Infections, Dermatologic Conditions in the Returned Pediatric Traveler

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Infections,
Dermatologic Conditions
in the Returned Pediatric Traveler
Gregory Juckett, MD, MPH
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EDUCATIONAL OBJECTIVES
1. Review infectious and non-infectious
causes of dermatologic problems in
returning pediatric travelers.
2. Learn how to take a travel history
recording geographic and environmental exposures, rash onset and
rash evolution and characteristics.
3. Identify primary skin lesion and
secondary characteristics.
Gregory Juckett, MD, MPH, is Professor of Family Medicine at the West
Virginia University School of Medicine,
Morgantown, WV.
Address correspondence to: Gregory
Juckett, MD, MPH, fax: 304-293-2713;
email: gjuckett@hsc.wvu.edu
Dr. Juckett has disclosed no relevant
financial relationships.
doi: 10.3928/00904481-20110615-09
D
ermatologic problems are the
third most common cause of
post-travel consultation at GeoSentinel travel clinics, after febrile illness and diarrhea.1 At these sites, typical
skin problems in returning travelers included cutaneous larva migrans (9.8%);
insect bites (8.2%); abscesses (7.7%);
infected insect bites (6.8%); allergic rash
(5.5%); dengue fever (3.4%); and leish-
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maniasis (3.3%).2 Other pyodermas and
skin infestations (scabies, myiasis, tungiasis) were also routinely seen.
Skin conditions in returning travelers
can be divided into infectious and noninfectious etiologies. Infectious skin conditions may be tropical in origin (25%),
although the majority are cosmopolitan
(75%).3 Rash with fever should always
be distinguished from rash without, since
the former implies potentially serious
illness. Although most skin conditions
in travelers are self-limited, dengue and
chikungunya fevers, rickettsial diseases,
hemorrhagic fevers and meningococcemia may be life threatening.
EXPOSURE HISTORY
Travel rashes may be acquired from
exposure to sun, heat, insects, marine life
and/or an array of infectious causes: viruses, bacteria, fungi and parasites. Taking a detailed travel history is therefore
a critical first step, since many of these
diagnoses are dependent on specific exposures and locales. What was the exposure (location and environment), when
did the rash begin, where did it spread,
and how has it changed?
The predominant skin symptom is an
important clue: Itching suggests an allergic etiology; tenderness at the site suggests infection. Another clue is how the
rash progresses. Centrifugal rashes start
on the trunk and spread to the extremities (varicella), whereas centripetal rashes
(dengue fever, rickettsial infections) do the
opposite. Topical treatment by the patient
may alter the appearance of the rash (tinea
incognito with steroid use) or even exacerbate it (Neosporin contact dermatitis). An
oral medication history is also essential, as
travelers frequently experience drug eruptions or photosensitivity reactions.
PHYSICAL EXAM
Determining the identity of the primary skin lesion based on its appearance
and size (macule/patch, papule/plaque,
etc.) and any secondary characteristics
(scaling, hypopigmentation, lichenification, etc.) will help narrow the differential diagnosis (Sidebar, see page 364).
Pattern recognition is key. One author
suggests identifying eight different categories of skin lesions as starting points:
ulcers; pruritic lesions; papules; nodules;
vesicles; pigment change; linear lesions;
and rash with fever.3
TYPES OF INFECTIONS
Viral Infections
Dengue or “break-bone” fever is the
most common arbovirus (arthropodborne viral infection) in the world, the
others being yellow fever, Japanese en-
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Image courtesy of the Public Health Image Library/ James Gathany
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The Aedes albopictus mosquito, also known as the Asian tiger mosquito, has been found to be a vector of dengue fever.
cephalitis, and tick-borne encephalitis.
Most dengue infections in travelers are
acquired in Asia, increasingly followed
by the Americas, with a minority of cases
from Africa.4 Day-biting Aedes aegypti or
A. albopictus mosquitoes spread dengue,
which is now at a 20-year high throughout the Caribbean and Central America,
including recent non-travel-related cases
in the Florida Keys and Texas.
Symptoms include headache, fever,
retro-orbital pain, severe myalgias/arthralgias and a pink centripetal maculopapular
rash in 50% of patients.5 The characteristic
rash, usually appearing around the time of
defervescence, initially resembles a sunburn and blanches with pressure. Typically, small islands of normal skin are spared
(“white islands in a red sea”). It usually
resolves after 2 to 4 days with moderate
itching and desquamation.
A clinically similar illness, also associated with rash and joint pain, is
chikungunya fever, which can be distinguished from dengue by serology.
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Arthritis pain with chikungunya tends
to persist much longer (several months)
and the disease is much more prevalent
in Asia, where it co-exists with dengue,
than in the Americas. It is also spread
by day-biting Aedes mosquitoes. A major outbreak in India and Indian Ocean
islands occurred in 2005.6 Management
of both conditions is symptomatic; the
only practical prevention for travelers is
to use mosquito repellents.
Other viral exanthems, mostly nonspecific rashes associated with various
viral infections, are common and usually
self-limited. Enteroviruses (predominating in summer) and various winter-time
respiratory viruses (eg, adenoviruses)
are likely culprits in travelers.
Molluscum contagiosum is a common
childhood infection presenting as shiny
pearly-pink skin papules, often with a
characteristic central dimple. It is easily spread by any skin contact and may
also be acquired sexually. Treatment is
through destroying the lesions by abla-
tion, cryotherapy or, in the case of multiple lesions, by imiquimod cream.7
Cold sores (herpes simplex virus 1)
are easily provoked by sun exposure or
respiratory illness in travelers. Genital
herpes (HSV-2) may follow ill-advised
sexual encounters in adolescents. Both
infections often follow adolescent or
college-age spring break trips. Both
HSV-1 and HSV-2 appear as clustered
vesicles in their respective areas and are
managed by acyclovir or related antivirals, such as valcyclovir.
Bacterial Skin Infections
Pyodermas, either from Staphylococcus aureus or Streptococcus pyogenes,
are the most common bacterial skin
infections in travelers. Staph infections
may manifest as impetigo contagiosum
(honey-colored crusts and sores); bullous impetigo (blisters and erosions); folliculitis; furuncles (boils); or carbuncles
(aggregates of furuncles). Strep infections present also as impetigo contagio-
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SIDEBAR.
Travel Rashes by Symptom or Lesion Type
Ulcers: impetigo sores (vesicle/ulcer); HSV (vesicle/ulcer); CL; rickettsial infection (eschar); cutaneous anthrax (eschar).
Vesicles/Bullae: contact dermatitis; bullous impetigo; sunburn; HSV; varicella.
Pruritic Lesions: contact dermatitis; eczema; insect bites; CLM; scabies; swimmer’s itch; sea
bather’s eruption; tinea infections; urticaria.
Papules: molluscum contagiosum; insect bites; acne; pyodermas; myiasis (early); tungiasis; miliaria.
Nodules: boils; myiasis (late).
Pigment change: pityriasis versicolor; vitiligo; pityriasis alba (following eczema); phytophotodermatitis; fire coral injuries; post-inflammatory hyperpigmentation.
Linear lesions: CLM; contact dermatitis; phytophotodermatitis (streaks); jelly fish stings; larva
currens (strongyloides).
Fever: dengue; chikungunya; other viral exanthems; rickettsial infections (eschar); typhoid/enteric fever (rose spots); leptospirosis (jaundice; erythema nodosum; petechiae); brucellosis
(erythema nodosum); drug eruption.
Note some categories overlap (adapted in part from O’Brien classification)
CLM = cutameous larva migrants (creeping eruption); CL = cutaneous leishmaniasis.
Source: O’Brien; B. A practical approach to common skin problems in returning travelers. Travel Medicine and Infectious Disease
2009; 7: 125-146.
sum; ecthyma infectiosum (punched-out
sores); erysipelas; or cellulitis. Erysipelas appears raised with well-demarcated
margins, whereas cellulitis has none of
these features. Localized impetigo usually
responds to mupiricin ointment, but systemic beta-lactam antibiotics are usually
necessary for deeper or widespread infections. Methicillin-resistant Staphylococcus
aureus (MRSA) infections respond to sulfamethoxazole-trimethoprim, clindamycin
or vancomycin. In the event of a fluctuant
skin abscess, incision and drainage usually
cure the infection.
Rickettsial infections classically
present with fever, centripetal maculopapular rash and headache. A small
papule at the site of an infected bite develops into a black eschar or scab (tache
noire). Travelers to Asia may acquire
scrub typhus (Orienta tsutsugamushi),
spread by infected trombiculid mites or
“chiggers.” A black eschar with regional
lymphadenopathy and fever is a classic
presentation. Neurologic symptoms (obtunded mental state, deafness), meningitis and vasculitis may follow with up to
50% mortality if untreated.8 The similar
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African tick typhus (R. africae) is the
commonest rickettsial infection in South
Africa. Other tick typhus species with
similar symptoms occur in the Mediterranean (Rickettsia conorii), Australia
(R. australis) and the Americas (Rocky
Mountain Spotted Fever or Brazilian
Spotted Fever, both from R. rickettsiae).
Travelers returning from endemic areas
with headache, fever and rash warrant
prompt empiric treatment with doxycycline 100 mg twice a day for 14 days.
Doxycycline is usually avoided in children under 8 years of age but exceptions
are usually made for life-threatening
rickettsial infections. The usual pediatric
dose is 2.2 mg/kg orally every 12 hours
(maximum 100 mg per dose).
Typhoid or enteric fever (Salmonella
typhi or paratyphi), characterized by sustained high fever, abdominal discomfort
and sometimes “pea-soup” diarrhea, may
be associated with faint “rose spots,” actually bacterial emboli, visible only in lightskinned individuals. These 2- to 3-mm
macules are usually on the abdomen or
lower chest and last 3 to 4 days.9 Travelers
visiting friends and relatives (“VFR” trav-
elers) in South Asia are at particular risk,
and typhoid vaccines, even when used, are
only 50% to 80% protective.9 Diagnosis is
through culture of the blood or bone marrow. Although ciprofloxacin has been the
usual treatment, increasing quinolone resistance may warrant ceftriaxone therapy.9
Cutaneous anthrax (Bacillis anthracis) is characterized by a larger, painless
black eschar at the site of inoculation
surrounded by swollen red tissue (“malignant pustule”). Spores may infect
animal hides, and some infections have
been linked to imported skins used in
drumming workshops.10 The importation of animal hides from several countries (eg, Haiti) is prohibited for this
reason. Human-to-human spread of cutaneous anthrax is not known to occur.
Ciprofloxacin is curative.
Fungal Infections
The hot, humid conditions of the tropics favor the development of fungal infections. Tinea corporis (“ringworm”) infections usually appear as scaly, round, itchy
patches with central clearing and serpiginous margins. Tinea pedis (“athlete’s
foot”) causes itching and scaling of the
feet. Groin tinea or T. crurus (“jock itch”)
commonly affects post-pubescent males
and may be mimicked by erythrasma, a
bacterial infection that fluoresces coralred with Wood’s lamp. Tinea imbricata
from Trichophyton concentricum produces complex shingled patterns and is
acquired in the South Pacific and humid
areas of South and Southeast Asia. Most
tinea infections fail to fluoresce (Trichosporum spp.), although Microsporum spp.
lesions will fluoresce green with Wood’s
lamp.11 Diagnosis of fungal infection may
also be confirmed by seeing hyphae on
microscopic exam of skin scrapings (best
from the lesion border) with a drop of
20% potassium hydroxide (KOH). Treatment is usually with 2 weeks of a topical antifungal cream, although systemic
treatment is necessary for tinea capitis
(scalp ringworm) and tinea imbricata.
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Tinea versicolor (Malassezia furfura)
is a superficial fungal infection presenting as hypo- or hyperpigmented scaly
macules on the neck, chest and upper
back, fluorescing yellow-white under
Wood’s lamp. Vacation tanning accentuates the hypo-pigmentation. Skin scrapings reveal a characteristic “spaghettiand-meatball” hyphae/spore pattern.
Best treatment is with a short course of
oral ketoconazole because topical treatments usually result in recurrence.
Parasitic Infections
Visceral larval migrans (VLM), or
“creeping eruption,” caused by the dog
hookworm (Ancylostoma brasiliense),
is the most common dermatologic diagnosis in returning travelers.2 A disproportionate number of cases come
from the Caribbean, where dog feces on
the beach are the usual source of infection.2 The hookworm larvae enter the
vacationer’s feet or buttocks, causing an
itchy serpiginous rash as the larvae migrate within the skin. Fortunately, the infection is self-limited because the larvae
eventually die without developing. The
simplest treatment is oral single-dose albendazole or ivermectin.
Myiasis is a human botfly infestation producing a tender skin boil. Close
examination usually reveals a small central pore or breathing hole for the motile
maggot inside. The human botfly (Dermatobium hominis) from Latin America
attaches its eggs to mosquitoes that seek
out mammalian hosts. Usually only a few
lesions can be found on exposed skin and
they take 6 to 12 weeks to develop. 12
One type of botfly in Africa, the
Tumbu fly (Cordylobia anthropophaga),
lays its eggs on laundry drying outdoors.
Hence, there are many lesions on sites
covered by clothing containing these
larvae, which develop rapidly, typically within 9 days.12 For both botfly and
Tumbu fly infestation, surgical extraction for either species can be aided by
prior application of an occlusive sub-
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stance (bacon fatback or petroleum jelly), which induces upward migration of
the larvae, typically within 24 hours.13
Dermatobium infection can be reduced
through use of insect repellents while
Cordylobia eggs can be killed by ironing clothes before wearing them. A recent hotspot for Dermatobium infections
has been the Bolivian Amazon.14
Tungiasis (Tunga penetrans) describes a sand flea infestation of the feet.
This small burrowing flea of Africa, west
India and South America produces itchy
subcutaneous, dark 5- to 8-mm nodules
that may be observed to extrude tiny
eggs.15 The lesions last about a month
and often become secondarily infected.
Treatment involves excision. Proper
footwear is protective.
TYPES OF EXPOSURES
Insect exposures
Insect bites are ubiquitous in the tropics, but for most patients, result only in
transiently temporary pruritic papules.
However, bite severity depends on patient sensitivity. Bites on the ankles are
usually due to fleas. Persistent, red pruritic papules on the trunk may be due
to bed bugs (often in clusters of three:
“breakfast, lunch and dinner” sign) or
chiggers (found on belt or sock-lines).
Insect repellents containing either N, Ndiethyl-meta-toluamide (DEET) 35% or
picaridin (known overseas as icaridin)
15% to 20% reduce the number of bites,
whereas antihistamines relieve much of
the itching.16 Permethrin spray may be
used to protect clothing. Most insect
bites presenting after travel are complicated by secondary infection and may
thus require antibiotics.
Scabies or itch mites (Sarcoptes scabiei) may afflict travelers 4 to 6 weeks
after skin exposure when the mite population reaches symptomatic levels.17 An
allergic response to the burrowing of
female mites results in extremely itchy
papules in the finger webs, wrists, axillae,
breasts, buttocks, and genitals. Usually
the face is spared, except in heavier infestations. Pruritus may become intolerable
at night, resulting in insomnia. Sexually
acquired scabies presents as nodules on
the penis or scrotum. Therefore, sexual
partners, as well as family members,
should be treated along with the patient.
The most effective scabies treatment
is permethrin 5% cream applied from
the neck down and left overnight.18
Next morning, the cream is showered
off and all bedding and clothing should
be washed. Treatment may be repeated
in 7 to 14 days to ensure eradication.19
Gamma-benzene hexachloride lotion
(Lindane) is more toxic than permethrin
and is being abandoned for safety and
environmental reasons. In more hygienic conditions, oral ivermectin 200 mcg/
kg may be given as a single dose and,
if possible, repeated in 2 weeks, but this
therapy is not FDA approved.20 Itching
from the dead mites may persist for several weeks after any of these treatments.
Head lice infestation or pediculosis
(Pediculus humanis capitus) is easily
acquired through contact with infected
children. An itchy scalp is typical and
nits may be observed attached to hair
behind the ears and on the nape of the
neck. Nits hatch in a week, with lice
maturing in only 15 days. Nits attached
more than 5 mm out on the hair shaft are
usually nonviable, so school “no-nit”
policies are unnecessary.21
Pubic lice (“crabs”) may be acquired
from sexual contact and are confirmed by
finding nits on pubic hair. Although permethrin and pyrethroid shampoos (Nix,
Rid) have been the mainstay of treatment,
increasing drug resistance has led to the
development of newer therapies. Isopropyl myristate 50% (Resultz) dehydrates
the lice by damaging their exoskeleton.
Spinosad (Natroba topical solution), a
natural insecticide derived from the soil
bacterium Saccharopolyspora spinosa,
was just approved by the FDA for children older than age 4 years. Malathion
0.5% lotion is a much more toxic sec-
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ond-line therapy for resistant infections
approved only for children older than 6
years. Oral ivermectin also seems to work
at the same dosage for scabies. All family
members and any close contacts should
be treated, even if asymptomatic.
Cutaneous leishmaniasis is a parasitic skin infection spread by sand fly
bites: Phlebotomus sand flies in the Old
World (Europe, Africa, and Asia) or
Lutzomyia in the New (the Americas).
Travelers describe a bite papule developing into a persistent painless ulcer
with raised margins. The lesion’s edge
should be biopsied and sent for pathology and polymerase chain reaction
(PCR) testing. PCR is the diagnostic
method of choice because it identifies
the species involved.22
Treatment, usually with pentavalent
antimony or with intravenous amphotericin, is problematic but will speed lesion
healing. Most untreated lesions usually
heal with scarring, but this may take 12
to 18 months. New World L. braziliensis
ulcers appear to resolve but may recur
years later as mucocutaneous leishmaniasis, thus the decision to treat with antimonial drugs or amphotericin often
hinges on the likelihood of L. braziliensis re-infection.22
Aquatic Exposures
Because many travelers engage in
water sports, aquatic exposures pose a
particular risk. Bacterial infections may
result from marine skin abrasions, often contact with shellfish or coral. Serious cellulitis from Vibrio vulnificus, V.
parahemolyticus and Aeromonas may
follow. V. vulnificus is especially dangerous, causing high mortality in patients with liver disease. If blood pressure drops and hemorrhagic bullous
necrotic cutaneous lesions develop,
approximately 50% of V. vulnificus patients die within 48 hours.23 Treatment
of early marine infections in healthy
patients can be initiated with doxycycline, but more susceptible patients
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require doxycycline and a third-generation cephalosporin.
Leptospirosis is primarily a febrile
illness with jaundice, but it may provoke
an erythema nodosum rash or even mimic hemorrhagic fever.24 Mycobacterium
marinum infection presents as a persistent hand or foot nodule. Pseudomonas
aeruginosa, found in contaminated pools
or hot tubs, causes self-limited “hot-tub”
folliculitis with most lesions found in areas covered by bathing suits.
Coral injuries are especially troublesome in snorkelers and divers, often
taking months to heal. Fire coral (Millepora), actually a hydrozoan rather
than a true coral, is capable of stinging
on touch, producing long-lasting areas
of residual hyperpigmentation.
Sea bather’s eruption is the result of
microscopic Linuche jellyfish larvae or
“sea lice” trapped under a swimsuit. The
itchy maculopapular rash develops hours
after exposure and is treated symptomatically. “Swimmer’s itch” describes a
fresh-water dermatitis on exposed skin
caused by avian schistosome larvae (cercaria). Fortunately, these larvae are poorly adapted to humans, so the rash is selflimited. However, human schistosomiasis
may also begin with a swimmer’s itch
from fresh-water exposure in the tropics.
Most human schistosomiasis is acquired
in Africa, and in one series, 45% of cases
reported cutaneous symptoms.25
DRUG REACTIONS
Drug-related rashes accounted for
nearly 1% of rashes in returning travelers.2 Pruritic urticarial rashes are the most
common, but maculopapular rash, fixed
drug eruptions, erythema multiforme,
Stevens-Johnson syndrome and even
anaphylaxis may occur. The incidence
of antimalarial skin reactions in travelers to Africa was 8% for chloroquineproguanil; 3% for doxycycline; 2% for
Malarone; and 1% for mefloquine.26
Photosensitivity-type drug reactions require additional UVA exposure
so the rash is limited to exposed areas.
Photosensitizing drugs include tetracyclines (doxycycline); quinolones
(ciprofloxacin); antimalarials (chloroquine); sulfonamides; sulfonylureas;
phenothiazines; and acne medications.
Discontinuation of the offending drug
and use of antihistamines to control
itching are often all the treatment that
is required. More severe reactions respond to prednisone.
ENVIRONMENTAL SKIN CONDITIONS
Contact dermatitis is an allergic
contact reaction from plants or other
allergens in the environment. Although
poison ivy, poison oak and poison sumac (all in the genus Toxicodendron)
are the usual US suspects, many other
plants can trigger this response. Mango
sap, present in the unpeeled fruit, crossreacts with urushiol (the allergenic
component in poison ivy sap), causing
a pruritic, erythematous rash. Other
sensitizing plants include poisonwood
(Metopium toxiferum); cashew fruit
(Anacardium); Japanese lacquer trees
(Toxicodendron); African poison ivy
(Smodingium); and Indian marking nut
(Semecarpus anacardium).
Phytophotodermatitis describes a
plant sensitivity reaction requiring UVA
light exposure. Lemon or lime juice on
the skin frequently produces a hyperpigmented persistent rash where the juice
dripped on an exposed extremity. Other
culprits include figs, rue, and giant hogweed (Heracleum).27
Sunburn ruins many trips, especially if the burn occurs during the first
few days. Usually, this is the result of
sunscreen being applied in insufficient quantities or not being reapplied
after swimming. Ideally, 1 oz of 30+
SPF sunscreen is needed (if wearing
a bathing suit) at least 30 minutes before exposure. Direct sun during peak
intensity, between the hours of 10 a.m.
and 3 p.m., should be avoided. Symptoms of sunburn range from erythema
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to intense blistering. Chills, fever, and
dehydration may accompany severe
cases (“sun poisoning”). Treatment involves anti-inflammatory agents such
as aspirin or nonsteroidal anti-inflammatory agents, cool compresses, aloe
vera lotion, topical steroids and, rarely,
prednisone. Topical anesthetics should
be avoided because they often induce
sensitization. Although some of these
treatments provide symptomatic relief,
none of them appear to shorten recovery
time or reduce epithelial cell damage.28
Continued protection from further sun
exposure is mandatory.
Solar urticaria (sun-induced hives)
is a pruritic eruption induced by sunlight in susceptible individuals. Polymorphous light eruption, appearing as a
variable itchy maculopapular eruption,
is a sensitivity reaction to intense UVA
exposure in an un-acclimated individual. Rash and pruritus occur shortly after
exposure. The condition usually subsides later in the summer after the skin
becomes desensitized to sunlight.
Excess sweating also produces skin
problems. Pitted keratolysis or “sweaty
socks syndrome” is caused by the bacteria Kytococcus (Micrococcus) sedentarius and appears as tiny crater-like
pits on weight-bearing areas of the foot.
A foul smell is associated. Keeping the
feet dry or using topical antibiotics is
curative. Miliaria rubra, better known
as “prickly heat,” is a self-limited intensely pruritic skin reaction caused by
trapped sweat. Multiple tiny erythematous papules are noted under clothing.
Miliaria profunda describes a more
persistent form that occurs only in hot,
humid climates. Treatment involves removal of clothing, air conditioning, and
cool compresses.
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CONCLUSION
Rashes in returning pediatric travelers require a careful history and exam to
exclude multiple infectious and environmental causes. Many of these are nontropical conditions, but it is important
to know what the patient may have been
exposed to in their travels. Identifying
the primary lesion, time of rash onset,
key symptoms (itching or tenderness),
and the presence or absence of fever will
assist in making an accurate diagnosis.
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