, on mats or benches and will be discharged directly from there.
Severely dehydrated persons or those with uncontrollable vomiting should be hospitalized
directly: see hospitalization.
Hospitalisation of severely dehydrated patients
Patients with severe dehydration and/or uncontrollable vomiting must be hospitalized for
immediate rehydration.
Each patient lies on a pierced bed with 1 bucket for stool collection underneath + 1 bucket
for vomit besides the bed.
Patients needing specific management (children, elderly, pregnant women) should be
regrouped in specific wards.
Do not exceed 20 patients per ward.
Recovery
For oral rehydration after hospitalisation when less surveillance is required. Patients stay
on mats or benches, as in the observation area.
Neutral area
Includes office space, rest area, changing room for staff, pharmacy and logistic stores,
water storage, preparation of chlorine solutions, kitchen.
Logistic store and pharmacy must be organized to ensure at least 7 days autonomy. In case
of reduced access/security constraints, stocks should be increased to avoid any shortage.
Mortuary
Must be isolated from other areas.
Water, Hygiene and Sanitation
➠ 60 litres of safe (chlorinated) water are needed per 1 CTC patient per day (this includes
DIARRHOEAL DISEASES – CHOLERA
needs for drinking water, food, hygiene of the patient and the caregiver).
➠ S u fficient storage capacity for 3 days must be ensured in order to avoid any shortage.
➠ Label and clearly differentiate each container (drinking water, ORS, chlorine solutions).
➠ 0.05% chlorine for hand washing, dish rinsing and bathing of soiled patients, 0.2%
chlorine for disinfecting floors, beds, clothes and footbaths, and 2% for disinfecting
of vomit, faeces and corpses.
97
chapter 3
Management of acute
and chronic malnutrition
General Objective
Introduce the basic principles of medical management and program intervention in acute
or chronic malnutrition crises using the most recent innovations in the field.
At the end of the session, participants will be familiar with:
➠ Epidemiological and socioeconomic framework of malnutrition
➠ The physiological basis of acute and chronic malnutrition and its impact on health
status
➠ Analysis of the later technical innovations and their impact in the development of
newer approaches to the management of malnutrition at individual and polulation
level
➠ Future challenges, technical and political developments
Content
➠ Global burden of acute and chronic malnutrition and the socio-political context
➠ Physiological basis of acute and chronic malnutrition
➠ The CTC (Community-based Therapeutic Care) model and the classic TFC (Treatment
Feeding Center aproach)
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Specific Objectives
99
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
➠
➠
➠
➠
100
Short presentation of the CTC model WHO guidelines for inpatient care
RUTF (Ready-to-Use-Therapeutic-Feeding)
Set up and resources needed for TFCs (Therapeutic Feeding Centers)
Hierarchy of nutritional interventions in emergency contexts
Future developments and the funding gap
Examples of case studies
Worldwide there are approximately 13 million children suffering from severe acute
malnutrition, and estimates are expected to climb to approximately 20 million when the new
WHO growth standards are applied. In 2006, two publications in Lancet highlighted the global
burden of acute malnutrition and emphasized that it is not just a by-product of conflict or
famine. In fact, two-thirds of the world’s wasted children live in India, Pakistan and
Bangladesh. Rates of wasting do not automatically decline with political and economic growth
India and Brazil both have good economic growth but rates of wasting remain high. Moreover,
in sub-Saharan Africa a high proportion of severely malnourished children admitted for care
are HIV positive. While development programs have traditionally focused on preventing
malnutrition and must continue to do so, high rates of acute malnutrition and improved
treatment protocols are demanding that we re-examine our efforts to address the needs of
acutely malnourished children. Our neglect to do so may contribute to considerable numbers
of avoidable deaths.
Severe malnutrition has traditionally been managed in inpatient facilities. However, in
several large-scale humanitarian crises in the 1990’s, it became evident that the traditional
therapeutic feeding centre (TFC) model of inpatient care was unable to provide an effective
response. For example, during the famine in south Sudan in 1998, only a small proportion
of acutely malnourished people were treated in NGO-run TFCs. Access was a considerable
obstacle, and coverage was very limited. Community-based Therapeutic Care (CTC) was
designed to address these limitations. Its underlying aims are to maximise coverage and
access. In practice, this means prioritising providing care for the majority of the acutely
malnourished over inpatient care for a few extreme cases. This can only be done by providing
treatment in people’s homes. Community mobilisation techniques are used to engage the
affected population and maximise coverage.
Within this new conceptions outlined above, participants will be introduced to treatment
and management protocols, admission and discharge criteria, assessment tools and the
hierarchy of nutrition interventions in emergencies. They will also be presented with case
study examples that will assist summarize the module.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Introduction
101
Methodology
➠ Lecture/discussion format
➠ Case studies
➠ Post learning assessment questions
Global burden of acute and chronic
malnutrition and the socio-political context 1
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Malnutrition is rarely regarded as an emergency, the children affected are not facing famine
and betray few or no obvious signs. Yet the largely invisible crisis of malnutrition is implicated
in more than half of all child deaths worldwide and violates children’s rights in profound ways,
compromising their physical and mental development and helping perpetuate poverty. More
widespread than many suspect –with one out of every three children affected– malnutrition
lowers the productivity and abilities of entire societies. This chapter examines the scale of this
intractable tragedy, the approaches that are helping resolve it and the new light that scientific
research is shedding on it.
102
Global burden and consequences of malnutrition
Malnutrition is usually the result of a combination of inadequate dietary intake and infection.
In children, malnutrition is synonymous with growth failure — malnourished children are
shorter and lighter than they should be for their age. To get a measure of malnutrition in a
population, young children can be weighed and measured and the results compared to those
of a reference population known to have grown well. Measuring weight and height is the
most common way of assessing malnutrition in populations. Although many people still refer
to growth failure as “protein-energy malnutrition”, or PEM, it is now recognized that poor
growth in children results not only from a deficiency of protein and energy but also from an
inadequate intake of vital minerals (such as iron, zinc and iodine) and vitamins (such as vitamin
A), and often essential fatty acids as well.
1. Adapted from the document “Progress for Children”, UNICEF Report on Nutrition, April 2006.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
These minerals are needed in tiny quantities, on the order of a few thousands of a gram
or less each day. They are consequently called micronutrients. Micronutrients are needed for
the production of enzymes, hormones and other substances that are required to regulate
biological processes leading to growth, activity, development and the functioning of the
immune and reproductive systems. All of the minerals that the body needs –calcium,
phosphorous, iron, zinc, iodine, sodium, potassium and magnesium, for example– have to
come either from the food we eat or from supplements. While the body manufactures many
of the complex organic molecules it needs from simpler building blocks, the vitamins – A,
the B complex, C and so on – are not synthesized. Vitamin D is exceptional in that it can be
made in the skin, providing a person has sufficient exposure to direct sunlight. While
micronutrients are needed at all ages, the effects of inadequate intake are particularly serious
during periods of rapid growth, pregnancy, early childhood and lactation. We are learning
more every day about the importance of micronutrients for the physical and the cognitive
development of children. While widespread moderate malnutrition may not be obvious unless
children are weighed and measured, some severely malnourished children develop clinical
signs that are easily observed – severe wasting (or marasmus) and the syndrome known as
kwashiorkor, with skin and hair changes and swelling of arms and legs. Despite years of
research, the reasons why some children develop kwashiorkor and why others develop
marasmus remains a mystery. What is clear is that left untreated, children with either
condition are at high risk of dying from severe malnutrition, and that both kwashiorkor and
marasmus can be prevented by ensuring an adequate intake of nutritious food and freedom
from repeated infections. Less severe forms of malnutrition also cause death, mostly because
they weaken children’s resistance to illness.
The 1990 World Summit for Children singled out deficiencies of three micronutrients –iron,
iodine, and vitamin A– as being particularly common and of special concern for children and
women in developing countries. Recently, knowledge of the prevalence and importance of
zinc for child growth and development has placed it in that league as well. Vitamin D
deficiency is now recognized as a major problem of children in countries such as Mongolia,
the northern parts of China and some of the countries of the Commonwealth of Independent
States that have long winters. Throughout this module, the term malnutrition is used to refer
to the consequences of the combination of an inadequate intake of protein energy,
micronutrients and frequent infections.
Malnutrition is implicated in more than half of all child deaths worldwide – a proportion
unmatched by any infectious disease since the Black Death in the middle ages. Yet it is not an
infectious disease. Millions of survivors are left crippled, chronically vulnerable to illness – and
intellectually disabled. It imperils women, families and, ultimately, the viability of whole
societies. It undermines the struggle of the United Nations for peace, equity and justice. It
is a violation of child rights that undermines virtually every aspect of UNICEF’s work for the
survival, protection and full development of the world’s children. Yet the worldwide crisis
of malnutrition has stirred little public alarm, despite substantial and growing scientific
103
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
104
evidence of the danger. More attention is lavished on world stock markets than on
malnutrition’s vast destructive potential – or on the equally powerful benefits of sound
nutrition, including mounting evidence that improved nutrition, such as an adequate intake
of vitamin A and iodine, can bring profound benefits to entire populations. Malnutrition is
a silent emergency.
But the crisis is real, and its persistence has profound and frightening implications for
children, society and the future of humankind. Malnutrition is not, as many think, a simple
matter of whether a child can satisfy her appetite. A child who eats enough to satisfy
immediate hunger can still be malnourished. And malnutrition is not just a silent emergency
– it is largely an invisible one as well. Three quarters of the children who die worldwide of
causes related to malnutrition are what nutritionists describe as mildly to moderately
malnourished and betray no outward signs of problems to a casual observer. Malnutrition’s
global toll is also not mainly a consequence of famines, wars and other catastrophes, as is
widely thought; in fact, such events are responsible for only a tiny part of the worldwide
malnutrition crisis. But such emergencies, like the ongoing crises in the Great Lakes region
of Central Africa and in the Democratic People’s Republic of Korea, often result in the severest
forms of malnutrition. Meeting food needs in these situations is essential, but so is protecting
people from illness and ensuring that young children and other vulnerable groups receive
good care. Child malnutrition is not confined to the developing world. In some industrialized
countries, widening income disparities, coupled with reductions in social protection, are
having worrying effects on the nutritional well-being of children.
Whatever the misconceptions, the dimensions of the malnutrition crisis are clear. It is a
crisis, first and foremost, about death and disability of children on a vast scale, about women
who become maternal mortality statistics partly because of nutritional deficiencies and about
social and economic costs that strangle development and snuff out hope. Malnutrition has
long been recognized as consequence of poverty. It is increasingly clear that it is also a cause.
In some parts of the world, notably Latin America and East Asia, there have been dramatic
gains in reducing child malnutrition. But overall, the absolute number of malnourished
children worldwide has grown. Half of South Asia’s children are malnourished. In Africa, one
of every three children is underweight, and in several countries of the continent, the
nutritional status of children is worsening. Malnourished children are much more likely to die
as a result of a common childhood disease than those who are adequately nourished. And
research indicates a link between malnutrition in early life –including the period of foetal
growth– and the development later in life of chronic conditions like coronary heart disease,
diabetes and high blood pressure, giving the countries in which malnutrition is already a major
problem new cause for concern. The most critically vulnerable groups are developing foetuses,
children up to the age of three and women before and during pregnancy and while they are
breastfeeding. Among children, malnutrition is especially prone to strike those who lack
nutritionally adequate diets, are not protected from frequent illness and do not receive
adequate care.
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Illness is frequently a consequence of malnutrition – and malnutrition is also commonly
the result of illness. Malaria, a major cause of child deaths in large parts of the world, also
takes a major toll on child growth and development. In parts of Africa where malaria is
common, about one third of child malnutrition is caused by malaria. The disease also has
dangerous nutritional consequences for pregnant women. In addition, pregnant women are
more susceptible to malaria, and children born to mothers with malaria run a greater chance
of being born underweight and anaemic. There is no one kind of malnutrition. It can take a
variety of forms that often appear in combination and contribute to each other, such as
protein energy malnutrition (PEM), iodine deficiency disorders and deficiencies of iron and
vitamin A, to name just a few. Many involve deficiencies of “micronutrients” – substances like
vitamin A and iodine that the human body cannot make itself but that are needed, often in
only tiny amounts, to orchestrate a whole range of essential physiological functions. Each type
of malnutrition is the result of a complex interplay of factors involving such diverse elements
as household access to food, child and maternal care, safe water and sanitation and access to
basic health services.
And each wreaks its own particular kind of havoc on the human body. Iodine deficiency
can damage intellectual capacity; anaemia is a factor in the pregnancy and childbirth
complications that kill 585,000 women annually; folate deficiency in expectant mothers can
cause birth defects in infants, such as spina bifida; and vitamin D deficiency can lead to poor
bone formation, including rickets. Vitamin A deficiency, which affects about 100 million young
children worldwide, was long known to cause blindness. But it has become increasingly clear
that even mild vitamin A deficiency also impairs the immune system, reducing children’s
resistance to diarrhoea, which kills 2.2 million children a year, and measles, which kills nearly
1 million annually. And new findings strongly suggest that vitamin A deficiency is a cause of
maternal mortality as well, especially among women in impoverished regions. At its most basic
level, malnutrition is a consequence of disease and inadequate dietary intake, which usually
occur in a debilitating and often lethal combination.
But many more elements-social, political, economic, cultural – are involved beyond the
physiological. Discrimination and violence against women are major causes of malnutrition.
Women are the principal providers of nourishment during the most crucial periods of children’s
development, but the caring practices vital to children’s nutritional well-being invariably suffer
when the division of labour and resources in families and communities favours men, and when
women and girls face discrimination in education and employment. A lack of access to good
education and correct information is also a cause of malnutrition. Without information
strategies and better and more accessible education programmes, the awareness, skills and
behaviours needed to combat malnutrition cannot be developed. There is, in short, nothing
simple about malnutrition – except perhaps the fact of how vast a toll it is taking. Of the
nearly 12 million children under five who die each year in developing countries mainly from
preventable causes, the deaths of over 6 million, or 55 per cent, are either directly or indirectly
attributable to malnutrition.
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Some 2.2 million children die from diarrhoeal dehydration as a result of persistent
diarrhoea that is often aggravated by malnutrition. And anaemia has been identified as a
contributing factor, if not a principal cause, in 20 per cent to 23 per cent of all post-partum
maternal deaths in Africa and Asia, an estimate many experts regard as conservative. If there
were no other consequences of malnutrition, these horrific statistics would be more than
enough to make its reduction an urgent global priority – and inaction a scandalous affront to
the human right to survival. But the issue goes beyond child survival and maternal mortality
and morbidity. Malnourished children, unlike their well-nourished peers, not only have lifetime
disabilities and weakened immune systems, but they also lack the capacity for learning that
their well-nourished peers have. In young children, malnutrition dulls motivation and curiosity
and reduces play and exploratory activities. These effects, in turn, impair mental and
congnitive development by reducing the amount of interaction children have both with their
environment, and with those who provide care.
Malnutrition in an expectant mother, especially iodine deficiency, can produce varying
degrees of mental retardation in her infant. In infancy and early childhood, iron deficiency
anaemia can delay psychomotor development and impair cognitive development, lowering IQ
by about 9 points. Anaemic pre-schoolers have been found to have difficulty in maintaining
attention and discriminating between visual stimuli. Poor school achievement among primary
school and adolescent children has also been linked to iron deficiency. Low-birthweight babies
have IQs that average 5 points below those of healthy children. And children who were not
breastfed have IQs that are 8 points lower than breastfed children. The depletion of human
intelligence on such a scale –for reasons that are almost entirely preventable– is a profligate,
even criminal, waste. Robbed of their mental as well as physical potential, malnourished
children who live past childhood face diminished futures. They will become adults with lower
physical and intellectual abilities, lower levels of productivity and higher levels of chronic
illness and disability, often in societies with little economic capacity for even minimal
therapeutic and rehabilitative measures.
At the family level, the increased costs and pressures that malnutrition linked disability
and illness place on those who care for them can be devastating to poor families –especially
to mothers, who receive little or no help from strained social services in developing countries.
And when the losses that occur in the microcosm of the family are repeated millions of times
at the societal level, the drain on global development is staggering. In 1990 alone, the
worldwide loss of social productivity caused by four overlapping types of malnutrition
–nutritional stunting and wasting, iodine deficiency disorders and deficiencies of iron and
vitamin A– amounted to almost 46 million years of productive, disability-free life, according
to one reckoning.
Vitamin and mineral deficiencies are estimated to cost some countries the equivalent of
more than 5 per cent of their gross national product in lost lives, disability and productivity.
By this calculation, Bangladesh and India forfeited a total of $18 billion in 1995. Malnourished
children’s low resistance to illness diminishes the effectiveness of the considerable resources
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that are spent to ensure that families have access to basic health services and sanitation. And
investments in basic education by governments and their partners are compromised by
malnutrition’s pernicious effects on brain development and intellectual performance. Iodine
deficiency and iron deficiency anaemia, which threaten millions of children, are especially
worrisome factors as countries strive to improve their educational systems. Iron-deficient
children under the age of two years show problems with coordination and balance and appear
more withdrawn and hesitant. Such factors can hinder a child’s ability to interact with and
learn from the environment and may lead to lower intellectual abilities. Severe iodine
deficiency in utero can cause the profound mental retardation of cretinism. But milder
deficiencies also take an intellectual toll. In the republic of Georgia, for instance, a widespread
iodine deficiency, recently detected, is estimated to have robbed the country of 500,000 IQ
points in the 50,000 babies born in 1996 alone.
Many children suffer from multiple types of malnutrition, so numbers tend to overlap. But
it is reliably estimated that globally 226 million children are stunted – shorter than they should
be for their age, and shorter than could be accounted for by any genetic variation. Stunting
is particularly dangerous for women, as stunted women are more likely to experience
obstructed labour and are thus at greater risk of dying while giving birth. Stunting is
associated with a long-term reduction in dietary intake, most often closely related to repeated
episodes of illness and poor-quality diets.
A study in Guatemala found that severely stunted men had an average of 1.8 fewer years
of schooling than those who were non-stunted, while severely stunted women had, on
average, one year less. The differences are important since every additional year of schooling
translated into 6 per cent more in wages. Some 67 million children are estimated to be
wasted, which means they are below the weight they should be for their height – the result
of reduced dietary intake, illness, or both. About 183 million children weigh less than they
should for their age. In one study, children who were severely underweight were found to be
two to eight times more likely to die within the following year as children of normal weight
for their age. More than 2 billion people –principally women and children– are iron deficient
and the World Health Organization (WHO) has estimated that 51 per cent of children under
the age of four in developing countries are anaemic. In most regions of the developing world,
malnutrition rates have been falling over the last two decades, but at markedly different
paces. The exception is sub-Saharan Africa, where malnutrition rates began increasing in most
countries during the early 1990s, following the regional economic decline that began in the
late 1980s. As government budgets shrank, basic social services and health services were hit
particularly hard. Per capita incomes also declined, affecting people’s ability to purchase food.
In the United States, researchers estimate that over 13 million children –more than one
in every four under the age of 12– have a difficult time getting all the food they need, a
problem that is often at its worst during the last week of the month when families’ social
benefits or wages run out. Over 20 per cent of children in the United States live in poverty,
more than double the rate of most other industrialized countries. In the United Kingdom,
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children and adults in poor families face health risks linked to diet, according to a recent study
that cited high rates of anaemia in children and adults, and of premature and low-weight
births, dental diseases, diabetes, obesity and hypertension. In Central and Eastern Europe,
economic dislocations accompanying the transition to market economies and major cutbacks
in state-run social programmes are having a more profound effect on the most vulnerable.
In the Russian Federation, the prevalence of stunting among children under two years of
age increased from 9 per cent in 1992 to 15 per cent in 1994. And in the Central Asian
republics and Kazakstan, 60 per cent of pregnant women and young children are now
anaemic. The effects of malnutrition also cross generations. The infants of women who are
themselves malnourished and underweight are likely to be small at birth. Overall, 60 per cent
of women of childbearing age in South Asia –where half of all children are underweight–
are themselves underweight. In South-East Asia, the proportion of underweight women is 45
per cent; it is 20 per cent in sub-Saharan Africa.
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The power of good nutrition
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The devastation of malnutrition is hard to overstate, but so is the countervailing power of
nutrition. Not only is good nutrition the key to the healthy development of individuals,
families and societies, but there is also growing reason to believe that improving the nutrition
of women and children will contribute to overcoming some of the greatest health challenges
the world is facing , including the burden of chronic and degenerative disease, maternal
mortality, malaria and AIDS. The most obvious proof of the power of good nutrition can be
seen in the taller, stronger, healthier children of many countries, separated by only a
generation from their shorter, less robust parents, and by the better diets and more healthful,
nurturing environments they enjoy. Stronger children grow into stronger, more productive
adults. Well nourished girls grow into women who face fewer risks during pregnancy and
childbearing, and whose children set out on firmer developmental paths, physically and
mentally.
And history shows that societies that meet women’s and children’s nutritional needs also
lift their capacities for greater social and economic progress. Approximately half of the
economic growth achieved by the United Kingdom and a number of Western European
countries between 1790 and 1980, for example, has been attributed to better nutrition and
improved health and sanitation conditions, social investments made as much as a century
earlier. Even in countries or regions where poverty is entrenched, the health and development
of children and women can be greatly protected or improved. In parts of Brazil, for example,
the percentage of underweight children plummeted from 17 per cent in 1973 to just under
6 per cent in 1996, at a time when poverty rates almost doubled. Much has already been
achieved. For example, 12 million children every year are being spared irreversible mental
Why time is of the essence
A child’s organs and tissues, blood, brain and bones are formed, and intellectual and physical
potential is shaped, during the period from conception through age three. Since human
development proceeds particularly rapidly for the first 18 months of life, the nutritional status
of pregnant and lactating mothers and young children is of paramount importance for a child’s
later physical, mental and social development. It is not an exaggeration to say that the
evolution of society as a whole hinges on the nutrition of mothers and children during this
crucial period of their lives.
The healthy newborn who develops from a single cell –roughly the size of the period at
the end of this sentence– will have some 2 billion cells and weigh an average of 3,250 grams.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
impairment from iodine deficiency because of iodized salt. And more than 60 per cent of
young children around the world are receiving vitamin A supplements.
Some effects of even severe malnutrition on a child’s mental development can be at least
partially reversed. The intelligence of severely malnourished children was found to improve
markedly, for example, when health care, adequate food and stimulation were provided
continually. And there is increasing evidence that good nutrition helps the body resist
infection; that when infection occurs, nutrition relieves its severity and seriousness; and that
it speeds recovery. Thirty years ago, most people could readily accept the notion that a ‘good
diet’ was beneficial to overall health. But the idea that specific nutrients could help fend off
–or, even more outlandishly, help treat– specific diseases smacked of “fringe science”. Today,
through clinical trials and studies, the fringe is edging closer to the mainstream, as nutrition
scientists as well as immunologists, paediatricians and gerontologists test the implications for
public policy of large-scale interventions to improve nutrition and its effects on an array of
critical physiological processes.
Malnutrition, reflected in the poor growth of children and adolescents and the high
prevalence of low-birth weight babies, already has well-known effects on a child’s capacity to
resist illness. It is thus reasonable to argue that in the global fight to reduce childhood death
and illness, initiatives to improve nutrition may be as powerful and important as, for example,
immunization programmes. There are now numerous scientific studies that suggest, but do
not yet prove, that vitamin A deficiency in a mother infected with the human immunodeficiency virus (HIV) may increase her risk of transmitting the virus to her infant.
The world is obligated to ease child malnutrition on the basis of international law, scientific
knowledge, practical experience and basic mortality. The ravages caused by malnutrition on
individuals, families and societies are preventable. The measures needed to reduce and end it
are becoming increasingly well understood. And the gains for humanity from doing so –in
greater creativity, energy, productivity, well-being and happiness– are immeasurable.
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110
Under optimal conditions, the infant will double its birth weight in the first four months of
life; by its third birthday, a healthy child will be four and a half times as heavy. Brain cells
proliferate at the rate of 250,000 a minute, beginning in the third week of gestation. By the
time of birth, a child will have 100 billion neurons, linked by synapses, the complex nerve
junctions that begin forming in the 13th week of gestation. Proliferating most rapidly after
birth, in large part because of the stimulation and care a child receives, millions upon millions
of these junctions will be forged by the time a healthy child reaches the age of two and a half.
Physical, mental and cognitive development depend on these communication links
between neurons. Without them, messages would dead-end, muscles would not flex, and the
complex processes of thought and learning would not be possible. Growth during the foetal
stage depends on how well nourished a woman was before pregnancy, as well as how much
weight she gains while she is pregnant. Gains in weight are essential for the development
of new maternal and foetal tissues, and for maternal body maintenance and energy. Since the
foetus relies entirely on the mother for nutrients, pregnant women not only need to gain
weight but also must maintain an optimal intake of essential nutrients such as iron and iodine.
But fulfilling these interlocking food, health and care needs can be a struggle for many
women in the developing world, where economic, social and cultural factors may be a barrier
to good nutrition. Currently about 24 million low birth weight babies are born every year,
which is about 17 per cent of all live births. Most are born in developing countries, where the
main cause of low birth weight is not premature birth, as it is in the industrialized world,
but poor foetal growth. Low-birth weight babies, defined as weighing less than 2.5 kilograms,
are at greater risk of dying than infants of average weight. If they survive, they will have more
episodes of illness, their cognitive development may be impaired, and they are also more likely
to become malnourished. Evidence is also mounting that low birth weight predisposes
children to a high risk of diabetes, heart disease and other chronic conditions later in life.
The measures that are essential for an expectant mother –care and rest, a reduced
workload and a well balanced diet that affords ample energy, protein, vitamins, minerals and
essential fatty acids– are equally important when a woman is breastfeeding her child.
Breastfeeding perfectly combines the three fundamentals of sound nutrition –food, health
and care– and is the next critical window of nutritional opportunity after pregnancy. While
not all children are breastfed, it remains an important protection for children. Because breast
milk contains all the nutrients, antibodies, hormones and antioxidants an infant needs to
thrive, it plays a pivotal role in promoting the mental and physical development of children.
Breastfed infants not only show better immune responses to immunizations, but their intake
of breast milk also protects the mucous membranes that line their gastrointestinal and
respiratory tracts, thus shielding them against diarrhoea and upper respiratory tract infections.
In countries where infant mortality rates are high or moderately high, a bottle-fed baby in a
poor community is 14 times more likely to die from diarrhoeal diseases and 4 times more likely
to die from pneumonia than a baby that is exclusively breastfed.
Breastfeeding also has cognitive benefits. In one study, breastfed subjects generally had
IQs that were about 8 points higher than children who had been bottle-fed, and higher
achievement scores as well. Nutritionists theorize that the effect may be the result of the
growth-promoting long-chain fatty acids of breast milk. It may also be related to the fact that
breastfed infants have fewer infections and, as healthier infants, they take a greater interest
in their environment and thus learn more than ill infants.
However, for mothers infected with HIV, breastfeeding’s enormous value as a bulwark
against malnutrition, illness and death must be weighed against the 14 per cent risk that they
may transmit the virus to their infants through breastmilk – and the vastly greater risk, especially
in poor communities with inadequate water and sanitation, that feeding their children artificially
will lead to infant deaths from diarrhoeal dehydration and respiratory infections.
During the second half of a child’s first year, synaptic growth in the prefrontal cortex of
the brain, the seat of forethought and logic, consumes twice the amount of energy required
by an adult brain. Much of this synaptic growth is believed to result from the caring
stimulation that an infant and young child receives — the nurturing, feeding and learning play
in which parents engage their children. After about six months, for optimal growth and
development, a child needs to be fed frequently with energy rich, nutrient-dense foods. The
failure to make such investments at the right time can never be remedied later. An adequate
intake of micronutrients, especially iodine, iron, vitamin A and zinc, remains crucial.
An understanding of the complex and subtle causes of malnutrition is important to appreciate
the scale and depth of the problem, the progress achieved to date and the possibilities for
further progress that exist. Malnutrition, clearly, is not a simple problem with a single, simple
solution. Multiple and interrelated determinants are involved in why malnutrition develops,
and a similarly intricate series of approaches, multifaceted and multi- sectoral, are needed
to deal with it.
Immediate causes
The interplay between the two most significant immediate causes of malnutrition
–inadequate dietary intake and illness– tends to create a vicious circle: A malnourished child,
whose resistance to illness is compromised, falls ill, and malnourishment worsens. Children
who enter this malnutrition-infection cycle can quickly fall into a potentially fatal spiral as one
condition feeds off the other. Malnutrition lowers the body’s ability to resist infection by
undermining the functioning of the main immune-response mechanisms. This leads to longer,
more severe and more frequent episodes of illness. Infections cause loss of appetite,
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Spotlighting the causes
111
malabsorption and metabolic and behavioural changes. These, in turn, increase the body’s
requirements for nutrients, which further affects young children’s eating patterns and how
they are cared for.
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Basic causes
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It is often said that poverty at the family level is the principal cause of child malnutrition.
While it is true that a lack of resources and malnutrition often go hand in hand, this statement
tells only part of the story. Many poor families do in fact receive adequate nutrition, and
malnutrition is found in many better-off families. The broader explanation lies within a fuller
understanding of the different types of resources necessary for good nutrition, and of the
factors that affect families’ ability to access and control these resources. The three components
of nutrition –food, health and care– interact closely in their influence on family life.
Often efforts to fulfil one precondition for good nutrition compete for the same resources
required to fulfil another condition. For example, if a woman has to spend excessive time in
producing food to achieve household food security, her ability to provide adequate child care
can be compromised. The result may be malnutrition in her young child. Political, legal and
cultural factors at the national and regional levels may defeat the best efforts of households
to attain good nutrition for all members. These include the degree to which the rights of
women and girls are protected by law and custom; the political and economic system that
determines how income and assets are distributed; and the ideologies and policies that govern
the social sectors.
For example, where it is known and appreciated by everyone in society –men and boys,
women and girls, teachers and religious leaders, doctors and nurses– that women in the late
stages of pregnancy need rest and protection from overwork, families are more apt to receive
the social support they need to ensure this protection.
In places where there is a tradition of non-discrimination against women in law and
custom, women are more likely to have good access to resources, including credit, and to the
decision-making power that can enable them to make the best use of services for themselves
and their children.
There is no doubt that while economic poverty is not the only kind of poverty that
eventually affects nutrition, it is still an important factor. Overcoming entrenched poverty and
underdevelopment requires resources and inputs that few developing countries, particularly
the poorest, can muster, either on their own, through existing levels of private external
investment and loans, or through current patterns of official assistance and loans. In 1996, for
example, aggregate resource flows to the developing world from all sources totalled $232
billion, $59 billion of which was official development loans and grants and the rest, $156
billion, was private. Middle income countries were the biggest recipients of the private
investments and loans: Two thirds went to them and one third to low-income countries.
Underlying causes
Three clusters of underlying causes lead to inadequate dietary intake and infectious
disease: inadequate access to food in a household; insufficient health services and an
unhealthful environment; and inadequate care for children and women.
Household food security
This is defined as sustainable access to safe food of sufficient quality and quantity –including
energy, protein and micronutrients– to ensure adequate intake and a healthy life for all members
of the family. In rural areas, household food security may depend on access to land and other
agricultural resources to guarantee sufficient domestic production. In urban areas, where food
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
The two regions of the world with the highest rates of childhood malnutrition –subSaharan Africa and South Asia– received only $1.6 billion and $5.2 billion respectively. And
although bright spots exist in terms of investment and trade in sub- Saharan Africa, the
problems of the continent’s economies remain stark, including relatively low levels of internal
demand and the import quotas industrialized countries impose on African manufactured
goods. At the same time, developing countries overall owed more than $2 trillion in external
debt in 1995. Sub-Saharan Africa, for example, paid $13.6 billion in debt servicing in 1995 –
nearly double what it spent on health services. And developing countries bear by far the
greatest proportion of the global burden of disease, which drains their human and economic
resources. One potentially optimistic note in this dismal picture of declining aid flows and
increasing debt is the new ‘Heavily Indebted Poor Countries (HIPC) Debt Initiative’ launched
by the World Bank and the International Monetary Fund in 1996. This initiative is designed to
assist poor countries to achieve sustainable levels of debt based on an established track record
of implementing social and economic reform and on the condition additional resources are
channelled to basic social services.
If the basic causes of malnutrition are to be addressed, greater and better targeted
resources and improved collaboration, participation and dialogue are needed. Awareness and
information must be generated: between sections of national governments; between
governments; with all development partners, donors, UN agencies, nongovernmental
organizations (NGOs) and investors; and above all with those whose circumstances are rarely
understood or noticed, the poor themselves.
Action against malnutrition is both imperative and possible. The world, as the next part
of this report explains, has already accumulated a wealth of experience and insights on which
progress can be built.
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is largely bought on the market, a range of foods must be available at accessible prices to ensure
food security. Other potential sources of food are by exchange, gifts from friends or family and
in extreme circumstances food aid provided by humanitarian agencies. Household food security
depends on access to food –financial, physical and social– as distinct from its availability. For
instance, there may be abundant food available on the market, but poor families that cannot
afford it are not food secure. For the poor, therefore, household food security is often extremely
precarious. Agricultural production varies with the season and longer-term environmental
conditions. Families selling crops may find themselves paid fluctuating prices depending on a
variety of factors beyond their control, while those who need to buy food may encounter
exorbitant prices. Families living on the edge of survival have few opportunities to build up
sufficient stocks of food, or to develop alternatives that would cushion them in times of hardship.
So while poor families may have adequate access to food for one month, what is essential
is access that is consistent and sustainable. Women have a special role to play in maintaining
household food security. In most societies, they are solely responsible for preparing, cooking,
preserving and storing the family’s food – and in many societies they have the primary
responsibility of producing and purchasing it. For household food security to translate into
good nutrition, this often overwhelming burden of work must be redistributed or reduced so
that other needs of children, also related to nutrition, can be met.
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Health services, safe water and sanitation
114
An essential element of good health is access to curative and preventive health services that
are affordable and of good quality. Families should have a health centre within a reasonable
distance, and the centre’s staff should be qualified and equipped to give the advice and care
needed. According to the United Nations Development Programme (UNDP), access varies
widely, but in as many as 35 of the poorest countries 30 to 50 per cent of the population may
have no access to health services at all.
In Africa, the programme known as the Bamako Initiative was launched in 1987 to address
the crisis in health care that came on the heels of budget cuts and economic decline in the
1980s. It is a strategy for improving health services by moving their control, management
and even some of their financing out of central jurisdiction and into communities. Now in place
in a number of countries in Africa, the Initiative’s principles are being adopted and adapted
in other regions as well. The results are promising: The supply of basic drugs in health centres
is more consistent, and management committees, composed of village residents, help ensure
that people pay reasonable fees for basic services and that the funds generated are well used.
Nevertheless, the fact remains that many people do not have access to health care and may be
further deterred from seeking timely and appropriate care by user fees for health care services.
The additional challenge of creating a climate where preventive health and nutritional care
Solutions
Caring practices
Experience has taught that even when there is adequate food in the house and a family
lives in a safe and healthful environment and has access to health services, children can still
become malnourished. Inadequate care for children and women, the third element of
malnutrition’s underlying causes, has only recently been recognized and understood in all
its harmful ramifications. Care is manifested in the ways a child is fed, nurtured, taught and
guided. It is the expression by individuals and families of the domestic and cultural values that
guide them. Nutritionally, care encompasses all measures and behaviours that translate
available food and health resources into good child growth and development.
This complex of caring behaviours is often mistakenly assumed to be the exclusive domain
of mothers. It is, in fact, the responsibility and domain of the entire family and the community,
and both mothers and children require the care of their families and communities. In
communities where mothers are supported and cared for, they are, in turn, better able to care
for young children. Among the range of caring behaviours that affects child nutrition and
health, the following are most critical:
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components are also integrated into the Bamako model is harder to realize. Because they
are less tangible to communities, preventive health and nutrition services are also often less
in demand than curative care. Prevention, nonetheless, is vital and cost-effective. In terms
of environmental health, the lack of ready access to a safe water supply and proper sanitation
and the unhygienic handling of food as well as the unhygienic conditions in and around
homes, which cause most childhood diarrhoea, have significant implications for the spread of
infectious diseases.
Moreover, when food is handled under unhygienic conditions and the environment is
unhealthful, littered with animal and human wastes, young children are also more prone to
infection by intestinal parasites, another cause of poor growth and malnutrition. Also, women
and children are usually responsible for fetching the water needed for domestic use, a task
that drains considerable time and energy. Depending on how much the distance to the water
source is shortened, it has been estimated that women could conserve large reserves of
energy, as many as 300 to 600 calories a day. Progress has been made in improving access
to safe water. But more than 1.1 billion people lack this fundamental requirement of good
nutrition. As for sanitary waste disposal, the world is actually losing ground, with the rate
of coverage falling in both urban and rural areas. Only 18 per cent of rural dwellers had access
to adequate sanitation services at the end of 1994 and overall some 2.9 billion people lack
access to adequate sanitation.
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Feeding
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As we have seen, exclusive breastfeeding for about six months, and then continued
breastfeeding with the addition of safe, high-quality complementary foods into the second
year of life, provides the best nourishment and protects children from infection. The
introduction of complementary foods is a critical stage. A child will be put at increased risk of
malnutrition and illness if these foods are introduced much before the age of six months, or
if the preparation and storage of food in the home is not hygienic. On the other hand, a child
must have complementary foods at the six month point, since breastmilk no longer meets
all nutritional needs.
Delaying the switch-over much beyond six months of age can cause a child’s growth to
falter. From about 6 months to 18 months of age, the period of complementary feeding, a
child needs frequent feeding –at least four times daily, depending on the number of times a
child is breastfed and other factors– and requires meals that are both dense in energy and
nutrients and easy to digest. The foods a family normally eats will have to be adapted to
the needs of small children, and time must be made available for preparing the meals and
feeding children.
Good caring practices need to be grounded in good information and knowledge and free
of cultural biases and misperceptions. In many cultures, for instance, food and liquids are
withheld during episodes of diarrhoea in the mistaken belief that doing so will end the
diarrhoea. The practice is dangerous because it denies the child the nutrients and water vital
for recovery.
Other behaviours that affect nutrition include whether children are fed first or last among
family members, and whether boys are fed preferentially over girls. In a number of cultures
and countries, men, adult guests and male children eat before women and girls. The level
of knowledge about hygiene and disease transmission is another important element of care.
It involves food preparation and storage, and whether both those who prepare the food
and those who eat it wash their hands properly before handling it. Ideas concerning
appropriate child behaviour are also important. If, for instance, it is considered disrespectful
for a child to ask for food, feeding problems can occur.
Protecting children’s health
Similarly rooted in good knowledge and information is the caring act of seeing that children
receive essential health care at the right time. Early treatment can prevent a disease from
becoming severe. Immunizations, for example, have to be carried out according to a specific
schedule. Sound health information needs to be available to communities, and families and
those caring for children need to be supported in seeking appropriate and timely health care.
Therapeutic treatment for a severely malnourished child in the hospital is far more
expensive than preventive care. According to a 1990 US Department of Agriculture study,
nutrition investments for pregnant women were very cost-effective: Every $1 spent on
prenatal nutrition care yielded an average savings of about $3 in reduced medical costs for
the children during the first two months after birth. A study in Ghana has also found savings
in health care costs: Children receiving vitamin A supplements made fewer clinic visits and had
lower hospital admission rates than children not receiving the supplement.
For optimal development, children require emotional support and cognitive stimulation,
and parents and other caregivers have a crucial role in recognizing and responding to the
actions and needs of infants. The link between caring stimulation and malnourished children
is also important: Several studies have found that malnourished children who were given
verbal and cognitive stimulation had higher growth rates than those who were not.
Breastfeeding affords the best early occasion to provide support and stimulation. It enables
mothers and their infants to develop a close emotional bond that benefits both. All children
need –and delight in– the kind of play and stimulation that is essential for their cognitive,
motor and social development. Verbal stimulation by caregivers is particularly important for
a child’s linguistic development. Sick or malnourished children who are in pain and have lost
their appetite need special attention to encourage them to feed and take a renewed interest
in their surroundings during recovery. In addition to improved nutrient intake, optimal
cognitive development also requires stimulation of, and regular interaction with, young
children.
The quality of these actions can be enhanced through education of parents and other
caregivers. Child-to-child programmes, for example, can provide simple resources to older
children to improve the care, development and nutritional well-being of their younger siblings.
Policy makers need to recognize the significance of such measures and actions and take them
into account when devising policy and programmes. But the timing must be carefully planned:
Many early child development activities concentrate on children who are age three and older
when the focus should be on children up to the age of three and should link care, good
feeding and psychosocial activities.
Care and support for mothers
As long as the unequal division of labour and resources in families and communities
continues to favour men, and as long as girls and women face discrimination in education and
employment, the caring practices vital to the nutritional well-being of children will suffer.
Women, on average, put nearly twice the hours of men into family and household
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Support and cognitive stimulation for children
117
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
118
maintenance. In Bangladesh, India and Nepal, for example, girls and women spend three to
five hours more a week than boys and men in tasks such as carrying fuel and growing and
processing food. They then spend an additional 20 to 30 hours a week performing other
unpaid household work. If the burdens they carry are not better and more equitably
distributed, both they and their caring role will suffer. The elements of care most critical for
women during pregnancy and lactation include extra quantities of good-quality food, release
from onerous labour, adequate time for rest, and skilled and sensitive pre- and post-natal
health care from trained practitioners.
The AIDS pandemic has introduced new and volatile considerations and aspects of care
into already sensitive areas of human behaviour and interaction. High priority should be given
to improving access to services that help minimize the risk of HIV transmission to women
before, during and after pregnancy, as well as to their partners. Cultural norms and
misconceptions affect the care women receive during pregnancy. In some culturally
conservative communities in parts of Asia, for example, fish, meat, eggs and fat are not part
of the diets of pregnant women because it is feared they will make a baby too large and
difficult to deliver. Research shows, however, that better maternal diet can improve the birth
weight of children in many cases without causing significantly increased head circumference
of the newborn, which is the factor most likely to put small women at risk.
The adjustment of workload is another aspect of the care accorded women during
pregnancy –and one with powerful ramifications. A survey in one village in the Gambia, for
example, found that even during periods of relatively low seasonal agricultural activity,
women gained on average just 5.5 kilograms during pregnancy– only about half of the
recommended weight gain that women need to sustain their developing foetus. Reductions
in a woman’s workload during pregnancy, combined with more food of good quality, improve
the nutritional status of a woman and her unborn child and reduce the risk that the child will
have a low birth weight. In Viet Nam, when men assumed some of their pregnant wives’
responsibilities during the third trimester of pregnancy, women rested more, and their infants
weighed more at birth.
In Indonesia, infants born to women who received a food supplement did not weigh more
at birth, but they developed better during the first year of life. The fact that women are
usually the primary caregivers does not mean that men, families and communities are exempt
from care-giving responsibilities. The often oppressive and demanding patriarchal environment
in which millions of women live must give way to an equal partnership in which women enjoy
autonomy and the sense of accomplishment that comes from building skills and capacities.
At the same time, girls need to be free from pressures to marry early. A study in West
Africa, for example, found that nearly 20 per cent of girls in rural areas of the Gambia and
Senegal and 45 per cent of girls in Niger marry before the age of 15. Figures such as these
underscore the great need for girls and women to be involved in major personal decisions,
including not only their marrying age but also how closely the births of their children will
be spaced. Adolescent pregnancy is a major risk factor for both mother and infant, as the
girl may not have finished growing before her first pregnancy, making childbirth dangerous.
The infant of a very young mother may have a low birth weight. Higher risks of toxaemia,
haemorrhage, anaemia, infection, obstructed labour and perinatal mortality are all associated
with childbearing in adolescence. A number of measures are essential, therefore, to enable
women and girls to develop their skills and abilities. These include ensuring their access to
family and community resources, such as credit, and to education and information.
The CTC model 2:
Community-based Therapeutic Care
Severe malnutrition has traditionally been managed in inpatient facilities. In the 1990’s, it
became evident that the traditional therapeutic feeding centre (TFC) model of inpatient care
was unable to provide an effective response in terms of coverage due to the heavy demand
for resources in several large-scale humanitarian crises. For example, during the famine in
south Sudan in 1998, only a small proportion of the population in need had access to NGOrun TFCs. TFCs, due to congestion, were raising the risk of cross infection for the ones that
managed to get access to care. Additionally the opportunity costs for care givers and their
family were very high as mainly mothers of small children had to stay there for several weeks,
leaving their other children with inadequate support.
Community-based Therapeutic Care (CTC) was designed to address those issues. It was
designed to maximise coverage and access, reducing the risk of nosocomial infection and
facilitating families and care givers to get timely treatment. In practice, this means prioritising
providing timely care for the majority of the acutely malnourished at a community level over
inpatient care for a few extreme cases. This can only be done by providing treatment in
people’s homes.
Community mobilisation strategies are used to engage the affected population, reduce
the demand for resource use and thus maximise coverage and timely access to care.
Programmes try to build on local capacity and existing structures and systems, in order to
assist communities to deal with future periods of vulnerability (Collins, 2001). Acutely
malnourished children are identified through screening of the affected population or by
2. Compiled and adapted from “CTC – A field manual”, Valid International 2006.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Introduction
119
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
community volunteers or self-referral. Three forms of treatment are provided according to the
severity of the child’s condition:
➠ Those with moderate acute malnutrition and no medical complications are treated in a
supplementary feeding programme (SFP) which provides dry take-home rations enriched
with micronutrients and simple medicines
➠ Those with severe acute malnutrition (SAM) with no medical complications are treated
in an Outpatient Therapeutic Programme (OTP), which provides ready-to-use therapeutic
food (RUTF) and routine medicines to treat simple medical conditions. These are taken
at home, and the child attends an OTP site weekly for check ups and more supplies of
RUTF
➠ Those who are acutely malnourished and have medical complications are treated in an
inpatient stabilisation centre (SC) until they are well enough to be referred to an outpatient
care.
120
The first pilot CTC programme was implemented out of necessity during the famine in
Ethiopia in 2000. The local government in Ethiopia had prohibited TFCs and malnourished
people had to be treated as outpatients during the 2000 famine. The impact of the
programme was positive, demonstrating that, for individual children, the clinical effectiveness
of the outpatient therapeutic approach was equivalent to, or better than that achieved in
TFCs (Collins and Sadler, 2002). The experience was repeated at a larger scale in Darfur, Sudan
in 2001, treating a total of 25,000 malnourished children (Grellety, 2001).
In 2002, Valid International formalised the development of the CTC model, and Concern
Worldwide agreed to fund a three-year research and development programme. In 2002,
FANTA/AED also provided financial support and technical assistance to Valid International for
the further development of the model.
In 2004-5 MSF applied the model at a very big scale in Maradi, Niger treating more than
60,000 people with documented results that surpassed the classical approach. A focus on
operational research, systematic analysis and documentation has resulted in a strong evidence
base. All those efforts provided governments, donors and implementing agencies with the
necessary technical documentation to make an informed choice regarding acute malnutrition.
Over 25,000 severely acutely malnourished children and over 130,000 moderately acutely
malnourished children have now been successfully treated in CTC programmes in a variety
of contexts and with a range of partners.
At the same time through the efforts of organizations such as Concern Worldwide and
MSF, a strong lobbying effort has taken place influencing the approach of UN bodies and
International Organizations in shifting policies under the light of the new technical and
scientific evidence produced. RUTF (Ready-to-Use-Treatment-Food) production has been on
the rise and many efforts are taking place to go for local production, price reduction and
expansion of availability. In this chapter we are going to present the overall management of
severe, moderate malnutrition and nutrition therapy based on the CTC model. A short
presentation of the RUTFs will be made. Medicines required and follow up protocols and
strategies will be presented. There will be also special mention to the admission and exit
criteria, treatment protocols and the rehabilitation of patients.
Short presentation of the CTC model
CTC is based on the basic principle that people at risk from death and health consequences
due to malnutrition have a right to receive appropriate care and assistance. Provision of CTC
services is meant to be impartial, based solely on need of individuals and communities. These
basic humanitarian principles translate into a commitment and moral obligation to provide
the maximum coverage possible for the acutely malnourished population. Thus the core
operating principles of CTC are:
CTC aims to reach the entire severely malnourished population as a priority. At a second
phase targeting the moderately malnourished individuals and preventing further development
to severe and complicated malnutrition , is of great importance. Making services accessible to
the highest possible proportion of the population in need at a lower cost is at the core of
the philosophy of the CTC model.
Timeliness
CTC aims to achieve case-finding and treatment before the escalation of malnutrition
prevelance and the rise in the occurrence of additional medical complications
Appropriate care
CTC aims to provide effective care at an outpatient basis for those without complications
and inpatient care and treatment for those with severe or moderate complicated malnutrition.
By maximazing access to treatment, CTC makes sure that children stay in the programme until
they have fully recovered either at an inpatient or outpatient basis of care. CTC builds local
capacity and integrates the programme within existing health and community structures,
so that effective treatment remains available and accessible to population for as long as acute
malnutrition is present in the community.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Maximum coverage and access
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MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
122
The CTC model is founded on the principle that if children get appropriate care early on
and before complications appear, the recovery rates and impact get maximized and the use
of resources is reduced, so that better coverage can be achieved. If children present late and
are discouraged to stay in the programme for as long as needed, recovery rates are lower,
defaulters rates higher, impact is reduced and coverage falls shorter than the true needs of
the population. The basis of this understanding is that malnutrition is the result of complex
social, economic, cultural, medical and public health factors. The severity of the condition and
the complexity of its management depends on the stage of evolution it is caught.
The serious metabolic and immunological complications of the condition appear late in its
evolution. At that stage where people face life-threatening conditions, management is
complicated, costly, resource demanding and must be treated at an inpatient basis. Treatment
has more chances of failing. Opportunity and economic costs are high for both patients, their
families and the providers. As a result, default rates are higher and services are often
inadequate.
However, if malnutrition is addressed early on, the technical aspects of treatment are very
simple. All that is required is a balanced diet in sufficient quality and quantity in terms of
proteins, carbohydrates, fats and micro-nutrients. Such diets are well known and they are
relatively cheap to produce and easy to administer to patients. Therefore, CTC programmes
focus on addressing acute malnutrition early in the progression of the condition, before its
metabolic and immunological aspects require inpatient complex care. In order to achieve
this and to ensure that children can stay in the programme with few costs to them or their
families, programmes are designed to remove barriers of access to care. Services are provided
close to where target population live. Social and cultural barriers are taken into account when
designing the programme in relation to the local social and cultural environment. Community
participation in developing and implementing the programme ensures that the population
understands the services that are available to them, reinforcing health-seeking behaviour. This
in turn helps locate cases of malnutrition at an early on stage.
Innovations
The CTC model has been enabled by a series of technical innovations introduced into field
practice recently such as:
➠ Ready-to-use therapeutic food (RUTF)
➠ A new classification of acute malnutrition
➠ Screening and admission by mid upper arm circumference (MUAC)
RUTF was invented in the late 1990’s by research scientist Andre Briend and Nutriset, a
private company making nutritional products for humanitarian relief. RUTF is an energy-dense
mineral/vitamin-enriched food, specifically designed to treat severe acute malnutrition (Briend
et al.,1999). It is equivalent in formulation to Formula 100 (F100), which is recommended by
the World Health Organisation (WHO) for the treatment of malnutrition (WHO, 1999/a).
However, recent studies have shown that RUTF promotes a faster rate of recovery from severe
acute malnutrition than standard F100 (Diop et al., 2003).
RUTF is extremely useful in treating malnutrition. It is usually oil-based and contains little
available water, which means that it is microbiologically safe and will keep for several months
in simple packaging. As it is eaten uncooked, it is ideal for delivering many micronutrients that
might otherwise be broken down by heat. Due to these properties, RUTF has enabled the
treatment of severe acute malnutrition to move outside of feeding centres and into the
community. These properties also make it potentially useful for the management of chronic
illnesses such as HIV/AIDS. Further research is underway aiming expand RUTF use into
HIV/AIDS, TB and adult chronic malnutrition care. Oil-based Ready-to-Use Foods (RUF) (RUTF,
RUSF etc.) can also be made easily using low-tech production methods. They therefore lend
themselves to local production which can reduce the price of the product and ensure local
availability.
Therapeutic foods such as BP100 (produced by COMPACT) are sometimes used in
emergency situations. BP100 is a solid food based on the F100 formula with some iron added.
It can be eaten as a biscuit or as a porridge mixed with water or breast milk (the porridge is
recommended for children under two years of age). Because of this need to mix the BP100
biscuit with water for the younger age group, CTC programmes recommend that where BP100
is used it is in combination with oil-based RUTF. This ensures that the younger children are
also treated with a ready-to use food that does not require mixing.
A New Classification of Acute Malnutrition
The existing WHO classification of malnutrition has two categories:
➠ severe acute malnutrition
➠ moderate acute malnutrition
defined according to anthropometry and the presence of bilateral pitting oedema (see
further in text). This classification is operationally useful when there are two modes of
treatment:
➣ inpatient therapeutic feeding centres for children with severe acute malnutrition
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Ready–to-Use Therapeutic Food (RUTF)
123
➣ outpatient supplementary feeding programmes for those with moderate acute
malnutrition and adults with malnutrition
CTC, however, has a third treatment mode:
➣ outpatient therapeutic feeding for children who are acutely malnourished but do not
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
have additional complications
124
A new classification of malnutrition has therefore been devised to include the new
category: acute malnutrition with complications. The new classification is used to decide
whether a child needs inpatient or outpatient treatment. It ensures that all those who can be
treated as outpatients are treated as outpatients, and only those who need inpatient care are
treated in inpatient centres (Collins and Yates, 2003).
The new classification is used to decide whether a child needs inpatient or outpatient
treatment. The additional category enables programmes to avoid many possible negative
consequences for the child and the programme. If children with severe acute malnutrition
without complications are admitted into inpatient centres, they are exposed unnecessarily to
additional risk of infections. The carer, usually the mother, has to spend a substantial period
away from her family including other children. This may result in increased malnutrition in the
other children and undermine the economic activity and food security of the household. Space
and resources in resource-intensive inpatient centres will be allocated to children who do not
need inpatient care, so reducing the programme’s impact and increasing its costs. On the other
hand, if cases of moderate acute malnutrition with complications are not admitted for
inpatient care, morbidity and mortality will increase.
Screening and Admission by MUAC
In order to give access to care to the largest possible proportion of the acutely malnourished population, a programme needs to be very effective at identifying children who need
care and admitting them to the programme. Screening must take place in the community,
using a simple, low cost method that is easy for community volunteers to use and which
communities can accept as fair and transparent.
Therapeutic feeding programmes typically use weight-for-height percentage of median
(WHM) and/or the presence of bilateral pitting oedema as admission criteria. Mobile teams
screen communities in a two-stage process using both WHM and MUAC measurement. Twostage community screening can, however, be a lengthy and resource-intensive process.
Normally it requires three people to perform and record the necessary measurements
accurately. They need to be literate and numerate, equipped with scales, height boards,
electronic calculators and special standard tables. Teams often need vehicles to transport them
and their equipment to screening sites and they must deal with crowd control and the
provision of temporary shelter for people attending the sites. In some cases it may be possible
to store equipment locally, but skilled staff still need transport of some kind.
These requirements tend to limit screening activity to particular areas, reduce the
frequency of screening and make the timely identification of malnourished children more
difficult. CTC programmes recommend the same MUAC criteria for community referral and
admission to allow a community-based strategy for referral to be adopted whereby all children
who are referred from the community by outreach workers or volunteers, and who arrive at
a programme site, are admitted.
The CTC Model Outline
A MUAC band
The recommended criteria for children >65cm height (and/or
age >6 months4) are (Myatt et al., 2006): MUAC < 110mm and/or
oedema: refer and admit to OTP MUAC ≥ 110mm and < 125mm:
refer and admit to SFP Using only MUAC for screening and
admission instead of a combination of MUAC and WHM has
important practical benefits: The interface between the programme
and the beneficiary community is strengthened. MUAC is simple to
use, and allows community volunteers to refer children directly to
the programme. It is a one-stage process, in which community
A MUAC
referral entitles an individual to admission to a programme.
band
Experience shows that a two stage process using a sufficientlysensitive MUAC threshold for community referral, followed by
admission using WHM, leads to many children being referred but
not admitted. This results in reduced coverage by creating confusion and disillusionment. It is
simple and cheap.
Other service providers can also screen and refer using MUAC without greatly increasing
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
First, potential cases are identified using a sensitive MUAC threshold (e.g. 130mm or with
higher sensitivity, eg. 123mm, when applicable according hierarchy of interventions context,
see further in text), or by the presence of bilateral pitting oedema; second, children with a
MUAC below the threshold are weighed and measured and their WHM (Weight-for-height
measurement) calculated. Children with a WHM below an admission threshold (usually 70%
WHM) and those with bilateral pitting oedema are referred for admission. In this scheme,
all children who are referred and arrive at a centre are admitted.
125
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
126
their workload. Links between the CTC programme and other sectors and services are
therefore facilitated. The confusion caused by using different weight-based indicators (e.g.
weight-forage and weight-for-height in growth monitoring and mother and child health,
MCH, programmes) is avoided. It enables programme sites to function more efficiently. Delays
and overcrowding are reduced because people do not need to be re-screened for admission.
It is less prone to mistakes. Comparative studies have shown that MUAC is subject to fewer
errors than weight for height (Myatt et al, 2006). It is more sensitive. MUAC is a better
indicator of mortality risk associated with malnutrition than WHM. It is therefore a better
measure by which to identify children most in need of treatment.
There are situations where WHM must still be used for admission to programmes – where
national strategies dictate the use of it, for instance, where other agencies working in the
area are using it, and links between programmes need to be fostered. In these cases,
compensation (soap, for example, supplementary rations or preventative services such as an
extended programme of immunisation, EPI, or de-worming from the clinic) should be offered
to people turned away, so that the visit to the clinic is still worthwhile.
Using a MUAC cut-off for referral and admissions, particularly in supplementary feeding
programmes, can have implications for the size of the programme and for reporting. Ideally,
a context-specific analysis of need, based on MUAC data collected during standard nutrition
surveys would be conducted to estimate the expected programme size for SFP based on
specific cut-offs. Tools are available to select the most appropriate MUAC cut-off to use for
a given situation/population group (SCUK, 2004). Cut-offs for SFP can then be adjusted (e.g.
reduced to 120mm) based on capacity and resources so that priority is given to identifying
children most at risk of death and therefore most in need of treatment.
Programme Components
The CTC model has four key components:
➠ Community mobilisation stimulating the understanding, engagement and participation
of the target population.
➠ Supplementary feeding programmes providing dry take-home rations and routine basic
treatment for children with moderate acute malnutrition without complications.
➠ Outpatient therapeutic programmes providing RUTF and routine treatment using
simple medical protocols for children with severe acute malnutrition without
complications.
➠ Stabilisation centres providing inpatient care for acutely malnourished children with
medical complications.
In addition to these four components, CTC links the provision of care for the malnourished
An acutely malnourished child is selected for admission through community mobilisation
and active case-finding. If screening measurements and assessment indicate s/he has moderate
acute malnutrition but no medical complications, s/he is admitted into the SFP and receives
regular dry rations for consumption at home until fully recovered. If s/he has severe acute
malnutrition with no medical complications, s/he is admitted into the OTP and receives RUTF
and medicines to treat simple medical conditions. These are taken at home and the child
attends an OTP site weekly for check-ups and to be re-supplied with food and medicines. If
s/he is acutely malnourished and has medical complications, s/he is transferred from the OTP
or SFP to the SC for inpatient treatment until well enough to return to outpatient care in
the OTP. When the condition has improved, s/he is discharged into the SFP for supplementary
feeding until fully recovered. A small number of children may also arrive directly at the SC and
would be referred to the appropriate programme component from there.
Programme Evolution
The sequence in which the various CTC components are established varies according
to the particular circumstances in which the programme is implemented. Ideally, a
programme evolves as follows. In the initial stage of an emergency CTC programme, the
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
with measures aimed at addressing some of the underlying causes of malnutrition, such as
public health, hygiene and food security
127
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
128
population is sensitised and mobilised. Key community figures (traditional and political
leaders, traditional healers, religious leaders, representatives of women’s groups) are
contacted and community meetings are held to provide information about the programme’s
aims, methods and target group, and to solicit help in mobilising the population. An SFP
can be rapidly established through multiple access points and the outpatient element (OTP)
is then added (at existing health facilities where possible). The initial stage can occur within
days.
As the programme evolves, resources can be put into selecting and mobilising volunteers
from the community, supported by outreach workers employed by the programme. These
volunteers are responsible for finding new cases, tracing defaulters and encouraging them to
return to the programme, and following up with particular malnourished children in their
homes. The aim is to increase programme coverage, improve compliance with treatment
regimes and increase the participation of the community in order to provide a platform for
the longer term.
When the SFP and OTP have achieved good coverage of the target population, resources
can be invested in creating stabilisation centres. Where possible, these are located within
existing structures. If competent local
Early Stages
healthcare structures exist, needing
relatively limited resources to strengthen
Outpatient
them, it is appropriate to do this at the
Therapeutic
early stages of the programme, so long
Programme
Supplementary
(OTP)
as this does not detract from the
Feeding
(SFP)
resourcing of the outpatient community
Community
components. Where local infrastructure
Mobilisation and
Participation
does not exist or is very weak, it is
important not to divert resources to
establish SCs before the OTP and SFP
Fully Evolved
elements have achieved good coverage.
Links with food security and
As the CTC programme evolves into the
other sectoral interventions
final stages, efforts are made to increase
SC
the links between the programme and
(OTP)
work in other sectors, particularly public
(SFP)
health and hygiene and food security
Community
interventions, as well as initiating the
Mobilisation and
Local RUTF
Participation
local production of RUTF.
Production
Programme evolution
Integration, Collaboration and Coordination
A wide range of interventions are required to ensure an effective nutritional response. CTC
offers a common framework within which agencies, local/regional/national government and
communities can collaborate to implement the various CTC programme components. It also
includes the promotion of links with interventions in other sectors to take into account the
social, economic and political aspects of food insecurity and malnutrition.
Intra-Sectoral Collaboration and Integration
A CTC programme demands a wide range of skills and capacities. An agency can
implement one or more of the CTC components while working closely with local ministries,
organisations and other agencies implementing other elements of the programme. CTC can
thus be complementary to traditional TFC/SFP programmes by integrating these elements into
a broader framework. Effective collaboration can ensure that the various components combine
to form a coherent and comprehensive response, thus achieving the greatest possible impact
for the target population. Collaboration may include:
care services.
➠ Integration of the SC into hospitals and health centres with an existing inpatient
facility.
➠ Links with health interventions such as Integrated Management of Childhood Illness
(IMCI), immunisation (EPI), malaria prevention, growth monitoring, micronutrient
supplementation, health and nutrition education, ante-natal programmes and family
planning programmes.
➠ Implementation of different CTC components by different agencies
Integration of CTC with Existing Clinical Health Systems
CASE STUDY 1:
Concern Wollo, Ethiopia 2003 onwards.
At initial programme set-up, plans were made to establish a stabilisation centre for children
requiring inpatient care in the local health centre. However, this was revised after a visit to the
zonal referral hospital which found that there was a 50-bed paediatric ward with one room
already allocated as a nutrition unit. Practices were out of date, for example a “kwash” milk
recipe containing eggs and milk which was being used. It was being made once a day in the
morning and left in a container beside the bed for 24 hours. Concern helped the hospital obtain
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
➠ Integration of the OTP into existing health facilities to run alongside primary health
129
F100 and F75 and supplies such as nasogastric tubes that were not available in the hospital,
and worked closely with the medical director to revise and update protocols. The medical
director also attended training on updated Ethiopia National protocols for inpatient treatment
of severe malnutrition and was then able to pass this training on to all the hospital paediatric
staff. Concern appointed one hospital liaison assistant (deliberately nonmedical) to facilitate
the admission, stay and discharge of children. No incentives or per diems were provided to
health staff. Concern also facilitated the transfer of children to and from hospital and paid
for medical expenses incurred while in hospital.
This investment in building local capacity and working within the current system paid
off. Results are extremely encouraging. 168 children were treated during the first year
period by the hospital staff as part of their normal workload. The hospital death rate for
severely malnourished children dropped from an estimated 50% before the start of the
project to 9.5% in this time. An excellent relationship has developed between Concern and
the hospital and long-term capacity for the hospital to treat severe malnutrition has been
markedly increased.
Source: (Mates, 2004)
CASE STUDY 2:
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Collaboration in Darfur, 2004.
130
During the emergency in Darfur in 2004, six different NGOs implemented the various
components of the CTC programme in El Geneina. TFC interventions were run by MSF-France
and MSF-Switzerland; medical care was provided through clinics operated by MSF-Switzerland
and Medair; outpatient therapeutic care was provided by Concern, Tearfund and SC-US and
outreach by Medair, Concern and MSF-Switzerland. Collaboration between the NGOs for
coherent protocols and referral was facilitated by Valid and United Nations International
Children’s Emergency Fund (UNICEF). This cooperation resulted in the decongestion of
inpatient care and the more efficient use of resources. It enhanced case-finding, case followup and hygiene promotion. Case fatality rates for severely malnourished individuals fell and
programme coverage increased dramatically.
Source: (Walsh and Faroug, 2004)
Inter-Sectoral Collaboration and Linkages
Nutritional crises are caused by a combination of factors including conflict, economic
deprivation, social exclusion, chronic vulnerability and individual pathological changes.
Activities in a variety of different sectors are needed to restore acceptable levels of nutrition
and health. A CTC programme does not provide this range of support, instead, it aims to form
links with local structures, services and agencies in different sectors in order to contribute
to a more comprehensive response.
The relevance of particular sectoral links depends on local morbidity and existing services.
Usually, links are made with the public health, agriculture and water and sanitation sectors.
The kind of links that might be considered include:
➠ Links with HIV/AIDS programmes such as voluntary counselling and testing (VCT)
By forming intersectoral links, a CTC programme can capitalise on existing programmes
and services to increase coverage and effectiveness while helping to strengthen other
programmes and services, thus also increasing their coverage and impact. CTC can also provide
an entry point for other interventions. Strategies and joint protocols can be developed to
enable CTC and programmes in other sectors to support each other’s activities. For example,
existing volunteer networks put in place by food security or water and sanitation programmes
can be mobilised for mutual objectives so that public messages about the various sectoral
activities can be delivered more efficiently.
Potential links should be identified early in the planning process and should be incorporated in programmes as soon as is appropriate. In an emergency, when a rapid response
is required, a staged approach is needed: priority is given to the most urgent elements and
components and links are developed with food security and public health interventions only
after the SFP, OTP and SC have been established. In developmental contexts, a comprehensive
approach can be taken from the outset.
CASE STUDY 3:
Sectoral Links in Malawi, Linking CTC with HIV/AIDS Interventions
Severe malnutrition and HIV/AIDS are inextricably linked. In many countries, a sizable
proportion of the caseload of severely malnourished in inpatient facilities is infected, or
otherwise affected by HIV/AIDS. CTC has proven to be a viable entry point for nutritional care
and support for people living with HIV/AIDS. For example, the CTC programme in Dowa
Malawi, has built up a strong community base. This has allowed it to make links with other
community-based interventions aimed at people with HIV/AIDS, such as home-based care. As
a result, there has been high uptake of voluntary counselling and testing for children and their
families, and effective links to treatment.
Source: (WHO, 2005/a)
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
programmes, home-based care (HBC) and mitigation interventions.
➠ Links with water and sanitation interventions.
➠ Links with food security and agricultural interventions.
131
Coordination
The requirements for collaboration and integration that are inherent in the CTC model require
strong coordination systems to promote discussion and information sharing. Agencies need
to be willing to coordinate effectively, on two levels:
➠ Working together on the ground – taking responsibility for complementary programmes
and running shared training exercises.
➠ Working together on joint monitoring and on establishing standards of best practice,
and developing locally appropriate tools to ensure the quality and accountability of
programming.
As a new and highly-designed model, CTC offers implementing agencies and donors a
unique opportunity to establish high standards in CTC programming to ensure the best
possible impact. Interagency collaboration might involve developing a code of good practice,
training and inter-agency mentoring, a system of collective self-regulation whereby agencies
are recognised for meeting agreed CTC standards, and the incorporation of CTC into
international technical guidelines such as those from WHO.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Implications for Implementers
132
Implementing CTC entails some important changes in impact assessment, funding, staffing
and logistics.
Assessment of Impact and Funding
As CTC is based on public health priorities, implementing agencies, donors and other
stakeholders need to develop and evaluate interventions according to population-level impact,
rather than the clinic-level outcome indicators that currently prevail. In order to rapidly achieve
high coverage, CTC programmes give priority to resourcing and establishing outpatient
services (SFP and OTP) and admitting high numbers of malnourished people. Overall, mortality
in a CTC programme is lower, but agencies and donors need to be prepared for the possible
political and emotional repercussions of reporting higher initial number of deaths.
Donor policy also needs to take account of the longer-term benefits of the CTC model.
Relatively long-term funding cycles are required to enable the integration of CTC services into
existing health services, and to allow for the gradual handover to local control. This applies
to CTC programmes financed from emergency as well as developmental sources.
Staffing
CTC programmes are carefully tailored to the context in which they operate. Adapting
programmes to fit the context is not work for inexperienced managers or advisors, and
programmes therefore require managers with extensive experience of humanitarian or
development programming and cultural understanding. They also call for expert technical
advice. On the other hand, the actual implementation of CTC requires few, if any, imported
specialist medical staff, and only a small number of skilled local staff. CTC protocols are short,
simple and easy to teach to primary healthcare workers.
Logistics
CTC IN CONTEXT 3
CTC is a highly adaptable model, and can be used to address acute malnutrition in most
contexts. This chapter describes CTC’s place within the hierarchy of interventions necessary
for an effective nutritional response and how CTC can be adapted to individual contexts.
Hierarchy of Nutritional Interventions
in an Emergency
In an emergency, CTC programmes take place within a hierarchy of interventions needed to
address the nutrition crisis. The impact of therapeutic feeding on levels of severe acute
3. Compiled and adapted from “CTC – Afield Manual”, Valid International 2006.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
In comparison with TFC programmes, CTC interventions require relatively little support
infrastructure. However, the highly decentralised nature of the CTC approach, with its numerous
OTP/SFP points, creates major logistical demands, particularly where programme areas are
remote and travel is difficult. Challenges include transporting programme teams, supervisory
staff and supplies to sites, and finding suitable storage space for RUTF and supplementary food
at programme sites. Establishing a functioning logistics system and ensuring its continuity over
the life of a programme calls for expertise in transport and procurement.
133
malnutrition is considerably reduced if appropriate general support for the population is not
in place (for example, if there is a failure in the general food pipeline or acute food insecurity).
The hierarchy of nutrition intervention therefore prioritises the provision of basic food stuffs
to the majority of the population over intensive, specialised nutritional support to
malnourished individuals. Once the majority of the population has access to adequate
quantities of food, the second priority is to provide high quality supplementary food to
individuals with acute moderate malnutrition. When adequate supplementary rations are
available to the majority of people affected by moderate acute malnutrition, therapeutic care
for those with severe acute malnutrition can then be effective. CTC programmes should
complement the provision of general food to the population. It may be necessary for the
agency implementing CTC to take a strong advocacy role to try to ensure the provision of a
general ration where appropriate. Starting a CTC programme may itself act as a powerful tool
for advocacy.
Higher priority
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
General access to
adequate rations
(eneral ration)
134
Lower priority
Supplementary feeding
Therapeutic feeding
Increasing coverage and population level impact
Better cost benefit
Increasingly intensive individual treatment
Poorer cost benefit
Hierarchy of interventions in nutritional emergencies
Emergency and Development Contexts
When there are large-scale, life-threatening needs in the context of a humanitarian crisis, the
design and implementation of the CTC programme needs to give priority to overarching
humanitarian principles that ensure rapid response for those in immediate need. In practice
this entails using the quickest, most effective means to establish immediate life-saving
components, regardless of issues of longer-term sustainability. During conflict, for example,
the programme may have to operate independently of national or international authorities
and/or government services if they are a party to the conflict (working directly with
Target Groups
The objective of selective feeding programmes is to reduce the prevalence of malnutrition and
mortality among vulnerable groups. Increased malnutrition and mortality in emergencies
are normally observed in children under five years of age. Children are more susceptible to
malnutrition because of their higher nutritional requirements in relation to their weight in
comparison with adults, mainly as a result of a different body composition. Increased exposure
to infections contributes to the higher mortality. Exclusively breastfed children below six
months are less affected by malnutrition and infections. Children aged six months to five years
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
communities can facilitate this). While community mobilisation, participation and capacity
building are perfectly feasible during emergency interventions, when communities are weak
or fragmented, or when community structures are subject to manipulation by political or
military actors, the potential for community participation and mobilisation is likely to be
reduced. In extreme circumstances –in Rwanda in 1994, for example– liaison with formal
community structures may be impossible or counter-productive.
The CTC model can also be adapted to stable development situations. The treatment of
severe acute malnutrition is regarded by many as specialised and expensive and is therefore
often ignored by health systems. Many children in developing countries die as a result. It is
not difficult to integrate OTP protocols into existing primary health care protocols and thus
have a substantial impact on child mortality. Positive results achieved in developmental as well
as emergency settings strongly suggest that OTP, SC and community mobilisation components
of CTC should be an essential component of the primary health care system in developing
countries.
When acute malnutrition is the result of chronic poverty and lack of development in a stable
situation, the CTC programme should emphasise developmental principles and approaches sustainability, ownership and capacity-building – that will address needs in the long term. In
practice, this is likely to mean planning and implementing the programme in close cooperation
with relevant actors, and building local capacity from the start. It may mean taking a demanddriven approach, in which the programme is implemented first in locations with the
infrastructure and level of local commitment that give it a good chance of success. Such ‘starter
sites’ can be used as demonstration and training facilities to introduce potential actors and
beneficiaries to the methods and benefits of CTC. In many situations, the context combines
elements of humanitarian crisis with long-term underdevelopment. In these situations,
experienced, well-informed programme planners and managers are essential to ensure that the
programme has the appropriate strategic balance for the context. The initial design and setting
up of the programme is particularly important, as the directions and working arrangements
established at the start can affect a programme for months or even years.
135
are therefore given by WHO as the priority target group for nutritional assistance in any food
emergency.
This manual reflects this prioritisation by focusing on treatment for children in the 6-59
months age group. To date, CTC has not been implemented in a situation where there are a
large number of malnourished individuals in other age groups. Guidelines for other groups
are therefore not included here. However, this does not mean that adolescents, adults and
the elderly cannot be treated using the CTC model with modified protocols. The treatment of
acutely malnourished infants under six months of age in emergencies is an area of continued
research and debate. CTC programmes have treated infants by referring them to the
stabilisation centre and using recommended protocols. However, the number of malnourished
infants encountered in this age group has been small. WHO is developing guidelines for this
age group, in consultation with other members of the international nutrition community
(Interagency Working Group, 2001) and (ENN et al., 2004). It is hoped that in the future, these
guidelines can be incorporated into CTC protocols. SFP protocols include support for infants
through nutritional support to breastfeeding mothers
Intervention Criteria and Decision-Making Tools
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
The decision about whether and when it is necessary to intervene with a CTC programme
is based on four main considerations:
136
➤ The prevalence of, and trends in, malnutrition.
➤ The context – including the causes of the malnutrition, the socioeconomic situation,
the food security situation, general ration quantity and allocation, the presence of
other interventions and projected future needs.
➤ Available resources – human, material and financial.
➤ Public health priorities – i.e. the hierarchy of intervention.
Prevalence of and Trends in Malnutrition
The decision to start a CTC programme can be based solely on the presence of a large
number of severely acutely malnourished children requiring immediate life saving treatment.
(WHO, 2000a). The following factors in relation to prevalence should also be taken into account:
➠ Levels of global acute malnutrition (GAM) and severe acute malnutrition (SAM) and the
relationship between the two. For example, if SAM is high while GAM remains relatively
low, it is likely that non-food factors such as disease, particularly HIV/AIDS, are important
determinants of malnutrition. It may be that a particular group (e.g. recently displaced
people) is at much higher risk compared to other groups, or there may be high levels of
kwashiorkor.
➠ Trends in malnutrition prevalence. When available, the findings of earlier surveys in the same
or a similar area can be compared and trends plotted. This allows judgements to be made
about the ‘normality’ of the malnutrition levels found. Information on trends may also come
from routine nutritional surveillance collected from clinics where these systems exist.
➠ The geographical spread of the affected population. It may be dispersed and mobile or
higher levels of malnutrition may be present in particular areas that should be targeted.
➠ The reliability of the data. Sources of possible bias must be identified and the implications
taken into account. However, this bias based on the prevalence of wasting and food
availability, does not take account of oedema prevalence, and includes a limited number
of aggravating factors. It is therefore essential that these criteria are adapted to the local
context, and that additional aggravating factors are considered
* The malnutrition rate is defined as
the percentage of the child
population (six months to five
years) who are less than -2SD
(Standard Deviations or z scores)
below the median weight-forheight of the international
reference distribution, or less than
80% of the reference median
weight-for-height.
** For WHO aggravating factors are:
ñ General food ration below the
mean energy requirement
(<2100kcal/person/day).
ñ Crude Death Rate greater than
1/10,000/day.
ñ Epidemic of measles or whooping
cough.
*** The CTC model falls within both
the therapeutic and supplementary
feeding categories. It can also
fit into the category of “attention
to malnourished individuals
through regular community
services”, as it has the potential
for implementation through
existing services. By strengthening
existing services, it creates capacity
to treat acute malnutrition in the
long term where prevalence is.
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Decision chart for the implementation
of Selective Feeding Programmes (SFPs)-WHO/2000a
137
The Context in which Malnutrition is Occurring
Different factors cause malnutrition in a population and it can be difficult to determine
the most important factors. The UNICEF conceptual framework for the determinants of
nutrition is a useful tool. It provides the basis for a causal analysis of malnutrition in a
particular population and can help in prioritising interventions.
It is important to know whether death rates are above acceptable levels, whether
there has been an increase in death rates or morbidity and whether there has been, or
there is a risk of, epidemics of measles or whooping cough. Consideration of death rates
is important as in some cases a survey can find misleadingly low malnutrition rates
because of high death rates among malnourished children.
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Death Rates and Stage Alert (adapted from SPHERE 2004,and USAID 2000
138
The crude death rate (CDR): is the most specific and useful health indicator in a
disaster situation. A doubling of the baseline CDR indicates a significant public health
emergency, requiring an immediate response. Socio/economic context: Livelihoods, market
trends and debt levels are important for an understanding of the current and future
vulnerability of the community. Cultural context: caring practices and beliefs concerning food
and disease. For example, in some contexts children’s nutrition is protected to such an extent
during periods of food insecurity that high malnutrition rates are not seen in this group,
though they exist in other groups, such as adults. In this case a CTC programme with wider
targeting criteria may be required.
Including climate patterns, harvest calendar, food security situation (food access,
availability and future vulnerability of agricultural production). For example, high levels of
malnutrition after a harvest are more alarming than similar levels immediately preceding the
harvest period.
Coping strategies: types of coping strategy, trends in their use, who is applying them,
how well they work and their potential adverse consequences. This provides an
understanding of the current situation and the extent to which current behaviour may be
creating future vulnerability. In such situations a feeding intervention can help to prevent
future deterioration.
Additional potential aggravating factors that could increase vulnerability and the risks
of malnutrition-related mortality. These may include insecurity, population movements,
climate, the availability of shelter, vaccination and water and sanitation. Such factors may
necessitate intervention even at relatively low rates of malnutrition prevalence. The
consequences of some aggravating factors can be measured against the SPHERE standards;
others require judgements by experienced staff. An estimate of the population’s future needs.
Including future food prospects, potential disease outbreaks and potential changes in caring
practices.
Other interventions being carried out or planned in the area. Intervention is necessary only
if services are not being provided already. Rather than starting a new CTC programme, it may
be appropriate to support or supplement an existing programme, for instance by providing
an OTP to work alongside an existing SFP. The presence and adequacy of general food
distributions (GFDs) is a key factor: if a population is highly dependent on food aid, the
adequacy of the general ration is crucial.
Available Resources
Decisions about whether to implement CTC, and the form the programme should take,
are also determined by the resources available, including staff, supplies, logistics, funding and
the capacity of the local health system. An understanding of existing capacity is essential to
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Agricultural/ecological context
139
ensure that, whenever possible, programmes build on and strengthen existing systems
capacity to treat severe acute malnutrition. The main considerations are:
➤ The personnel, expertise, supplies, logistics capacity and funding of the Implementing
agency.
➤ The personnel, supplies and logistics capacity of existing services, including govern-
ment health services, other government departments, international and local NGO
programmes and religious groups. They may be able to provide resources such as
seconded staff or community workers who can help to disseminate information
about CTC.
➤ A reliable supply of RUTF.
Information Sources
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
The information needed to make decisions about whether to implement a CTC programme
may come from secondary data or fresh data may be collected in the field. The more sources
of information that are available, the better informed the decision will be. Information sources
include:
140
➠
➠
➠
➠
➠
➠
➠
➠
➠
➠
Host government documentation/resources on the current situation and context.
Nutrition surveys.
Food security assessments.
Interviews and focus group discussions with key informants and community members.
Routine screenings.
Monitoring data on therapeutic and supplementary feeding programmes.
Clinic records.
Routine health surveillance.
The population records of the local authority.
Information from other programmes in the area (general ration provisions, food
security, health and health education, water and sanitation).
Treatment protocols 4
This chapter provides guidelines for the management of patients with severe malnutrition.
It tries to promote the best available management in order to reduce the risk of death or
relapse and reduce the time spent in the hospital. It focuses mainly on the management of
severely malnourished children. In the end there is a brief outline for the management of
adolescents and adults as well. It has been based on the WHO manual but followed by the
specific alterations in admission and exit criteria, classification and management that the CTC
model, presented before has brought about.
Severe malnutrition is both a medical and social disorder. Malnutrition is the endpoint
outcome of chronic neglect of the child’s needs (nutritional, medical and emotional) at home
by carers that ignore the importance of appropriate care or do not have access to the
resources needed for such care. If the illness is viewed as a mere medical problem, the child
will relapse once it returns home and the other children in the family remain at high risk of
presenting with severe malnutrition and complications as well (Table page 142).
Management of a child with severe malnutrition does not require sophisticated facilities
or equipment. It does however require that each phase of treatment will be cared out by
personnel that is adequately trained on the implementation of guidelines and dedicated enough
to offer proper care and affection. This way risk of death is reduced to acceptable levels 5.
There are three phases for the management of a child with severe malnutrition:
➠ Initial treatment: in a hospital or residential care facility environment life-threatening
problems are identified and addressed, metabolic and specific nutritional deficiencies
are corrected and gradual feeding is started
➠ Rehabilitation phase: most of the lost weight is recovered by intensive feeding,
emotional and physical stimulation is increased, the carer is being trained to care for
the child properly at home and all needed preparations before discharge take place
➠ Follow-up : the child and its family are being followed-up at an outpatient basis to
prevent relapse and offer support for continued physical, emotional and mental
development of the child.
4. Compiled and adapted from: ‘’Management of severe malnutrition: a manual for physicians and other
seniour health workers’’, WHO, Geneva, 2000
5. A case fatality rate of >20% is considered unacceptable, 11-20% is poor, 5-10% is moderate, 1-4% good
and <1% is excellent. Historically an average of 3-10% has been achieved by nutrition interventions by NGOs
in emergencies.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Introduction
141
Time frame overview for the management of a child with severe malnutrition
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Source: Management of severe malnutrition: a manual for physicians and other senior health workers, WHO,
Geneva, 1999.
142
Treatment facilities
Residential care is essential for initial treatment and for the beginning of rehabilitation
of a child with severe malnutrition. The child is admitted to a Treatment Feeding Center
TFC (usually run by an NGO) or a special unit of the hospital preferably with experience in
management of malnutrition. After the initial phase and if the child has no complications
and is eating satisfactorily (usually after 2-3 weeks of initial treatment), it can be discharged
under the responsibility of a day care unit (Primary Health Care Unit or special nutritional day
care facility) that provides day care by trained staff in the rehabilitation of malnourished
children. The child is brought in every morning and spends the night at home. Close
collaboration between the Hospital or the TFC is required to ensure continuity of care. If
there are no other specialized care units in the area, it is the responsibility of the hospital
to provide care for the phase of rehabilitation and follow up by its outpatient units or
supportive services.
Advantages and disadvantages of residential and non-resindential facilities
for severely malnourished children
Evaluation of the malnourished child
Assessment of nutritional status and criteria for admission
Children whose weight-for-height or length is below -3SD or less than 70% of the
median WHO references (termed severely wasted or stunted) or who have symmetrical
oedema involving at least the feet are severely malnourished. The are in need of hospital
care for management of complications, correction of metabolic and physiological imbalances
around the clock. Stunted children are usually considered to have a milder, chronic form
of malnutrition. They are at immediate risk of complications and resulting death at any
time as their condition can worsen rapidly with diarrhoea, respiratory infections or
measles. Stunted children can satisfactorily be managed at an outpatient basis in the
community. For those children guidelines for ‘’preparation of discharge’’ apply for their care
and follow up.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Source: Management of severe malnutrition: a manual for physicians and other senior health workers, WHO,
Geneva, 1999.
143
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History and physical examination
144
Source: Management of severe malnutrition: a manual for physicians and other senior health workers, WHO,
Geneva, 1999.
Laboratory tests
Laboratory facilities and relevant tests could be used where available, however malnutrition
can alter interpretation of laboratory tests and results and they can misguide an inexperienced
health worker. Careful, repeated assessment and clinical examination of the child is the
cornerstone of diagnosis and medical follow up in the case of malnutrition. You can find below
a table presenting main laboratory tests and their significance in malnutrition.
Initial treatment
Principles of management
Children with severe malnutrition are often seriously ill when they present for treatment.
Wasting, anorexia and infections are common. Frequent and careful evaluation is necessary
for early anticipation and management of complications in order to reduce death rates. They
are in need of constant monitoring.
Special care should be given to prevent hypothermia. Children should be washed during
daytime and dried immediately. Windows must be kept closed at night and children away
from windows and draughts. They should be clothed properly, including head coverage. Room
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Source: Management of severe malnutrition: a manual for physicians and other senior health workers, WHO,
Geneva, 1999.
145
temperature should be at 25-30 C or 77-86 F, that is uncorfotable for fully clothed active
adults.
Intravenous infusions should be given only when absolutely necessary (septic shock, severe
dyhydration) and intramuscular injections should be given with care at the bottocks and with
the smallest possible fluid volume, using the smallest available gauge needle. To avoid
nosocomial infections, children should be kept at a special unit or place, away from other
admitted patients if possible.
Initial treatment begins with admission into the hospital or Treatment Feeding Center (TFC)
and lasts 2-7 days until the child can be fed easily and appetite has returned. If this initial
phase takes longer than 10 days, the child is failing to respond and additional measures are
required.
Main tasks during initial treatment include:
➠
➠
➠
➠
➠
➠
treat or prevent hypoglycaemia and hypothermia
treat or prevent dehydration and restore electrolyte balance
treat incipient or developed septic shock if present
start feeding the child
treat infection
identify and treat any other problems, including vitamin deficiency, severe anaemia
and heart failure as indicated
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Those tasks will be further analyzed below in detail.
146
Hypoglycaemia
All malnourished children are at risk of developing hypoglycaemia (Gluc <54mg/dl or
3mmol) which is an important cause of death during the first 2 days of treatment.
Hypoglycaemia can be triggered by a serious infection or if the child has not been fed for 46 hours as it usually happens during the trip to the hospital. To prevent this, a child should be
fed every 2-3 hours around the clock.
Signs of hypoglycaemia
➤
➤
➤
➤
➤
➤
low body temperature <36 Æ C
lethargy
limpness
conciousness loss
sweating and pallor are usually absent
drowsiness (usually before death)
If hypoglycaemia is suspected treatment should be given immediately without laboratory
confirmation: it can do no harm, even if diagnosis is incorrect. If the patient is conscious or
can be roused and is able to drink, give 50 ml of 10% glucose or sucrose, or give F-75 diet
by mouth, whichever is available most quickly. If only 50% glucose solution is available, dilute
one part to four parts of sterile water. Stay with the child until he or she is fully alert. If the
child is losing consciousness, cannot be aroused or has convulsions, give 5 ml/kg of body
weight of sterile 10% glucose intravenously (IV), followed by 50 ml of10% glucose or sucrose
by nasogastric (NG) tube. If IV glucose cannot be given immediately, give the NG dose first.
When the child regains consciousness, immediately begin giving F-75 diet or glucose in water
(60 g/l). Continue frequent oral or NG feeding with F-75 diet to prevent a recurrence. All
malnourished children with suspected hypoglycaemia should also be treated with broadspectrum antimicrobials for serious systemic infection.
Infants under 12 months, and those with marasmus, large areas of damaged skin or
serious infections are highly susceptible to hypothermia. If the rectal temperature is below
35.5 C (95.9 F) or the underarm temperature is below 35.0 C (95.0 F), the child should be
warmed. Either use the “kangaroo technique” by placing the child on the mother’s bare chest
or abdomen (skin-to-skin) and covering both of them, or clothe the child well (including the
head), cover with a warmed blanket and place an incandescent lamp over, but not touching,
the child’s body. Fluorescent lamps are of no use and hotwater bottles are dangerous.
The rectal temperature must be measured every 30 minutes during rewarming with a
lamp, as the child may rapidly become hyperthermic. The underarm temperature is not a
reliable guide to body temperature during rewarming. All hypothermic children must also
be treated for hypoglycaemia and for serious systemic infection.
Dehydration and septic shock
Dehydration and septic shock are difficult to differentiate in a child with severe
malnutrition. Signs of hypovolaemia are seen in both conditions, and progressively worsen
if treatment is not given. Dehydration progresses from “some” to “severe”, reflecting 5-10%
and >10% weight loss, respectively, whereas septic shock progresses from “incipient” to
“developed”, as blood flow to the vital organs decreases. Moreover, in many cases of septic
shock there is a history of diarrhoea and some degree of dehydration, giving a mixed clinical
picture.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Hypothermia
147
Diagnosis
Many of the signs that are normally used to assess dehydration are unreliable in a child with
severe malnutrition, making it difficult or impossible to detect dehydration reliably or
determine its severity. Moreover, many signs of dehydration are also seen in septic shock. This
has two results:
➠ dehydration tends to be overdiagnosed and its severity overestimated; and
➠ it is often necessary to treat the child for both dehydration and septic shock.
(a) Signs of dehydration and/or septic shock that are reliable in a child with severe
malnutrition include:
HISTORY OF DIARRHOEA
A child with dehydration should have a history of watery diarrhoea. Small mucoid stools
are commonly seen in severe malnutrition, but do not cause dehydration. A child with signs
of dehydration, but without watery diarrhoea, should be treated as having septic shock.
THIRST
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Drinking eagerly is a reliable sign of “some” dehydration. In infants this may be expressed
as restlessness. Thirst is not a symptom of septic shock.
148
HYPOTHERMIA
When present, this is a sign of serious infection, including septic shock. It is not a sign of
dehydration.
SUNKEN EYES
These are a helpful sign of dehydration, but only when the mother says the sunken
appearance is recent.
WEAK OR ABSENT RADIAL PULSE
This is a sign of shock, from either severe dehydration or sepsis. As hypovolaemia develops,
the pulse rate increases and the pulse becomes weaker. If the pulse in the carotid, femoral
or brachial artery is weak, the child is at risk of dying and must be treated urgently.
COLD HANDS AND FEET
This is a sign of both severe dehydration and septic shock. It should be assessed with the
back of the hand.
URINE FLOW
Urine flow diminishes as dehydration or septic shock worsens. In severe dehydration or
fully developed septic shock, no urine is formed.
(b) Signs of dehydration that are not reliable include:
MENTAL STATE
A severely malnourished child is usually apathetic when left alone and irritable when
handled. As dehydration worsens, the child progressively loses consciousness. Hypoglycaemia,
hypothermia and septic shock also cause reduced consciousness.
MOUTH, TONGUE AND TEARS
The salivary and lacrimal glands are atrophied in severe malnutrition, so the child usually
has a dry mouth and absent tears. Breathing through the mouth also makes the mouth dry.
SKIN ELASTICITY
The loss of supporting tissues and absence of subcutaneous fat make the skin thin and
loose. It flattens very slowly when pinched, or may not flatten at all. Oedema, if present, may
mask diminished elasticity of the skin. The clinical features of dehydration and septic shock
are compared in table in page 52.
INCIPIENT SEPTIC SHOCK
The child is usually limp, apathetic and profoundly anorexic, but is neither thirsty nor
restless.
DEVELOPED SEPTIC SHOCK
The superficial veins, such as the external jugular and scalp veins, are dilated rather than
constricted. The veins in the lungs may also become engorged, making the lungs stiffer than
normal. For this reason the child may groan, grunt, have a shallow cough and appear to have
difficulty breathing. As shock worsens, kidney, liver, intestinal or cardiac failure may occur.
There may be vomiting of blood mixed with stomach contents (“coffee-ground vomit”), blood
in the stool, and abdominal distension with “abdominal splash”; intestinal fluid may be visible
on X-ray. When a child reaches this stage, survival is unlikely.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
(c) Additional signs of septic shock:
149
Treatment of dehydration
Whenever possible, a dehydrated child with severe malnutrition should be rehydrated orally.
IV infusion easily causes overhydration and heart failure and should be used only when there
are definite signs of shock.
Oral rehydration salts (ORS) solution
for severely malnourished children
Because severely malnourished children are deficient in potassium and have abnormally
high levels of sodium, the oral rehydration salts (ORS) solution should contain less sodium and
more potassium than the standard WHO-recommended solution. Magnesium, zinc and copper
should also be given to correct deficiencies of these minerals. The composition of the
recommended ORS solution for severely malnourished children (ReSoMal) is given below.
ReSoMal is available commercially. However, ReSoMal can also be made by diluting one packet
of the standard WHO-recommended ORS in 2 litres of water, instead of 1 litre, and adding 50
g of sucrose (25 g/l) and 40 ml (20 ml/l) of mineral mix solution.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Comparison of clinical signs of dehydration
and septic shock in the severely malnourished child
150
Amount of ReSoMal to give
Between 70 and 100 ml of ReSoMal per kg of body weight is usually enough to restore
normal hydration. Give this amount over 12 hours, starting with 5 ml/kg every 30 minutes for
the first 2 hours orally or by NG tube, and then 5–10 ml/kg per hour. This rate is slower than
for children who are not severely malnourished. Reassess the child at least every hour. The
exact amount to give should be determined by how much the child will drink, the amount
of ongoing losses in the stool, and whether the child is vomiting and has any signs of
overhydration, especially signs of heart failure. ReSoMal should be stopped if:
➠ the respiratory and pulse rates increase;
➠ the jugular veins become engorged; or
➠ there is increasing oedema (e.g. puffy eyelids).
Rehydration is completed when the child is no longer thirsty, urine is passed and any other
signs of dehydration have disappeared. Fluids given to maintain hydration should be based
on the child’s willingness to drink and, if possible, the amount of ongoing losses in the stool.
As a guide, children under 2 years should be given 50–100 ml (between one-quarter and onehalf of a large cup) of ReSoMal after each loose stool, while older children should receive
100–200 ml. Continue this treatment until diarrhoea stops.
How to give ReSoMal
Children who can drink may be given the required amount as sips or by spoon every few
minutes. However, malnourished children are weak and quickly become exhausted, so they
may not continue to take enough fluid voluntarily. If this occurs, the solution should be given
by NG tube at the same rate. An NG tube should be used in all weak or exhausted children,
and in those who vomit, have fast breathing or painful stomatitis.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Comparison of oral rehydration salts solution for severely malnourished children (ReSoMal)
151
Intravenous rehydration
The only indication for IV infusion in a severely malnourished child is circulatory collapse
caused by severe dehydration or septic shock. Use one of the following solutions (in order
of preference):
➠ half-strength Darrow’s solution with 5% glucose (dextrose)
➠ Ringer’s lactate solution with 5% glucose
➠ 0.45% (half-normal) saline with 5% glucose
Give 15 ml/kg IV over 1 hour and monitor the child carefully for signs of overhydration.
While the IV drip is being set up, also insert an NG tube and give ReSoMal through the tube
(10 ml/kg per hour). Reassess the child after 1 hour. If the child is severely dehydrated, there
should be an improvement with IV treatment and his or her respiratory and pulse rates should
fall. In this case, repeat the IV treatment (15 mg/kg over 1 hour) and then switch to ReSoMal
orally or by NG tube (10 ml/kg per hour) for up to 10 hours. If the child fails to improve after
the first IV treatment and his or her radial pulse is still absent, then assume that the child
has septic shock and treat accordingly.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Feeding during rehydration
152
Breastfeeding should not be interrupted during rehydration. Begin to give the F-75 diet
as soon as possible, orally or by NG tube, usually within 2–3 hours after starting orally. IV
infusion easily causes overhydration and heart failure and should be used only when there are
definite signs of shock.
Oral rehydration salts (ORS) solution
for severely malnourished children
Because severely malnourished children are deficient in potassium and have abnormally
high levels of sodium, the oral rehydration salts (ORS) solution should contain less sodium and
more potassium than the standard WHO-recommended solution. Magnesium, zinc and copper
should also be given to correct deficiencies of these minerals. ReSoMal is available
commercially.
Feeding during rehydration
If the child is alert and drinking, give the F-75 diet immediately, even before rehydration
is completed. Usually the diet and ReSoMal are given in alternate hours. If the child vomits,
give the diet by NG tube. When the child stops passing watery stools, continue feeding.
Treatment of septic shock
All severely malnourished children with signs of incipient or developed septic shock should
be treated for septic shock. This includes especially children with:
➠ signs of dehydration, but without a history of watery diarrhoea;
➠ hypothermia or hypoglycaemia;
➠ oedema and signs of dehydration.
Incipient septic shock
The child should be fed promptly to prevent hypoglycaemia, using the F-75 diet with
added mineral mix. As these children are nearly always anorexic, the diet must be given by
NG tube. The amounts to be given and frequency of feeding are described in page 157.
Developed septic shock
Begin IV rehydration immediatelly. Give 15 ml/kg per hour. Observe the child carefully
(every 5-10 minutes) for signs of overhydration and congestive heart failure. As soon as the
radial pulse becomes strong and the child regains consciousness, continue rehydration orally
or by NG tube. If signs of congestive heart failure develop or the child does not improve after
1 hour of IV therapy, give a blood transfusion (10ml/kg) slowly over at least 3 hours). If blood
is not available, give plasma. If there are signs of liver failure (e.g. purpura, jaundice, enlarged
tender liver), give a single dose of 1mg of vitamin K intramuscularly.
During the blood transfusion, nothing else should be given, so as to minimize the risk of
congestive heart failure. If there is any sign of congestive heart failure (e.g. distension of
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Every child with septic shock should immediately be given broad-spectrum antibiotics and
be kept warm to prevent or treat hypothermia. The child should not be handled any more
than is essential for treatment. Nor should the child be washed or bathed; after the child
has defecated, his or her bottom can be cleaned with a damp cloth. Iron supplements should
not be given. Other treatment is described below.
153
the jugular veins, increasing respiratory rate or respiratory distress), give a diuretic and slow
the rate of transfusion. Steroids, epinephrine or nikethamide are of no value and should never
be used.
After the transfusion, begin to give F-75 diet by NG tube (see page 157). If the child
develops increasing abdominal distension or vomits repeatedly, give the diet more slowly.
If the problem does not resolve, stop feeding the child and give only fluids by IV infusion
at a rate of 2–4 ml/kg per hour. Also give 2 ml of 50% magnesium sulfate solution
intramuscularly (IM).
Dietary treatment
Children who do not require other emergency treatment, especially for hypothermia,
dehydration or septic shock, should immediately be given a formula diet. They should also
continue to be breastfed.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Formula diets for severely malnourished children
154
Almost all severely malnourished children have infections, impaired liver and intestinal
function, and problems related to imbalance of electrolytes when first admitted to hospital.
Because of these problems, they are unable to tolerate the usual amounts of dietary protein,
fat and sodium. It is important, therefore, to begin feeding these children with a diet that is
low in these nutrients, and high in carbohydrate.
Two formula diets, F-75 and F-100, are used for severely malnourished children. F-75 (75
kcalth or 315 kJ/100 ml), is used during the initial phase of treatment, while F-100 (100 kcalth
or 420 kJ/100 ml) is used during the rehabilitation phase, after the appetite has returned.
These formulas can easily be prepared from the basic ingredients: dried skimmed milk, sugar,
cereal flour, oil, mineral mix and vitamin mix. They are also commercially available as powder
formulations that are mixed with water. The mineral mix supplies potassium, magnesium and
other essential minerals; it must be added to the diet. The potassium deficit, present in all
malnourished children, adversely affects cardiac function and gastric emptying. Magnesium is
essential for potassium to enter cells and be retained. The mineral mix does not contain iron
as this is withheld during the initial phase.
Feeding on admission
Nasogastric feeding
Despite coaxing and patience, many children will not take sufficient diet by mouth during
the first few days of treatment. Common reasons include a very poor appetite, weakness and
painful stomatitis. Such children should be fed using a NG tube. However, NG feeding should
end as soon as possible. At each feed, the child should first be offered the diet orally. After
the child has taken as much as he or she wants, the remainder should be given by NG tube.
The NG tube should be removed when the child is taking three-quarters of the day’s diet
orally, or takes two consecutive feeds fully by mouth. If over the next 24 hours the child fails
to take 80 kcalth or 336 kJ/kg, the tube should be reinserted. If the child develops abdominal
distension during NG feeding, give 2 ml of a 50% solution of magnesium sulfate IM.
The NG tube should always be aspirated before fluids are administered. It should also be
properly fixed so that it cannot move to the lungs during feeding. NG feeding should be done
by experienced staff.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
To avoid overloading the intestine, liver and kidneys, it is essential that food be given
frequently and in small amounts. Children who are unwilling to eat should be fed by NG tube
(do not use IV feeding). Children who can eat should be given the diet every 2, 3 or 4 hours,
day and night. If vomiting occurs, both the amount given at each feed and the interval
between feeds should be reduced. The F-75 diet should be given to all children during the
initial phase of treatment. The child should be given at least 80 kcalth or 336 kJ/kg, but no
more than 100 kcalth or 420 kJ/kg per day. If less than 80 kcalth or 336 kJ/kg per day are given,
the tissues will continue to be broken down and the child will deteriorate. If more than 100
kcalth or 420 kJ/kg per day are given, the child may develop a serious metabolic imbalance.
For example, if a child weighing 7.0 kg is given the F-75 diet every 2 hours, each feed
should be 75 ml. During the initial phase of treatment, maintain the volume of F-75 feed at
130 ml/kg per day, but gradually decrease the frequency of feeding and increase the volume
of each feed until you are giving the child feeds 4-hourly (6 feeds per day). Nearly all
malnourished children have poor appetites when first admitted to hospital. Patience and
coaxing are needed to encourage the child to complete each feed. The child should be fed
from a cup and spoon; feeding bottles should never be used, even for very young infants,
as they are an important source of infection. Children who are very weak may be fed using
a dropper or a syringe. While being fed, the child should always be held securely in a sitting
position on the attendant’s or mother’s lap. Children should never be left alone in bed to feed
themselves.
155
Preparation of F-75 and F-100 diets
a-d
e-f
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Ingredient Amount in F-75a-d, F-100e-f
156
a. To prepare the F-75 diet, add the dried skimmed milk, sugar, cereal flour and oil to some water and mix. Boil
for 5–7 minutes. Allow to cool, then add the mineral mix and vitamin mix and mix again. Make up the
volume to 1000 ml with water.
b. A comparable formula can be made from 35 g of whole dried milk, 70 g of sugar, 35 g of cereal flour, 17
g of oil, 20 ml of mineral mix, 140 mg of vitamin mix and water to make 1000 ml. Alternatively, use 300
ml of fresh cows’ milk, 70 g of sugar, 35 g of cereal flour, 17g of oil, 20 ml of mineral mix, 140 mg of vitamin
mix and water to make 1000 ml.
c. Isotonic versions of F-75 (280 mOsmol/l), which contain maltodextrins instead of cereal flour and some of
the sugar and which include all the necessary micronutrients, are available commercially.
d. If cereal flour is not available or there are no cooking facilities, a comparable formula can be made from
25 g of dried skimmed milk, 100 g of sugar, 27 g of oil, 20 ml of mineral mix, 140 mg of vitamin mix and
water to make 1000 ml. However, this formula has a high osmolarity (415 mOsmol/l) and may not be well
tolerated by all children, especially those with diarrhoea.
e. To prepare the F-100 diet, add the dried skimmed milk, sugar and oil to some warm boiled water and mix.
Add the mineral mix and vitamin mix and mix again. Make up the volume to 1000 ml with water.
f. A comparable formula can be made from 110 g of whole dried milk, 50 g of sugar, 30 g of oil, 20 ml of
mineral mix, 140 mg of vitamin mix and water to make 1000 ml. Alternatively, use 880 ml of fresh cows’
milk, 75 g of sugar, 20 g of oil, 20 ml of mineral mix, 140 mg of vitamin mix and water to make 1000 ml.
g. If only small amounts of feed are being prepared, it will not be feasible to prepare the vitamin mix because
of the small amounts involved. In this case, give a proprietary multivitamin supplement. Alternatively, a
combined mineral and vitamin mix for malnourished children is available commercially and can be used in
the above diets.
Feeding after the appetite improves
If the child’s appetite improves, treatment has been successful. The initial phase of
treatment ends when the child becomes hungry. This indicates that infections are coming under
control, the liver is able to metabolize the diet, and other metabolic abnormalities are
improving. The child is now ready to begin the rehabilitation phase. This usually occurs after
2–7 days. Some children with complications may take longer, whereas others are hungry from
the start and can be transferred quickly to F-100. Nevertheless, the transition should be gradual
to avoid the risk of heart failure which can occur if children suddenly consume large amounts
of feed. Replace the F-75 diet with an equal amount of F-100 for 2 days before increasing the
volume offered at each feed. It is important to note that it is the child’s appetite and general
condition that determine the phase of treatment and not the length of time since admission.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Determining the amount of diet to give at each feed to achieve a daily intake
of 100 kcalth or 420 kJ/kg
157
Milk intolerance
Clinically significant milk intolerance is unusual in severely malnourished children.
Intolerance should be diagnosed only if copious watery diarrhoea occurs promptly after milkbased feeds (e.g. F-100) are begun, the diarrhoea clearly improves when milk intake is reduced
or stopped, and it recurs when milk is given again. Other signs include acidic faeces (pH 5.0)
and the presence of increased levels of reducing substances in the faeces. In such cases, the
milk should be partially or totally replaced by yoghurt or a commercial lactose-free formula.
Before the child is discharged, milk-based feeds should be given again to determine whether
the intolerance has resolved.
Recording food intake
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
The type of feed given, the amounts offered and taken, and the date and time must be
recorded accurately after each feed. If the child vomits, the amount lost should be estimated
in relation to the size of the feed (e.g. a whole feed, half a feed), and deducted from the total
intake. Once a day the energy intake for the past 24 hours should be determined and
compared with the child’s weight. If the daily intake is less than 80 kcalth or 336 kJ/kg, the
amount of feed offered should be increased. If more than 100 kcalth or 420 kJ/kg have been
given, the amount of feed offered should be reduced. A sample form for recording food intake
is given.
158
Infections
Bacterial infections
Nearly all severely malnourished children have bacterial infections when first admitted
to hospital. Many have several infections caused by different organisms. Infection of the lower
respiratory tract is especially common. Although signs of infection should be carefully looked
for when the child is evaluated, they are often difficult to detect. Unlike well-nourished
children, who respond to infection with fever and inflammation, malnourished children with
serious infections may only become apathetic or drowsy. Early treatment of bacterial infections
with effective antimicrobials improves the nutritional response to feeding, prevents septic
shock and reduces mortality.
Because bacterial infections are common and difficult to detect, all children with severe
malnutrition should routinely receive broad-spectrum antimicrobial treatment when first
admitted for care. Each institution should have a policy on which antimicrobials to use.These
are divided into those used for first-line treatment, which are given routinely to all severely
malnourished children, and those used for second-line treatment, which are given when a
child is not improving or a specific infection is diagnosed. Although local resistance patterns
of important bacterial pathogens and the availability and cost of the antimicrobials will
determine the policy, a suggested scheme is given below.
First-line treatment
Children with no apparent signs of infection and no complications should be given
cotrimoxazole (25 mg of sulfamethoxazole 5 mg of trimethoprim/kg) orally twice daily for 5
days.
Children with complications (septic shock, hypoglycaemia, hypothermia, skin infections,
respiratory or urinary tract infections, or who appear lethargic or sickly) should be given:
➠ ampicillin, 50mg/kg IM or IV every 6 hours for 2 days, followed by amoxicillin, 15mg/kg
orally every 8 hours for 5 days (if amoxicillin is unavailable, give ampicillin, 25mg/kg
orally every 6 hours) and
➠ gentamicin, 7.5 mg/kg IM or IV once daily for 7 days.
If the child fails to improve within 48 hours, add chloramphenicol, 25mg/kg IM or IV every
8 hours (or every 6 hours if meningitis is suspected) for 5 days. Further details of antimicrobial
treatment are given The duration of treatment depends on the response and nutritional status
of the child. Antimicrobials should be continued for at least 5 days. If anorexia still persists
after 5 days of treatment, give the child another 5-day course. If anorexia still persists after
10 days of treatment, reassess the child fully. Examine the child for specific infections and
potentially resistant organisms, and check that vitamin and mineral supplements have been
correctly given.
If specific infections are detected for which additional treatment is needed, for example
dysentery, candidiasis, malaria or intestinal helminthiasis, this should also be given.
Tuberculosis is common, but antituberculosis drugs should be given only when tuberculosis is
diagnosed.
Note: Some institutions routinely give malnourished children metronidazole, 7.5 mg/kg
every 8 hours for 7 days, in addition to broad-spectrum antimicrobials. However, the efficacy
of this treatment has not been established by clinical trials.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Second-line treatment
159
Measles and other viral infections
All malnourished children should receive measles vaccine when admitted to hospital. This
protects other children in hospital from catching the disease, which is associated with a high
rate of mortality. A second dose of vaccine should be given before discharge. There is no
specific treatment for measles, disseminated herpes or other systemic viral infections.
However, most children with these infections develop secondary systemic bacterial infections
and septic shock. If fever is present, antipyretics should be given.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Vitamin A deficiency
160
Severely malnourished children are at high risk of developing blindness due to vitamin A
deficiency. For this reason a large dose of vitamin A should be given routinely to all
malnourished children on day 1, unless there is definitive evidence that a dose has been given
during the past month. The dose is as follows:1 50 000 International Units (IU) orally for
infants <6 months of age, 100 000 IU orally for infants 6-12 months of age and 200000 IU
orally for children >12 months of age. If there are any clinical signs of vitamin A deficiency
(e.g. night blindness, conjunctival xerosis with Bitot’s spots, corneal xerosis or ulceration, or
keratomalacia), a large dose should be given on the first 2 days, followed by a third dose at
least 2 weeks later. Oral treatment is preferred, except at the beginning in children with severe
anorexia, oedematous malnutrition or septic shock, who should be given IM treatment. For
oral treatment, oil-based preparations are preferred, but water-miscible formulations may
be used if oil-based formulations are not available. Only water-miscible formulations should
be used for IM treatment. Great care must be taken during examination of the eyes, as they
easily rupture in children with vitamin A deficiency. The eyes should be examined gently for
signs of xerophthalmia, corneal xerosis and ulceration, cloudiness and keratomalacia. If there
is ocular inflammation or ulceration, protect the eyes with pads soaked in 0.9% saline.
Tetracycline eye drops (1%) should be instilled four times daily until all signs of inflammation
or ulceration resolve. Atropine eye drops (0.1%) should also be applied and the affected eye(s)
should be bandaged, as scratching with a finger can cause rupture of an ulcerated cornea.
More details on the management of vitamin A deficiency are given elsewhere.
Other vitamin deficiencies
All malnourished children should receive 5 mg of folic acid orally on day 1 and then 1mg
orally per day thereafter. Many malnourished children are also deficient in riboflavin, ascorbic
acid, pyridoxine, thiamine and the fat-soluble vitamins D, E and K. All diets should be fortified
with these vitamins by adding the vitamin mix.
Treatment of clinical vitamin A deficiency in children
a. For oral administration, preferably in an oil-based preparation, except in children with severe anorexia,
oedematous malnutrition or septic shock.
b. The international standard (or reference preparation) of vitamin A has been discontinued. However, the
international units for vitamin A are still used extensively, particularly in the labelling of capsules and
injectable preparations.
If the haemoglobin concentration is less than 40 g/l or the packed-cell volume is less than
12%, the child has very severe anaemia, which can cause heart failure. Children with very
severe anaemia need a blood transfusion. Give 10 ml of packed red cells or whole blood per
kg of body weight slowly over 3 hours. Where testing for HIV and viral hepatitis B is not
possible, transfusion should be given only when the haemoglobin concentration falls below
30 g/l (or packed-cell volume below 10%), or when there are signs of life-threatening heart
failure. Do not give iron during the initial phase of treatment, as it can have toxic effects
and may reduce resistance to infection.
Congestive heart failure
This is usually a complication of overhydration (especially when an IV infusion or standard
ORS solution is given), very severe anaemia, blood or plasma transfusion, or giving a diet with
a high sodium content. The first sign of heart failure is fast breathing (50 breaths per minute
or more if the child is aged 2 months up to 12 months; 40 breaths per minute or more if the
child is aged 12 months up to 5 years). Later signs are respiratory distress, a rapid pulse,
engorgement of the jugular vein, cold hands and feet, and cyanosis of the fingertips and
under the tongue. Heart failure must be differentiated from respiratory infection and septic
shock, which usually occur within 48 hours of admission, whereas heart failure usually occurs
somewhat later. When heart failure is caused by fluid overload, the following measures should
be taken:
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Very severe anaemia
161
➠ Stop all oral intake and IV fluids; the treatment of heart failure takes precedence over
feeding the child. No fluid should be given until the heart failure is improved, even if
this takes 24-48 hours.
➠ Give a diuretic IV. The most appropriate choice is furosemide (1 mg/kg).
➠ Do not give digitalis unless the diagnosis of heart failure is unequivocal (jugular venous
pressure is elevated) and the plasma potassium level is normal. In that case, 5mg/kg of
body weight of digoxin may be given IV as a single dose, or orally, if the IV preparation
is not available.
There is no reported experience in malnourished children of angiotensin-converting
enzyme inhibitors or other drugs used to treat congestive heart failure. Diuretics should never
be used to reduce oedema in malnourished children.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Dermatosis of kwashiorkor
162
This is characterized by hypo- or hyperpigmentation, shedding of the skin in scales or
sheets, and ulceration of the skin of the perineum, groin, limbs, behind the ears and armpits.
There may be widespread weeping skin lesions which easily become infected. Spontaneous
resolution occurs as nutrition improves. Atrophy of the skin in the perineum leads to severe
diaper dermatitis, especially if the child has diarrhoea. The diaper area should be left
uncovered. If the diaper area becomes colonized with Candida spp., it should be treated with
nystatin ointment or cream (100000 IU (1 g)) twice daily for 2 weeks and the child should
be given oral nystatin (100 000 IU four times daily). In other affected areas, application of zinc
and castor oil ointment, petroleum jelly or paraffin gauze dressings helps to relieve pain and
prevent infection. The zinc supplement contained in the mineral mix is particularly important
in these children, as they are usually severely deficient. Bathe the affected areas in 1%
potassium permanganate solution for 10–15 minutes daily. This dries the lesions, helps to
prevent loss of serum, and inhibits infection. Polyvidone iodine, 10% ointment, can also be
used. It should be used sparingly, however, if the lesions are extensive, as there is significant
systemic absorption. All children with kwashiorkor-related dermatosis should receive systemic
antibiotics.
Rehabilitation
The child is deemed to have entered the rehabilitation phase when his or her appetite has
returned. A child who is being fed by NG tube is not considered ready to enter the rehabilitation phase.
Principles of management
The principal tasks during the rehabilitation phase are:
➠
➠
➠
➠
to encourage the child to eat as much as possible;
to re-initiate and/or encourage breastfeeding as necessary;
to stimulate emotional and physical development; and
to prepare the mother or carer to continue to look after the child after discharge.
The child should remain in hospital for the first part of the rehabilitation phase. When
all the criteriabelow have been met (usually 2–3 weeks after admission), the child can be
transferred to a nutrition rehabilitation centre.
Criteria for transfer to a nutrition rehabilitation centre
Eating well
Mental state has improved: smiles, responds to stimuli, interested in surroundings
Sits, crawls, stands or walks (depending on age)
Normal temperature (36.5-37.5 ÆC)
No vomiting or diarrhoea
No oedema
Gaining weight: >5 g/kg of body weight per day for 3 successive days
Nutritional rehabilitation
The most important determinant of the rate of recovery is the amount of energy
consumed. However, at the start of the rehabilitation phase, the child is still deficient in
protein and various micronutrients, including potassium, magnesium, iron and zinc. These
must also be given in increased amounts. Infants under 24 months can be fed exclusively on
liquid or semi-liquid formulas. It is usually appropriate to introduce solid foods for older
children.
Feeding children under 24 months
During rehabilitation, F-100 diet should be given every 4 hours, night and day. Transition
to the rehabilitation phase involves increasing the amount of diet given at each feed by 10 ml
(e.g. if the first feed is 60 ml, the second should be 70 ml, the third 80 ml, and so on) until the
child refuses to finish the feed. When a feed is not finished, the same amount should be
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
➤
➤
➤
➤
➤
➤
➤
163
offered at the next feed. If that feed is finished, the amount offered for the following feed
should be increased by 10 ml. Continue this process until some food is left after most feeds.
The amount being offered should then be dispensed for the child at each feed on subsequent
days. The amounts of each feed offered and taken should be recorded on the feeding chart
and any food not taken should be discarded; never reuse it for the next feed. During
rehabilitation most children take between 150 and 220 kcalth/kg (630–920 kJ/kg) per day. If
intake is below 130 kcalth or 540 kJ/kg per day, the child is failing to respond.
The attitude of those feeding the child is crucial to success. Sufficient time must be spent
with the child to enable him or her to finish each feed. The child must be actively encouraged
to eat while sitting comfortably on the mother’s or nurse’s lap. Children must never be left
alone to “take what they want”.
During the first few days of rehabilitation, children with oedema may not gain weight,
despite an adequate intake. This is because oedema fluid is being lost while tissue is being
restored. Thus, progress in these children is seen as decreased oedema rather than rapid
weight gain. If the child is neither gaining weight nor showing decreased oedema, or if there
is increasing oedema, the child is failing to respond. F-100 should be continued until the child
achieves >1 SD (90%) of the median NCHS/WHO reference values for weight-for-height. When
this occurs appetite diminishes and increasing amounts of food are left uneaten. The child
is now ready for the discharge phase of treatment.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Feeding children over 24 months
164
Children over 24 months can also be successfully treated with increasing quantities of F100; it is not essential to use a different diet. This has practical value in refugee camps where
it is important to keep the number of different diets to a minimum. For most older children,
however, it is appropriate to introduce solid food, especially for those who want a mixed diet.
Most traditional mixed diets have a lower energy content than F-100. They are also relatively
deficient in minerals, particularly potassium and magnesium, and contain substances which
inhibit the absorption of zinc, copper and iron. Moreover, the diets are usually deficient in
various vitamins. Thus, local foods should be fortified to increase their content of energy,
minerals and vitamins. Oil should be added to increase the energy content, and the mineral
and vitamin mixes used in F-100 should be added after cooking. Other ingredients, such as
dried skimmed milk, may also be added to increase the protein and mineral content. The
energy content of mixed diets should be at least 1 kcalth or 4.2 kJ/g. To avoid the effects of
food substances which reduce the absorption of minerals, F-100 should be given between
feeds of the mixed diet. For example, if the mixed diet is given three times daily, F-100 should
also be given three times daily, making six feeds a day. Water intake is not usually a problem
in children over 2 years because they can ask for it when they are thirsty.
At the beginning of rehabilitation, the children should be fed every 4 hours, day and night
(six feeds per 24 hours). When they are growing well and are no longer at risk of developing
hypothermia or hypoglycaemia, one of the night-time feeds can be omitted, making five feeds
per 24 hours. This allows the child longer undisturbed sleep and makes it much easier to
manage the child as a day-patient. It is also less taxing for those caring for the child.
Folic acid and iron
Nearly all severely malnourished children have anaemia and should be given supplementary folic acid and iron. They should also continue to receive the vitamin and mineral
mixes in their food throughout rehabilitation. Iron should never be given during the initial
phase of treatment, but must be given during the rehabilitation phase. It should only be given
orally, never by injection. Children with moderate or severe anaemia should be given
elemental iron, 3 mg/kg per day in two divided doses, up to a maximum of 60mg daily, for
3 months. It is preferable to give iron supplements between meals using a liquid preparation.
All children must be given 5 mg of folic acid on day 1 and then 1mg per day thereafter.
Assessing progress
The child should be weighed daily and the weight plotted on a graph. It is useful to mark
weight-for-height on the graph, which is the target weight for discharge. The usual weight
gain is about 10-15 g/kg per day. A child who does not gain at least 5 g/kg per day for 3
consecutive days is failing to respond to treatment . With high-energy feeding, most severely
malnourished children reach their target weight for discharge after 2-4 weeks.
Emotional and physical stimulation
Severely malnourished children have delayed mental and behavioural development, which,
if not treated, can become the most serious long-term result of malnutrition. Emotional and
physical stimulation through play programmes that start during rehabilitation and continue
after discharge can substantially reduce the risk of permanent mental retardation and
emotional impairment.
Care must be taken to avoid sensory deprivation. The child’s face must not be covered; the
child must be able to see and hear what is happening around him or her. The child should
never be wrapped or tied to prevent him or her moving around in the cot. It is essential that
the mother (or carer) be with her child in hospital and at the nutrition rehabilitation centre,
and that she be encouraged to feed, hold, comfort and play with her child as much as
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
the point that is equivalent to 1 SD (90%) of the median NCHS/WHO reference values for
165
possible. The number of other adults who interact with the child should be as few as possible.
Each adult should talk, smile and show affection towards the child. Medical procedures, such
as venepuncture, should be done by the most skilled person available, preferably out of
earshot and sight of the other children. Immediately after any unpleasant procedure the child
should be held and comforted.
The environment
The austerity of a traditional hospital has no place in the treatment of malnourished
children. Rooms should be brightly coloured, with decorations that interest children. Colourful
mobiles should be hung over every cot, if possible. The staff should wear normal clothing
rather than uniforms. Brightly coloured aprons may be used to protect their clothing. A radio
can provide background music. The atmosphere in the ward should be relaxed, cheerful and
welcoming. Toys should always be available in the child’s cot and room, as well as in the
play area; they should be changed frequently. Toys should be safe, washable and appropriate
for the child’s age and level of development. Inexpensive toys made from cardboard boxes,
plastic bottles, tin cans and similar materials are best, because mothers can copy them.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Play activities
166
Malnourished children need interaction with other children during rehabilitation. After
the initial phase of treatment, the child should spend prolonged periods with other children
on large play mats, and with the mother or a play guide. The child can also be fed in the play
area. These activities do not increase the risk of cross-infection appreciably and the benefit
for the child is substantial. One person, usually a nurse or volunteer, should be responsible
for developing a curriculum of play activities and for leading the play sessions. Activities
should be selected to develop both motor and language skills, and new activities and
materials should be introduced regularly. One aim should be to play with each child,
individually, for 15–30 minutes each day, in addition to informal group play. Mothers can
be trained to supervise play sessions. Learning through play should be fun for children. A
child’s efforts to perform a task should always be praised and never criticized. When a child
is taught a skill, the nurse or volunteer should demonstrate the skill first, then help the child
do it, and finally let the child do it alone. This sequence should be repeated until the child
has mastered the skill.
Physical activities
Physical activities promote the development of essential motor skills and may also enhance
growth during rehabilitation. For those children who are unable to move, passive limb
movements and splashing in a warm bath are helpful. For other children, play should include
such activities as rolling on a mattress, running after and tossing a ball, climbing stairs, and
walking. The duration and intensity of physical activities should increase as the child’s
nutritional status and general condition improve. If there is sufficient space, an outdoor
playground should be developed.
All parents should know how to prevent malnutrition from recurring. Before the child is
discharged, ensure that the parents or carers understand the causes of malnutrition and how
to prevent its recurrence, including correct feeding and continuing to stimulate the child’s
mental and emotional development. They must also know how to treat, or obtain treatment
for, diarrhoea and other infections, and understand the importance of regular (every 6
months) treatment for intestinal parasites. The parents have much to learn; teaching them
should not be left until a few days before the child is discharged.
The mother (or carer) should spend as much time as possible at the nutrition
rehabilitation centre with her child. This may be facilitated by providing the mother with
money for transportation and meals. The mother, in turn, should help prepare her child’s
food, and feed and look after her child. A rotation of mothers may also be organized to help
with general activities on the ward, including play, cooking, feeding, bathing and changing
the children, under supervision. This will enable each mother to learn how to care for her
child at home; she will also feel that she is contributing to the work of the centre. Teaching
of mothers should include regular sessions at which important parenting skills are
demonstrated and practised. Each mother should be taught the play activities that are
appropriate for her child, so that she and others in the family can continue to make toys
and play with the child after discharge. The staff must be friendly and treat the mothers
as partners in the care of the children. A mother should never be scolded, blamed for her
child’s problems, humiliated or made to feel unwelcome. Moreover, helping, teaching,
counselling and befriending the mother are an essential part of the long-term treatment of
the child.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Teaching parents how to prevent malnutrition from recurring
167
Preparation for discharge
During rehabilitation, preparations should be made to ensure that the child is fully
reintegrated into the family and community after discharge. As the child’s home is the
environment in which severe malnutrition developed, the family must be carefully prepared
to prevent its recurrence. If possible, the child’s home should be visited by a social worker
or nurse before discharge to ensure that adequate home care can be provided. If the child is
abandoned or conditions at the child’s home are unsuitable, often because of death or
absence of a carer, a foster home should be sought.
Criteria for discharge
A child may be considered to have recovered and be ready for discharge when the child’s
weight-for-height has reached 1 SD (90%) of the median NCHS/WHO reference values. To
achieve this goal, it is essential that the child receives as many meals as possible per day. In
some instances, a child may be discharged before he or she has reached the target weightfor-height for discharge; however, since the child is not yet recovered, he or she will need
continuing care (as an outpatient). To ensure that relapse does not occur, it is important that
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
all the criteria have been met before the child is discharged.
168
Appropriate diets
During rehabilitation the child should be fed at least five times daily. After reaching 1
SD of the median NCHS/WHO reference values, the child should be fed at least three times
daily at home. Adjustment to this change in frequency of feeding should take place under
supervision before discharge. This is done by gradually reducing and eventually stopping the
supplementary feeds of F-100 and adding or increasing the mixed diet until the child is eating
as he or she will at home.
Before discharge, the mother (or carer) must practise preparing the recommended foods
and feeding them to the child. It is essential that the mother demonstrates that she is able
and willing to do these tasks, and that she understands the importance of continued correct
feeding for her child. Appropriate mixed diets are the same as those normally recommended
for a healthy child. They should provide at least 110 kcalth or 460 kJ/kg per day and also
sufficient vitamins and minerals to support continued growth. Breast-feeding should be
continued; animal milk is also an important source of energy and protein. Solid foods should
include a well-cooked staple cereal, to which vegetable oil should be added (5–10 ml for each
100 g serving) to enrich its energy content. The cereal should be soft and mashed; for infants
use a thick pap. A variety of well-cooked vegetables, including orange and dark-green leafy
ones, should be given. If possible, include fruit, meat, eggs or fish. The mother should be
encouraged to give the child extra food between meals.
Immunization
Before discharge, the child should be immunized in accordance with national guidelines.
The mother should be informed of where and when to bring the child for any required booster
doses.
Planning follow-up
Follow-up
Although much improved at the time of discharge, the child usually remains stunted and
mental development is delayed. Management of these conditions and preventing the
recurrence of severe malnutrition requires sustained improvement in feeding of the child and
in other parenting skills. Planned follow-up of the child at regular intervals after discharge
is essential. This should include an efficient strategy for tracing children who fail to attend
follow-up appointments. Such children are at increased risk of recurrence of malnutrition or
of developing other serious illnesses.
As the risk of relapse is greatest soon after discharge, the child should be seen after 1
week, 2 weeks, 1 month, 3 months and 6 months. Provided the child’s weight-for-height is
no less than 1SD (90%) of the median NCHS/WHO reference values, progress is considered
satisfactory. If a problem is found, visits should be more frequent until it is resolved. After 6
months, visits should be twice yearly until the child is at least 3 years old. Children with
frequent problems should remain under supervision longer. The mother should know the
location and regular opening hours of the nearest nutrition clinic and be encouraged to bring
her child without an appointment if the child is ill or a previous appointment was missed.
At each visit the mother should be asked about the child’s recent health, feeding practices
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Before discharge, make an appointment to see the child 1 week after discharge. Followup
visits should preferably take place at a special clinic for malnourished children, not at a general
paediatric clinic.
If possible, arrange for a health worker or field nurse trained to provide practical advice
on health and nutrition to visit the family at home. Also arrange for a social worker to visit
the family, in order to find a way of solving the family’s social and economic problems.
169
and play activities. The child should be examined, weighed and measured, and the results
recorded. Any needed vaccine should be given. Training of the mother should focus on areas
that need to be strengthened, especially feeding practices, and mental and physical
stimulation of the child. Attention should also be given to feeding practices for other children
in the family, and for pregnant or lactating women, as these are likely to be inadequate. If
vitamins or medicines are needed, they should be provided.
Failure to respond to treatment
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
General principles
170
When the treatment guidelines in this manual are followed, a severely malnourished child
without complications should show definite signs of improvement within a few days and
should continue to improve thereafter. Failure to achieve initial improvement at the expected
rate is termed primary failure to respond, whereas deterioration of the child’s condition, when
a satisfactory response has been established, is termed secondary failure to respond.
A child who meets any of the criteria should be diagnosed as failing to respond. When this
diagnosis is made it is essential that practices in the treatment unit are carefully reviewed and
the child is thoroughly re-evaluated. The objective is to identify the cause for failure to
respond and to correct the problem by making specific changes to practices in the unit or
to the child’s treatment. Treatment should never be changed blindly; this is more likely to
be harmful than to help the child. The most frequent causes of failure to respond are listed
below.
Frequent causes of failure to respond
Problems with the treatment facility:
➠
➠
➠
➠
Poor environment for malnourished children
Insufficient or inadequately trained staff
Inaccurate weighing machines
Food prepared or given incorrectly
Problems of individual children:
➠ Insufficient food given
➠ Vitamin or mineral deficiency
➠ Malabsorption of nutrients
➠
➠
➠
➠
Rumination
Infections, especially diarrhoea, dysentery, otitis media, pneumonia, tuberculosis,
urinary tract infection, malaria, intestinal helminthiasis and HIV/AIDS
Serious underlying disease
Problems with the treatment facility
TYPE OF FACILITY
Failure to respond is more likely when a malnourished child is treated in a general
paediatric ward than in a special nutrition unit. This is because the risk of crossinfection is
increased in a general ward, it is more difficult to provide the necessary care and attention,
and staff are less likely to have the essential skills and attitudes for management of
malnourished children. Wherever possible, malnourished children should be managed in a
special nutrition unit. If this is not possible, they should be treated in a specially designated
area of a paediatric ward, by staff specifically trained in the treatment of severe malnutrition.
The special nutrition unit must, however, be well organized. If essential food supplies or
medications are not available, weighing scales do not work properly, diagnostic facilities or
administrative procedures are inadequate, or there are insufficient trained staff, treatment
failure and mortality will be high. An effective management system should ensure careful
monitoring of each child, proper training of nurses and auxiliary staff, use of the most
experienced staff as supervisors, reliable supplies of drugs and food supplements, and reliable
record-keeping.
STAFF
Experienced staff (including junior staff) who understand the needs of malnourished
children and are familiar with the important details of their management are essential for a
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Criteria for failure to respond to treatment
171
well-functioning treatment facility. It is important, therefore, that loss of experienced staff be
avoided wherever possible. For this reason, staff of the treatment facility should not take part
in the routine rotation of staff that is practised in many hospitals. If staff must be changed,
this should be done one person at a time so as to minimize disruption of routines in the
facility.
The attitude of staff towards a particular child can determine whether treatment of the
child will succeed or fail. If staff believe that a child is beyond helping, they may give less
attention to the child. Such children often fail to respond to treatment, which seems to
confirm the opinion of the staff. This “clinical prejudice” may be difficult to correct, especially
when it reflects the views of the most experienced staff. It is essential that staff are reminded
frequently that each child’s well-being depends on their efforts and that every child must
be given their full attention.
INACCURATE WEIGHING MACHINES
Machines used for weighing children easily become inaccurate and, thus, give misleading
information on the progress of children in the facility. Weighing machines must be checked
and adjusted daily following a standard procedure. Records of daily checks should be kept.
Weighing machines used for preparing food or for measuring the ingredients of the mineral
mix should be checked and adjusted weekly.
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Problems with preparing or giving food
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Standard hygiene practices should be used when storing, preparing and handling food
in the kitchen of the hospital or nutrition rehabilitation centre. Hands should be washed with
soap after defecation and before food is handled. Foods should be thoroughly cooked and
served promptly. Any cooked food that will be stored for more than 2 hours should be
refrigerated (after allowing it to cool to room temperature) and re-heated until it is thoroughly
hot (and then allowed to cool) before being served. Persons with infections on their hands
should not handle food. Each person involved in preparing food should be checked to ensure
that they are following the correct procedures for weighing, measuring, mixing, cooking
and storing the food. Observe the feeds being made; check that the recipes are correct and
all ingredients are added.
Ensure that sufficient time is allocated to feeding each child and that there are enough
staff, day and night, for this task. Remember that feeding a malnourished child takes more
time and patience than feeding a normal child. If it is assumed that it takes about 15 minutes
to feed each child and that food is given every 3 hours, one person is needed, day and night,
to feed 12 children. When food is given every 2 hours, more staff are needed. If there are
not enough staff, treatment of a child may fail because insufficient time is taken for feeding.
Having the mother help with feeding her child can relieve this situation.
Problems with individual children
FEEDING
Are sufficient vitamins and minerals being given?
Nutrient deficiency can result from the increased requirements related to the synthesis of
new tissue during rapid growth. When this happens, there is usually an initial period of rapid
growth, after which growth slows or stops even though food intake is adequate. Deficiencies
of potassium, magnesium, zinc, copper or iron may be responsible. Diets are often deficient
in these minerals and commercial vitamin and mineral preparations do not provide them in
sufficient amounts for severely malnourished children. This problem can be avoided by ensuring
that the mineral and vitamin mixes described in are added to the child’s food every day.
Is the child ruminating?
Rumination is a condition that occurs in up to 10% of severely malnourished, emotionally
impaired children. It should be suspected when a child eats well, but fails to gain weight.
Children with this condition regurgitate food from the stomach into the mouth, and then
vomit part of it and swallow the rest. This usually happens when they are ignored, so it may
not be observed. Such children are usually thought to have vomiting without diarrhoea
because they often smell of vomit, and may have vomit-stained clothes or bedding. They
are often unusually alert and suspicious, may make stereotyped chewing movements, and do
not appear distressed by vomiting. Rumination is best treated by staff members who have
experience with this problem and give special attention to the child. They need to show
disapproval whenever the child begins to ruminate, without being intimidating, and to
encourage other less harmful behaviours.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Is enough food being given?
Recalculate the food requirement for the child. Ensure that the correct amount is being
offered at the required times, and that the amount taken by the child is measured and
recorded accurately. Observe the measuring and giving of food. Check the calculation of the
daily energy intake of the child.
Review the feeding guidelines giving particular attention to feeding during the night, as
this is often done less well than during the day.
A child treated at a nutrition rehabilitation centre may fail to respond because the feeds
provided at home are too few or too small, or incorrectly prepared. Such failures usually
indicate that the family was not adequately counselled initially. If, despite corrective measures,
the child fails to respond, the child should be readmitted to hospital.
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Infection
Unrecognized infections are a frequent cause of failure to respond. Those most often
overlooked include pneumonia, urinary tract infection, otitis media and tuberculosis. Others
include malaria, dengue, viral hepatitis B and HIV infection. Children who fail to respond to
treatment should be investigated for infection as follows:
➠ Examine the child carefully. Measure the child’s temperature, pulse rate and respiration
rate every 3 hours. As already mentioned, infection in a malnourished child often
causes hypothermia.
➠ If possible, obtain a chest X-ray. Examine the urine for pus cells. Examine and culture the
sputum or a tracheal aspirate for tubercle bacilli. Examine the stool for signs of blood,
Giardia trophozoites or cysts and Strongyloides stercoralis larvae, and culture for bacterial
pathogens. Culture the blood and test for the presence of viral hepatitis B and malaria.
Examine
and culture the cerebrospinal fluid.
➠
➠ Specific infections are discussed below.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Persistent diarrhoea
174
This is diarrhoea that occurs every day for at least 14 days. Weight loss is common.
ReSoMal should be given to prevent or treat dehydration. If the stool contains visible blood,
treat the child with an oral antimicrobial that is effective against most local strains of Shigella
(see treatment guidelines for dysentery below). If cysts or trophozoites of Giardia are found
in the stool, treat the child with metronidazole, 5 mg/kg orally three times daily for 5 days.
Blind antimicrobial therapy, however, is ineffective and should not be given.
Every child with persistent diarrhoea should be examined for non-intestinal infections,
such as pneumonia, sepsis, urinary tract infection and otitis media. Antimicrobial treatment
of these infections should follow standard guidelines. Antidiarrhoeal drugs should never be
used. Such drugs are not effective in children and some may be dangerous. Feeding guidelines
are the same as for severe malnutrition. Breast-feeding should be continued as often and
for as long as the child wants. Milk intolerance is rare when the recommended feeding
guidelines for malnutrition are followed. However, if it occurs, replace the animal milk with
yoghurt or a commercial lactose-free formula. Persistent diarrhoea usually resolves when
the child begins to gain weight. Further details of treatment of diarrhoea are available
elsewhere.
Dysentery
This is diarrhoea with visible blood in the stool. Shigella is the most frequent cause,
especially of cases that are severe. Treatment is with an oral antibiotic to which most local
strains of Shigella are sensitive. Unfortunately, the choice of antimicrobials for treatment of
shigellosis has narrowed considerably in recent years as the prevalence of antimicrobial
resistance has increased. Resistance to ampicillin and cotrimoxazole (sulfamethoxazole
trimethoprim), formerly the drugs of choice, is now widespread.
Nevertheless, cotrimoxazole (25mg of sulfamethoxazole 5mg of trimethoprim/kg orally
twice daily for 5 days) and, in a few areas, ampicillin (25mg/kg four times daily for 5 days) may
still be effective against most endemic strains. Nalidixic acid (15mg/kg four times daily for 5
days), which was formerly reserved for the treatment of resistant cases of shigellosis, is now
the drug of choice in many areas. If there is no improvement (less blood in the stool or passage
of fewer stools) after 2 days, the antibiotic should be changed to another to which local
strains of Shigella are sensitive.
Accordingly, health facilities in areas where there is a high incidence of bloody diarrhoea
should ensure that several antimicrobials known to be effective against most local strains of
Shigella spp. are kept in stock.
Amoebiasis can cause dysentery, liver abscess and other systemic complications, but is rare
in children under 5 years. Treatment for amoebiasis should be given when motile trophozoites
of Entamoeba histolytica containing ingested erythrocytes are found in a fresh stool sample
or when bloody diarrhoea continues after successive treatment with two antibiotics that
are usually effective for Shigella. The finding of amoebic cysts in the stools is not sufficient for
a diagnosis of amoebiasis. Treatment is with metronidazole oral suspension, 10 mg/kg three
times daily for 5–10 days.
Giardiasis
Intestinal infection with Giardia is common and usually has no adverse effect on wellnourished children. However, in severely malnourished children, treatment for giardiasis
should be given when cysts or trophozoites of Giardia are seen in the stool. Treatment is with
metronidazole, 5 mg/kg orally three times daily for 5 days.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Amoebiasis
175
Otitis media
Otitis media occurs frequently in children, often in connection with hospital-acquired
upper respiratory infection. There are no specific clinical signs, except when the eardrum has
ruptured, causing drainage from the ear. The diagnosis usually requires examination of the
ears with an otoscope, looking for loss of the tympanic light reflex or perforation of the
eardrum. Typical signs of inflammation may not be present. Treatment is with cotrimoxazole
(25mg of sulfamethoxazole 5mg of trimethoprim/kg twice daily), ampicillin (25 mg/kg four
times daily) or amoxicillin (15 mg/kg three times daily) for 5 days. A cotton wick should be
used to dry any drainage from the ear.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Pneumonia
176
Pneumonia is manifested by fast breathing and, sometimes, chest indrawing. Cough,
crackly breath sounds and abnormalities on chest X-ray are frequently absent. The cut off
for fast breathing is 50 times per minute or more if the child is aged 2–12 months, or 40 times
per minute or more if the child is aged 12 months to 5 years. Children with fast breathing
should be diagnosed as having pneumonia and given an oral antimicrobial for 5 days.
Cotrimoxazole (sulfamethoxazole trimethoprim), ampicillin or amoxicillin is usually effective.
Children with fast breathing and chest indrawing should be treated with benzylpenicillin,
50 000 IU/kg IM four times daily for at least 5 days, until they improve, and then with oral
ampicillin or amoxicillin. Oxygen should also be given if the breathing rate is over 70 breaths
per minute.
Urinary tract infections
Urinary tract infections occur frequently, with a similar incidence in boys and girls. Such
infections are usually asymptomatic and are diagnosed using dip-stick tests or by finding large
numbers of leukocytes on microscopic examination of fresh urine (at least 10 leukocytes per
microscope field (X40 magnification)). Cotrimoxazole (25mg of sulfamethoxazole 5 mg of
trimethoprim/kg twice daily for 5 days) is usually effective. Alternatively, ampicillin (25 mg/kg
four times daily for 5 days) can be given.
Skin infections
These include pustules, impetigo, infected fissures (especially behind the ears) and indolent
ulcers. Treatment should include washing the affected area with soap and water, and gently
removing debris and crusts by soaking in warm saline or clean warm water. Dry the child
carefully and apply polyvidone iodine, 10% ointment, or chlorhexidine, 5% lotion, to the
affected area. Widespread superficial and deep-seated infections should be treated with
benzylpenicillin, 50000 IU/kg IM four times daily for at least 10 days. If abscesses are present,
they should be drained surgically.
Candidiasis
Oral candidiasis causes creamy-white lesions in the mouth and may be painful, making
feeding difficult. The diagnosis is confirmed by the presence of typical yeast forms on Gram
staining of scrapings from the lesion. Candidiasis can also involve the oesophagus, stomach,
rectum and moist tissues (e.g. axillae, groin). In systemic candidiasis, the respiratory tract and
blood may be involved. Nystatin oral suspension, 100 000 IU four times daily is recommended
for oral, oesophageal and rectal candidiasis. Nystatin cream (100 000 IU (1 g)) should be
applied to affected areas of skin twice daily for 2 weeks. Children over 2 years with systemic
candidiasis should be given ketoconazole, 5 mg/kg orally daily until remission is obtained.
Scabies is caused by a mite that burrows superficially into the skin and causes intense
itching; the scratched lesions often become secondarily infected. Lindane, 0.3% lotion, should
be applied to affected areas once daily for 2 days. If this is not available, benzyl benzoate,
25% lotion, may be used. Although cheaper, it is more irritating; it should be avoided in
malnourished children, unless there is no alternative available. Family members should also
be treated to prevent infestation or reinfestation.
Tuberculosis
Tuberculosis is an important cause of failure to respond. The diagnosis is made by chest Xray and examination or culture of sputum or tracheal secretions. Occasionally, typical
tuberculous lesions can be seen in the fundus of the eye. The Mantoux test is often negative
owing to anergy, but may become positive as the child’s nutritional status improves.
Antituberculosis drugs should be given only when tuberculosis is diagnosed, and
treatment should follow guidelines published by WHO or national guidelines. Children with
HIV infection are at increased risk of tuberculosis and should be treated if tuberculosis is
suspected. As the recommended drugs are hepatotoxic, they should be used with caution
in any child with an enlarged or tender liver.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Scabies
177
Helminthiasis
Ascariasis, hookworm infection and trichuriasis. Infection with Ascaris lumbricoides
(roundworm), Ancylostoma duodenale or Necator americanus (hookworm), and Trichuris
trichiura (whipworm) is common in children who play outside. Whipworm infections can cause
dysentery, anaemia and, occasionally, prolapse of the rectum.
Hookworm infections can cause severe anaemia. Treatment of these infections should
be delayed until the rehabilitation phase of treatment for severe malnutrition. Albendazole
(400 mg in a single dose) and mebendazole (100 mg twice daily for 3 days for inpatient
treatment or 500 mg in a single dose for outpatient treatment) are both effective in children
over 2 years. If these drugs are not available or the child is under 2 years, hookworm can be
treated with pyrantel (10 mg/kg in a single dose) and ascariasis with pyrantel or piperazine.
Piperazine is also effective in whipworm infections. Children aged 2–12 years should be given
75 mg/kg of piperazine in a single dose to a maximum of 2.5 g, while those under 2 years
should receive 50 mg/kg in a single dose administered under medical supervision.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Strongyloidiasis
178
Infection with Strongyloides stercoralis is also common in children who play outside. The
diagnosis is made by detecting typical larvae in the faeces. In patients whose immune systems
are depressed by disease, the larvae may become widely disseminated, giving rise to lifethreatening pulmonary, cerebral and hepatic complications. Albendazole is the drug of choice
for children over 2 years; 400 mg should be given in a single oral dose. If albendazole is
unavailable or the child is under 2 years, ivermectin should be given; the dosage is 200 g/kg
in a single oral dose. Tiabendazole is effective, but causes severe anorexia, which is dangerous
for malnourished children.
Malaria
Malaria is diagnosed by microscopic examination of a blood smear for malarial parasites.
Malaria often appears during the rehabilitation phase of treatment for malnutrition.
Malnourished children with malaria should receive a full course of antimalarial therapy with
the dosage based on body weight. National protocols should guide the anti-malarial therapy
used. However, it is recommended that paracheck is carried out then Fansidar given as a
combination therapy with Artesunate for positive cases. Paracheck should be carried out on
all children in a malaria endemic area. In other areas, testing should be carried out only on
those with a strong index of suspicion.
HIV infection and AIDS
Children with acquired immunodeficiency syndrome (AIDS) are likely to present with
severe malnutrition. In some countries up to half of the children presenting with severe
malnutrition have AIDS. Treatment of malnutrition in children with HIV infection or AIDS is
the same as in children who are HIV-negative. Interstitial lymphocytic pneumonia is specifically
associated with HIV infection. If findings on X-ray are typical of interstitial lymphocytic
pneumonia, an HIV test should be performed. Treatment is with steroids.
Severely malnourished children should not be tested routinely for HIV. Knowledge of HIV
status plays no role in management of the child, except to diagnose interstitial lymphocytic
pneumonia. When an HIV test is done, the results should not be revealed to the staff.
Otherwise, a positive test may cause them to neglect the child.
Serious underlying disease
Learning from failure
Accurate records should be kept of all children who fail to respond to treatment and of all
deaths. These should include, as a minimum, details of the child’s age, sex, date of admission,
weight-for-height (or length) on admission, principal diagnoses, treatment and, where
appropriate, date and time of death, and apparent cause of death. Periodic review of these
records can help to identify areas where case management practices should be carefully
examined and improved. For example, deaths that occur within the first 2 days are often
due to hypoglycaemia, unrecognized or mismanaged septic shock, or other serious infection,
whereas deaths that occur after day 2 are often due to heart failure. An increase in deaths
occurring at night or at weekends suggests that monitoring and care of children at those
times should be reviewed and improved. The objective should be to achieve a case-fatality
rate of <5%.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Malnutrition may result from unrecognized congenital abnormalities, inborn errors of
metabolism, malignancies, immunological diseases and other diseases of the major organs.
Examination of a child who fails to respond to treatment should include a search for serious
underlying disease. Any problem identified should be treated appropriately; however, the
associated malnutrition should be managed according to the guidelines in this manual.
179
References
ñ Valid International. Community-based Therapeutic Care (CTC): A field manual, 2006.
ñ WHO. Management of severe malnutrition: A manual for physicians and other senior health workers,
WHO, 1999.
ñ M.S. Chaiken et al. The promise of a community based approach to managing severe malnutrition:
a case study from Ethiopia.
ñ Scrimshaw NS. Historical concepts of interactions, synergism, and antagonism between nutrition and
infection. J Nutr 2003;133:316S-21S.
ñ Briend A. History of Plumpy’nut. Proceedings of an interdisciplinary workshop. Dublin, Ireland:
Emergency Nutrition Network, 2003.
ñ Field Exchange Emergency Nutrition Network Online. Available at: http://ennonline.net/. Accessed
20 March 2006.
ñ Collins S, Sadler K. Outpatient care for severely malnourished children in emergency relief
programmes: a retrospective cohort study. Lancet 2002; 360:1824-30.
ñ Sphere Project. Humanitarian charter and minimum standards in disaster response. London: Sphere
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
Project, 2000.
180
ñ Field Exchange. Emergency Nutrition Network. Scaling up the treatment of acute childhood
malnutrition in Niger. Issue 28; July 2006.
ñ Field Exchange. Emergency Nutrition Network. Management of moderate acute malnutrition with
RUTF in Niger. Issue 31; September 2007.
ñ A Retrospective Study of Emergency Supplementary Feeding Programmes. Dr. Carlos NavarroColarado. June 2007. ENN and SC UK. Available at http://www.ennonline.net/research
ñ http://www.who.int/childgrowth/en/
ñ WFP in Statistics 2006. World Food Programme 2007.
ñ Enhancing the Nutritional Quality of Relief Diets Workshop Proceedings. SUSTAIN 1999
http://www.sustaintech.org/publications/pubq6.pdf (accessed October 1st, 2007)
ñ Community-Based Management of Severe Acute Malnutrition. A Joint Statement by the World
Health Organization, the World Food Programme, the United Nations Standing Committee on
Nutrition and the United Nations Children’s Fund. May 07 http://www.who.int/child-adolescenthealth/New_Publications/CHILD_HEALTH/Severe_Acute_Malnutrition_en.pdf
ñ UNICEF, The State of the World’s Children 2006 Progress for Children, UNICEF Report on Nutrition,
April 2006.
ñ Pelletier-DL, The relationship between child anthropometry and mortality in developing countries,
implications for policy, programs and future research. The Journal of Nutrition, supplement, 1994.
2047S-2018S.
MANAGEMENT OF ACUTE AND CHRONIC MALNUTRITION
ñ Progress for Children, UNICEF Report on Nutrition, April 2006
ñ UNICEF, The State of the World’s Children 2006
ñ MSF: Food is not enough. http://www.msf.org
181
chapter 4
Neonatal and
Childhood Care
General Objective
To provide participants with introductive knowledge of Standards for Neonatal Care, as well
as the Integrated Management of Childhood Illnesses (IMCI).
Specific Objectives
Content
Altogether more than 10 million children die each year in developing countries before they
reach their fifth birthday. Seven in ten of these deaths are due to acute respirator infections
(mostly pneumonia), diarrhoea, measles, malaria, or malnutrition – and often to a combination
of these conditions.
Every day, millions of parents take children with potentially fatal illnesses to first-level
health facilities such as clinics, health centers and outpatient departments of hospitals. In
some countries, three in four episodes of childhood illness are caused by one of these five
conditions.
NEONATAL AND CHILDHOOD CARE
At the end of the session, participants will be familiar with:
➠ Assessment, classification and treatment of sick children accurately following the
IMCI case
➠ Administration of pre-referral treatment correctly and referral of seriously ill children
183
Participants will get familiar with clinical guidelines, which are based on expert clinical
opinion and research results and designed for the management of sick children aged 1 week
up to 5 years. They promote evidence-based assessment and management, using a syndromic
approach that supports the rational, effective and affordable use of drugs. They include
methods for assessing signs that indicate severe disease; assessing a child’s nutrition,
immunization, and feeding; teaching parents how to care for a child at home; counselling
parents to solve feeding problems; and advising parents about when to return to a health
facility.
➠ The sick child age 2 months up to 5 years (assess and classify)
ñ General danger signs
ñ Cough or difficult breathing (severe pneumonia, cold)
ñ Diarrhoea (classification of dehydration)
ñ Fever (malaria, measles)
ñ Ear problem (mastoiditis, acute and chronic ear infection)
ñ Malnutrition and Anaemia
ñ Immunization status
➠ The sick child age 1 week up to 2 months (assess and classify)
ñ Possible bacterial infection
ñ Diarrhoea
ñ Feeding problem, low weight
NEONATAL AND CHILDHOOD CARE
Methodology
184
➠
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➠
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PPt Presentations
Lecture/discussion format
Case studies
Attendance of pediatric wards and pediatric outpatients’ department
Post learning assessment questions
References
Since the 1970s, the estimated annual number of deaths among children less than 5 years old
has decreased by almost a third. This reduction, however, has been very uneven.
And in some countries rates of childhood mortality are increasing. In 1998, more than
50 countries still had childhood mortality rates of over 100 per 1000 live births. (World Health
Organization. World health report 1999: Making a difference. Geneva: WHO, 1999)
Altogether more than 10 million children die each year in developing countries before they
reach their fifth birthday. Seven in ten of these deaths are due to acute respirator infections
(mostly pneumonia), diarrhoea, measles, malaria, or malnutrition – and often to a combination
of these conditions.
Every day, millions of parents take children with potentially fatal illnesses to first-level
health facilities such as clinics, health centers and outpatient departments of hospitals. In
some countries, three in four episodes of childhood illness are caused by one of these five
conditions.
And most sick children present with signs and symptoms related to more than one. This
overlap means that a single diagnosis may not be possible or appropriate, and that treatment
may be complicated by the need to combine therapy for several conditions. Surveys of the
management of sick children at these facilities reveal that many are not properly assessed and
treated and that their parents are poorly advised. (World Health Organization. Report of the
Division of Child Health and Development 1996-1997. Geneva: WHO, 1998)
At this level, in most developing countries, diagnostic supports such as radiology and
laboratory services are minimal or non-existent; and drugs and equipment are scarce. Limited
supplies and equipment, combined with an irregular flow of patients, leave health care
providers at first-level facilities with few opportunities to practice complicated clinical
procedures. Instead, they must often rely on history and signs and symptoms to determine
a course of management that makes the best use of available resources.
The clinical guidelines, which are based on expert clinical opinion and research results, are
designed for the management of sick children aged 1 week up to 5 years. They promote
evidence- based assessment and management, using a syndromic approach that supports the
rational, effective and affordable use of drugs. They include methods for assessing signs that
indicate severe disease; assessing a child’s nutrition, immunization, and feeding; teaching
parents how to care for a child at home; counselling parents to solve feeding problems; and
advising parents about when to return to a health facility.
The guidelines also include recommendations for checking the parents’ understanding
of the advice given and for showing them how to administer the first dose of treatment.
NEONATAL AND CHILDHOOD CARE
Intergrated Management
of Childhood Illness (IMCI)
185
When assessing a sick child, a combination of individual signs leads to one or more
classifications, rather than to a diagnosis. IMCI classifications are action oriented and allow
a health care provider to determine if a child should be urgently referred to another health
facility, if the child can be treated at the first-level facility (e.g. with oral antibiotic,
antimalarial, ORS, etc.), or if the child can be safely managed at home.
The complete IMCI case management process involves the following:
➠ The health worker assesses a child by checking first for danger signs, asking questions
about common conditions (cough or difficult breathing, diarrhoea, fever, and ear
problems), examining the child, and checking the nutrition and immunization status.
The health worker also assesses the child for other health problems.
➠ The health worker classifies a child’s illnesses using a colour-coded triage system:
ñ urgent pre-referral treatment and referral (red colour),
ñ specific medical treatment and advice (yellow colour),
ñ simple advice on home management (green colour).
➠ Because children often have more than one condition, the health worker classifies each
illness according to whether it requires urgent pre-referral treatment and referral,
specific medical treatment and advice, or simple advice on home management.
➠ After classification, the health worker identifies specific treatments and develops an
integrated treatment plan for each child. If a child requires urgent referral, the health
worker gives essential treatment before the patient is transferred. If a child needs
treatment at home, the health worker gives the first dose of drugs to the child.
➠ The health worker provides practical treatment instructions, including advising the
NEONATAL AND CHILDHOOD CARE
caretaker on how to give oral drugs, how to feed and give fluids during illness, and
how to treat local infections at home. The health worker asks the caretaker to return
for follow-up on a certain date, and teaches them how to recognize signs that indicate
that the child should return immediately to the health facility.
186
➠ If a child is underweight, the health worker identifies treatment or refers the child,
when appropriate. The health worker also provides counselling to solve feeding
problems, including assessment of breastfeeding practices. If a child should be
immunized, the health worker gives immunizations.
➠ When a child is brought back to the clinic as requested, the health worker gives followup care and, if necessary, reassesses the child for new problems.
4
NEONATAL AND CHILDHOOD CARE
Summary of the Intergrated case management process
187
The Sick Child Age 2 Months up
to 5 Years. Assess and Classify
The steps on the ASSESS AND CLASSIFY THE SICK CHILD chart describe what you should
do when a mother brings her child to the clinic because her child is sick. The chart should
not be used for a well child brought for immunization or for a child with an injury or burn.
When patients arrive at most clinics, clinic staff identify the reason for the child’s visit. Clinic
staff obtain the child’s weight and temperature and record them on a patient chart, another
written record, or on a small piece of paper. Then the mother and child see a health worker.
The ASSESS AND CLASSIFY chart summarizes how to assess the child, classify the child’s
illnesses and identify treatments. The ASSESS column on the left side of the chart describes
how to take a history and do a physical examination. The instructions in this column begin
with ASK THE MOTHER WHAT THE CHILD’S PROBLEMS ARE.
6
General danger signs
NEONATAL AND CHILDHOOD CARE
Moving down the left side of the ASSESS AND CLASSIFY chart, you find a box titled CHECK
FOR GENERAL DANGER SIGNS. Ask the questions and look for the clinical signs described in
this box.
A child with a general danger sign has a serious problem. Most children with a general
danger sign need URGENT referral to hospital. They may need lifesaving treatment with
injectable antibiotics, oxygen or other treatments that may not be available in a first-level
health facility. Complete the rest of the assessment immediately.
When you check for general danger signs make the following questions:
188
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➠
➠
Is the child able to drink or breastfeed?
Does the child vomit everything?
Has the child had convulsions?
Is the child lethargic or unconscious?
Cough or difficult breathing
Respiratory infections can occur in any part of the respiratory tract such as the nose,
throat, larynx, trachea, air passages or lungs. A child with cough or difficult breathing may
have pneumonia or another severe respiratory infection.
Pneumonia is an infection of the lungs. Both bacteria and viruses can cause pneumonia.
In developing countries, pneumonia is often due to bacteria. The most common are
Streptococcus pneumoniae and Hemophilus influenzae. Children with bacterial pneumonia
may die from hypoxia (too little oxygen) or sepsis (generalized infection).
Many children are brought to the clinic with less serious respiratory infections. Most
children with cough or difficult breathing have only a mild infection. For example, a child
who has a cold may cough because nasal discharge drips down the back of the throat. Or
the child may have a viral infection of the bronchi called bronchitis. These children are not
seriously ill. They do not need treatment with antibiotics. Their families can manage them at
home.
You need to identify the few, very sick children with cough or difficult breathing who need
NEONATAL AND CHILDHOOD CARE
Summary of Assess and Classify
189
treatment with antibiotics. Fortunately, you can identify almost all cases of pneumonia by
checking for these two clinical signs: fast breathing and chest indrawing.
When children develop pneumonia, their lungs become stiff. One of the body’s responses
to stiff lungs and hypoxia (too little oxygen) is fast breathing. When the pneumonia becomes
more severe, the lungs become even stiffer. Chest indrawing may develop. Chest indrawing
is a sign of severe pneumonia.
Moving down the left side of the ASSESS AND CLASSIFY chart, you find the first main
symptom box. Each main symptom box contains two parts: an assessment section on the left
side and a colour-coded classification table on the right. The assessment section lists questions
and clinical signs under the headings ask, look, listen, check and feel.
Before entering a main symptom box, ask if the child has the main symptom. For example,
ask, “Does the child have cough or difficult breathing?” If the answer is NO, leave the box and
move down the chart to the next main symptom box. If the answer is YES, ask the questions
and check the clinical signs in the assessment section of the box. Then follow the classify arrow
across the page to the classification table.
For ALL sick children ask:
➠ Does the child have cough or difficult breathing?
➠ For how long?
➠ How many breaths in one minute?
➠ Chest drawing?
➠ Stridor?
NEONATAL AND CHILDHOOD CARE
SEVERE PNEUMONIA OR VERY SEVERE DISEASE
190
A child with cough or difficult breathing and with any of the following signs—any general
danger sign, chest indrawing or stridor in a calm child—is classified as having SEVERE
PNEUMONIA OR VERY SEVERE DISEASE.
A child with chest indrawing usually has severe pneumonia. Or the child may have another
serious acute lower respiratory infection such as bronchiolitis, pertussis, or a wheezing
problem. Chest indrawing develops when the lungs become stiff. The effort the child needs
to breathe in is much greater than normal.
A child with chest indrawing has a higher risk of death from pneumonia than the child
who has fast breathing and no chest indrawing. If the child is tired, and if the effort the
child needs to expand the stiff lungs is too great, the child’s breathing slows down.
Therefore, a child with chest indrawing may not have fast breathing. Chest indrawing may
be the child’s only sign of severe pneumonia.
A child classified as having SEVERE PNEUMONIA OR VERY SEVERE DISEASE is seriously ill.
He or she needs urgent referral to a hospital for treatments such as oxygen, a bronchodilator,
or injectable antibiotics. Before the child leaves, give the first dose of an appropriate antibiotic.
The antibiotic helps prevent severe pneumonia from becoming worse. It also helps treat other
serious bacterial infections such as sepsis or meningitis.
PNEUMONIA
A child with cough or difficult breathing who has fast breathing and no general danger
signs, no chest indrawing and no stridor when calm is classified as having PNEUMONIA.
A child with PNEUMONIA needs treatment with an appropriate antibiotic.
NO PNEUMONIA: COUGH OR COLD
A child with cough or difficult breathing who has no general danger signs, no chest
indrawing, no stridor when calm and no fast breathing is classified as having NO PNEUMONIA:
COUGH OR COLD. A child with NO PNEUMONIA: COUGH OR COLD does not need an antibiotic.
The antibiotic will not relieve the child’s symptoms. It will not prevent the cold from
developing into pneumonia.
Instead, give the mother advice about good home care. A child with a cold normally
improves in one to two weeks. However, a child who has a chronic cough (a cough lasting
more than 30 days) may have tuberculosis, asthma, whooping cough or another problem. A
child with a chronic cough needs to be referred to hospital for further assessment.
Diarrhoea occurs when stools contain more water than normal. Diarrhoea is also called
loose or watery stools. It is common in children, especially those between 6 months and 2
years of age. It is more common in babies under 6 months who are drinking cow’s milk or
infant formulas. Frequent passing of normal stools is not diarrhoea. The number of stools
normally passed in a day varies with the diet and age of the child. In many regions diarrhoea
is defined as three or more loose or watery stools in a 24-hour period.
Mothers usually know when their children have diarrhoea. They may say that the child’s
stools are loose or watery. Mothers may use a local word for diarrhoea. Babies who are
exclusively breastfed often have stools that are soft; this is not diarrhoea. The mother of a
breastfed baby can recognize diarrhoea because the consistency or frequency of the stools
is different than normal.
Ask about diarrhoea in ALL children:
➤
➤
➤
➤
➤
➤
Does the child have diarrhoea?
For how long?
Blood in the stool?
How is child’s general condition?
Does the child have sunken eyes?
Pinch the skin of the abdomen.
CLASSIFY DEHYDRATION
There are three possible classifications for dehydration in a child with diarrhoea: SEVERE
DEHYDRATION, SOME DEHYDRATION and NO DEHYDRATION
NEONATAL AND CHILDHOOD CARE
Diarrhoea
191
Fever
A child with fever may have malaria, measles or another severe disease. Or, a child with
fever may have a simple cough or cold or other viral infection.
9
NEONATAL AND CHILDHOOD CARE
MALARIA
192
Malaria is caused by parasites in the blood called “plasmodia.” They are transmitted
through the bite of anopheline mosquitoes. Four species of plasmodia can cause malaria,
but the most dangerous one is Plasmodium falciparum. Fever is the main symptom of malaria.
It can be present all the time or go away and return at regular intervals. Other signs of
falciparum malaria are shivering, sweating and vomiting. A child with malaria may have
chronic anaemia (with no fever) as the only sign of illness.
Signs of malaria can overlap with signs of other illnesses. For example, a child may have
malaria and cough with fast breathing, a sign of pneumonia. This child needs treatment for
both falciparum malaria and pneumonia. Children with malaria may also have diarrhoea.
They need an antimalarial and treatment for the diarrhoea.
In areas with very high malaria transmission, malaria is a major cause of death in children.
A case of uncomplicated malaria can develop into severe malaria as soon as 24 hours after the
fever first appears. Severe malaria is malaria with complications such as cerebral malaria
or severe anaemia. The child can die if he does not receive urgent treatment.
MEASLES
Fever and a generalized rash are the main signs of measles. Measles is highly infectious.
Maternal antibody protects young infants against measles for about 6 months. Then the
protection gradually disappears. Most cases occur in children between 6 months and 2 years
of age. Overcrowding and poor housing increase the risk of measles occurring early. Measles
is caused by a virus. It infects the skin and the layer of cells that line the lung, gut, eye, mouth
and throat. The measles virus damages the immune system for many weeks after the onset
of measles. This leaves the child at risk for other infections.
Complications of measles occur in about 30% of all cases. The most important are:
diarrhoea (including dysentery and persistent diarrhoea)
pneumonia
stridor
mouth ulcers
ear infection and
severe eye infection (which may lead to corneal ulceration and blindness).
Encephalitis (a brain infection) occurs in about one in one thousand cases. A child with
encephalitis may have a general danger sign such as convulsions or lethargic or unconscious.
Measles contributes to malnutrition because it causes diarrhoea, high fever and mouth
ulcers. These problems interfere with feeding. Malnourished children are more likely to have
severe complications due to measles. This is especially true for children who are deficient in
vitamin A. One in ten severely malnourished children with measles may die.
For this reason, it is very important to help the mother to continue to feed her child during
measles.
Ask (or measure) fever in ALL children:
➠ Does the child have fever?
➠ What is the malaria risk?
➠ For how long? If more than 7 days, has been present every day?
➠ Has the child had measles within the last 3 months?
➠ Stiff neck?
➠ Runny nose?
➠ Are there signs suggesting measles?
➠ Mouth ulcers? (Are they deep and extensive?)
➠ Draining from the eye? Clouding of the cornea?
NEONATAL AND CHILDHOOD CARE
➠
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193
Very severe febrile disease
If a child with fever has any general danger sign or a stiff neck, classify the child as having
VERY SEVERE FEBRILE DISEASE.
A child with fever and any general danger sign or stiff neck may have meningitis, severe
malaria (including cerebral malaria) or sepsis. It is not possible to distinguish between these
severe diseases without laboratory tests. A child classified as having VERY SEVERE FEBRILE
DISEASE needs urgent treatment and referral. Before referring urgently, you will give several
treatments for the possible severe diseases.
MALARIA
If a general danger sign or stiff neck is not present, look at the yellow row.
Because the child has a fever (by history, feels hot, or temperature 37.5ÆC or above) in a
high malaria risk area, classify the child as having MALARIA. When the risk of malaria is high,
the chance is also high that the child’s fever is due to malaria.
Most viral infections last less than a week. A fever that persists every day for more than
7 days may be a sign of typhoid fever or other severe disease. If the child’s fever has persisted
every day for more than 7 days, refer the child for additional assessment.
Treat a child classified as having MALARIA with an oral antimalarial. If the child also has
cough and fast breathing, the child may have malaria or pneumonia, or both. It is not possible
without laboratory tests to find out if the child has malaria or pneumonia. Cotrimoxazole is
effective as both an antibiotic and an antimalarial.
NEONATAL AND CHILDHOOD CARE
SEVERE COMPLICATED MEASLES
194
If the child has any general danger sign, clouding of cornea, or deep or extensive mouth
ulcers, classify the child as having SEVERE COMPLICATED MEASLES. This child needs urgent
treatment and referral to hospital.
If there is clouding of the cornea, or pus draining from the eye, apply tetracycline ointment.
If it is not treated, corneal clouding can result in blindness. Ask the mother if the clouding
has been present for some time. Find out if it was assessed and treated at the hospital. If it
was, you do not need to refer the child again for this eye sign.
MEASLES WITH EYE OR MOUTH COMPLICATIONS
If the child has pus draining from the eye, or mouth ulcers which are not deep or extensive,
classify the child as having MEASLES WITH EYE OR MOUTH COMPLICATIONS.
A child with this classification does not need referral.
Identifying and treating measles complications early in the infection can prevent many
deaths. Treat the child with vitamin A. It will help correct any vitamin A deficiency and decrease
the severity of the complications. Teach the mother to treat the child’s eye infection or mouth
ulcers at home. Treating mouth ulcers helps the child to more quickly resume normal feeding.
MEASLES
A child with measles now or within the last 3 months and with none of the complications
listed in the pink (top) or yellow (middle) rows is classified as having MEASLES.
Give the child vitamin A to help prevent measles complications. All children with measles
should receive vitamin A.
Ear problem
➠
➠
➠
➠
➠
Does the child have an ear problem?
Does the child have ear pain?
Is there ear discharge? For how long?
Pus draining from the ear?
Tender swelling behind the ear?
There are four classifications for ear problem: MASTOIDITIS, ACUTE EAR INFECTION, CHRONIC
EAR INFECTION, NO EAR INFECTION.
MASTOIDITIS
If a child has tender swelling behind the ear, classify the child as having MASTOIDITIS.
Refer the child urgently to hospital. This child needs treatment with injectable antibiotics.
He may also need surgery. Before the child leaves for hospital, give the first dose of an
appropriate antibiotic.
NEONATAL AND CHILDHOOD CARE
A child with an ear problem may have an ear infection.
When a child has an ear infection, pus collects behind the eardrum and causes pain and
often fever. If the infection is not treated, the eardrum may burst. The pus discharges, and the
child feels less pain. The fever and other symptoms may stop, but the child suffers from poor
hearing because the eardrum has a hole in it. Usually the eardrum heals by itself. At other
times the discharge continues, the eardrum does not heal and the child becomes deaf in
that ear.
Sometimes the infection can spread from the ear to the bone behind the ear (the mastoid)
causing mastoiditis. Infection can also spread from the ear to the brain causing meningitis.
These are severe diseases. They need urgent attention and referral.
Ear infections rarely cause death. However, they cause many days of illness in children. Ear
infections are the main cause of deafness in developing countries, and deafness causes
learning problems in school. The ASSESS & CLASSIFY chart helps you identify ear problems due
to ear infection.
Ask about ear problem in ALL sick children:
195
ACUTE EAR INFECTION
If you see pus draining from the ear and discharge is reported present for less than two
weeks, or if there is ear pain, classify the child’s illness as ACUTE EAR INFECTION. Give a child
with an ACUTE EAR INFECTION an appropriate antibiotic. Antibiotics for treating pneumonia
are effective against the bacteria that cause most ear infections.
Give paracetamol to relieve the ear pain (or high fever). If pus is draining from the ear, dry
the ear by wicking.
CHRONIC EAR INFECTION
If you see pus draining from the ear and discharge has been present for two weeks or
more, classify the child’s illness as CHRONIC EAR INFECTION.
Most bacteria that cause CHRONIC EAR INFECTION are different from those that cause acute
ear infections. For this reason, oral antibiotics are not usually effective against chronic
infections. Do not give repeated courses of antibiotics for a draining ear.
NO EAR INFECTION
If there is no ear pain and no pus is seen draining from the ear, the child’s illness is classified
as NO EAR INFECTION. The child needs no additional treatment.
NEONATAL AND CHILDHOOD CARE
Malnutrition and Anaemia
196
A mother may bring her child to clinic because the child has an acute illness. The child may
not have specific complaints that point to malnutrition or anaemia. A sick child can be
malnourished, but you or the child’s family may not notice the problem. A child with malnutrition has a higher risk of many types of disease and death. Even children with mild and
moderate malnutrition have an increased risk of death.
Identifying children with malnutrition and treating them can help prevent many severe
diseases and death. Some malnutrition cases can be treated at home. Severe cases need
referral to hospital for special feeding, blood transfusion, or specific treatment of a disease
contributing to malnutrition (such as tuberculosis).
Check ALL children for malnutrition and anaemia:
➠ Look for visible severe wasting.
➠ Look for palmar pallor
➠ Look and feel for oedema of both feet
➠ Determine weight for age.
SEVERE MALNUTRITION OR SEVERE ANAEMIA
If the child has visible severe wasting, severe palmar pallor or oedema of both feet, classify
the child as having SEVERE MALNUTRITION OR SEVERE ANAEMIA.
Children with oedema of both feet may have other diseases such as nephrotic syndrome.
It is not necessary to distinguish these other conditions from kwashiorkor since they also
require referral.
Children classified as having SEVERE MALNUTRITION OR SEVERE ANAEMIA are at risk of
death from pneumonia, diarrhoea, measles, and other severe diseases. These children need
urgent referral to hospital where their treatment can be carefully monitored.
They may need special feeding, antibiotics or blood transfusions. Before the child leaves
for hospital, give the child a dose of vitamin A.
ANAEMIA OR VERY LOW WEIGHT
If the child is very low weight for age or has some palmar pallor, classify the child as having
ANAEMIA OR VERY LOW WEIGHT. A child classified as having ANAEMIA OR VERY LOW WEIGHT
has a higher risk of severe disease. When you record this classification, you can just write
ANAEMIA if the child has only palmar pallor or VERY LOW WEIGHT if the child is only very
low weight for age.
Assess the child’s feeding and counsel the mother about feeding her child according to the
instructions and recommendations in the FOOD box on the COUNSEL THE MOTHER chart.
A child with some palmar pallor may have anaemia. Treat the child with iron. The anaemia
may be due to malaria, Hookworm or Whipworm. When there is a high risk of malaria, give
an antimalarial to a child with signs of anaemia. Hookworm and whipworm infections
contribute to anaemia because the loss of blood from the gut results in iron deficiency. Give
the child mebendazole only if there is hookworm or whipworm in the area. Only give
mebendazole if the child with anaemia is 2 years of age or older and has not had a dose of
mebendazole in the last 6 months.
13
If the child is not very low weight for age and there are no other signs of malnutrition,
classify the child as having NO ANAEMIA AND NOT VERY LOW WEIGHT. Children less than 2
years of age have a higher risk of feeding problems and malnutrition than older children do.
If the child is less than 2 years of age, assess the child’s feeding.
Immunization status
In the past some health workers thought minor illness was a contraindication to
immunization (a reason to not immunize the child). They sent sick children away and told
the mothers to bring them back when the children were well. This is a bad practice because
it delays immunization. The mother may have travelled a long distance to bring her sick child
to the clinic and cannot easily bring the child back for immunization at another time. The
child is left at risk of getting measles, polio, diphtheria, pertussis, tetanus or tuberculosis.
It is very important to immunize sick and malnourished children against these diseases.
NEONATAL AND CHILDHOOD CARE
NO ANAEMIA AND NOT VERY LOW WEIGHT
197
There are only three situations at present that are contraindications to immunization:
➣ Do not give BCG to a child known to have AIDS.
➣ Do not give DPT 2 or DPT 3 to a child who has had convulsions or shock within 3 days
of the most recent dose.
➣ Do not give DPT to a child with recurrent convulsions or another active neurological
disease of the central nervous system.
In all other situations, here is a good rule to follow: There are no contraindications to
immunization of a sick child if the child is well enough to go home.
If a child is going to be referred, do not immunize the child before referral. The hospital
staff at the referral site should make the decision about immunizing the child when the child
is admitted. This will avoid delaying referral.
Children with diarrhoea who are due for OPV should receive a dose of OPV (oral polio
vaccine) during this visit. However, do not count the dose. The child should return when the
next dose of OPV is due for an extra dose of OPV.
Advise the mother to be sure that the other children in the family are immunized. Give the
mother tetanus toxoid, if required.
NEONATAL AND CHILDHOOD CARE
The Sick Child Infante Age 1 Week
to 5 Month. Assess and Classify
198
In this section you will learn to assess a sick young infant age 1 week up to 2 months and
to classify the infant’s illnesses. The process is very similar to the one you learned for the
sick child age 2 months up to 5 years. All the steps are described on the chart titled ASSESS,
CLASSIFY AND TREAT THE SICK YOUNG INFANT.
Ask the mother what the young infant’s problems are. Determine if this is an initial or
follow-up visit for these problems. If this is a follow-up visit, you should manage the infant
according to the special instructions for a follow-up visit.
Young infants have special characteristics that must be considered when classifying their
illnesses. They can become sick and die very quickly from serious bacterial infections.
They frequently have only general signs such as few movements, fever, or low body
temperature. Mild chest indrawing is normal in young infants because their chest wall is soft.
For these reasons, you will assess, classify and treat the young infant somewhat differently than
an older infant or young child. The ASSESS, CLASSIFY AND TREAT THE SICK YOUNG INFANT chart
lists the special signs to assess, the classifications, and the treatments for young infants.
The chart is not used for a sick newborn that is a young infant who is less than 1 week of
age. In the first week of life, newborn infants are often sick from conditions related to labour
and delivery, or have conditions which require special management. Newborns may be suffering
from asphyxia, sepsis from premature ruptured membranes or other intrauterine infection,
or birth trauma. Or they may have trouble breathing due to immature lungs. Jaundice also
requires special management in the first week of life. For all these reasons, management of a
sick newborn is somewhat different from caring for a young infant age 1 week up to 2 months.
15
Assess and classify the sick young infant
The steps to assess and classify a sick young infant during an initial visit are:
➠ Check for signs of possible bacterial infection. Then classify the young infant based on
the clinical signs found.
NEONATAL AND CHILDHOOD CARE
Summary of Assess and Classify
199
➠ Ask about diarrhoea. If the infant has diarrhoea, assess for related signs. Classify the
young infant for dehydration. Also classify for persistent diarrhoea and dysentery if
present.
➠ Check for feeding problem or low weight. This may include assessing breastfeeding.
Then classify feeding.
➠ Check the young infant’s immunization status.
➠ Assess any other problems.
NEONATAL AND CHILDHOOD CARE
If you find a reason that a young infant needs urgent referral, you should continue the
assessment. However, skip the breastfeeding assessment because it can take some time.
Check a young infant for possible bacterial infection
200
NEONATAL AND CHILDHOOD CARE
Assess and classify a young infant for diarrhoea
201
202
NEONATAL AND CHILDHOOD CARE
References
ñ Handbook: IMCI Integrated management of childhood Illness. Geneva, World Health Organization,
2005 http://www.who.int/child-adolescent health/New_Publications/IMCI/WHO_FCH_CAH_00.12/
IMCI_Handbook.pdf)
ñ Clinical Guidelines: Diagnosis and Treatment Manual for Curative Programmes in Hospitals and
Dispensaries, 7th edition. Medecins sans Frontieres, 2006 http://www.msf.org/source/refbooks/
msf_docs/en/Essential_ drugs/ED_en.pdf)
ñ Model Chapter for Textbook IMCI integrated management of childhood illness (WHO, UNICEF 2001)
ñ Management of severe malnutrition: a manual for physicians and other senior health care workers.
Geneva, World Health Organization, 1999 http://www.who.int/nutrition/publications/en/manage
severe _malnutrition_eng.pdf
ñ Manual for the health care of children in humanitarian emergencies (WHO 2008)
ñ EFFECTIVE TEACHING A Guide for Educating Healthcare ProvidersGuide for Facilitators WHO, JHPIEGO
Field-Test Version 2005
ñ Integrated Management of Childhood Illness. Trainer’s guide (WHO, UNICEF, CARE)
ñ Management of the child with serious infection or severe malnutrition: guidelines for care at the firstreferral level in developing countries. Geneva, World Health Organization, 2000 http://www.who.int/
childadolescent- health/publications/referral_care/Referral_Care_en.pdf
ñ Malaria Control During Mass Population Movements and Natural Disasters. Peter B. Bloland and Holly
A. Williams. Roundtable on the Demography of Forced Migration. Committee on Population, Division
of Behavioral and Social Sciences and Education and Program on Forced Migration and Health at the
Mailman School of Public Health of Columbia University, Washington, DC. National Research Council.
The National Academies Press, 2003.
ñ WHO guidelines for epidemic preparedness and response to measles outbreaks. Geneva, World
children2.pdf
ñ Pocket book of hospital care for children: guidelines for the management of common illnesses with
limited resources. Geneva, World Health Organization, 2005 http://www.who.int/child-adolescenthealth/New_ Publications/CHILD_HEALTH/PB/00.PB_full_low.pdf
ñ HIV/AIDS prevention and care in resource-constrained settings: a handbook for the design and
management of programs. Inter-Agency Standing Committee. http://www.fhi.org/en/HIVAIDS/pub/
guide/HIVAIDSPreventionCare.htm
NEONATAL AND CHILDHOOD CARE
Health Organization, 1999 http://www.who.int/mental_health/mental_health_food_shortage_
203
chapter 5
Maternity Health
Care in Normal Birth –
Obstetrics
The session provides participants with introductive knowledge of standards for routine care
for women during pregnancy, labour and delivery, as well as key preventive measures required
to reduce the incidence of endemic and other diseases like malaria, anaemia, HIV/AIDS and
TB, which add to maternal and perinatal morbidity and mortality.
Specific Objectives
At the end of the session, participants will be familiar with:
➠
➠
➠
➠
Core components of basic care and basic care provision
The concept of “normality” in labour and delivery
General aspects of care in labour
Pregnancy-related pathologies and pathological pregnancy
Content
Despite considerable debate and research over many years the concept of “normality” in
labour and delivery is not standardized or universal. Recent decades have seen a rapid
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
General Objective
205
expansion in the development and use of a range of practices designed to start, augment,
accelerate, regulate or monitor the physiological process of labour, with the aim of improving
outcomes for mothers and babies, and sometimes of rationalizing work patterns in
institutional birth.
➠ Maternity health
ñ Core components of basic care (quick check, basic assessment)
ñ Physical Examination
ñ Basic Care Provision (general elements, life-threatening complications)
➠ Normal Birth
ñ Introduction – general aspects of care in labour
ñ Care during the four stages of labour
➠ Obstetrics in Remote Settings
ñ Bleeding during he first half of Pregnancy (diagnosis, management)
ñ Bleeding during the second half of Pregnancy
ñ Pregnancy-related pathologies and pathological pregnancy (iron deficiency anaemia,
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
pregnancy induced hypertension, premature rupture of membranes, threatened
preterm delivery, intrauterine fetal death, bacterial – parasitic – viral infections)
➠ Pregnancy and HIV infection
206
Methodology
➠
➠
➠
➠
➠
PPt Presentations
Lecture/discussion format
Case studies
Attendance of maternity ward and operating theatre
Post learning assessment questions
References
Maternity Health
Core Components of Basic Care
The core components of basic care are the services that all women and newborn babies should
receive to ensure, support and maintain a normal childbearing cycle and newborn period.
At a minimum basic care includes the following:
➠ Targeted assessment to ensure normal progress of the childbearing cycle and newborn
period and facilitate the early detection of complications, chronic conditions and other
problems/potential problems and;
➠ Individualized care provision to help maintain normal progress, consisting of preventive
measures, supportive care, health messages and counseling and birth preparedness
and complication readiness planning.
The quick check ensures that a woman or newborn in need of immediate medical
attention is identified, stabilized (if necessary) and treated or referred/ transferred as quickly
as possible. Every woman or newborn who comes to the healthcare facility for care (or is cared
for at home) undergoes a quick check immediately upon arrival. If danger signs are identified,
the skilled provider performs a rapid assessment to determine the degree of illness (if any)
and the need for stabilization or emergency care before proceeding. The quick check is also
used to recognize the respond appropriately to signs of advanced labor in the pregnant
woman and to danger signs in the newborn.
Basic assessment
If it is determined through the quick check that the woman or newborn does not have
an emergent condition the skilled provider may proceed to the assessment. Through the
assessment process, the skilled provider works to:
➠ Ensure maternal or newborn well-being and/or normal pregnancy
➠ Gather information that can be used to individualize a plan of care to best meet the
woman’s or newborn’s needs
➠ Identify common discomforts/ concerns and special needs
➠ Detect conditions beyond the scope of basic care, including life-threatening complications
➠ Establish a trusting and respectful relationship with the woman and her companion/
partner/family
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Quick check
207
During the assessment the skilled provider takes the woman’s or newborn’s history,
performs a physical examination and conducts any necessary test.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 1. Rationales for Elements of Maternal History
208
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 1. Rationales for Elements of Maternal History (continued)
209
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 1. Rationales for Elements of Maternal History (continued)
210
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 2. Rationales for Elements of Newborn History
211
Table 2. Rationales for Elements of Newborn History (continued)
Physical Examination
Physical examination helps the skilled provider detect and identify abnormal signs, special
needs, and other potential problems that should be considered during further assessment and
when planning and implementing care.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 3. Rationales for Elements of Maternal Physical Examination
212
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 3. Rationales for Elements of Maternal Physical Examination (continued)
213
Table 3. Rationales for Elements of Maternal Physical Examination (continued)
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 4. Rationale for Elements of Newborn Physical Examination/Observation
214
Basic Care Provision
General Elements
If all findings of the assessment are normal, the woman or newborn is a suitable candidate
for basic care provision. All of the components of basic care provision should be addressed
during the first visit, if possible, and reinforced or addressed as needed during subsequent
visits. During this part of the basic care visit, the skilled provider helps support and maintain
a normal childbearing cycle and newborn period by doing the following:
➠ Helping to prevent conditions that can adversely affect the woman, fetus, or newborn
through preventive measures
➠ Assisting the woman and her family in preparing for normal birth and possible
complications
➠ Empowering the woman with information that promotes her overall health and
protects her life, as well as the health and life of her baby
➠ Continuing to build a trusting and respectful relationship with the woman and her
companion/partner/family
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 4. Rationale for Elements of Newborn Physical Examination/Observation (continued)
215
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 5. Rationales for Elements of Maternal Basic Care Provision
216
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 5. Rationales for Elements of Maternal Basic Care Provision (continued)
217
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 6. Rationales for Elements of Newborn Basic Care Provision
218
Life-Threatening Complications
Some women and newborn babies may present with danger signs that indicate a lifethreatening condition or one whose diagnosis or management lies beyond the scope of this
manual. Identifying those who have such conditions is just as important as identifying women
and newborn babies who are progressing normally through the childbearing cycle and
newborn period. Initial care for these women and newborn babies, includes the following:
➠ Rapid initial assessment
➠ Stabilization and other initial management measures, as needed
➠ Urgent referral/transfer to a specialist or facility that has comprehensive essential
obstetric care services
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Table 7. Rationales for Ongoing Assessment during the Four Stages of Labor
219
RAPID INITIAL ASSESSMENT AND STABILIZATION PROCEDURES
When danger signs are identified, the skilled provider immediately performs a rapid initial
assessment to determine the degree of illness, need for emergency care/stabilization, and
immediate course of action that must be taken. The skilled provider will assess the woman or
newborn for signs of the following:
➠ Respiratory distress
➠ Shock
➠ Convulsions or loss of consciousness (and, for newborn babies, spasms)
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
If the woman or newborn is in need of stabilization, the skilled provider performs the
designated life-saving measures to stabilize the woman or newborn before proceeding with
care or urgent referral/transfer. If the woman or newborn is not in need of stabilization, the
skilled provider should conduct a further assessment per presenting danger sign to determine
whether the woman or newborn requires urgent referral/transfer or specialized care, or
whether the woman or newborn can continue with basic care.
220
Normal Birth
Normal Bi
rth
Despite considerable debate and research over many years the concept of “normality” in
labour and delivery is not standardised or universal. Recent decades have seen a rapid
expansion in the development and use of a range of practices designed to start, augment,
accelerate, regulate or monitor the physiological process of labour, with the aim of improving
outcomes for mothers and babies, and sometimes of rationalising work patterns in
institutional birth. In developed countries where such activity has become generalized,
questions are increasingly raised as to the value or desirability of such high levels of
intervention. In the mean time, developing countries are seeking to make safe, affordable
delivery care accessible to all women. The uncritical adoption of a range of unhelpful,
untimely, inappropriate and/or unnecessary interventions, all too frequently poorly evaluated,
is a risk run by many who try to improve the maternity services. After establishing a working
definition of “normal birth” this text identifies the commonest practices used throughout
labour and attempts to establish some norms of good practice for the conduct of noncomplicated labour and delivery.
The text addresses issues of care in normal birth irrespective of the setting or level of care.
Its recommendations on those interventions, which are or should be used to support the
processes of normal birth, are neither country nor region specific. Enormous variations exist
worldwide as to the place and level of care, the sophistication of services available and the
status of the caregiver for normal birth.
Definition of Normal Birth
In defining normal birth two factors must be taken into consideration: the risk status of the
pregnancy, and the course of labour and delivery. The predictive value of risk scoring is far
from being 100% – a pregnant woman who is at low risk when labour starts may eventually
have a complicated delivery. On the other hand, many high-risk pregnant women ultimately
have an uncomplicated course of labour and delivery. In this text our primary target is the
large group of low-risk pregnancies.
We define normal birth as: spontaneous in onset, low-risk at the start of labour and
remaining so throughout labour and delivery. The infant is born spontaneously in the
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Introduction
221
vertex position between 37 and 42 completed weeks of pregnancy. After birth mother and
infant are in good condition.
However, as the labour and delivery of many high-risk pregnant women have a normal
course, a number of the recommendations in this paper also apply to the care of these
women.
Aim of the Care in Normal Birth,
Tasks of the Caregiver
The aim of the care is to achieve a healthy mother and child with the least possible level of
intervention that is compatible with safety. This approach implies that:
In normal birth there should be a valid reason to interfere with the natural process.
The tasks of the caregiver are fourfold:
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
➠ support of the woman, her partner and family during labour, at the moment of
222
childbirth and in the period thereafter
➠ observation of the labouring woman; monitoring of the fetal condition and of the
condition of the infant after birth; assessment of risk factors; early detection of
problems
➠ performing minor interventions, if necessary, such as amniotomy and episiotomy; care
of the infant after birth.
➠ referral to a higher level of care, if risk factors become apparent or complications
develop that justify such referral.
This description assumes that referral to a higher level of care can be easily realized. In
many countries that is not the case; special regulations are then necessary to enable primary
caregivers to perform life saving tasks. This implies additional training, and adaptation of
legislation to support the caregiver in these tasks. It also implies agreement amongst
caregivers regarding their responsibilities (Kwast 1992, Fathalla 1992).
General Aspects of Care in Labour
Assessing the Well-being of the Woman during Labour
Where the onset of labour is spontaneous women themselves usually initiate care, either
by sending for their birth attendant or by making arrangements to be admitted to a health
facility.
Wherever birth takes place the establishment of good rapport between the woman and
her caregiver is vital, whether or not they have met previously. The quality of welcome
extended to a woman who seeks institutional care may well determine the level of trust which
she and her family feel able to put in her carers.
Throughout labour and delivery the woman’s physical and emotional well-being should
be regularly assessed. This implies measuring of temperature, pulse and blood pressure,
checking fluid intake and urine output, assessing pain and need of support. This monitoring
should be maintained until the conclusion of the birthing process.
The assessment of the woman’s well-being also comprises attention to her privacy during
labour, respecting her choice of companions and avoiding the presence of unnecessary persons
in the labour room.
Labour Pain
Almost all women experience pain during labour, but the responses of individual women
to labour pain are widely different. According to clinical experience, abnormal labour,
prolonged or complicated by dystocia, induced or accelerated by oxytocics, or terminated
by instrumental delivery, seems to be more painful than “normal labour”. Nevertheless, even
completely normal labour is painful too.
An important task of the birth attendant is to help women cope with labour pain. This
may be achieved by pharmacological pain relief, but more fundamental and more important
is the non- pharmacological approach, starting during prenatal care by providing reassuring
information to the pregnant woman and her partner, and if need be to her family. Empathetic
support, before and during labour, from caregivers and companions, can reduce the need
for pharmacological pain relief and thus improve the childbirth experience.
PHARMACOLOGICAL PAIN RELIEF IN LABOUR
Pharmacological methods of pain relief have gained ample application, especially in the
developed countries. The effects of several techniques have been investigated by clinical trials;
the benefits of pain relief became obvious, but the possible adverse effects on mother or
infant have received less attention.
Systemic agents
A number of drugs have been and are being used for pain relief: opioid alkaloids, of which
by far the most popular is pethidine, followed by phenothiazine derivatives (promethazine),
benzodiazepines (diazepam) and others. In some countries inhalation analgesia for normal
labour has decreased in recent years (it has been replaced by epidural analgesia); the most
commonly used agent is nitrous oxide combined with 50 percent oxygen. All these agents can
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
NON-PHARMACOLOGICAL METHODS OF PAIN RELIEF
223
provide reasonable pain relief, but at the cost of unwanted side-effects (Dickersin 1989).
Maternal side effects of pethidine are orthostatic hypotension, nausea, vomiting, and
dizziness. All of the systemic drugs used for pain relief cross the placenta and all except nitrous
oxide are known to cause respiratory depression in the baby and neonatal behavioural
abnormalities, including reluctance to breast-feed.
Diazepam can cause neonatal respiratory depression, hypotonia, lethargy and hypothermia
(Dalen et al 1969, Catchlove and Kafer 1971, Flowers et al 1969, McCarthy et al 1973,
McAllister 1980).
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Epidural analgesia
Of the different techniques of regional analgesia (epidural, caudal, paracervical, spinal)
epidural analgesia is the method most widely used in normal labour. Its effects have been
investigated in a number of trials, all of which compare epidural analgesia with other
techniques of pain control (Robinson et al 1980, Philipsen and Jensen 1989, 1990, Swanstrom
and Bratteby 1981, Thorp et al 1993). It provides better and more lasting pain relief than
systemic agents. The adoption of epidural analgesia in obstetric care is resource-intensive and
calls for several important facilities: labour and delivery should take place in a well-equipped
hospital, the technical apparatus should be sufficient, an anaesthetist should be available at
all times and constant skilled supervision of the mother is called for. Pharmacological methods
should never replace personal attention to the labouring woman and tender loving care.
39
224
Monitoring the Fetus during Labour
Monitoring fetal well-being is part of essential care during labour. The occurrence of fetal
distress, usually through hypoxia, can never be fully excluded, even though a labour may meet
the criteria for “normal” that is: it starts at term, after an uneventful pregnancy without
factors indicating an increased risk of complications. The risk of fetal distress is somewhat
higher during the second stage of labour and in the case of prolonged labour.
Assessment of amniotic fluid
The passage of meconium may reflect fetal distress and is associated with intrapartum
stillbirth and neonatal morbidity or death. Where services permit, the passage of meconium
during labour is considered an indication for referral of the labouring woman by the primary
caregiver. Thick meconium recognized after rupture of the membranes carries the worst
prognosis; undiluted meconium also reflects reduced amniotic fluid volume, which is a risk
factor in itself. The absence of amniotic fluid at the time of rupturing the membranes should
also be considered a risk factor. Slight staining of the amniotic fluid probably reflects a far less
serious risk, but this has not been fully investigated.
Monitoring the fetal heart rate
The relation between fetal well-being and fetal heart rate has been investigated in
numerous studies. It is clear that fetal distress may express itself in abnormalities of the heart
rate: bradycardia (<120/min), tachycardia (>160/min), reduced variability or decelerations.
There are two methods of monitoring the heart rate: intermittent auscultation and continuous
electronic surveillance.
Wherever labour and delivery are managed, cleanliness is a first and foremost requirement.
There is no need for the form of sterility commonly used in an operating theatre, but nails
must be short as well as clean and hands must be carefully washed with soap and water.
Attention should be paid to the personal hygiene of birthing women and birth attendants
as well as to the cleanliness of the environment and all materials used during birth. In some
countries masks and terile gowns are used traditionally to protect labouring woman from
infection. For that purpose they are useless (Crowther et al 1989). However, in regions with a
high prevalence of HIV and hepatitis B and C virus protective clothing is useful to protect
the caregiver from contact with contaminated blood and other materials (WHO 1995).
The programmes already in place to advocate the positive effect of the use of the “three
cleans” (hands, perineal area, umbilical area) need to be maintained or expanded. The
contents of the clean delivery kit may vary from country to country, but they must fit the
specific needs of the women giving birth and be easily obtainable at every street corner and
in all remote regions of a country. These simple but effective kits can even be assembled at
home and include a new, sterile razor blade for the umbilical cord. The clean delivery kit itself
and its contents should indeed be clean and need not be sterilized. The disposable materials
in the kit should not be reused.
Care during the first stage of labour
Assessing the Start of Labour
Assessing the start of labour is one of the most important aspects of the management
of labour. Signs of the start of labour are:
➠ painful contractions with a certain regularity
➠ effacement and/or dilatation of the cervix
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Cleanliness
225
➠ leakage of amniotic fluid
➠ bloody discharge
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Rupture of the membranes is a clear sign that something irreversible has occurred. The
other symptoms are less obvious: contractions may be felt long before labour actually starts,
and cervical dilatation may be present weeks before the end of pregnancy, and may progress
slowly to the time of labour (Crowther 1989). Notwithstanding these difficulties the birth
attendant should be able to distinguish between false labour and the beginning of labour;
usually a vaginal examination is necessary to detect alterations of the cervix. The
establishment of the onset of labour is, inevitably, the basis for identifying prolonged labour
requiring action. If the diagnosis “start of labour” is made erroneously, the result may be
unnecessary interventions, such as amniotomy or oxytocin infusions. The diagnosis “prolonged
latent phase” is usually better substituted by “false labour”, because actually labour has not
yet started. Sometimes the distinction between “start of labour” and “false labour” can only
be made after a short period of observation. In the WHO multicentre trial of the partograph
(WHO 1994b) only 1.3% of the women were reported to have a prolonged latent phase.
The cause of this small percentage can be twofold: at the introduction of the partograph in
the hospitals a discussion of labour management took place which may have affected the way
the latent phase is perceived. Also, active intervention in the latent phase is postponed by 8
hours in the partograph.
226
Vaginal Examination
This is one of the essential diagnostic actions in the assessment of the start and the progress
of labour. It should only be conducted by trained birth attendants, with clean hands, covered by
sterile gloves. The number of vaginal examinations should be limited to the strictly necessary;
during the first stage of labour usually once every 4 hours is enough, as prescribed in the manual
for the use of the partograph (WHO 1993). If labour passes off smoothly, experienced birth
attendants can sometimes limit the number of examinations to one. Ideally, that would be the
one examination necessary to establish active labour, i.e. to confirm the fact that there is
dilatation of the cervix (the most objective criterion of active labour). Another practice in the
management of labour is to only perform a vaginal examination when there is an indication for
the need, for example when the intensity and frequency of the contractions decrease or at signs
of heavy show or the urge to push, or before the administration of analgesia.
Monitoring the Progress of Labour
The assessment of the progress of labour is made by observation of the woman; her
appearance, behaviour, contractions, and the descent of the presenting part. The most
accurate measure is dilatation of the cervix. Deviation from an arbitrarily defined normal
rate of dilatation should be an indication for review of the labour management plans. In the
partograph method of WHO (WHO 1993) the alert line is passed if the dilatation is slower than
1 cm per hour; if the woman is in a health centre this is reason to refer her to a hospital.
The action line is passed if delay in progress continues for four more hours. Then a critical
assessment of the cause of delay should be made, and a decision taken about the appropriate
management. Although these strict rules are not followed in all countries, they form valuable
guidelines, especially in those situations where distances to a referral centre are great, and
birth attendants are isolated.
Prevention of Prolonged Labour
Early amniotomy
This intervention has been recommended as a routine procedure 1 hour after admission
in labour (O’Driscoll et al 1973). In a controlled study a considerable increase of type I
decelerations of the fetal heart rate was found after early amniotomy (Schwarcz et al 1973).
Several randomized trials suggest that amniotomy early in labour leads to a reduction, on
average, of between 60 and
120 minutes in the duration of labour, without effects on the use of analgesia and rates
of operative delivery. The trials provide no evidence that early amniotomy has a favourable or
unfavourable effect on the condition of the neonate (Fraser et al 1991, 1993, Barrett et al
1992). It is not possible to conclude that early amniotomy has a clear advantage over
expectant management, or the reverse. Therefore, in normal labour there should be a valid
reason to interfere with the spontaneous timing of the rupture of the membranes.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Several measures have been proposed to prevent delay in the progress of labour;
sometimes these actions are taken long before the action line or even the alert line of the
partograph are reached. The most active interventions are early amniotomy and early oxytocin
infusion, or a combination of the two. Early amniotomy interferes with the physiological
timing of fetal membranes’ rupture. Under normal conditions, the membranes remain intact
until full dilatation in 75% of the cases (Schwarcz et al 1995). Amniotomy before full dilatation
is frequently practised as a method to expedite labour.
227
Care during the second stage of labour
Physiological Background
During the second stage of labour the oxygenation of the fetus is gradually reduced
because the fetus is being expelled from the uterine cavity, with resulting retraction of the
uterus and decrease in placental circulation. Moreover, strong contractions and strenuous
pushing may further reduce the uteroplacental circulation. The decrease in oxygenation is
accompanied by acidosis. There are however large individual differences in the rate and
seriousness of this process, and therefore the caregiver should carefully monitor the condition
of the fetus.
The Onset of the Second Stage
The beginning of the second stage is marked by the following symptoms:
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
➠ the woman feels the urge to bear down, because the amniotic sac or the presenting
228
part protrudes through the dilated cervix and presses against the rectum;
➠ often the membranes rupture spontaneously;
➠ usually there is full dilatation of the cervix, but sometimes the woman feels the urge
to push at an earlier stage of dilatation. If a rim of cervix is left it will be pushed aside
by the presenting part.
From the above-mentioned it becomes clear that often the onset of the second stage is
not exactly known. A woman may feel the urge to bear down before complete dilatation or
she may not yet feel it at the moment complete dilatation is diagnosed. If complete dilatation
is diagnosed by vaginal examination, it remains uncertain how long this condition has been
present before.
In some hospitals it is customary to transport the woman from the labour room to a
specific “delivery room” at the onset of the second stage. The delivery room is usually
equipped with large bright lamps, instruments and a delivery bed fitted lithotomy poles and
stirrups or metal gutters. Although such a setting is more convenient for the caregiver if
an operative delivery is contemplated, for the woman any unnecessary transportation is
unpleasant. In normal labour there is no need to move the woman to a different room at the
onset of the second stage. Labour and delivery can very well be attended to in the same
room.
The Onset of Pushing during the Second Stage
Caregivers often decide on the onset of the second stage by encouraging the woman to
push, either when full dilatation has been diagnosed, or sometimes even earlier. The physiological approach is to wait until the woman feels the urge to bear down herself. At full
dilatation sometimes the urge is not yet present, and by waiting ten or twenty minutes the
expulsion phase may start spontaneously. There are no controlled trials about early versus late
pushing in normal labour, but some trials have been done with epidural analgesia. Because
the bearing down reflex is suppressed it is easy to delay the pushing efforts until the vertex
is visible in the introitus.
Care of the Perineum
Perineal damage is one of the traumas most frequently suffered by women during delivery,
even during labour and delivery that are considered normal. There are several techniques and
practices aimed at reducing the damage, or modifying it to manageable proportions.
Many textbooks describe the practice of guarding the perineum during delivery of the fetal
head: the fingers of one hand (usually the right) support the perineum, while the second hand
applies pressure to the fetal head to control the speed of crowning, thus trying to prevent
or reduce damage to the perineal tissues. It is possible that by this manoeuvre a perineal
tear may be prevented, but it is also conceivable that the pressure on the fetal head impedes
the extension movement of the head and diverts it from the pubic arch to the perineum, thus
increasing the chance of perineal damage.
Perineal tear and episiotomy
Perineal tears occur frequently, especially in primiparous women. First-degree tears
sometimes do not even need to be sutured, second-degree tears usually can be sutured easily
under local analgesia, and as a rule heal without complications. Third-degree tears can have
more serious consequences and should, where at all possible, be sutured by an obstetrician in
a well-equipped hospital, in order to prevent faecal incontinence and/or faecal fistulas.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
“Guarding the perineum” during delivery
229
Care during the third stage of labour
Background
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
In this stage of labour placental separation and expulsion take place; for the mother the
main risks are haemorrhage during or after separation of the placenta, and retention of the
placenta.
Postpartum haemorrhage is one of the main causes of maternal mortality; the large
majority of these cases occur in developing countries. The incidence of postpartum haemorrhage and retention of the placenta is increased if predisposing factors are present, such as
multiple pregnancy or polyhydramnios, and complicated labour: augmentation of labour,
obstructed labour, or vaginal operative delivery. Postpartum haemorrhage and placental
retention also occur more frequently if these complications were present in the obstetric
history of the woman. To a certain extent therefore it is possible to select during pregnancy
and in the course of labour those women with an increased risk of complications in the third
stage. But even in low-risk pregnancies and after an uneventful first and second stage of
labour serious haemorrhage and/or placental retention may sometimes occur. The
management of the third stage may influence the incidence of these complications, and the
amount of blood lost. Several measures aiming at the prevention of complications have been
proposed, have been tested in randomized trials and are discussed below.
230
Prophylactic use of Oxytocics
Oxytocics may be given prophylactically at various moments during the third stage. Most
often they are administered intramuscularly immediately with the delivery of the anterior
shoulder, or after delivery of the infant. The drugs usually given, and investigated in trials, are
oxytocin and ergot derivatives like ergometrine, or a combination of the two, syntometrine.
Complications of oxytocics are nausea, vomiting, headache and hypertension postpartum.
These complications occur more often with ergot derivatives.
Controlled Cord Traction
Controlled cord traction involves traction on the cord, combined with counterpressure
upwards on the uterine body by a hand placed immediately above the symphysis pubis.
Active Versus Expectant Management of the Third Stage
The combined effects of oxytocics and controlled cord traction are sometimes summarized
by the term “active management of the third stage”, as opposed to expectant or physiological
management. Sometimes early clamping of the cord is included too, especially because in
controlled cord traction early clamping is mandatory.
44
Directly after birth there should be attention to the condition of the newborn. Such
attention is an integral part of care in normal birth, and the World Health Organization
stresses the importance of a unified approach to care of the mother and the baby. Immediate
care involves ensuring that the airway is clear, taking measures to maintain body temperature,
clamping and cutting the cord and putting the baby to the breast as early as possible.
Immediately after the birth the baby has to be dried with warm towels or cloths, while
being placed on the mother’s abdomen or in her arms. The baby’s condition is assessed and
the existence of a clear airway is ensured (if necessary) simultaneously. Maintaining the body
temperature of the baby is important; newborn babies exposed to cold delivery rooms may
experience marked drops in body temperature, and concurrent metabolic problems. A fall in
infant temperature can be reduced by skin-to-skin contact between baby and mother.
Early skin-to skin contact between mother and baby is important for several other reasons.
Psychologically it stimulates mother and baby to get acquainted with each other. After birth
babies are colonized by bacteria; it is advantageous that they come into contact with their
mothers’ skin bacteria, and that they are not colonized by bacteria from caregivers or from
a hospital. All these advantages are difficult to prove, but nevertheless they seem plausible.
Early suckling/breast-feeding should be encouraged, within the first hour after birth.
Care of the Mother Immediately after Delivery of the Placenta
The placenta should be examined carefully to detect abnormalities (infarcts, haematomas,
abnormal insertion of the umbilical cord), but above all to ensure that it is complete. If there
is a suspicion that part of the placenta is missing, preparations should be made to explore the
uterine cavity. If part of the membranes are missing exploration of the uterus is not necessary.
In some countries it is customary for birth attendants routinely to explore the uterine
cavity after every delivery, “uterine revision”. There is not the slightest evidence that such
policy is useful; on the contrary, it can cause infection or mechanical trauma or even shock.
The same holds true for another practice, the “lavage of the uterus”, the rinsing out or
douching of the uterine cavity after delivery. The mother should be observed carefully during
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Immediate Care of the Newborn
231
the first hour postpartum. The most important observations include the amount of blood lost,
and uterine fundal height: if the uterus contracts insufficiently blood may accumulate in the
uterine cavity. If the blood loss is abnormal and the uterus is contracting poorly, gentle
abdominal massage of the uterus can be helpful. It is essential to ensure that uterine
contraction is not inhibited by the presence of a full bladder.
Abnormal blood loss, estimated more than 500 ml, should be treated with oxytocics:
ergometrine or oxytocin intramuscularly. The condition of the mother is also important: blood
pressure, pulse and temperature, and general well-being should be assessed.
MATERNAL AND NEWBORN HEALTH/
SAFE MOTHERHOOD DIVISION
OF REPRODUCTIVE HEALTH WORLD HEALTH ORGANIZATION
GENEVA
WHO/FRH/MSM/96.24
Distr.: General
Orig.: English
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Obstetrics in remote settings
232
Look for pregnancy in any case of vaginal bleeding in a woman of childbearing age.
The two diagnoses to firstly consider during the first half of pregnancy are abortion and
ectopic pregnancy.
Abortion
Spontaneous or induced interruption of pregnancy before the end of the sixth month.
Induced abortions are often clandestine: consider the possibility of local infection, perforation,
and tetanus. The main differential diagnosis, in a context of amenorrhea, is ectopic pregnancy,
examination and follow-up are therefore essential.
DIAGNOSIS
– Light bleeding, pelvic pain, closed cervix: threatened abortion
– More or less severe bleeding, pelvic pain, uterine contractions, expulsion of the embryo
and membranes or products, open cervix: incomplete abortion
MANAGEMENT
Threatened abortion
➠ Look for foreign bodies or vaginal wound consistent with induced abortion; remove
foreign bodies, clean the wound; update tetanus immunization.
➠ Place the patient on rest. Either the threat of abortion recedes, or abortion is inevitable.
➠ Treat pain if necessary: oral paracetamol or antispasmodic.
Incomplete abortion
take pulse and BP, assess the severity of bleeding;
treat pain: oral or injectable anti-inflammatory or antispasmodic;
tetanus prophylaxis
Monitor pulse, BP, bleeding;
Insert an IV line, administer Ringer lactate;
Prepare for a possible transfusion (determine patient’s blood group and identify
potential donors). If transfusion is necessary, only use blood that has been screened (at
least for HIV-1, HIV-2, hepatitis B and C).
– For septic abortion (fever, abdominal pain, tender uterus, foul-smelling discharge), add:
amoxicillin-clavulanic acid (co-amoxiclav) IV: 6 g amoxicillin/day divided in 3 injections
administered 8 hours apart
+ gentamicin IM: 5 mg/kg once daily
Continue for 48 hours (until the fever disappears), then change to co-amoxiclav PO: 3
g/day in 3 divided doses, to complete 5 days of treatment
or
ampicillin IV: 6 g/day divided in 3 injections administered 8 hours apart
+ metronidazole IV: 1.5 g/day divided in 3 infusions administered 8 hours apart
+ gentamicin IM: 5 mg/kg once daily
Continue for 48 hours (until the fever disappears), then change to amoxicillin PO: 3 g/day
in 3 divided doses + metronidazole PO: 1.5 g/day in 3 divided doses, to complete 5 days of
treatment.
Ectopic pregnancy
Implantation of the fertilized egg outside of the uterine cavity, usually in the fallopian
tube, less frequently in the ovary or abdomen. Predisposing factors are history of peritonitis
or pelvic infection
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
➠
➠
➠
➠
➠
➠
233
Tubal pregnancy
Ampullary prenancy
Three clinical presentations:
– haematosalpinx: accumulation of blood in the fallopian tube;
– haematocele: progressive bleeding with haematoma formation in the Pouch of
Douglas, haemodynamic parameters preserved;
– haemoperitoneum: bloody effusion into the peritoneal cavity secondary to rupture
of the fallopian tube and its blood vessels. This is the clinical picture seen most
commonly in rural areas.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
A pregnancy test is only valuable if it is positive; a negative result does not rule out the
diagnosis.
234
Molar pregnancy (hydatidiform mole)
Pathological pregnancy due to cystic degeneration of the placenta, common in Asia and
North Africa. The mole presents in the form of translucent vesicles, 1 to 2 cm in diameter,
connected by filaments like a cluster of grapes. In most cases there is neither foetus nor
amniotic sac.
Mole
DIAGNOSIS
Before abortion
➤ Spontaneous bleeding of variable severity.
➤ Uterus that is larger and softer than expected for gestational age.
➤ No foetal heartbeat, movements, or poles at five months.
➤ Nausea and vomiting.
➤ Possible oedema, proteinuria, or hypertension if the pregnancy is advanced.
➤ Occasionally: expulsion of vesicles during bleeding episodes; enlarged ovaries, weight
loss, mild jaundice.
Abortion
Slow, fragmentary, incomplete, and occasionally accompanied by heavy bleeding with
expulsion of vesicles.
In next table there is a summary of history and clinical signs occurring in bleeding during
the second half of pregnancy.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Bleeding during the second half of pregnancy
235
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
236
Pregnancy-related pathologies
and pathological pregnancy
Iron deficiency anaemia
Anaemia is defined as a haemoglobin level below 11 g/dl (below 10.5 g/dl from the 6th
month of pregnancy).
Pregnancy aggravates pre-existing anaemia due, for example, to nutritional deficiency or
malaria.
Anaemia increases the risk of intrauterine growth retardation and preterm birth. It
increases vulnerability in the event of haemorrhage (particularly postpartum haemorrhage).
Diagnosis
– Pallor of the conjunctivae, mucous membranes, palms, and the soles of the feet; fatigue,
dizziness, tachycardia, heart murmur
– If possible, measure heamoglobin
– Signs of serious illness: intense pallor, lethargy, dyspnoea, haemoglobin < 7g/dl.
Pregnancy-induced hypertension and pre-eclampsia
Normally, blood pressure (BP) goes down during pregnancy. In a pregnant woman,
hypertension (HBP) is defined as BP 140/90 mmHg. The BP should be checked several times,
with the woman seated and at rest.
Chronic HBP is defined as hypertension predating the pregnancy or appearing before 20
weeks LMP.
Pregnancy-induced hypertension (PIH) is defined as isolated hypertension, without
proteinuria, that appears after 20 weeks LMP.
Pre-eclampsia refers to HBP accompanied by proteinuria during pregnancy. Preeclampsia
carries a significant risk of foetal growth retardation, foetal distress, foetal death, placental
abruption and eclampsia.
The goal of antihypertensive treatment is to prevent the maternal complications of severe
hypertension. Treatment is administered when BP is 180/110 mmHg or higher; the objective
is to lower it to about 140/90 mmHg. Antihypertensive treatment does not improve the foetal
prognosis.
Hypertensive treatment in pregnant women should be carried out with caution as it is
essential to preserve placental perfusion and to avoid excessive fall in maternal BP.
– Usually, elevated BP with diastolic BP constantly 3 90 mmHg
– Proteinuria (3 ++ on dipstick test); dark urine, low output
– Oedema (legs, hands) that appears suddenly or rapidly worsens
CLINICAL SIGNS OF SEVERE PRE-ECLAMPSIA
–
–
–
–
–
–
–
–
Diastolic BP 3 110 mmHg persistently elevated in spite of treatment
Proteinuria > 3.5 g/day (3 +++ on dipstick test)
Oliguria (urine output < 400 ml/day or < 30 ml/hour)
Hyperreflexia
Epigastric pain, nausea, vomiting
Significant oedema, facial oedema, pulmonary oedema
Intense headaches not relieved by paracetamol
Buzzing in the ears, visual disturbances
Eclampsia
Convulsions during the third trimester of pregnancy, most commonly in a context of preeclampsia. Eclampsia can also occur after delivery.
Consider other causes of convulsions, such as meningitis and cerebral malaria (increased
incidence in pregnant women).
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
CLINICAL SIGNS OF PRE-ECLAMPSIA
237
Abnormally large uterus
Fundal height greater than the presumed gestational age. The possible causes are:
incorrect due date, multiple pregnancy, a large-for-gestational-age (LGA) foetus, polyhydramnios, or molar pregnancy.
Polyhydramnios
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Excess amniotic fluid (more than 2 litres at term), generally reflecting a severe foetal
abnormality. There are two clinical situations:
– In the second trimester: acute polyhydramnios
– In the third trimester: chronic polyhydramnios
238
Acute polyhydramnios (rare but serious)
Diagnosis
– Rapid increase in the size of the uterus
– Painful abdomen, abdominal pressure, dyspnoea
– Distended, hard uterus, foetus cannot be palpated
Usually associated with foetal malformation, sometimes a complicated twin pregnancy.
Management
Wait until labour begins. Let the abortion/delivery take its course; rupture the membranes
as soon as possible.
Chronic polyhydramnios Diagnosis
– More moderate increase in the size of the uterus, occurring in spurts
– Foetus cannot be palpated
– Foetal heartbeat muffled
– Receding head on vaginal exam, fluid wave Management
– Do nothing during the pregnancy but monitor.
– Look for diabetes and treat if found.
– Amniotomy carries risk of cord prolapse.
– Examine the newborn for foetal malformation.
Premature rupture of membranes
Discharge of amniotic fluid before the onset of labour, due to a leak or frank rupture of
the amniotic sac.
DIFFERENTIAL DIAGNOSIS
– Urinary incontinence
– Expulsion of the mucus plug
– Leucorrhoea
RISKS
➠ Intra-amniotic infection; suspect infection if there is maternal fever, persistent foetal
tachycardia or loss of foetal heartbeat, or discoloured amniotic fluid.
Never administer a tocolytic agent, no matter what the gestational age, when
intraamniotic infection is suspected.
➠ Pre-term birth, if the rupture occurs before 37 weeks LMP.
Threatened preterm delivery
Regular uterine contractions and cervical changes before 37 weeks LMP.
➠
➠
➠
➠
➠
➠
Premature rupture of membranes
Incompetent cervix, immature uterus in the young primipara
Infection, fever
Pregnancy-related disorder: pre-eclampsia, polyhydramnios, placenta praevia
Malnutrition
Twin pregnancy
INTRAUTERINE FETAL DEATH
Foetal death during the 2nd or 3rd trimester of pregnancy, outside of labour.
Diagnosis
➣ Absence or cessation of foetal movements-the usual reason for consultation.
➣ Fundal height too small for gestational age, or decrease in fundal height from a prior
visit.
➣ Absence of foetal heartbeat.
➣ Sometimes, breast engorgement indicating the end of the pregnancy.
None of these signs is sufficiently sensitive to justify a hasty, rash decision. Errors are
common. Repeat the exam, do not rush. Diagnosis can be confirmed by ultrasound.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
CAUSATIVE FACTORS
239
Bacterial infections
Fever above 38.5ÆC, no matter what its cause, should be treated with paracetamol PO: 3 g/day
in 3 divided doses.
Meningitis
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
– In an epidemic context:
ceftriaxone IM: 100 mg/kg as a single dose (4 g maximum)
Administer a second dose after 24 to 48 hours in the following cases:
ñ failure to regain consciousness since admission, or Glasgow Coma Scale score < 11 at
24 hours, or < 13 at 48 hours;
ñ onset or worsening of neurological signs after admission;
ñ recurrent, persistent convulsions;
ñ axillary temperature above 38.5ÆC at 48 hours.
– In a non-epidemic context:
ceftriaxone IM: 2 g once daily for 5 to 7 days
or, failing that:
ampicillin IV: 12 g/day divided in 3 injections administered 8 hours apart, then
amoxicillin PO: 6 g/day in 2 or 3 divided doses, to complete 7 days of treatment
240
Typhoid
Typhoid fever poses a major risk of complications both for the mother (gastrointestinal
perforation, peritonitis, septicaemia) and the foetus (spontaneous abortion, preterm birth,
intrauterine death).
– In cases of drug resistance or severe infection:
ceftriaxone IM or IV2: 2 to 4 g once daily for 10 to 14 days
– In the absence of drug resistance:
amoxicillin PO: 3 g/day in 3 divided doses for 14 days
The fever persists 4 to 5 days after beginning treatment, even when effective. It is
essential to treat the fever and monitor for maternal and foetal complications.
52
Shigellosis
ceftriaxone IM: 1 g once daily for 3 to 5 days
Gonorrhoea
Gonorrhoea can cause premature rupture of membranes, preterm delivery, and neonatal
conjunctivitis, which can be fulminant.
Suspect gonorrhoea in the event of urethral or vaginal discharge. Use a speculum to look
for purulent discharge from the cervix. Quite often, gonorrhoea is associated with chlamydial
infection.
Treat the mother simultaneously for gonorrhoea and chlamydia: cefixime PO 400 mg as a
single dose + azithromycin PO 1 g as a single dose. The sexual partner should receive the
same treatment.
For the newborn infant of an infected mother, at the time of birth: ceftriaxone IM: 50
mg/kg as a single dose; up to a maximum dose of 12 5 mg.
Syphilis screening is essential and should be performed routinely at the first prenatal visit,
as early as possible in pregnancy.
Syphilis can cause spontaneous abortion, polyhydramnios, intrauterine death, and
congenital syphilis.
For the mother:
benzathine benzylpenicillin IM: 2.4 MIU as a single dose (half-dose in each buttock); same
treatment for the sexual partner.
In a penicillin-allergic patient, use erythromycin PO: 2 g/day in 2 or 4 divided doses, for
14 days
For the newborn:
– No treatment if the mother was treated more than 30 days before childbirth.
– If the mother was treated less than 30 days before childbirth:
benzathine benzylpenicillin IM: 75 mg/kg (or 100,000 IU/kg) as a single dose
– If the newborn is symptomatic, treat for congenital syphilis.
Cystitis
Increase fluid intake: at least 1.5 litres per day
fosfomycin-trometamol PO: 3 g as a single dose
or
nitrofurantoin PO (except during the last month of pregnancy): 300 mg/day in 3 divided
doses for 5 to 7 days
or
cefixime PO: 400 mg/day in 2 divided doses for 5 days
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Syphilis
241
Pyelonephritis
Hospitalize; bed rest required due to risk of preterm delivery
Increase fluid intake: at least 1.5 litres per day
In the absence of signs of serious illness:
ceftriaxone IM: 1 g once daily for at least 3 days, then ceftriaxone PO: 400 mg/day in 2
divided doses to complete 14 days of treatment
If signs of serious illness are present, or failure after 48 hours of treatment:
ceftriaxone: 1 to 2 g once daily by IM injection (1 g in each buttock if the dose is 2 g),
or by slow IV injection (over 3 minutes) or by infusion (over 30 minutes)
+ gentamicin: 5 mg/kg once daily by IM or slow IV injection (over 3 minutes) or by slow
infu sion (over 30 minutes) for a maximum of 5 days
Parasitic infections
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Malaria
242
The diagnosis should, if possible, be confirmed by rapid test or microscopic examination
(thick or thin smear).
Artemisinin derivatives (artesunate, artemether) may be administered in the 2nd and 3rd
trimesters, but data regarding their use in the first trimester is limited. Nevertheless, in case
of life-threatening malaria or uncontrolled hypoglycaemia on IV quinine, the mother’s survival
takes precedence over the potential teratogenic risk.
Doxycycline is contra-indicated at any time during pregnancy and mefloquine is contraindicated during the first trimester.
Amoebiasis
The disease is worsened by pregnancy. There is a risk of postnatal transmission to the
newborn.
The diagnosis should be established by microscopic examination of fresh stools. If the
result of the examination is positive:
secnidazole PO: 2 g as a single dose
or
tinidazole PO: 2 g once daily for 3 days
or
metronidazole PO: 1.5 g/day in 3 divided doses for 5 to 7 days
Giardiasis
Like amoebiasis, giardiasis can be severe: dysenteric syndrome, profuse bloody diarrhoea
with dehydration.
The diagnosis should be established by microscopic examination of fresh stools. If the
result of the examination is positive:
secnidazole PO: 2 g as a single dose
or
tinidazole PO: 2 g as a single dose
or
metronidazole PO: 2 g once daily for 3 days
Ascariasis and ancylostomiasis
Viral infections
Genital herpes
If mother has visible lesions at time of childbirth:
– Limit vaginal exams; no artificial rupture of membranes.
– Discuss caesarean section on a case-by-case basis.
For the mother:
– Local disinfection (polyvidone iodine)
– Pain management: paracetamol PO, 3 g/day in 3 divided doses
– Antiviral treatment: aciclovir PO, 400 mg 3 times per day for 7 days; in munocompromised patients, continue the treatment until clinical resolution
For the child:
– If the mother has active infection at the time of birth: monitor the newborn (risk of
keratitis, disseminated herpes infection, herpes encephalitis, etc.).
– Systematic prophylactic treatment for herpes keratitis with aciclovir 3% ophthalmic
ointment: a single application in each eye at birth. Clean the eyes with 0.9% sodium chloride;
apply aciclovir; wait 12 hours before applying ophthalmic tetracycline for prevention of
gonococcal neonatal conjunctivitis.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
For symptomatic infection or infection proven by faecal exam:
albendazole PO: 400 mg as a single dose
Do not administer during the 1st trimester of pregnancy.
In the event of ancylostomiasis, treat the associated anaemia (iron + folic acid).
243
Hepatitis B
For the mother:
No specific treatment; no special obstetric measures.
For the child:
– Hepatitis B vaccination
In areas where there is a high probability of perinatal transmission: one dose at birth, at
6 weeks, and at 14 weeks.
If perinatal transmission is unlikely: one dose at 6, 10 and 14 weeks
– Specific immunoglobulin for the prevention of hepatitis B, if available and the mother’s
status is known to be positive.
55
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
Hepatitis E
244
Hepatitis E carries a very high mortality rate for pregnant women (20% during the 3rd
trimester). It can also cause spontaneous abortion, preterm delivery, and intrauterine foetal
death. The virus is transmitted by fecal-oral route (contaminated drinking water, primarily).
The virus can cause epidemic outbreaks, especially in situations where large numbers of
people are gathered (refugees, displaced persons), when hygiene and sanitation are poor.
There is no specific curative treatment. Prevention (water, hygiene, sanitation) is the only
protection against the disease.
HIV infection
With no intervention, the risk of mother-to-child transmission is on the order of 20 to 45%
for HIV-1, and 0 to 4% for HIV-2. There are several ways to reduce mother-to-child
HIV transmission: antiretroviral therapy (ART), reducing the number of traumatic
obstetrical procedures, elective caesarean section, and replacement feeding.
ANTIRETROVIRAL THERAPY
The following protocols are examples. In all cases, check national recommendations and
refer to specific guidelines.
1. Pregnant HIV+woman receiving effective ART prior to pregnancy
– For the mother Continue antiretroviral treatment. If the treatment includes efavirenz
(teratogenic risk), replace it with nevirapine as early as possible, in the 1st trimester.
If the treatment includes stavudine (d4T) and didanosine (ddI), it is advisable to change
at least one of these two drugs, because the combination is not recommended.
If possible, replace stavudine with zidovudine.
– For the child
zidovudine (syrup): 8 mg/kg/day in 2 divided doses for 7 days
With this treatment, the HIV transmission rate is less than 2% if the child is fed artificially
immediately from birth.
3. Pregnant HIV + woman not needing triple therapy herself
– For the mother
zidovudine PO: 600 mg/day in 2 divided doses. Begin at 28 weeks LMP, or as soon as
possible after that.
When labour begins: one dose of zidovudine 600 mg + nevirapine 200 mg
Continue zidovudine 600 mg/day in 2 divided doses + lamivudine 300 mg/day in 2 divided
doses for 7 days after childbirth.
– For the child
nevirapine (syrup): 2 mg/kg as a single dose within 72 hours after birth
+ zidovudine (syrup): 8 mg/kg/day in 2 divided doses for 7 days
+ lamivudine (syrup): 4 mg/kg/day in 2 divided doses for 7 days If the mother’s treatment
began less than one month before childbirth, continue giving the infant zidovudine for one
month.
4. Pregnant HIV + woman for whom treatment could not best arted during pregnancy
– For the mother
When labour begins: one dose of zidovudine 600 mg + nevirapine 200 mg
Then, zidovudine + lamivudine: 600 mg + 300 mg/day in 2 divided doses for 7 days after
childbirth.
– For the child
zidovudine (syrup): 8 mg/kg/day in 2 divided doses for one month + nevirapine (syrup):
2 mg/kg as a single dose within 72 hours of birth.
5. Pregnant woman needing triple therapy herself, when not available
If possible, follow instructions for case #3, failing that, for case #4.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
2. Pregnant HIV+woman not receiving ART prior to pregnancy, requiring treatment
herself (WHO clinical stage 3 or 4, or stage 1 or 2 with CD4 < 200)
– For the mother
Beginning at 12 weeks LMP: triple therapy with zidovudine (or stavudine) + lamivudine
+ nevirapine4 (do not use efavirenz), lifelong treatment.
– For the child
zidovudine (syrup): 8 mg/kg/day in 2 divided doses for 7 days
If the mother’s treatment began less than one month before childbirth, continue giving
the infant zidovudine for one month.
245
OTHER MEASURES
ñ It is also important to keep traumatic obstetric procedures that facilitate transmission
of the virus to an absolute minimum:
– keep the membranes intact as long as possible
– avoid episiotomy and instrument extraction (vacuum extractor, forceps) if possible
ñ In certain situations, where the context allows, an elective caesarean section (prior
to commencement of labour or rupture of membranes), under antiretroviral cover, can
reduce mother-to-child transmission. It is absolutely imperative to consider the risk
of a caesarean section against the benefit of this intervention.
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
FEEDING
246
Breastfeeding is one of the ways that HIV is transmitted. The additional risk conferred
by this feeding method is in the order of 12%, which represents one third to one half of the
overall transmission rate. There is a risk of transmission as long as breastfeeding lasts.
Mastitis and/or cracked nipples increase the risk: prevent them, look for them, and actively
treat them.
Whenever possible, replacement feeding should be encouraged and supported (provided
the caretaker has access to clean water, continuous availability of infant formula, and knows
how to prepare the milk correctly). Otherwise, recommend exclusive breastfeeding with rapid
weaning at 6 months. Mixed feeding (breast milk plus other liquids, including water, other
milks, or solid food) carries the greatest risk of viral transmission. This method is therefore
highly inadvisable; it is very important to explain this to the mother.
References
ñ Basic Maternal and Newborn Care: A Guide for Skilled Providers Maternal & Neonatal Health, USAID,
JHPIEGO 2004.
ñ JHPIEGO/Maternal and Neonatal Health Program Guidelines for Assessment of Skilled Providers after
Training in Maternal and Newborn Healthcare, 2004.
ñ Foundation module: The midwife in the community. Education material for teachers of midwifery,
Department of Making Pregnancy Safer Family and Community Health. World Health Organization,
Geneva, 2006. http://www.who.int/making_pregnancy_safer/publications/midwifery_modules/
en/index.html
ñ Obstetrics in remote settings. Practical guide for non-specialized health care professionals, MSF 2007.
ñ Integrated Management of Pregnancy and Childbirth. Pregnancy, Childbirth, Postpartum and
Newborn Care: a guide for essential practice, WHO, UNFPA, UNICEF, The World Bank Group, Geneva
2006.
ñ WHO Recommended Interventions for Improving Maternal and Newborn Health. http://whqlibdoc.
who.int/hq/2007/WHO_MPS_07.05_eng.pdf
ñ WHO Recommendations for the Prevention of Postpartum Haemorrhage. Department of Making
Pregnancy Safer, WHO 2007. http://whqlibdoc.who.int/hq/2007/WHO_MPS_07.06_eng.pdf
the Collaborative Safe Motherhood Pre Congress Workshop International Confederation of Midwives,
Brisbane, Australia, July 21 - 23, 2005 http://whqlibdoc.who.int/hq/2007/WHO_MPS_07.09_eng.pdf
ñ Obstetric Fistula. Guiding principles for clinical management and programme development,
Department of Making Pregnancy Safer, WHO 2006. http://www.who.int/making_pregnancy_
safer/publications/ obstetric_fistula.pdf
ñ MALARIA IN PREGNANCY Guidelines for measuring key monitoring and evaluation indicators, WHO
2007. http://whqlibdoc.who.int/publications/2007/9789241595636_eng.pdf
ñ Monitoring and Evaluation of Maternal and Newborn Health and Services at the District Level,
Department of Making Pregnancy Safer, WHO 2007. http://whqlibdoc.who.int/hq/2007/WHO_
MPS_07.04_eng.pdf
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
ñ Promoting the health of mothers and newborns during birth and the postnatal period Report of
247
Post learning assessment questions
1. Tests that should be performed for every woman during antenatal care include
a. ____ Hemoglobin
b. ____ Test for syphilis
c. ____ Ultrasound of baby
d. ____ A and B only
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
2. One way to prevent transmission of HIV from an infected mother to her baby (vertical
transmission) is to
a. ____ Use condoms
b. ____ Give AZT to the woman after the baby is born
c. ____ Rupture membranes early in labor
d. ____ Give a single dose of nevirapine to the woman in labor and to the baby after birth
248
3. The appropriate order of steps in active management of the third stage of labor include
a. ____ Controlled cord traction, fundal massage, and oxytocin
b. ____ Intravenous oxytocin, cord clamping and cutting, and fundal massage
c. ____ Cord clamping and cutting, controlled cord traction, ergometrine administration,
andinspection to be sure the placenta is intact
d. ____ Intramuscular injection of oxytocin, controlled cord traction with countertraction to the
uterus, and uterine massage
4. If bleeding continues after delivery of the placenta using active management, th first thing the
provider should do is call for help and
a. ____ Start an IV
b. ____ Massage the uterus
c. ____ Insert a urinary catheter
d. ____ Check the placenta to make sure that it is complete
5. Which of the following will help to decrease the risk of infection during childbirth?
a. ____ Performing frequent vaginal examinations
b. ____ Rupturing membranes as soon as possible in the first stage of labor
c. ____ Routine catheterization of the bladder before childbirth
d. ____ Reducing prolonged labor
6. The first step in thermal protection for the newborn includes
a. ____ Drying the baby thoroughly immediately after birth
b. ____ Drying the baby thoroughly after the cord has been cut
c. ____ Covering the baby with a clean, dry cloth immediately after birth
d. ____ Covering the baby with a clean, dry cloth after the cord has been cut
7. Immediate care for anormal new born includes
a. ____ Skin-to-skin contact followed by placing the baby in a warming incubator
b. ____ Drying the baby, removing the wet cloth, and covering the baby with a clean, dry cloth
c. ____ Stimulating the baby by slapping the soles of the baby’s feet
d. ____ Deep suctioning of the airway to remove mucus
8. Which of the following can contribute to hypothermia in newborns?
a. ____ The baby is not dried thoroughly immediately after birth
b. ____ The baby is bathed immediately after birth
c. ____ The baby is dried and placed in skin-to-skin contact with the mother
d. ____ A and B
10. Care of the umbilicus should include
a. ____ Cleansing with alcohol
b. ____ Covering with a sterile compress
c. ____ Cleansing with cooled, boiled water and leaving uncovered
d. ____ Applying antibiotic cream
11. The best way to determine if an newborn needs resuscitation is to
a. ____ Wait until 1 minute after birth and assign the Apgar score
b. ____ Listen to the baby’s heart rate
c. ____ Observe respirations immediately and begin resuscitation if they are less than 30/minute
d. ____ Perform resuscitation only if central cyanosis is present
12. Breast feeding should begin
a. ____ After the baby’s first bath
b. ____ When the baby starts to cry
c. ____ Within the first hour following birth
d. ____ When the mother’s milk comes in
13. Each post partum examination should include
a. ____ Measurement of blood pressure and temperature, and assessment of conjunctiva,
breasts, abdomen, perineum, and legs
b. ____ Observation of breastfeeding
c. ____ Information about contraception, safer sex, and counseling and testing for HIV
d. ____ All of the above
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
9. To maintain the newborn’s axillary temperature between 36.5ÆC and 37.5ÆC it is important to
a. ____ Place the baby in an incubator
b. ____ Bathe the baby in warm water immediately after birth
c. ____ Rub the baby vigorously with a blanket
d. ____ Cover the baby’s head, place
249
14. Carry out rapid initial assessment
a. ____ Only for women who present with abdominal pain and vaginal bleeding
b. ____ Only for women who present with abdominal pain
c. ____ Only for women who present with vaginal bleeding
d. ____ For all women of childbearing age who present with a danger sign
15. Immediate post partum hemorrhage can be due to
a. ____ Uterine atony
b. ____ Genital trauma
c. ____ Retained placenta
d. ____ All of the above
16. The most effective way to immediately control eclamptic convulsionsis to
a. ____ Give diazepam
b. ____ Give magnesium sulfate
c. ____ Deliver the baby as soon as possible
d. ____ Give nifedipine
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
17. A woman with a ruptured uterus has which of the following signs and symptoms
a. ____ Rapid maternal pulse
b. ____ Persistent abdominal pain and suprapubic tenderness
c. ____ Fetal distress
d. ____ All of the above
250
18. Treatment of post part ummetritis includes
a. ____ Discontinuing breastfeeding
b. ____ Bedrest and adequate hydration
c. ____ Intravenous ampicillin, gentamicin, and metronidazole until fever free for 48 hours
d. ____ B AND C only
19. Of the following signs, which on esare general danger signs (2answers)
a. ____ fast breathing
b. ____ chest indrawing
c. ____ convulsions
d. ____ neck stiffness
e. ____ vomiting everything
f. ____ severe wasting
20. A 6 month old classified as SEVERE PNEUMONIA or VERY SEVERE DISEASE:
a. ____ should be assessed for HIV
b. ____ may have severe pneumonia or may not
c. ____ needs to be given first dose of antibiotic before urgent referral
d. ____ may have stridor or chest indrawing or any general danger sign
e. ____ all of the above
21. To check for malnutrition (three answers)
a. ____ look for visible severe wasting
b. ____ feel for oedema of both feet
c. ____ look for palmar pallor
d. ____ determine weight for age
22. An infanth as good attachment if
a. ____ chin touching breast
b. ____ Mouth wide open
c. ____ lower lip turned outward
d. ____ more areola visible below than above the mouth
e. ____ all the above
f. ____ none of the above
23. An infant may be said to have feeding problem if
a. ____ not well attached
b. ____ not suckling effectively
c. ____ having less than 8 breastfeeds in 24 hours
d. ____ receives other foods or drinks
e. ____ low weight for age
f. ____ has mouth ulcers
h. ____ none of the above
24. A child with HIV infection may usually present with
a. ____ pneumonia
b. ____ persistent diarrhoea
c. ____ very low weight for age
d. ____ enlargement of the lymph nodes in at least two sites or parotid gland enlargement
e. ____ oral thrush
f. ____ all the above
g. ____ none of the above
MATERNITY HEALTH / CARE IN NORMAL BIRTH – OBSTETRICS
g. ____ all the above
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chapter 6
Viral Hemorrhagic fevers
(VHF), Onchocerciasis
and Leprosy
To familiarize participants with the epidemiological and clinical characteristics of viral
hemorrhagic fevers (VHF), Oncocerciasis and Leprosy.
Specific Objectives
At the end of the session, participants will be familiar with:
➠ The biology and epidemiology of Viral hemorrhagic fevers (VHF), Oncocerciasis and
Leprosy
➠ The management of VHF, Oncocerciasis and Leprosy
➠ Appropriate interventions during outbreaks of VHF
Content
➠ Biology, epidemiology and management of Viral hemorrhagic fevers (VHF)
➠ Biology, epidemiology and management of Oncocerciasis and Leprosy
➠ Surveillance and outbreak control
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
General Objective
253
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Introduction
254
Viral Hemorrhagic fevers (VHF) are caused by a number of different viruses some of which are
associated with arthropods (ARBO) and rodents but may also infect humans. They mostly
cause mild disease but they are capable of causing severe disease with high fatality rates nd
some of them can lead to devastating epidemics in certain areas of the world. Each VHF has
its own distinct clinical profile but all of them share a common clinical profile of fever and a
bleeding tendency with an often devastating result such as severe hemorrhage and shock.
These diseases can cause a serious public health threat as they can have a high epidemic
potential, high fatality rate up to 50-80% in the case of Ebola and extreme difficulties in
treatment and prevention measures. By consequence they warrant strict safety procedures in
health facilities, labs and the community. Effective vaccines exist only in the case of yellow
fever and Rift Valley fever indicated only for high risk individuals. Antiviral treatment is not
available except in the case of Lassa fever (ribavirin) and thus, treatment is symptomatic.
Management of fluid and electrolyte balance from the onset is the most significant measure.
Onchocerciasis is a parasitic disease caused by the filarial worm Onchocerca volvulus. It is
transmitted through the bites of infected blackflies of Simulium species, which carry immature
larval forms of the parasite from human to human. In the human body, the larvae form nodules
in the subcutaneous tissue, where they mature to adult worms. After mating, the female adult
worm can release up to 1000 microfilariae a day. These move through the body, and when they
die they cause a variety of conditions, including blindness, skin rashes, lesions, intense itching
and skin depigmentation. In a number of countries, onchocerciasis has been controlled through
spraying of blackfly breeding sites with insecticide. In addition, a drug is available that kills the
microfilariae, alleviating symptoms and reducing transmission. An international control effort
aims to bring annual treatment with this drug to all populations at risk by the year 2010. When
that is achieved, onchocerciasis may cease to be a public health problem.
Leprosy is caused by a slow-growing bacillus, Mycobacterium leprae. It is transmitted via
droplets from the nose and mouth of untreated patients with severe disease, but is not highly
infectious. If left untreated, the disease can cause nerve damage, leading to muscle weakness
and atrophy, and permanent disabilities. Leprosy can be easily treated with a 6–12-month
course of multidrug therapy. The treatment is highly effective, and has few side-effects and
low relapse rates; there is no known drug resistance.
Methodology
➠ PPt Presentations
➠ Lecture/discussion format
➠ Case study presentation (Marburg/Ebola)
Yellow fever 1
Yellow fever is a viral disease that has caused large epidemics in Africa and the Americas. It
can be recognized from historic texts stretching back 400 years. Infection causes a wide
spectrum of disease, from mild symptoms to severe illness and death. The “yellow” in the
name is explained by the jaundice that affects some patients. Although an effective vaccine
has been available for 60 years, the number of people infected over the last two decades
has increased and yellow fever is now a serious public health issue again.
Cause
Symptoms
The virus remains silent in the body during an incubation period of three to six days. There
are then two disease phases. While some infections have no symptoms whatsoever, the first,
“acute”, phase is normally characterized by fever, muscle pain (with prominent backache),
headache, shivers, loss of appetite, nausea and/or vomiting. Often, the high fever is
paradoxically associated with a slow pulse. After three to four days most patients improve
and their symptoms disappear.
However, 15% enter a “toxic phase” within 24 hours. Fever reappears and several body
systems are affected. The patient rapidly develops jaundice and complains of abdominal pain
with vomiting. Bleeding can occur from the mouth, nose, eyes and/or stomach. Once this
happens, blood appears in the vomit and faeces. Kidney function deteriorates; this can range
from abnormal protein levels in the urine (albuminuria) to complete kidney failure with no
urine production (anuria). Half of the patients in the “toxic phase” die within 10-14 days. The
remainder recover without significant organ damage.
Yellow fever is difficult to recognize, especially during the early stages. It can easily be
1. All information on disease from WHO Health Topics site, http://www.who.int
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
The disease is caused by the yellow fever virus, which belongs to the flavivirus group. In Africa
there are two distinct genetic types (called topotypes) associated with East and West Africa.
South America has two different types, but since 1974 only one has been identified as the
cause of disease outbreaks.
255
confused with malaria, typhoid, rickettsial diseases, haemorrhagic viral fevers (e.g. Lassa),
arboviral infections (e.g. dengue), leptospirosis, viral hepatitis and poisoning (e.g. carbon
tetrachloride). A laboratory analysis is required to confirm a suspect case. Blood tests (serology
assays) can detect yellow fever antibodies that are produced in response to the infection.
Several other techniques are used to identify the virus itself in blood specimens or liver tissue
collected after death. These tests require highly trained laboratory staff using specialized
equipment and materials.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Regions affected
256
The virus is constantly present with low levels of infection (i.e. endemic) in some tropical areas
of Africa and the Americas. This viral presence can amplify into regular epidemics. Until the
start of this century, yellow fever outbreaks also occurred in Europe, the Caribbean islands
and Central and North America. Even though the virus is not felt to be present in these areas
now, they must still be considered at risk for yellow fever epidemics.
Thirty-three countries, with a combined population of 508 million, are at risk in Africa.
These lie within a band from 15ÆN to 10ÆS of the equator. In the Americas, yellow fever is
endemic in nine South American countries and in several Caribbean islands. Bolivia, Brazil,
Colombia, Ecuador and Peru are considered at greatest risk.
There are 200,000 estimated cases of yellow fever (with 30,000 deaths) per year. However,
due to underreporting, only a small percentage of these cases are identified. Small numbers
of imported cases also occur in countries free of yellow fever. Although yellow fever has never
been reported from Asia, this region is at risk because the appropriate primates and
mosquitoes are present.
Transmission
Humans and monkeys are the principal animals to be infected. The virus is carried from one
animal to another (horizontal transmission) by a biting mosquito (the vector). The mosquito
can also pass the virus via infected eggs to its offspring (vertical transmission). The eggs
produced are resistant to drying and lie dormant through dry conditions, hatching when the
rainy season begins. Therefore, the mosquito is the true reservoir of the virus, ensuring
transmission from one year to the next.
Several different species of the Aedes and Haemogogus (S. America only) mosquitoes
transmit the yellow fever virus. These mosquitoes are either domestic (i.e. they breed around
houses), wild (they breed in the jungle) or semi-domestic types (they display a mixture of
habits). Any region populated with these mosquitoes can potentially harbour the disease.
Control programmes successfully eradicated mosquito habitats in the past, especially in South
America. However, these programmes have lapsed over the last 30 years and mosquito
populations have increased. This favours epidemics of yellow fever.
Infection of humans
There are three types of transmission cycle for yellow fever: sylvatic, intermediate and urban.
All three cycles exist in Africa, but in South America, only sylvatic and urban yellow fever occur.
that are infected by wild mosquitoes. The infected monkeys can then pass the virus
onto other mosquitoes that feed on them. These infected wild mosquitoes bite
humans entering the forest resulting in sporadic cases of yellow fever. The majority
of cases are young men working in the forest (logging, etc). On occasion, the virus
spreads beyond the affected individual.
➠ Intermediate yellow fever: In humid or semi-humid savannahs of Africa, small-scale
epidemics occur. These behave differently from urban epidemics; many separate
villages in an area suffer cases simultaneously, but fewer people die from infection.
Semi-domestic mosquitoes infect both monkey and human hosts. This area is often
called the “zone of emergence”, where increased contact between man and infected
mosquito leads to disease. This is the most common type of outbreak seen in recent
decades in Africa. It can shift to a more severe urban-type epidemic if the infection is
carried into a suitable environment (with the presence of domestic mosquitoes and
unvaccinated humans).
➠ Urban yellow fever: Large epidemics can occur when migrants introduce the virus into
areas with high human population density. Domestic mosquitoes (of one species,
Aedes aegypti) carry the virus from person to person; no monkeys are involved in
transmission. These outbreaks tend to spread outwards from one source to cover a
wide area.
Treatment
There is no specific treatment for yellow fever. Dehydration and fever can be corrected with
oral rehydration salts and paracetamol. Any superimposed bacterial infection should be
treated with an appropriate antibiotic. Intensive supportive care may improve the outcome
for seriously ill patients, but is rarely available in poorer, developing countries.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➠ Sylvatic (or jungle) yellow fever: In tropical rainforests, yellow fever occurs in monkeys
257
Prevention
Vaccination is the single most important measure for preventing yellow fever. In populations
where vaccination coverage is low, vigilant surveillance is critical for prompt recognition and
rapid control of outbreaks. Mosquito control measures can be used to prevent virus
transmission until vaccination has taken effect.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Vaccination
258
Yellow fever vaccine is safe and highly effective. The protective effect (immunity) occurs within
one week in 95% of people vaccinated. A single dose of vaccine provides protection for 10
years and probably for life. Over 300 million doses have been given and serious side effects
are extremely rare. However, recently a few serious adverse outcomes, including deaths, have
been reported in Brazil, Australia and the United States. Scientists are investigating the cause
of these adverse events, and monitoring to ensure detection of any similar incidents.
The risk to life from yellow fever is far greater than the risk from the vaccine, so those who
may be exposed to yellow fever should be protected by immunization. If there is no risk of
exposure, for example, if a person will not be visiting an endemic area, there is no necessity
to receive the vaccine. Since most of the other known side effects have occurred in children
less than six months old, vaccine is not administered to this age group. The vaccine should
only be given to pregnant women during vaccination campaigns in the midst of an epidemic.
Vaccination can be part of a routine preventive immunization programme or can be done
in mass “catch-up” campaigns to increase vaccination coverage in areas where it is low. The
World Health Organization (WHO) strongly recommends routine childhood vaccination. The
vaccine can be administered at age nine months, at the same time as the measles vaccine.
Eighteen African nations have agreed to incorporate yellow fever vaccine into their routine
national vaccination programmes. This is more cost effective and prevents more cases (and
deaths) than when emergency vaccination campaigns are performed to control an epidemic.
Past experience shows the success of this strategy. Between 1939 and 1952 yellow fever
cases almost vanished from French West Africa after intensive vaccination campaigns.
Similarly, Gambia instituted mass routine vaccination after its 1979/1980 epidemic and later
incorporated yellow fever vaccine into its childhood immunization programme. Gambia
reported 85% vaccine coverage in 2000. No cases have been reported since 1980, yet the virus
remains present in the environment.
To prevent an epidemic in a country, at least 80% of the population must have immunity
to yellow fever. This can only be achieved through the effective incorporation of yellow fever
into childhood immunization programmes and the implementation of mass catch-up
campaigns. The latter is the only way to ensure that coverage of all susceptible age groups
is achieved and will prevent outbreaks from spreading. Very few countries in Africa have
achieved this level to date.
Vaccination is highly recommended for travellers to high-risk areas. A vaccination
certificate is required for entry to many countries, particularly for travellers arriving in Asia
from Africa or South America. Fatal cases in unvaccinated tourists have been reported.
Because vaccination coverage in many areas is not optimal, prompt detection of yellow fever
cases and rapid response (emergency vaccination campaigns) are essential for controlling
disease outbreaks. Improvement in yellow fever surveillance is needed as evidenced by the
gross underreporting of cases (estimates as to the true number of cases vary widely and have
put the underreporting factor between three- and 250-fold). A surveillance system must be
sensitive enough to detect and appropriately investigate suspect cases. This is facilitated by a
standardized definition of possible yellow fever cases, that is “acute fever followed by
jaundice within two weeks of onset of symptoms, or with bleeding symptoms or with death
within three weeks of onset”. Suspect cases are reported to health authorities on a
standardized case investigation form.
Ready access to laboratory testing is essential for confirming cases of yellow fever, as many
other diseases have similar symptoms. WHO has recently recommended that every at-risk
country have at least one national laboratory where basic yellow fever blood tests can be
performed. Training programmes are being conducted and test materials are provided by
WHO.
Given the likelihood that other cases have occurred (but have not been detected), one
confirmed case of yellow fever is considered to be an outbreak. An investigation team should
subsequently explore and define the outbreak. This produces data for analysis, which guides
the epidemic control committee in preparing the appropriate outbreak response (e.g.
emergency vaccination programmes, mosquito control activities). This committee should also
plan for the long term by implementing or strengthening routine childhood yellow fever
vaccination.
Mosquito control
In general, eliminating potential mosquito breeding sites is an important and effective means
for controlling mosquito-transmitted diseases. For prevention and control of yellow fever,
priority is placed on vaccination programmes. For example, mosquito control programmes
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Surveillance
259
against wild mosquitoes in forested areas are not practical or cost-effective for preventing
sylvatic infections. Spraying to kill adult mosquitoes during epidemics may have value by
interrupting virus transmission. This “buys time” for immunity to develop after an emergency
vaccination campaign.
In summary
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Over the last 20 years the number of yellow fever epidemics has risen and more countries are
reporting cases. Mosquito numbers and habitats are increasing. In both Africa and the
Americas, there is a large susceptible, unvaccinated population. Changes in the world’s environment, such as deforestation and urbanization, have increased contact with the mosquito/virus.
Widespread international travel could play a role in spreading the disease. The priorities are
vaccination of exposed populations, improved surveillance and epidemic preparedness.
260
Dengue and dengue haemorrhagic fever
Key facts
ñ Dengue is a mosquito-borne infection that causes a severe flu-like illness, and sometimes
a potentially lethal complication called dengue haemorrhagic fever.
ñ Global incidence of dengue has grown dramatically in recent decades.
ñ About two fifths of the world’s population are now at risk.
ñ Dengue is found in tropical and sub-tropical climates worldwide, mostly in urban and semiurban areas.
ñ Dengue haemorrhagic fever is a leading cause of serious illness and death among children
in some Asian countries.
ñ There is no specific treatment for dengue, but appropriate medical care frequently saves
the lives of patients with the more serious dengue haemorrhagic fever.
ñ The only way to prevent dengue virus transmission is to combat the disease-carrying
mosquitoes.
Dengue is a mosquito-borne infection that in recent decades has become a major international public health concern. Dengue is found in tropical and sub-tropical regions around
the world, predominantly in urban and semi-urban areas.
Dengue haemorrhagic fever (DHF), a potentially lethal complication, was first recognized
in the 1950s during dengue epidemics in the Philippines and Thailand. Today DHF affects most
Asian countries and has become a leading cause of hospitalization and death among children
in the region.
There are four distinct, but closely related, viruses that cause dengue. Recovery from
infection by one provides lifelong immunity against that virus but confers only partial and
transient protection against subsequent infection by the other three viruses. There is good
evidence that sequential infection increases the risk of developing DHF.
The incidence of dengue has grown dramatically around the world in recent decades.
Some 2.5 billion people – two fifths of the world’s population – are now at risk from dengue.
WHO currently estimates there may be 50 million dengue infections worldwide every year.
In 2007 alone, there were more than 890 000 reported cases of dengue in the Americas,
of which 26 000 cases were DHF.
The disease is now endemic in more than 100 countries in Africa, the Americas, the Eastern
Mediterranean, South-east Asia and the Western Pacific. South-east Asia and the Western
Pacific are the most seriously affected. Before 1970 only nine countries had experienced DHF
epidemics, a number that had increased more than four-fold by 1995.
Not only is the number of cases increasing as the disease is spreading to new areas, but
explosive outbreaks are occurring. In 2007, Venezuela reported over 80 000 cases, including
more than 6 000 cases of DHF.
Some other statistics:
➠ During epidemics of dengue, infection rates among those who have not been
previously exposed to the virus are often 40% to 50%, but can reach 80% to 90%.
➠ An estimated 500 000 people with DHF require hospitalization each year, a very large
proportion of whom are children. About 2.5% of those affected die.
➠ Without proper treatment, DHF fatality rates can exceed 20%. Wider access to medical
care from health providers with knowledge about DHF - physicians and nurses who
recognize its symptoms and know how to treat its effects - can reduce death rates
to less than 1%.
The spread of dengue is attributed to expanding geographic distribution of the four
dengue viruses and their mosquito vectors, the most important of which is the predominantly
urban species Aedes aegypti. A rapid rise in urban mosquito populations is bringing ever
greater numbers of people into contact with this vector, especially in areas that are favourable
for mosquito breeding, e.g. where household water storage is common and where solid waste
disposal services are inadequate.
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Global burden of dengue
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DengueNet: WHO surveillance
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Transmission
Dengue viruses are transmitted to humans through the bites of infective female Aedes
mosquitoes. Mosquitoes generally acquire the virus while feeding on the blood of an infected
person. After virus incubation for eight to 10 days,
an infected mosquito is capable, during probing and
blood feeding, of transmitting the virus for the rest
of its life. Infected female mosquitoes may also
transmit the virus to their offspring by transovarial
(via the eggs) transmission, but the role of this in
sustaining transmission of the virus to humans has
not yet been defined.
Infected humans are the main carriers and
WHO/TDR/Stammers
multipliers of the virus, serving as a source of the virus
for uninfected mosquitoes. The virus circulates in the
blood of infected humans for two to seven days, at approximately the same time that they
have a fever; Aedes mosquitoes may acquire the virus when they feed on an individual during
this period. Some studies have shown that monkeys in some parts of the world play a similar
role in transmission.
Characteristics
Dengue fever is a severe, flu-like illness that affects infants, young children and adults, but
seldom causes death.
The clinical features of dengue fever vary according to the age of the patient. Infants
and young children may have a fever with rash. Older children and adults may have either a
mild fever or the classical incapacitating disease with abrupt onset and high fever, severe
headache, pain behind the eyes, muscle and joint pains, and rash.
Dengue haemorrhagic fever (DHF) is a potentially deadly complication that is characterized
by high fever, often with enlargement of the liver, and in severe cases circulatory failure.
The illness often begins with a sudden rise in temperature accompanied by facial flush and
other flu-like symptoms. The fever usually continues for two to seven days and can be as high
as 41ÆC, possibly with convulsions and other complications.
In moderate DHF cases, all signs and symptoms abate after the fever subsides. In severe
cases, the patient’s condition may suddenly deteriorate after a few days of fever; the
temperature drops, followed by signs of circulatory failure, and the patient may rapidly go
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into a critical state of shock and die within 12 to 24 hours, or quickly recover following
appropriate medical treatment (see below).
Treatment
There is no specific treatment for dengue fever.
For DHF, medical care by physicians and nurses experienced with the effects and
progression of the complicating haemorrhagic fever can frequently save lives - decreasing
mortality rates from more than 20% to less than 1%. Maintenance of the patient’s circulating
fluid volume is the central feature of DHF care.
Immunization
There is no vaccine to protect against dengue. Although progress is underway, developing
a vaccine against the disease –in either its mild or severe form– is challenging.
against all four types to be effective.
➠ There is limited understanding of how the disease typically behaves and how the virus
interacts with the immune system.
➠ There is a lack of laboratory animal models available to test immune responses to
potential vaccines.
Despite these challenges, two vaccine candidates have advanced to evaluation in human
subjects in countries with endemic disease, and several potential vaccines are in earlier stages
of development. WHO provides technical advice and guidance to countries and private
partners to support vaccine research and evaluation.
Prevention and control
At present, the only method of controlling or preventing dengue virus transmission is to
combat the vector mosquitoes.
In Asia and the Americas, Aedes aegypti breeds primarily in man-made containers like
earthenware jars, metal drums and concrete cisterns used for domestic water storage, as well
as discarded plastic food containers, used automobile tyres and other items that collect
rainwater. In Africa the mosquito also breeds extensively in natural habitats such as tree holes,
and leaves that gather to form “cups” and catch water.
In recent years, Aedes albopictus, a secondary dengue vector in Asia, has become
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➠ With four closely related viruses that can cause the disease, the vaccine must immunize
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established in the United States, several Latin
American and Caribbean countries, parts of Europe
and Africa. The rapid geographic spread of this
species is largely attributed to the international trade
in used tyres, a breeding habitat.
Vector control is implemented using environmental management and chemical methods. Proper
solid waste disposal and improved water storage
WHO/TDR/Crump
practices, including covering containers to prevent
access by egg-laying female mosquitoes are among
methods that are encouraged through community-based programmes.
During outbreaks, emergency vector control measures can also include broad application
of insecticides as space sprays using portable or truck-mounted machines or even aircraft.
However, the mosquito-killing effect is transient, variable in its effectiveness because the
aerosol droplets may not penetrate indoors to microhabitats where adult mosquitoes are
sequestered, and the procedure is costly and operationally difficult. Regular monitoring of the
vectors’ susceptibility to widely used insecticides is necessary to ensure the appropriate choice
of chemicals. Active monitoring and surveillance of the natural mosquito population should
accompany control efforts to determine programme effectiveness.
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Lassa fever
Lassa viral haemorrhagic fever is an acute illness of 1-4 weeks duration that occurs in West
Africa. Though first described in the 1950s, the virus causing the disease was not identified
until 1969. The virus is a single-stranded RNA virus belonging to the virus family Arenaviridae.
Lassa fever is known to be endemic in Guinea (Conakry), Liberia, Sierra Leone and parts of
Nigeria, but probably exists in other West African countries as well.
Signs and symptoms
About 80% of human infections are asymptomatic; the remaining cases have severe multisystem disease, where the virus affects several organs in the body, such as the liver, spleen and
kidneys. The incubation period of Lassa fever ranges from 6-21 days. The onset of the disease
is usually gradual, starting with fever, general weakness, and malaise. After a few days,
headache, sore throat, muscle pain, chest pain, nausea, vomiting, diarrhoea, cough, and
abdominal pain may follow. Severe cases may progress to show facial swelling, fluid in the
lung cavity, bleeding from mouth, nose, vagina or gastrointestinal tract, and low blood
pressure. Protein may be noted in the urine. Shock, seizures, tremor, disorientation, and coma
may be seen in the late stages. Deafness occurs in 25% of patients of whom half recover some
function after 1-3 months. Transient hair loss and gait disturbance may occur during recovery.
Morbidity and mortality
Animal reservoir
Lassa fever is a zoonotic disease, meaning that humans become infected from contact with
infected animals. The animal reservoir, or host, of Lassa virus is a rodent of the genus
Mastomys, commonly known as the “multimammate rat.” Mastomys infected with Lassa virus
do not become ill, but they can shed the virus in their excreta (urine and faeces).
People at risk
Lassa fever occurs in all age groups and in both men and women. Persons at greatest risk
are those living in rural areas where Mastomys are usually found, especially in areas of poor
sanitation or crowded living conditions. Health care workers are at risk if proper barrier
nursing and infection control practices are not maintained.
Transmission
Humans usually become infected with Lassa virus from exposure to excreta of infected
Mastomys. Both direct exposure, (touching the excreta) and Lassa virus may also be spread
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Some studies indicate that 300 000 to 500 000 cases of Lassa fever and 5000 deaths occur
yearly across West Africa. The overall case-fatality rate is 1%, up to 15% among hospitalized
patients. Death usually occurs within 14 days of onset in fatal cases. The disease is especially
severe late in pregnancy, with maternal death and/or fetal loss occurring in greater than 80%
of cases during the third trimester.
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between humans through direct contact with the blood, urine, faeces, or other bodily
secretions of a person with Lassa fever. There is no epidemiological evidence supporting
airborne spread between humans. Person-to-person transmission occurs in both community
and health care settings, where the virus may be spread by contaminated medical equipment,
such as re-used needles. Sexual transmission of Lassa virus has been reported.
Diagnosis
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Because the symptoms of Lassa fever are so varied and non-specific, clinical diagnosis is often
difficult, especially early in the course of the disease. Lassa fever is difficult to distinguish from
many other diseases which cause fever, including malaria, shigellosis, typhoid fever, yellow
fever and other viral haemorrhagic fevers.
Definitive diagnosis requires testing that is available only in highly specialized laboratories.
Laboratory specimens may be hazardous and must be handled with extreme care. Lassa fever
is diagnosed by detection of Lassa antigen, anti-Lassa antibodies, or virus isolation techniques.
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Treatment and prophylaxis
The antiviral drug ribavirin is effective treatment for Lassa fever if given early on in the course
of clinical illness. There is no evidence to support the role of ribavirin as post-exposure
prophylactic treatment for Lassa fever.
Prevention
Prevention of Lassa fever in the community centers on promoting good “community hygiene”
to discourage rodents from entering homes. Effective measures include storing grain and
other foodstuffs in rodent-proof containers, disposing of garbage far from the home,
maintaining clean households and keeping cats. Because Mastomys are so abundant in
endemic areas, it is not possible to completely eliminate them from the environment.
Infection control
Family members and health care workers should always be careful to avoid contact with blood
and body fluids while caring for sick persons. Routine barrier nursing precautions probably
protect against transmission of Lassa virus in most circumstances. However, for added safety,
patients suspected to have Lassa fever should be cared for under specific “isolation
precautions,” which include the wearing of protective clothing such as masks, gloves, gowns,
and face shields, and the systematic sterilization of contaminated equipment (see also detailed
guidelines in “Infection Control for Viral Hemorrhagic Fevers in the African Health Care
Setting”)
Civil unrest in many of the countries where Lassa fever is endemic has impeded effective
control. However, recent peace initiatives have opened new opportunities to combat the
problem. The Ministries of Health of Guinea, Liberia and Sierra Leone, WHO, the Office of
United States Foreign Disaster Assistance, the United Nations, and other partners have worked
together to establish the Mano River Union Lassa Fever Network. The programme supports
these three countries in developing national prevention strategies and enhancing laboratory
diagnostics for Lassa fever and other dangerous diseases. Training in laboratory diagnosis,
clinical management, and environmental control is also included. In addition, a new ward
dedicated to the care of patients with Lassa fever is under construction in Sierra Leone,
sponsored by the European Union.
International public health implications
On rare occasions, travellers from areas where Lassa fever is endemic export the disease to
other countries. Although malaria, typhoid fever, and many other tropical infections are much
more common, the diagnosis of Lassa fever should be considered in febrile patients returning
from West Africa, especially if they have had exposures in rural areas or hospitals in countries
where Lassa fever is known to be endemic. Health care workers seeing a patient suspected to
have Lassa fever should immediately contact local and national experts for advice and to
arrange for laboratory testing.
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Ongoing initiatives
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Crimean-Congo haemorrhagic fever
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Crimean-Congo haemorrhagic fever (CCHF) is a viral haemorrhagic fever of the Nairovirus
group. Although primarily a zoonosis, sporadic cases and outbreaks of CCHF affecting humans
do occur. The disease is endemic in many countries in Africa, Europe and Asia, and during
2001, cases or outbreaks have been recorded in Kosovo, Albania, Iran, Pakistan, and South
Africa.
The disease was first described in the Crimea in 1944 and given the name Crimean
haemorrhagic fever. In 1969 it was recognized that the pathogen causing Crimean haemorrhagic
fever was the same as that responsible for an illness identified in 1956 in the Congo, and
linkage of the 2 place names resulted in the current name for the disease and the virus. CCHF
is a severe disease in humans, with a high mortality rate. Fortunately, human illness occurs
infrequently, although animal infection may be more common.
The geographical distribution of the virus, like that of its tick vector, is widespread.
Evidence of CCHF virus has been found in Africa, Asia, the Middle East and Eastern Europe.
Healthcare workers in endemic areas should be aware of the illness and the correct infection
control procedures to protect themselves and their patients from the risk of nosocomial
(hospital-acquired) infection.
CCHF virus
The virus which causes CCHF is a Nairovirus, a group of related viruses forming one of the five
genera in the Bunyaviridae family of viruses. All of the 32 members of the Nairovirus genus
are transmitted by argasid or ixodid ticks, but only three have been implicated as causes of
human disease: the Dugbe and Nairobi sheep viruses, and CCHF, which is the most important
human pathogen amongst them.
CCHF reservoirs and vectors
➠ The CCHF virus may infect a wide range of domestic and wild animals. Many birds are
resistant to infection, but ostriches are susceptible and may show a high prevalence of
infection in endemic areas. Animals become infected with CCHF from the bite of infected
ticks.
➠ A number of tick genera are capable of becoming infected with CCHF virus, but the most
➠
➠
➠
➠
➠
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➠
efficient and common vectors for CCHF appear to be members of the Hyalomma genus.
Trans-ovarial (transmission of the virus from infected female ticks to offspring via eggs) and
venereal transmission have been demonstrated amongst some vector species, indicating
one mechanism which may contribute to maintaining the circulation of the virus in nature.
However, the most important source for acquisition of the virus by ticks is believed to
be infected small vertebrates on which immature Hyalomma ticks feed. Once infected, the
tick remains infected through its developmental stages, and the mature tick may transmit
the infection to large vertebrates, such as livestock. Domestic ruminant animals, such as
cattle, sheep and goats, are viraemic (virus circulating in the bloodstream) for around
one week after becoming infected.
Humans who become infected with CCHF acquire the virus from direct contact with blood
or other infected tissues from livestock during this time, or they may become infected from
a tick bite. The majority of cases have occurred in those involved with the livestock
industry, such as agricultural workers, slaughterhouse workers and veterinarians.
CLINICAL FEATURES
The length of the incubation period for the illness appears to depend on the mode of
acquisition of the virus. Following infection via tick bite, the incubation period is usually
one to three days, with a maximum of nine days. The incubation period following contact
with infected blood or tissues is usually five to six days, with a documented maximum
of 13 days.
Onset of symptoms is sudden, with fever, myalgia (aching muscles), dizziness, neck pain
and stiffness, backache, headache, sore eyes and photophobia (sensitivity to light). There
may be nausea, vomiting and sore throat early on, which may be accompanied by
diarrhoea and generalised abdominal pain. Over the next few days, the patient may
experience sharp mood swings, and may become confused and aggressive. After two to
four days, the agitation may be replaced by sleepiness, depression and lassitude, and the
abdominal pain may localize to the right upper quadrant, with detectable hepatomegaly
(liver enlargement).
Other clinical signs which emerge include tachycardia (fast heart rate), lymphadenopathy
(enlarged lymph nodes), and a petechial rash (a rash caused by bleeding into the skin),
both on internal mucosal surfaces, such as in the mouth and throat, and on the skin. The
petechiae may give way to ecchymoses (like a petechial rash, but covering larger areas)
and other haemorrhagic phenomena such as melaena (bleeding from the upper bowel,
passed as altered blood in the faeces), haematuria (blood in the urine), epistaxis
(nosebleeds) and bleeding from the gums. There is usually evidence of hepatitis. The
severely ill may develop hepatorenal (i.e., liver and kidney) and pulmonary failure after the
fifth day of illness.
The mortality rate from CCHF is approximately 30%, with death occurring in the second
week of illness. In those patients who recover, improvement generally begins on the ninth
or tenth day after the onset of illness.
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Diagnosis
➤ Diagnosis of suspected CCHF is performed in specially-equipped, high biosafety level
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
laboratories. IgG and IgM antibodies may be detected in serum by enzyme-linked
immunoassay (the “ELISA” or “EIA” methods) from about day six of illness. IgM remains
detectable for up to four months, and IgG levels decline but remain detectable for up to
five years.
➤ Patients with fatal disease do not usually develop a measurable antibody response and
in these individuals, as well as in patients in the first few days of illness, diagnosis is
achieved by virus detection in blood or tissue samples. There are several methods for doing
this. The virus may be isolated from blood or tissue specimens in the first five days of
illness, and grown in cell culture. Viral antigens may sometimes be shown in tissue samples
using immunofluorescence or EIA.
➤ More recently, the polymerase chain reaction (PCR), a molecular method for detecting the
viral genome, has been successfully applied in diagnosis.
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Treatment
➠ General supportive therapy is the mainstay of patient management in CCHF. Intensive
monitoring to guide volume and blood component replacement is required.
➠ The antiviral drug ribavirin has been used in treatment of established CCHF infection with
apparent benefit. Both oral and intravenous formulations seem to be effective.
➠ The value of immune plasma from recovered patients for therapeutic purposes has not
been demonstrated, although it has been employed on several occasions.
Prevention and control
➣ Although an inactivated, mouse brain-derived vaccine against CCHF has been developed
and used on a small scale in Eastern Europe, there is no safe and effective vaccine widely
available for human use. The tick vectors are numerous and widespread and tick control
with acaricides (chemicals intended to kill ticks) is only a realistic option for well-managed
livestock production facilities.
➣ Persons living in endemic areas should use personal protective measures that include
avoidance of areas where tick vectors are abundant and when they are active (Spring to
Fall); regular examination of clothing and skin for ticks, and their removal; and use of
repellents.
➣ Persons who work with livestock or other animals in the endemic areas can take practical
Marburg haemorrhagic fever
Marburg haemorrhagic fever is a severe and highly fatal disease caused by a virus from the
same family as the one that causes Ebola haemorrhagic fever. Viewed under electron microscopy, the viruses show particles shaped like elongated filaments, sometimes coiled into
strange shapes, that give the Filoviridae family its name. These viruses are among the most
virulent pathogens known to infect humans.
Though caused by different viruses, the two diseases are clinically similar. Both diseases
are rare, but have a capacity to cause dramatic outbreaks with high fatality. Historically,
outbreaks have tended to reach the attention of health authorities only after transmission
has been amplified by inadequate infection control in health care settings.
Neither disease has a vaccine or specific treatment. Ecological studies are in progress to
identify the natural reservoir of both Marburg and Ebola. There is evidence that bats are
involved, but much work remains to be done to definitively describe the the natural
transmission cycle. Monkeys are susceptible to infection but are not considered plausible
reservoir hosts as virtually all infected animals die too rapidly to sustain survival of the virus.
Infection of humans occurs sporadically.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
measures to protect themselves. These include the use of repellents on the skin (e.g. DEET)
and clothing (e.g. permethrin) and wearing gloves or other protective clothing to prevent
skin contact with infected tissue or blood.
➣ When patients with CCHF are admitted to hospital, there is a risk of nosocomial spread of
infection. In the past, serious outbreaks have occurred in this way and it is imperative that
adequate infection control measures be observed to prevent this disastrous outcome.
➣ Patients with suspected or confirmed CCHF should be isolated and cared for using barrier
nursing techniques. Specimens of blood or tissues taken for diagnostic purposes should
be collected and handled using universal precautions. Sharps (needles and other
penetrating surgical instruments) and body wastes should be safely disposed of using
appropriate decontamination procedures.
➣ Healthcare workers are at risk of acquiring infection from sharps injuries during surgical
procedures and, in the past, infection has been transmitted to surgeons operating on
patients to determine the cause of the abdominal symptoms in the early stages of (at that
moment undiagnosed) infection. Healthcare workers who have had contact with tissue or
blood from patients with suspected or confirmed CCHF should be followed up with daily
temperature and symptom monitoring for at least 14 days after the putative exposure.
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Natural history and clinical features
Causative agent. Marburgvirus of the Filoviridae family.
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Geographical occurrence. A large, 2-centre outbreak in Marburg , Germany, and Belgrade,
former Yugoslavia, in 1967 led to the initial recognition of the disease. The outbreak was
associated laboratory work using African green monkeys (Cercopithecus aethiops) imported
from Uganda. Subsequently, outbreaks and sporadic cases have been reported in Angola,
Democratic Republic of the Congo, Kenya, South Africa (in a person with a recent travel
history to Zimbabwe) and Uganda.
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Transmission. Transmission of the virus from person to person requires close contact with
a patient. Transmission does not occur during the incubation period. Infection results from
contact with blood or other body fluids (faeces, vomitus, urine, saliva, and respiratory
secretions) with high virus concentration, especially when these fluids contain blood.
Transmission via infected semen can occur; virus has been detected in semen up to seven
weeks after clinical recovery.
Patients become increasingly infectious as their illness progresses, and are most infectious
during the phase of severe illness. Close contact with a severely ill patient, during care at home
or in hospital, and certain burial practices are common routes of infection. Transmission via
contaminated injection equipment or through needle-stick injuries is associated with more
severe disease, rapid deterioration, and possibly higher fatality.
Incubation period. 3 to 9 days.
Susceptibility. All age groups are susceptible to infection, but most cases have occurred in
adults. Prior to the present outbreak in Angola (2004), paediatric cases were considered extremely
rare. In the largest outbreak previously recorded, which occurred in the Democratic Republic of
the Congo from late 1998 to 2000, only 12 (8%) of the cases were under the age of 5 years.
Clinical features. Illness caused by Marburg virus begins abruptly, with severe headache
and severe malaise. Muscle aches and pains are a common feature.
A high fever usually appears on the first day of illness, followed by progressive and rapid
debilitation. A severe watery diarrhoea, abdominal pain and cramping, nausea, and vomiting
begin about the third day. Diarrhoea can persist for a week. The appearance of patients at
this phase has been described as showing “ghost-like” drawn features, deep-set eyes,
expressionless faces, and extreme lethargy. In the 1967 European outbreak, a non-itchy rash
was a feature noted in most patients between days 2 and 7 after symptom onset.
Many patients develop severe haemorrhagic manifestations between days 5 and 7 and
fatal cases usually have some form of bleeding, often from multiple sites. Findings of fresh
blood in vomitus and faeces are often accompanied by bleeding from the nose, gums, and
vagina. Spontaneous bleeding at venipuncture sites can be particularly troublesome. During
the severe phase of illness, patients have sustained high fevers. Involvement of the central
nervous system can result in confusion, irritability, and aggression. Orchitis has been reported
occasionally in the late phase of disease (day 15).
In fatal cases, death occurs most often between 8 and 9 days after symptom onset, usually
preceded by severe blood loss and shock.
Natural reservoir of the virus. Unknown.
1967: Germany and Yugoslavia. Marburg haemorrhagic fever was initially detected following
simultaneous outbreaks in Marburg and Frankfurt, Germany and Belgrade, former
Yugoslavia. The initial cases occurred in laboratory workers handling African green
monkeys imported from Uganda. The outbreaks involved 25 primary infections, with 7
deaths, and 6 secondary cases, with no deaths. The primary infections were in laboratory
staff exposed to Marburg virus while working with monkeys or their tissues. The secondary
cases involved two doctors, a nurse, a post-mortem attendant, and the wife of a
veterinarian. All secondary cases had direct contact, usually involving blood, with a primary
case. Both doctors became infected through accidental skin pricks when drawing blood
from patients.
1975: South Africa, possibly via Zimbabwe. In mid-February 1975, an Australian, aged 20
years, was admitted to a hospital in Johannesburg, South Africa. During early February, he
and a companion had travelled extensively through Zimbabwe, often camping outdoors.
He died of Marburg haemorrhagic fever four days after hospital admission. His travelling
companion became infected, as did a nurse who attended both patients. Both secondary
cases recovered.
1980: Kenya. In January 1980, a 56-year-old Frenchman, who had visited Kitum Cave in
Kenya’s Mount Elgon National Park, became infected. Despite specialized care in Nairobi
and aggressive resuscitation attempts, he died on 15 January. The doctor who attempted
resuscitation developed symptoms 9 days later. He recovered.
1987: Kenya. In August 1987, a 15-year old Dane, was admitted to a hospital in Kenya,
suffering from Marburg haemorrhagic fever. His illnes proved fatal.Nine days prior to
symptom onset, he had visited Kitum Cave in Mount Elgon National Park. No further cases
were detected.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
History of recorded outbreaks
273
1998-2000: Democratic Republic of the Congo. The outbreak in DRC marked the first large
outbreak of this disease under natural conditions. The outbreak, which occurred from late
1998 to 2000, involved 154 cases, of which 128 were fatal, representing a case fatality
of 83%. The majority of cases occurred in young male workers at a gold mine in Durba, in
the north-eastern part of the country, which proved to be the epicentre of the outbreak.
Cases were subsequently detected in the neighbouring village of Watsa. Family members
involved in the close care of patients accounted for some cases, but secondary transmission
appeared to be rare. Subsequent virological investigation indicated that virus of several
different strains was introduced to human populations, from some yet unknown
environmental source, on more than seven separate occasions.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
2004-2005: Angola. In what was to become the largest outbreak of MHF in history, this
outbreak is believed to have begun in Uige Province in October 2004. By the time the
last laboratory-confirmed case was identified in July 2005, the Ministry of Health had
reported a total of 374 cases, including 329 deaths (CFR 88%) countrywide. Of these, 368
cases, including 323 deaths, were reported in Uige Province. All cases detected in other
provinces have been linked directly to the outbreak in Uige.
274
2008. In July 2008, a Dutch tourist developed Marburg four days after returning to the
Netherlands from a three-week holiday in Uganda. To-date, the source of the exposure
has not been confirmed, although it is known that the woman visited caves in western
Uganda where bats were present.
Ebola haemorrhagic fever
The Ebola virus belongs to the Filoviridae family (filovirus) and is comprised of five distinct
species: Zaïre, Sudan, Côte d’Ivoire, Bundibugyo and Reston.
Zaïre, Sudan and Bundibugyo species have been associated with large Ebola hemorrhagic
fever (EHF) outbreaks in Africa with high case fatality ratio (25–90%) while Côte d’Ivoire and
Reston have not. Reston species can infect humans but no serious illness or death in humans
have been reported to date.
Human infection with the Ebola Reston subtype, found in the Western Pacific, has only
caused asymptomatic illness, meaning that those who contract the disease do not experience
clinical illness. The natural reservoir of the Ebola virus seems to reside in the rain forests of the
African continent and in areas of the Western Pacific.
Transmission
➠ The Ebola virus is transmitted by direct contact with the blood, secretions, organs or
other body fluids of infected persons.
➠ Burial ceremonies where mourners have direct contact with the body of the deceased
person can play a significant role in the transmission of Ebola.
➠ The infection of human cases with Ebola virus through the handling of infected
chimpanzees, gorillas, and forest antelopes –both dead and alive– has been
documented in Côte d’Ivoire, the Republic of Congo and Gabon. The transmission of
the Ebola Reston strain through the handling of cynomolgus monkeys has also been
reported.
➠ Health care workers have frequently been infected while treating Ebola patients,
through close contact without correct infection control precautions and adequate
barrier nursing procedures.
Symptoms
Ebola is characterized by the sudden onset of fever, intense weakness, muscle pain, headache
and sore throat. This is often followed by vomiting, diarrhoea, rash, impaired kidney and liver
function, and in some cases, both internal and external bleeding. Laboratory findings show
low counts of white blood cells and platelets as well as elevated liver enzymes.
Diagnosis
Specialized laboratory tests on blood specimens detect specific antigens and/or genes of the
virus. Antibodies to the virus can be detected, and the virus can be isolated in cell culture.
Tests on samples present an extreme biohazard risk and are only conducted under maximum
biological containment conditions. New developments in diagnostic techniques include noninvasive methods of diagnosis (testing saliva and urine samples) and testing inactivated
samples to provide rapid laboratory diagnosis to support case management during outbreak
control activities.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Incubation period: two to 21 days.
275
Therapy and vaccine
➤ Severe cases require intensive supportive care, as patients are frequently dehydrated and
in need of intravenous fluids or oral rehydration with solutions containing electrolytes.
➤ No specific treatment or vaccine is yet available for Ebola haemorrhagic fever. Several
potential vaccines are being tested but it could be several years before any is available.
A new drug therapy has shown some promise in laboratory studies and is currently
being evaluated. But this too will take several years.
➤ Experimental studies using hyper-immune sera on animals have shown no protection
against the disease.
Containment
➠ Suspected cases should be isolated from other patients and strict barrier nursing
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➠
276
➠
➠
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techniques implemented.
Tracing and following up people who may have been exposed to Ebola through close
contact with patients is essential.
All hospital staff should be briefed on the nature of the disease and its transmission
routes. Particular emphasis should be placed on ensuring that invasive procedures such
as the placing of intravenous lines and the handling of blood, secretions, catheters and
suction devices are carried out under strict barrier nursing conditions. Hospital staff
should have individual gowns, gloves, masks and goggles. Non-disposable protective
equipment must not be reused unless they have been properly disinfected.
Infection may also spread through contact with the soiled clothing or bed linens from
a patient with Ebola. Disinfection is therefore required before handling these items.
Communities affected by Ebola should make efforts to ensure that the population is
well informed, both about the nature of the disease itself and about necessary
outbreak containment measures, including burial of the deceased. People who have
died from Ebola should be promptly and safely buried.
Contacts
➤ As the primary mode of person-to-person transmission is contact with contaminated
blood, secretions or body fluids, people who have had close physical contact with
patients should be kept under strict surveillance. Their body temperature should be
checked twice a day, with immediate hospitalization and strict isolation in case of
the onset of fever.
➤ Hospital staff who come into close contact with patients or contaminated materials
without barrier protection measures be considered as contacts and followed up
accordingly.
History
The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby
region of Zaïre (now the Democratic Republic of the Congo) in 1976 after significant epidemics
in Yambuku in northern Democratic Republic of the Congo, and Nzara in southern Sudan.
➣
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causing 151 deaths. In the Democratic Republic of the Congo, there were 318 cases
and 280 deaths in September and October. An isolated case occurred in the Democratic
Republic of the Congo in 1977, and there was another outbreak in Sudan in 1979 (33
cases, including 22 deaths).
In 1989, Reston, an Ebola virus subtype, was isolated in quarantined laboratory
cynomolgus monkeys (Macacca fascicularis) in Reston, Virginia, USA. From 1989 to
1996, several outbreaks caused by the Ebola Reston subtype occurred in monkeys
imported from the Philippines to the USA (Reston in Virginia, Alice in Texas and
Pennsylvania) and to Italy. Investigations traced the source of all Ebola Reston
outbreaks to one export facility near Manila in the Philippines, but the mode of
contamination of this facility was not determined. Several monkeys died, and at least
four people were infected, although none of them suffered clinical illness.
One human case of Ebola haemorrhagic fever of the Cote d’Ivoire subtype and several
cases in chimpanzees were confirmed in Côte d’Ivoire in November 1994.
A large epidemic occurred in Kikwit, the Democratic Republic of the Congo in 1995
with 315 cases, 250 of whom died.
In Gabon, Ebola haemorrhagic fever was first documented in 1994 (19 cases including
9 deaths). Successive outbreaks occurred in February (37 cases including 21 deaths) and
July of 1996 (60 cases including 45 deaths).
In October 2000, Ebola was reported in Gulu district in northern Uganda. Between
September 2000 and January 2001, the Sudan subtype of the Ebola virus infected
425 cases, including 224 deaths, making this the largest epidemic so far documented
of Ebola. This was the first reported emergence of the Sudan Ebola virus since 1979.
From October 2001 to December 2003, several Ebola outbreaks of the Zaïre subtype were
reported in Gabon and the Republic of the Congo with a total of 302 cases and 254 deaths.
About 1850 cases with over 1200 deaths have been documented since the Ebola virus was
discovered.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➣ Between June and November 1976, the Ebola virus infected 284 people in Sudan,
277
Natural reservoir
➠ The natural reservoir of the Ebola virus is unknown despite extensive studies, but it
seems to reside in the rain forests on the African continent and in the Western Pacific.
➠ Although non-human primates have been a source of infection for humans, they are
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
not thought to be the reservoir. They, like humans, are believed to be infected directly
from the natural reservoir or through a chain of transmission from the natural reservoir.
➠ On the African continent, Ebola infections of human cases have been linked to direct
contact with gorillas, chimpanzees, monkeys, forest antelope and porcupines found
dead in the rainforest. So far, the Ebola virus has been detected in the wild in carcasses
of chimpanzees (in Côte-d’Ivoire and the Republic of the Congo), gorillas (Gabon and
the Republic of the Congo) and duikers (the Republic of the Congo).
➠ Different hypotheses have been developed to explain the origin of Ebola outbreaks.
Laboratory observation has shown that bats experimentally infected with Ebola do not
die, and this has raised speculation that these mammals may play a role in maintaining
the virus in the tropical forest.
➠ Extensive ecological studies are under way in the Republic of the Congo and Gabon to
identify the Ebola’s natural reservoir.
278
Case studies-Ebola outbreaks
1. Ebola of outbreak
in the Democratic Republic of the Congo
http://www.who.int/csr/don/2009_02_17/en/index.html
17 February 2009 – The Ministry of Health of the Democratic Republic of the Congo (DRC) has
on 16 February 2009 declared the end of the Ebola epidemic in the Mweka and Luebo health
zones in the Province of Kasai Occidental . The last person to be infected by the virus died
on 1 January 2009. This is more than double the maximum incubation period (42 days) for
Ebola.
As of today, the health authorities have reported a total of 32 cases, including 15 deaths
from Ebola. These 32 cases include confirmed, probable and suspect cases. During this
outbreak, the Ebola virus was confirmed by laboratory tests at the Institut National de
Recherches Biologiques (INRB) in Kinshasa, the Centre International de Recherches Médicales
de Franceville (CIRMF) in Gabon, and the National Institute for Communicable Diseases (NICD),
South Africa.
The WHO Country Office, Regional Office and Headquarters supported the MoH in
Kinshasa and in the field at the location of the outbreak. The international response to the
outbreak also involved UNICEF, the United Nations Organization Mission in the Democratic
Republic of the Congo (MONUC), and the World Food Programme (WFP), as well as support
from Caritas (Belgium), and the Congolese (DRC) Red Cross, together with partners in the
Global Outbreak Alert and Response Network (GOARN), including the National Microbiology
Laboratory (NML) of the Public Health Agency of Canada (PHAC), CIRMF, and NICD, and
Médecins Sans Frontières (Belgium).
2. Outbreak of Ebola hemorrhagic fever, Uganda,
Aug 2000-Jan 2001
An outbreak of an unusual severe febrile illness characterized by gastroenteritis, headache,
conjunctivitis and occasional haemorrhagic signs, with significant mortality, was reported to
the Ministry of Health in Kampala on 8 October 2000, by both the medical superintendent
of St Mary’s hospital in Lacor and the acting district director of health services, Gulu district,
Uganda. A preliminary assessment of the situation by the Ministry of Health revealed
additional evidence of disease in the community as well as in Gulu hospital, the regional
referral hospital for the north-eastern region.
On 10 October, an isolation ward was put in place in Lacor hospital. The clinical suspicion
of haemorrhagic fever was confirmed on 15 October, when the National Institute of Virology,
Johannesburg (South Africa) identified Ebola virus infection among specimens from a cluster
of cases including student nurses at St Mary’s hospital. The laboratory testing included a
combination of virus antigen detection and antibody.
ELISA tests, and reverse transcriptase polymerase chain reaction (RT-PCR). The virus
associated with this outbreak is Ebola-Sudan and differed at the nucleotide sequence level
from earlier Ebola-Sudan isolates by 3.3% and 4.2% in the polymerase (362 nucleotides)
and nucleocapsid (146 nucleotides) protein encoding genes, respectively. The Ministry of
Health requested WHO to coordinate the international response of health organizations
worldwide.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
9 Feb 2001, 76th YEAR , No. 6, 2001, 76, 41-48, http://www.who.int/wer
279
Epidemic response
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Control activities were organized around surveillance and epidemiology, clinical case
management, social mobilization, coordination and logistic support. An active surveillance
system for Ebola haemorrhagic fever (EHF) was initiated to determine the extent and
magnitude of the outbreak, identify foci of disease activity, and detect cases early. The system
was designed to be very sensitive and detect all persons whose illness might be EHF. Ill persons
were encouraged to be assessed at a hospital and, if indicated, to be hospitalized to diminish
further community transmission. Targeted prevention activities included: following up
contacts for 21 days (maximum incubation period), establishment of trained burial teams
for all potential and confirmed EHF deaths, community education, cessation of traditional
healing practices and burials and of large public gatherings, and updating hospital infection
control measures. Initial laboratory testing was performed at a field laboratory established at
St Mary’s hospital, by the Centers for Disease Control and Prevention (CDC), Atlanta, United
States, and supplemented by additional testing at CDC and the National Institute of Virology
(South Africa).
280
Surveillance
A reinforced active surveillance system was established during the third week of October, with
3 case notification categories: alert, suspect, probable. The alert. category was restricted to
community use for notification to mobile teams, peripheral health units, private clinics and
pharmacies, of individuals with sudden onset of high fever, sudden death, or any haemorrhagic signs. The suspect case definition was used by the mobile teams and peripheral
health units to categorize potential cases and to determine if any patient required transport
to an isolation ward. This category included all persons with fever and contact with a potential
case of EHF, all persons with unexplained bleeding of any kind, all persons with fever and 3
or more specified symptoms (i.e. headache, vomiting, anorexia, diarrhoea, weakness or severe
fatigue, abdominal pain, body aches or joint pains, difficulty in swallowing, difficulty in
breathing and hiccoughs), and all unexplained deaths. The probable case definition was
identical to the suspect definition but with the requirement that it was described by a
physician. Where possible, verbal autopsies were conducted on unexplained community
deaths to obtain additional clinical and epidemiological information. If laboratory samples
were obtained at an appropriate time during the illness, these notification categories were
reclassified into laboratory-confirmed. cases and .not a case.. Laboratory-confirmed cases were
either positive for Ebola virus antigen or Ebola IgG antibody; not a case had no Ebola specific
detectable antibody or antigen. Individuals identified with isolated IgG antibodies without
symptoms were not included as cases.
An independent rapid reporting system which was initially established to estimate the
magnitude of the outbreak at the national level was also continued. New admissions at
hospital isolation wards, in addition to incident deaths identified in those wards and the
community, were reported every morning as clinical EHF cases. This system formed the basis
of daily press briefings and resource allocation and mobilization.
Among 62 patients with laboratory-confirmed EHF admitted to Gulu hospital between 5
October and 27 November 2000, the most commonly reported signs and symptoms on
admission included diarrhoea (66%), asthenia (64%), anorexia (61%), headache (63%), nausea
and vomiting (60%), abdominal pain (55%) and chest pain (48%). Patients presented for care
a mean of 4.2 days after the onset of symptoms. Bleeding was seen in only about 20% of
patients and primarily involved the gastrointestinal tract. A preliminary analysis of these
laboratory-confirmed cases compared with 92 laboratory-negative patients showed the
following signs and symptoms to be significantly (p<0.05) more common among Ebola cases
than in patients presenting with other illnesses: asthenia, anorexia, sore throat, right upper
quadrant abdominal tenderness, conjunctival injection or haemorrhage, fine papular rash, and
gingival bleeding.
The cumulative case-fatality rate in this hospitalized group was 58%, but was higher (80%)
in children aged < 15 years. Spontaneous abortions were noted among pregnant women
infected with Ebola virus. Fatal cases usually exhibited a rapid progression of shock, increasing
coagulopathy, and loss of consciousness.
Epidemiology
As of 23 January 2001, a total of 425 presumptive cases of Ebola haemorrhagic fever were
recorded from 3 districts in Uganda: 393 (93%) from Gulu, 27 (6%) from Masindi, and 5 (1%)
from Mbarara with a combined area of 31 000 kmÇ and an estimated current population of
1.8 million (based on the 1991 census and movement of displaced persons) (page 284). The
earliest reported presumptive case had disease onset on 30 August 2000, and the last case on
9 January 2001 (Fig. in page 284). There were 269 (63%) women and 156 (37%) men with 224
deaths (case-fatality rate = 53%). The mean age was 27 years ± 16 years; the youngest was
aged 3 days and the oldest 72 years; 20% of presumptive cases were aged < 13 years. There
were 29 infected health care workers.
The mean time from symptom onset until death was 8 ± 5 days. Laboratory confirmation
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Case description
281
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
was established for 218 (51%) of the presumptive cases. As of 23 January 2001, a total of 428
clinical EHF cases were reported to and by the Ministry of Health. However, the number of
reported deaths was 173. Although the discrepancy in deaths was expected because of the
addition of retrospective unexplained deaths in the reinforced active surveillance system and
updating of the final outcome of admissions, the concordance in the two systems of
estimating the magnitude of the outbreak in the community was remarkable. The smaller
total number can be explained by subsequent laboratory testing of admissions that excluded
Ebola infection.
Although the outbreak was reported following a cluster of cases including health care
workers, it was retrospectively recognized among sporadic cases in the hospital and
community.
The 3 most important defined means of amplification were: attendance at funerals of
presumptive EHF cases where ritual contact with the deceased was the norm; patients with
multiple familial care providers; or nosocomial transmission from other patients or staff
members. Four- teen (64%) of 22 health care workers in Gulu district were infected after
establishing the isolation wards which required subsequent reinforcement of infection control
measures. Two distant focal outbreaks were initiated by movement of infected contacts of
EHF cases from Gulu to Mbarara and Masindi districts. National notification and surveillance
efforts led to the quick identification of these foci and their effective containment.
282
Editorial note
Ebola haemorrhagic fever is a viral haemorrhagic fever associated with infection with any 3
of the 4 members of the genus Ebola virus in the family Filoviridae. The purported zoonotic
reservoir for the viruses remains unknown. However, outbreaks of EHF are most often
associated with the introduction of the virus into the community via a single infected human
followed by dissemination by human-to-human transmission, often within medical facilities.
This is the largest reported EHF outbreak, and only the third known Ebola-Sudan virusassociated outbreak. The first occurred in 1976 in southern Sudan in the towns of Nzara and
Maridi, and was concurrent with an Ebola-Zaire outbreak in Zaire. The second Ebola-Sudan
outbreak occurred in 1979 in the same locations. As in this outbreak, both the 1976 and 1979
outbreaks had a case fatality of approximately 50%. Also similar to previous Ebola outbreaks,
the current outbreak seems to have been initiated by the introduction of the virus into Gulu
municipality followed by transmission in the community and in medical care facilities.
However, the early cases of this outbreak remain obscure, which has limited the ability
to track back to the initial case to allow any further investigation of the possible reservoir
of the virus.
Transmission in the community was eliminated by recognition of the outbreak and
The international outbreak response team, working with the Ministry of Health of
Uganda under the leadership of WHO, was made up of partners in the Global Alert
and Response Network. The international team included: International Committee of
the Red Cross, International Federation of Red Cross and Red Crescent Societies,
International Rescue Committee, Médecins sans frontières (Holland and Belgium); and
teams from the following countries: Belgium (Institute for Tropical Medicine, Antwerp);
Canada (Health Canada); France (Epicentre, Paris); Germany (Tropical Medicine
Institute, Hamburg); Italy (Istituto superiore di sanità, Italian Cooperation); Japan
(Nagoya City University Medical School, National Institute of Infectious Diseases,
Ministry of Health, Labour and Welfare, Institute of Medical Science, Tokyo); South
Africa (National Institute of Virology, Johannesburg); Uganda (Red Cross); United
Kingdom (National Health Service and Public Health Laboratory Services); United States
(Centers for Disease Control and Prevention, Atlanta). The Global Outbreak Alert and
Response Network is a technical partnership of national and international institutions
and networks that mobilize and pool resources to detect, verify and respond effectively
and efficiently to outbreaks of potential international importance.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
initiation of case finding and hospitalization of identified cases in medical care facilities where
barrier nursing was implemented. Education of the community about the dangers of close
contact with symptomatic and deceased EHF cases and awareness of the disease among
medical staff were all employed to diminish further transmission. Despite the inauguration of
barrier nursing practices in special isolation wards, transmission to medical care providers
occurred during this outbreak.
However, the use of isolation facilities to diminish community transmission of the virus
and reduce the overall burden of EHF in the community remains the single most effective
means of controlling outbreaks of EHF. National efforts limited the scope of this outbreak .
during the course of the outbreak approximately 5 600 contacts were under surveillance for
21-day periods in Gulu district by over 150 trained volunteers. Efforts have been initiated to
better understand this outbreak, identify specific risk factors for disease acquisition in the
community and hospital, determine antibody prevalence in selected groups, and examine
virological and clinical parameters of infection to refine future prevention activities. Efforts
are also under way to include and increase the frequency of reporting of additional diseases
of epidemic potential such as EHF into the national integrated disease surveillance system.
283
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Cases of Ebola Haemorrhagic fever meeting criteria, Uganda
284
Sites of outbreak of Ebola haemorrhagic fever, Uganda, Aug 2000-Jan 2001
Leprosy
Cause
➤ Leprosy is a chronic disease caused by a bacillus, Mycobacterium leprae;
➤ M. leprae multiplies very slowly and the incubation period of the disease is about five
years. Symptoms can take as long as 20 years to appear;
➤ Leprosy is not highly infectious. It is transmitted via droplets, from the nose and mouth,
during close and frequent contacts with untreated cases.
Symptoms
and eyes.
History
➤ Leprosy was recognized in the ancient civilizations of China, Egypt and India;
➤ The first known written mention of leprosy is dated 600 BC;
➤ Throughout history, the afflicted have often been ostracized by their communities and
families.
Treatment today
➠ Leprosy is a curable disease and treatment provided in the early stages averts disability;
➠ With minimal training, leprosy can be easily diagnosed on clinical signs alone;
➠ A World Health Organization (WHO) Study Group recommended multidrug therapy
(MDT) in 1981. MDT consists of three drugs: dapsone, rifampicin and clofazimine. This
drug combination kills the pathogen and cures the patient;
➠ MDT is safe, effective and easily administered under field conditions. MDT is available
in convenient monthly calendar blister packs to all patients;
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➠ Leprosy mainly affects the skin and nerves;
➠ If untreated, there can be progressive and permanent damage to the skin, nerves, limbs
285
➠ Since 1995, WHO provides free MDT for all patients in the world, initially through
the drug fund provided by the Nippon Foundation and since 2000, through the MDT
donation provided by Novartis and the Novartis Foundation for Sustainable
Development.
High effectiveness of multidrug therapy
➤ PB patients treated with MDT are cured within six months;
➤ MB patients treated with MDT are cured within 12 months;
➤ Patients are no longer infectious to others after the first dose of MDT. In other words,
transmission of leprosy is interrupted;
➤ There are virtually no relapses, i.e. recurrences of the disease after treatment is
completed;
➤ No resistance of the bacillus to MDT has been detected;
➤ WHO estimates that early detection and treatment with MDT has prevented about
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
four million people from being disabled. This suggests great cost-effectiveness of MDT
as a health intervention, considering the economic and social loss averted.
286
History of treatment
➠ The first breakthrough occurred in the 1940s with the development of the drug
dapsone, which arrested the disease. But the duration of the treatment of leprosy was
many years, even a lifetime, making it difficult for patients to follow;
➠ In the 1960s, M. leprae started to develop resistance to dapsone, the world’s only
known anti-leprosy drug at that time;
➠ Rifampicin and clofazimine, the other two components of MDT, were discovered in the
early 1960s.
The elimination of leprosy as a public health problem
➤ In 1991 World Health Assembly passed a resolution to eliminate leprosy as a public
health problem by the year 2000. Elimination of leprosy as a public health problem is
defined as a prevalence rate of less than one case per 10 000 persons; The target was
achieved on time.
➤ The widespread use of MDT has reduced the disease burden dramatically;
➤ Over the past 20 years, more than 14 million leprosy patients have been cured about
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4 million since 2000.
The prevalence rate of the disease has dropped by 90% – from 21.1 per 10 000
inhabitants to less than 1 per 10,000 inhabitants in 2000.
A dramatic decrease in the global disease burden: from 5.2 million in 1985 to 805 000
in 1995 to 753 000 at the end of 1999 to 286 000 cases at the end of 2004.
Leprosy has been eliminated from 113 countries out of 122 countries where leprosy
was considered as a public health problem in 1985. An additional 13 countries achieved
the elimination target since 2000.
A 20% annual decrease in new cases detected globally since 2001.
Absence of resistance to drugs used in MDT.
Efforts currently focus on eliminating leprosy at a national level in the remaining
endemic countries and at a sub-national level from the others.
Figures on the current leprosy situation
to a peak of 804 000 in 1998. At the beginning of 2005, 290 000 cases were
undergoing treatment;
➠ In 9 countries in Africa, Asia and Latin America leprosy is still considered a public health
problem; These countries account for about 75% of the global disease burden.
➠ According to the latest available information, intensive efforts are still needed to reach
the leprosy elimination target in five countries: Brazil, India, Madagascar, Mozambique,
and Nepal.
Actions and resources required
➤ Political commitment needs to be sustained in countries where leprosy remains a public
health problem;
➤ In order to reach all patients, treatment of leprosy needs to be fully integrated into
general health services. This is a key to successful elimination of the disease;
➤ Partners in leprosy elimination need to continue to ensure that human and financial
resources are made available for the elimination of leprosy;
➤ The age-old stigma associated with the disease remains an obstacle to self-reporting
and early treatment. The image of leprosy has to be changed at the global, national
and local levels. A new environment, in which patients will not hesitate to come
forward for diagnosis and treatment at any health facility, must be created.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
➠ Approximately 410 000 new cases of leprosy were detected during 2004 compared
287
The strategy for leprosy elimination
The following actions are part of the ongoing leprosy elimination campaign:
➠ Ensuring accessible and uninterrupted MDT services available to all patients through
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
flexible and patient-friendly drug delivery systems;
➠ Ensuring the sustainability of MDT services by integrating leprosy services into the
general health services and building the ability of general health workers to treat
leprosy;
➠ Encouraging self-reporting and early treatment by promoting community awareness
and changing the image of leprosy;
➠ Monitoring the performance of MDT services, the quality of patients’ care and the
progress being made towards elimination through national disease surveillance
systems.
288
Onchocerciasis (river blindness)
Definition
Onchocerciasis is an insect-borne disease caused by a parasite Onchocerca volvulus and
transmitted by blackflies of the species Simulium damnosum. Onchocerciasis is often called
“river blindness” because the blackfly which transmits the disease abounds in fertile riverside
areas, that frequently remain uninhabited for fear of infection. O. volvulus is almost exclusively
a parasite of man. Adult worms live in nodules in a human body where the female worms
produce high numbers of first-stage larvae known as microfilariae. They migrate from the
nodules to the sub-epidermal layer of the skin where they can be ingested by blackflies. They
further develop in the body of the insect from which more people can be infected. Eye lesions
in humans are caused by microfilariae. They can be found in all internal tissues of the eye —
except the lens — where they cause eye inflammation, bleeding, and other complications that
ultimately lead to blindness.
Magnitude
Onchocerciasis is a major cause of blindness in many African countries. As a public health
problem, the disease is most closely associated with West and Central Africa, but it is also
prevalent in Yemen and six countries in Latin America. Onchocerciasis has in the past greatly
reduced the economic productivity in infected areas and left vast tracts of arable land
abandoned. It is estimated that there are about half a million blind people due to river
blindness.
Prevention and treatment
References
ñ WHO, Health Topics site, http://www.who.int/
ñ E. Giamarellou et al. Infections and Antimicrobial Therapy. 3rd Volume. Litsas 2005
ñ Up-to-date, 16.3
ñ Salvaggio MR, Baddley JW. Other viral bioweapons: Ebola and Marburg hemorrhagic fever, Dermatol
Clin 2004; 22:291-302
ñ Solomon T. Flavivirus encephalitis. N Engl J Med 2004; 351:370-8
ñ Current diagnosis and treatment of infectious diseases. McGrawHill, 2001
ñ WHO. Emergency preparedness and response. Rapid health assessment in outbreaks of viral
haemorrhagic fever, including yellow fever. Geneva: WHO, 1990. ERO/EPR/90.1.4.
ñ CDC, WHO, Zairian Ministry of Health. Barrier nursing handbook. Strategies for managing patients
with VHF. CDC, 1995.
ñ Cook, G. Manson’s tropical diseases. Expert consult. 22nd edition. London: WB Saunders, 2008
ñ WHO. Viral hemorrhagic fever. Management of suspected cases. Wkly Epidemiol Ec, 1995, 70(35):
249-52.
VIRAL HEMORRHAGIC FEVERS (VHF), ONCHOCERCIASIS AND LEPROSY
Much progress has been made in fighting the disease in several countries through control
of the blackfly, however, the disease can now also be treated with an annual dose of the drug
ivermectine, Mectizan®, which also relieves the severe skin itching caused by the disease.
289
chapter 7
Malaria care, health
policy and research
General Objective
To introduce participants to malaria care along with issues of health policy and research
initiatives
Specific Objectives
➠ Epidemiology and global burden of malaria
➠ Clinical management of malaria
➠ Health policy issues and research initiatives
Content
➠ Epidemiology and global burden of malaria disease
➠ Medical Management of malaria
Uncomplicated malaria
Complicated malaria
Malaria and pregnancy and other aspects of treatment
➠ Research initiatives for malaria control, malaria elimination and research
MALARIA CARE, HEALTH POLICY AND RESEARCH
At the end of the session, participants will be familiar with:
291
Introduction
Each year more than 300 million malaria cases occur worldwide. More than one million deaths
from malaria occur each year-90% of them in Africa south of the Sahara. Around 30% of
Africa’s malaria deaths are in countries experiencing acute, chronic or post-conflict complex
emergency situations. Since the 90’s the AIDS pandemic, breakdown of vector control
measures and inefficient drugs due to widespread plasmodium resistance have contributed
to a huge rise in the impact malaria has to health and survival of the most affected
populations. Since 2004 new effective combination drugs called ACT (Artemisin-derived
Combination Therapy), have been available. However access to these new drugs is not yet
universal.
Participants will be presented with biology, epidemiology, clinical spectrum of disease,
diagnosis and management of malaria. Resistance issues, barrier measures and public health
interventions will be addressed. Finally current directions of research in clinical management,
prevention and vector control will be presented.
Methodology
MALARIA CARE, HEALTH POLICY AND RESEARCH
➠ PPt Presentations
➠ Lecture/discussion format
292
Artemisinin-based combination therapy (ACT). A combination of artemisinin or one if its
derivatives with an antimalarial or antimalarials of a different class.
Asexual cycle. The life-cycle of the malaria parasite in host red blood cells (intraerythrocytic
development) from merozoite invasion to schizont rupture (merozoite stage, trophozoite,
schizont, merozoites). Duration approximately 48 h in Plasmodium falciparum, P. ovale and
P. vivax; 72 h in P. malariae.
Asexual parasitaemia. The presence in host red blood cells of asexual parasites. The level
of asexual parasitaemia can be expressed in several different ways: the percentage of
infected red blood cells, the number of infected cells per unit volume of blood, the number
of parasites seen in one microscopic field in a high-power examination of a thick blood
film, or the number of parasites seen per 200–1000 white blood cells in a high-power
examination of a thick blood film.
Cerebral malaria. Severe falciparum malaria with coma (Glasgow coma scale <11, Blantyre
coma scale <3). Malaria with coma persisting for >30 min after a seizure is considered to
be cerebral malaria.
Combination treatment (CT). A combination of two or more different classes of antimalarial
medicines with unrelated mechanisms of action.
Cure.Elimination of the symptoms and asexual blood stages of the malaria parasite that
caused the patient or carer to seek treatment.
Drug resistance. Reduced susceptibility of the causal agent to a drug. WHO define resistance
to antimalarials as the ability of a parasite strain to survive and/or multiply despite the
administration and absorption of a medicine given in doses equal to –or higher than–
those usually recommended but within the tolerance of the subject, with the caveat that
the form of the drug active against the parasite must be able to gain access to the parasite
or the infected red blood cell for the duration of the time necessary for its normal action.
Resistance to antimalarials arises because of the selection of parasites with genetic
mutations or gene amplifications that confer reduced susceptibility.
Gametocytes. Sexual stages of malaria parasites present in the host red blood cells, which are
infective to the anopheline mosquito.
Hypnozoites. Persistent liver stages of P. vivax and P. ovale malaria that remain dormant in
host hepatocytes for a fixed interval (3–45 weeks) before maturing to hepatic schizonts.
These then burst and release merozoites, which infect red blood cells. Hypnozoites are the
source of relapses.
Malaria pigment (haemozoin). A dark brown granular pigment formed by malaria parasites
as a by-product of haemoglobin catabolism. The pigment is evident in mature trophozoites
and schizonts.
Merozoites. Parasites released into the host bloodstream when a hepatic or erythrocytic
schizont bursts. These then invade the red blood cells.
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Glossary
293
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294
Monotherapy. Antimalarial treatment with a single medicine (either a single active compound
or a synergistic combination of two compounds with related mechanism of action).
Plasmodium. A genus of protozoan vertebrate blood parasites that includes the causal agents
of malaria. Plasmodium falciparum, P. malariae, P. ovale and P. vivax cause malaria in humans.
Pre-erythrocytic development. The life-cycle of the malaria parasite when it first enters the
host. Following inoculation into a human by the female anopheline mosquito, sporozoites
invade parenchyma cells in the host liver and multiply within the hepatocytes for 5–12
days, forming hepatic schizonts. These then burst liberating merozoites into the
bloodstream, which subsequently invade red blood cells.
Radical cure. In P. vivax and P. ovale infections only, this comprises cure as defined above plus
prevention of relapses.
Rapid diagnostic test (RDT). An antigen-based stick, cassette or card test for malaria in which
a coloured line indicates that plasmodial antigens have been detected.
Recrudescence. The recurrence of asexual parasitaemia after treatment of the infection with
the same infection that caused the original illness (in endemic areas now defined by
molecular genotyping). This results from incomplete clearance of parasitaemia by
treatment and is therefore different to a relapse in P. vivax and P. ovale infections.
Recurrence. The recurrence of asexual parasitaemia following treatment. This can be caused
by a recrudescence, a relapse (in P. vivax and P. ovale infections only) or a new infection.
Relapse. The recurrence of asexual parasitaemia in P. vivax and P. ovale malaria deriving from
persisting liver stages. Relapse occurs when the blood stage infection has been eliminated
but hypnozoites persist in the liver and mature to form hepatic schizonts. After a variable
interval of weeks (tropical strains) or months (temperate strains) the hepatic schizonts
burst and liberate merozoites into the bloodstream.
Ring stage. Young usually ring-shaped intra-erythrocytic malaria parasites, before malaria
pigment is evident under microscopy.
Schizonts. Mature malaria parasites in host liver cells (hepatic schizonts) or red blood cells
(erythrocytic schizonts) that are undergoing nuclear division. This process is called
schizogony.
Selection pressure. Resistance to antimalarials emerges and spreads because of the selective
survival advantage that resistant parasites have in the presence of antimalarials that they
are resistant to. Selection pressure describes the intensity and magnitude of the selection
process; the greater the proportion of parasites in a given parasite population exposed to
concentrations of an antimalarial that allow proliferation of resistant, but not sensitive
parasites, the greater is the selection pressure.
Severe anaemia. Haemoglobin concentration of <5 g/100 ml.
Severe falciparum malaria. Acute falciparum malaria with signs of severity and/or evidence
of vital organ dysfunction.
Sporozoites. Motile malaria parasites that are infective to humans, inoculated by a feeding
female anopheline mosquito. The sporozoites invade hepatocytes.
Transmission intensity. The intensity of malaria transmission measured by the frequency with
which people living in an area are bitten by anopheline mosquitoes carrying sporozoites.
This is often expressed as the annual entomological inoculation rate (EIR), which is the
number of inoculations of malaria parasites received by one person in one year.
Trophozoites. Stage of development of the malaria parasites within host red blood cells from
the ring stage and before nuclear division. Mature trophozoites contain visible malaria
pigment.
Uncomplicated malaria. Symptomatic infection with malaria parasitaemia without signs of
severity and/or evidence of vital organ dysfunction.
ACT artemisinin-based combination therapy
AL artemether-lumefantrine combination
AQ amodiaquine
AS artesunate
AS+AQ artesunate + amodiaquine combination
AS+MQ artesunate + mefloquine combination
AS+SP artesunate + sulfadoxine-pyrimethamine combination
CI confidence interval
CQ chloroquine
EIR entomological inoculation rate
HIV/AIDS human immunodeficiency virus/
acquired immunodeficiency syndrome
HRP2 histidine-rich protein 2
IC50 concentration providing 50% inhibition
MIC minimum inhibitory concentration
MQ mefloquine
OR odds ratio
PCR polymerase chain reaction
pLDH parasite-lactate dehydrogenase
RCT randomized controlled trial
RDT rapid diagnostic test
RR relative risk
SP sulfadoxine–pyrimethamine
WHO World Health Organization
WMD weighted mean difference
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Abbreviations
295
MALARIA: “The rapidly spreading disease is
affecting more people than ever before, but
until recently the outcry has been muted”
By Michael Finkel, July 2007
National Geographic Magazine
A story on malaria through Zambia’s plight
MALARIA CARE, HEALTH POLICY AND RESEARCH
http://www.ngm.nationalgeographic.com/2007/07/malaria/finkel/text
296
Executive summary notes
Some figures
Malaria is endemic in more than 106 countries, accounting for 400-500 million cases yearly,
affecting 50% of the world’s population
➠ >1 million deaths, especially among pregnant women, <5yrs and PLWHA
➠ 20% of deaths in <5 in sub-saharan Africa, 1.6-5.4 episodes per child/year or 1 dead
child every 30 sec
➠
➠
➠
➠
1.3% of GNP lost per year in highly endemic regions
Twice the annual death rate compared with a generation ago
125.000.000 travelers visit malaria endemic zones
10.000 cases yearly among returning travelers, whereas the true figure is estimated
around 30.000 casecases
➠ 10%-12% of the population in Greece is by now immigrants/refugees, ~20% of them
from endemic countries
➠ Greece is among the regions at risk due to the expansion of the malaria zone caused
by climate change
Rising prevalence figures and expansion of the malaria zone
➠
➠
➠
➠
➠
➠
Increasing resistance to anti-malarials
Increasing resistance of mosquitoes to pesticides
Ecologic, social, financial and urbanization processes
The AIDS pandemic
1969 ban on DDT-20million children lost due to just this intitiative
Increasing travel and migration wave from the tropics
Risk of malaria by duration of stay
➤ Oceania > 1/30
➤ Sub-Saharan Africa 1/50
➤ Indian peninsula 1/250
➤ SA Asia 1/1.000
➤ S. America 1/2.500
➤ C. America 1/10.000
Fever in traveler or immigrant pt
Fever within 3 months in the returning traveler is a MEDICAL EMERGENCY due to the high
morbidity and mortality in the non-immune adult in P. falciparum malaria (parasitemia>
2-5%), that with the exception of a small number of countries cannot easily by ruled out.
➤ If in the smallest doubt, treat as if resistant P. falciparum malaria
➤ P. vivax and P. ovale cause more mild disease
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➤ Risk calculated for 1 month of stay in endemic area with no chemoprophylaxis taken
297
➤ (<parasitemia <1%)
➤ Infection by P. malariae is rare causing more mild disease with a long duration up to
40 years if left untreated
Transmission
➠ Female Anopheles mosquito, biting mainly at dask and dawn, higher prevalence during
➠
➠
➠
➠
➠
➠
➠
the rainy season in the zones of steady endemicity (prevalence of parasitemia>50%
during the year, accounting for up to 50-100 bites per person per month)
Transmission decreases at altitudes above 2,000 metres
“Airport malaria” and “Autochthonous malaria”
Bloodborne (sharps, transfusions etc), Vertical trasmission, A and B thalassemia
Sickle cell anaemia
Ovalocytosis
Duffy factor mainly in W. Africa
“Semi immunity” after the age of five in areas of steady endemicity
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P. Falciparum and sporozoite in the gut of female anopheles mosquito
298
Sourse: WHO
The parasite cycle
Clinical presentation-uncomplicated malaria
➠ Fever,fatigue, myalgias, headache,chills, sweating, anorexia, vomiting, nausea, diarrhea,
Clinical characteristics
➤ Incubation period 7-35 days (mean 12-14d), but up to 12 months if ‘’semi-immune’’ or
on chemoprophylaxis
➤ Erythrocyte cycle is the symptomatic phase lasting 48hrs (fever) for all species except for
P.malariae that lasts 72 lasts hrs
➤ P. vivax and P. ovale produce hypnozoites in the liver and if not treated with primaquine
(mind G-6PD deficiency) may cause recrudence
➤ P. falciparum infects erythrocytes of all stages inflicting greater parasitemia and thus more
severe infection
MALARIA CARE, HEALTH POLICY AND RESEARCH
abdominal cramps, lower back pain, cough, gastroenteritis presentation
➠ Irregular fever – may become periodic after 15 days in 30% of cases
299
Laboratory findings
➠
➠
➠
➠
➠
➠
➠
➠
➠
Anaemia (normocytic)
Leucocytosis in severe disease
Increased CRP
Mild thrombocytopenia
Intravascular hemolysis
PT prolongation, DIC (Diffuse intravascular coangulation)
Hyperglobulinemia
Abnormal LFTs, RFTs (Liver and Renal functions tests)
Hypoglycemia (children, adults under tx)
Pathogenesis of clinical presentation and complications
➤ Defragmentation of erythrocyte proteins
➤ Glucose consumption with anaerobic glycolysis causing hypoglycemia and lactic acidosis
➤ Hemolysis, spleen sequestration, splenomegaly
➤ P. falciparum induces Knots production on erythrocyte cell membrane causing tissue
ischaemia/hypoxia
➤ Induction of TNF-a production that supresses haemopoeisis
➤ Intense immune stimulation= Tropical splenomegaly, neuropathy by immunocomplexes (P.
MALARIA CARE, HEALTH POLICY AND RESEARCH
malariae) features as a common cause of Chronic Renal Failure
300
Increased vulnerability
➠
➠
➠
➠
➠
➠
Non-immunity
<5 yrs and pregnancy
PLWHIA
Malnutrition
Splenectomy
Immunity gets lost when in non-endemic countries anytime between 6 months and five yrs
Complicated malaria, P. falciparum
➤ Celebral malaria
➤ GI complications
➤ Acute hepatic failure
➤ Septic shock
➤ Acute Pulmonary oedema / ARDS
➤ Renal failure
➤ Hypoglycemia and lactic acidosis
➤ Haematologic complications
➤ Spleen rupture and infracts
Differential diagnosis
➠
➠
➠
➠
➠
➠
➠
➠
➠
➠
Influenza
Gastroenteritis
Enteric fever (typhoid)
Viral hepatitis
Dengue
Visceral leishmaniasis (kala-azar)
Amoebic liver abscess
Babesiosis
Leptospirosis
Any other febrile ilness
➤ Blood Cultures
➤ Thick and Thin Blood Slide
➤ Myelogram and peripheral blood smear
➤ FAs (Serology)
➤ PCR
➤ RTDs (Plasmodium Ags detected by monoclonal Abs)
Diagnosis and monitoring of treatment
Golden standard:
Direct microscopy and recently PCR, however only microscopy offers ability for monitoring
and f/up of treatment and paracitaemia
➤ At least 3 blood smears quasi 6-12 hrs before excluding infection
➤ >95% positive from 1st sample
MALARIA CARE, HEALTH POLICY AND RESEARCH
Diagnosis
301
➤ If smear positive and/or neurologic signs, but high suspicion, then treat as if malaria but
be alert for alternative diagnosis
➤ P. falciparum induces >2-5% of parasitemia in immune adults, other species <1%
➤ Adult from endemic area needs to have >2% of parasitemia to be considered clinical
infection (P. falciparum)
Celebral malaria
➠
➠
➠
➠
Mortality 20%
Neurologic sequelae 1-10% (mostly children)
Headache, coma, neurologic focal signs, seizures, meningoencephalitis, retinal bleeding
Be alert on: DDx from hypoglycemia due to parasite use of cell glucose or quinine tx
(mostly children)
➠ Corticosteroids have no place in treatment
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Malaria transmission area and reported P. falciparum resistance, 2004
302
Areas where malaria transmission occurs (high / low)
P. falciparum chloroquine resistance
P. falciparum sulfadoxine pyrimethamine resistance
P. falciparum mefloquine treatment failures
Malaria-free areas
Malaria transimission areas and the distribution of reported resistance or treatment failures with selected
antimalarial drugs, September 2004 (mefloquine resistance in Africa is currently being further reviewed)
Sourse: WHO
Principles of treatment
➠ Based on knowledge of epidemiology and resistance patterns reported at local level
➠ If in doubt, treat as if resistant P. falciparum
➠ Non-immune pts need daily monitoring of parasitemia by quantification
➠ Double tx to prevent failure, relapse and development of resistance
➠ Chemoprophylaxis and IPT (Interminent preventive treatment, eg Fansidar for pregnant
women) regimens cannot be used for treatment
➠ Should parasitemia not reduce by 25% within 48 hrs or disappear within 7 days= suspect
resistance to tx regimen, select specimen for PCR analysis and report to nearest WHO
supervised authority according to National Protocol not your medical textbooks!!!!
Note:
1: expected to reduce normally by 75% in most cases within 48 hrs
2: not your medical textbooks!
Treatment for uncomplicated malaria, ACTs
➤ Artemether 20mg + lumefantrine 120mg (Co-artem) 3d/ 4tls 0,8,24,36,48,60 hrs (not for
pregnant or <5)
➤ Artesunate 4mg/kg + amodiaquine 10mg/kg D1-3 OD
➤ Artesunate 4mg/kg + mefloquine 15-10-0 mg/kg D1-3 OD
➤ Artesunate 4mg/kg + SP 25mg/kg D1-3/OD-SD
➠ Quinine 600mgX3 + doxycycline 100mgx2/ clind
➠ Atovaquone 250mg/ proguanil100mg 4tbls X 1 3d
➠ Mefloquine 750 mg (3tbls X1) at O hrs 500mg (2tblsX1) at 12hrs
Complicated malaria, pregnancy, <5
➤ Quinine IV 10mg/kg ÛÂ 1hr, 24mg/kg ÛÂ 4hrs (0,02mg/kg/min), 2mg/kg within 4hrs, q8hrs
in continuous infusion until parasitemia<1% or patient able to feed
➤ If not available administer quinidine under cardiac monitoring (~25% QT-prolongation)
➤ Artemether im 3.2 mg/kg IM D1, 1.6mg/kg, better tolerated, however greatest risk of
relapses
➤ artesunate 2.4 mg/kg bw i.v. or i.m. given on admission (time = 0), then at 12 h and 24
h, then once a day
Recently a number of studies have proved artesunate superior to artemether in complicated
malaria.
MALARIA CARE, HEALTH POLICY AND RESEARCH
If ACTs not available (countries in EE or USA)
303
Chemoprophylaxis and mechanical preventive
measures for travellers
➠ Chloroquine 300mg PO wk (very few areas in the world)
➠ Mefloquine 250mg PO wk, Doxycycline 100mg PO daily
➠ Atovaquone-Proguanil 250mg/100mg PO daily (SA Asia), 1 day before, one day after (for
➠
➠
➠
➠
➠
short stay in endemic areas)
Mefloquine 2-4wks before departure, 4wks after return (for expats)
Does not confer total protection, protects from celebral malaria attacks
DEET 40-50% q8hrs on the skin
ITN (Insecticide treated bednets), Residual Spraying of buildings
Covering of exposed body parts at dask and dawn
Mefloquine Side effects and tolerance
➤ No alchocol intake
➤ Not advised on individuals with psychiatric past history
➤ Tolerated well after 2-4 wks
➤ CNS complications: depression, suicidal tendency, psychosis, paranoia, abnormal dreaming,
confusion
MALARIA CARE, HEALTH POLICY AND RESEARCH
Malaria and HIV/AIDS
304
➠ Malaria induces temporally increased Viral Loads, decreased immunity, increased risk of
MTCT (Mother-to-child transmission of HIV)
➠ Huge effect on epidemiological transmissibility of both diseases
➠ Clinical course of malaria and long term prognosis of HIV/AIDS disease progression does
not seem to be affected but not sufficient data exist
➠ Measures to reduce malaria episodes among seropositive and pregnant women are
considered golden standard approach (provision of free ITN bednets, active screening for
malaria, IPT (Interminent preventive treatment) of pregnant women through MCH
(Mother and Child Health) services
ACCESS AND AVAILABILITY ISSUES
1.000.000 cases of malaria episodes
ñ Coverage with use of ITN bednets remains low in most of Sub-saharan Africa
ñ Malaria vaccine research if successful could assist reverse the epidemic along with renewed
interest in vector control research targeting different areas of intervention (viral
paratrangenesis, insecticides etc)
New initiatives aim to combine several approaches
to developing effective malaria vaccines
MVI (Malaria vaccine initiative) is working with a range of partners to develop and study
combinations of pre-erythrocytic and blood-stage antigens, to introduce new immunopotentiators and vaccine technologies, and to develop needed assays and models.
MALARIA CARE, HEALTH POLICY AND RESEARCH
ñ As of today only 80 million ACT treatments per year are available out of a total of 400
305
New initiatives answer R&D questions
ADJUVANTS/FORMULATIONS
ñ Infectious Disease Research Institute (IDRI)
MALARIA CARE, HEALTH POLICY AND RESEARCH
ANTIGENS
306
ñ Seattle Biomedical Research Institute (SBRI)
ñ Walter and Eliza Hall Institute of Medical Research (WEHI)
EVALUATION TECHNOLOGIES
ñ Center for Biologics Evaluation and Research (CBER), US Food and Drug Administration (FDA)
ñ Seattle Biomedical Research Institute (SBRI)
http://www.malariavaccine.org
Malaria remains one of the main global health problems of our time, causing more than 1
million deaths per year, with about 90% of deaths and 60% of cases occurring in Africa south
of the Sahara. It is caused by the protozoan parasite Plasmodium and transmitted by
Anopheles mosquitoes, which bite mainly between sunset and sunrise.
There are four species of malaria parasites that infect people – P. falciparum, P. vivax, P.
malariae and P. ovale. Of these, P. falciparum and P. vivax are the most common. Falciparum
malaria can be fatal. Severe falciparum malaria has a case-fatality rate of around 10% in
reasonably well-equipped hospitals.
Vivax malaria is an acute but not life-threatening illness and is associated with anaemia
and splenomegaly. Like P. falciparum, it causes low birth weight in neonates. Unlike P.
falciparum, P. vivax and P. ovale can stay dormant in the liver as hypnozoites for up to several
months or even years after inoculation by the mosquito. Forms of malaria caused by P.
malariae and P. ovale are less severe and rarely life-threatening; the former can lead to chronic
immunopathological sequelae.
The four human malaria species are not evenly spread across the malaria affected areas of
the world, and their relative importance varies between and within different areas, by
zoogeographical region. P. falciparum is the most common species and predominates across
Africa south of the Sahara. P. vivax predominates in the subtropics and coexists with P.
falciparum in tropical Asia, the tropical Americas and the Horn of Africa. P. ovale is found in
Africa and sporadically in South-East Asia and the western Pacifi c. P. malariae has a similar
geographical distribution to P. falciparum but its incidence is patchy.
Unlike the other malaria parasites, blood infection with P. malariae can continue
undetected for decades. The risk of contracting malaria is highly variable from country to
country and even between areas in a country.
The female Anopheles mosquito is the vector of malaria parasites. There are more than
400 different species of Anopheles mosquitoes throughout the world, but only some 60 of
these are vectors of malaria under natural conditions, of which 30 are vectors of major
importance. Each species has a different behaviour pattern. Most areas have multiple species
of Anopheles, and different ones occur in different parts of the world. Highly effi cient species
such as A. gambiae, A. arabiensis and A. funestus predominate in Africa south of the Sahara.
Less efficient vectors such as A. stephensi in urban settings, and A. minimus and A. dirus in
hilly or mountainous zones predominate in Asian countries.
The transmission cycle of malaria is represented in the figure that follows. After a human
1. Adapted from: Malaria elimination: a field manula for loe and moderate endemic countries, WHO, 2007.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Epidemiology and biology of malaria1
307
308
Adapted, by perimission of the publishers,
from Life cycle of Plasmodium spp. (4) and Sullivan (5)
MALARIA CARE, HEALTH POLICY AND RESEARCH
is infected, the parasites pass through the human liver phase and blood cycle onto the next
phase, in the mosquito.
P. falciparum takes 8-11 days to complete the mosquito phase (sporogony) at an optimal
ambient temperature of 28 ÆC and 22 days at 20 ÆC. The temperature of the mosquito gut
equals the ambient temperature: a low environmental temperature therefore results in a
longer development time for the parasite in the mosquito. Below 20 ÆC, P. falciparum is unable
to develop. Thus, in mountainous areas of East Africa above 2000 metres, there is little malaria
transmission because it is too cold. P. vivax can develop in the mosquito at lower ambient
temperatures, so P. vivax transmission is found in some areas where the average temperature
is too low to allow P. falciparum transmission (for example, in the Russian Federation). The
human liver phase and blood cycle combined take P. falciparum 15.5–17 days.
In total, the incubation interval of P. falciparum is 23.5–39 days depending on ambient
temperatures. The same interval takes P. vivax about 20 days, making the control of P. vivax
more complex than that of P. falciparum. The liver-stage hypnozoites of P. vivax are
responsible for late relapses, which are strain-dependent.
A total of 107 countries and areas were considered to have malarious zones. Of these,
15 have never had or no longer have local P. falciparum transmission. Seven countries reported
no indigenous cases; two of these countries have reported no such cases since 1998. The
United Arab Emirates finalized the requirements for certification of malaria elimination in
2006. In January 2007, it was the first formerly endemic country to be certified by WHO as
malaria-free since Australia and Singapore in the 1980s.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Intensity of malaria transmission, WHO, 2007
309
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Global burden of disease and
background information2
310
Malaria is an important cause of death and illness in children and adults in tropical countries.
Mortality, currently estimated at over a million people per year, has risen in recent years,
probably due to increasing resistance to antimalarial medicines. Malaria control requires an
integrated approach comprising prevention including vector control and treatment with
effective antimalarials. The affordable and widely available antimalarial chloroquine that was
in the past a mainstay of malaria control is now ineffective in most falciparum malaria endemic
areas, and resistance to sulfadoxine–pyrimethamine is increasing rapidly. The discovery and
development of the artemisinin derivatives in China, and their evaluation in South-East Asia
and other regions, have provided a new class of highly effective antimalarials, and have
already transformed the chemotherapy of malaria in South-East Asia. Artemisinin-based
combination therapies (ACTs) are now generally considered as the best current treatment
for uncomplicated falciparum malaria.
These treatment guidelines recommend antimalarials for which there is adequate evidence
of efficacy and safety now, and which are unlikely to be affected by resistance in the near
future. Much of the world’s symptomatic malaria is treated in peripheral health centres or
remote villages, where facilities are limited. The aim is therefore to provide simple and
straightforward treatment recommendations based on sound evidence that can be applied
effectively in most settings.
These guidelines are based on a review of current evidence and are developed in
accordance with WHO’s standard methodology. Clinical evidence has been assessed in an
objective way using standard methods. The number of antimalarial drug trials published has
doubled in the past seven years, so these guidelines have a firmer evidence base than previous
treatment recommendations.
Inevitably, information gaps remain, however, and so the guidelines will remain under
regular review and will be updated as new evidence becomes available. There are also
difficulties when comparing results from different areas, as levels of drug resistance and
background immunity vary. Where transmission levels and, consequently, immunity are high,
the malaria symptoms are selflimiting in many patients, in particular in adults, so that drugs
that are only partially effective may appear still to work well in many cases, misleading
patients and doctors alike. But in the same location, the young child who lacks immunity to
illness caused by P. falciparum may die if ineffective drugs are given.
The treatment recommendations given in these guidelines aim for effective treatment for
2. Adapted from: Guidelines for the treatment of malaria, WHO, 2006
the most vulnerable and therefore take all the relevant factors into account. These factors
include laboratory measures, such as tests for in vitro antimalarial susceptibility and validated
molecular markers of resistance, the pharmacokinetic and pharmacodynamic properties of the
different antimalarials, and clinical trial results. Cost is a factor that has been taken into
consideration in antimalarial treatment policy and practices. However, there are increasing
international subsidies for antimalarials. Efficacy (both now and in the future) and safety have
therefore taken precedence when making the recommendations. The malaria treatment
guidelines given below are brief; for those who wish to study the evidence base in more detail,
a series of annexes is provided.
Malaria is caused by infection of red blood cells with protozoan parasites of the genus
Plasmodium. The parasites are inoculated into the human host by a feeding female anopheline
mosquito. The four Plasmodium species that infect humans are P. falciparum, P. vivax, P. ovale
and P. malariae. Occasional infections with monkey malaria parasites, such as P. knowlesi, also
occur. The first symptoms of malaria are nonspecific and similar to the symptoms of a minor
systemic viral illness. They comprise: headache, lassitude, fatigue, abdominal discomfort and
muscle and joint aches, followed by fever, chills, perspiration, anorexia, vomiting and
worsening malaise. This is the typical picture of uncomplicated malaria. Residents of endemic
areas are often familiar with this combination of symptoms, and frequently self-diagnose.
Malaria is therefore frequently overdiagnosed on the basis of symptoms alone. Infection
with P. vivax and P. ovale, more than with other species, can be associated with well-defined
malarial paroxysms, in which fever spikes, chills and rigors occur at regular intervals. At this
stage, with no evidence of vital organ dysfunction, the case-fatality rate is low (0.1% for P.
falciparum infections – the other human malarias are rarely fatal) provided prompt and
effective treatment is given. But if ineffective drugs are given or treatment is delayed in
falciparum malaria, the parasite burden continues to increase and severe malaria may ensue.
A patient may progress from having minor symptoms to having severe disease within a few
hours. This usually manifests with one or more of the following: coma (cerebral malaria),
metabolic acidosis, severe anaemia, hypoglycaemia and, in adults, acute renal failure or acute
pulmonary oedema. By this stage, mortality in people receiving treatment has risen to 1520%. If untreated, severe malaria is almost always fatal.
The nature of the clinical disease depends very much on the pattern and intensity of
malaria transmission in the area of residence, which determines the degree of protective
immunity acquired and, in turn, the clinical disease profile. Where malaria transmission is
“stable” – meaning where populations are continuously exposed to a fairly constant rate of
malarial inoculations – and if the inoculation rates are high – entomological inoculation rate
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The clinical disease
311
(EIR) >10/year –, then partial immunity to the clinical disease and to its severe manifestations
is acquired early in childhood. In such situations, which prevail in much of sub-Saharan Africa
and parts of Oceania, the acute clinical disease described above is almost always confined
to young children who suffer high parasite densities and acute clinical disease. If untreated,
this can progress very rapidly to severe malaria. In stable and high-transmission areas,
adolescents and adults are partially immune and rarely suffer clinical disease, although they
continue to harbour low blood-parasite densities. Immunity is reduced in pregnancy, and
can be lost when individuals move out of the transmission zone.
In areas of unstable malaria, the situation prevailing in much of Asia and Latin America
and the remaining parts of the world where malaria is endemic, the rates of inoculation
fluctuate greatly over seasons and years. EIRs are usually <5/year and often <1/year. This
retards the acquisition of immunity and results in people of all ages, adults and children alike,
suffering acute clinical malaria, with a high risk of progression to severe malaria if untreated.
Epidemics may occur in areas of unstable malaria when inoculation rates increase rapidly.
Epidemics manifest as a very high incidence of malaria in all age groups and can overwhelm
health services. Severe malaria is common if effective treatment is not made widely available.
Thus in areas of high transmission, it is children who are at risk of severe malaria and
death, whereas in areas of low or unstable transmission, all age groups are at risk.
Treatment objectives
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Uncomplicated malaria
312
The objective of treating uncomplicated malaria is to cure the infection. This is important
as it will help prevent progression to severe disease and prevent additional morbidity
associated with treatment failure. Cure of the infection means eradication from the body of
the infection that caused the illness. In treatment evaluations in all settings, emerging
evidence indicates that it is necessary to follow patients for long enough to document cure.
In assessing drug efficacy in high-transmission settings, temporary suppression of infection
for 14 days is not considered sufficient by the group.
The public health goal of treatment is to reduce transmission of the infection to others,
i.e. to reduce the infectious reservoir. A secondary but equally important objective of treatment is to prevent the emergence and spread of resistance to antimalarials. Tolerability, the
adverse effect profile and the speed of therapeutic response are also important
considerations.
Severe malaria
The primary objective of antimalarial treatment in severe malaria is to prevent death.
Prevention of recrudescence and avoidance of minor adverse effects are secondary. In treating
cerebral malaria, prevention of neurological deficit is also an important objective. In the
treatment of severe malaria in pregnancy, saving the life of the mother is the primary objective.
Diagnosis of malaria
Clinical diagnosis
The signs and symptoms of malaria are nonspecific. Malaria is clinically diagnosed mostly
on the basis of fever or history of fever. The following WHO recommendations are still
considered valid for clinical diagnosis.
➠ In general, in settings where the risk of malaria is low, clinical diagnosis of
uncomplicated malaria should be based on the degree of exposure to malaria and a
history of fever in the previous 3 days with no features of other severe diseases.
➠ In settings where the risk of malaria is high, clinical diagnosis should be based on
a history of fever in the previous 24 h and/or the presence of anaemia, for which pallor
of the palms appears to be the most reliable sign in young children.
The WHO/UNICEF strategy for Integrated Management of Childhood Illness (IMCI) has also
developed practical algorithms for management of the sick child presenting with fever where
there are no facilities for laboratory diagnosis.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Prompt and accurate diagnosis of malaria is part of effective disease management and will,
if implemented effectively, help to reduce unnecessary use of antimalarials. High sensitivity of
malaria diagnosis is important in all settings, in particular for the most vulnerable population
groups, such as young children, in which the disease can be rapidly fatal. High specificity
can reduce unnecessary treatment with antimalarials and improve differential diagnosis of
febrile illness.
The diagnosis of malaria is based on clinical criteria (clinical diagnosis) supplemented by
the detection of parasites in the blood (parasitological or confirmatory diagnosis). Clinical
diagnosis alone has very low specificity and in many areas parasitological diagnosis is not
currently available. The decision to provide antimalarial treatment in these settings must be
based on the prior probability of the illness being malaria. One needs to weigh the risk of
withholding antimalarial treatment from a patient with malaria against the risk associated
with antimalarial treatment when given to a patient who does not have malaria.
313
Parasitological diagnosis
The introduction of ACTs has increased the urgency of improving the specificity of malaria
diagnosis. The relatively high cost of these drugs makes waste through unnecessary treatment
of patients without parasitaemia unsustainable. In addition to cost savings, parasitological
diagnosis has the following advantages:
➠ improved patient care in parasite-positive patients owing to greater certainty that the
➠
➠
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➠
➠
314
patient has malaria;
identification of parasite-negative patients in whom another diagnosis must be sought;
prevention of unnecessary exposure to antimalarials, thereby reducing side-effects,
drug interactions and selection pressure;
improved health information;
confirmation of treatment failures.
The two methods in use for parasitological diagnosis are light microscopy and rapid
diagnostic tests (RDTs). Light microscopy has the advantage of low cost and high sensitivity
and specificity when used by well-trained staff. RDTs for detection of parasite antigen are
generally more expensive, but the prices of some of these products have recently decreased
to an extent that makes their deployment cost-effective in some settings. Their sensitivity and
specificity are variable, and their vulnerability to high temperatures and humidity is an
important constraint. Despite these concerns, RDTs make it possible to expand the use of
confirmatory diagnosis. Deployment of these tests, as with microscopy, must be accompanied
by quality assurance. Practical experience and operational evidence from large-scale
implementation are limited and, therefore, their introduction should be carefully monitored
and evaluated. The results of parasitological diagnosis should be available within a short time
(less than 2 h) of the patient presenting. If this is not possible, the patient must be treated on
the basis of a clinical diagnosis.
The choice between RDTs and microscopy
The choice between RDTs and microscopy depends on local circumstances, including the
skills available, the usefulness of microscopy for other diseases found in the area, and the caseload. Where the case-load of fever patients is high, microscopy is likely to be less expensive
than RDTs. Microscopy has further advantages in that it can be used for speciation and
quantification of parasites, and identification of other causes of fever. However, most malaria
patients are treated outside the health services, for example, in the community, in the home
or by private providers; microscopy is generally not feasible in such circumstances, but RDTs
may be.
Where malaria transmission is low to moderate and/or unstable
Parasitological confirmation of the diagnosis of malaria is recommended. This should be
provided by microscopy or, where not available, RDTs. Low to moderate transmission settings
include many urban areas in Africa, and the low transmission season in areas with seasonal
malaria.
In settings where malaria incidence is very low, parasitological diagnosis for all fever cases
may lead to considerable expenditure to detect only a few patients who are actually suffering
from malaria. In such settings, health workers should be trained to identify, through the history,
patients that have been exposed to malaria risk before they conduct a parasitological test.
Malaria is usually the most common cause of fever in children under 5 years of age in these
areas. Antimalarial treatment should therefore be given to children with fever (>37.5 oC) or
a history of fever and no other obvious cause.
Malaria is the most likely cause of their illness and there is as yet no evidence to show that
the benefits of parasitological diagnosis in this highly vulnerable group outweigh the risks
of not treating false negatives. In children of 5 years of age and above, malaria becomes
progressively less likely as a cause of fever, as immunity is acquired. In these older children and
in adults, malaria diagnosis should be based on a parasitological confirmation. Parasitological
diagnosis should be promoted in pregnant women, to improve the differential diagnosis of
fever and to reduce unnecessary use of antimalarials in pregnancy. Parasitological diagnosis
is also particularly important in settings with a high prevalence of HIV/AIDS because of the
high incidence of febrile disease that is not malaria in HIV-infected patients.
Transmission intensity is conventionally expressed in terms of EIR (Entomological
Inoculation Rate). There is as yet no consensus on criteria for determining the thresholds
between high, and low to moderate transmission settings. Suggested criteria include: the
proportion of all children under 5 years of age with patent parasitaemia, and the incidence of
individuals with the spleen palpable below the umbilicus in children aged 2–9 years. The IMCI
(Integrated Management of Childhood Ilness) guidelines recommend that areas in which
fewer than 5% of young children with fever have malaria parasitaemia should be considered
as low-transmission settings.
Malaria parasite species identification
In areas where two or more species of malaria parasites are common, only a parasitological
method will permit a species diagnosis. Where mono-infection with P. vivax is common and
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In stable high-transmission settings
315
microscopy is not available, it is recommended that a combination RDT which contains a panmalarial antigen is used. Alternatively, RDTs specific for falciparum malaria may be used, and
treatment for vivax malaria given only to cases with a negative test result but a high clinical
suspicion of malaria. Where P. vivax, P.malariae or P.ovale occur almost always as a co-infection
with P. falciparum, an RDT detecting P. falciparum alone is sufficient. Anti-relapse treatment
with primaquine should only be given to cases with confirmed diagnosis of vivax malaria.
SUMMARY OF RECOMMENDATIONS ON PARASITOLOGICAL DIAGNOSIS
✓ In areas of low to moderate transmission, prompt parasitological confirmation of the
diagnosis is recommended before treatment is started. This should be achieved through
microscopy or, where not available, RDTs.
✓ In areas of high stable malaria transmission, the prior probability of fever in a child being
caused by malaria is high. Children under 5 years of age should therefore be treated on
the basis of a clinical diagnosis of malaria. In older children and adults including in
pregnant women, a parasitological diagnosis is recommended before treatment is started.
✓ In all suspected cases of severe malaria, a parasitological confirmation of the diagnosis
of malaria is recommended. In the absence of or a delay in obtaining parasitological
diagnosis, patients should be treated for severe malaria on clinical grounds.
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Resistance to antimalarial medicines
316
Resistance has arisen to all classes of antimalarials except, as yet, to the artemisinin
derivatives. This has increased the global malaria burden and is a major threat to malaria
control. Widespread and indiscriminate use of antimalarials places a strong selective pressure
on malaria parasites to develop high levels of resistance. Resistance can be prevented, or its
onset slowed considerably, by combining antimalarials with different mechanisms of action
and ensuring very high cure rates through full adherence to correct dose regimens.
Impact of resistance
Initially, at low levels of resistance and with a low prevalence of malaria, the impact of
resistance to antimalarials is insidious. The initial symptoms of the infection resolve and the
patient appears to be better for some weeks. When symptoms recur, usually more than two
weeks later, anaemia may have worsened and there is a greater probability of carrying
gametocytes (which in turn carry the resistance genes) and transmitting malaria. However,
the patient and the treatment provider may interpret this as a newly acquired infection. At
this stage, unless clinical drug trials are conducted, resistance may go unrecognized. As
resistance worsens the interval between primary infection and recrudescence shortens, until
eventually symptoms fail to resolve following treatment. At this stage, malaria incidence may
rise in low transmission settings and mortality is likely to rise in all settings.
Global distribution of resistance
Resistance to antimalarials has been documented for P. falciparum, P. vivax and, recently,
P. malariae. In P. falciparum, resistance has been observed to almost all currently used
antimalarials (amodiaquine, chloroquine, mefloquine, quinine and sulfadoxine– pyrimethamine) except for artemisinin and its derivatives. The geographical distributions and rates
of spread have varied considerably.
P. vivax has developed resistance rapidly to sulfadoxine–pyrimethamine in many areas.
Chloroquine resistance is confined largely to Indonesia, East Timor, Papua New Guinea and
other parts of Oceania. There are also documented reports from Peru. P. vivax remains
sensitive to chloroquine in South-East Asia, the Indian subcontinent, the Korean peninsula,
the Middle East, north-east Africa, and most of South and Central America.
Assessing resistance
The following methods are available for assessing resistance to antimalarials:
Criteria for antimalarial treatment policy change
These malaria treatment guidelines recommend that antimalarial treatment policy should
be changed at treatment failure rates considerably lower than those recommended previously.
This major change reflects the availability of highly effective drugs, and the recognition both
of the consequences of drug resistance, in terms of morbidity and mortality, and the
importance of high cure rates in malaria control.
It is now recommended that a change of first-line treatment should be initiated if the total
failure proportion exceeds 10%. However, it is acknowledged that a decision to change may
be influenced by a number of additional factors, including the prevalence and geographical
distribution of reported treatment failures, health service provider and/or patient
dissatisfaction with the treatment, the political and economical context, and the availability
of affordable alternatives to the commonly used treatment.
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➠ in vivo assessment of therapeutic efficacy,
➠ in vitro studies of parasite susceptibility to drugs in culture,
➠ molecular genotyping.
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Treatment of uncomplicated P. falciparum malaria
P. falciparum malaria
Assessment
Uncomplicated malaria is defined as symptomatic malaria without signs of severity or
evidence of vital organ dysfunction. In acute falciparum malaria there is a continuum from
mild to severe malaria. Young children and non-immune adults with malaria may deteriorate
rapidly. Detailed definitions of severe malaria are available to guide practitioners and for
epidemiological and research purposes but, in practice, any patient whom the attending
physician or health care worker suspects of having severe malaria should be treated as such
initially. The risks of under-treating severe malaria considerably exceed those of giving
parenteral or rectal treatment to a patient who does not need it.
Antimalarial combination therapy
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To counter the threat of resistance of P. falciparum to monotherapies, and to improve
treatment outcome, combinations of antimalarials are now recommended by WHO for the
treatment of falciparum malaria.
318
Definition
Antimalarial combination therapy is the simultaneous use of two or more blood
schizontocidal drugs with independent modes of action and thus unrelated biochemical
targets in the parasite. The concept is based on the potential of two or more simultaneously
administered schizontocidal drugs with independent modes of action to improve therapeutic
efficacy and also to delay the development of resistance to the individual components of
the combination.
What is not considered to be combination therapy
Drug combinations such as sulfadoxine–pyrimethamine, sulfalene–pyrimethamine,
proguanil-dapsone, chlorproguanil-dapsone and atovaquone-proguanil rely on synergy
between the two components. The drug targets in the malaria parasite are linked. These
combinations are operationally considered as single products and treatment with them is not
considered to be antimalarial combination therapy. Multiple-drug therapies that include a nonantimalarial medicine to enhance the antimalarial effect of a blood schizontocidal drug (e.g.
chloroquine and chlorpheniramine) are also not antimalarial combination therapy.
Rationale for antimalarial combination therapy
The rationale for combining antimalarials with different modes of action is twofold: (1)
the combination is often more effective; and (2) in the rare event that a mutant parasite
that is resistant to one of the drugs arises de novo during the course of the infection, the
parasite will be killed by the other drug. This mutual protection is thought to prevent or delay
the emergence of resistance.
To realize the two advantages, the partner drugs in a combination must be independently
effective. The possible disadvantages of combination treatments are the potential for
increased risk of adverse effects and the increased cost.
Artemisinin and its derivatives (artesunate, artemether, artemotil, dihydroartemisinin)
produce rapid clearance of parasitaemia and rapid resolution of symptoms. They reduce
parasite numbers by a factor of approximately 10 000 in each asexual cycle, which is more
than other current antimalarials (which reduce parasite numbers 100- to 1000-fold per cycle).
Artemisinin and its derivatives are eliminated rapidly. When given in combination with rapidly
eliminated compounds (tetracyclines, clindamycin), a 7-day course of treatment with an
artemisinin compound is required; but when given in combination with slowly eliminated
antimalarials, shorter courses of treatment (3 days) are effective. The evidence of their
superiority in comparison to monotherapies has been clearly documented.
trials comparing monotherapies with ACTsa
The choice of artemisinin-based combination therapy options
Although there are some minor differences in oral absorption and bioavailability between
the different artemisinin derivatives, there is no evidence that these differences are clinically
significant in current formulations. It is the properties of the partner medicine that determine
the effectiveness and choice of combination.
ACTs with amodiaquine, atovaquone-proguanil, chloroquine, clindamycin, doxycycline,
lumefantrine, mefloquine, piperaquine, pyronaridine, proguanil-dapsone, sulfadoxinepyrimethamine and tetracycline have all been evaluated in trials carried out across the malariaaffected regions of the world. Some of these are studies for product development. Though
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Artemisinin-based combination therapy (ACT)
319
there are still gaps in our knowledge, there is reasonable evidence on safety and efficacy on
which to base recommendations.
The following ACTs are currently recommended (alphabetical order):
➠
➠
➠
➠
artemether-lumefantrine,
artesunate + amodiaquine,
artesunate + mefloquine,
artesunate + sulfadoxine–pyrimethamine.
An advantage of this combination is that lumefantrine is not available as a monotherapy
and has never been used by itself for the treatment of malaria. Recent evidence indicates that
the therapeutic response and safety profile in young children of less than 10 kg is similar to
that in older children, and artemether-lumefantrine is now recommended for patients > 5 kg.
Lumefantrine absorption is enhanced by co-administration with fat. Low blood levels, with
resultant treatment failure, could potentially result from inadequate fat intake, and so it is
essential that patients or carers are informed of the need to take this ACT with milk or fatcontaining food – particularly on the second and third days of treatment.
Alternative 2nd line treatment for uncomplicated
P. falciparum malaria
MALARIA CARE, HEALTH POLICY AND RESEARCH
➠ alternative ACT known to be effective in the region,
➠ artesunate + tetracycline or doxycycline or clindamycin,
➠ quinine + tetracycline or doxycycline or clindamycin.
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Incorrect approaches to treatment
In endemic regions, some semi-immune malaria patients could be cured using partial
treatment with effective medicines (i.e. use of regimens that would be unsatisfactory in
patients with no immunity). This had led in the past to different recommendations for patients
considered to be semi-immune and those considered to be non-immune. Another potentially
dangerous practice is to give only the first dose of the treatment course for patients with
suspected but unconfirmed malaria, with the intention of giving full treatment if the diagnosis
is eventually confirmed. Neither practice is recommended. If malaria is suspected and the
decision to treat is made, then a full effective treatment is required whether or not the
diagnosis is confirmed by a test.
With the exception of artemether-lumefantrine, the partner medicines of all other ACTs
have been previously used as monotherapies, and still continue to be available as such in many
countries. Their continued use as monotherapies can potentially compromise the value of ACTs
by selecting for drug resistance. The withdrawal of artemisinins and other monotherapies is
recommended.
Pregnant women with symptomatic acute malaria are a high-risk group, and must receive
effective antimalarials. Malaria in pregnancy is associated with low birth weight, increased
anaemia and, in low-transmission areas, an increased risk of severe malaria. In hightransmission settings, despite the adverse effects on fetal growth, malaria is usually
asymptomatic in pregnancy. There is insufficient information on the safety and efficacy of
most antimalarials in pregnancy, particularly for exposure in the first trimester, and so
treatment recommendations are different to those for non-pregnant adults.
Organogenesis occurs mainly in the first trimester and this is therefore the time of greatest
concern for potential teratogenicity, although nervous system development continues
throughout pregnancy. The antimalarials considered safe in the first trimester of pregnancy are
quinine, chloroquine, proguanil, pyrimethamine and sulfadoxine–pyrimethamine. Of these,
quinine remains the most effective and can be used in all trimesters of pregnancy including the
first trimester. In reality women often do not declare their pregnancies in the first trimester and
so, early pregnancies will often be exposed inadvertently to the available firstline treatment.
Inadvertent exposure to antimalarials is not an indication for termination of the pregnancy.
There is increasing experience with artemisinin derivatives in the second and third
trimesters (over 1000 documented pregnancies). There have been no adverse effects on the
mother or fetus. The current assessment of benefits compared with potential risks suggests
that the artemisinin derivatives should be used to treat uncomplicated falciparum malaria
in the second and third trimesters of pregnancy, but should not be used in the first trimester
until more information becomes available. The choice of combination partner is difficult.
Mefloquine has been associated with an increased risk of stillbirth in large observational
studies in Thailand, but not in Malawi. Amodiaquine, chlorproguanil- dapsone, halofantrine,
lumefantrine and piperaquine have not been evaluated sufficiently to permit positive
recommendations. Sulfadoxine-pyrimethamine is safe but may be ineffective in many areas
because of increasing resistance. Clindamycin is also safe, but both medicines (clindamycin
and the artemisinin partner) must be given for 7 days. Primaquine and tetracyclines should
not be used in pregnancy.
Despite these many uncertainties, effective treatment must not be delayed in pregnant
women. Given the disadvantages of quinine, i.e. the long course of treatment, and the
increased risk of hypoglycaemia in the second and third trimesters, ACTs are considered
suitable alternatives for these trimesters. In practice, if first-line treatment with an artemisinin
combination is all that is immediately available to treat in the first trimester of pregnancy
pregnant women who have symptomatic malaria, then this should be given.
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Pregnant women
321
Pharmacovigilance programmes to document the outcome of pregnancies where there has
been exposure to ACTs, and if possible documentation of the development of the infant,
are encouraged so that future recommendations can stand on a firmer footing.
FIRST TRIMESTER:
quinine + clindamycin to be given for 7 days. ACT should be used if it is the only effective
treatment available.
SECOND AND THIRD TRIMESTERS:
ACT known to be effective in the country/region or artesunate + clindamycin to be given
for 7 days or quinine + clindamycin to be given for 7 days.
Lactating women
The amounts of antimalarials that enter breast milk and are therefore likely to be
consumed by the breast-feeding infant are relatively small. The only exception to this is
dapsone, relatively large amounts of which are excreted in breast milk (14% of the adult
dose), and pending further data this should not be prescribed. Tetracyclines are also
contraindicated because of their effect on the infant’s bones and teeth.
Infants
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CHOICE OF ANTIMALARIAL DRUG
322
In endemic countries, malaria is common in infants and children under 2 years of age.
Immunity acquired from the mother wanes after 3–6 months of age, and the case-fatality rate
of severe malaria in infants is higher than in older children. Furthermore, there are important
differences between infants and older children in the pharmacokinetics of many medicines.
Accurate dosing is particularly important in infants. Despite this, few clinical studies focus
specifically on this age range, partly because of ethical considerations relating to the
recruitment of very young children to clinical trials, and also because of the difficulty of
repeated blood sampling. In the majority of clinical studies, subgroup analysis is not used to
distinguish between infants and older children. Infants are more likely to vomit or regurgitate
antimalarial treatment than older children or adults. Taste, volume, consistency and
gastrointestinal tolerability are important determinants of whether the child retains the
treatment. Mothers often need advice on techniques of medicine administration and the
importance of administering the medicine again if it is immediately regurgitated. With the
increasing failure of chloroquine and sulfadoxine– pyrimethamine as front-line antimalarials,
the challenge is now to find safe alternatives in this age group. Fortunately the artemisinin
derivatives appear to be safe in, and well tolerated by young children, and so the choice of
ACT will be determined largely by the safety and tolerability of the partner drug. The limited
information available does not indicate particular problems with currently recommended ACTs
in infancy.
DOSING
Although dosing based on body area is recommended for many drugs in young children, for
the sake of simplicity, dosing of antimalarials has been traditionally based on weight. The
weight-adjusted doses of antimalarials in infants are similar to those used in adults. For the
majority of antimalarials, however, the lack of an infant formulation necessitates the division of
adult tablets, which leads to inaccurate dosing. There is a need to develop infant formulations
for a range of antimalarials in order to improve the accuracy and reliability of dosing.
Delay in treating falciparum malaria may have fatal consequences, particularly for more
severe infections. Every effort should be made to give oral treatment and ensure that it is
retained. In situations where it is not possible to give parenteral treatment, a sick infant
who vomits antimalarial medicine treatment repeatedly, has a seizure or is too weak to
swallow reliably should be given artesunate by the rectal route, pending transfer to a facility
where parenteral treatment is possible. Large trials assessing the impact of this strategy on
mortality have recently been undertaken in remote rural areas, but results are not yet
available. Pharmacological and trial evidence concerning the rectal administration of
artesunate and other antimalarial drugs is provided
Travellers who acquire malaria are often non-immune adults either from cities with little
or no transmission within endemic countries, or visitors from nonendemic countries. Both are
likely to be at a higher risk of malaria and its consequences because they have no immunity
to malaria. Within the malaria endemic country they should in principle be treated according
to national policy.
Travellers who return to a non-endemic country and then develop malaria present
particular problems and, have a high case fatality rate. Doctors may be unfamiliar with malaria
and the diagnosis may be delayed, relevant antimalarials may not be registered and/or
therefore available. If the patient falls ill far from a major health facility, availability of
antimalarials can be a lifethreatening issue despite registration. On the other hand prevention
of emergence of resistance and transmission are of less relevance outside malaria endemic
areas. Thus monotherapy may be given if it can be assured to be effective. Furthermore cost
of treatment is usually not a limiting factor.
The principles underlying the recommendations given below are that effective medicines
should be used to treat travellers; if the patient has taken chemoprophylaxis, then the same
medicine should not be used for treatment.
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Travellers
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The treatment for P. vivax, P. ovale and P. malariae in travellers should be the same as
for these infections in patients from endemic areas. In the management of severe malaria
outside endemic areas, there may be delays in obtaining artesunate, artemether or quinine.
If parenteral quinidine is available but other parenteral drugs are not, then this should be
given with careful clinical and electrocardiographic monitoring. For travellers returning to nonendemic countires:
➠ atovaquone-proguanil (15/6 mg/kg, usual adult dose, 4 tablets once a day for 3 days
➠ arthemether-lumefantrine (adult dose, 4 tablets twice a day for 3 days)
➠ quinine (10mg salt/hg every 8 hours)+doxycycline3 (3.5mg/kg once a day) or
clindamycin (10mg/kg twice a day), all drugs for 7 days
For travellers with severe complicated malaria:
➠ the same as in severe malaria in endemic countries (see further)
➠ they should be managed in an intensive care unit
➠ haemofiltration or haemodialysis should be started early in acute renal failure or severe
metabolic acidosis
➠ positive pressure ventilation should be started early if there is any breathing pattern
abnormality, intractable seizure or acute respiratory distress syndrome
Coexisting morbidities
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HIV INFECTION
324
Increasing numbers of people in malaria endemic areas are living with HIV infection. It
is becoming increasingly apparent that, as HIV progresses and immunosuppression worsens,
the manifestations of malaria also worsen. In pregnant women, the adverse effects on birth
weight are increased. In patients with partial immunity to malaria, the severity of the
infection is increased. There is insufficient information at the present time on how HIV
infection modifies the therapeutic response to antimalarials. However, increasing parasite
burdens and reduced host immunity, both of which occur with HIV infection, are associated
with increased treatment failure rates. At this time, there is insufficient information to
modify the general malaria treatment recommendations for patients with HIV/AIDS. Current
UNAIDS/WHO recommendations on the prophylaxis of opportunistic infections with
cotrimoxazole (trimethoprimsulfamethoxazole) in people living with HIV/AIDS remain
unchanged.
However, treatment with sulfadoxine–pyrimethamine should not be given to patients
on cotrimoxazole as there is probably an increased risk of sulfa-related adverse effects (and in
3. Clindamycin not to be used in children less than 8 years of age.
any case as both medicines have similar antimalarial activity, the malaria infection is likely
to be resistant to sulfadoxine–pyrimethamine). Depending on the malaria transmission
setting, HIV-infected individuals are at increased risk of asymptomatic parasitaemia, clinical
malaria or severe and complicated malaria. Therefore, they have an even greater need for
malaria control measures than individuals not infected with HIV.
Treatment of complicated P. falciparum malaria
Definition
In a patient with P. falciparum asexual parasitaemia and no other obvious cause of their
symptoms, the presence of one or more of the following clinical or laboratory features
classifies the patient as suffering from severe malaria:
Prostration
Impaired consciousness
Respiratory distress (acidotic breathing)
Multiple convulsions
Circulatory collapse
Pulmonary oedema (radiological)
Abnormal bleeding
Jaundice
Haemoglobinuria
LABORATORY TEST:
➠
➠
➠
➠
➠
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Severe anaemia
Hypoglycaemia
Acidosis
Renal impairment
Hyperlactataemia
Hyperparasitaemia
Treatment objectives
The main objective is to prevent the patient from dying, secondary objectives are prevention
of recrudescence, transmission or emergence of resistance and prevention of disabilities.
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CLINICAL MANIFESTATION:
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The mortality of untreated severe malaria is thought to approach 100%. With antimalarial
treatment the mortality falls to 15–20% overall, although within the broad definition are
syndromes associated with mortality rates that are lower (e.g. severe anaemia) and higher
(metabolic acidosis). Death from severe malaria often occurs within hours of admission to
hospital or clinic, and so it is essential that therapeutic concentrations of antimalarial are
achieved as soon as possible. Management of severe malaria comprises four main areas:
clinical assessment of the patient, specific antimalarial treatment, adjunctive therapy and
supportive care.
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Clinical assessment
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Severe malaria is a medical emergency. The airway should be secured in unconscious
patients and breathing and circulation assessed. The patient should be weighed or body weight
estimated so that drugs, including antimalarials and fluids can be given on a body weight basis.
An intravenous cannula should be inserted and immediate measurements of blood glucose
(stick test), haematocrit/haemoglobin, parasitaemia and, in adults, renal function should be
taken. A detailed clinical examination should be conducted, with particular note of the level of
consciousness and record of the coma score. Several coma scores have been advocated. The
Glasgow coma scale is suitable for adults, and the simple Blantyre modification or children’s
Glasgow coma scale are easily performed in children. Unconscious patients should have a
lumbar puncture for cerebrospinal fluid analysis to exclude bacterial meningitis.
The degree of acidosis is an important determinant of outcome; the plasma bicarbonate
or venous lactate level should therefore be measured if possible. If facilities are available,
arterial or capillary blood pH and gases should be measured in patients who are unconscious,
hyperventilating or in shock.
Blood should be taken for cross-match, and (if possible) full blood count, platelet count,
clotting studies, blood culture and full biochemistry should be conducted. The assessment
of fluid balance is critical in severe malaria.
Respiratory distress, in particular with acidotic breathing in severely anaemic children,
often indicates hypovolaemia and requires prompt rehydration and, where indicated, blood
transfusion.
Specific antimalarial treatment
It is essential that antimalarial treatment in full doses is given as soon as possible in severe
malaria. Two classes of drugs are currently available for the parenteral treatment of severe
malaria: the cinchona alkaloids (quinine and quinidine) and the artemisinin derivatives
(artesunate, artemether and artemotil). Although there are a few areas where chloroquine
is still effective, parenteral chloroquine is no longer recommended for the treatment of severe
malaria because of widespread resistance. Intramuscular sulfadoxine– pyrimethamine is also
not recommended.
Quinine
Quinine treatment for severe malaria was established before modern trial methods were
developed. Several salts of quinine have been formulated for parenteral use, but the
dihydrochloride is the most widely used. Peak concentrations following intramuscular quinine
in severe malaria are similar to those following intravenous infusion. Pharmacokinetic
modelling studies suggest that a loading dose of quinine of twice the maintenance dose (i.e.
20 mg salt/kg bw) reduces the time to reach therapeutic plasma concentrations. After the first
day of treatment, the total daily maintenance dose of quinine is 30 mg salt/kg bw (usually
divided into three equal administrations at 8 h intervals).
Various artemisinin derivatives have been used in the treatment of severe malaria including
artemether, artemisinin (rectal), artemotil and artesunate. The pharmacokinetic properties
of artesunate are superior to those of artemether and artemotil as it is water soluble and
can be given either by intravenous or intramuscular injection. Randomised trials comparing
artesunate and quinine from South-East Asia show clear evidence of benefit with artesunate.
In the largest multi-centre trial, which enrolled 1461 patients (including 202 children <15 years
old), mortality was reduced by 34.7% compared to the quinine group. The results of this
and smaller trials are consistent and suggest that artesunate is the treatment of choice for
adults with severe malaria.
There are, however, still insufficient data for children, particularly from high transmission
settings to make the same conclusion. An individual patient data meta-analysis of trials
comparing artemether and quinine showed no difference in mortality in African children.
Although artesunate has better pharmacokinetic properties than artemether or artemotil,
there are relatively few published comparative clinical trials.
Concerns have been raised, regarding the possibility that the intrinsic benefits of
artemether as an antimalarial may have been negated by its erratic absorption following
intramuscular injection. Artemotil is very similar to artemether, but very few trials have been
conducted.
Recommendation: there is insufficient evidence to recommend rectal administration of
quinine unless parenteral administration is not possible and no other effective options are
available.
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Artemisinin derivatives
327
Quinidine
Quinidine commonly causes hypotension and concentration-dependent prolongation of
ventricular repolarization (QT prolongation). Quinidine is thus considered more toxic than
quinine and should only be used if none of the other effective parenteral drugs are available.
Electrocardiographic monitoring and frequent assessment of vital signs are required if
quinidine is used.
Summary of recommendations
on the treatment of severe malaria
Severe malaria is a medical emergency. After rapid clinical assessment and confirmation of the
diagnosis, full doses of parenteral antimalarial treatment should be started without delay with
whichever effective antimalarial is first available.
Artesunate 2.4 mg/kg bw i.v. or i.m. given on admission (time = 0), then at 12 h and 24
h, then once a day is the recommended choice in low transmission areas or outside malaria
endemic areas
For children in high transmission areas, the following antimalarial medicines are
recommended as there is insufficient evidence to recommend any of these antimalarial
medicines over another for severe malaria:
MALARIA CARE, HEALTH POLICY AND RESEARCH
➠ artesunate 2.4 mg/kg bw i.v. or i.m. given on admission (time = 0), then at 12 h and
328
24 h, then once a day;
➠ artemether 3.2 mg/kg bw i.m. given on admission then 1.6 mg/kg bw per day;
➠ quinine 20 mg salt/kg bw on admission (i.v. infusion or divided i.m. injection), then 10
mg/kg bw every 8 h; infusion rate should not exceed 5 mg salt/kg bw per hour.
Practical aspects of treatment
Artemisinins
Artemisinin is formulated as a suppository for rectal administration. Artemether and
artemotil are formulated in oil and are given by intramuscular injection.
They are both absorbed erratically, particularly in very severely ill patients. Artesunate is
soluble in water and can be given either by intravenous or intramuscular injection. There
are also rectal formulations of artesunate, artemether and dihydroartemisinin.
The dosing of artemisinin derivatives has been largely empirical. The doses recommended
here are those that have been most widely studied. The only recent change is the higher
maintenance dose of parenteral artesunate recommended (2.4 mg/kg bw), which is based on
pharmacokinetic and pharmacodynamic studies and by extrapolation from studies with oral
artesunate. Expert opinion is that the previously recommended maintenance dose of 1.2
mg/kg bw may have been insufficient in some patients.
Artesunate is dispensed as a powder of artesunic acid. This is dissolved in sodium
bicarbonate (5%) to form sodium artesunate. The solution is then diluted in approximately
5 ml of 5% dextrose and given by intravenous injection or by intramuscular injection to the
anterior thigh. The solution should be prepared freshly for each administration and should
not be stored.
Artemether and artemotil are dispensed dissolved in oil (groundnut, sesame seed) and
given by i.m. injection into the anterior thigh.
Whereas many antimalarials are prescribed in terms of base, for historical reasons quinine
doses are often recommended in terms of salt (usually sulphate for oral use and
dihydrochloride for parenteral use). Recommendations for doses of this and other antimalarials
should state clearly whether the salt or base is being referred to (doses with different salts
must have the same base equivalents).
Quinine must never be given by intravenous injection, as lethal hypotension may result.
Quinine dihydrochloride should be given by rate-controlled infusion in saline or dextrose
solutions at a rate not exceeding 5 mg salt/kg bw per hour. If this is not possible then it should
be given by intramuscular injection to the anterior thigh, not the buttock (to avoid sciatic
nerve injury).
The first dose should be split, 10 mg/kg bw to each thigh. Undiluted quinine dihydrochloride
at a concentration of 300 mg/ml is acidic (pH 2) and painful when given by intramuscular
injection, so it is best either formulated or diluted to concentrations of 60–100 mg/ml for
intramuscular injection. Gluconate salts are less acidic and better tolerated than the
dihydrochloride salt when given by the intramuscular and rectal routes.
As the first dose (loading dose) is the most important in the treatment of severe malaria,
this should be reduced only if there is clear evidence of adequate pretreatment before
presentation. Although quinine can cause hypotension if administered rapidly, and overdose
is associated with blindness and deafness, these adverse effects are rare in the treatment of
severe malaria. The dangers of insufficient treatment (i.e. death from malaria) exceed those
from excessive treatment initially. After the second day of parenteral treatment, if there is no
clinical improvement or in acute renal failure, the maintenance doses of quinine given by
infusion should be reduced by one-third to avoid accumulation.
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Quinine
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Adjustment of dosing in renal failure or hepatic dysfunction
The dosage of artemisinin derivatives does not need adjustment in vital organ dysfunction.
Quinine (and quinidine) levels may accumulate in severe vital organ dysfunction. If there is no
clinical improvement or the patient remains in acute renal failure the dose should be reduced
by one-third after 48 h. Dosage adjustments are not necessary if patients are receiving either
haemodialysis or haemofiltration. Dosage adjustment by one-third is necessary in patients
with hepatic dysfunction.
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Follow-on treatment
330
Following initial parenteral treatment, once the patient can tolerate oral therapy, it is
essential to continue and complete treatment with an effective oral antimalarial. Current
practice is to continue the same medicine orally as given parenterally to complete a full 7 days
of treatment. In non-pregnant adults, doxycycline is added to either quinine, artesunate or
artemether and should also be given for 7 days. Doxycycline is preferred to other tetracyclines
because it can be given once daily, and does not accumulate in renal failure. But as treatment
with doxycycline only starts when the patient has recovered sufficiently, the doxycycline
course finishes after the quinine, artemether or artesunate course. Where available,
clindamycin may be substituted in children and pregnant women, as doxycycline cannot be
given to these groups. Although following parenteral treatment with a full course of oral ACT
(artesunate + amodiaquine or artemether-lumefantrine) is theoretically a good alternative,
this has not been evaluated in clinical trials.
The recommendation from experts’ opinion is to complete treatment in severe malaria
following parenteral drug administration by giving a full course of combination therapy, ACT
or quinine + clindamycin or doxycycline. Regimens containing mefloquine should be avoided
if the patient presented initially with impaired consciousness. This is because of an increased
incidence of neuropsychiatric complications associated with mefloquine following cerebral
malaria.
Pre-referral treatment options
The risk of death from severe malaria is greatest in the first 24 h, yet in most malaria
endemic countries, the transit time between referral and arrival at appropriate health facilities
is usually prolonged thus delaying the commencement of appropriate antimalarial treatment,
during which time the patient may deteriorate or die. It is recommended that patients are
treated with the first dose of one of the recommended treatments by the parenteral route
if possible or by the intra-rectal route before referral (unless the referral time is very short).
This could be intramuscular artemether, artesunate or quinine, or a rectal formulation of
artemisinin or artesunate.
Pre-referral and continued treatment with rectal artemisinins
The administration of an artemisinin by the rectal route as pre-referral treatment is feasible
even at the community level. There is insufficient evidence to show whether rectal artesunate
is as good as intravenous or intramuscular options in the management of severe malaria.
The recommendation, therefore, is to use artesunate or artemisinin suppositories only
as pre-referral treatment and to refer the patient to a facility where complete parenteral
treatment with artesunate, quinine or artemether can be instituted. If, however, referral is
impossible, rectal treatment should be continued until the patient can tolerate oral
medication, at which point a full course of the recommended ACT for uncomplicated malaria
in the locality can be administered.
Dosing for antimalarials given by suppository
ARTEMISININ DERIVATIVES
Artemisinin suppositories are not widely available. Doses used have been variable and
empiric: 10-40 mg/kg bw (at 0, 4 or 12, 24, 48 and 72 h). Some studies have given a maintenance
dose of one- to two-thirds of the initial dose. Artesunate suppositories* are given in a dose
artesunate.
INITIAL (PRE-REFERRAL) TREATMENT WITH RECTAL ARTESUNATE
The appropriate single dose of artesunate given by suppository should be administered
rectally as soon as the presumptive diagnosis of severe malaria is made. In the event that
an artesunate suppository is expelled from the rectum within 30 min of insertion, a second
suppository should be inserted and, especially in young children, the buttocks should be held
together, for 10 min to ensure retention of the rectal dose of artesunate.
For adults::
one or more artesunate suppositories inserted in the rectum, dose as indicated in The dose
should be given once and followed as soon as possible by definitive therapy for malaria.
Dosage* for initial (pre-referral) treatment in adult patients (aged ≥16 years)
* It should be noted that the clinical trial data with rectal artesunate relate to a single suppository
formulation and presentation which has well characterized absorption kinetics and so cannot necessarily be
extrapolated to other rectal formulations of artesunate.
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of 10 mg/kg bw daily. The individual suppositories contain either 50, 100 or 400 mg of
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Artesunate dose Regimen (single dose)
Use appropriate no. of 100-mg rectal suppositories
Weight (kg)
<40 Kg
10 mg/kg bw
40–59 Kg
400 mg One 400-mg suppository
60–80 Kg
800 mg Two 400-mg suppositories
>80 Kg
1200 mg Three 400-mg suppositories
For children::
one or more artesunate suppositories inserted in the rectum as indicated. The dose should
be given once and followed as soon as possible by definitive therapy for malaria.
Dosage for initial (pre-referral) treatment in children (aged 2–15 years) and weighing at
least 5 kg
MALARIA CARE, HEALTH POLICY AND RESEARCH
Weight (kg) Age Artesunate dose (mg)
5–8.9 0–12 months 50 One 50-mg suppository
9–19 13–42 months 100 One 100-mg suppository
20–29 43–60 months 200 Two 100-mg suppositories
30–39 6–13 years 300 Three 100-mg suppositories
>40 >14 years 400 One 400-mg suppository
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Quinine
The intrarectal dose used in treatment trials in Africa was either 12 mg/kg bw quinine base
every 12 h without a loading dose, or 8 mg/kg bw every 8 h, also without a loading dose. The
retention and absorption of quinine is dependent on pH. Results with gluconate salts (pH 4.5)
cannot be extrapolated to more acidic solutions (such as the dihydrochloride salt, pH 2).
Continuing supportive care
Patients with severe malaria require intensive nursing, in an intensive care unitif possible.
Following the initial assessment and the start of antimalarial treatment, clinical observations
should be made as frequently as possible. These should include recording of vital signs, with
an accurate assessment of respiratory rate and pattern, coma score, and urine output. Blood
glucose should be checked, using rapid stick tests every 4 h if possible, particularly in
unconscious patients. Convulsions should be treated promptly with intravenous or rectal
diazepam or intramuscular paraldehyde.
Fluid requirements should be assessed individually. Adults with severe malaria are very
vulnerable to fluid overload and there is a thin dividing line between underhydration, and
thus worsening renal impairment, and overhydration, with the risk of precipitating pulmonary
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Immediate clinical management of severe manifestations
and complications of falciparum malaria
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334
oedema. If the patient becomes oliguric (<0.4 ml of urine/kg bw per hour) despite adequate
rehydration, and the blood urea or creatinine are rising or already high, then fluids should
be restricted to replace insensible losses only. Children, on the other hand, are more likely
to be dehydrated and may respond well to a bolus of fluid. The fluid regimen must also be
tailored around infusion of the antimalarial drugs. Central venous pressure should be
maintained at 0–5 cm. If the venous pressure is elevated (usually because of excessive fluid
administration), the patient should be nursed with the head raised at an angle of 45o and,
if necessary, intravenous furosemide should be given. If available, heamofiltration should be
started early for acute renal failure or severe metabolic acidosis unresponsive to rehydration.
If blood glucose is <2.2 mmol/l then hypoglycaemia should be treated immediately (0.3–0.5
g/kg bw of glucose). Hypoglycaemia should be suspected in any patient who deteriorates
suddenly. Stick tests may overestimate the frequency of hypoglycaemia, so laboratory
confirmation may be necessary.
Patients with acute pulmonary oedema should be nursed in an upright position and given
oxygen, and filling pressures on the right side of the heart should be reduced with whichever
treatments are available (loop diuretics, opiates, venodilators, venesection, haemofiltration,
dialysis). The right-sided pressure should be reduced to the lowest level compatible with an
adequate cardiac output. Positive pressure ventilation should be started (if available) early if
the patient becomes hypoxic.
Fewer than 5% of patients with severe malaria develop clinically significant disseminated
intravascular coagulation. These patients should be given fresh blood transfusions and vitamin
K. Patients with secondary pneumonia should be given empirical treatment with a thirdgeneration cephalosporin, unless admitted with clear evidence of aspiration, in which case
penicillin or clindamycin is adequate. Children with persistent fever despite parasite clearance
may have a systematic Salmonella infection, although in the majority of cases of persistent
fever no other pathogen is identified after parasite clearance. Urinary tract infections are
common in catheterized patients. Antibiotic treatments should take account of likely local
antibiotic sensitivity patterns.
Additional aspects of clinical management
Diagnosis
The differential diagnosis of fever in a severely ill patient is broad. Coma and fever may
result from meningoencephalitis or malaria. Cerebral malaria is not associated with signs of
meningeal irritation (neck stiffness, photophobia, Kernig sign) but the patient may be
opisthotonic. As untreated bacterial meningitis is almost invariably fatal, a diagnostic lumbar
puncture should be performed to exclude this condition. There is also considerable clinical
overlap between septicaemia, pneumonia and severe malaria – and these conditions may
coexist. In malaria endemic areas particularly, where parasitaemia is common in the young age
group, it is often impossible to rule out septicaemia in a shocked or severely ill obtunded child.
Where possible, blood should always be taken on admission for culture, and if there is any
doubt, empirical antibiotic treatment should be started immediately along with antimalarial
treatment.
Many other supportive strategies and interventions have been proposed in severe malaria,
but very few are supported by evidence of benefit, and many have proved harmful. Heparin,
prostacyclin, deferoxamine, pentoxifylline, low molecular weight dextran, urea, high-dose
corticosteroids, acetylsalicylic acid, deferoxamine, anti-tumour necrosis factor antibody,
cyclosporin, dichloroacetate, adrenaline and hyperimmune serum have all been suggested –
but none of these is recommended.
Evidence on use of corticosteroids is summarized in below. Severe metabolic acidosis is
common but apart from correction of hypovolaemia and anaemia, no specific treatment is
of proven value. Significant electrolyte abnormalities are relatively unusual, and potassium
supplementation is often not required in the acute phase. The optimum fluid resuscitation
regimens, the thresholds for blood transfusion, the role of exchange transfusion, and the
management of seizures remain areas of uncertainty, and these are discussed in more detail
below. The optimum body positioning in comatose patients, and the timing and type of
feeding in patients who remain unconscious for > 24 h have not been studied. It is generally
agreed that early ventilation for respiratory abnormalities and early management of renal
failure or severe metabolic acidosis are beneficial. In acute renal failure, haemofiltration is
associated with a lower mortality, and more rapid correction of biochemical abnormalities
compared with peritoneal dialysis. There have been no comparative trials of haemodialysis
and haemofiltration.
Summary of recommendations for use of corticosteroids
Interventions: corticosteroids i.v.
Summary of RCTs: one systematic review and no additional trials. No significant difference in
mortality; increased risk of gastrointestinal bleeding.
Expert comment: no additional information.
Basis of decision: systematic review.
Recommendation: do not use corticosteroids.
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Other treatments
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Fluid therapy
Patients, especially children with severe malaria may be dehydrated. However, the degree
of fluid depletion varies considerably. As a result, it is not possible to give general
recommendations on fluid replacement. Each patient must be individually assessed and fluid
resuscitation based on estimated deficit. In hightransmission settings where severe malaria is
confined to childhood, children commonly present with severe anaemia and hyperventilation
(sometimes termed “respiratory distress”). In the past this was ascribed to “anaemic heart
failure” (i.e. pulmonary oedema), and sometimes diuretics were administered. It is now clear
that this syndrome is not a result of anaemic heart failure, but results from severe metabolic
acidosis and anaemia, and so should be treated by blood transfusion. In general children
tolerate rapid fluid resuscitation better than adults, and are less likely to develop pulmonary
oedema. In adults, there is a very thin dividing line between overhydration, which may
produce pulmonary oedema, and underhydration contributing to shock and worsening
acidosis and renal impairment.
Careful and frequent evaluations of the jugular venous pressure, peripheral perfusion,
venous filling, skin turgor and urine output should be made. Where there is uncertainty over
the jugular venous pressure, and if nursing facilities permit, a central venous catheter should
be inserted and the central venous pressure measured directly. The optimum rate of
resuscitation, the role of colloids compared with crystalloids, and the optimum electrolyte
composition of the replacement fluid have not been determined.
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Blood transfusion
336
Severe malaria is associated with rapid development of anaemia as infected and
uninfected erythrocytes are removed from the circulation. In areas of high stable transmission,
severe anaemia in young children is the principal manifestation of severe falciparum malaria.
Ideally fresh blood should be transfused, and the patient’s relatives are often willing donors.
However, in most settings cross-matched virus-free blood is in short supply. As with fluid
resuscitation, there have not been enough studies to provide strong evidence-based
recommendations, so the recommendations given here are based on expert opinion.
In high-transmission settings, blood transfusion is recommended for children with a
haemoglobin level of <5 g/100 ml (haematocrit <15%). Mortality as a direct result of anaemia
rises at lower haemoglobin levels. In low-transmission settings, a threshold of 20%
(haemoglobin 7 g/100ml) is recommended. These general recommendations still need to be
tailored to the individual, as the pathological consequences of rapid development of anaemia
are worse than those of acute on chronic anaemia, where there has been adaptation and a
compensatory right shift in the oxygen dissociation curve.
Exchange blood transfusion (EBT)
There have been many anecdotal reports and several series claiming benefit for EBT in
severe malaria but no comparative trials, and there is no consensus on whether it reduces
mortality or how it might work. The rationale for EBT has been variously proposed as:
➠ removing infected red blood cells from the circulation and therefore lowering the
parasite burden (although only the circulating relatively non-pathogenic stages are
removed – and this is also achieved rapidly with artemisinin derivatives);
➠ reducing rapidly both the antigen load and the burden of parasite-derived toxins,
metabolites and toxic mediators produced by the host;
➠ replacing the rigid unparasitized red cells by more deformable cells and therefore
alleviating microcirculatory obstruction.
EBT requires intensive nursing and a relatively large volume of blood, and carries significant
risks. There is no consensus on the indications, benefits and dangers involved, or on practical
details such as the volume of blood that should be exchanged. It is therefore not possible
to make any recommendation regarding the use of EBT.
Seizures are common in cerebral malaria, particularly in children. The treatment of
convulsions in cerebral malaria with intravenous (or, if not possible, rectal) benzodiazepines
or intramuscular paraldehyde is similar to that for repeated seizures from any cause. In a large
double-blind placebo-controlled evaluation of a single intramuscular injection of 20 mg/kg bw
of phenobarbital (phenobarbitone) in children with cerebral malaria there was a reduction
in seizures but a significant increase in mortality in phenobarbital recipients. This resulted from
respiratory arrest, and was associated with additional benzodiazepine use. Clearly the 20
mg/kg dose of phenobarbital should not be given without respiratory support, but it is not
known, whether a lower dose would be effective and safer or whether, if ventilation is given,
mortality would not be increased. In the absence of further information, prophylactic
anticonvulsants are not recommended.
Interventions: phenobarbital i.v.
Summary of RCTs: systematic review of three trials. In the two trials with adequate
blinding, death was more common with phenobarbital.
Expert comment: no additional information.
Basis of decision: systematic review.
Recommendation: avoid routine use of phenobarbital
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Use of anticonvulsants
337
Concomitant use of antibiotics
The threshold for administering antibiotic treatment should be low in severe malaria.
Septicaemia and severe malaria are associated and there is diagnostic overlap, particularly
in children. Unexplained deterioration may result from a supervening bacterial infection.
Although enteric bacteria (notably Salmonella) have predominated in most trial series, a
variety of bacteria have been cultured from the blood of patients diagnosed as having severe
malaria, and so broadspectrum antibiotic treatment should be given initially.
EVIDENCE: trials on use of phenobarbital for the treatment of
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Treatment during pregnancy
338
Pregnant women, particularly in the second and third trimesters of pregnancy are more likely
to develop severe malaria than other adults, often complicated by pulmonary oedema and
hypoglycaemia. Maternal mortality is approximately 50%, which is higher than in nonpregnant adults. Fetal death and premature labour are common. The role of early Caesarean
section for the viable live fetus is unproven, but is recommended by many authorities.
Obstetric advice should be sought at an early stage, the paediatricians alerted, and blood
glucose checked frequently. Hypoglycaemia should be expected and is often recurrent if the
patient is receiving quinine. Antimalarials should be given in full doses. Severe malaria may
also present immediately following delivery. Postpartum bacterial infection is a common
complication in these cases. Falciparum malaria has also been associated with severe midtrimester haemolytic anaemia in Nigeria. This often requires transfusion, in addition to
antimalarial treatment and folate supplementation.
Parenteral antimalarials should be given to pregnant women with severe malaria in full
doses without delay. Artesunate or artemether are preferred over quinine in the second and
third trimesters because quinine is associated with recurrent hypoglycaemia. Recent evidence
shows that in non pregnant adults with severe malaria in areas of low transmission,
artesunate was superior to quinine, reducing mortality by 35% compared to quinine, which
makes artesunate the preferred option in the second and third trimesters. In the first trimester,
the risk of hypoglycaemia associated with quinine is lower, and the uncertainties over the
safety of the artemisinin derivatives are greater.
However, weighing these risks against the above evidence in favour of the efficacy of
artesunate, and until more evidence becomes available, both artesunate and quinine may
be considered as options. Treatment must not be delayed so if only one of the drugs
artesunate, artemether or quinine is available it should be started immediately.
Interventions: oral AS+MQ, oral CQ alone, oral quinine, oral
quinine+clindamycin
Summary of RCTs: four randomized and two quasi-randomized trials with 513 pregnant
participants. There were fewer treatment failures with AS+MQ than with quinine in one
trial (day 63: RR: 0.09; 95% CI: 0.02–0.38; 106 participants). Data for other comparisons
are scant. Where trials reported adverse outcomes, there were no differences reported
between treatments in terms of effect on the mother or the fetus.
Expert comment: systematic summaries of safety suggest that the artemisinin derivatives are
safe in the second and third trimesters of pregnancy. One large observational study in
Thailand suggests an increased risk of stillbirth associated with MQ but this was not found
in a study conducted in Malawi. There are as yet insufficient safety data about the use
of artemisinin derivatives in the first trimester of pregnancy.
Basis of decision: expert opinion.
Recommendations: for the first trimester of pregnancy: quinine +/– clindamycin.
For second and third trimesters:
1. the ACT being used in the country/region, or
2. artesunate + clindamycin,
3. quinine + clindamycin.
SUMMARY OF RECOMMENDATIONS FOR PREGNANT WOMEN
First trimester: quinine + clindamycina to be given for 7 days. ACT should be used if it
is the only effective treatment available.
Second and third trimesters: ACT known to be effective in the country/region or
artesunate + clindamycin to be given for 7 days or quinine + clindamycin to be given for 7 days.
Management of severe falciparum malaria in epidemic situations will often take place in
temporary clinics or in situations in which staff shortages and high workloads make intensive
care monitoring difficult. Drug treatment should therefore be as simple and safe as possible,
with simple dosing schedules and a minimum need for monitoring. Artesunate has been
shown to reduce mortality of severe malaria, but with the current artesunate formulation,
drawing the drug into a syringe takes two dissolution-dilution steps. In some circumstances
this may not be possible. Parenteral quinine requires either intravenous infusions or a three
times a day intramuscular regimen, plus monitoring of blood glucose.
Thus the simple once a day regimens and the ease of drawing up and administering
intramuscular artemether make this a suitable alternative for severe malaria in most epidemic
situations. Experience with artesunate suppositories in epidemic situations is limited. Their
use may be appropriate in severely ill patients who are unable to swallow oral medication
when intramuscular artemether (or quinine by intravenous infusion) is unavailable. If
artesunate suppositories are used, patients should be moved as soon as possible to a facility
where intramuscular or intravenous therapy can be started.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Management in epidemic situations
339
Interventions: AS, artemether, quinine (all parenteral)
Summary of RCTs: none.
Expert comment: complications of severe malaria are more frequent in pregnant women than
in non-pregnant adults. Artesunate reduces the mortality of severe malaria in non
pregnant adults compared with quinine in low transmission situations. The artemisinin
derivatives (artesunate and artemether) may also have safety advantages compared with
quinine in the second and third trimesters of pregnancy because they do not cause
recurrent hypoglycaemia. In the first trimester, the risk of hypoglycaemia associated with
quinine is lower, and the uncertainties over the safety of the artemisinin derivatives are
greater.
Basis of decision: expert opinion.
Recommendation: use the parenteral antimalarial treatment locally available for severe
malaria in full doses. Where available, AS is the first, and artemether the second option in
the second and third trimesters. In the first trimester, until more evidence becomes
available, both artesunate and quinine may be considered as options. When the patient
cannot be moved, continued treatment with rectal artesunate is appropriate until oral
drugs can be taken. It is essential that a full course of antimalarial treatment is completed.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Hyperparasitaemia
340
Patients with high parasite counts are known to be at increased risk of dying, although the
relationship between parasite counts and prognosis varies at different levels of malaria
endemicity. Many hyperparasitaemic patients have evidence of vital organ dysfunction but
there is a large subgroup in which no other manifestations of severe disease are present. These
patients have symptoms and signs compatible with a diagnosis of uncomplicated malaria in
association with a high parasite count (sometimes termed uncomplicated hyperparasitaemia).
The relevance for treatment is firstly the increased risk of progressing to severe malaria, and
secondly the generally higher treatment failure rates. This is of particular concern as resistance
to antimalarials is most likely to arise in patients with heavy parasite burdens and little or
no immunity.
In a low-transmission area in north-west Thailand, the overall mortality of uncomplicated
falciparum malaria was 0.1%, but in patients with parasitaemia of >4% it was 3%. In areas
of moderate or high transmission, much higher parasitaemias are often well tolerated,
however. There is not enough evidence to provide a firm recommendation on the definition
of hyperparasitaemia, although >5% parasitaemia in a low-transmission setting and >10% in
a higher transmission setting are commonly used.
Treatment of hyperparasitaemia
Available evidence indicates that use of oral treatment under close supervision is effective
in the treatment of patients with hyperparasitaemia who have no other features of severe
malaria. Parenteral treatment should, however, be substituted at any time if there is concern.
The rapidity of action of the artemisinin derivatives makes them ideal drugs. The standard
treatment course should be given, as there is insufficient information on the safety of higher
doses of the partner drug. Alternatively, the first dose of artemisinin derivative can be given
parenterally or rectally to ensure adequate absorption, followed by a full course of ACT.
Mefloquine-containing regimens in which the tablets are dispensed separately should be given
such that mefloquine is given on days 2 and 3, rather than day 1, when it is better tolerated,
with a lower incidence of early vomiting.
The optimum duration of treatment for hyperparasitaemia is still unresolved. Data to
support the suggestion that patients should be treated conservatively with 7 days of an
artemisinin derivative, plus a full course of partner medicine (e.g. artesunate 7 days +
mefloquine 25 mg/kg bw divided over 2 days) are lacking. A longer ACT course than is
recommended for uncomplicated malaria may not be possible in places where only fixed-dose
combinations are available.
SUMMARY OF RECOMMENDATIONS ON THE TREATMENT OF HYPERPARASITAEMIA
IN FALCIPARUM MALARIA
➠ patients must be monitored closely for the first 48 h after the start of treatment,
➠ if the patient does not retain oral medication, parenteral treatment should be given
without delay.
Non-immune patients with parasitaemia of >20% should receive parenteral antimalarial
treatment.
Treatment of malaria caused
by P. vivax, P. Ovale or P. malariae
P. vivax, the second most important species causing human malaria, accounts for about 40%
of malaria cases worldwide and is the dominant malaria species outside Africa. It is prevalent
in endemic areas in the Middle East, Asia, Oceania and Central and South America. In Africa,
it is rare except in the Horn and it is almost absent in West Africa. In most areas where P. vivax
is prevalent, malaria transmission rates are low, and the affected populations therefore
achieve little immunity to this parasite. Consequently, people of all ages are at risk.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Hyperparasitaemic patients with no other signs of severe disease should be treated with
oral artemisinin derivatives under the following conditions:
341
The other two human malaria parasite species P. malariae and P. ovale are generally less
prevalent but are distributed worldwide especially in the tropical areas of Africa. Among the
four species of Plasmodium that affect humans, only P. vivax and P. ovale form hypnozoites,
parasite stages in the liver that can result in multiple relapses of infection, weeks to months
after the primary infection. Thus a single infection causes repeated bouts of illness. This affects
the development and schooling of children and debilitates adults, thereby impairing human
and economic development in affected populations. The objective of treating malaria caused
by P. vivax and P. ovale is to cure both the blood stage and the liver stage infections, and
thereby prevent both relapse and recrudescence.
This is called radical cure. Infection with P. vivax during pregnancy, as with P. falciparum,
reduces birth weight. In primigravidae, the reduction is approximately two-thirds of that
associated with P. falciparum (110 g compared to 170 g), but this adverse effect does not
decline with successive pregnancies as with P. falciparum infections. Indeed, in the one large
series in which this was studied, it increased. Reduction in birth weight (<2500 g) increases
the risk of neonatal death.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Diagnosis
342
The clinical features of uncomplicated malaria are too non-specific for a clinical diagnosis
of the species of malaria infection to be made. Diagnosis of P. vivax malaria is based on
microscopy. Although rapid diagnostic tests based on immunochromatographic methods are
available for the detection of non-falciparum malaria, their sensitivities below parasite
densities of 500/Ìl are low. Their relatively high cost is a further impediment to their wide use
in endemic areas. Molecular markers for genotyping P. vivax parasites have been developed
to assist epidemiological and treatment studies but these are still under evaluation.
Susceptibility of P. vivax, P. ovale and P. malariae to antimalarials
There are very few recent data on the in vivo susceptibility of P. ovale and P. malariae to
antimalarials. Both species are regarded as very sensitive to chloroquine, although there is a
single recent report of chloroquine resistance in P. malariae. Experience indicates that P. ovale
and P. malariae are also susceptible to amodiaquine, mefloquine and the artemisinin
derivatives. Their susceptibility to antifolate antimalarials such as sulfadoxine-pyrimethamine
is less certain. P. vivax susceptibility has been studied extensively, and now that short-term
culture methodologies have been standardized, clinical studies have been supported by in
vitro observations. P. vivax is still generally very sensitive to chloroquine, although resistance
is prevalent and increasing in some areas, notably Oceania, Indonesia and Peru. Resistance
to pyrimethamine has increased rapidly in some areas, and sulfadoxinepyrimethamine is
consequently ineffective. There are insufficient data on current susceptibility to proguanil and
chlorproguanil, although resistance to proguanil was selected rapidly when it was first used
in P.vivax endemic areas.
In general, P. vivax is sensitive to all the other antimalarial drugs; it is more sensitive than
P. falciparum to the artemisinin derivatives, and slightly less sensitive to mefloquine (although
mefloquine is still effective). In contrast to P. falciparum, asexual stages of P. vivax are
susceptible to primaquine. Thus chloroquine + primaquine can be considered as a combination
treatment. The only drugs with significant activity against the hypnozoites are the 8aminoquinolines (bulaquine, primaquine, tafenoquine). There is no standardized in
vitromethod of drug assessment for hypnozoiticidal activity. In vivo assessment suggests that
tolerance of P. vivax to primaquine in East Asia and Oceania is greater than elsewhere.
Treatment of uncomplicated vivax malaria
There have been fewer studies on the treatment of malaria caused by P. vivax than of
falciparum malaria – only 11% of 435 published before 2004. For
chloroquine-sensitive
vivax malaria (i.e. in most places where P. vivax is prevalent) the conventional oral chloroquine
dose of 25 mg base/kg bw is well tolerated and effective. Some have advocated lower total
doses, but this is not recommended as it might encourage the emergence of resistance.
Chloroquine is given in an initial dose of 10 mg base/kg bw followed by either 5 mg/kg bw at
6 h, 24 h and 48 h or, more commonly, by 10 mg/kg bw on the second day and 5 mg/kg bw
on the third day. It is also clear that if ACT treatment is given, the response is as good as or
better than in falciparum malaria. The exception to this is a regimen containing sulfadoxinepyrimethamine. It appears that P. vivax has developed resistance to sulfadoxinepyrimethamine more rapidly than has P. falciparum, so that artesunate + sulfadoxine
pyrimethamine may not be effective against P. vivax in many areas.
Chloroquine-resistant vivax malaria
There are relatively few data on treatment responses in chloroquine-resistant vivax
malaria. Studies from Indonesia indicate that amodiaquine is efficacious, and there is some
evidence that mefloquine and quinine can also be used. The artemisinin derivatives would also
be expected to be highly effective, and artemether-lumefantrine could be an alternative
treatment. However, there are insufficient clinical data to confirm this.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Blood stage infection
343
Liver stage infection
To achieve radical cure, relapses must be prevented by giving primaquine. The frequency
and pattern of relapses varies geographically, however. It has become clear in recent years that
whereas 50–60% of P. vivax infections in South- East Asia relapse, the frequency is lower in
Indonesia (30%) and the Indian subcontinent (15–20%). Some P. vivax infections in the Korean
peninsula (now the most northerly of human malarias) have an incubation period of nearly
one year. Thus the preventive efficacy of primaquine must be set against the prevalent relapse
frequency. It appears that the total dose of 8-aminoquinoline given is the main determinant
of curative efficacy against liver-stage infection.
There is no evidence that the short courses of primaquine widely recommended (such as
5-day regimens) have any efficacy. Primaquine should be given for 14 days. The usual adult
oral dose is 15 mg base (0.25 mg/kg bw per day) but in South-East Asia, particularly Indonesia,
and in Oceania, higher doses (0.5 mg base/kg bw per day) are required. Primaquine causes
abdominal discomfort when taken on an empty stomach; it should always be taken with food.
There has been debate as to whether primaquine should be given in endemic areas.
Repeated vivax malaria relapses are debilitating at any age, but if reinfection is very frequent,
then the risks of widespread use of primaquine may exceed the benefits. In low-transmission
areas, the benefits of deploying primaquine are considered to exceed the risks, but in areas
of sustained high transmission (such as on the island of New Guinea), P. vivax infection is very
frequent, immunity is acquired, and the risks of widespread deployment of primaquine are
considered to outweigh the benefits.
MALARIA CARE, HEALTH POLICY AND RESEARCH
PRIMAQUINE AND GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY
344
The inherited sex-linked deficiency in glucose-6-phosphate dehydrogenase (G6PD) is
associated with some protection against falciparum malaria, but increased susceptibility to
oxidant haemolysis. The prevalence of G6PD deficiency varies but can be as high as 30%.
There are many different genotypes, each with different levels of deficiency. Primaquine is an
oxidant and causes variable haemolysis in G6PD-deficient individuals. Fortunately primaquine
is eliminated rapidly and so haemolysis is self-limiting provided no further medicine is taken.
Screening for G6PD deficiency is not generally available outside hospitals, although rapid tests
are under development. Many patients are therefore unaware of their G6PD status. If a
patient is known to be severely G6PD deficient then primaquine should not be given. For
the majority of patients with mild variants of the deficiency, primaquine should be given in
a dose of 0.75 mg base/kg bw once a week for 8 weeks. If significant haemolysis occurs on
treatment then primaquine should be stopped.
SUMMARY OF RECOMMENDATIONS ON THE TREATMENT OF UNCOMPLICATED VIVAX MALARIA
Chloroquine 25 mg base/kg bw divided over 3 days, combined with primaquine 0.25 mg
base/kg bw, taken with food once daily for 14 days is the treatment of choice for chloroquine-
sensitive infections. In Oceania and South-East Asia the dose of primaquine should be 0.5
mg/kg bw.
Amodiaquine (30 mg base/kg bw divided over 3 days as 10 mg/kg bw single daily doses)
combined with primaquine should be given for chloroquine-resistant vivax malaria.
In moderate G6PD deficiency, primaquine 0.75 mg base/kg bw should be given once a
week for 8 weeks. In severe G6PD deficiency, primaquine should not be given.
Where ACT has been adopted as the first-line treatment for P. falciparum malaria, it may
also be used for P. vivax malaria in combination with primaquine for radical cure. Artesunate
+ sulfadoxine-pyrimethamine is the exception as it will not be effective against P. vivax in
many places.
Treatment of severe vivax malaria
Treatment of malaria caused by P. ovale and P. malariae
Resistance of P. ovale and P. malariae to antimalarials is not well characterized and
infections caused by these two species are considered to be generally sensitive to chloroquine.
Only one study, conducted in Indonesia, has reported resistance to chloroquine in P. malariae.
The recommended treatment for the relapsing malaria caused by P. ovale is the same as that
given to achieve radical cure in vivax malaria, i.e. with chloroquine and primaquine. P. malariae
should be treated with the standard regimen of chloroquine as for vivax malaria, but it does
not require radical cure with primaquine as no hypnozoites are formed in infection with this
species.
P.ovale mainly occurs in areas of high stable transmission where the risk of re-infection
is high. In such settings, primaquine treatment is not indicated.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Although P. vivax malaria is considered to be a benign malaria, with a very low casefatality ratio, it may still cause a severe and debilitating febrile illness. It can also very
occasionally result in severe disease as in falciparum malaria. Severe vivax malaria
manifestations that have been reported are cerebral malaria, severe anaemia, severe
thrombocytopenia and pancytopenia, jaundice, spleen rupture, acute renal failure and acute
respiratory distress syndrome.
Severe anaemia and acute pulmonary oedema are not uncommon. The underlying
mechanisms of severe manifestations are not well understood. Prompt and effective
treatment and case management should be the same as for severe and complicated falciparum
malaria.
345
Monitoring therapeutic efficacy for vivax malaria
The antimalarial sensitivity of vivax malaria needs monitoring, to track and respond to
emerging resistance to chloroquine. The 28-day in vivo test for P. vivax is similar to that for P.
falciparum although the interpretation is slightly different. Genotyping may distinguish a
reinfection from a recrudescence and from acquisition of a new infection, but it is not possible
to distinguish reliably between a relapse and a recrudescence as they derive from the same
infection. If parasitaemia recurs within 16 days of administering treatment then relapse is
unlikely, but after that time, relapse cannot be distinguished from a recrudescence. Any P.
vivax infection that recurs within 28 days, whatever its origin, must be resistant to chloroquine
(or any other slowly eliminated antimalarial) provided adequate treatment has been given. In
the case of chloroquine, adequate absorption can be confirmed by measurement of the whole
blood concentration at the time of recurrence. Any P. vivax infection that has grown in vivo
through a chloroquine blood concentration 100 ng/ml must be chloroquine resistant. Shortterm in vitro culture allows assessment of in vitro susceptibility. There are no molecular
markers yet identified for chloroquine resistance. Antifolate resistance can be monitored by
molecular genotyping of the gene that encodes dihydrofolate reductase (Pvdhfr).
MALARIA CARE, HEALTH POLICY AND RESEARCH
Mixed malaria infections
346
Mixed malaria infections are common. In Thailand, despite low levels of malaria
transmission, one-third of patients with acute P. falciparum infection are co-infected with P.
vivax, and 8% of patients with acute vivax malaria have simultaneous P. falciparum infection.
Mixed infections are underestimated by routine microscopy. Cryptic P. falciparum infections
can be revealed in approximately 75% of cases by the RDTs based on the histidine-rich protein
2 (HRP2) antigen, but such antigen tests are much less useful (because of their lower
sensitivity) in detecting cryptic vivax malaria. ACTs are effective against all malaria species and
are the treatment of choice. Radical treatment with primaquine should be given to patients
with confirmed P. vivax and P. ovale infections except in high transmission settings where the
risk of re-infection is high.
Complex emergencies and epidemics
When large numbers of people are displaced within malaria endemic areas there is an
increased risk of a malaria epidemic, especially when people living in an area with little or
no malaria transmission move to an endemic area (e.g. displacement from highland to lowland
areas). The lack of protective immunity, concentration of population, breakdown in public
health activities and difficulties in accessing insecticides, insecticide-treated nets and effective
treatment, all conspire to fuel epidemic malaria, in which morbidity and mortality are often
high. Such circumstances are also ideal for the development of resistance to antimalarials. For
these reasons, particular efforts must be made to deliver effective antimalarial treatment to
the population at risk.
Diagnosis
In epidemic and complex emergency situations, facilities for laboratory diagnosis may be
either unavailable or so overwhelmed with the case-load that parasite-based diagnosis is
impossible. In such circumstances, it is impractical and unnecessary to demonstrate parasites
before treatment in all cases of fever.
Once an epidemic of malaria has been confirmed, and if case numbers are high, treatment
based solely on the clinical history is appropriate in most cases, using a full treatment course.
However, parasite-based diagnosis is essential to:
➠ diagnose the cause of an epidemic of febrile illness,
➠ monitor and confirm the end of an epidemic,
➠ follow progress in infants, pregnant women, and those with severe malaria.
Use of rapid diagnostic tests in epidemic situations
RDTs offer the advantage of simplicity and speed in epidemic situations, but heat stability
may be a problem and false-negative results may be seen. A negative result should not
automatically preclude treatment, especially in severe clinical disease. Current experience with
RDTs indicates that they are useful for confirming the cause and end-point of malaria
epidemics, but they should not be relied on as the sole basis for treatment. They should also
be backed up with adequate quality assurance, including temperature stability testing.
MALARIA CARE, HEALTH POLICY AND RESEARCH
As the epidemic wanes, the proportion of fever cases investigated parasitologically can be
increased. It is important to monitor the clinical response to treatment wherever possible,
bearing in mind that other infections may also be present. In mixed falciparum/vivax
epidemics, parasitaemia should be monitored in order to determine a species-specific
treatment.
347
Eradication efforts and prospects
Some 35 years after the effort to eradicate malaria worldwide was abandoned, malaria
elimination features again on the global health agenda. In recent years, an increasing number
of countries with low and moderate transmission areas have decided to eliminate malaria
transmission from their entire territory. In January 2007, the United Arab Emirates was the
fi rst formerly endemic country since the 1980s to be certifi ed by the World Health
Organization (WHO) as malaria-free. Certification of malaria elimination is granted to
countries that have successfully maintained their malaria-free status for a period of at least
three years. It is recognition of a considerable operational achievement.
Effective malaria elimination programmes set realistic targets and follow a comprehensive
and funded plan of action, backed up by government commitment at the highest levels. Such
programmes:
MALARIA CARE, HEALTH POLICY AND RESEARCH
➠
➠
➠
➠
➠
➠
348
detect and cure malaria patients;
interrupt local mosquito-borne malaria transmission;
identify and clear up residual foci of malaria transmission;
develop and implement vigilance systems for maintaining the malaria-freestatus;
prevent re-establishment of transmission despite continuing importation of parasites;
collaborate with neighbouring endemic countries to reduce malaria transmission in the
region.
Malaria elimination evolves from a successful countrywide malaria control effort that has
been able to eliminate malaria as a public health problem. In its early phases, the elimination
programme temporarily becomes a specialized vertical programme that focuses on the spatial
distribution of malaria, vector control, case-fi nding and case investigation. When the goal of
elimination is almost reached, the focus shifts back to the general health services, which are
key to a good vigilance system.
Malaria transmission is particularly diffi cult to interrupt in areas with effi - cient mosquito
vectors, a long or year-round transmission season, poor state of overall development,
marginalized populations and weak health systems with inadequate coverage of health
services, as well as in areas with civil unrest, illegal cross-border movement, or areas that
border high-burden neighbouring countries and experience intense cross-border population
movement. Each of these factors will reduce the feasibility of malaria elimination.
Malaria elimination cannot be detached from overall development efforts, including the
2015 Millennium Development Goals. Most countries that have successfully achieved
interruption of malaria transmission have also achieved an improvement in the overall
socioeconomic situation, health services coverage and living standards of the population. The
4. Adapted from: Malaria elimination: a field manula for loe and moderate endemic countries, WHO, 2007.
MALARIA CARE, HEALTH POLICY AND RESEARCH
malaria-free status adds to these developments by removing barriers to investment and tourism.
The aims of the global fight against malaria are not only to (i) reduce the burden of malaria
in endemic areas, but also (ii) reduce and confi ne the geographical extent of malaria-endemic
areas in the world. The latter entails the elimination of malaria from countries and localities
where this is feasible. The elimination of malaria is indeed the end goal of the fi ght against
the disease, and is a process which starts with good malaria control.
An increasing number of endemic countries have been successful in interrupting local
mosquito-borne malaria transmission – seen as vital for public health, business and tourism.
Others have reduced their malaria burden to levels where elimination is a possibility. Of the
107 malaria-endemic countries and areas worldwide, 7 are currently reporting no more locally
acquired infections. In January 2007, the United Arab Emirates was offi cially certifi ed by
the World Health Organization (WHO) as malaria-free, a fi rst since Australia and Singapore
in the 1980s.
The aim of an elimination programme is to identify and treat all people who carry malaria
parasites in their blood and reduce the onward transmission of infection. As part of essential
programmatic elimination requirements, malaria transmission hot spots are identifi ed and
mapped by the national programme.
Targeted, custom-tailored mosquito control interventions are used to reduce the vectorial
capacity and human–vector contact in these areas, and eventually halt transmission
nationwide.
In the continuum from malaria control to elimination, two important programme
reorientations take place. The fi rst starts once high coverage with effective malaria control
interventions and overall socioeconomic development are starting to reduce transmission to
a marginal level, with a patchy and focalized geographical spread. At that point, coverage
of good-quality laboratory and clinical services, reporting and surveillance must be reinforced,
followed by other programme adjustments aimed at halting transmission nationwide.
The second programme reorientation starts when locally acquired malaria cases are close
to zero, and malaria parasites that are brought into the coun try by people who became
infected abroad may pose a bigger threat of continuation or resumption of transmission than
the last dwindling local parasite strains. The prevention of re-establishment of local malaria
transmission from imported cases relies heavily on the watchfulness of the general health
services, under the guidance of a small group of malaria experts at central level backed up
by national and local authorities, in collaboration with other sectors such as private industry,
tourism and foreign affairs. Nationals who plan to travel abroad are provided with health
information, chemoprophylaxis and measures to protect against mosquito bites, aimed at
reducing the importation of parasites at source. Visitors and migrants from endemic areas are
informed of the risks of malaria and given easy access to free-of-charge diagnostic and
treatment facilities. Vector control is used to contain local outbreaks and protect areas that
are known to be receptive to the resumption of transmission as well as exposed to frequent
importation of malaria parasites.
349
Once a country is proven to be free from local transmission for at least three consecutive
years, WHO can grant certifi cation of its malaria-free status. The world is increasingly
interconnected. When malaria is eliminated from a country, it still remains at risk from
imported cases. The dedication of both the government and programme personnel that was
necessary to eliminate malaria must be sustained so that the requisite knowledge and skills
are maintained and the health service organized in such a way that these attributes can be
used as and when necessary. Continuous active involvement of local authorities with budget
power1 will be required, as well as engagement from the tourism and construction industries
and other private sectors that employ immigrants from endemic countries or respond to an
infl ux of refugees, as well as agricultural businesses and others designing projects that have
an environmental impact. It will be the role of the ministry of foreign affairs to increase
intercountry collaboration on malaria and the role of regional political or socioeconomic
powers to boost regional approaches for malaria control.
Transitions from malaria control to elimination
HIGH TRANSMISSION AREAS
MALARIA CARE, HEALTH POLICY AND RESEARCH
In areas where the geographical distribution of malaria cases is country- or area-wide, the
prime objective is to reduce malaria mortality, morbidity and transmission intensity. In these
areas, the malaria control programme should make all possible eff orts to achieve universal
coverage of cost-eff ective preventive and treatment interventions.
In addition, monitoring, health information systems, and intercountry and crossborder
collaboration are critical to reduce the burden of malaria to consistently less than 5% of all
patients with febrile disease.
350
LOW TRANSMISSION AREAS
In some areas, natural conditions and/or control eff orts have limited the transmission
intensity to a marginal point where risk is low and localized in well-defi ned geographical
areas. An almost universal access to antimalarial measures and their documented impact
on the malaria burden make it possible to envision programme reorientation towards
elimination. The fi rst aim at this pre-elimination stage is to reduce the malaria burden to
manageable levels at an annual malaria incidence of less than 1 case per 1000 people at risk.
This is achievable by perfecting the quality and targeting of case management and vector
control operations, and introducing/ maintaining activities aimed at consistently reducing
the onward transmission from existing cases in residual and new active foci. A strong
surveillance system, with the cooperation of all health-care providers, must be established
at this stage. These areas can subsequently aim to halt local malaria transmission through
incremental stages.
AREAS WHERE TRANSMISSION HAS BEEN INTERRUPTED
In areas where interruption of malaria transmission has been achieved, the goal will be to
prevent re-establishment of local transmission through prevention of onward transmission
from imported cases. Once the entire country has been free from local malaria transmission
for three consecutive years, the process for certification of the malaria-free status can be
started.
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ñ Bloland PB, Wirima JJ, Steketee RW, Chilima B, Higtower A, Breman JG: Maternal HIV infection
and infant mortality in Malawi: evidence for increased mortality due to placental malaria infection.
AIDS. 1995; 9(7):721-726.
ñ Mount AM, Mwapasa V, Elliott SR, Beeson JG, Tadesse E, Lema VN, Molyneux ME, Meshnick SR,
Rogerson SJ: Impairnment of humoral immunity to P. falciparum malaria in pregnancy by HIV
infection. Lancet. 2004;4:363(9424)1860-1867.
ñ Ter Kuite FO, Parise ME, Verhoeff FH, Udhayakumar V, Newman RD, van Eijk AM et al: The burden
of coinfection with human immunodeficiency virus type 1 and malaria in pregnant women in subSaharan Africa. Am J Trop Med Hyg. 2004; 71(2 suppl):41-54.
ñ Kublin JG, Patnaik P, Jere CS, Miller WC, Hoffman IF, Chimbiya N et al: Effect of P. falciparum malaria
on concentration of HIV-1-RNA in the blood of adults in rural Malawi: a prospective cohort study.
MALARIA CARE, HEALTH POLICY AND RESEARCH
Lancet. 2005;15:365(9455): 233-240.
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chapter 8
Vaccination programmes
and campaigns
in emergencies
Outline the principles of vaccination programs and the delivery of campaigns in emergency
situations.
Specific Objectives
At the end of the session, participants will be familiar with:
➠ Principles of vaccination programs
➠ Vaccination campaigns in emergency situations
Content
➠ Vaccination programmes
➠ Vaccination campaigns delivery models in emergency situations:
ñ Measles
ñ Meningococcal meningitis
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
General Objective
353
Immunization against diseases
of public health importance1
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
The benefits of immunization
354
Vaccines –which protect against disease by inducing immunity– are widely and routinely
administered around the world based on the common-sense principle that it is better to keep
people from falling ill than to treat them once they are ill. Suffering, disability, and death
are avoided. Immunization averted about two million deaths in 2002. In addition, contagion
is reduced, strain on health-care systems is eased, and money is frequently saved that can
be used for other health services.
Immunization is a proven tool for controlling and even eradicating disease. An
immunization campaign carried out by the World Health Organization (WHO) from 1967 to
1977 eradicated the natural occurrence of smallpox. When the programme began, the disease
still threatened 60% of the world’s population and killed every fourth victim. Eradication of
poliomyelitis is within reach. Since the launch by WHO and its partners of the Global Polio
Eradication Initiative in 1988, infections have fallen by 99%, and some five million people have
escaped paralysis. Between 1999 and 2003, measles deaths dropped worldwide by almost
40%, and some regions have set a target of eliminating the disease. Maternal and neonatal
tetanus will soon be eliminated in 14 of 57 high-risk countries.
New vaccines also have been introduced with significant results, including the first vaccine
to help prevent liver cancer, hepatitis B vaccine, which is now routinely given to infants in 77%
of WHO’s Member States. Rapid progress in the development of new vaccines means protection
will be available in the near future against a wider range of serious infectious diseases.
History
Introducing a small amount of smallpox virus by inhaling through the nose or by making a
number of small pricks through the skin (variolation) to create resistance to the disease
appears to have begun in the 10th or 11th century in Central Asia. The practice spread; in Asia
and Africa, the method was nasal, while in Europe it involved skin punctures. Variolation was
introduced into England in 1721. There, in 1798, Edward Jenner, having studied the success
of variolation with cowpox –a mild illness– in protecting against smallpox, began to carry out
1. Http:// www.who.int/mediacentre/factsheets/fs288/en/index.html
inoculations against smallpox, the first systematic effort to control a disease through
immunization.
In 1885, Louis Pasteur developed the first vaccine to protect humans against rabies.
Toxoids against diphtheria and tetanus were introduced in the early 1900s; the bacillus
Calmette-Guérin vaccine (against tuberculosis) in 1927; the Salk polio vaccine in 1955; and
vaccines against measles and mumps in the 1960s.
Routine vaccination is now provided in all developing countries against measles, polio,
diphtheria, tetanus, pertussis, and tuberculosis. To this basic package of vaccines, which served
as the standard for years, have come new additions. Immunization against hepatitis B is now
recommended by WHO for all nations, and currently is offered to infants in 147 of 192 WHO
Member States. Immunization against Haemophilus influenzae type b (Hib) is recommended
where resources permit its use and the burden of disease is established; it is provided in 89
countries (only in selected parts of two of those countries). Yellow fever vaccine is offered
in about two-thirds of the nations at risk for yellow fever outbreaks. Routine immunization
against rubella is provided in 111 countries.
In industrialized countries a wider span of protection is typically provided than in
developing countries, often including vaccines against influenza, predominant strains of
pneumococcal disease, and mumps (usually in combination with measles and rubella vaccine).
Immunization programmes may be aimed at adolescents or adults –depending on the disease
concerned– as well as at infants and children.
Global immunization coverage
Coverage has greatly increased since WHO’s Expanded Programme on Immunization began
in 1974. In 2003, global DTP3 (three doses of the diphtheria-tetanus-pertussis combination
vaccine) coverage was 78% – up from 20% in 1980. However, 27 million children worldwide
were not reached by DTP3 in 2003, including 9.9 million in South Asia and 9.6 million in subSaharan Africa. Those who miss out on routine vaccination programmes tend to be people
living in remote locations, urban slums and border areas. They also include indigenous groups,
displaced populations, those lacking access to vaccination because of various social barriers,
those lacking awareness or motivation to be vaccinated and those who refuse.
An estimated 2.1 million people around the world died in 2002 of diseases preventable by
widely used vaccines. This toll included 1.4 million children under the age of five. Among these
childhood deaths, over 500 000 were caused by measles; nearly 400 000 by Hib; nearly 300
000 by pertussis; and 180 000 by neonatal tetanus.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Commonly used vaccines
355
Vaccines under development
Numerous new vaccines with major potential for improving health in developing countries
are in the research and development pipeline. They include vaccines for rotavirus diarrhoea,
which kills 300 000 to 600 000 children under age five every year; human papillomavirus, a
leading cause of cervical cancer, which afflicts some 500 000 women each year, 80% of them
in developing countries; and pneumococcal disease, which causes a large fraction of the world’s
approximately two million annual deaths from childhood pneumonia. In addition, a conjugate
vaccine now in development should be much more effective against Group A meningococcal
disease (Men A), a frequently fatal form of meningitis that causes recurring epidemics in a
number of countries in sub-Saharan Africa. Several of these vaccines –those against rotavirus,
pneumococcal disease, and Men A– may be available in developing countries by 2008-2009.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
How vaccines work
356
Vaccines typically provide the immune system with harmless copies of an antigen: a
portion of the surface of a bacterium or virus that the immune system recognizes as “foreign.”
(An antigen often plays a role in causing disease – for example by enabling a virus or
bacterium to attach to cells.) A vaccine may also provide a non-active version of a toxin –a
poison produced by a bacterium– so that the body can devise a defence against it.
Once an antigen is detected by the immune system, white blood cells called B-lymphocytes
create a protein called an antibody that is precisely designed to attach to that antigen. Many
copies of this antibody are produced. If a true infection of the same disease occurs, still more
antibodies are created, and as they attach to their targets they may block the activity of the
virus or bacterial strain directly, thus combating infection. In addition, once in place, the
antibodies make it much easier for other components of the immune system (particularly
phagocytes) to recognize and destroy the invading agent.
Immune systems are designed to “remember” –once exposed to a particular bacterium or
virus, they retain immunity against it for years, decades, or even a lifetime– and so are prepared
to defeat a later infection, and to do so quickly. This ability, and the speed with which it occurs,
is a huge benefit: a body encountering a germ for the first time may need from seven to 12
days to mount an effective defence, and by then serious illness and even death may occur.
Types of vaccines
Vaccines come in different forms. The injected polio vaccine is a killed, intact virus; the oral
polio vaccine is a live, weakened virus. The vaccine for typhoid is a killed, intact bacteria.
Vaccines for measles and the other standard “childhood” diseases –mumps, chickenpox, and
rubella — are live, attenuated (or weakened) viruses. Vaccines for diphtheria and tetanus
consist of toxins that have been “inactivated.” Influenza vaccines often consist of killed,
“disrupted” viruses (that is, the proteins on the coat of the virus have been released into a
solution by solvents). Vaccines against Hib, pneumococcal disease, and meningococcal disease
consist of highly purified complex sugars taken from bacterial coats or capsules.
Vaccines are frequently administered as combinations of antigens. The most widely used
combinations are diphtheria-tetanus-pertussis (DTP); diphtheria-tetanus-pertussis-hepatitis B
(DTP-HepB); pentavalent vaccine: diphtheria-tetanus-pertussis-hepatitis B-Hib; and measlesmumps-and rubella (MMR).
All vaccines used for routine immunization are very effective in preventing disease,
although no vaccine attains 100% effectiveness. More than one dose of a vaccine is generally
given to increase the chance of developing immunity.
Vaccines are very safe, and side effects are minor – especially when compared to the
diseases they are designed to prevent. Serious complications occur rarely. For example, severe
allergic reactions result at a rate of one for every 100 000 doses of measles vaccine. Two to
four cases of vaccine-associated paralytic polio have been reported for every one million
children receiving oral polio vaccine.
The cost-effectiveness of immunization
Immunization is considered among the most cost-effective of health investments. There is
a well-defined target group; contact with the health system is only needed at the time of
delivery; and vaccination does not require any major change of lifestyle.
A recent study estimated that a one-week “supplemental immunization activity” against
measles carried out in Kenya in 2002 –in which 12.8 million children were vaccinated– would
result in a net saving in health costs of US$ 12 million over the following ten years; during
that time it would prevent 3 850 000 cases of measles and 125 000 deaths. In the United
States, cost-benefit analysis indicate that every dollar invested in a vaccine dose saves US$
2 to US$ 27 in health expenses.
The cost of immunizing a child
In mid-1990s, vaccines to provide “basic” coverage for tuberculosis, polio, diphtheria,
tetanus, pertussis, and measles cost about US$ 1 per child. Inclusion of vaccines for hepatitis
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Effectiveness and safety
357
B and Hib, raises the vaccine cost alone to US$ 7-13 per child (not including administration
and injection equipment) in the developing world. When vaccine administration is included,
the costs amount to between US$ 20-40 per child. It has become a significant challenge for
low-income countries and international health agencies to find ways to introduce more highlypriced vaccines such as those for hepatitis B and Hib, which can greatly increase the costs of
national immunization programmes. With many new vaccines expected to be available in the
near future, issues of financing and financial sustainability will become ever more important.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Financing immunization
358
Many developing countries have difficulties affording vaccines. International initiatives such
as the Expanded Programme on Immunization and the Global Alliance for Vaccines and
Immunization (GAVI) have provided impetus, funding, and technical support that have helped
increase immunization coverage and the number of vaccines provided. The proposed WHOUNICEF Global Immunization Vision and Strategies, intended to run from 2006-2015, would
further this existing coordination, aim to expand vaccination coverage, and enable the
logistical systems set up for that purpose to provide other health care services as well.
The economics of vaccine development have tended to run against the interests of the
world’s poorer countries. Vaccines are much less profitable than medicines, and
pharmaceutical firms understandably have been reluctant to make the high investments
necessary to research and develop vaccines against infectious diseases, realizing that the
largest pool of potential customers are governments that likely could not afford to pay
enough for these products to ensure a profit. For the same reason, when new vaccines have
been developed, limited quantities often have been manufactured, increasing the cost per
dose. Part of the difficulty for manufacturers is in forecasting demand and in accounting for
various market uncertainties.
Steps have been taken to deal with these challenges. The UNICEF Vaccine Independence
Initiative, established in 1991, sets up a revolving fund for each participating country, allows
these countries to buy vaccines through UNICEF’s procurement system using local currencies,
and enables them to pay for the vaccines only after delivery. A more recent approach is to
guarantee a large market and a reasonable price in advance to pharmaceutical firms which
develop vaccines that will have great health benefits for poor nations. This “push-pull”
approach is being financed and progressively fine-tuned by a coalition of international donors,
bilateral aid programmes, private philanthropists, and some governments.
WHO immunization work
In the field of immunization WHO works with partners including governments, United
Nations agencies and other international organizations, bilateral government health and
development agencies, non-governmental organizations, professional groups and the private
sector. WHO’s specific responsibilities include:
➠
➠
➠
➠
Supporting and facilitating research and development;
Ensuring the quality and safety of vaccines;
Developing policies and strategies for maximizing the use of vaccines;
Reducing financial and technical barriers to the introduction of vaccines and
technologies; and
➠ Supporting countries in acquiring the skills and infrastructure needed to achieve
disease control and eradication.
Measles
Measles remains a major cause of childhood mortality throughout the world, especially in
developing countries. However, the disease can be prevented by vaccination. Measles
immunization has been established since the ‘70s as part of the Expanded Programme on
Immunization (EPI) and has significantly contributed to reducing child mortality. Despite a high
level of global vaccination coverage in 1993 (78%, WHO reporting), there were an estimated
45 million cases and 1.2 million deaths through out the world. One reason could be the wide
variation for vaccination coverage across regions: 19 countries, most of them in Africa, report
vaccine coverage below 50%.
Measles is one of the main contributors to child mortality and one of the most urgent
health problems in refugee populations. Measles outbreaks are frequent, especially in camp
settings as overcrowding is one of the most important risk factor for measles transmission.
Complications such as pneumonia, diarrhoea and croup are very common and case fatality
rates can reach very high figures, exceeding 10%.
However, high mortality due to measles is preventable, and mass immunization against
measles, coupled with vitamin A distribution, is one of the top priorities in the initial phase
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Vaccination campaigns delivery
models in emergency situations
359
of a refugee influx, even if refugees are coming from areas with high vaccination coverage
rates. The vaccine seems to offer good protection but not perfect as it protects 85% of
children if administered at the age of 9 months. This means that there is still a significant
number of people susceptible to measles and therefore vulnerable to outbreaks, given the
extreme infectiousness of the virus. It is therefore essential to aim for a coverage near 100%.
Objective
The objective of a mass vaccination campaign is to prevent measles outbreaks and in this
way to prevent avoidable deaths. To achieve this, it is essential to aim for 90-100% coverage
in the age group from 6 months to 15 years. If the outbreak occurs before the mass
vaccination campaign takes place, the objective is to prevent measles deaths as exposed
individuals can experience less severe disease if vaccinated within 3 days of exposure.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Target population
360
The vaccine has to be administered when there is no longer risk of interfering with
maternal antibodies in order to achieve optimal response. The recommended age of
vaccination according to EPI (Expanded Programme of Immunization) in developing countries
is from 9 months to 2-5 years. At 6 months vaccine efficacy drops from 85% (at 9 months)
to 50%. In refugee settings, overcrowding and other factors, increase the risk of infection
in young children and the severity of disease in all age groups. The target group has to be
expanded: 6 months to 15 years in the emergency phase. In open situations, the same age
group among the local population should also be immunized. However, every child that has
been vaccinated between 6 and 9 months of age, should receive a second dose after 9
months. Children up to 12-15 years of age should be included, as they are susceptible and
there is a shift to older groups recently. Measles related mortality and morbidity can be quite
high in this group, too. If an outbreak occurs, and if age groups older than 15 years of age are
affected, the target population can be expanded further. Measles vaccination is only contraindicated in pregnant women because the vaccine contains a live attenuated virus.
Malnutrition, HIV/AIDS, previous vaccination, infection are not contra-indications. A 2nd dose
given to children previously immunized provides an even better protection.
Planning an immunization campaign
The resources required to implement mass immunization should be available as soon as
refugees begin to gather on sites. One agency should take overall responsibility for the
programme and coordinate the various efforts involved. Responsibility for each component
of the programme needs to be clearly assigned to the different partners involved (health
agencies, Ministry of Health and local EPI representatives and refugee leaders). The national
EPI of the host country should be involved from the beginning.
Main tasks include:
➠
➠
➠
➠
➠
➠
Estimation of the target population
Obtain a map of the site
Define the vaccination strategies
Estimation of resources needed: staff, vaccines, equipment
Procurement and management of resources
Cold chain
Mass immunization campaign
➠
➠
➠
➠
➠
Training session 2-3 days before the campaign
Dissemination of information among the target population
Selection and preparation of immunization sites (1 or 2 sites for every 10,000 refugees)
Issue of individual cards for each child
Daily record of the numbers vaccinated per day
Fixed immunization sites should be integrated to existing health structures if available.
Evaluation is an integral part of the whole effort. Routinely collected data, vaccination
coverage survey and a study for vaccine efficacy (if failures are suspected) are various methods
to be used. Routinely collected data must always be evaluated, but vaccination coverage
survey and a study for vaccine efficacy do not have to be undertaken systematically after each
campaign, unless the accuracy of results is under question.
Meningococcal meningitis
Meningitis is an infection of the meninges, the thin lining that surrounds the brain and the
spinal cord. Several different bacteria can cause meningitis and Neisseria meningitidis is one
of the most important because of its potential to cause epidemics. Meningococcal disease was
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
One immunization team includes 20 people: 1 supervisor, 1 logistics officer, 4 staff
preparing vaccines, 2 staff members administering the vaccines, 6 staff members to register
and tally, 6 staff members to maintain order (crowd control). Such a team can immunize 500700 people/hour.
Main aspects of organization are:
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VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
362
first described in 1805 when an outbreak swept through Geneva, Switzerland. The causative
agent, Neisseria meningitidis (the meningococcus), was identified in 1887.
Large outbreaks of meningitis are exclusively due to meningococcus (Neisseria meningitides). More than 13 serogroups of meningococcus have been isolated and differ in epidemic
potential. Only serogroups A, B and C can cause outbreaks. The serogroups are divided into
serotypes, sub-types and clones. 90% of outbreaks are due to serogroup A. Serogroup B (in
Europe and South America) generally causes only sporadic cases or small outbreaks. Serogroup
C has been responsible for a few outbreaks in Africa, Asia and South America. Haemophilus
influenza and Streptococcus pneumoniae are other frequent causes of sporadic meningitis
cases and other etiologic agents can also be found.
Traditionally, most meningitis outbreaks occurred in the region described as the
“meningitis belt” in sub-Saharan Africa. Outbreaks used to occur every 8 to 12 years and
stopped at the onset of the rainy season. However, epidemiological patterns have changed
since the 80s and outbreaks increasingly occur in African countries located outside the
“meningitis belt”. This change may be due to the arrival of a new clone (Neisseria meningitis
serogroup A clone III-1), climate changes or increased mobility of the populations, including
refugee movements. It is now reported that epidemics occur at any time of the year and in
any region. There is increasing evidence of serogroup W135 being associated with outbreaks
of considerable size. In 2000 and 2001 several hundred pilgrims attending the Hajj in Saudia
Arabia were infected with N. meningitidis W135. Then in 2002, W135 emerged in Burkina
Faso, striking 13,000 people and killing 1,500.
The African meningitis belt
The highest burden of meningococcal disease occurs in sub-Saharan Africa, which is known
as the “Meningitis Belt”, an area that stretches from Senegal in the west to Ethiopia in the
east, with an estimated total population of 300 million people. This hyperendemic area is
characterized by particular climate and social habits. During the dry season, between
December and June, because of dust winds and upper respiratory tract infections due to
cold nights, the local immunity of the pharynx is diminished increasing the risk of meningitis.
At the same time, the transmission of N. meningitidis is favoured by overcrowded housing
at family level and by large population displacements due to pilgrimages and traditional
markets at regional level. This conjunction of factors explains the large epidemics which occur
during this season in the meningitis belt area. Due to herd immunity (whereby transmission
is blocked when a critical percentage of the population had been vaccinated, thus extending
protection to the unvaccinated), these epidemics occur in a cyclic mode. N. meningitidis A,
C and W135 are now the main serogroups involved in the meningococcal meningitis activity
in Africa.
In major African epidemics, attack rates ranges from 100 to 800 per 100 000 population,
How is the disease transmitted
The bacteria are transmitted from person to person through droplets of respiratory or
throat secretions. Close and prolonged contact (e.g. kissing, sneezing and coughing on
someone, living in close quarters or dormitories (military recruits, students), sharing eating or
drinking utensils, etc.) facilitate the spread of the disease. The average incubation period is
4 days, ranging between 2 and 10 days.
N. meningitidis only infects humans; there is no animal reservoir. The bacteria can be
carried in the pharynx and sometimes, for reasons not fully known, overwhelm the body’s
defences allowing infection to spread through the bloodstream and to the brain. It is
estimated that between 10 to 25% of the population carry N.meningitidis at any given time,
but of course the carriage rate may be much higher in epidemic situations.
The disease
The most common symptoms are stiff neck, high fever, sensitivity to light, confusion,
headaches and vomiting. Even when the disease is diagnosed early and adequate therapy
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
but individual communities have reported rates as high as 1000 per 100 000. While in endemic
disease the highest attack rates are observed in young children, during epidemics, older
children, teenagers and young adults are also affected.
In 1996, Africa experienced the largest recorded outbreak of epidemic meningitis in history,
with over 250 000 cases and 25 000 deaths registered. Between that crisis and 2002, 223,000
new cases of meningococcal meningitis were reported to the World Health Organization. The
countries most affected countries have been Burkina Faso, Chad, Ethiopia and Niger; in 2002,
the outbreaks occurring in Burkina Faso, Ethiopia and Niger accounted for about 65% of
the total cases reported in the African continent. Furthermore, the meningitis belt appears to
be extending further south. In 2002, the Great Lakes region was affected by outbreaks in
villages and refugees camps which caused more than 2,200 cases, including 200 deaths.
The population at risk is classically the age group below 30, in which 80% of cases occur.
Nevertheless, during epidemics in the 90’, clone Neisseria meningitis serogroup A clone III-1,
high attack rates and case fatality rates were reported in those of over 30 years (Uganda
and Burundi, 1992). The overall attack rate ranges from 10 to 1,000 per 100,000 and varies
widely. Variability may exist from one epidemiological week to another: a range from 30360 cases per 100,000 have been reported. The CFR (case fatality rate), without treatment can
reach 70%. With treatment varies from 5-15%. Outbreaks usually last 10-14 weeks, but can
vary from 4 to 20 weeks. The peak is normally reached 4 weeks after the onset (range:2-8
weeks).
363
instituted, 5% to 10% of patients die, typically within 24-48 hours of onset of symptoms.
Bacterial meningitis may result in brain damage, hearing loss, or learning disability in 10 to
20% of survivors. A less common but more severe (often fatal) form of meningococcal disease
is meningococcal septicaemia which is characterized by a haemorrhagic rash and rapid
circulatory collapse.
Diagnosis
The diagnosis of meningococcal meningitis is suspected by the clinical presentation and
a lumbar puncture showing a purulent spinal fluid; sometimes the bacteria can be seen in
microscopic examinations of the spinal fluid. The diagnosis is confirmed by growing the
bacteria from specimens of spinal fluid or blood. More specialised laboratory tests are needed
for the identification of the serogroups as well as for testing susceptibility to antibiotics.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Treatment
364
Meningococcal disease is potentially fatal and should always be viewed as a medical
emergency. Admission to a hospital or health centre is necessary. Isolation of the patient is
not necessary. Antimicrobial therapy must be commenced as soon as possible after the lumbar
puncture has been carried out (if started before, it may be difficult to grow the bacteria from
the spinal fluid and thus confirm the diagnosis).
A range of antibiotics may be used for treatment including penicillin, ampicillin,
chloramphenicol, and ceftriaxone. Under epidemic conditions in Africa, oily chloramphenicol
is the drug of choice in areas with limited health facilities because a single dose of this longacting formulation has been shown to be effective.
Prevention
Several vaccines are available to prevent the disease. Polysaccharide vaccines, which have
been available for over 30 years, exist against serogroups A, C, Y, W135 in various
combinations. A monovalent conjugate vaccine against serogroup C, has recently been
licensed in developed countries for use in children and adolescents. This vaccine is
immunogenic, particularly for children under 2 years of age whereas polysaccharide vaccines
are not. All these vaccines have been proven to be safe and effective with infrequent and mild
side effects. The vaccines may not provide adequate protection for 10 to 14 days following
injection.
Routine vaccination: Routine preventive mass vaccination has been attempted and its
effect has been extensively debated. Saudi Arabia, for example, offers routine immunization
of its entire population. Sudan and other countries routinely vaccinate school children.
Preventive vaccination can be used to protect individuals at risk (e.g. travellers, military,
pilgrims).
Protection of close contacts: When a sporadic case occurs, the close contacts need to be
protected by a vaccine and chemoprophylaxis with antibiotics to cover the delay between
vaccination and protection (see above). Antibiotics used for chemoprophylaxis are rifampicin,
minocycline, spiramycin, ciprofloxacin and ceftriaxone.
Vaccination for epidemic control: In the African Meningitis Belt context, enhanced
epidemiological surveillance and prompt case management with oily chloramphenicol are used
to control the epidemics. Routine immunization is not possible with the current available
vaccines as the polysaccharide vaccines provide protection for only three to five years and
cannot be used in children under 2 years of age because they lack the ability to develop
antibodies. Furthermore, even large scale coverage with current vaccines does not provide
sufficient “herd immunity”. Consequently, the current WHO recommendation for outbreak
control is to mass vaccinate every district that is in an epidemic phase, as well as those
contiguous districts that are in alert phase. It is estimated that a mass immunization campaign,
promptly implemented, can avoid 70 % of cases.
Emergence of W135: Bivalent AC vaccine is commonly used in Africa but the emergence
of N. meningitidis W135 as an epidemic strain involves revising this control strategy. A
tetravalent ACYW135 polysaccharide vaccine exists but its high price and limited availability
restricts its use in the African context. In 2003, WHO reached an agreement with a
manufacturer to produce an affordable polysaccharide vaccine for Africa which would protect
against A, C and W135 strains.
WHO’s strategy
WHO promotes a two-pronged strategy which involves epidemic preparedness and
epidemic response. Preparedness focuses on surveillance, from case detection and investigation and laboratory confirmation. This implies strengthening of surveillance and laboratory
capacity for early detection of epidemics, the establishment of national and sub-regional
stocks of vaccine, and the development or updating of national plans for epidemic
management (including preparedness, contingency and response). WHO regularly provides
technical support in the field, in the countries facing epidemics.
Following large outbreaks in Africa in 1995-96, WHO was instrumental in establishing the
International Coordinating Group (ICG) on Vaccine Provision for Epidemic Meningitis Control
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Vaccination use
365
to ensure rapid and equal access to vaccines, injection material and oily chloramphenicol, as
well as for their adequate use when the stocks are limited. The ICG is composed of partners
from the UN, including WHO, nongovernmental organizations, technical partners and the
private sector. WHO is committed to eliminating meningococcal disease as a public health
problem and ensuring control of sporadic cases through routine health services in the shortest
possible time. The only way to reach this goal will be with an improved vaccine. WHO supports
the development of such a vaccine.
Surveillance
Meningitis surveillance should always be part of the routine surveillance system to detect
any outbreak and initiate control measures at the earliest possible stage. There should be a
standard case definition. Lumbar puncture is necessary to confirm the diagnosis, and identify
the meningococcus in the first suspected cases. It must be remembered that clinical diagnosis
does not differentiate serogroup A meningococcal meningitis from other causes of sporadic
meningitis.
Suspected case:
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
➠ <12 months with fever and bulging fontanel
➠ >12 months and adults with sudden onset of fever with stiff neck and/or petechial
366
or purpular rash
Probable case:
➠ Suspected case with turbid CSF (with or without Gram stain)
➠ Suspected case with ongoing outbreak
Confirmed case:
➠ Suspected or probable case and CSF antigen detection (positive latex agglutination
test)
➠ Suspected or probable case with positive culture
The number of cases should be followed closely, and the data to be collected for each
patient should include full demographic data, onset, type of diagnosis (clinical, CSF etc),
treatment, outcome, immunization status and date of immunization. The number of case per
week per 100,000 refugees should be computed and compared with epidemic threshold and
age of cases is needed in order to define target groups for vaccination campaign.
Outbreak identification and control
In an outbreak prioritization has to be given to the determination of the aetiology and
serogroup, since establishing the presence of serogroup A or C is crucial for planning further
steps. Laboratory investigation should always be performed on the first suspected cases and
may be done using a rapid test (latex agglutination test CSF), that should be available in all
refugee settings. Confirmation by culture is difficult to attain in the field – the meningococcus
is fragile – but could be essential for antibiotic resistance patterns.
It is not possible to define a universal epidemic threshold due to variations in incidence
rates due to climate, season or geography. Thresholds should be defined for each specific
setting. In a large refugee population (over 30,000) it is generally recommended to use a
threshold of 15 cases/100,000/persons/week during 2 consecutive weeks. In smaller
populations it can be as low as 2-3 cases per week. In very large populations the general
threshold of 15 cases/100,000/persons/week may be unsuitable due to very low attack rates
that could obscure higher attack rates within subgroups of the overall population. Once an
epidemic is confirmed, mass immunization and treatment must be rapidly and effectively
organized to prevent cases, deaths and reduce CFR.
A mass immunization campaign can be effective in controlling outbreaks of meningococcus A and C, but it will only have an impact if implemented early on. It should implemented
within the first 4-8 weeks. However, recent data, suggest that this delay might be too long
to allow time for protective levels of antibodies. Mass vaccination is not recommended if it
is definitely too late and the epidemic curve is clearly decreasing. The appropriateness of a
mass vaccination campaign during an emergency phase with high mortality rates or scarce
resources should always be questioned and weighed against the alternative strategy of
focusing on early case detection and treatment. If an epidemic due to a classic clone (other
than the III-1) in the meningitis belt occurs in proximity to the rainy season, might also lead
to a decision not to undertake a mass immunization campaign.
Immunization should not be limited to the refugee population but should cover the whole
area affected, as well the surrounding ones. The same holds of course for open situations with
refugees living among the local communities. Target groups should be decided based on age
specific attack rates, but it is preferable to consider mass vaccination of the entire population
above 6 months. If resources and time are limited, prioritization should be given to the age
group 6 months to 30 years of age.
Good organization is crucial for a successful campaign. Teams of 20 members can
vaccinate 350-600 people/hour. Immunization starts from the center of the outbreak and
includes all contacts spreading out in near locations.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
Mass immunization campaign
367
Surveillance during an outbreak
After confirming an outbreak, surveillance should increase to detect new cases using a
case definition on clinical grounds (preferably with visual CSF detection. Weekly compilation
of cases allows the drawing of an epidemic curve. Collecting information on vaccination status
of cases, allows evaluation of vaccine efficacy to take place.
Simplified treatment protocol
for bacterial meningitis
Meningitis is an emergency:
the earlier the treatment, the better the chances of a cure.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
CLINICAL FEATURES
368
Children more than one year old and adults: sudden fever > 38.5ÆC, stiffness of the neck,
headaches, vomiting
Children less than one year old: fever > 38.5ÆC, hypotonia, dehydration and bulging
fontanelle
TREATMENT
Antibotic treatment
●
Children more than one year old and adults
oily chloramphenicol IM
Children: 100 mg/kg
Adults: 3 g (6 vials of 500 mg)
Age
12-23 months
2.5 years
6-9 years
10-14 years
>14 years
Dose
1g
1.5 g
2g
2.5 g
3g
Volume
4 ml
6 ml
8 ml
10 ml
12 ml
This single dose should be administered in 2 injections – one in each buttock – as the
product is viscous.
●
Pregnant and lactating women
The use of ceftriaxone or ampicillin is preferred, if available; if not available, oily
chloramphenicol can be used, as the priority is to administer treatment quickly.
●
Children between 2 months and one year old
ceftriaxone IM: 80 mg/kg once daily (i.e. about 250 mg/day) for 5 days
IV solvent can be used by IM route, but never use IM solvent by IV route as
it contains lidocaine.
✓ If ceftriaxone is not available, oily chloramphenicol can be used.
●
Children under 2 monthsof age
ampicillin slow IV: 200 mg/kg/day in 3 divided doses for 5 days
Use IV route for 5 days before changing to the IM route (same dosage) or oral route with
amoxicillin PO: 100 mg/kg/day) for a further 3 to 5 days.
Treatment of fever
Age
0 Adult
1 months
1 years
5 years
15 years
Weight
0
4g
8g
15 g
35 g
100-mg tablet
ó tab x 3
3/4 to 11/2 tab x 3
11/2 to 3 tab x 3
–
–
500-mg tablet
–
–
1/4 to ó tab x 3
ó to 11/2 tab x 3
2 tab x 3
Do not administer aspirin in the presence of purpura.
PREVENTION AND TREATMENT OF DEHYDRATION
✓ Make the patient drink to avoid dehydration.
✓ Use oral rehydration solution (ORS) if dehydrated.
Notes:
➠ If transfer is necessary, give the first injection BEFORE transferring, with a letter
indicating the treatment administered.
➠ Oily choramphenicol is the treatment of choice for meningitis and should not be used
for other pathologies. Leftover vials should be returned to the regional authorities at the
end of the epidemic. In the event that stocks run out, contact the regional authorities.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
– Either bathe the child or keep him/her damp with a cloth.
– Administer paracetamol PO:
369
References
ñ MSF. Conduite a tenir en cas d’ epidemie de meningite a meningocoque, 1993.
ñ MSF. Refugee Health: An approach to emergency situations. MacMillan, 2008.
ñ http://www.who.int/mediacentre/factsheets/fs141/en/
ñ WHO. Control of epidemic meningococcal disease. WHO practical guidelines. Lyon: Editions Fondation
Marcel Merieux, 1995.
ñ Flachet L, Boelaert M, Henkens M et al. Intervention en cas d’ epidemie de meningite: indications et
limites. Etudes des interventions realisees par MSF, 1985-91. Journees scientifiques 1991-1992. Paris:
Epicentre, AEDES, Medecins Sans Frontieres, 1992.
ñ CDC. Famine-affected, refugee, and displaced populations: Recommendations for public health issues.
MMWR, 1992, 41 (RR-13): 1-76.
ñ Moore, P S, Reeves, M W, Schwartz, B, Gellin, B G, Broome, C V. Intercontinental spread of an
epidemic group A Neisseria meningitides strain. The Lancet, 1989, 2(8657):2 260-2.
ñ WHO in collaboration with CDC, CRED and FINNPREP. Emergency preperadeness and response: Rapid
health assessment in mengitis outbreaks. Emergency Relief Operations, 1990.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
ñ Hussey, G. A discussion document presented at WHO clinical research meeting. Banjul, Gambia: 1993.
370
ñ CDC. Famine-affected, refugee, and displaced populations: Recommendations for public health issues.
MMWR, 1992, 41 (RR-13): 1-76.
ñ MSF. Conduite a tenir en cas d’ epidemie de rougeole. Paris: Medecins Sans Frontieres, 1996.
ñ Measles-Recent trends and futur prospects. Wkly Epidemiol Rec, 1994, 69(33): 245-52.
ñ
WHO. Responding to a suspected polio outbreak: Case investigation, surveillance and control.
Geneva: WHO, 1991. WHO/EPI/POL/91.3.
ñ Benenson, A. Control of communicable diseases manual. 16 th edition. Washington DC: American
Public Health Association, 1995.
ñ Van Niekerk, Vries, J B et al. Outbreak of paralytic poliomyelitis in Namimbia. The Lancet, 1994,
344: 661-4.
Study questions
1. Describe the composition of an immunization team for a mass vaccination campaign
2. An immunization team can immunize
❏
❏
❏
❏
100-150/hour
500/day
400-700/hour
50-100/hour
3. Measles vaccine is 50% protective at age 9 months. True or false?
4. Meningococcal vaccination is effective
❏
❏
❏
❏
1 day after vaccination
5-14 days after vaccination
1 week after vaccination
None of the above
5. During a meningitis epidemic the peak is usually reached within
2-8 weeks
1 week
2 months
1-3 weeks
6. During a meningitis epidemic there should always be undertaken a
mass immunization
campaign. True or false?
7. Which is the target group prioritized in a measles vaccination campaign?
8. Which is the target group prioritized in a mengitis vaccination campaign?
9. Which meningococcal serogroups cause epidemics?
10. Meningitis cases should always be diagnosed by laboratory diagnosis with gram stain and
culture. True or false and why?
11. In meningitis epidemics the threshold is always 15 cases/100,000/persons/week. True or false?
12. Attack rate in mengitis epidemics ranges from:
❏
❏
❏
❏
10-1000 cases/100,000 population
50-100 cases/100,000 population
2-10 cases/100,000 population
None of the above
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
❏
❏
❏
❏
371
13. CFR in mengitis without treatment can be as high as:
❏
❏
❏
❏
90%
10%
40%
70%
14. CFR in measles is usually:
❏
❏
❏
❏
<5%
1-6%
90%
10-20%
15. Measles vaccine is contra-indicated in:
❏
❏
❏
❏
Pregnancy
Malnutrition
HIV/AIDS
All of the above
16. 2 dosages of measles vaccination should be given at children at 9 months and 2 years of age.
VACCINATION PROGRAMMES AND CAMPAIGNS IN EMERGENCIES
True or false?
372
17. Routine meningitis vaccination is recommended as routine practice in overcrowding situations
in order to achieve herd immunity. True or false?
18. Children 2 months to 1 year of age with meningitis should be treated with:
❏
❏
❏
❏
Ampicilline
Ceftriaxone
Chloramphenicol
Amoxicillin
chapter 9
Sexually Transimitted
Infections
General Objective
To introduce the basic social, public health and medical aspects of the common Sexually
Transmitted Infections (STIs).
Specific Objectives
➠ the burden of STIs throughout the world and the relationship with HIV
➠ the basic biology, clinical presentations and diagnostic procedures used in STIs medicine
➠ the syndromic management approach
➠ general principles of education and counselling of the patients and the partner
management
Content
➠ Introduction to STI Prevention and Control introduces participants to the size and
scope of the epidemic of STIs, how they are transmitted and the burden they place on
SEXUALLY TRANSIMITTED INFECTIONS
At the end of the session, participants will be familiar with:
individuals, society, health services and national economies.
373
➠ Introducing STI Syndromic Case Management deals with the syndromic approach to
STI case management and explains why syndromic case management is an effective
approach to treating and preventing STIs. The module also introduces flowcharts and
explains how to use them.
➠ History-taking and Examination is a step-by-step approach of STI patients through
what toask, how to ask it and how to examine them.
➠ Diagnosis and Treatment cover seach syndromic flow chart in detail, explaining the
specific signs and symptoms to help participants diagnose and treat each patient. It
also lists the drug options recommended by WHO for each condition identified.
➠ Educating and Counselling the Patient explore show to educate and motivate
patients about STI prevention and treatment. Partner Management is about managing
and treating the patient’s sexual partners. It discusses why partner management is
so important.
Methodology
➠ PPT presentations – Case studies
➠ Attendance in OPDs
➠ Post learning assessment questions
SEXUALLY TRANSIMITTED INFECTIONS
References
374
Introduction to STI Prevention
and Control
Sexually transmitted infections (STIs) are very common. The most widely known are gonorrhoea, syphilis and HIV but there are more than 20 others.
➠ The World Health Organization (WHO) estimated that in 1999 there were 340 million
new cases of curable STIs. In other words, almost one million new infections occur
every day.
According
to the Joint United Nations Programme on HIV/AIDS (UNAIDS) and WHO,
➠
in 2005 an estimated 4.9 million people were newly infected with HIV. Another 40.3
million people were already living with HIV.
This first part will explain the severity and impact of the STI epidemic.
You will learn how STIs are transmitted, what biological and social factors influence
theirtransmission, their epidemiology and social and behavioral impact, and about the links
between STIs and HIV.
The transimission of STIs
➠ How are STIs transmitted?
➠ What factors increase the risk of transmission?
➠ Which population groups, if any, are particularly vulnerable?
How are STIs transmitted?
By far the most common mode of transmission of STIs is through unprotected penetrative
sexual intercourse (vaginal or anal). Other, more rare modes of transmission include:
➠ from mother to child:
ñ during pregnancy (e.g. HIV and syphilis);
ñ at delivery (e.g. gonorrhoea, chlamydia and HIV);
ñ after birth (e.g. HIV);
ñ through breast milk (e.g. HIV);
SEXUALLY TRANSIMITTED INFECTIONS
This section will help you to answer three questions:
375
➠ through the unsafe (unsterile) use of needles or injections or other contact with blood
or blood products (e.g. syphilis, HIV and hepatitis).
It is important to remember that HIV is transmitted in the same ways as any other STI.
What factors increase the risk of transmission?
Not all acts of unprotected sexual intercourse result in the transmission of an STI from
an infected person to a partner. Whether or not a person will be infected depends on many
factors, both biological and behavioural.
SEXUALLY TRANSIMITTED INFECTIONS
BIOLOGICAL FACTORS
376
Certain biological factors influence the transmission of STIs. They are age, sex, immune
status of the host and the virulence of the organism.
Age: The vaginal mucosa and cervical tissue in young women is immature and makes
them more vulnerable to STIs than older women. This is due to cervical ectopy, a
normal condition for young women, when cervical surface cells more readily allow
infections to occur. Young women are especially at risk in cultures where they marry
or become sexually active during early adolescence. On average, women become
infected at a younger age than men.
Sex: Infections enter the body most easily through a mucosal surface such as the lining
of the vagina. Since the mucosal surface that comes into contact with the infective
agent is much greater in women than in men, women can be more easily infected
than men.
Immune status: The immune status of the host and virulence of the infective agent affect
transmission of STIs. Certain STIs increase the risk of transmission of HIV (itself a
sexually transmitted infection). HIV, in its turn, facilitates the transmission of some
STIs and worsens the complications of STIs by weakening the immune system.
BEHAVIOURAL FACTORS
Many behavioural factors may affect the chance of getting an STI. Such behaviours are
known as “risky”. Risky behaviours include the following.
Personal risky sexual behaviours include:
➠ changing sexual partners frequently;
➠ having more than one sexual partner;
➠ having sex with “casual” partners, sex workers or their clients:
recent or frequent change of sexual partner, having more than one sexual partner or
having sex with sex workers or their clients makes it more likely that a person will come
into contact with someone who has an STI;
ñ having unprotected penetrative sexual intercourse in a situation where either
partner has an infection;
ñ having had an STI in the last year:
people who have had an STI in the last year are at risk of getting infected again if
they have not been able to change their sexual behaviour.
SOCIAL FACTORS
OTHER PERSONAL BEHAVIOURS MAY BE ASSOCIATED WITH INCREASED RISK, INCLUDING:
➠ skin piercing; this refers to a wide range of practices including the use of unsterile
needles to give injections or tattoos, scarification or body piercing and circumcision
using shared knives;
use
of alcohol or other drugs before or during sex; alcohol or drug use may negatively
➠
affect condom use; alcohol may diminish the perception of risk, resulting in not using
a condom; or if a condom is used it may not be used correctly.
RISKY BEHAVIOUR OF PARTNER(S) INCLUDES:
➠ having sex with others
➠ having an STI
➠ injecting drugs
➠ male partner having sex with other men.
A partner with one or more of these behaviours is more exposed to STIs, and in turn is
more likely to transmit an STI.
SEXUALLY TRANSIMITTED INFECTIONS
A number of social factors link sex and behavioural issues and may affect a person’s risk
of getting an STI, for example:
➠ in most cultures women have very little power over sexual practices and choices, such
as use of condoms;
women
tend to be economically dependent on their male partners and are therefore
➠
more likely to tolerate men’s risky behaviour of multiple sexual partners, thus putting
themselves at risk of infection;
➠ sexual violence tends to be directed more towards women by men, making it difficult
for women to discuss STIs with their male counterparts;
➠ in some societies the girl-child tends to be married off to an adult male at a very young
age, thus exposing the girl to infection;
➠ in some societies a permissive attitude is taken towards men allowing them to have
more than one sexual partner.
377
Which population groups are particularly vulnerable?
In most countries some groups of people are particularly vulnerable to STIs. This may be
because they are exposed to infected partners more frequently, or because they are more
susceptible to getting infected each time they are exposed. Such groups include:
➤ sexually active teenage girls;
➤ sex workers and their clients;
➤ men or women who have multiple sexual partners; men or women whose jobs
separate them from their regular sex partners for long periods of time, such as longdistance drivers, soldiers and migrant workers.
For various reasons, these people may hesitate to go to health facilities for treatment.
Special effort may be necessary to reach them and make services acceptable to them.
STIs – the problem
In this section, we explore the extent of STIs, their complications and sequelae when
untreated or not treated effectively, and the links between STIs and HIV, which make it so
important to control their spread.
It will enable you to:
SEXUALLY TRANSIMITTED INFECTIONS
➠ discuss the frequency and distribution of STIs;
➠ identify the range of serious complications which some STIs can cause;
➠ explain the links between STIs and HIV.
378
The distribution of STIs
Worldwide, WHO estimated that in 1999 there were 340 million new cases of curable
STIs.
Figure 1 on the next page illustrates the global spread of new cases among adults.
It shows that the largest number of new infections occurred in the region of South and
South-East Asia, followed by sub-Saharan Africa, then Latin America and the
Caribbean.
Figure 2 represents the estimated prevalence of curable STIs among adults in 1999. Both
prevalence and incidence of STIs are higher in the developing world than in the industrialized
world.
Figure 2 Estimated prevalence of curable STIs among adults, 1999*
* colours denote which countries are included in regional calculations
SEXUALLY TRANSIMITTED INFECTIONS
Figure 1 Estimated new cases of curable STIs among adults, 1999*
379
“The STDs that are caused by bacterial, mycological and protozoal agents have ... continued
to be a public health problem in both industrialized and developing countries. Equilibrium
has been reached, however, in most industrialized countries, with low (and often still falling)
rates of infection. In contrast, the equilibrium reached in many developing countries has been
with highly endemic levels of disease. In many developing countries STDs have for several
decades ranked among the top five diseases for which adults seek health care services.”
Sexually transmitted diseases: policies and principles for
prevention and care. UNAIDS/WHO, 1999.
Any global figures will mask widely different incidence and prevalence in different regions
and countries. Even within countries, prevalence may be high within specific, high-risk groups
or within the general population.
In general, the prevalence of STIs tends to be higher in urban areas than in rural ones, and
higher in unmarried people and younger adults. STIs, including HIV, occur in both males and
females. However, statistics rare show an equal distribution between men and women, nor
do they show an equal distribution between different age groups.
DISTRIBUTION BY AGE
Most children under 14 years of age are not affected by STIs, other than by congenital
syphilis, ophthalmia neonatorum and HIV infection. New STI cases begin to occur during
adolescence and tend to be most frequent in the 15-44 age group, decreasing in older adults.
DISTRIBUTION BY SEX
SEXUALLY TRANSIMITTED INFECTIONS
Upon first thought, it would be reasonable to assume that men and women are equally
vulnerable to STIs. However, cases occur:
➠ more frequently among females than males between the ages of 14 and 19 years;
➠ slightly more frequently among males than females over the age of 19 years.
380
Why are there differences?
The higher frequency among females aged 14–19 years may be attributable to several
factors:
➠ the start of sexual activity is usually earlier for girls than for boys;
➠ girls tend to have sex with older male partners, who have more sexual experience
and are more likely to carry infections;
➠ due to the characteristics of the genital tract of young girls, they are especially
vulnerable to infection with STIs.
After the age of 19 years, the slight male preponderance may be for one or more reasons,
as follows.
➠ Sexually transmissible infections often produce no symptoms or only mild symptoms in
women. For example, more women than men are symptom-free:
ñ Up to 70% of women and 30% of men infected with Chlamydia may not have
symptoms.
ñ Up to 80% of women and 10% of men infected with gonorrhoea may also have no
symptoms (some studies in Africa have show asymptomatic infections with
gonorrhoea and Chlamydia in men to be higher than those shown above. Clearly,
more research will elucidate the extent of asymptomatic infection in men).
This means that as few as 20% of the women infected will come forward for treatment
– so the rest do not appear in statistics.
➠ Services in general may be more accessible to men than women. For example, where
men migrate to urban areas for employment, they have access to the urban services
– and therefore are more likely to appear in statistics.
➠ Cultural and economic constraints might also prevent a proportion of women from
attending for treatment.
➠ A large number of men might be infected after practising unsafe sex with a small
number of sex workers.
➠ Older men may be more sexually active than women of the same age.
➠ Men are more likely to change partners than women.
In many developing countries, the best available indicators of STI levels in women are
surveys taken by antenatal, family planning or gynaecological clinics.
Sexually transmitted infections are of public health concern not only because of their high
prevalence worldwide, but also because of their potential to cause serious and permanent
complications in infected people who are not treated in a timely and effective way. In addition
they are known to facilitate HIV.
A UNAIDS Technical Update in May 1998 states that:
“Both symptomatic and asymptomatic infections can lead to the development of serious
complications.
The most serious complications and sequelae (long-term consequences) of untreated
STI tend to be in women and newborn babies. These can include cervical cancer, pelvic
inflammatory disease (salpingitis), chronic pelvic pain, fetal wastage, ectopic pregnancy and
related maternal mortality.
Chlamydial infections and gonorrhoea are important causes of infertility, particularly
in women, with far-reaching social consequences. Chlamydial infection is an important
SEXUALLY TRANSIMITTED INFECTIONS
The complications of STIs
381
cause of pneumonia in infants. Neonatal gonococcal infections of the eyes can lead to
blindness.
Congenital syphilis is an important and significant cause of infant morbidity and
mortality. In adults, syphilis can cause serious cardiac, neurological and other consequences,
which can ultimately be fatal.”
The public health approach to STD control May 1998.
UNAIDS/WHO Technical Update.
The complications that may result from STIs are summarized in Table below.
SEXUALLY TRANSIMITTED INFECTIONS
The effect on society
382
The social and economic burden of STIs can be enormous. Untreated STIs can lead to loss
of employment and broken marriage. For example, one of the biological effects of pelvic
inflammatory disease (PID) is infertility – the effect of childlessness can mean divorce and
disruption of the family.
Below is a simple example.
In a family of two adults and three children, first one parent and then the other loses
work due to the complications of untreated STIs. The oldest daughter gives up her teaching
job to care for her parents: the younger son stops going to school for financial reasons. To
raise some money for the family he takes on poorly paid and unskilled work whenever he
can.
The state not only loses three skilled workers, but also its investment in a potentially
skilled worker.
STIs can therefore place a heavy financial burden on families, communities and health
services. If an epidemic of STIs is uncontrolled, the loss to the national income can be
significant. For example, in one African country more than 70% of the budget for antibiotic
drugs was used for STI treatment.
The link between STIs and HIV/AIDS
In fact, the interrelationship between STIs and HIV is more complex, in that:
➠ certain STIs facilitate the transmission of HIV;
➠ the presence of HIV can make people more susceptible to the acquisition of STIs;
➠ the presence of HIV increases the severity of some STIs and their resistance to
treatment.
WHICH STIS SEEM TO FACILITATE THE TRANSMISSION OF HIV?
A person with open sores in the genital area is much more likely both t contract and to
transmit HIV. Chancroid and syphilis are the main bacteria causes of sores: if promptly
diagnosed and treated, these links can b reduced.
Genital herpes also facilitates HIV transmission.
“There is evidence that genital herpes, an incurable viral infectio in which patients have
recurrent genital ulcers, may play a more important part than previously thought ...
In high-income countries, genital herpes – infection with the herpes simplex virus-2
(HSV-2) – is the leading cause of genital ulcers, though rates are low. HSV-2 is now
assuming that position in sub- Saharan Africa too ... An ulcer in the genital area provides
an ‘open door’ through which HIV can easily pass. Unfortunately, HSV-2 is lifelong and
incurable ...The best way to deal with the exponentially rising risks of HIV and HSV-2
infection is to increase efforts to prevent them both, particularly by increasing condom
Report on the global HIV/AIDS epidemic. UNAIDS, 2000, p. 71-72.
Chlamydia, gonorrhoea and trichomoniasis can also facilitate the transmission of HIV. This
may be for one or both of two reasons:
➠ These non-ulcerative diseases stimulate the body’s immune system to increase the
number of white blood cells, which are both targets and sources of HIV.
➠ Genital inflammation associated with these STIs can cause microscopic cuts in genital
tissues, creating potential sites where HIV can enter the body.
HIV MAKES INFECTION WITH OTHER STIS MORE LIKELY
It is also true that people infected with HIV are more vulnerable to getting multiple
infections. This is because changes in their bodies make them more vulnerable to infection
in general.
SEXUALLY TRANSIMITTED INFECTIONS
use.”
383
HIV AND INCREASED SEVERITY OF STIS AND RESISTANCE TO TREATMENT
The severity and resistance of STIs are increased by the presence of HIV infection.
“An additional relationship between HIV and other STIs ... is the alteration of the
natural history of an STI in an individual with coexistent immunodeficiency associated with
HIV. The severity of the manifestations may be increased, infectiveness prolonged and
increased, and the response to conventional regimens reduced.”
Sexually transmitted diseases: policies and principles
for prevention and care. UNAIDS/WHO, 1999.
The links between HIV and STIs are summarized in figure below
10
Introducing STI Syndromic Case Management
SEXUALLY TRANSIMITTED INFECTIONS
Commonest sexually transmissible pathogens and clinical presentation
384
Introduction to STI Prevention
and Control
Syndromic Case Management
In this section we introduce you to a third approach to STI treatment (the other two are the
etiological approach and the clinical diagnosis) known as syndromic case management.
This section will help you to answer three questions:
➠ How does syndromic case management differ from the two other approaches?
➠ What features and advantages does it offer?
➠ How the flowcharts work?
SEXUALLY TRANSIMITTED INFECTIONS
Commonest sexually transmissible pathogens and clinical presentation (continued)
385
The key features of syndromic case management
The key features of syndromic case management are that it:
➤ is problem-oriented (it responds to the patient’s symptoms);
➤ is highly sensitive and does not miss mixed infections;
➤ treats the patient at the first visit;
➤ makes STI care more accessible as it can be implemented at primary health-care level;
➤ uses flowcharts that guide the health worker through logical steps;
➤ provides opportunity and time for education and counselling.
Identifying the syndromes
A number of different organisms that cause STIs give rise to only a limited number of
syndromes. A syndrome is simply a group of the symptoms a patient complains about and the
clinical signs you observe during examination.
The table below explains the signs and symptoms for the main STI syndromes and their
causes. The aim of syndromic management is to identify one of these seven syndromes and
manage it accordingly.
SEXUALLY TRANSIMITTED INFECTIONS
Syndromic flowcharts
386
The syndromes are relatively easy to identify and it is possible to devise a flowchart for
each one. A flowchart is a diagram or type of map representing steps to be taken through a
process of decision-making.
A major benefit of the flowcharts is that, once trained, service providers find them easy
to use – so non-STI specialists at any health facility are able to manage STI cases.
In turn, this means that:
➠ you can offer prompt treatment because patients with STIs are treated at their first
visit;
➠ many more patients with STIs have access to treatment;
➠ there are opportunities for introducing preventive and promotive measures such as
education and condom distribution.
Treatment for all the causative agents
While a clinical or etiological diagnosis tries to identify just one causative agent, syndromic
diagnosis leads to immediate treatment for all the most important causative agents. This is
important because mixed infections occur frequently.
respond to treatment and lead to severe consequences if left untreated. Other STI syndromes,
such as vesicular lesions (herpes), genital warts and dysuria in women (painful passing urine),
are not included.
This means that, if the necessary drugs are available and affordable, syndromic treatment
can quickly render the patient non-infectious.
Here is an example of syndromic diagnosis and treatment in practice.
A patient complains of a discharge from the penis. Upon examination, you notice a
discharge from the urethra. The sign and symptom together suggest urethral discharge
syndrome.
SEXUALLY TRANSIMITTED INFECTIONS
Important This module is concerned only with STI syndromes caused by organisms, which both
387
Urethral discharge syndrome is commonly caused by gonorrhoea and/or chlamydial
infection. Not only can these cause serious complications, but also they can facilitate the
transmission and acquisition of HIV. It is therefore essential that we treat the patient for
both.
Such agents as Ureaplasma urealyticum and Trichomonas vaginalis can also cause
urethral discharge syndrome. Should the patient be treated for these causes as well? Not
necessarily, because both are less common and neither leads to complications. If symptoms
persist in this male patient, you can always treat these infections on follow-up.
As this example shows, we can use syndromic management to identify the most likely
causes of a patient’s symptoms and signs and treat the patient for those that have serious
complications or sequelae.
Here is another example that you might like to work on.
A young woman complains of a sore. Upon examination you notice an ulcer on the
outer labia. This indicates the syndrome of genital ulcer.
There are two main bacterial causes of genital ulcer: chancroid and syphilis.
Responding to criticisms of the syndromic approach
Below we answer the main criticisms of the syndromic approach. Many of our comments
touch on points we have already raised, so the activity was partly intended to help you review
the arguments – though it adds more detail.
SEXUALLY TRANSIMITTED INFECTIONS
THE SYNDROMIC APPROACH IS NOT SCIENTIFIC.
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On the contrary, it is based on a wide range of epidemiological studies in both the
industrialized and developing world. This case management approach has been used and
adapted in more than 20 countries throughout the world.
Validation studies have compared syndromic and laboratory diagnosis to assess the
accuracy of syndromic diagnosis and found their results to be similar, so syndromic diagnosis
is accurate, with limitations relating to only one of the syndromes, vaginal discharge, which
we will discuss later in this module.
Other studies have thrown light on the possible impact of syndromic case management
on the incidence of STIs and HIV in a given population.
14This was a trial in 1995 in the Mwanza region of the United Republic of Tanzania, which
aimed to learn what impact STI case management and treatment-seeking behaviour would
have on HIV transmission and STIs in a population. After two years, findings in the trial areas
compared with control areas included:
➠ a reduction of 50% in the prevalence of symptomatic urethritis in men;
➠ a significant reduction in the prevalence of serological syphilis;
➠ a 38% reduction in HIV incidence.
Consultations on STD interventions for preventing HIV:
what is the evidence?
UNAIDS, 2000.
Another trial, three years later, in the Rakai district of Uganda had different findings but
was not about syndromic case management (it took the wider approach of offering homebased treatment to everyone between 15 and 59 years of age regardless of symptoms). This
was found to reduce some STIs but had no impact on HIV infection.
As usual, more research is needed, but positive lessons were learnt from these studies.
SYNDROMIC DIAGNOSIS IS FAR TOO SIMPLE FOR A PHYSICIAN TO USE –
IT CAN EVEN BE USED BY NURSES.
Simplicity does not prevent physicians from using other tools including the thermometer
or stethoscope. It is an important advantage that other service providers, in addition to
doctors, can use the syndromic approach to make a diagnosis. A streamlined diagnosis and
treatment process also allows health workers more time to offer education for behaviour
change.
THE SYNDROMIC APPROACH FAILS TO MAKE USE OF A SERVICE PROVIDER’S
CLINICAL SKILLS AND EXPERIENCE.
Many clinicians rely heavily on their own clinical judgement, but a number of studies have
shown that clinicians using their judgement get the diagnosis wrong in up to 50% of cases:
“Studies have shown that even highly experienced STD specialists using this system
infections in a significant number of cases.”
Sexually transmitted diseases: policies and principles
of prevention and care. WHO/UNAIDS, 1999.
IT WOULD BE BETTER TO TREAT THE PATIENT FIRST FOR THE MOST COMMON CAUSE
AND THEN, IF THE SYMPTOMS DO NOT IMPROVE, TREAT FOR A SECOND CAUSE.
Many patients required to return to a health centre for treatment do not do so. They may
even seek treatment elsewhere. If the first course of treatment is not effective, the patient
may continue to transmit the STI – at best for a few days but at worst for years.
15
SEXUALLY TRANSIMITTED INFECTIONS
of clinical diagnosis will fail to make the correct diagnosis and/or will miss concurrent
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THE SYNDROMIC APPROACH RESULTS IN A WASTE OF DRUGS, BECAUSE PATIENTS
ARE BEING OVER-TREATED.
In fact studies have shown that the syndromic approach is less expensive than clinical or
etiological diagnoses. This is because, in weighing the alternatives, we need to include not
only the high cost of etiological diagnosis or wrong clinical diagnosis but also the biological
and social costs, including infertility, loss of income, family breakdown and so on.
Over-treatment in syndromic management could be said to be a waste when patients
are treated for a syndromic cause which is not the cause of the discharge. This includes, for
example, treatment for gonorrhoea and/or chlamydial infection as the causes of vaginal
discharge in areas where they are not the predominant cause.
GOOD, SIMPLE LABORATORY TESTS SUCH AS GRAM STAIN SHOULD BE INCLUDED
IN STI DIAGNOSIS.
Laboratory diagnosis must never be at the expense of delayed treatment or the risk of
patient non-return. It continues to play an important role for selective cases, but is costly and
needs external controls to ensure maintenance of the technically demanding procedures.
The vaginal discharge flowchart is the least positive at predicting etiology, especially for
populations with lower rates of STIs.
Using the flowcharts
This section explains what a flowchart is and how to use it. It also suggests a number of
exercises for you to familiarize yourself with the process.
SEXUALLY TRANSIMITTED INFECTIONS
What is a flowchart?
390
A flowchart is a diagrammatic map that guides you through a series of decisions and
actions you need to make. Each decision or action is enclosed in a box, with one or two routes
leading out of it to another box, with another decision or action.
Upon learning a patient’s symptoms, you would turn to the relevant flowchart and work
through the decisions and actions it suggests.
Each flowchart is made up of a series of three sorts of step:
➠ the clinical problem – the patient’s presenting symptom at the top – this is the starting
point;
➠ a decision to make, usually by answering “yes” or “no” to a question;
➠ an action to take: what you need to do (different boxes suggest treatment, education
and condom promotion, etc, and patient referral if necessary).
This module is about two very important skills in syndromic case management of sexually
transmitted infections (STIs): taking the medical history from a patient with STIs and conducting
the physical examination.
Even if you have a good deal of experience of interviewing patients, interviewing someone
with symptoms of an STI can be difficult. Their symptoms occur in the genital area and
patients must describe their sexual behaviour, so embarrassment can make the encounter
challenging.
Such feelings can prompt patients to withhold sensitive information or have difficulty
answering questions accurately.
You will need to win the patient’s trust and confidence quickly in order to take an accurate
history in the short time available.
This module will, therefore, help you to refine your knowledge so that you can successfully
take a history and carry out a physical examination.
SEXUALLY TRANSIMITTED INFECTIONS
History – Taking and Examination
391
The needs of the patient with STIs
The patient may be concerned or embarrassed, so it is important that the service provider and
the environment set him or her at ease.
The environment
Confidentiality and privacy are crucial: somewhere to talk where others cannot see or hear
– and a particular need for patient confidentiality.
The service provider
Perhaps most important of all: patients need to feel that the service provider understands
and respects them and wants to listen. To do this, you need to develop a rapport with the
patient and be non-judgemental.
Establishing a good rapport with the patient
This section will enable you to:
➠ identify a number of skills, both verbal and non-verbal, that you can use to establish
SEXUALLY TRANSIMITTED INFECTIONS
good rapport with a patient;
➠ list four non-verbal techniques you can use to demonstrate respect and attention.
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How can we establish a good rapport with a patient? Communication skills are the first
ones we need. These include:
➠ verbal skills: the way we talk to the patient and ask questions;
➠ non-verbal skills: how we behave towards the patient.
A first step should be to greet the patient in an appropriately friendly manner and
introduce yourself – as you would like anyone to do who interviewed you. For example:
➠
➠
➠
➠
➠
smile and use a welcoming tone of voice;
introduce yourself;
use the patient’s name if you have it;
offer the patient a seat;
begin the history-taking only when you have privacy;
➠ make eye contact if culturally appropriate;
➠ be respectful and understanding – especially when the patient, like Swati, stammers
and hesitates.
■
■
■
■
■
Maintain appropriate eye contact. Where culturally appropriate, eye contact shows
that you are interested in the patient’s issues. We transmit a considerable amount of
information by non-verbal communication, such as facial expression and eye movements. Watch and listen and pay attention to feelings as well as facts.
Listen carefully to what the patient says. Active listening is a function of what we
pay attention to in the person we are trying to help. Real communication occurs when
we listen with understanding. Listening intelligently, understandingly and skilfully to
another person is not that easy. For example, it is believed that the brain can process
about 500 words per minute. An average person talks at the rate of 150 words per
minute. This leaves the brain the capacity to process 350 words per minute. The trick
is to use this capacity to actively listen and not to let it wander to “what’s for dinner
tonight” and “I wonder what I should say to this person at the end of this”.
Listening involves the use of both verbal and non-verbal gestures and signals. For
example, is your facial expression relaxed rather than tense? What are your hands and
feet doing during the session? If your hands are waving about too much, your client
may find this distracting. Fingers tapping on the table are a sure sign of impatience
or nervousness. If your legs and feet are swinging, dancing and tapping, this can be
a sign of agitation and can be off-putting to the client.
These gestures are sometimes done subconsciously, but training and role-playing can
help us observe and control them. Body posture is also important. Slumping gives
the impression of boredom, fatigue or lack of interest. Counsellors need to understand
the situation, themselves and their reactions and prejudices in order to act
appropriately on them. To show that you are listening, lean slightly towards the
patient; nod your head or comment occasionally to encourage him/her. Avoid fidgeting
or writing while the patient is talking and do not interrupt unless it is necessary to
clarify a point.
Reflect the patient’s behaviour. For example, sit if the patient is sitting and stand when
the patient stands; lean forwards or back when the patient does. This is a useful way
to show that you share the patient’s feelings. It also shows that you are equal –
standing over someone can sometimes seem threatening.
Stay as close to the patient as is culturally acceptable. A desk or table forms a barrier
between patient and service provider, so it is better to sit at the corner of the desk
or table if you can.
SEXUALLY TRANSIMITTED INFECTIONS
The key to effective non-verbal behaviour is to treat each patient with respect and give
him or her your full attention.
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These four points are very simple, but they can mean the difference between gaining
and losing the patient’s trust or confidence. Can any of us be sure that we demonstrate
supportive behaviour with all patients?
Verbal skills in history-taking
➣ Always phrase your questions politely and respectfully, however busy or rushed you
➣
➣
➣
➣
➣
SEXUALLY TRANSIMITTED INFECTIONS
➣
394
may be;
Use words that the patient understands. Avoid using medical terms that he/she may not
understand;
Make your questions specific, so that the patient knows exactly how to answer you;
Ask one question at a time: double questions confuse;
Keep your questions free of moral judgments;
Avoid “leading” questions that ask the patient to agree with you: let people answer in
their own words;
Ask the patient’s permission before asking about his/her STI or sexual behaviour.
Open-ended questions enable patients to explain something in their own words, and to
say everything they think is important. This means that it is possible to gather much more
information from one open question than from several closed ones. Also, because patients
often have trouble talking about their own sexuality, open questions can help them to feel
more in control and comfortable.
Closed questions, on the other hand, ask the patient to answer a precise question based
on the service provider’s words. Closed questions are normally better saved for later in the
interview, when you have won the patient’s confidence and are checking particular
details.
Experts in interviewing patients with STIs suggest that it is important to ask the second
question, “Anything else?”, several times. This is because some patients are so embarrassed
about STI symptoms that they describe other, unrelated symptoms, such as a headache, before
they are comfortable enough to describe an STI-related problem. Giving them a chance to
describe a range of complaints often reveals useful information.
Once you are sure that you have a complete understanding of the patient’s problem as he
or she sees it, closed questions may be very helpful to draw out specific details that you need
to know.
In addition to positive non-verbal behaviour and appropriate, respectful questioning, some
specific techniques and skills can be extremely useful when interviewing patients with STIs.
They can help you to deal supportively with the patient’s emotions as well as to gather
information effectively.
These are the six skills:
➠ facilitation;
➠ direction;
➠ summarizing and checking;
➠ empathy;
➠ reassurance;
➠ expressing partnership.
Gathering information
The section will enable you to:
➤ identify general information that you need to gather;
➤ explain why this information is necessary;
➤ match the information you need to the questioning skills you have learned.
Improving your ability to gather information about a patient is useful because it will help
you to make an accurate diagnosis of STIs in the time available. The information collected will
be the starting point for understanding the patient’s behavioural risks of transmitting or
contracting STIs in the future, as well as for partner referral and treatment.
First, it is worth reminding ourselves of why we are taking the patient’s history. It is to:
1. make an accurate syndromic STI diagnosis;
2. establish the patient’s risk of transmitting or contracting STIs;
3. find out about partners who may have been infected.
1.
2.
3.
4.
20
The patient’s general details.
The patient’s present illness.
His or her medical history.
His or her sexual history.
SEXUALLY TRANSIMITTED INFECTIONS
This is the information you need to collect, in more or less this order:
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Guide for history-taking
1. General details
ñ Age
ñ Number of children
ñ Locality or address
ñ Employment
SEXUALLY TRANSIMITTED INFECTIONS
2. Present illness
ñ Presenting complaints and duration:
Men:
– If an inguinal bubo
– is it painful? Associated with genital ulcer? Swellings elsewhere in the body?
– If a urethral discharge – pain while passing urine? Frequency?
– If scrotal swelling – history of trauma?
Women:
– If a vaginal discharge – pain while passing urine? Frequency? Risk assessment positive?*
– Lower abdominal pain – vaginal bleeding or discharge?
– Painful or difficult pregnancy or childbirth?
– Painful or difficult or irregular menstruation?
– Missed or overdue period?
Men and women:
– If a genital ulcer – is it painful? Recurrent? Appearance? Spontaneous onset?
– Other symptoms, such as itching or discomfort?
396
3. Medical history
ñ Any past ST – type? Dates? Any treatment and response? Results of tests?
ñ Other il lness – type? Dates? Any treatment and response? Results of tests?
ñ Medications being taken currently.
ñ Drugallergies.
4. Sexual history
ñ Currently active sexually?
ñ New partner in the last three months?
ñ Risk assessment.*
Note: Risk assessment is a specific set of questions to ask female patients who complain of vaginal
discharge. The questions were devised to help service providers decide on the etiology; they
should be adapted for local social and behavioural situations.
Examination
The purpose of a physical examination is to confirm any STI symptoms the patient has
described by checking for signs of STIs. This section explains what to do when examining male
and female patients.
Examining the most private parts of a person’s body requires tact, sensitivity and respect
on the part of the service provider. Patients may be embarrassed or uncomfortable. We
suggest ways to help the patient understand the importance of the examination and
overcome his or her embarrassment.
This section will help you to:
➠ behave professionally with the patient before and during the examination;
➠ reassure the patient who is reluctant to be examined and gain his/her confidence and
cooperation;
➠ conduct an efficient examination of both male and female patients.
Because people may be shy and even reluctant to have their genitals examined, you must
be professional in your behaviour. Be sure to:
➠
➠
➠
➠
➠
ensure privacy;
explain what you are going to do and why an examination is important;
ask the patient for his or her permission to make an examination;
be patient, even though you may have little time to examine the patient;
approach the examination in a confident way yet sensitive to the patient’s needs.
Three general principles
for syndromic examination
Before discussing the steps for examining male and then female patients, please remember:
1. Syndromic diagnosis requires good history-taking an dinspection of the external
genitalia.
2. We recommend the use of gloves.
SEXUALLY TRANSIMITTED INFECTIONS
For most syndromes, the examination is important in order to arrive at a diagnosis.
However, we must never force someone to be examined. So what can you say to a patient
who is unwilling to be examined?
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3. As else where in the STI case management programme, this section focuses on
examination for seven STI syndromes only. It does not take account of STIs such as
scabies or lice, treatment of which should be a normal part of your responsibilities.
When examining the abdomen, take care not to cause the patient any undue pain. Palpate
the abdomen gently making sure you observe for any signs of pain or tenderness in the
patient. Take note that the differential diagnoses of pelvic inflammatory disease (PID) are
acute appendicitis, pelvic abscesses or intestinal obstruction.
Three general principles for syndromic examination
Examining male patients for STI syndromes
1. We recommend that you ask both male and female patients to lie down comfortably on
a couch for a genital examination. Ask male patients to remove their shirt first, then to lie
down on the couch and pull their lower garment down to expose the area from the hip
to knees. The patient should be covered with a sheet to maintain dignity and respect.
Where a couch is not available a male patient may be examined standing up, but this is
not ideal. In such a case an explanation should be given. The patient should be asked to
expose the area from the chest to knees for examination.
2. Palpate the inguinal region in order to detect the presence or absence of enlarged lymph
nodes and buboes.
SEXUALLY TRANSIMITTED INFECTIONS
3. Palpate the scrotum, feeling for individual parts of the anatomy:
– testes;
– spermatic cord;
– epididymis.
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4. Examine the penis, noting any rashes or sores.Then retract the foreskin if present, and look
at the:
– glans penis;
– urethral meatus.
If you cannot see an obvious urethral discharge, milk the urethra or ask the patient to milk
the urethra gently in order to express any discharge. If a discharge is present, wipe it with a
swab and dispose of it in a leak-proof container, ready for incineration.
5. Record the presence or absence of:
– buboes;
– ulcers;
– urethral discharge, noting the colour and amount.
Examining female patients for STI syndromes
1. Were commend that you ask both male and female patients to lie down comfortably on
a couch for genital examination. Ask female patients to expose the area from the chest to
knees for examination. The patient should be covered with a sheet to maintain dignity
and respect.
2. Palpate the abdomen for pelvic masses and tenderness, taking great care not to hurt the
patient.
3. Palpate the inguinal region in order to detect the presence or absence of enlarged
lymphnodes and buboes.
4. Ask the patient to bend her knees and separate her legs, then examine the vulva, anus
and perineum.
5. The physical examination may include, where possible, an internal pelvic examination in
volving (a) bimanual examination to check for active PID; shape, size and position of uterus
for uterine masses, for example, pregnancy and (b) speculum examination to check for the
nature of the vaginal discharge, purulent cervicitis and/or erosions. If a microscope or
laboratory facilities are available, obtain specimens of cervical and vaginal secretions for
diagnostic studies.
A special note: risk assessment –
only if you will use the vaginal discharge flowchart
Using vaginal discharge as an entry point to manage cervical infection is far from ideal.
While vaginal discharge is highly indicative of vaginal infection, it is poorly predictive of
cervical infection with gonorrhoea and/or chlamydia.
The flowchart may become more predictive of cervical infection if a number of risk factors
are included. In the literature a number of risk factors have been shown to be indicative of
cervical infection. Some of those demonstrated to be significant, but not necessarily all in the
same setting, were:
➠ being under 21 years of age (or 25 in some settings);
➠ being unmarried;
➠ having more than one sexual partner in the last three months;
SEXUALLY TRANSIMITTED INFECTIONS
6. Record the presence or absence of:
– buboes;
– ulcers;
– vaginal discharge, noting the type, colour and amount.
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➠ having a new partner in the last three months;
➠ the current partner having a sexually transmitted infection;
➠ recent use of condoms by the partner.
Diagnosis and Treatment
This section provides you with a practical, step-by-step guide to using each of the global
syndromic flowcharts for the management of sexually transmitted infections (STIs). It explains
all the important decisions and actions to take.
There are seven main syndromic flowcharts, as indicated by the WHO guidelines for the
management of the STIs:
1.
2.
3.
4.
5.
6.
7.
Urethral Discharge
Genital Ulcer
Vaginal Discharge
Lower Abdominal Pain
Scrotal Swelling
Inguinal Bubo
Neonatal Conjuctivitis
Important
SEXUALLY TRANSIMITTED INFECTIONS
GENITAL ULCER DISEASE AND HIV INFECTION
400
An ulcer in the genital area offers easy access for HIV. In an HIV-infected person, the
natural history of syphilis and chancroid may change, so that their respective lesions are
atypical. In chancroid, the ulcers can be more extensive and even multiple, sometimes
accompanied by fever and chills; reference should be made to the local treatment guidelines
in such settings.
In areas where HIV infection is prevalent, an increasing number of cases of genital ulcer
may harbour genital herpes, which also becomes more prevalent. A person with HIV may
have atypical HSV-2 ulcers, which are persistent, multiple ulcers requiring medical
attention. Antiviral treatment becomes important for the patient’s comfort; this treatment
protocol in patients with HIV may require adapting, which you must refer to in your local
setting:
“HSV-2 and HIV appear to operate in a vicious circle, each increasing the risk of
contracting and passing on the other. Unfortunately, HSV_2 infection is lifelong and
incurable. Drugs that suppress the genital ulcers and viral shedding associated with HSV2 do exist, but they are very expensive, and their widespread use in poor countries is
problematic. Thus, the only practicable option for HSV-2 is prevention.”
Report on the global AIDS epidemic. UNAIDS, 2000.
VAGINAL DISCHARGE
Unfortunately, it is not easy to distinguish between cervicitis and vaginitis, especially when
it is not possible to do an internal examination. Cervicitis is more likely in areas where the
prevalence of gonorrhoea and/or chlamydia is high. The higher the prevalence, the stronger
the justification for treatment.
In areas where gonorrhoea and chlamydia are highly prevalent, risk assessment questions
may help to identify women with a higher risk of cervical infection.
LOWER ABDOMINAL PAIN
The term pelvic inflammatory disease (PID) refers to infections of the female upper
genital tract: the uterus, fallopian tubes, ovaries or pelvic cavity. It occurs as a result of
SEXUALLY TRANSIMITTED INFECTIONS
It is normal for women to have some vaginal discharge. Women may notice it more during
certain phases of the menstrual cycle, during and after sexual activity and during pregnancy
and lactation. Usually women complain of vaginal discharge when they think it is unusual for
them or if it causes itching or discomfort. In general, they will not seek medication for a
discharge they consider normal.
Women develop the symptom of vaginal discharge if they have either vaginitis (infection
of the vagina) or cervicitis (infection of the cervix), or both. It is important to distinguish
between these conditions because one of them, cervicitis, leads to serious complications, so
the patient’s sexual partner(s) must also be treated to avoid reinfection.
The differences between vaginitis and cervicitis can be summarized with the table below.
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SEXUALLY TRANSIMITTED INFECTIONS
infection going through the cervix. It can be caused by gonorrhoea, chlamydia and some
anaerobic bacteria.
PID includes endometritis, salpingitis, tubo-ovarian abscess and pelvic peritonitis. It can also
lead to generalized peritonitis, a potentially fatal condition. Salpingitis may lead to a blocked
fallopian tube, resulting in decreased fertility or total infertility if both tubes become infected.
It may also lead to partial tubal obstruction, allowing spermatozoa to pass through, but not
the relatively larger fertilized ovum. The result can be a tubal or ectopic pregnancy, which
will eventually rupture, causing massive intra-abdominal haemorrhage and, possibly, death.
Women with PID usually have a history of lower abdominal pain and vaginal discharge.
However, in addition, some women with PID or endometritis will not complain of lower
abdominal pain. Other suggestive symptoms include pain during intercourse, vaginal
discharge, abnormal bleeding from the womb at any time including during a period, painful
urination, pain during menstruation, fever and sometimes nausea and vomiting.
Although difficult to diagnose, PID becomes more probable when one or more of the
symptoms above combine with lower abdominal tenderness, vaginal discharge and cervical
motion tenderness.
In the history, you need to check for other symptoms, such as erratic bleeding, missed or
overdue period, recent delivery, abortion or miscarriage. Erratic bleeding might be an early
symptom of ectopic pregnancy. Ask questions similar to these:
➠ Are there any problems with your periods?
➠ Do you have any vaginal bleeding not related to normal menstruation?
➠ Have you had a miscarriage, abortion or delivery in the last six weeks?
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When examining the patient:
➠ Check the patient’s temperature. A high temperature indicates infection.
➠ Palpate the abdomen for tenderness, rebound tenderness, guarding and detection
of a mass. Abdominal palpation should first be superficial to detect pain on light
palpation. Pain on palpation is referred to as tenderness.
➠ Then make a careful and deep palpation. In the area where you found tenderness to
light palpation, press down slowly and very gently and release the pressure suddenly.
Any severe pain that results is known as rebound tenderness.
When the peritoneum is inflamed, upon palpation the abdominal muscles will become
rigid and will not allow you to apply pressure.
This is known as guarding. Guarding and rebound tenderness are features of peritonitis
or an intra-abdominal abscess.
Light abdominal palpation will also enable you to detect a swelling or lump in the patient’s
abdomen. This is known as a mass. Upon deep palpation of the lower right and lower left
abdomen, you might detect a tender mass deep in the pelvic cavity. This may be a tuboovarian abscess.
➠ Check for vaginal bleeding. This should alert you to the possibility of an ectopic
pregnancy or abortion.
➠ Finally, check for abnormal vaginal discharge.
SERIOUSLY CONSIDER HOSPITALIZING PATIENTS WITH PID WHEN:
➠
➠
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the diagnosis is uncertain;
surgical emergencies such as appendicitis and ectopic pregnancy cannot be excluded;
a pelvic abscess is suspected;
severe illness precludes management on an outpatient basis;
the patient is pregnant;
the patient is unable to follow or tolerate an outpatient regimen;
the patient has failed to respond to outpatient therapy.
Many experts recommend that all patients with PID should be admitted to hospital for
treatment.
SCROTAL SWELLING
Examine the patient:
1. Inspect the scrotal sac and compare the two sides for swelling of the testis. Palpate and
note any tenderness.
2. What is the position of the testis in the scrotal sac? Is it elevated or rotated? If so, this is
characteristic of testicular torsion.
3. Is there bruising of the scrotal skin which could indicate trauma?
4. Is there an obvious urethral discharge? If not, ask the patient to gently squeeze the penis
and milk the urethra in order to express any discharge.
5. Is there evidence of any other STI such as an ulcer?
6. Is there swelling in the inguinal area or does the scrotal swelling increase when the patient
raises the intra-abdominal pressure (straining as if passing stools)? This may point to a
hernia and requires referral to a surgical facility.
SEXUALLY TRANSIMITTED INFECTIONS
Infection of the testis or epididymis is a serious complication of gonococcal urethritis and
chlamydial urethritis. When infected, the testis becomes swollen, hot and very painful. If early
and effective therapy is not given, the inflammation will heal with fibrous scarring and
destruction of testicular tissue. This may lead to infertility.
It is important to consider possible non-infectious causes of scrotal swelling and pain, as
well as non-sexually transmitted infections.
Non-infectious causes include trauma, tumour and testicular torsion and all require
referral. The following two questions are particularly important.
➠ Has the patient sustained any injury to the scrotal region?
➠ FHas the patient had an STI in the last six weeks?
403
Inguinal Bubo
This is a painful, often fluctuant, swelling of the lymph nodes in the inguinal region (groin).
Buboes are usually caused by either chancroid or lymphogranuloma venereum (LGV).
In many, but not all, cases of chancroid, a genital ulcer may be visible. If so, you should
refer to the genital ulcer flowchart and treat the patient for that syndrome.
Infections of the lower limb and other non-STIs can also cause swelling of the inguinal
lymph nodes.
When examining the patient, try and determine whether the swelling is really a bubo or
simply enlarged lymph nodes or any other pathology, which has enlarged nodes in other sites.
A bubo is usually painful, warm, tender when palpated and fluctuant.
There may be one large mass or a collection of smaller painful swellings. Occasionally
the bubo might have ruptured and a sinus, discharging pus, will be present.
In order to ease patient’s symptoms, you may aspirate through healthy skin.
If a bubo is present, make sure to look for genital ulcers:
➠ FIn men, remember to examine the underside of the foreskin and the parts normally
covered by the foreskin. If the patient cannot retract the foreskin because of swelling,
assume there is a genital ulcer and use the appropriate flowchart.
➠ FIn women, examine the skin of the external genitalia and then separate the labia and
look at the mucous surface for ulcers.
SEXUALLY TRANSIMITTED INFECTIONS
Neonatal Conjuctivitis
404
Neonatal conjunctivitis (ophthalmia neonatorum) is defined as purulent conjunctivitis
occurring in a baby less than one month of age. The most important causes of this
potentially sight-threatening condition are gonorrhoea and chlamydia. If caused by
gonorrhoea, blindness often follows.
In developing countries, gonorrhoea accounts for 20–75% and Chlamydia for 15–35%
of cases of neonatal conjunctivitis. Newborn babies are generally presented because of
redness and swelling of the eyelids, discharge from the eye or “sticky eyes”.
For babies older than one month, the cause is unlikely to be an STI.
Prompt eye prophylaxis at delivery should prevent gonococcal neonatal conjunctivitis.
All newborn babies should have preventive therapy carried out as follows:
➠ As soon as the baby is born, carefully wipe both eyes with dry, clean cotton wool.
➠ Then apply 1% silver nitrate solution or 1% tetracycline eye ointment into the infant’s
eyes.
➠ Remember that the baby’s eyes are usually swollen soon after birth and may be
difficult to open. Therefore, the eyes should be opened and the eye ointment placed
in the lower conjunctival sacs and not on the eyelids.
Diagnosis and Treatment
Case Studies
Based on WHO guidelines for the management of the Sexually Transmitted Infections and the
national guidelines of the country, where available, participants have to deal with the
following study cases and treat the patients accordingly.
www.who.int/reproductive-health/publications/mngt_stis/index.html
a) Mas is an adolescent boy of 15 years who lives in the slum area of a large town. He has
been brought to the district hospital because his scrotum is swollen and he is vomiting.
What flowchart do you use? On examination, the scrotum is swollen and painful; the
testes elevated and rotated. How do you manage this patient?
b) Gloria took her four-day-old baby to the clinic when she noticed that his right eye was
swollen and there was pus in both eyes (the right eye more than the left).
a) Doris, aged 22, attended the family planning clinic for her usual check-up while on the
contraceptive pill. She tells the nurse about a yellow, itchy vaginal discharge that she
has had for the past four days. What flowchart do you use? Doris says she has no
abdominal pain or urination pain. She had her period two weeks ago and it was normal.
Shyly, she discloses that she had sex with an old school friend a week ago, and that she
did not use a condom because she was on the pill. She last had sex with her regular
boyfriend a month ago, as he was out of town.
For what do you treat Doris?
d) An18-year-old dock worker named Mark attends your clinic complaining that he had
adischarge yesterday. What flowchart do you use?
On examination, you can find no discharge, even after milking the urethra.
However, you do find an ulcer on his penis.
What do you do now? For what do you treat this patient?
e) 24-year-old Puloka states that she began seeing Hopi, her new partner, three months ago.
She is now experiencing a dull persistent abdominal pain, which she thinks has been
brought on by her excessive sexual activity with Hopi.
What flowchart do you use?
Puloka tells you that her periods are normal and she has never been pregnant.
SEXUALLY TRANSIMITTED INFECTIONS
What flowchart do you use?
What treatment do you offer, to whom?
405
She thought that there might be some increase in what she considers to be normal vaginal
discharge. On examination, she has no rebound tenderness or guarding, but clearly feels
pain when you palpate the lower abdomen.
What treatment do you give to her, using which flowchart?
f) Richard says he noticed a slight pain in his left groin. Two days later, he noticed that it
looked swollen. He has rushed to the clinic after work.
What flowchart do you use?
On examination, you find that he has a small sore on his penis. His left groin is tender and
swollen.
For what do you treat Richard, using which flowchart?
Below there are a few case studies to give you more practice in diagnosing the cause or
causes of vaginal discharge. Please decide whether you need to treat each woman for vaginitis
only, or for both vaginitis and cervical infection.
1. Sara moved in with her present partner four months ago. She is 22 years old. In
addition to the discharge, she says her lower abdomen feels tender. Her partner has
no symptoms.
2. Jasmincomplainsofaslightvaginaldischarge.Sheis25yearsoldandhasbeenmarriedfor eight
years. Her third child was born four months ago, so she’s been busy caring for him at
home. Apart from this discharge, she feels well and has no other symptoms.
3. Ami is 17 years old, living in an urban area. She reports a slight discharge but no other
symptoms. She has lived with her current boyfriend for nine months.
SEXUALLY TRANSIMITTED INFECTIONS
4. 34-year-old Sharma complains of a slight yellow discharge. She has not been with
anyone since her husband left home six months ago. She has no other symptoms.
406
5. 25-year-old Palantina complains of a watery vaginal discharge. She has had this for two
weeks and it is getting worse. She does not know whether her partner has a penile
discharge because she has not seen him for two weeks. She has no other symptoms.
6. A two-week-old baby is brought into the clinic with an obvious eye infection. One eye
appears swollen, the other is swollen and discharging yellow pus. The mother brings
the baby back after the weekend complaining that the eye infection is no better.
7. For the last four days Jon, a young businessman, has had pain when he passes urine.
You note a slight watery discharge from the tip of his penis. Jon’s wife is in their village
150 kilometres away: he has not seen her for three months.
8. Sofi’s partner has informed her that he has gonorrhoea. She has no discharge and no
fever. She has pain in her left lower abdomen. On palpation, her abdomen is soft, with
tenderness on the left side but no guarding. One week later, she returns at your
request and is still tender on palpation.
9. A young man called Tram comes into the health centre complaining of a painful groin.
The testes are swollen and painful, with no history or evidence of trauma or torsion.
10. Mrs Bogatsu complains of a painful vulva. Her husband is her only partner. She appears
ill and feverish. On examination, she has many small sores filled with a clear liquid
on both labia majora and minora, and no visible ulcer.
11. Ahmed, 32 years old, attends the centre because of severe pain in the groin. He has
had several different sexual partners over the last few months and does not use
condoms on a regular basis. There is no visible sore on the penis, but there is a large,
swollen node in the right groin.
Preparing to use STI flowcharts in your health centre
Check what drugs are available and effective for each condition
Confirm the risk factors that you will use
For specific places, the risk factors for vaginal discharge may need to be amended. If you
have not already consulted your trainer on this matter, please do so.
30
SEXUALLY TRANSIMITTED INFECTIONS
This is an important priority so, if you have not done so already, find out what drugs are
available to treat each syndrome. At the back of the module, you will find space to record
locally recommended drugs.
Make sure you have easy access to a list of the locally recommended drugs. You might, for
example, write them on a piece of paper or card that you could keep on your desk, or use a
permanent marker to note them on each flowchart.
407
Education and Counselling
the patient Partner management
Health education and counselling are closely linked. Both activities may take place at the same
time. In health education, the aim is to make the patient better informed, so that he/she can
make an informed choice of sexual behaviour and practices. Counselling relates more to issues
of anxiety and coping with the infection or its consequences, biomedical as well as social.
Health education is the provision of accurate and truthful information so that a person
can become knowledgeable about the subject and make an informed choice.
SEXUALLY TRANSIMITTED INFECTIONS
For example, a young woman with an STI needs to know how she contracted the infection
in order to decide to change her sexual practice.
The service provider should inform her about STIs and their prevention.
408
Counselling is a two-way interaction between a client and a provider. It is an
interpersonal, dynamic communication process that involves a kind of contractual agreement
between a client and a counsellor who is trained to an acceptable standard and who is bound
by a code of ethics and practice. It requires empathy, genuineness and the absence of any
moral or personal judgement.
Counselling can be applied to any life situation, for example, when a nurse is listening and
talking to grieving relatives; or a colleague is talking to someone who wants to quit their
job and even commit suicide because of it! In other words, counselling is not peculiar only
to STIs and HIV.
Counselling aims to encourage healthy living and requires the client to explore important
personal issues and to identify ways of living with the prevailing situation, whether it is an
infection or bereavement. It is not about providing advice or guidance, nor does it mean
befriending someone.
In STIs and HIV, the counselling process assesses and addresses the client’s needs to enable
the person to cope with any anxiety and stress brought about by the diagnosis. The
counselling process should also evaluate the person’s risk of STI transmission and explore
preventive behaviour in future. So, counselling helps clients understand themselves better
as individuals, exploring their feelings, attitudes, values and beliefs.
Equipped with the right knowledge, the client should seek to change behaviour as a result
of counselling.
For example, a man may have infected his wife with gonorrhoea after being infected
elsewhere and he now needs to tell her about this. He may need counselling to deal with this
particular problem.
Another example might be where a male patient is found to have genital herpes. The
service provider educates him about this infection. The patient might panic when told that
the infection is incurable, so counselling would be necessary.
Health education happens when health-care providers share their knowledge with the
aim of increasing a client’s awareness and understanding. In health education the same facts
are given to everyone.
As with any other type of patient, people with an STI need to know about their condition
and its management because the goals of patient education are to:
➠ help the patient resolve any current infections;
➠ prevent future infections;
➠ make sure that sex partners are also treated and educated.
As a health-care provider, you may feel uncomfortable using certain words about sexual
matters. It is important to become familiar with using these words so you can feel comfortable
when you speak to and educate your patients.
Educate on prevention of future infection
Once you are sure that the patient understands his or her infection and what treatment
to follow, he or she next needs to appreciate the risk of becoming reinfected. This means that
you assist the patient to assess his/ her own risk level.
Remember: high-risk behaviour is behaviour that exposes the patient to sex fluids and
blood. Therefore, changing from high-risk to low-risk sexual behaviour is one way to prevent
future infection. Reducing the number of sex partners or the rate of change of sex partners is
important. Sexual abstinence virtually guarantees against contracting or transmitting an STI.
This is particularly important during treatment for STIs.
CONDOMS
Another practice for preventing the spread of STIs is the use of condoms.
Male latex condoms can reduce the risk of contracting or transmitting STIs if consistently
and correctly used. The health-care provider must demonstrate the correct use of condoms,
using a penile model where available. Let the clients practise on the model so that they
understand how to put the condom on, can demonstrate this skill and feel confident about
handling a condom.
SEXUALLY TRANSIMITTED INFECTIONS
CHANGING SEXUAL BEHAVIOUR
409
SEXUAL PRACTICE
It is also important to inform clients that some sexual practices have a higher risk of
infection. For example, anal sex, whether it is male to female or male to male, carries a higher
risk than penile – vaginal sex.
OTHER BARRIER METHODS
Inform your clients of any other existing prevention methods such as the use of spermicides that may also be bactericidal; microbicides or vaccines (e.g. for hepatitis B).
PERSONAL HYGIENE AND CULTURAL PRACTICES
Vaginal douching, for example, may remove protective bacteria in the vagina increasing
the risk of getting some STIs, e.g. HIV. Washing with soap and water may help prevent colonization with parasites, such as pubic lice or scabies.
32
SEXUALLY TRANSIMITTED INFECTIONS
The need to treat sexual partners
410
This is the theme of Module 6, so we need not discuss it in any detail here.
Remember: always inform patients how important it is to have all their known sex partners
treated.
Reassure patients that you will maintain confidentiality and discuss how they can persuade
their partner(s) to attend for treatment. Stress that treatment will benefit both partners
because there will be no risk of reinfection and the partner, who may not be aware of the
infection, will have the STI treated and avoid future serious complications.
This is all factual information and you could supplement it with a brochure that patients
can take home to read at leisure. Once the patients have assimilated the information, they
will know about STIs and how to prevent them.
However, knowledge and information alone are not sufficient to bring about behaviour
change. We also need to bring about behaviour change, and counselling is one strategy that
can be used to achieve this.
References
ñ Guidelines for the Management of Sexually Transmitted Infections, WHO Geneva 2003
http://www.who.int/reproductive-health/publications/mngt_stis/guidelines_mngt_stis.pdf
ñ Sexually transmitted and other reproductive tract infections: a guide for essential practice, WHO
Geneva 2005. http://www.who.int/reproductive-health/publications/rtis_gep/rtis_gep.pdf
ñ Training Modules for the Syndromic Management of Sexually Transmitted Infections 2007.
http://www.who.int/reproductive-health/stis/training.htm
ñ Periodic presumptive treatment for sexually transmitted infections: experience from the field and
recommendations for research, WHO Geneva 2008
http://www.who.int/reproductive-health/publications/ppt/ppt.pdf
ñ Sexually transmitted infections among adolescents - the need for adequate health services, WHO
Geneva 2005 http://www.who.int/reproductive-health/publications/stis_among_adolescents/stis_
among_ adolescents_adequate_health_services.pdf
ñ The global elimination of congenital syphilis: rationale and strategy for action, WHO Geneva 2007
http://www.who.int/reproductive-health/publications/congenital_syphilis/strategy_
congenitalsyphilis.pdf
ñ Human papillomavirus and HPV vaccines: technical information for policy-makers and health
professionals, WHO Geneva 2007
http://www.who.int/reproductive-health/publications/ hpvvaccines_techinfo/hpvtechinfo.pdf
ñ GLOBAL PREVALENCE AND INCIDENCE OF SELECTED CURABLE SEXUALLY TRANSMITTED INFECTIONS –
SEXUALLY TRANSIMITTED INFECTIONS
OVERVIEW AND ESTIMATES. http://www.who.int/hiv/pub/sti/who_hiv_aids_2001.02.pdf
411
SEXUALLY TRANSIMITTED INFECTIONS
Case Study: Rivas District Outbreak
412
1.
Three biological factors influence the transmission of STIs. The first two are age and sex.
What is the third?
2.
Sex workers and their clients are clearly very vulnerable to infection by STIs. Which other two
population groups are also particularly vulnerable? (2 answers)
a. Sexually active teenage girls.
b. Sexually active teenage boys.
c. Adult men who are sexually active with more than one partner.
d. Adult women who are sexually active with more than one partner.
3.
Are these two statements about STIs and HIV TRUE or FALSE?
a. There is asyet no evidence to show that STIs such as syphilis or chancroid can facilitate
the transmission of HIV. b. HIV infection makes infection with other STIs more likely.
4.
Which of these state ments about comprehensive case management of patients with STIs
is true?
a. The two main topics in patient education are the nature of the infection and treatment
compliance.
b. Diagnosing an STI syndrome and providing effective antimicrobial treatment are two
features of syndromic case management.
c. Because all health facilities can diagnose and treat STI syndromes, the specialist STI clinic
(genito-urinary centre) has no further role to play.
d. Partner management is difficult and should not form part of the case management of
patients with STIs.
5.
Briefly note three problems with the etiological approach to STI diagnosis and treatment.
6.
CFR in Which of the four most accurately completes this statement?
Syndromic case management aims to treat patients with STIs upon:
a. their first visit to a specialist STI clinic;
b. their first visit to the health centre;
c. their return to a health centre after etiological diagnosis;
d. their return to a health centre after syndromic, and etiological diagnosis.
7.
CFR in Which STIs accurately complete this statement?
The most common causes of urethral discharge are:
a. gonorrhoeaandchlamydia;
b. syphilis and chlamydia;
c. syphilis and chancroid;
d. gonorrhoea and chancroid.
8.
Validation studies have found syndromic diagnosis to be accurate, except for limitations
concerning one syndrome: which is it?
a. Urethraldischarge.
b. Genital ulcer.
c. Scrotal swelling.
d. Vaginal discharge.
e. Neonatal conjunctivitis.
9.
CFR in Patients coming to discuss a possible STI have particular needs of the health-care
environment and the provider. Briefly:
a. Name their two basic needs of the environment. (2 points)
b. Name their two key requirements of the health-care provider.
10. When is it best to use closed questions? Tick the box you think correct.
a. To help the client open up on a particular issue.
b. When you want to collect answers to many precise questions.
c. To help the patient relax and feel more confident.
d. To check particular details towards the interview’s end.
11. Which of these is an openquestion? Tick the box you think correct.
a. When did your symptoms begin?
b. What can you tell me about this sore?
c. Have you completed your course of medication?
d. Does it feel tender?
12. What question is it useful to ask several times when taking a patient’s history?
reassurance. What are the other three?
Listening Direction Control
Empathy Affection Enthusiasm
Motivation Partnership Expectation
14. A male patient does not want to be examined by a female health-care worker. No male healthcare workers are available this afternoon. What should you do about this?
a. Suggest that a male working at the centre accompany the patient.
b. Tactfully try to find out why the patient feels so strongly about this, so that your can
persuade him of the need for examination in those terms.
c. Explain why it is so important to make an examination if you are to get the diagnosis right.
d. Explainthat, if the patient can not agreet to be examined, you can not provide any
treatment.
SEXUALLY TRANSIMITTED INFECTIONS
13. Three of the six verbal skills in history-taking are summarizing/checking, facilitation and
413
15. If a patient complain so fabdominal pain and you suspect PID, which of the factors or
symptoms below would suggest possible PID and which would suggest referring the patient
for surgical or gynaecological assessment?
TREAT FOR PID
REFER
a. Recentdelivery, abortion or miscarriage.
b. Abdominal guarding and/or rebound tenderness.
c. Vaginal discharge.
d. Cervical excitation tenderness.
e. Abnormalvaginalbleeding.
f. Lower abdominal tenderness.
g. Missed/overdue period.
16. If a person with symptoms of genital ulcer is also HIV-positive, what effect might this have
on the appearance of the ulcer?
17. Which of these statements about vaginal discharge and risk assessment is FALSE?
a. Vaginitis can lead to serious complications.
b. Vaginal discharge alone is poorly predictive of cervical infection.
c. Cervicitis can lead to serious complications.
d. In areas with a high prevalence of gonorrhoea and chlamydia, local risk assessment factors
help identify women at higher risk of infection.
18. A young man complains of a painful scrotum. You learn that he has several casual girl friends.
Upon gentle palpation, you confirm pain and some swelling. There is no discharge, torsion
or apparent trauma. How would you treat this patient?
a. Referthepatientimmediatelyforasurgicalopinion.
b. Treat for syphilis and chancroid and review in seven days.
SEXUALLY TRANSIMITTED INFECTIONS
c. Treat for lymphogranuloma venereum and review in five days.
414
d. Treat for gonorrhoea and chlamydia and review in three days.
19. A young man complains of a lump in his groin. Upon examination, you confirm a painful,
fluctuant bubo but no other STI syndromes.
a. For what two causes do you treat this patient?
b. What else could you do to help ease the patient’s symptoms?
20. What is the maximum age of a young child for purulent conjunctivitis to be caused by an STI?
a. Twoweeks.
b. One month.
c. Six weeks.
d. Two months.
chapter 10
Unintentional Injuries
General Objective
To introduce the basic social and medical aspects of trauma (other than the war trauma) in
developing countries (described as Low and Middle Income Countries – LMICs).
Specific Objectives
At the end of the session, participants will be familiar with:
➠ the burden and causes of unintentional injuries (UIs) throughout the developing
countries
Content
This session examines the issue of unintentional injuries which consist of that subset of injuries
for which there is no evidence of predetermined intent. Other categories such as psycosociological trauma or war trauma and the neglected issue of the sexual violence will not
be part of this session.
➠ Burden of Unintentional Injuries
➠ Economic Burden of Unintentional Injuries
UNINTENTIONAL INJURIES
➠ the clinical presentations and diagnostic procedures used
➠ potential interventions
415
➠ Causes of Unintentional Injuries in LMICs (risk factors for Road Traffic Injuries,
Poisonings, Fall-related Injuries, Burn-related Injuries, Drowning
➠ Potential Interventions
Methodology
➠ PPT presentations
➠ Lecture-discussion format
UNINTENTIONAL INJURIES
References
416
Introduction
Trauma is defined as any wound or shock produced by sudden physical or psychological
injury, as from accident, injury, or impact. This study examines the issue of unintentional
injuries which consist of that subset of injuries for which there is no evidence of
predetermined intent. Other categories such as psyco- sociological trauma or war trauma
and the neglected issue of the sexual violence will not be part of the study. The causespecific unintentional injuries examined here include those that the World Health
Organization (WHO) routinely analyzes and publishes data on and that individually account
for the greatest unintentional injury burden in terms of mortality and disability-adjusted
life years (DALYs). These include road traffic injuries (RTIs), poisonings, falls, burns, and
drowning.
Burden and Causes
of Unintentional Injuries
This section provides a brief outline of the burden of unintentional injuries and then reviews
the available evidence about known and potential causes of such injuries.
Worldwide, unintentional injuries accounted for more than 3.5 million deaths in 2001, or
about 6 percent of all deaths and 66 percent of all injury deaths. Unintentional injuries were
also responsible for more than 113 million DALYs in 2001, or about 8 percent of all DALYs and
some 70 percent of all injury DALYs. More than 90 percent of unintentional injury deaths
occurred in low –and middle– income countries (LMICs), accounting for around 7 percent of
all deaths in those countries. Similarly, more than 90 percent of DALYs that were attributed
to unintentional injuries occurred in LMICs, accounting for about 8 percent of all DALYs in
those countries. Injury death rates per 100,000 population were higher in LMICs (62 per
100,000) than globally (57 per 100,000).
Compared with other age groups, young people age 15 to 29 accounted for the largest
UNINTENTIONAL INJURIES
Burden of Unintentional Injuries
417
proportion of deaths from unintentional injuries in LMICs (figure 2). RTIs accounted for the
greatest burden of deaths from unintentional injuries in LMICs in 2001, or about 34 percent
of the total burden, and the greatest burden of DALYs from unintentional injuries in LMICs in
2001, accounting for 28 percent of the burden (figure 1). Whereas young people age 15 to 29
years accounted for the highest proportion of all unintentional injuries, those age 45 to 59
accounted for the highest proportion of injuries from poisonings, while those age 70 to 79
accounted for the highest proportion of injuries from falls (figure 2).
RTIs accounted for the greatest burden of deaths from unintentional injuries in LMICs in
2001, or about 34 percent of the total burden, and the greatest burden of DALYs from
unintentional injuries in LMICs in 2001, accounting for 28 percent of the burden (figure 1).
Whereas young people age 15 to 29 years accounted for the highest proportion of all
unintentional injuries, those age 45 to 59 accounted for the highest proportion of injuries
from poisonings, while those age 70 to 79 accounted for the highest proportion of injuries
from falls (figure 2).
Economic Burden of Unintentional Injuries
Estimates of the burden of unintentional injuries as measured in terms of economic costs
are almost nonexistent. The best estimates available are for RTIs. Using road crash costs from
21 developed and developing countries, the Transport Research Laboratory Ltd. finds that the
average annual cost of road crashes was equivalent to about 1.0 percent of gross national
product in developing countries, 1.5 percent in transition countries, and 2.0 percent in highly
motorized countries. The annual burden of road crash costs is about US$518 billion globally
and about US$65 billion in LMICs, exceeding the total annual amount these countries receive
in development assistance (Jacobs, Aeron-Thomas, and Astrop 2000).
40
UNINTENTIONAL INJURIES
Causes of Unintentional Injuries in LMICs
418
As in the case of most diseases, unintentional injuries are caused by multiple factors. The
traditional epidemiological paradigm of host, vector, and environmental factors that in
combination contribute to the incidence of disease has been adapted and applied in
determining the causes of unintentional injury.
Figure 1 Distribution of Unintentional Injuries, Low –and Middle– Income Countries, 2001
Risk Factors for Road Traffic Injuries
The increasing volume of traffic is one of the main factors contributing to the increase
in RTIs in LMICs. Motorization rates rise with income and a number of LMICs experiencing
growth have seen a corresponding increase in the number of motor vehicles (Ghaffar and
others 1999). In some LMICs, this growth has been led by an increase in motorized twowheeled vehicles, one of the least safe forms of travel, which has resulted in concurrent
increases in related injuries (Zhang and others 2004).
UNINTENTIONAL INJURIES
Figure 2 Distribution of Unintentional Injuries by Type of Injury and Age Group, LMICs, 2001
419
The rapid growth in motor vehicles in many LMICs has not been accompanied by
improvements in facilities for these road users or by facilities that respond to the continued
predominance of nonmotorized traffic. Many of the technical aspects of planning, highway
design, traffic engineering, and traffic management that are the hallmarks of transportation
systems in many HICs are absent in LMICs.
Data obtained from routinely collected police reports in a number of LMICs show that
speed is listed as the leading cause of road traffic crashes, accounting for up to 50 percent
of all crashes.
Studies conducted in LMICs showed that drivers had consumed alcohol in 33 to 69 percent
of crashes in which drivers were fatally injured and in 8 to 29 percent of crashes in which
drivers were not fatally injured.
A recent case-control study from China shows that the risks of a crash doubled with
chronic sleepiness on the part of the driver (G. F. Liu and others 2003), and surveys of
commercial and public road transport in a number of African countries have shown that
drivers often work long hours and go to work exhausted. Road –and vehicle– related factors
may also increase the risk of crash involvement. Specific factors related to road planning
include traffic passing through residential areas, conflicts between pedestrians and vehicles,
schools located on busy roads, lack of median barriers to prevent dangerous passing on twolane roads, and lack of barriers to prevent pedestrian access on to high-speed roads, although
few studies have specifically examined the risks associated with those factors.
Although the severity of crash injuries is related to in-vehicle crash protection, evidence
indicates that many engineering advances found in vehicles in HICs are not present in vehicles
in LMICs.
A significant risk factor for increased severity of injuries of users of motorized two-wheeled
vehicles is riders’ failure to use motorcycle helmets. Studies in a number of Asian countries
have shown that failure to use helmets, use of nonstandard helmets, and use of improperly
secured helmets are not uncommon, even in countries with mandatory helmet laws (Conrad
and others 1996; Kulanthayan and others 2000).
UNINTENTIONAL INJURIES
Risk Factors for Poisonings
420
The literature on poisonings in LMICs includes comprehensive information about
intentional poisonings; significant information about occupation-related poisonings, especially
pesticide poisonings; and a growing body of information about lead poisoning. The literature’s
focus on risk factors for childhood poisoning probably reflects the fact that child- poisoning
victims are seen more often than adults in most hospital settings (Ellis and others 1994; Nhachi
and Kasilo 1992).
The most common agents involved in childhood poisonings are paraffin (or kerosene) and
other household chemicals; pesticides; and various plants or animals, including snakes.
Risk Factors for Fall-related Injuries
Fall related injuries usually have to do with labor accidents. Lack of precautions and under
qualified labor conditions are the main reasons.
Risk Factors for Burn-related Injuries
Despite the focus of WHO’s data on burn-related injuries sustained as a result of fires, a
number of country-specific surveys conducted in medical facilities suggest that scalds from
hot water may be equally important or more important causes of burn-related injuries.
However, in some countries, including China and particularly India, fire related injuries clearly
outweigh scald-related injuries.
Overall, women are at greater risk of fire-related burn injuries than are men. In many
studies, burn-related injuries account for a much higher proportion of injuries in young
children compared with other age groups.
Rural location appears to be a consistent risk factor for burn-related injuries, as is the
home.
Most drowning incidents in LMICs are not associated with recreation or leisure, as is
commonly the case in HICs, but instead are associated with everyday activities near bodies of
water, including rivers, wells, and buckets.
Men account for a higher proportion of drowning incidents than women, and children age
one to four and young people appear to be at greatest risk, with drowning accounting for
a high proportion of injury-related deaths in those age groups (Celis 1997; Kibel and others
1990; Kozik and others 1999; Tan, Li, and Bu 1998). Some surveys also suggest that older
people may be at particularly high risk.
Surveys indicate that those living in rural areas are at greater risk than those living in urban
areas probably indicating greater exposure to unprotected water surfaces. A number of
studies find that most adult drowning incidents appear to be associated with positive blood
alcohol tests.
UNINTENTIONAL INJURIES
Risk Factors for Drowning
421
Interventions
Interventions to prevent unintentional injuries have traditionally been considered in terms
of the three E’s –education, enforcement, and engineering– and within the framework of the
Haddon matrix. That is, interventions are considered in terms of preventing the occurrence of
the injury, minimizing the severity of injury at the time of the injury, and minimizing the
severity of injury following the injury event.
Interventions shown to be effective in LMICs can be summarized in table 2.
UNINTENTIONAL INJURIES
Table 2
422
References
ñ Assum, T. 1998.“Road Safety in Africa: Appraisal of Road Safety Initiatives in Five African Countries.”
Sub- Saharan Africa Transport Policy Program. Working Paper 33,World Bank,Washington, DC.
ñ Bangdiwala, S. I., and E. Anzola-Perez. 1990. “The Incidence of Injuries in Young People: II. Log-Linear
Multivariable Models for Risk Factors in a Collaborative Study in Brazil, Chile, Cuba, and Venezuela.”
International Journal of Epidemiology 19 (1): 125-32.
ñ Carlini-Cotrim, B., and A. A. da Matta Chasin. 2000. “Blood Alcohol Content and Death from Fatal
Injury: A Study in Metropolitan Area of Sào Paulo, Brazil.” Journal of Psychoactive Drugs 32
(3): 269-75.
ñ Conrad, P., Y. S. Bradshaw, R. Lamsudin, N. Kasniyah, and C. Costello. 1996. “Helmets, Injuries,
and Cultural Definitions: Motorcycle Injury in Urban Indonesia.” Accident Analysis and Prevention
28: 193-200.
ñ Elvik, R., and T.Vaa. 2004. Handbook of Road Safety Measures. Amsterdam: Elsevier.
ñ European Road Safety Action Program. 2003. Halving the Number of Road AccidentVictims in the
EuropeanUnion by 2010: A Shared Responsibility. Brussels: European Commission.
ñ Forjuoh, S. N. 2003. “Traffic-Related Injury Prevention Interventions for Low Income Countries.” Injury
Control and Safety Promotion 10 (1-2): 109-18.
ñ Global Forum for Health Research. 2002. The 10/90 Report on Health Research 2001-2002. Geneva:
Global Forum for Health Research.
ñ Haddon, W. Jr. 1968. “The Changing Approach to the Epidemiology, Prevention, and Amelioration of
Trauma: The Transition to Approaches Etiologically Rather Than Descriptively Based.” American
Journal of Public Health and the Nation’s Health 58 (8): 1431-38.
ñ Liu, B., R. Ivers, R. Norton, S. Blows, and S. K. Lo. 2004. “Helmets for Preventing Injury in Motorcycle
Riders.” Cochrane Database of Systematic Reviews (4) CD004333.
ñ Nhachi, C. F., and O. M. Kasilo. 1992. “The Pattern of Poisoning in Urban Zimbabwe.” Journal of
Applied Toxicology 12 (6): 435-38.
ñ Tan, Z., X. Li, and Q. Bu. 1998. “Epidemiological Study on Drowning in Wujin, Jiangsu, 1997.”
ñ UNDP (United Nations Development Programme). 1998. Human Development Report 1998. New
York: Oxford University Press.
ñ van Beeck, E. F., G. J. Borsboom, and J. P. Mackenbach. 2000. “Economic Development and Traffic
Accident Mortality in the Industrialized World, 1962-1990.” International Journal of Epidemiology
29 (3): 503-9.
UNINTENTIONAL INJURIES
Zhonghua Liu Xing Bing Xue Za Zhi 19 (4): 208-10.
423
chapter 11
Sexual Violence
General Objective
To introduce the basic social and medical aspects of Sexual Violence (SV) and rise up both
physical and psychological effects on health and well-being.
Specific Objectives
At the end of the session, participants will be familiar with:
➠
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the prevalence and consequences of SV
myths about rape and the Rape Trauma Syndrome
the assessment and examination of adult victims of SV
the treatment and follow-up care
Sexual violence is ubiquitous; it occurs in every culture, in all levels of society and in every
country of the world. Data from country and local studies indicate that, in some parts of the
world at least, one woman in every five has suffered an attempted or completed rape by an
intimate partner during her lifetime.
➠ Prevalence
➠ Health Consequences Myths and the Rape Trauma Syndrome
➠ Assessment and Examination (general medical history, gynaecological history, the
assault itself
SEXUAL VIOLENCE
Content
425
➠ Treatment and Follow-up care (Physical Injuries, Pregnancy Prevention and Management, Emergency Contraception, Sexually Transmitted Infections)
➠ Medical review of follow-up care
Methodology
➠ PPT presentations
➠ Lecture-discussion format
SEXUAL VIOLENCE
References
426
Sexual Violence: a Global Problem
Sexual violence is ubiquitous; it occurs in every culture, in all levels of society and in every
country of the world. Data from country and local studies indicate that, in some parts of the
world at least, one woman in every five has suffered an attempted or completed rape by an
intimate partner during her lifetime.
Furthermore, up to one-third of women describe their first sexual experience as being
forced. Although the vast majority of victims are women, men and children of both sexes also
experience sexual violence. Sexual violence can thus be regarded as a global problem, not only
in the geographical sense but also in terms of age and sex.
Sexual violence takes place within a variety of settings, including the home, the workplace,
schools and the community. In many cases, it begins in childhood or adolescence. High rates
of forced sexual initiation have been reported in population-based studies conducted in such
diverse locations as Cameroon, the Caribbean, Peru, New Zealand, South Africa and Tanzania.
According to these studies, between 9% and 37% of adolescent females, and between 7%
and 30% of adolescent males, have reported sexual coercion at the hands of family members,
teachers, boyfriends or strangers.
Sexual violence has a significant negative impact on the health of the population. The
potential reproductive and sexual health consequences are numerous – unwanted pregnancy,
sexually transmitted infections (STIs), human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/ AIDS) and increased risk for adoption of adoption of risky sexual
behaviours (e.g. early and increased sexual involvement, and exposure to older and multiple
partners). The mental health consequences of sexual violence can be just as serious and long
lasting. Victims of child sexual abuse, for example, are more likely to experience depression,
substance abuse, post-traumatic stress disorder (PTSD) and suicide in later life than their nonabused counterparts. Worldwide child sexual abuse is a major cause of PTSD, accounting for
an estimated 33% of cases in females and 21% of cases in males.
The terms “rape”, “sexual assault”, “sexual abuse” and “sexual violence” are generally considered to be synonymous and are often used interchangeably.
However, these terms may have very different meanings (and implications) in varying
situations and locations. More significantly, legal definitions of specific types of sexual violence
may differ from the medical and social definitions, and furthermore, can vary between
countries and even within countries. It is important, therefore, that health care professionals
SEXUAL VIOLENCE
Definition of sexual violence
427
are aware of the legal definitions of sexual violence within their own jurisdiction, particularly
as it applies to the age of consent and marriage.
Sexual violence is defined as, “any sexual act, attempt to obtain a sexual act, unwanted
sexual comments or advances, or acts to traffic women’s sexuality, using coercion, threats
of harm or physical force, by any person regardless of relationship to the victim, in any setting,
including but not limited to home and work”. According to this definition, a very wide range
of behaviours, from rape at gun-point to sexual coercion under a threat of dismissal (i.e. with
false agreement), would be classed as an act of sexual violence.
False agreement to sexual activity can be obtained in a variety of ways; for instance,
through threats of physical violence, threats of withholding benefits (such as a promotion
at work or a good grade), psychological pressure or blackmail. Agreement in such circumstances does not amount to freely given consent. The same is true in cases of sexual acts
involving individuals who are unable to give consent, that is to say, individuals who are not
capable of understanding the significance of the act or of indicating their consent or refusal
(e.g. those who are incapacitated due to the effects of alcohol and/or drugs, or those with
a mental disability); such acts would also be described as nonconsensual.
SEXUAL VIOLENCE
Prevalence
428
Sexual violence is a reality for millions of people worldwide, and for women in particular.
Research indicates that the vast majority of victims of sexual violence are female, most
perpetrators are male, and that most victims know their attacker. This does not, however,
negate that fact that sexual violence against men and boys is also widespread.
While it is generally acknowledged that sexual violence against women is pervasive in
all countries and in all levels of society, reliable statistics concerning the prevalence of sexual
violence around the world are very limited. Population based studies of abuse by intimate
partners indicate that between 6% and 46% of women report that they have experienced
attempted or completed forced sex by an intimate partner or ex-partner at some time in their
lives. Rape and domestic violence account for an estimated 5–16% of healthy years of life lost
to women of reproductive age.
There is significant underreporting of sexual violence. Published statistics are therefore
unlikely to provide an accurate picture of the true scale of the problem. This also creates
difficulties when attempting to compare studies.
The reasons for non-reporting are complex and multifaceted but typically include fear of
retribution or ridicule, and a lack of confidence in investigators, police and health workers.
Men are even less likely than women to report being a victim of sexual violence and for this
reason information about the extent of sexual violence against males is especially limited.
Health consequences
The health consequences of sexual violence are numerous and varied, and include physical
and psychological effects, both in the short-term and in the long-term.
Most significantly perhaps, sexual abuse can have devastating long-term psychological
effects, influencing and radically altering a person’s entire life course.
Physical consequences
Individuals who have experienced sexual assault may suffer a range of physical injuries,
genital and non-genital, or in extreme cases, death. Mortality can result either from the act
of violence itself, or from acts of retribution (e.g. “honour” killings or as a punishment for
reporting the crime) or from suicide.
In addition, rape victims are at an increased risk from:
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unwanted pregnancy;
unsafe abortion;
sexually transmitted infections (STIs), including HIV/AIDS;
sexual dysfunction;
infertility;
pelvic pain and pelvic inflammatory disease;
urinary tract infections.
Genital injuries in women are most likely to be seen in the posterior fourchette, the labia
minora, the hymen and/or the fossa navicularis. The most common types of genital injuries
include:
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tears;
ecchymosis (i.e. bruising);
abrasions;
redness and swelling.
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bruises and contusions;
lacerations;
ligature marks to ankles, wrists and neck;
pattern injuries (i.e. hand prints, finger marks, belt marks, bite marks);
anal or rectal trauma.
SEXUAL VIOLENCE
Non-genital physical injuries typically include the following:
429
Psychological consequences
Just as there is no typical victim, there is no typical reaction to the experience of sexual
violence; psychological effects vary considerably from person to person.
Generally speaking, however, sexual abuse should be suspected in individuals who present,
particularly repeatedly, with the following health problems:
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rape trauma syndrome (see below);
post-traumatic stress disorder (see below);
depression;
social phobias (especially in marital or date rape victims);
anxiety;
increased substance use or abuse;
suicidal behaviour.
In the longer-term, victims may complain of the following:
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chronic headaches;
fatigue;
sleep disturbances (i.e. nightmares, flashbacks);
recurrent nausea;
eating disorders;
menstrual pain;
sexual difficulties.
In adult survivors of child sexual abuse, symptoms are often an extension of those found
in children, and may include:
SEXUAL VIOLENCE
➠ depression;
➠ anxiety;
➠ post-traumatic stress disorder;
➠ cognitive distortions;
➠ externalized emotional distress;
➠ interpersonal difficulties, including sexual problems.
430
Myths and the Rape Trauma Syndrome
Common myths about rape
SEXUAL VIOLENCE
Common myths about rape
431
Rape trauma syndrome
Many victims of sexual violence experience rape trauma syndrome (RTS).
This is defined as “...the stress response pattern of... a person who has experienced sexual
violence”. RTS may be manifested in somatic, cognitive, psychological and/or behavioural
symptoms and usually consists of two phases: the acute and the long term.
THE ACUTE PHASE. The acute phase is a period of disorganization. It begins immediately
after the rape and persists for approximately 2-3 weeks. During the acute phase, a person
usually experiences strong emotional reactions and may present with physical symptoms.
Emotional responses tend to be either expressed or controlled, for example:
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crying and sobbing;
smiling and laughing;
calm and very controlled;
a flat affect.
SEXUAL VIOLENCE
Emotions may be expressed as anger, fear or anxiety. Some individuals may show feelings
of shock and numbness; others may mask their feelings and act as though everything is fine.
The acute reaction is rooted in a fear of physical injury, mutilation or death. Once victims
feel safe again they may begin to experience:
432
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➠
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mood swings;
feelings of humiliation;
degradation;
shame;
guilt;
embarrassment;
self-blame;
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defencelessness;
hopelessness;
anger;
revenge;
fear of another assault.
THE LONG-TERM PHASE. The subsequent phase is one of reorganization, and ordinarily,
begins approximately 2–3 weeks after the event. At this time the person starts to reorganize
their lifestyle; this reorganization may be either adaptive or maladaptive. Reactions during
this phase vary markedly from person to person, depending on:
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the age of the survivor;
their life situation;
the circumstances surrounding the rape;
specific personality traits;
the response of support persons.
Victims often initiate lifestyle changes, such as moving to a new residence, changing their
telephone number, or obtaining an unlisted telephone number.
Some individuals choose to embark on a period of travel.
Some individuals may experience difficulties in functioning at work, home or school.
Phobias, such as fear of crowds or a fear of being alone, may begin to appear depending on
where the rape took place.
Sexual dysfunction or changes in a person’s sex life are very common.
Frequently, the person may terminate an existing relationship with an intimate partner.
Some of the sexual problems that women often encounter post assault include:
sexual aversion;
flashbacks of the rape during sex;
vaginismus;
orgasmic dysfunction.
Assessment and Examination
General medical history
The primary purpose of taking a medical history is to obtain information that may assist
in the medical management of the patient or may help to explain subsequent findings, e.g.
easy bruising or loss of consciousness or memory loss. Health professionals are advised to refer
SEXUAL VIOLENCE
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433
to national guidelines or standards for conducting clinical examinations to ensure that they
are in compliance.
As a minimum, the medical history should cover any known health problems (including
allergies), immunization status and medications. In terms of obtaining information about the
patient’s general health status, useful questions to ask would be:
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Tell me about your general health.
Have you seen a nurse or doctor lately?
Have you been diagnosed with any illnesses?
Have you had any operations?
Do you suffer from any infectious diseases?
When seeking information about medications that your patient may be taking, the
following questions may be helpful:
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Do you have any allergies?
Do you take tablets given to you by a health worker?
Do you take herbal preparations?
Do you take any other potions?
Gynaecological history
A patient’s recent gynaecological history is of particular relevance in cases of sexual assault.
Questions that could be asked include:
➤ When was the first day of your last menstrual period?
➤ Have you had any sexual relationship prior to this event?
➤ Have you had any pregnancies? How many and how were they delivered?
➤ How many children do you have?
➤ Were there any complications during delivery?
➤ Have you had pelvic surgery?
➤ Do you use contraception? What type?
➤ Do you have a current sexual partner?
SEXUAL VIOLENCE
➤ When did you last have intercourse that you agreed to? (Details may be required if
434
DNA analysis is to be performed.)
The assault itself
The main aims of obtaining an account of the violence inflicted are to:
➠ detect and treat all acute injuries;
➠ assess the risk of adverse consequences, such as pregnancy and STIs;
➠ guide relevant specimen collection;
➠ allow documentation (the history should be precise, accurate, without unnecessary
information that may result in discrepancies with police reports);
➠ guide forensic examination.
When interviewing the patient about the assault, ask her to tell you in her own words
what happened to her. Document her account without unnecessary interruption; if you need
to clarify any details, ask questions after your patient has completed her account. Avoid
questions commencing with the word, “Why?” as this tends to imply blame; instead use openended, non-leading questions. Be thorough, bearing in mind that some patients may
intentionally avoid particularly embarrassing details of the assault (for example, patients may
omit details of oral sexual contact or anal penetration); others may find it difficult to talk
about the assault. Explain to the patient that you are interested in different aspects of the
event to the police; as her health worker you are particularly concerned about any physical
contacts between the patient and her assailant(s).
Always address patient questions and concerns in a non-judgmental, empathetic manner;
for instance:
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use a very calm tone of voice;
maintain eye-contact as is culturally appropriate;
don’t express shock or disbelief;
avoid using victim-blaming statements such as, “What did you think would happen?”,
“What were you doing out alone?”, “What were you wearing?” or “You should have
known better.”
Note that some victims experience involuntary orgasms during the assault; this may cause
much confusion for the patient. The fact that a patient experienced orgasm does not imply
consent.
The following details about the alleged assault must be documented, preferably in an
examination proforma:
➤ the date, time and location of the assault, including a description of the type of surface
on which the assault occurred;
➤ the nature of the physical contacts and detailed account of violence inflicted;
➤ use of weapons and restraints;
➤ use of medications/drugs/alcohol/inhaled substances;
➤ how clothing was removed.
Details of actual or attempted sexual activity should also be carefully recorded, in particular
whether or not the following occurred:
SEXUAL VIOLENCE
➤ the name, identity and number of assailants;
435
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vaginal penetration of victim by offender’s penis, fingers or objects;
rectal penetration of victim by offender’s penis, fingers or objects;
oral penetration of victim by offender’s penis or other object;
oral contact of offender’s mouth with victim’s face, body or genito-anal area;
forced oral contact of victim’s mouth with offender’s face, body or genitoanal area;
ejaculation in victim’s vagina or elsewhere on body the victim’s body or at the scene.
The use of condoms and lubricant should be noted. Any subsequent activities by the
patient that may alter evidence, for example, bathing, douching, wiping, the use of tampons
and changes of clothing, should also be documented. Finally, details of any symptoms that
have developed since the assault must be recorded; these may include:
➠ genital bleeding, discharge, itching, sores or pain;
➠ urinary symptoms;
➠ anal pain or bleeding;
➠ abdominal pain.
Treatment and follow-up care
Physical injuries
Patients with severe, life-threatening conditions should be referred for emergency
treatment immediately. Patients with less severe injuries, for example, cuts, bruises and
superficial wounds can usually be treated in situ by the examining health care worker or other
nursing staff. Any wounds should be cleaned and treated as necessary. The following
medications may be indicated:
➤ antibiotics to prevent wounds from becoming infected;
➤ a tetanus booster or vaccination (according to local protocols);
➤ medications for the relief of pain, anxiety or insomnia.
SEXUAL VIOLENCE
5
436
Pregnancy prevention and management
Most female victims of sexual violence are concerned about the possibility of becoming
pregnant as a result of the assault. If a woman seeks health care within a few hours and up
to 5 days after the sexual assault, emergency contraception should be offered. If she presents
more than 5 days after the assault she should be advised to return for pregnancy testing if
she misses her next menstrual period.
Inspection sites
for a “top-to-toe”
physical examination of
victims of sexual violence.
Emergency contraception
➤ a risk of pregnancy;
➤ patient presents for treatment within 5 days of the assault and wants to prevent
pregnancy;
➤ patient has a negative pregnancy test or it has been determined that she is not
currently pregnant (if pregnancy cannot be ruled out with certainty, ECPs can still be
prescribed so long as the patient is informed that if she is already pregnant, the pills
will not be effective but neither will they affect the pregnancy nor harm the foetus).
SEXUAL VIOLENCE
The most widely used means of pregnancy prevention is the oral administration of the
emergency contraceptive pill (ECP), otherwise known as the “morning after pill”. ECPs act
by preventing or delaying ovulation, by blocking fertilization, or by interfering with
implantation. They are not abortion pills and do not affect an existing pregnancy.
Criteria for administering ECPs include:
437
There are no known medical conditions for which ECP use is contraindicated.
Medical conditions that limit the continuous use of oral contraceptive pills are not relevant
for the use of ECPs. Some jurisdictions require the patient to sign an informed consent form
for emergency contraception.
Sexually transmitted infections
Victims of sexual violence may contract a sexually transmitted infection (STI) as a direct
result of the assault. Infections most frequently contracted by sexual violence victims, and for
which there are effective treatment options, are:
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chlamydia;
gonorrhoea;
syphilis;
trichomoniasis.
Victims of sexual violence may also be at risk of contracting human papilloma virus (HPV),
herpes simplex virus type 2 (HSV-2), HIV and the hepatitis B virus;
PROPHYLACTIC TREATMENT FOR STIS
The decision to offer prophylactic treatment should be made on a case-bycase basis after
the physical examination (see Tables 11 and 12 for recommended treatment regimens that
can also be used for prophylaxis). Routine prophylactic treatment of patients who have been
sexually assaulted is not recommended, as evidence regarding the effectiveness of this
strategy is scant. Practitioners should follow national and local protocols on this matter.
Further guidance on STI treatment (including prophylactic treatment) is provided in the latest
edition of the WHO Guidelines for the Management of Sexually Transmitted Infections.
SEXUAL VIOLENCE
HIV/AIDS
438
Although there are no accurate data on the number of victims of sexual violence who
become infected with HIV as a result of an assault, the risk of contracting HIV from sexual
violence is estimated to be relatively low.
The likelihood of acquiring HIV from sexual assault depends on several factors:
➤ type of assault (i.e. vaginal, oral, anal);
➤ vaginal or anal trauma (including bleeding);
➤ whether and where on, or in, the body ejaculation occurred;
➤ viral load of ejaculate;
➤ presence of STI(s);
➤ presence of genital lesions in either the victim or perpetrator;
➤ intravenous drug use by perpetrator;
➤ frequency of assaults;
➤ number of perpetrators;
➤ HIV status of perpetrator(s);
➤ high prevalence of HIV in the area;
➤ whether a barrier contraceptive method was used.
Male victims of sexual violence have a higher risk of acquiring HIV from an assault as
they are usually penetrated anally. Incarcerated males are likely to be at greater risk, given the
high prevalence of HIV in prison populations and the fact that incarcerated males are at an
increased risk of sexual violence relative to the general population.
HIV testing
Sexual assault victims should be offered a baseline test for HIV. If there are appropriate
facilities for confidential HIV testing and counselling, this could be done on-site. Alternatively,
the patient could be referred to a HIV specialist or to a centre that specializes in confidential
HIV testing and counselling.
Appropriate counselling services should be made available before and after HIV testing.
Ideally, these services should be available on site. If not, the appropriate referrals should be
arranged.
POST-EXPOSURE PROPHYLAXIS
■
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■
■
the limited data regarding the efficacy of PEP;
possible side effects of the medications;
the need for strict compliance when taking the medications;
length of treatment;
importance of follow-up;
the need to begin treatment immediately for maximal effect of medications.
SEXUAL VIOLENCE
At the present time, routine prophylaxis for HIV is a matter of considerable controversy
and not a universally accepted standard of practice. The risk factors for acquiring HIV from
a sexual assault will determine whether or not PEP should be offered to a patient. Health
workers should refer to local protocols dealing with PEP, if they exist. The patient and health
worker must evaluate the risks and benefits of initiating or refraining from post-exposure
prophylactic (PEP) treatment and decide together the best option for the patient.
The patient needs to be fully informed of the following:
439
If prescribed, PEP should be initiated within 72 hours of an assault and be given for 28
days. Antiemetics should be offered to counteract the side effects of the medication. Patient
liver enzyme levels should be measured and a complete blood count (CBC) made prior to
the commencement of PEP (to establish baseline values) and then monitored at regular
intervals until the treatment has been completed.
If the initial test results for HIV were negative, patients should have the test repeated at
6, 12 and 24 weeks after the assault.
Hepatitis B
Victims of sexual violence may be at risk for hepatitis B and should therefore be offered
testing and immunization. A variety of hepatitis B vaccines, with varying dosages and
immunization schedules, are available throughout the world. Health workers should use the
appropriate type of vaccine, dosage and immunization schedule for their local area.
Generally speaking, it is not necessary to administer hepatitis B immune globulin (HBIG)
unless the perpetrator is known to have acute hepatitis B. The administration of HBIG or
the hepatitis vaccine is not contraindicated in pregnant women.
Follow-up care (medical review)
Follow-up visits are recommended at 2 weeks, 3 months and 6 months post assault.
The 2-week follow-up visit
As part of the 2-week post-assault visit, the following routine tasks and checks should
be performed:
SEXUAL VIOLENCE
➣ Examine any injuries for proper healing.
➣ Photograph injuries if indicated (i.e. to document healing, comparisons in court).
➣ Check that the patient has completed the course of any medications given for STIs.
440
➣ Obtain cultures and draw blood to assess STI status, especially if prophylactic
antibiotics were not given at the initial visit.
➣ Discuss results of any tests performed.
➣ Test for pregnancy if indicated. If pregnant, advise about options.
➣ Remind patients to return for their hepatitis B vaccinations in 1 month and 6 months,
other immunizations as indicated, and HIV testing at 3 and 6 months or to follow-up
with their usual health care provider.
➣ Make follow-up appointments.
➣ Assess the patient’s emotional state and mental status, and encourage the patient
to seek counselling if they have not yet done so.
The 3-month follow-up visit
At 3 months post assault:
➤ Test for HIV. Make sure that pre- and post-testing counselling is available or make
the appropriate referral. Assess pregnancy status and provide advice and support.
➤ Discuss results.
➤ Draw blood for syphilis testing if prophylactic antibiotics were not given previously.
➤ Assess patient’s emotional state and mental status and encourage the patient to seek
counselling if they have not yet done so.
The 6-month follow-up visit
At 6 months post assault:
➠ Test for HIV. Make sure that pre- and post-testing counselling is available or make an
SEXUAL VIOLENCE
appropriate referral.
➠ Discuss results.
➠ Administer the third dose of the hepatitis B vaccine.
➠ Assess the patient’s emotional health and refer as necessary.
58
441
References
ñ Clinical Management of Rape Survivors. Developing protocols for use with refugees and internally
displaced persons, WHO, UNFPA 2004. http://www.who.int/reproductive-health/publications/clinical_
mngt_rapesurvivors/clinical_mngt_rapesurvivors.pdf
ñ Guidelines for Gender-based Violence Interventions in Humanitarian Settings. Focusing on Prevention
of and Response to Sexual Violence in Emergencies, IASC Taskforce on Gender in Humanitarian
Assistance 2005. http://www.humanitarianreform.org/humanitarianreform/Portals/1/cluster%
20approach%20page/clusters %20pages/Gender/tfgender_GBVGuidelines2005.pdf
ñ WHO Ethical and safety recommendations for researching, documenting and monitoring sexual
violence in emergencies, WHO Geneva 2007. http://www.who.int/gender/documents/OMS_
Ethics&Safety10Aug07.pdf
ñ Preventing violence. A guide to implementing the recommendations of the World report on violence
and health. WHO Geneva 2004. http://whqlibdoc.who.int/publications/2004/9241592079.pdf
ñ Clinical Care for Sexual Assault Survivors. International Rescue Committee/University of CaliforniaLos Angeles, 2008.
ñ Emergency Contraception for Conflict Affected Settings: A Reproductive Health Response in Conflict
Consortium Distance Learning Module. Developed by the Women’s Commission for Refugee Women
and Children on behalf of the RHRC Consortium, 2004 . http://www.rhrc.org/resources/general_
fieldtools/er_contraception/welcome.html
ñ Facilitator’s Guide: Training Manual for Multisectoral and Interagency Prevention and Response to
Gender-based Violence. JSI/RHRC 2004. http://www.rhrc.org/resources/gbv/gbv_manual/gbv_
manual_toc.html
ñ Gender Based Violence Communication Skills Manual. Family Health International (FHI), the RHRC
Consortium, and the IRC, December 2004. http://www.rhrc.org/resources/gbv/comm_manual/comm_manual_toc.html
ñ IASC Gender Handbook for Humanitarian Action: Women, Girls, Boys & Men, Different Needs – Equal
Opportunities. IASC 2006. http://www.humanitarianinfo.org/iasc/pageloader.aspx?page=contentdocuments-subsidi-tf_gender-iasc%20gender%20handbook%20(feb%202007).pdf
ñ Sexual and Gender-Based Violence (Guinea, Liberia). UNHCR 2001. http://www.rhrc.org/resources/
SEXUAL VIOLENCE
h2g007.pdf – http://www.rhrc.org/resources/h2g008.pdf
442
chapter 12
Neglected Tropical
Diseases
General Objective
To provide background information on a group of infections that are highly prevalent in the world
but which do not gain as much attention as other serious infections and gain an understanding
of the epidemiology, clinical manifestations and treatment challenges of these infections.
Specific Objectives
At the end of the session, participants will be familiar with:
General characteristics
The transmission cycle
Diagnosis and
Treatment of most neglected tropical diseases (Human African Trypanosomiasis, Buruli
Ulcer disease, Leishmaniasis and Chagas disease).
Content
MAlthough medically diverse, tropical diseases like trypanosomiasis, leishmaniasis and specific
myco- bacterium infections share futures that allow them to persist in condition of poverty,
where they cluster and frequently overlap. Because of the low profile and status in public
health priorities, these diseases are called neglected.
NEGLECTED TROPICAL DISEASES
➠
➠
➠
➠
443
Human African Trypanosomiasis
➠
➠
➠
➠
General characteristics
The transmission cycle
Diagnosis
Treatment – main drug chalacteristics (history, indications, adverse effects, storage)
Buruli ulcer disease
(Mycobacterium ulcerans infection)
➠
➠
➠
➠
➠
➠
History
Cause – transmission
Epidemiology – prevalence
Signs and symptoms – diagnosis
Treatment
Social and cultural aspects
Leishmaniasis
➠
➠
➠
➠
➠
➠
History
Epidemiology – geographical distribution
Leishmania/HIV co-infection
Cutaneous, mucocutaneous and visceral forms
Diagnosis
Treatment – vector control, development of new drugs
NEGLECTED TROPICAL DISEASES
Chagas Disease (American Trypanosomiasis)
444
➠
➠
➠
➠
➠
Introduction
Clinical signs
Laboratory diagnosis
Prevention
Treatment
Methodology
Lecture/discussion format, Manual textbook, Annexes
Introduction
Today, neglected tropical diseases are a symptom of poverty and disadvantage. Those most
affected are the poorest populations often living in remote, rural areas, urban slums or in
conflict zones. With little political voice, neglected tropical diseases have a low profile and
status in public health priorities. Lack of reliable statistics and unpronounceable names of
diseases have all hampered efforts to bring them out of the shadows.
Although medically diverse, neglected tropical diseases share features that allow them
to persist in conditions of poverty, where they cluster and frequently overlap. Over 1 billion
people –one sixth of the world’s population– suffer from one or more neglected tropical
diseases. Conflict situations or natural disasters aggravate conditions that are conducive to
the spread of these diseases.
http://www.who.int/neglected_diseases/en/
Human African Trypanosomiasis –also called “sleeping sickness”– is caused by a parasite and
is fatal if left untreated. Trypanosomes are transmitted by the insect Glossina called the tsetse
fly. The disease affects mostly poor populations living in remote rural areas of Africa. Travelers
visiting the sub-Saharan part of the continent may also become infected when they travel
through tsetse fly habitat. There is basically no risk of sleeping sickness transmission in urban
areas; however, peri- urban transmission has been recently described in Kinshasa and Luanda.
Following the bite of the infected fly the parasite will multiply in the lymph and the blood
causing headaches, fever, weakness, sweating, pain in the joints, and stiffness; over time, it
will cross the blood-brain barrier migrating to the central nervous system causing a panoply
of neurological disorders including psychiatric disorders, seizures, coma and ultimately death.
People who become infected may or may not show signs of illness immediately. In the case
of T.b. rhodesiense infections, the disease is acute, lasting from a few weeks to several months
while in T.b. gambiense infections the disease is chronic, generally lasting several years
without any major signs or symptoms. However, in both cases without proper diagnosis and
treatment the outcome is death.
WHO estimated that in 2000 that some 50 to 60 million people in Africa were exposed
to the bite of the tsetse fly. At that time WHO considered that close to 300 000 children,
NEGLECTED TROPICAL DISEASES
Human African Trypanosomiasis
445
women, and men on the African continent were affected by the disease, a figure which is
much larger than the 27 000 cases diagnosed and treated that year.
When infected individuals remain undiagnosed or diagnosed but untreated they are a
source of infection for flies, which will become infected when biting them. The parasite will
then multiply in the salivary glands of the fly, which will spread the infection to the next flybite individual thus closing the transmission cycle. Animals can also become infected and
harbor the human infective parasites which substantially complicates the transmission cycle
since infected animals become parasite reservoirs for the uninfected flies. Commonly, in the
case of T.b. rhodesiense transmission the cycle involves wild and domestic animals while in
T.b. gambiense the transmission cycle is mostly human to human, involving animals to a much
lesser extent.
The T.b. rhodesiense acute infections occur in eastern and south eastern part of the
continent. The chronic form of the disease due to T.b. gambiense is found in west, central and
south western part of Africa. The distribution of the disease is focal occurring in circumscribed
areas. Since the beginning of the 20th century, as soon as the disease was clearly identified
and its epidemiology better understood, some 260 foci were described. Today only a number
of these foci are recognized active, meaning where transmission is taking place.
NEGLECTED TROPICAL DISEASES
The transmission Cycle
446
T.b. gambiense sleeping sickness is transmitted from human to human by the tsetse fly
which is the most common form of transmission. As some animals can host the human
pathogenic parasite, transmission can occasionally take place directly from animals to humans,
which is believed to be one of the cause of the long term maintenance of the disease in
endemic areas, however the epidemiological importance of such zoonotic transmission is
poorly understood.
4
Diagnosis
Diagnosis of HAT requires confirming the presence of the parasite. The disease is difficult
to diagnose early by both, lack of specific signs and symptoms in the first stage of the disease
and lack of sensitivity of the parasitological methods available. Serological tests available
NEGLECTED TROPICAL DISEASES
T.b. rhodesiense sleeping sickness transmission cycle involves to a great extent domestic
and wild animals. Intensified man to man transmission occurs during epidemics. The strong
zoonotic character of the T.b. rhodesiense form of the disease substantially complicates surveillance and control issues, requiring action on the fly or on the animals hosting the parasite.
447
today are only useful for screening and establishing suspicion of infection. Confirmation of
infection will require the performance of parasitological tests to demonstrate the presence of
trypanosomes in the patient. The parasites can be present in any body fluids. However, the
number of parasite can be so low (mainly in the gambiense form of the disease) that available
parasitological methods may not be sensitive enough to find them. Thus a negative
parasitological result in the presence of a positive serological test does not necessarily indicate
absence of infection, and tests may have to be repeated over time to achieve diagnosis.
Treatment
Only four drugs are registered for the treatment of Human African Trypanosomiasis:
pentamidine, suramin, melarsoprol and eflornithine. None of them are anodyne since all have
a certain level of toxicity. Pentamidine and suramin are used in the first or early stage of
respectively T.b. gambiense and T.b. rhodesiense infections. Melarsoprol is used in the second
or advanced stage of both form of the disease and eflornithine is only used in the second
stage of the T.b.gambiense infections since it has been found not to be effective in the disease
due to T.b rhodesiense. All four drugs are described in a separate section.
Drugs
NEGLECTED TROPICAL DISEASES
PENTAMIDINE
448
Powder for injection 200 mg of pentamidine isethionate.
Pentamidine was registered in 1950 as pentamidine mesylate but has been used against
Trypanosomiasis since 1937 (Lourie 1942) and against leishmaniasis since 1940. Its effect on
Pneumocystis carinii was evidenced by Goa (1987), and the drug was reevaluated and
commercialized in its actual isethionate form in 1984. Pentamidine isethionate is a diamidine
compound with antiprotozoal activity. It is administered parenterally since it is unreliably
absorbed from the gastrointestinal tract. It does not enter the cerebrospinal fluid at curative
levels. Detectable amounts remain in the liver and kidney for many months as a result of
selective binding. Only a small fraction is excreted unchanged in the urine within 24 hours.
Used in the treatment of the first stage of T. b. gambiense African trypanosomiasis.
Some of the observed adverse effects are mild nephrotoxicity which is usually completely
reversible and pancreatic damage resulting in hypoglycaemia due to excessive insulin
release, subsequent insulin insufficiency and pancreatitis have been reported. Other adverse
effects include hypocalcaemia, gastrointestinal effects, confusion, hallucinations, cardiac
dysrhythmias, local induration and, occasionally, sterile abscess. Rarely, thrombocytopenia,
leukopenia, abnormal hepatic function tests and Stevens-Johnson syndrome have been
reported.
Storage: Vials of dry powder should be stored below 30 Æ C. Reconstituted sterile solutions
should be stored between 2 and 8 Æ C (for short periods) and any unused portion should be
discarded within 24 hours of preparation.
SURAMIN SODIUM
Powder for injection 1 g
A complex derivative of urea with antiprotozoal activity that has also been used in the
treatment of onchocerciasis. It enters the extracellular space but does not cross the bloodbrain barrier. Because it forms stable complexes with protein, suramin is not absorbed from
the gastrointestinal tract and must be administered by intravenous injection. It dissociates
slowly from plasma proteins and is detectable unchanged in the urine for up to 3 months after
the last dose.
Used in the treatment of first stage T. b. rhodesiense African trypanosomiasis
Some of the observed adverse effects are heavy proteinuria, stomal ulceration, exfoliative
dermatitis, severe diarrhoea, prolonged high fever and prostration. Lesser symptoms,
which are common, include tiredness, anorexia, malaise, polyuria, increased thirst and
tenderness of the palms and soles.
Storage: Vials of suramin powder for injection should be kept in well-closed containers
protected from light.
Injection 36 mg/ml solution in propylene glycol (1,2 – propanediol)
Melarsoprol is an organic arsenical compound that is used in African trypanosomiasis when
the central nervous system is involved. It is administered intravenously because it is unreliably
absorbed from the gastrointestinal tract and is too irritant for intramuscular administration.
However, it enters the central nervous system in sufficiently high quantities to kill the
trypanosomes. It is largely metabolized to nontoxic pentavalent compounds and is excreted
in the urine and faeces within a few days.
Used in the treatment of confirmed second stage cases (meningoencephalitic involvement)
of T. b. gambiense or T. b. rhodesiense African trypanosomiasis. Relapse occurs in less than
5% of cases, however in certain endemic areas rate of relapses have been much higher (up to
20%). Because drug-induced fatalities occasionally occur, melarsoprol should be used only
in hospitals and specialized treatment centres.
Some of the observed adverse effects are a reactive encephalopathy characterized by
headache, tremor, slurring of speech, convulsions and ultimately coma, this is the most serious
complication. Frequent, less severe, adverse effects include myocardial damage, albuminuria and
hypertension. Agranulocytosis is a particularly dangerous but rare reaction. Dose-related renal
and hepatic dysfunction can occur during the later phases of treatment. Other adverse effects
include hyperthermia, urticarial rashes, headache, diarrhoea and vomiting.
Storage: Ampoules are kept at room temperature and should be protected from light.
NEGLECTED TROPICAL DISEASES
MELARSOPROL
449
EFLORNITHINE
Injection 200 mg of eflornithine hydrochloride/ml solution in 100-ml bottle.
Eflornithine is an ornithine derivative with activity that is specific against T. b. gambiense.
It acts by inhibiting the enzyme ornithine decarboxylase, which is involved in polyamine
synthesis in trypanosomes. The plasma half-life is 3.0-3.5 hours. Eflornithine readily crosses
the blood-brain barrier to enter the brain and is mainly excreted by the kidneys.
Used for the treatment of T. b. gambiense African trypanosomiasis in both the early and
the late stages. Eflornithine is not effective for the treatment of T.b. rhodesiense infections.
The most common adverse effects reported include diarrhoea, anaemia, leukopenia,
thrombocytopenia and convulsions. Impaired hearing has also been reported. Less
commonly, vomiting, anorexia, alopecia, abdominal pain, headache, facial oedema,
eosinophilia and dizziness have occurred. These are reversible on withdrawal of the drug.
Storage: Ampoules should be stored at ambient temperatures.
http://www.who.int/trypanosomiasis_african/en/
NEGLECTED TROPICAL DISEASES
Buruli ulcer disease
(Mycobacterium ulcerans infection)
450
Buruli ulcer, a disease caused by infection with Mycobacterium ulcerans, is one of the most
neglected but treatable tropical diseases. The causative organism is from the family of
bacteria which causes tuberculosis and leprosy but Buruli ulcer has received less attention
than these diseases. Infection leads to extensive destruction of skin and soft tissue with
the formation of large ulcers usually on the legs or arms. Patients who are not treated early
often suffer long-term functional disability such as restriction of joint movement as well as
the obvious cosmetic problem. Early diagnosis and treatment are vital in preventing such
disabilities.
Buruli ulcer has been reported in over 30 countries mainly with tropical and subtropical
climates but it may also occur in some countries where it has not yet been recognized. Limited
knowledge of the disease, its focal distribution and the fact that it affects mainly poor rural
communities contribute to low reporting of cases. Steady progress is being made now to
develop tools for diagnosis, to understand exactly how infection is transmitted and to develop
treatment and prevention, and these offer the prospect of better disease control.
History
In 1897, Sir Albert Cook, a British physician working at the Mengo Hospital in Kampala,
Uganda, described skin ulcers that were consistent with Buruli ulcer (BU). In 1948, Professor
Peter MacCallum and his colleagues in Australia provided a detailed description of the disease
among six patients from the Bairnsdale area near Melbourne. They were the first scientists to
isolate the causative organism, Mycobacterium ulcerans. In southern Australia, the disease
is still referred to as the Bairnsdale ulcer. In the 1960s, many cases occurred in Buruli County
(now called Nakasongola District) in Uganda, giving rise to the most widely used name for the
disease – Buruli ulcer. Since 1980, the disease has emerged rapidly in several parts of the
world, particularly in West Africa, prompting action by WHO in 1998. Given the increasing
geographical spread, severe consequences and limited knowledge of the disease, the World
Health Assembly (WHA) in 2004 adopted a resolution1 to improve the surveillance and control
of BU and accelerate research to develop better tools for its control.
Cause
Transmission
The exact mode of transmission is still under investigation. Some patients state that lesions
develop at the site of antecedent trauma. Research suggests that in Africa, some aquatic
insects of the order Hemiptera (Naucoridae and Belostomatidae) can harbour M. ulcerans in
their salivary glands and transmit the disease to experimental animals. More recent data from
Australia suggest that salt marsh mosquitoes test positive for M. ulcerans DNA, although
transmission by this type of mosquito has not been established. Further research is in progress
to establish the exact role of insects and other factors in the transmission of the disease to
NEGLECTED TROPICAL DISEASES
M. ulcerans is an environmental mycobacterium. Recent information suggests that the
organism does not live freely in the environment, as previously thought, but is likely to occupy
a specific niche within aquatic environments (e.g. small aquatic animals, biofilms) from where
it is transmitted to humans by an unknown mechanism. Although slow growing, M. ulcerans
can be cultured from human lesions on media used for mycobacteria, provided the incubation
temperature is kept between 29-33 ÆC (lower than that for M. tuberculosis). There is some
variation among strains of M. ulcerans from different geographical areas (Africa, America, Asia
and Australia), but the relationship between the different strains and virulence in humans has
not been established. M. ulcerans produces a destructive toxin, mycolactone, which causes
tissue damage and inhibits the immune response. The toxic effects of mycolactone explain
most of the virulence of this organism.
451
humans. If confirmed, BU will be the only known mycobacterial disease to be transmitted
by insects.
Epidemiology
Buruli ulcer frequently occurs near water bodies – slow flowing rivers, ponds, swamps and
lakes; cases have also occurred following flooding. Activities that take place near water bodies,
such as farming, are risk factors, and wearing protective clothing appears to reduce the risk
of the disease. The reasons for the growing spread of BU remain unclear. All ages and sexes
are affected, but most patients are among children under 15 years. In general, there is no
difference in the infection rate among males and females. The disease can affect any part of
the body, but in about 90% of cases the lesions are on the limbs, with nearly 60% of all lesions
on the lower limbs. Unlike tuberculosis (TB), there is no evidence to suggest that infection
with the human immunodeficiency virus (HIV) predisposes individuals to BU infection. There
is also no evidence that the disease can be transmitted from person to person. There is little
seasonal variation in the incidence of the disease.
NEGLECTED TROPICAL DISEASES
Prevalence
452
Buruli ulcer has been reported from 30 countries in Africa, the Americas, Asia and the
Western Pacific, mainly in tropical and subtropical regions. In Côte d’Ivoire, approximately
24 000 cases have been recorded between 1978 and 2006. In Benin, nearly 7000 cases have
been recorded between 1989 and 2006; in Ghana more than 11 000 cases have been recorded
since 1993. In Australia, more cases of BU are being reported recently – 25 in 2004, 47 in 2005
and 72 in 2006. Most of the recent cases have come from the State of Victoria and the town
of Point Lonsdale. Increasing number of cases are being reported from Cameroon, Congo,
Gabon, Sudan, Togo and Uganda. After 30 years of no official report, an assessment carried
out in south-eastern Nigeria in November 2006 confirmed some BU cases. Some patients have
been reported from China, but the extent of the disease is not known. Recent reports suggest,
for the first time, that Brazil may be endemic in the areas bordering French Guyana. These
numbers may only be an indication of the presence of the disease but do not reveal the
magnitude of the problem.
Considerable research would be required to determine the exact prevalence and burden
of the disease for reasons including:
➠ insufficient knowledge of the disease among both health workers and the general
public, leading to significant underreporting;
➠ people most affected by BU living in remote, rural areas with little contact with the
health system;
➠ variability in the clinical presentation of the disease leading to BU being mistaken for
other tropical skin diseases and ulcers; and
➠ BU not being a notifiable disease in many countries.
9
For these and other reasons, it is difficult to establish the exact number of people affected
by the disease and the size and location of all endemic areas. Vigilance is required in the
surveillance systems of both endemic countries and countries that have not reported BU but
which share borders with endemic countries. Other tropical and subtropical countries have
the potential to become endemic; again, vigilant surveillance is important. Occasionally,
travellers who have returned from endemic areas to North America or Europe develop BU,
which can pose a significant diagnostic challenge for clinicians unfamiliar with the disease.
Signs and Symptoms
Diagnosis
Buruli ulcer is often diagnosed and treated based mainly on clinical findings by experienced
health workers in endemic areas. Laboratory diagnoses are infrequently used to make
decisions about treatment because of logistic and operational difficulties. However, laboratory
diagnoses can be used to confirm the clinical diagnosis retrospectively on swabs and tissues
taken during treatment, but this is seldom done.
Four laboratory confirmatory methods are commonly used:
●
Direct smear examination. An examination done on swabs from ulcers or smears from
tissue biopsies that can be carried out rapidly at local health facilities where TB microscopy
NEGLECTED TROPICAL DISEASES
Buruli ulcer often starts as a painless, mobile swelling in the skin called a nodule. The
disease can present as a large area of induration or a diffuse swelling of the legs and arms.
Strains of M. ulcerans isolated from the different clinical forms of the disease in a particular
geographical region appear identical, suggesting that host factors may play an important role
in determining the different clinical presentations. Because of the local immunosuppressive
properties of mycolactone, or perhaps as a result of other unknown mechanisms, the disease
progresses with no pain and fever, which may partly explain why those affected often do not
seek prompt treatment. However, without treatment, massive ulcers result, with the classical,
undermined borders. Sometimes, bone is affected causing gross deformities. When lesions
heal, scarring may cause restricted movement of limbs and other permanent disabilities in
about a quarter of patients. Other conditions that may mimic BU include: tropical phagedenic
ulcers, often referred to as tropical ulcers; leishmaniasis, particularly in South America;
onchocerciasis nodules; and fungal skin infections.
453
●
●
●
is also done. The sensitivity of this method, however, is low (about 40%) because M.
ulcerans bacilli are not uniformly located within tissue and because their numbers tend to
decrease over time.
Culture of M. ulcerans. A procedure done on swabs from ulcers or tissue biopsies that
takes 6–8 weeks or more; sensitivity is approximately 20-60%.
Polymerase chain reaction (PCR). A test whose results can be obtained within two days
on swabs of ulcers or tissue biopsies; sensitivity is around 98%.
Histopathology. A method that requires tissue biopsies; sensitivity is about 90% and is
useful also for differential diagnoses when the results of methods 1 to 3 are negative.
However, methods 2 to 4 are confined to reference and research laboratories, which are
often remote from endemic areas. Recently, an innovative dry-reagent-based PCR has been
developed that may be used in district hospital laboratories.
A simple and rapid diagnostic field test for BU is urgently needed because early disease
–nodule– can be treated locally and inexpensively. However, early disease poses the greatest
clinical diagnostic challenge. M. ulcerans toxin is more widely distributed within a lesion than
the bacilli, suggesting that the development of an antibody to mycolactone could lead to a
rapid diagnostic field test. Equally, the genome sequencing of M. ulcerans has revealed
proteins that appear to be unique to M. ulcerans. The testing of these proteins as potential
antigens to be used in the development of a simple diagnostic blood test and the development of antimycolactone antibodies are high research priorities.
Treatment
Current recommendations for treatment are as follows:
NEGLECTED TROPICAL DISEASES
➠ A combination of rifampicin and streptomycin/amikacin for eight weeks as a first-line
454
treatment for all forms of the active disease. Nodules or uncomplicated cases can be
treated without hospitalization.
➠ Surgery to remove necrotic tissue, cover skin defects and correct deformities.
➠ Interventions to minimize or prevent disabilities. Cumulative experience of treating
about 300 patients in Benin, Cameroon and Ghana has shown that treatment with
rifampicin and streptomycin (RS) for eight weeks according to WHO guidelines leads
to complete healing of nearly 50% Buruli lesions. Interestingly, it is also possible to
treat some of the patients on ambulatory basis. Recurrences after antibiotic treatment
is less than 2% compared to 16-30% with surgical treatment alone. These encouraging
developments are changing the strategy for BU control and treatment which until 2004
focused on surgical treatment.
Social and cultural aspects
In developing countries, sociocultural beliefs and practices strongly influence the healthseeking behaviours of people affected by BU. The first recourse is often traditional treatment.
In addition to the high cost of surgical treatment, fear of surgery and concerns about the
resulting scars and possible amputations may also prevail. Due to the disfiguration, stigma
is a problem that also prevents people from seeking treatment. As a consequence, most
patients seek treatment too late, and both the direct and indirect costs are considerable.
The impact of the disease on the few health facilities in the affected areas is enormous. The
long hospital stay, often more than three months per patient, represents a huge loss in
productivity for adult patients and family caregivers, and loss of educational opportunities for
children. The long-term care of those disabled, most of whom are children aged 15 years,
places an additional costly burden on affected families.
http://www.who.int/buruli/en/
Leishmaniasis
Although cutaneous leishmaniasis can be traced back many hundreds of years, one of the
first and most important clinical descriptions was made in 1756 by Alexander Russell following
an examination of a Turkish patient. The disease, then commonly known as “Aleppo boil”,
was described in terms which are relevant: “After it is cicatrised, it leaves an ugly scar, which
remains through life, and for many months has a livid colour. When they are not irritated, they
seldom give much pain. It affects the natives when they are children, and generally appears
in the face, though they also have some lesions on their extremities. In strangers, it commonly
appears some months after their arrival in an endemic area; very few escape having lesions,
but they seldom affect the same person above once.”
Representations of skin lesions and facial deformities have been found on pre-Inca
potteries from Ecuador and Peru dating back to the first century AD. They are evidence that
cutaneous and mucocutaneous forms of leishmaniasis prevailed in the New World as early
as this period.
Texts from the Inca period in the 15th and 16th centuries, and then during the Spanish
colonization, mention the risk run by seasonal agricultural workers who returned from the
Andes with skin ulcers which, in those times were attributed to “valley sickness” or
NEGLECTED TROPICAL DISEASES
History
455
“Andean sickness”. Later, disfigurements of the nose and mouth become known as “white
leprosy” because of their strong resemblance to the lesions caused by leprosy. In the Old
World, Indian physicians applied the Sanskrit term kala azar (meaning “black fever”) to an
ancient disease later defined as visceral leishmaniasis. In 1901, Leishman identified certain
organisms in smears taken from the spleen of a patient who had died from “dum-dum
fever”. At the time “Dum-dum”, a town not far from Calcutta, was considered to be
particularly unhealthy. The disease was characterized by general debility, irregular and
repetitive bouts of fever, severe anaemia, muscular atrophy and excessive swelling of the
spleen. Initially, these organisms were considered to be trypanosomes, but in 1903 Captain
Donovan described them as being new. The link between these organisms and kala azar was
eventually discovered by Major Ross, who named them Leishmania donovani. The Leishmania
genus had been discovered.
NEGLECTED TROPICAL DISEASES
http://www.who.int/leishmaniasis/history_disease/en/index.html
456
The disease and its epidemiology
THE VECTOR
The leishmaniases are caused by 20 species pathogenic for humans belonging to the genus
Leishmania, a protozoa transmitted by the bite of a tiny 2 to 3 millimetre-long insect vector,
the phlebotomine sandfly.
Of 500 known phlebotomine species, only some 30 of them have been positively identified
as vectors of the disease. Only the female sandfly transmits the protozoa, infecting itself with
the Leishmania parasites contained in the blood it sucks from its human or mammalian host
in order to obtain the protein necessary to develop its eggs. During a period of 4 to 25 days,
the parasite continues its development inside the sandfly where it undergoes a major
transformation. When the now infectious female sandfly feeds on a fresh source of blood, its
painful sting inoculates its new victim with the parasite, and the transmission cycle is
completed.
The insect vector of leishmaniasis, the
phlebotomine sandfly, is found throughout the
world’s inter-tropical and temperate regions.
The female sandfly lays its eggs in the burrows of
certain rodents, in the bark of old trees, in ruined
buildings, in cracks in house walls, in animal
shelters and in household rubbish, as it is in such
environments that the larvae will find the
organic matter, heat and humidity which are
necessary for their development. In its search for
blood (usually in the evening and at night), the female sandfly covers a radius of a few to
several hundred metres around its habitat.
Various forms of leishmaniasis
Leishmaniasis currently threatens 350 million men, women and children in 88 countries
around the world. The leishmaniases are parasitic diseases with a wide range of clinical
symptoms: cutaneous, mucocutaneous and visceral.
Cutaneous forms of the disease normally produce skin ulcers on the
exposed parts of the body such as the face, arms and legs. The
disease can produce a large number of lesions –sometimes up to
200– causing serious disability and invariably leaving the patient
permanently scarred, a stigma which can
cause serious social prejudice.
MUCOCUTANEOUS FORMS
In mucocutaneous forms of leishmaniasis,
lesions can lead to partial or total destruction of the mucous
membranes of the nose, mouth and throat cavities and surrounding
tissues. These disabling and degrading forms of leishmaniasis can
result in victims being humiliated and cast out from society.
NEGLECTED TROPICAL DISEASES
CUTANEOUS FORMS
457
VISCERAL FORMS
Visceral leishmaniasis –also known as kala azar– is characterized
by irregular bouts of fever, substantial weight loss, swelling of the
spleen and liver, and anaemia (occasionally serious). If left untreated,
the fatality rate in developing countries can be as high as 100%
within 2 years.
http://www.who.int/leishmaniasis/en/
Geographical distribution
Currently the leishmaniases, prevalent in four continents, are considered to be endemic in
88 countries, 72 of which are developing countries:
➠ 90% of all visceral leishmaniasis cases occur in Bangladesh, Brazil, India, Nepal and
Sudan;
➠ 90% of mucocutaneous leishmaniasis occurs in Bolivia, Brazil and Peru;
➠ 90% of cutaneous leishmaniasis cases occur in Afghanistan, Brazil, Iran, Peru, Saudi
Arabia and Syria.
NEGLECTED TROPICAL DISEASES
Magnitude of the problem
458
Over the last 10 years, endemic regions have been spreading further and there has been
a sharp increase in the number of recorded cases of the disease. As declaration is compulsory
in only 32 of the 88 countries affected by leishmaniasis, a substantial number of cases are
never recorded. In fact, 2 million new cases (1.5 million for CL and 500 000 for VL) are
considered to occur annually, with an estimated 12 million people presently infected
worldwide.
Leishmania/HIV co-infection
In a particularly ominous trend, the spread of HIV infection is bringing the severe visceral
form of leishmaniasis to new geographical areas and changing the epidemiology of this
disease in dangerous ways. The two infections coexist in a deadly synergy. Where
leishmaniasis occurs in urban areas, conditions often favour explosive epidemics – thus
transforming leishmaniasis from a sporadic to an epidemic threat. In persons infected with
HIV, leishmaniasis accelerates the onset of AIDS by cumulative immunosuppression and by
stimulating replication of the virus. The epidemiological significance of asymptomatic carriers
of the parasite has also been amplified by the advent of HIV, as co-infection rapidly activates
disease in parasite carriers. Sharing of needles by intravenous drug users contributes to the
spread of leishmaniasis as well as HIV.
To date, co-infection with leishmaniasis and HIV has been reported in 34 countries in
Africa, Asia, Europe, and South America. The impact of this emerging public health problem
is readily apparent and increasingly severe. In southern Europe, for example, up to 70% of
adult cases of visceral leishmaniasis are associated with HIV infection. Users of injecting drugs
are the most seriously affected group. Analysis of trends is facilitated by use of a geographical
information system to map and monitor patterns of co-infection.
http://www.who.int/leishmaniasis/burden/en/
Diagnosis
DAT freeze-dried antigen, antigen detection in urine (of special interest in immunosuppressed VL patients) and dipsticks K39/K26.The dipstick K39 for serological diagnosis was
successfully used in Ethiopia, India, Nepal, and Sudan. An intercountry research programme
(Ethiopia, Kenya, Sudan), supported by TDR, aims at comparing tests for diagnosis of visceral
leishmaniasis in the field.
Treatment
VECTOR CONTROL
DEVELOPMENT OF NEW DUGS
Routine control currently depends on case management: early detection and prompt
treatment. Pentavalent antimonials have been the mainstay of case management since the
1940s. Although injection directly into the ulcers in the common cutaneous form brings good
results, management of all other forms has limitations imposed by the high cost of drugs, the
long course of treatment, and the serious side-effects. The development of resistance is of
particular concern. In India, for example, up to 60% of cases are now resistant to first-line
drugs, necessitating the use of even more expensive and more toxic second-line drugs.
All currently available drugs have serious drawbacks. Some are associated with severe
reactions, including chemical pancreatitis and cardiovascular toxicity. If used at high dosage,
NEGLECTED TROPICAL DISEASES
As an alternative vector control approach, insecticide-impregnated bednets in Syria were
used to cover a population of 10 000. A 50% reduction in yearly incidence of cutaneous
leishmaniasis was oberved. The insecticide-impregnated bednets were also used in Sudan.
459
one has been shown to cause diabetes in more than 10% of cases. Second-line drugs trigger
dangerous reactions, some of which can be lethal. Some treatments require injections while
others need to be administered intravenously over a period of 15 to 30 days under close
medical supervision, usually in a hospital setting. As leishmaniasis affects impoverished
populations, the high price of these drugs and long treatment courses preclude the treatment
of many patients.
http://www.who.int/leishmaniasis/research/en/
Chagas Disease
(American Trypanosomiasis)
Introduction
Chagas disease is a zoonosis (or an anthropozoonosis) due to the flagellated protozoan
parasite Trypanosoma cruzi. It is transmitted to man by infected faeces of a blood-sucking
triatomine bug through the insect sting, another skin break or through mucous membranes,
including conjunctiva or oral/digestive mucosa, occasionally causing outbreaks with
contaminated food. Transmission through blood transfusion, pregnancy and delivery are also
possible, and less frequently, through organ transplantation or laboratory accident.
NEGLECTED TROPICAL DISEASES
Clinical signs
460
The acute phase, with high parasitaemia, commonly lasts around two months. Most of the
cases are a- or oligosymptomatic, but depending on the inoculation site, the first sign can
be a skin chancre (chagoma) or unilateral purplish orbital oedema (Rom a sign) with local
lymphoadenopathies and fever over several weeks. That can be accompanied, among others,
by headache, pallor, myalgia, dyspnoea, oedema in inferior limbs or face, abdominal pain,
cough, hepatomegaly, rash, painful nodules, splenomegaly, generalized oedema, diarrhoea,
multiple lymphoadenopathies, myocarditis (chest pain, heart failure) and more rarely
meningoencephalitis (seizures, paralysis). Morbidity can be higher in children under five,
elderly, immunocompromised or in cases with possible high parasite inoculum, such as seen
in oral outbreaks. In AIDS the meningoencephalitis is the more frequent manifestation
(differential diagnosis with toxoplasmosis).
The chronic phase, with parasites hidden in target tissues – especially heart and digestive
smooth muscle, has different possible clinical forms: a) asymptomatic (indeterminate form),
more frequent, typically in the beginning of the chronic phase and lasting all life in most of
the patients; b) cardiac form, till 30% of the patients, with conduction dispreveorders,
arrhythmia, cardiomyopathy, heart failure and secondary thromboembolism; c) digestive
lesions (megaoesophagus and megacolon) or mixed forms (cardiac plus digestive), till 10% of
the patients, just seen south to the Amazon basin.
Laboratory diagnosis
In the acute phase (or in reactivation for immunosuppression) a blood wet smear or a blood
concentration technique such as microhaematocrit or Strout technique, must be used.
Stained preparations, such as malaria films, detect parasites when parasitaemia is high (acute
phase). In the Amazon basin microscospy technicians of malaria have been trained to detect
acute individual cases and through them possible oral outbreaks and areas of active
transmission (surveillance system). In the chronic phase serologic tests should be used: the
detection of anti-Trypanosoma cruzi antibodies through a conventional or recombinant
enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination assay, indirect
immunofluorescence assay, western blot, rapid diagnostic test (such as immunochromatography), among others. Especially for research purposes, haemoculture, xenodiagnosis
(faeces examination of uninfected triatomine bug fed with the patient’s blood) and
Polymerase Chain Reaction (PCR) are also used.
There is no any available vaccine. Depending on the region, key tools are vector control
(insecticide spraying), house improvement (such as plastered walls, cement floors, corrugatediron roofs) and personal preventive measures (such as bed nets) and good hygiene practices
in food preparation, transportation, storage and consumption bed nets), together with the
transmission control through blood transfusion and organ transplantation. Secondary
prevention is important in: congenital transmission – diagnosis of infected pregnant women
and detection of possible newborn infection with parasitological or serological tests after
eight months of age (with no longer existing mother antibodies); laboratory accident
prevention using safety standard protocols (laboratory coat, gloves, face mask, cap, glasses),
especially when dealing with trypomastigotes - the human infective form of the parasite.
NEGLECTED TROPICAL DISEASES
Prevention
461
Treatment
The etiological treatment is urgently indicated in the acute phase and reactivation (immunosuppression). At that moment parasitological cure rates are almost 100% and they decrease
with longer duration of the infection/disease. At younger age the prevalence of side-effects
is also lower. The etiological treatment is indicated, as well, in congenital infection and early
chronic phase. In adults, especially those with indeterminated form, etiological treatment
should be offered, but balancing potential benefits (to prevent or delay the development of
the Chagas disease) against a long treatment schedule together with frequent side effects.
The two available drugs are benznidazole and nifurtimox. Main contra-indications are
pregnancy and renal or hepatic failure. Especially with nifurtimox, also psychiatric or neuronal
disorders (such as seizures).
NEGLECTED TROPICAL DISEASES
http://www.who.int/neglected_diseases/diseases/chagas/en/index.html
462
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