Tropical Medicine 5: Dermatological Manifestations
The focus of this portal is the dermatological manifestations of tropical infectious diseases. The scope of dermatology includes far more than just infections, and this must be kept in mind when evaluating skin lesions in travelers and immigrants.
Macular, Popular, and Nodular Lesions
Arthropod Causes
Bites
One common cause of
dermatitis in the tropics is arthropod bites, including flies, spiders,
ticks, or mosquitoes. Localized reaction to the arthropod saliva often
occurs. Symptomatic treatment with antihistamines or topical steroids
is often adequate. Important to remember is that a number of tropical arthropods
are vectors for disease; keep this in mind in patients with evidence of arthropod
exposure.
Infestations
Scabies are
common in the tropics. The classic burrowing lesion may not be seen,
however, due to secondary infection. This should be on the top of the
differential
diagnosis in any tropically acquired dermatitis, especially in
children, and may be treated
topically with permethrin (5% cream) or ivermectin (200
µg/kg PO
single dose) as would
be done with domestically acquired scabies infestations.
Lice are another common infestation. Lice infestation is diagnosed by spotting either the nits or adult lice and treated similarly to scabies. It is important to thoroughly launder and dry clothing (including bedclothes) to prevent re-infection.
Myiasis is a unique infestation consisting of an arthropod (fly, flea, tick, etc.) laying its eggs on the host, and the larvae then invades the skin. Typically this appears to be a localized boil. However, upon opening the boil, the maggot is often visible. Tumbu fly (Africa), Bot fly (Central and South America), and Tunga chiggers/jiggers (Africa, Americas, Asia) are the most common syndromes. Treatment consists of removing the offending arthropod. Covering the lesion with petroleum jelly prompts the larvae to partially emerge, making grasp with instruments and extraction possible. Bot fly and chiggers are more difficult to remove and may require more aggressive, local, surgical extraction. Occasionally, body cavity myiasis (nose, urethra, anus, vagina, eyes, ears, wounds) may be seen, most often the result of the Old World screwworm fly. Again, physical removal of the screwworm is the approach to treatment, but may be challenging.
Fungal Causes
In the warm, humid setting of the
tropics, fungal infections abound. Tinea capitis, tinea cruris, tinea
corpora, tinea barbae, and tinea versicolor—all seen in
temperate zones—are
more common in the tropics. Clinically, they may be more
severe, but diagnosis and treatment
remains the same.
Madura foot, or mycetoma, is another noteworthy fungal syndrome that involves chronic swelling, involvement of the skin, subcutaneous tissues, and bone along with sinus formation and drainage of fungal spores. Madura foot may be caused by a number of organisms. Typically, the organisms are introduced transcutaneously (eg, via a thorn or other contaminated object) and are not contagious. This syndrome is slowly progressive and surprisingly painless. Diagnosis is through fungal stain or culture, and treatment is not terribly successful. Ketoconazole 200 mg twice daily for prolonged periods does help. Surgery (amputation) carries a high recurrence rate.
Other fungal infections transmitted via skin trauma include chromoblastomycosis and sporotrichosis. Microscopic exam is the diagnostic modality, and treatment is prolonged and of variable efficacy.
Parasitic
Infections
Onchocerciasis
The parasite
Onchocerca
is spread by the bite
of the blackfly. Larvae mature to
adults, which form subcutaneous nodules. The female
Onchocerca
sheds
countless larvae over her decades-long lifespan. These tiny larvae,
known as
microfilariae, migrate through subcutaneous tissues
from which they are taken
up in the blackfly bite. While alive, these microfilaria suppress the
immune
response locally; when they die, there is a minute, punctuate reaction
to their
corpse. Multiplied by the millions of microfilariae present, the
development of a significant dermatitis is understandable. It is
intensely pruritic, and may take
hyperkeratotic, atrophic, de-pigmented, or hyperpigmented forms. Sowda,
an
asymmetric hyperpigmentation of the lower extremity, is a trait
of onchocerciasis
in certain areas of Africa. Clinical
manifestations develop many months after
infection.
Diagnosis is obtained by taking a superficial skin biopsy, placing it in saline, and examining it microscopically for the emergence of the microfilariae. It is important that the skin snip be bloodless, for other filariae (discussed in later chapters) may be co-endemic with Onchocerca. Serological and DNA tests are also available.
Treatment is with ivermectin (see Vol III—TM13 Antiparasitic Primer). Occasionally, the Mazzotti reaction occurs with treatment, though less commonly with ivermectin than with older agents. This is basically an acute worsening of the dermatitis essentially resulting from the simultaneous demise of all the microfilariae
Cutaneous Larval
Migrans
Toxocara larvae (see
Vol III—TM4 Gastrointestinal and Abdominal Manifestations) in addition
to causing damage as
visceral larval migrans, are responsible for creeping lesion, when they
migrate
through the subcutaneous tissues. Rather unnerving, the worm is visible
as it
slowly snakes its way
along, causing local itching and irritation. This may be
treated with albendazole, or by cryotherapy of its leading end.
Bacterial and Mycobacterial Infections
Leprosy
A chronic granulomatous mycobacterial disease, leprosy may present as
chronic
or unusual acute skin lesions. The two types of leprosy are lepromatous
and
tuberculoid. Between these are intermediate (borderline, indeterminate)
forms.
Lepromatous leprosy is manifest by multiple hypopigmented macules and papules, which may be confluent. Lesions tend to be smooth and shiny. These patients have a high burden of the organisms, with dissemination throughout the body. The organisms gradually infiltrate the skin and thick, disfiguring nodules develop. Destruction of the nasal septum and other bony structures are pathognomonic. Testicular destruction may also result.
Tuberculoid leprosy has few lesions, which are flat macules or plaques with well-defined margins, are dry, scaly, and anesthetic. Hair loss is common in the affected area. Significant peripheral neuropathy develops, affecting the function of the motor system; the accompanying decrease in sensation leads to problems not unlike the diabetic foot.
For lepromatous leprosy, diagnosis is clinical, combined with acid-fast organisms identified in the skin. For tuberculoid leprosy, the organisms are fewer and may not be seen. Serology is often not helpful.
Treatment is a multidrug regimen. The World Health Organization (WHO) pharmacological treatment recommendations for tuberculoid leprosy are rifampin 600 mg monthly and dapsone 100 mg four times daily for 6 months. For lepromatous leprosy, the WHO recommends rifampin 600 mg monthly, dapsone 100 mg four times daily, and clofazimine 50 mg four times daily (or 300 mg monthly) for 2 years.
Pinta
A non-venereal treponemal infection, pinta is acquired by prolonged
close
contact. The lesion begins as a small, red papule and, over months,
progresses to
irregular, scaly patches up to 10 cm in diameter, progressing over many
months
to pintids, which are flat, hyperpigmented plaques, and ultimately to
hyperkeratotic de-pigmented plaques. Pinta may look like psoriasis,
lichen
planus, and
leprosy. Treat with benzathine penicillin
G 2.4 million units IM
(PEDS: 1.2 million units in
children).
Venereal Skin Conditions are discussed in Vol III—TM10 Urogenital Manifestations.
Ulcerous Lesions
Keep in mind that nearly any of the dermatoses noted in the preceding
section
may progress to an ulcerous lesion due to secondary infection,
excoriation, or
other causes.
Tropical Ulcer
This term
refers to ulcers of the lower leg found in the tropics that are not
attributable to
other etiologies described here. Although uncommon in tourists,
tropical ulcers are much more common in immigrants and refugees.
Administer
antibiotic treatment to
cover potential causes
such as anaerobes, spirochetes, or
Bacillus fusiformis.
Beljel
A subspecies of
Treponema pallidum
is transmitted non-venereally and is
responsible for endemic syphilis. Affecting children primarily, beljel
has a different geographic distribution (Middle East and North Africa)
than either
pinta (Caribbean and South America) or yaws (equatorial America,
Africa, and
Asia). Primary lesions
are painless white ulcers in the buccal
mucosa; secondary
lesions may be found in the mouth or spread
diffusely over the body. The
infection may cause long-term damage to
the cartilage, bones, and eyes. Serology
and microscopy do not distinguish between treponemal infections, so
epidemiological history is important. Treatment is benzathine
penicillin G 2.4 million units IM (PEDS:
50
000 units/kg in children).
Yaws
Yaws is another non-venereal treponemal infection and (PEDS) is most common
in children and adolescents.
In its primary stage, an ulcer full of spirochetes
forms at the site of exposure; in later stages, multiple similar
lesions occur, primarily on the palms and soles. There is a latent
phase, and the tertiary phase
may result in bone and soft tissue deformities. Diagnosis is
from history and
clinical exam. Serology and microscopy do not differentiate between
this and syphilis. Treatment is
benzathine penicillin
G 2.4 million units IM
(PEDS: 50
000 units/kg in children).
Leishmaniasis
Visceral leishmaniasis
is a protozoan parasitic infection caused by a flagellate of
the genus
Leishmania [L donovani]
and
transmitted by the sand fly bite. The same
organism causes dermatological and mucocutaneous disease. After sandfly
bite, a variable incubation period is followed by papule formation,
which
may be subclinical. This
progresses to a nodule and
ultimately an ulcer, which may
persist for years before healing. This is diagnosed by demonstration of
amastigotes within the tissue macrophages within biopsy samples from
the
margin of the lesion. Espundia
is a late complication of cutaneous leishmaniasis, occurring several
years after the skin lesions resolve, and believed to be due to
the hematological spread to nasal and oropharyngeal mucosa. Destruction
of
cartilage of the nose and palate are highly disfiguring. Several
treatment options
exist, but are fairly toxic. (See
Vol III—TM13 Antiparasitic Primer.)
Diffuse cutaneous leshmaniasis resembling lepromatous leprosy, in which ulceration is uncommon, presents another manifestation of infection by this organism. Diagnosis is via demonstration of the organisms, again intracellularly in biopsies of the nodules. Treatment is the same as localized cutaneous disease.
Dracuntiasis
The guinea worm larva is ingested in water and contaminated by its
intermediate host—a water flea. It migrates to the subcutaneous tissues
and
develops into the adult form there, ultimately
migrating to the lower
extremities. The female digests her
tail through the skin and releases larvae when exposed to
water. Typically, a burning blister appears suddenly, which
feels better when
immersed in water. Diagnosis is clinical; treatment is focused
primarily on
preventing secondary infection. Traditionally, the worms are slowly
wound out
of the skin lesion over
many days. This involves the end of the worm being
wrapped around a stick, and every few hours the slack (resulting from
the
worm’s slow emergence) is taken out by winding the stick a bit more.
Eventually, the entire
many-inches-long worm has been totally wound out of the
lesion. However, surgical removal is also a possibility. Anthelmintics
are of
questionable value.
Mycobacteria
Buruli Ulcer
This highly destructive lesion is caused by
Mycobacterium ulcerans
(M ulcerans), the third most significant mycobacterial
infection affecting immunocompetent
individuals. PEDS:
M
ulcerans
is most common in children. Following minor
penetrating injury, a papular lesion develops that painlessly ulcerates
and
rapidly spreads. Satellite ulcers may occur, and there may be extensive
undermining of the surrounding tissues. Secondary infection may
occur as well. Differential diagnosis is broad, and is confirmed by
acid-fast staining of the
ulcerous exudate. Antimycobacterial therapy
is only marginally effective but
worth trying.
Others
A cutaneous form of tuberculosis, known as
lupus vulgaris,
is a slowly
progressive, ulcerating nodule often on the face. Both
M bovis and
M tuberculosis
may cause this, although the former is most commonly the culprit.
Antimycobacterial therapy is effective. M marinum, M kansasii, M avium,
and
other mycobacteria all may also present dermatological manifestations.