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of
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74 Adedayo O, Grell G, Bellot P Hyperinfective strongyloidiasis in
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94- Matsen JM, Tumer JA Reinfection in enterobiasjs (pinworm infection): simultaneous
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Tlssue
Nematodes Including
Trichinosis, Dracunculiasis,
and the Filariases
DAVID I. GROVE
9;93:195_203.
a recombinant
nitiatiye. Int
2003:33:1 2.15- 1 258
NR IrnpacI of mass chemotherapy on the morbidity due to soil-trar.smitted
roes Acta Trop 2003;86:191-214
usnn LS. Optinising the benefifs
Dnr:rs 2001;3:495-508
Med Int Health 2001t6:915-921.
Grove DI Human strongyloidiasis Adv parasitol 1996;38:251-309
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acute infantile disease in Papua New Guinea. Trms R Soc Trop Med Hyg 1978:12:554.
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medical center, West Virginia, 1991-1998. CIin Infect Dis 2000;31:E5-E6.
68
mthelmintic treutment
in chiljrcn
J
The tissue-dwelling
roundworms constitute r ltr,tiol. global hezJrh
problem. They are widely scattered arould tho r.icrld, especially in ljte
tropics, and intect millions of people. Sorne are p.rrasites of hunlans
cnly, whereas others hf,ve an animai reservoir. A'll these pnrasites havcl
complex life cycles involving arthropod intermedjate hosts, except
Trichinella species, which are transmitted directly from one host to the
next by ingestion of infective larvae. Like most helminths, the adult
worms do not multiply in the human host; therefore the worm load and
severity of disease depend in large measure on the intensity and frequency of exposure to the infective forms. The relative pathogenicity
of the adult wofins versus the larval forms varies according to the
species of infecting worm. Deflnitive diagnosis requires isolation and
identiflcation of the parasite, but for some infections this is difficult.
Effective therapy is available for only some of these infections. Some
parasites present almost insurmountable control problems, whereas
others can be avoided by simple preventive measures.
Infections acquired by ingestion of contaminated food or water are
considered first, and then those transmitted by blood-sucking flies are
discussed. Historical information conceming all of these parasites, including the circumstances of their discovery and elucidation of their
life cycles together with the clinical illness they cause and modes of
treatment that have been developed can be found elsewhere.l
TRICHINOSIS
Trichinosis develops when undercooked flesh contaminated with infective larvae of Trichinell.a spp. is eaten. Most infections are asymptomatic, but heavy exposure may lead to diarrhea, periorbital edema,
myositis, fever, and prostration.
Tricltinella spiralis is the species that has been recognized for
years, but the genus has been revised taxonomically. Eight species
have now been described based on their genetic, biochemical, physical (tolerance to high and low temperatures), and biologic data (susceptibility of various hosts) (Table 286-1). In addition, three other
genotypes are acknowledged in the genus, but their taxonomic level is
uncertain at present.2'3
Life Cycle
When raw or inadequately cooked meat containing viable larvae of
Trichinella spp. is eaten, the organisms are freed from the cyst walls
by acid pepsin digestion in the stomach and pass into the small intestine. Larvae invade the colurnnar epithelium at the bases of the villi of
the small intestine and develop into adult worns. They are obligate intracellular parasiteS occupying the cytoplasm of a row of enterocytes.
The males are about 1.50 x 0.05 mm and the females about 3.50 x
0.06 mm. The number of larvae released by a fertilized female varies
with the species of both parasite and host. T. spiralis probably produces about 500 lar-vae over a period of 2 to 3 weeks and then the adult
wonns are expelled in the feces. The newbom larvae seed the skeletal
muscles via the bloodstream. They burrow into individual muscle'
fibers and over the next 3 weeks increase 10 times in length; they then
coil and become capable of infecting a new host. In many species) a
cyst wall develops around the larva that may eventually calcify (see
Table 286-1). Larvae may remain viable for several years.
T. spiralis
T. nafjya
T. britovi
T1
T2
T. pseudospiralis
T. murrell.i
Uncedain status
T. nel3oni
Uncertain status
Uncertain status
T. papuae
T. zimbawensis
.Except
T3
T4
T5
T6
T7
T8
T9
T10
T11
Worldwide'
Arctic, subarctic
Temperate, subarctic
Arctic, Tasmania
North America
Subarctic
Tropical Afnca
Southern Alrica
Japan
Papua New Guinea
Central Africa
Australia and New Zealand and some Pacific islands
Epidemiology
Trichinella spp. arc distributed throughout the world and
are
spread in nature among a large number of carnivorous animals;
being an incidental host (see Table 286-l).a The reservoir hoii
primarily the fauna present in that region. Humans are an,i
host, most infections being due to T. spiralis; a few are
britoyi, T. nativa, T. nelsoni, and T. pseudospiralis. T. spiralii
papuae are the species with the highest infectivity for
swine in the United States are fed with grain, and these
generally uninfected. The small proportion fed with garb
come infected when given uncooked trichinous scraps,
meat, or when the carcasses of infected wild animals suc
eaten.5 In Europe the fox is the primary reservoir of the
of Trichinella, and human infections usually occur in rural
traditional swine-rearing practices are used or raw horse meat.ii
Fewer than 100 human cases are usually reported each
United States. About three-fourths of them are due to
processed pork; most of the rest have been caused by
poorly cooked bear meat. walrus meat, or cougar jerk1,.
gence of the domestic cycle of
has resulted from the breakdo
owned farms in some countries.
has increased greatly in both de
,.,:::l
,_..
Pathologic Characteristics
the various species have ditrrfmt- ,..
er hosts.r For example. trichinocis itr
r ingestion of inlected walrus scrms
to be associated wrth prolonged diarrhea and few muscle
nativaprodnces primarily an enteral illness, whereas Z
few if any intestinal symptoms. T. nelsoni is of relatively
genicity during both its enteral and parenteral phases,
do.rpirolis may produce severe enteral and systemic sym. ptom$i'..-:1 :
"
During the flrst 2 to 3 weeks after infection, the sni.Lil[
shows mild, partial villous atrophy and an inflammatoryi
polymorphonuclear cells, eosinophils, lymphocytes, and rulft
in the mucosa and submucosa. Adult worrns may be seeii,lilithelial layer near the bases of the villi. The most striking
in the skeletal muscles. The fibers become edematous, loSe
striations, and undergo basophilic degeneration; in addidon;
clei proliferate. The typical coiled worm, the cyst wall dedi
the host cell, and the surrounding lymphocytic and eos
trate may be seen within the muscle fiber (Fig. 286-l). In
focal interstitial myocarditis, meningitis, and encephalitis
Clinical Features
Most infections are subclinical. The development of
pends
mainly on the size of the inoculum of vi4p!c,l;t
-Consequently,
the frequencies of the symptoms una srgry .-0j:
Pigs, rodents, horses, bears, foxes
Bears, foxes, dogs
Dogs, cats, bears
Birds, omrivorous mammals
Bears
Bears
Yes
Yes
Yes
No
Hyenas, cats
Yes
Yes
Yes
Lions, panthers
Yes
Sy)vatic camivores
Pigs
Crocodiles. mammals
No
No
Yes
particularly pork products or wildlife, the likelihood of the diAgnosis
is greatly increased.I0 Further confirmation is provided if others who
have eaten the same meat have similar symptoms. Eosinophilia is often found, beginning about the l0th day and sometimes reaching extremely high levels. The erythrocyte sedimentation rate is usually nor-
286-1.
Section of muscle showing two cysts, the larger
the coiled larva cut in cross section surrounded by the
derived from the host muscle fiber (the "nurse" cell) and a pre-
mononuclear infiltrate. H&E.
widely from outbreak to outbreak. Their relative frequenin Table 286-2.
attributable to adult worms in the intestines may be
the first week after infection.s Diarrhea is the most combut patients may also complain of abdominal discomvomiting. Patients with extremely heavy worm burdens may
lminating enteritis. Symptoms associated with systemic inlawae are much more corrunon and usually appear during
week after infection. Fever is frequently present, although
iable intensity and duration. Periorbital edema may be assosubconjunctival hemorrhages and chemosis. Myositis with
and weakness is also common; it usually develops first
muscles and then involves the masseters, neck musflexors, and lumbar muscles. Some patients complain of
cough, shortness of breath, hoarseness, and dysphagia.
a macular or petechial rash is observed. Retinal or subnter hemorrhages are sometimes seen. These systemic
usually peak 2 to 3 weeks after infection and then slowly
although malaise and weakness mdy persist for weeks.
, a patient dies, usually from myocarditis but sometimes
litis or pneumonia. It has been claimed that there may be
sequelae ofinfection, including muscle aches, eye disturcardiac complaints, and headaches.e
should be suspected in a patient who has any of the cardiof periorbital edema, myositis, fever, and eosinophilia. If
reveals the recent consumption of poorly cooked meat,
mal. Elevated serum creatine phosphokinase and lactic dehydrogenase
Ievels indicate considerable muscle involvement.
Antibodies are not detectable until at least 3 weeks after infection.
They may be measured by a variety of techniques including enzymelinked, immunofluorescence, indirect hemagglutinin, precipitin, and
bentonite flocculation assays. A rising antibody titer may help establish the diagnosis.s Tests for detecting Trichinella DNA in muscle or
blood using the polymerase chain reaction (PCR) are being developed.rt Muscle biopsy is usually unnecessary; if doubt remains, a
specimen obtained from a tender, swollen muscle may confirm the diagnosis, although Trichinella species must be differentiated from other
nerfiatodes sometimes found in muscles.
The protean manifestations of trichinosis require differentiation of
t[is infection from a large number of other diseases. The gastrointestinal symptoms may mimic those of gastroenteritis. Systemic symptoms may cause confusion with influenza, typhoid fever, sinusitis, dermatomyositis, glomerulonephritis, and angioneurotic edema. The rash
may resemble that found with measles, scarlet fever, and typhus.
Treatment
,l
There is no satisfactory treatment for trichinosis. In the rare instance that
a patient is known to have ingested trichinous meat within the past week
or so, mebendazole (5 mg/kg) or albendazole (5 mglkg) should be administered orally twice daily for 1 week.8,12 These drugs are active
against intestinal worms but have little effect on muscle-embedded lar-
vae.
In a
placebo-controlled trial, patients with trichinous myositis
treated with mebendazole or thiabendazole improved significantly compared with those given a placebo or the antifungal agent fluconazole.rl
However, the first cases were seen within a day of eating an infected pig,
and patients had been ill for a median of only 3 days when treatment was
started (G. Watt, personal communication). The apparent improvement
in patients given anthelmintics may have been due to accelerated elimination of adult worms from the gut and hence less seeding of muscles
by larvae. Furthermore, it has been shown that mebendazole fails to kill
parasites encapsulating in muscles.la The mainstays of treatment for systemic trichinosis are bed rest and salicylates. Corticosteroids may be
used for critically ill patients, but evidence of benefit is equivocal.
Prevention
The most efflective method for killing Trichinella larvae is proper
cooking: The thermal death point is 55o C, so meat should be cooked
until there is no trace of pink fluid or flesh. Storage in a home freezer
(-15'C) for 3 weeks usually sterilizes meat; smoking, salting, and
drying are unreliable. L5
OTHER MUSCLE NEMATODE INFECTIONS
H aycocknem
and malaise
edema
rash
leg edema
91
89
82
77
52
20
18
I6
l5
hemorrhage
splinter hemonhage
9
9
6
J
71-100
68-r00
50-94
29-100
0-100
o-67
0-75
0-48
0-67
0-65
0-60
0-40
0-13
a perplex u m lnfection
Two Australian patients have been described who presented with severe;
progressive muscle weakness, in one case over a period of 2 years.
Muscle biopsy disclosed predominantly adult nematodes within muscle
fibers and sparse larvae both within and outside ofthe fibers; capsules did
not form around parasites within myoflbers.16 These worms were subsequently described as a new genus and species, Haycocknemn perplexum.tl Ther life cycle is unknown. It is possible that autoinfection occurs, particularly in patients treated with corticosteroids for polymyositis.
Six weeks of treatment with albendazole appeared to be effective.
DRACUNCULIASIS
Dracunculiasis (dracontiasis, guinea worm infection) develops after
drinking water containing small crustaceans infected with
Dracunculus medinensis. It is characterized by a chronic cutaneous ulcer from which the worm protrudes.rE
Life Cycle
When water containing infected copepods is ingested, larvae are released in the host stomach, pass into the small intestine, penetrate the
mucosa, and reach the retroperitoneum, where they mature and mate.
Epidemiology
is now found mostly in tropical Africa.
Shallow ponds, cistems, and wells are the usual habitat of the crustacean
intermediate hosts. The disease is prevalent in areas where people bathe
or wade in water used for drinking putposes. Manifestations in a com_
al cycle
Dracunculus medinensis
ear, and
disabil-
ity resulting from infection may be of great socioeconomic importance.
Clinical Features
There are often no clinical signs until the worm reaches the surface and
after which the ulcer heals. Multiple ulcers are common, and secondary
infection is frequent. In endemic areas, patients are often bedridden for
a month or so. There is no immunity to reinfection.
FIGURE 2A6-2.
Diagnosis
The clinical picture is characteristic. Larvae can be found during mi_
croscopic examinatign of the discharge fluid.
Treatment
Thiabendazole,25 mg/kg twice daily for 2 days, and metronidazole, 5
mg/kg twice daily for I week to 10 days, have no effect on the worms
themselves but produce resolution of the inflammation within several
days. This permits easy removal of the worm over a week or so by pro_ ,
gressively rolling out the emerging worm onto a small stick. (As of
this writing, it is not clear whether thiabendazole will continue to be
available from its manufacturer, Merck.) Corticosteroid ointmenls.
shorten the time to complete healing, and the addition of topical antibiotics reduces the risk of secondary bacterial infection.re Ivermectin
has no effect on prepatent guinea worms. Mebendazole in high dosage
is not recommended because it does not lessen the duration of diseaie
H::il:'ff,lj:,"T:;
completely and pain-
th local
Secondary bacterial infection
anesthesia.2r
should be treated as necessary.
Prevention
cally from an estimated 4 million in 1981. By 2001 dracunculiasis had
been restricted to 13 African countries. During the first 6 months of
2002, only 21,000 cases were reported, 777a of those being in the
Guinea worm partially extruded frorii
the dorsum of the foot.
Sudan which is racked by civil war. Guinea worm diseasQ
become the second human infection to be eradicated.22 :
BANCROFTIAN AND BRUGIAN FILARIASIS
Bancroftian fllariasis and brugian (Malayan) filariasis are sii
ical conditions resulting from the transmission of
crofti, Brugia malayi, arld Brugia timori to humans
by,
Symptomatic patients have acute lymphatic inflammatrol
fects of chronic lymphatic obstruction such as hydrocele,
sis of the limbs, and chyluria.
Life Cycle
After the bite of an infected mosquito, infective larvae:
lymphatics and lymph nodes, where they mature over
months into white, thread-like adult worms. the males
X 0.1 mm and the females 100 x 0.25 mm. The adults
or more, and the fertilized females discharge microfilari
approximately 150 X 7 pm via the lymphatics into thp
The number of microfilariae found in the peripherat blood
is usually a surge of microfllariae into the blood during
the night, a phenomenon known as nocturnal periodicity,
the South Pacific with W. bancrofii infection have a
nounced peak that is maximal during the day. B. malayi
duce nocturnal peaks of varying intinsity. Ii microfilariae
by a mosquito during feeding, the organiims develop intovae ovet the next 2 weeks and are ready to repeat the
bancrofti is distributed widely throughout the tropics and
malail is restricted to South and Southeast Asia. and B.
is restricted to the eastern Indonesian archipelago. It is estithat 120 million people are infected with these parasites. There
B.
'animal reservoir for W. bancrofti, bttt B. malayi has been found
and primates.
in endemic areas, only a small proportion (less than l7o) of
ito bites are infective. It is probable that infections with microa are produced only when a susceptible person receives a large
of infective larvae and that obstmctive disease develops only
posure continues for many years. Although infection often bechildhood,23 clinical filariasis is mainly a disease of adults
more cofilmon in men.2a'2t The disability resulting from infechave profound sexual and socioeconomic effects.
Characteristics
s
harboring adult worms display lymphangiectasia but little inearly in the course ofinfection. Later, there may be endotheion, fibrin deposition, and a granulomatous inflammatory
of eosinophils, lymphocytes, and macrophages. Molting and the
worms exacerbate the inflammation, which is succeeded by fi-
obstruction of lymph flow26 All of these Processes are assoclith complex immunologic events.2? It is possible that a proportion
population in endemic areas generates protective immunity that
T cell-mediated. Secondary bacterial infection may be an imporin the development of elephantiasis.2s
been recognized recently that most filariae are infected with
rickettsial bacteria of the genus Wolbachia. These bactransmitted transovarially and appear to have evolved a muassociation with their fiIarial hosts.'ze Antibiotic treatment of
shown that clearance of bacteria results in embryotoxicity,
of molting, and eventually death of the worms. It is likely
released from these bacteria is a major activator
responses. Death of parasites, whether occurring
or as a result of antiparasitic treatment,30 is likely to release
of bacteria, which precipitate an acute inflammatory reFurthermore, chronic release of Wolbachia may cause progresto infected lymphatics and desensitization of the immune
Features
are asymptomatic despite the presence of microfilaremra.
manifestations are due to acute inflammation or chronic lymn. Attacks of lymphangitis or lymphadenitis with fever,
backache, and nausea occasionally occur. Acute funiculitis,
itis, or orchitis may be seen. These acute episodes usually suba few days to several weeks but may recur. Chronic lymtthy is frequently found and may be the only manifestation of
ln long-standing cases, lymphedema may develop. Chronic
is the most common feature and may cause considerable sexity. The lower limbs are involved less frequently; at first there
edema that is most marked pretibially, but eventually nonpitmay involve the whole limb (Fig. 286-3). With elephantiain of the leg or scrotum becomes thickened, flssured, and
ion and secondary infection may occur.32 Occasionally,
ices appear, especially in the genital region. Chyluria develops
lymphatics burst into the urinary tract.
diagnosis of bancroftian filariasis and brugian filariasls
on demonstrating the parasite. Unfortunately, microfl lariae
ently absent from the blood during both the early and late
lhe disease. A blood sample should be taken around midnight
Patient is from the South Pacific. The smear is stained and
for microfllariae (Fig. 286-4). Ifnone is found, a concentrashould be used.
FIGURE 246-3. Man with inguinal lymphadenopathy, large bilateral hydroceles, marked edema of the left lower limb (particularly the
leg and foot), and early signs of elephantiasis in the foot.
Microfilariae are occasionally found in hydrocele fluid or chylous
urine. Eosinophilia is usually absent except during episodes of acute
inflammation. Serologic tests for antibody such as bentonite flocculation, indirect hemagglutination, enzyme-linked immunosorbent assay,
and indirect fluorescent antibody tests may be of some help but do not
differentiate among the various forms of filariasis or between past and
current infection. A commercial card test to detect W. bancrofti arfii'
gen is available,33 and assays for brugian filariasis are being developed. Polymerase chain reaction (PCR) tests to detect W. bancrofii in
2a
blood may be available in research laboratories
Adult worms are sometimes found in Iymph node biopsy specimens, but this procedure is not generally justified. Microfilariae or
worm fragments may be seen with fine-needle aspiration cytology.3a
Ultrasonography of the lymphatic vessels in the scrotal area may reveal dilated lymphatics and motile adult worms, the so-called "fllarial
dance sign," examples of which may be viewed on the Internet.r5
Unfortunately, the adult worms of brugian filariasis are not easily detectable.36 Abnormal lymphatic drainage in the legs may be demonstrated by lymphoscintigraphy.3T If microfilariae cannot be lbund and
sophisticated imaging techniques are not available, the diagnosis must
be made on clinical grounds by excluding other causes.
Treatment
There is no satisfactory treatment for filariasis. Dethylcarbamazine in an
oral dose of 6 mg/kg daily for 2 weeks reduces the number of microflIariae in the peripheral blood but is no panacea. An altemative regimen is as
follows: day I 50 mg, day 2 50 mg tid, day 3 100 mg tid, then 6 mg/kg/day
in 3 divided doses for 4-14 days. Diethylcarbamazine kills some adult
complications that may be seen are endomyocardial f,brosis,
hy, encephalopathy, peripheral neuropathy, arthritis, pleural
tn, glomerulonephritis and nephrotic syndrome, venous thromand breast calciflcat'ion. Pulmonary infiltrates have also been as-
to loiasis, but it is difficult to differentiate this condition from
pulmonary eosinophilia,
ONCHOCERCIASIS
Onchocerciasis (river blindness) is caused by Onchocerca volvuhts
and is transmitted to humans by blackflies. It is characterizedby an
itchy dermatitis, subcutaneous nodules, keratitis, and chorioretinitis.
Life Cycle
After the bite of an infected Simulium blackfly, Iarvae penetrate the skin
should be suspected in a patient with a typical history who
in West or Central Africa. The diagnosis is established by findariae in the daytime blood, as described under "Bancroftian
Filariasis." Failure to find microfllariae does not rule out the
and the diagnosis is usually made on clinical grounds. Filarial
serology may be available in specialized laboratories.s'z A PCR
been described that is positive in some nonmicrofilaremic indi, but it is not generally available.s3 Occasionally, the adult worm
extracted from the eye or elsewhere, a therapeutic as well as di-
where they may live for years. Each female produces large numbers of
unsheathed microfilariae, 200 to 300 x 6 to 8 pm, that migrate through
the skin and connective tissues. The life cycle is continued when they are
ingested by female blackflies and develop into infective larvae.
Epidemiology
In the recent past, O. volyulus has infected 20 million people in West,
measure.
eliminates microfilariae from the blood but often
administered as described under
asis." Treatment with ivermectin in a single dose of 200
decreases microfrlarial densities in the peripheral blood.
albendazole has any effect is uncertain; conflicting results
bendazole at 600 to 800 mg daily for several days have been
by the same investigators.5a's5 Patients with high microfilarial
kill adult worrns. It is
(more than 30,000/m[) often experience fever, pruritus,
, and artfualgia within 36 hours of
diethylcarbamazine or
n therapy. Encephalopathy may be precipitated by treatment
of these drugs, especially if microfilarial loads are high.56
with doxycycline was unsuccessful in'two patients.sT
protection depends on avoiding places where biting flies are nuwearing protective clottring, and using insect repellents. Mass
Ont of villages intemrpts transmission; diethylcarbamazine is adin doses of 5 mg&g/day for 3 consecutive days each month,
n may be given at 3-month intervals. Diethylcarbamazine rn
of 300 mg once weekJy is effective in preventing loiasis in persons
residing temporarily in endemic regions.s8
SUBCONJUNCTIVAL NEMATODE INFECTIONS
repens lnfection
been a number of reports from around the world of ocular
with the nematode Dirofilaria repens, which is a parasite of
felids and is transmitted by mosquitoes. In humans, most
found in the subconjunctiva, but they may also be found inand in the orbit. Treatment is by excision.se
formosana lnfection
formosana is normally a filarial parasite infection of ca'monkeys (Macaca cyclopsis), probably transmitted by biting
(Culicoides species). A7.4 cm long worm was removed from
lunctiva of a Taiwanese woman; no microfilariae were seen
lupi lnfection
of subconjunctival infection with a filarial nemaOnchocerca lupi, a parasite of dogs, have been re-
cases
ly
and migrate into the connective tissues. They develop into white flliform
adults, the males being 3 X 0.2 mm and the females 400 X 0.3 mm. The
worns are often found tangled together in nodules of flbrous tissue,
Europe.6'
labi atopapillosa lnfection
of subconjunctival infection with Setaria labiatopillosa, a
have been described from Romania. The worms
,d, and the patients were treated with diethylcarbamazrne.
is unknown.62
Cenhal, and East Africa and another 1 million people in scattered foci in
Central America and South America. It is possible that the Onchocerca
causing sowda, which is prevalent inArabia, may be due to an as yet undescribed species.63 There is no known animal reservoir. Onchocerciasis
tends to haye a focal distribution in areas in which it is endemic. In Africa
the flies breed in faslflowing streams in both the savannah and rain forest
and tend to bite the lower body. [n the Americas thq,flies breed in small
streams on hillsides and bite more frequently around the head. Heavy parasite loads and severe disease are seen only with repeated infection.
Pathologic Gharacteristics
A granulomatous inflammatory reaction followed by fibrosis
develops
around the adult worms. The microfilariae in the subcutaneous tissues
may produce a low-grade inflammatory reaction, destruction of elastic
fibers, and fibrosis. Similarly, immunologically mediated processes
cause onchocercal keratitiss and retinal disease. As discussed earlier
(see "Bancroftian and Brugian Filariasis"), O. volvulus,like many other
filariae, is infected by Wolbachia bacteria.2e The inflammatory response
to microfiIariae is thought to be predominantly directed against
Wolbachia.6s Furthermore, when patients with onchocerciasis were
treated with doxycycline for 6 weeks and the worms excised 4 months
later, most bacteria were eliminated and embryogenesis was largely inhibited.66 When doxycycline was administered with ivermectin, embryogenesis was blocked completely for at least l8 months.67
Clinical Features
Early skin lesions produce an itchy, erythematous, papular rash. With
severe infections, cutaneous lymphedema with leathery thickening
and depigmentation may be seen.68 Ultimately, loss of elasticity with
chronic lymphadenopathy may produce pendulous sacs containing inguinal and femoral lymph nodes. There may be firm, nontender, freely
mobile fibrous nodules measuring several millimeters to centimeters
and containing the adult worrns. They are most commonly located
over bony prominences. In addition, there may be systemic changes
including weight loss and musculoskeletal pains. Sowda is a form of
onchocerciasis that is often localized to one limb with intensely itchy,
swollen, darkened skin covered with scaly papules.
Impaired visual acuity is the most serious complication of onchocerciasis. The most comrnon lesion is punctate keratitis followed
by pannus formation and corneal fibrosis. Slit lamp examination often
reveals microfilariae in the cornea and anterior chamber. Iridocyclitis,
glaucoma, choroiditis, and optic atrophy may develop.6e Not surprisingly, blindness in endemic areas is associated with a three- to fourfold increase in the mortality rate. It has been suggested that onchocerciasis is associated with an increased prevalence of epilepsy.
Diagnosis
The diagnosis is made by demonstrating microfilariae in skin snips or
in the comea or anterior chamber on slit-lamp examination or by flnding adult worms in a nodule biopsy specimen. Nonpalpable nodules
OTHER ONCHOCERCAL INFEL;TIONS
Fewer than 10 cases of zoonotic infections with various
Onchocerca have been reported. The reports have inc
worms in the subconjunctiva,6r cornea,Te wrist,8o and
under a microscope for microfilariae.
found in urine. Ultrasonographic deous humor has been described, and
for the detection of onchocercal antibodies and antigens and the PCR test for DNA are available in some
{ru_v-s*9Lv_+*14_!l!f,F*Q*I.tg-l!-s_
Mansonella ozzardi lnfection
research laboratories.To'7r
M anso nel I a
Treatment
Traditionally, patients with skin disease have been treated with di_
ethylcarbamazine. This drug kills microfilariae but has little effect on
the adult worm. Severe reactions such as rash, fever, generalized body
pains, keratitis, and iritis may occur, so the dose must be increased
gradually as follows: day 1, 50 mg; day 2,50 mg three rimes; day 3,
100 mg three times; and days 4 to 21,3 mg&g three times a day.
During the past few years, many studies have shown thai iver_
mectin is safer and more effective than diethylcarbamazine. The rate
of decrease in the number of microfilariae in the skin and anterior
chamber of the eye and the severity of Mazzotti reactions are less, and
treatment with 150 pg/kg repeated at 3-month intervals for 2 to 3
Years
stage and may cause
slow
si4gle and repeated
cours
n the number of mi_
crofilariae in skin and the anterior chamber of the eye, and there is a
significant reduction, in infection transmission.
Ivermectin therapy leads to alleviation of the severe skin disease and
regression of early lesions of the anterior segment of the eye, especially
iridocyclitis, but the posterior segment lesions remain stable. lndeed, a
Cochrane review has questioned whether ivermectin treatment prevents
loss of visuai acuity.Ta A practical approach to treatment is to administer
ivermectin, 150 pg/kg orally once and repeat it at 3-month intervals if ,
there are continuing symptoms or evidence of eye infection. Side effects
appear to be rel
areas but may be
more severe in i
op fever, prurinis,.
and an urticarial
cerciasis ind loiasis may develop ah encephalopathy when treated with ivermectin.Ts
Inadvertent administration of ivermectin during pregnancy was not as_
sociated with an increased number of birth defects.
Albendazole probably has little place in the treatment of onchocer_
ciasis. It may well be that by the time the next edition of this book ap_
pears doxycycline with or without ivermectin will be the standard
treatment
s.76 Nodules should be removed surgically
whenever
ophthalmologic advice should be iought
before tre
perstans nfection
I
Mansonella perstans, also transmitted by midges, is found
and South America. Adult worms live in the body cavities. U
microfilariae may be found in the peripheral blood, especiqily
Most patients are asymptomatic, although some have coniunct
ules. If teatment is required, diethylcarbamazine should tre
cause ivermectin is minimally effective.sa Albendazole may be;
value when given at a dose of 400 mg twice daily for at least l
M an so nel I a st re pto
cerca nfection
I
Mansonella streptocerca, transmitted to humans by biting
found in Central Africa. It is characterized by dermatitis. M
are found in skin snips. The traditional treatment is with
mazine, although iverrnectin also has some effect.85
Tropical pulmonary eosinophilia is a disease syndrome
crofilariae in the tissues, especially the lungs. It is probabl5z <
munologic hyperresponsiveness to W bancrofti or B. matayi:
tered throughout the tropics but is most commonly seen in.:
Asia.86 Patients have recurrent episodes of a paroxysmal d1
wheezing, and dyspnea. Malaise, anorexia, and weight loss are
Physical examination often reveals scattered wheezes aiili
Some patients may have hepatomegaly and lymphade
severity of the symptoms usually fluctuates over many
of microfilariae from the blood makes a definiti
absence
Prevention
ting flies are
control prois being athas been repeated mass administration of ivermectin. Although the parasite has
not been eradicated, major control has been achieved.?7 In 1991 a program was set in motion in the Americas with the aim of intemrpting
transmission within the next few yeals.78
FIGURE 286-6. Chest radiograph of a woman
,91aty eosinophilia. Reticulonodular opacities are
out both lung fields.
with
Eosinophilia is almost always present at more than 3000
ils/I, often at extremely high levels. Chest radiographs ususcattered reticulonodular opacities (Fig. 286-6). Antibodies
al worms are found in the serum. A presumptive clinical diagcan usually be made without recourse to lung biopsy, and the diis established by a successful response to therapy.
inistration of diethylcarbamazine orally in a dose of 3 mg/kg
times daily for 2 weeks is an effective treatment.sT There may be
ial exacerbation of symptoms, but the eosinophil level falls, and
radiograph clears over a few weeks. A small proportion of
, however, have persistent, subtle clinical, radiologic, or funcabnormalities indicating chronic low-grade alveolitis77; in such
nces, it may be appropriate to repeat the course of treatment with
ylcarbamazine. The role of ivermectin in the treatment of tropical
eosinophilia has not yet been determined.
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parallels the distribution of the specific freshwater snail that
its intermediate host (Table 287-1). Five major species of
somes infect more than 200 million persons, and more than 65
of other trematodes infect at least 40 mjllion persons.2-4
Trematodes vary in length from I mm to more than l0 cnr,
tened dorsoventrally, and have an anterior and ventral
blind bifurcate intestinal tract. Schistosomes differ from other
todes in several ways: The sexes of adult wofins are separa6
mission is via penetration of skin by larvae, and there is only a
intermediate host. whereas other trematodes are hermanhr;di,
are transmitted through ingestion of infected fish,
aquatic plants that serve as second intermediate hosts. Most
infections are subclinical, and in general it is only the small
ofpersons who have heavy worm burdens who develop severe
SCHISTOSOMES
Of an estimated 200 million persons infected with schi
countries and teritories, approximately 120 million have
20 million have severe disease, and 100,000 die each vear.2a
control programs and socioeconomic development have
nated schistosomiasis in some parts of the world, little
been made elsewhere, especially in Sub-Saharan Africa,
than 80Vo of cases occur. Moreover, water resource
jects and population movements have spread the disease into
where it was not previously endemic. In addition to the flV€
species that cause human schistosomiasis or bilharziasisi,i
Schistosoma mansonl S. japodcum, S. mekongi, S.
S. haematobium, othex species of animal schistosomes cause
infection, including schistosomes of birds and small
cannot mature in the human host but die in the skin where
a dermatitis.5'6
Life Cycle
Adult worms measuring I to2 cm in length and 0.3 to 0.6
Iive, mate, and feed on blood in the portal and mesentedG,
(5. japonicum, S. mekongi, S. mansoni, S. intercalatum)
plexus (S. haemntobium).7 The male worm folds around and
the female in its gynecophoral canal. Egg production varie!:
proximately 300 eggs per day for female S. mnnsoni auitd S;;
bium and 3000 eggs duly for
S.
japonicum (Fig. 287-1).
ing 145 X 55 pm for S. mansoni and S. h.oertatobium and85
for S. japonicum (Fig.287-2), are deposited in the venules.
their way into the urine or feces and hatch in fresh wate4,