Dermatologic Conditions

CDC Yellow Book 2024

Posttravel Evaluation

Author(s): Karolyn Wanat, Scott Norton

Skin and soft tissue problems, including rashes, are among the most frequent medical concerns of returned travelers. Several large reviews of dermatologic conditions in returned travelers have shown that cutaneous larva migrans, insect bite reactions, and bacterial infections (often superimposed on insect bites) represent the most common skin problems identified during posttravel medical visits (Table 11-12).

Clinicians can use several approaches to diagnose and manage skin conditions in returned travelers. One useful approach is to consider whether the condition is accompanied by an elevated temperature. Few travelers’ dermatoses are accompanied by fever, which could indicate a systemic infection, usually viral or bacterial, that requires prompt attention. A second consideration is the geographic and exposure elements of the travel history. A third consideration is the morphology of the lesions noted on physical examination. The most successful approach combines all 3 considerations supported by laboratory confirmation from cultures, serology, skin biopsy, or microscopy if required or indicated. Box 11-02 includes essential elements of the assessment of returned travelers presenting with skin problems.

Many dermatologic problems in returned travelers represent a flare of an existing condition, perhaps because of interruption in the usual treatment regimen while away from home. Other skin disorders might coincide with travel or appear shortly thereafter but are unrelated to travel itself.

Table 11-12 Most common causes of skin lesions in returned travelers


Cutaneous larva migrans


Insect bite


Skin abscess


Superinfected insect bite


Allergic rash


Rash, unknown origin


Dog bite


Superficial fungal infection








Spotted fever group rickettsiosis








Source: Modified from Lederman ER, Weld LH, Elyazar IR, von Sonnenburg F, Loutan L, Schwartz E, et al. GeoSentinel Surveillance Network. Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance Network. Int J Infect Dis. 2008;12(6):593–602.

Box 11-02 Assessing returned travelers presenting with skin problems: essential elements


  • Systemic diseases and chronic conditions, including preexisting skin conditions
  • Current medications and allergies


  • Time of onset of lesions (during or after travel)
  • Associated symptoms: fever, pain, pruritus


  • Location and duration of travel
  • Exposure history: freshwater, marine water, insects, animals, plants, occupational and recreational exposures, sexual and other human contact exposures
  • Companion travelers with similar findings
  • Vaccination status
  • Adherence to standard travel precautions (e.g., safe food and water precautions, insect bite precautions)
  • Medications taken during travel (could provide adequate prophylaxis for certain conditions or might have cutaneous side effects)


  • Shape of skin lesions (e.g., macules, nodules, papules, plaques, ulcers)
  • Number, pattern, and distribution of lesions
  • Location of lesions: exposed versus unexposed skin surfaces

Fever & Rash

Many illnesses fall into the category of fever with a rash. Consider the following infections in the differential diagnosis of febrile travelers with rashes: cytomegalovirus, enteroviruses (e.g., coxsackievirus, echovirus), Epstein-Barr virus, hepatitis B virus, histoplasmosis, leptospirosis, measles, syphilis, and typhus. Fever and rash in returned travelers are most often, though not exclusively, due to viral infections.

Systemic Viral Infections & Illnesses


A virus transmitted by Aedes spp. mosquitoes, chikungunya has caused major outbreaks of illness in southeast Africa, the Americas and the Caribbean, and South Asia (see Sec. 5, Part 2, Ch. 2, Chikungunya). The rash associated with chikungunya resembles that of dengue (discussed next), but hemorrhage, shock, and death are rare with chikungunya. A major distinguishing feature of chikungunya is its associated arthritis, arthralgia, or tenosynovitis that can persist for months, particularly in older adults. As with dengue, serologic testing is available for diagnosis. After ruling out dengue, treat arthritis with nonsteroidal anti-inflammatory drugs (NSAIDs).


Dengue is caused by 1 of 4 strains of dengue viruses (see Sec. 5, Part 2, Ch. 4, Dengue). The disease is transmitted by Aedes spp. mosquitoes often found in urban areas, and its incidence continues to increase. Disease is characterized by abrupt onset of high fever, frontal headache (often accompanied by retro-orbital pain), and myalgia. A widespread but faint macular rash interrupted by islands of uninvolved pallid skin commonly becomes evident 2–4 days after illness onset. A petechial rash might be found in classic and severe dengue.

Diagnostic methods include antigen and antibody detection tests, and PCR assays. A positive IgM serology helps support the diagnosis. Treatment is supportive; avoid NSAIDs, which can increase the risk of bleeding in patients with dengue.

Acute HIV

Acute retroviral syndrome can present as a flulike syndrome including fever, generalized lymphadenopathy, malaise, and a generalized skin eruption. Acute HIV infection–associated skin findings are often nonspecific and present as pink to deeply red macules or papules or as a morbilliform eruption, but urticarial and pustular lesions also have been described. Oral ulcers might be present.


Zika is a flavivirus transmitted by Aedes mosquitoes. It caused major outbreaks in the Western Hemisphere beginning in 2015 (see Sec. 5, Part 2, Ch. 27, Zika). Sexual transmission has been documented for months after infection. The course of the illness is generally subclinical or mild, characterized by arthralgia, conjunctivitis, fever, lymphadenopathy, and a morbilliform (“maculopapular”) rash. In pregnant people, Zika infection can cause fetal loss or fetal microcephaly and neurological damage. Zika-associated Guillain-Barré syndrome also has been reported after infection. Infection is usually diagnosed by using molecular diagnostics and serologic testing. Treatment involves supportive care.

Systemic Bacterial Infections & Illnesses


Invasive Neisseria meningitidis disease occurs worldwide and often is associated with outbreaks, especially in the meningitis belt of sub-Saharan Africa (see Sec. 5, Part 1, Ch. 13, Meningococcal Disease). Meningococcemia is characterized by acute onset of fever and petechiae that often expand into purpuric macules and patches, commonly accompanied by hypotension and multiorgan failure. Rapid diagnosis and immediate treatment can be lifesaving.


African Tick-Bite Fever

Rickettsia africae, the bacteria responsible for African tick-bite fever (South African tick typhus), is transmitted by the bite of a hard tick (Hyalomma spp.). Travelers who hike and camp outdoors or who are on safari are particularly at risk for this disease, a frequent cause of fever and rash in southern Africa (see Sec. 5, Part 1, Ch. 18, Rickettsial Diseases).

Disease is characterized by fever and an eschar at the site of the tick bite. The eschar, or tache noire, is a mildly painful black necrotic lesion with a red rim. Several lesions might be present because people often suffer multiple tick bites. Within a few days, patients develop a fine petechial or papular rash, associated with localized lymphadenopathy. Diagnosis is usually made through clinical recognition and is confirmed by serologic testing. Treatment is doxycycline.

Other rickettsial infections (e.g., Mediterranean spotted fever, rickettsialpox, scrub typhus) might present with eschars or maculopapular, vesicular, or petechial rashes. Each has distinctive geographic or epidemiologic exposure risks.

Rocky Mountain Spotted Fever

Rocky Mountain spotted fever (RMSF) is a tickborne rickettsial disease that is more severe than the other spotted fevers. RMSF occurs in North America (the United States and Mexico) and parts of Central and South America, but it is uncommon in travelers. Nevertheless, because of its potential severity and the need for early treatment, consider RMSF when evaluating patients with fever and rash.

Most patients with RMSF develop a rash 3–5 days after illness onset. The typical rash of RMSF begins on the ankles and wrists and spreads centrally and to the palms and soles. The rash commonly starts as a blanching maculopapular eruption that becomes petechial, although in some patients it begins with petechiae. Doxycycline is the treatment of choice.

Bacterial Skin Infections

Bacterial skin infections occur most frequently when the skin’s surface has been interrupted, often by abrasions, bites, or minor scratches, particularly when maintaining good hygiene is difficult. Common organisms responsible are Staphylococcus aureus and Streptococcus pyogenes. Resulting infections are collectively called pyodermas (Greek for “pus skin”) and can present as cellulitis and erysipelas, ecthyma (ulcers or open sores), folliculitis, furuncles (also called abscesses or boils), impetigo, and lymphangitis.

Cellulitis & Erysipelas

Cellulitis and erysipelas manifest as red, warm, edematous areas that might start at the site of a minor injury or opening in the skin, or without an obvious underlying suppurative focus. Unlike cellulitis, erysipelas tends to be raised, with a clear line of demarcation at the edge of the lesion due to involvement of superficial lymphatics, and is more likely to be associated with fever. Cellulitis, erysipelas, and lymphangitis are usually caused by β-hemolytic streptococci. S. aureus (including methicillin-resistant strains), and gram-negative aerobic bacteria also can cause cellulitis.


People whose skin or nasal mucosa is colonized with S. aureus are at risk for recurrent folliculitis or furunculosis. Boils can continue to occur weeks or months after a traveler returns; if associated with S. aureus, treatment usually involves a decolonization regimen with nasal mupirocin and a skin wash with an antimicrobial skin cleanser. Some decolonization protocols advise similar treatment for household members and close contacts.

Many travelers who develop boils when abroad mistakenly attribute the tender lesions to spider bites. Outside a few endemic areas, however, necrotizing spider bites are extremely rare. The lesions in these cases are far more likely to be abscesses caused by methicillin-resistant S. aureus and should be treated accordingly.


Impetigo is another common bacterial skin infection, especially in children in the tropics, and is caused by S. aureus or S. pyogenes. Impetigo is a highly contagious superficial skin infection that generally appears on the arms, legs, or face as golden or “honey-colored” crusting formed from dried serum. Streptococcal impetigo is usually what causes the classic crust seen in the mid-face of children. Staphylococcal impetigo often appears in body folds, especially the axillae, and might present as delicate pustules.


Use soap and water for local cleansing of bacterial skin infections. A topical antibiotic, preferably mupirocin, also can be used; bacitracin zinc and polymyxin sulfate (often in combination) are an alternative. Topical antibiotic ointments widely available in other countries contain neomycin (a known, common cause of acute allergic contact dermatitis) or gentamicin. Other “triple cream” type products available for purchase in low- and middle-income countries often contain ultra-potent steroids that can interfere with the healing of common infections and have their own side effects. In many low- and middle-income countries, an application of gentian violet or potassium permanganate is the treatment of choice for impetigo.

Minor skin abscesses often respond to incision and drainage without the need for antibiotics. Oral or parenteral antibiotics might be required if the skin infection is deep, expanding, extensive, painful, or associated with systemic symptoms (e.g., fever). Consider antibiotic resistance if the condition does not respond to empiric therapy. Bites and scratches from animals (both domestic and wild) can be the source of unusual gram-negative organisms and anaerobic bacteria; appropriate treatment might require care from specialists who can obtain bacterial cultures, prescribe focused antibiotic therapy, and perform surgical debridement, as needed (see Sec. 4, Ch. 7, Zoonotic Exposures: Bites, Stings, Scratches & Other Hazards).

Skin Lesion Morphology

Linear Lesions

Cutaneous Larva Migrans

Cutaneous larva migrans, a condition in which the skin is infested with the larval stage of cat or dog hookworm (Ancylostoma spp.), manifests as an extremely pruritic, serpiginous, linear lesion (see Sec. 5, Part 3, Ch. 4, Cutaneous Larva Migrans). The migrating larvae advance relatively slowly in the skin’s uppermost layers. A deeper lesion that resembles urticarial patches and that progresses rapidly might be due to larva currens (running larva), caused by cutaneous migration of filariform larva of Strongyloides stercoralis (see Sec. 5, Part 3, Ch. 21, Strongyloidiasis).

Lymphocutaneous or Sporotrichoid Spread of Infection

Lymphocutaneous or sporotrichoid spread of infection occurs when organisms ascend proximally along superficial cutaneous lymphatics, producing raised, cordlike, linear lesions. Alternatively, this condition can present as an ascending chain of discontinuous, sometimes ulcerated nodules (termed nodular lymphangitis) that occur after primary percutaneous inoculation of certain pathogens. Causative pathogens can be bacterial (e.g., Francisella tularensis; atypical Mycobacterium spp. [such as M. marinum after exposure to brackish water or rapidly growing Mycobacteria after pedicure footbaths]; Nocardia spp.), parasitic (e.g., Leishmania spp., particularly those responsible for causing Western Hemisphere leishmaniasis), or fungal (e.g., Coccidioides spp., Sporothrix).

Phytophotodermatitis & Other Noninfectious Exposures

Phytophotodermatitis is a noninfectious condition resulting from the interaction of natural psoralens, most common in the juice of limes, and ultraviolet A radiation from the sun. The result is the equivalent of an exaggerated sunburn that creates a painful line of blisters, after which asymptomatic hyperpigmented lines appear that can take weeks or months to resolve.

Long linear lesions caused by cnidarian envenomation (e.g., stings from the tentacles of jellyfish and the Portuguese man o’ war [Physalia physalis]), often resemble phytophotodermatitis. Another common, but self-evident, cause of an itchy, often blistering eruption, is acute contact dermatitis due to black henna. In places where temporary tattooing is practiced, paraphenylenediamine is added to red or brown henna to make a longer-lasting pigment, black henna. Travelers who receive temporary tattoos using black henna (rather than the red or brown), are at risk for developing a cutaneous reaction to paraphenylenediamine.

Macular Lesions

Macules and patches (flat lesions) are common, often nonspecific, and frequently due to drug reactions or viral exanthems. Purpura are typically macular, and any purpuric lesion associated with fever could indicate a life-threatening emergency (e.g., meningococcemia).

Coronavirus Disease 2019

Some patients with coronavirus disease 2019 (COVID-19), particularly young children and young adults, develop a condition known as COVID toes. The condition is characterized by the sudden onset of painful, dusky red macules and patches, typically on the plantar aspect of the distal phalanges of ≥1 toes. Clinically and histologically, COVID toes resembles conditions known as chilblains (a cold weather injury) or lupus pernio (a skin finding in some patients with systemic lupus erythematosus). Although an epidemiologic link with the COVID-19 pandemic seems apparent, viral, molecular, and serologic studies have not confirmed a causal relationship. Nevertheless, young travelers who develop this medical condition warrant further evaluation for COVID-19.

Leprosy / Hansen’s Disease

Leprosy frequently presents with hypopigmented or erythematous patches that are hypoesthetic to pin prick and associated with peripheral nerve enlargement. Newly diagnosed leprosy cases occur almost exclusively in immigrants arriving from low- or middle-income countries where the disease is endemic. Diagnosis is made by skin lesion biopsies. The National Hansen’s Disease Clinical Center in Baton Rouge, Louisiana, provides consultations (; 800-642-2477).

Lyme Disease

Lyme disease is caused by the spirochete Borrelia burgdorferi sensu lato (see Sec. 5, Part 1, Ch. 11, Lyme Disease). Endemic to temperate latitudes in North America, Asia, and Europe, the bacteria that causes Lyme disease is transmitted through the bite of infected hard ticks, genus Ixodes.

Infected travelers present with ≥1 large erythematous patch (erythema migrans). If ≥1 lesion is present, the first lesion to appear is where the tick bite occurred; subsequent lesions are due to secondary, probably hematogenous, spread of Borrelia, not multiple tick bites. Erythema migrans often is described as targetoid, but central clearing or red-and-white bands do not occur with every case. The lesions generally are asymptomatic. Pruritus, if present, is usually intermittent and very mild. Lesions that are severely or persistently pruritic are unlikely to be erythema migrans.


Tinea (ringworm) is caused by a variety of superficial fungi (e.g., Microsporum, Trichophyton). Typical lesions appear as expanding, red, raised rings, with an area of central clearing. Diagnostic methods include fungal culture, microscopy (prepare skin scraping samples using a 10% solution of potassium hydroxide [KOH]), and PCR. Treatment usually involves several weeks’ application of a topical antifungal (e.g., clotrimazole, ketoconazole, miconazole, terbinafine) or a course of an oral antifungal (e.g., fluconazole, griseofulvin, terbinafine). Nystatin-based topical agents are ineffective.

For recalcitrant tinea infections associated with international travel, consider obtaining culture for species identification. Prolonged courses of higher dose oral antifungals might be needed to treat severe or recurrent infections caused by emerging resistant Trichophyton species.

Topical medications that combine an antifungal agent with a potent corticosteroid (e.g., betamethasone, clobetasol) are available in many countries; caution travelers against their use. Adverse events associated with steroid-containing antifungal preparations include longer-lasting infections; more extensive spread of the infection over large areas of the body; invasion of the fungal pathogen into the deeper skin layers; unusual presentation of infection (making diagnosis more challenging); and severe redness and burning.

Tinea Versicolor

Caused by several species of the fungus Malassezia (e.g., M. furfur [previously Pityrosporum ovale], M. globosa), tinea versicolor is characterized by abundant, asymptomatic, round to oval skin patches. Lesions are often 1–3 cm in diameter, but dozens of lesions can coalesce to form a “map-like” appearance on the upper chest and back. Affected skin typically has a dry or dusty surface. Lesions can be skin-colored, slightly hypopigmented, or slightly hyperpigmented (versicolor means “changed color”), but all lesions on a person have a uniform color.

Tinea versicolor can be diagnosed in various ways. A clinical diagnosis often is based on the appearance of the lesions. Under the light of a Wood ultraviolet lamp, the lesion produces a subtle yellowish-green hue, corroborating the diagnosis. Microscopic examination using a KOH preparation can be confirmatory.

Topical azoles (e.g., clotrimazole cream, ketoconazole shampoo used as a body wash), selenium sulfide shampoo, or topical zinc pyrithione are recommended treatments. Systemic azoles (e.g., fluconazole) can be used for infections that are severe, relapsing, or recalcitrant to first-line therapies. In many countries, the most common treatment is Whitfield ointment (salicylic acid 3% and benzoic acid 6%, mixed in a vehicle such as petrolatum). Oral griseofulvin and oral terbinafine are ineffective against Malassezia.

Nodular & Subcutaneous Lesions


Gnathostomiasis is a nematode infection primarily occurring in equatorial Africa, along the Pacific coast of Ecuador and Peru, in parts of Mexico, and in Southeast Asia. Infection results from eating raw or undercooked freshwater fish, amphibians, or reptiles. Infected travelers experience transient, migratory, subcutaneous, pruritic, and painful nodules that can occur weeks or even years after exposure. Symptoms are due to migration of the nematode through the body; central nervous system involvement is possible. Eosinophilia is common, and serologic tests are available for diagnosis. Treat cutaneous gnathostomiasis with albendazole or ivermectin.


Caused by Loa loa, a deerfly-transmitted nematode, loiasis occasionally occurs in long-term travelers living in rural equatorial Africa. Infected travelers present with transient, migratory, subcutaneous, painful, or pruritic nodules (called Calabar swellings) produced by adult nematode migration through the skin. Rarely, the worm can be observed crossing the conjunctiva or eyelid. Peripheral eosinophilia is common.

Loiasis can be diagnosed by finding microfilariae in blood collected during daytime; because microfilaremia might be indetectable, however, serologic testing is useful. Treatment is complicated, and consultation with an expert is required for nearly all cases. Two medications are required to control both the larval microfilariae and the adult filariae; the most common regimen includes use of both albendazole and diethylcarbamazine (DEC).

Due to relative contraindications for DEC use in patients with onchocerciasis, special management considerations are warranted for travelers who visited areas endemic for both loiasis and onchocerciasis. Treating loiasis with ivermectin can cause adverse neurological side effects. For additional details regarding contraindications to use of DEC and ivermectin (and a recommendation to consult a specialist in tropical diseases for management advice and support), see Sec. 5, Part 3, Ch. 9, Lymphatic Filariasis, and Sec. 5, Part 3, Ch. 17, Onchocerciasis / River Blindness).


In sub-Saharan Africa, myiasis is caused by a skin infestation with the larva of the tumbu fly, also known as the mputsi fly (Cordylobia anthropophaga and related species). In the Western Hemisphere, larva of the botfly (Dermatobia hominis) cause furuncular myiasis; the botfly’s range extends from central Mexico to the northern half of South America. Solitary or multiple painful nodules resembling a furuncle might be present; each lesion holds only a single larva. The center of the lesion has a small punctum through which the larva both breathes and expels waste.

More mature larvae sometimes exit on their own to pupate, or can be gently squeezed out of nodules. Extracting larva can be difficult; obstructing the breathing punctum as a first step can be helpful and is easily achieved by applying an occlusive dressing or covering (e.g., a bottle cap filled with petroleum jelly), for several hours. Removal might require minor incision, carefully performed to avoid puncturing the larval body, after which newly vacant cavity should be flushed with sterile water. Treatment for secondary infection and appropriate prophylaxis for tetanus also could be required.


Tungiasis is a skin infestation caused by adult female sand fleas (Tunga penetrans). Gestating females burrow into the usually thick skin on the sole of the foot or around the toes. Most people with tungiasis have multiple lesions. Individual lesions have a strikingly uniform appearance with a round, 5 mm diameter, white, slightly elevated surface. In the center of the lesion, a minute, frequently black, opening is present, through which the embedded flea breathes, eliminates waste, and eventually extrudes eggs. Clustered lesions can appear as crusty, dirty, or draining plaques, which are typically itchy, painful, and continue to expand as the uterus of the sand flea fills with eggs.

Treatment includes extracting the burrowed fleas, empirical antibiotics for secondary bacterial infection, and appropriate prophylaxis for tetanus, if required. In many countries, extraction is performed at home using a heat-sterilized needle to pluck out the mature flea with eggs.

Papular Lesions

Arthropod Bites

Arthropod bites are probably the most common cause of papular lesions. Biting arthropods include bed bugs, fleas, headlice, midges, mosquitoes, and sandflies. Itching associated with arthropod bites is due to hypersensitivity reactions to proteins and other components in arthropod saliva.

Individual bites usually appear as small (4–10 mm diameter) edematous, pink to red papules with a gentle “watch-glass” profile. The center of many bites will have a small, subtle break in the epidermis where the arthropod’s mouth parts entered the surface of the skin. The pink to red color generally does not extend beyond the elevated part of the lesion, and often a subtle pale hypovascular surrounding halo is apparent.

Lesions are almost invariably quite pruritic; scratching will often excoriate or erode the skin’s surface. Such bites are vulnerable to secondary bacterial infections, usually with Staphylococcus spp. or Streptococcus spp. Many types of arthropods produce bite reactions with characteristic shapes, patterns, and distributions. For example, bites from bed bugs and fleas often appear as scattered clusters of discrete red papules on unclothed surfaces of the body.


Scabies infestation usually manifests as a generalized or regional pruritic papular rash with erythema, abundant excoriations, and secondarily infected pustules (see Sec. 5, Part 3, Ch. 19, Scabies). Scabies generally has regional symmetry and most commonly involves the volar wrists and finger web spaces. Most boys and men with scabies will have nodular lesions on the scrotum and penis. Scabies burrows are short, delicate, linear lesions involving just the most superficial part of the epidermis; they are pathognomonic but can be difficult to detect.

Other Papular Lesions

Many other conditions present as widespread, extremely pruritic eruptions, often with numerous fine, slightly elevated, somewhat indistinct papules. Examples include acute allergic contact dermatitis (perhaps due to plants) and photosensitive dermatitis (often associated with photosensitizing medications, e.g., doxycycline). Onchocerciasis (specifically onchocercal dermatitis due to microfilaria migrating through the skin) can occur in expatriates living in endemic areas in sub-Saharan Africa and manifests as a generalized pruritic, papular dermatitis (see Sec. 5, Part 3, Ch. 17, Onchocerciasis / River Blindness). Swimmer’s itch (cercarial dermatitis) and hookworm folliculitis are extremely itchy eruptions composed of papules on skin surfaces exposed to fresh water and fecally contaminated soils, respectively.

Ulcerative Lesions

Skin ulcers form when a destructive process damages or erodes the epidermis, the skin’s superficial layer, and then enters the dermis, the skin’s deeper, more leathery layer. The most frequent causes of acute (duration <1 month) cutaneous ulcers are the common pyogenic bacteria, staphylococci and streptococci. These create well-demarcated, shallow ulcers with sharp borders and are known as bacterial or common ecthyma; treatment is described earlier in this chapter.


Cutaneous anthrax produces a large, surprisingly painless edematous swelling. The surface develops a shallow ulcer that progresses into a necrotic black eschar. Nearly all cases of travel-associated anthrax are cutaneous and result from exposure to live cattle, goats, or sheep, or from handling unprocessed products made from animal hides or wool (see Sec. 5, Part 1, Ch. 1, Anthrax).

Buruli Ulcer

Buruli ulcer is a rare infection in travelers caused by Mycobacterium ulcerans, a freshwater bacterium found most commonly in equatorial Africa (especially Ghana and Nigeria) and in the Australian state of Victoria. Buruli ulcers typically start as edematous nodules that arise at sites of minor skin injury. The nodules ultimately break down into expanding invasive wounds. Tropical ulcer has a similar clinical presentation but is exceptionally painful. Unlike Buruli ulcer, tropical ulcer likely represents a polymicrobial bacterial infection, including some mycobacteria.

Cutaneous Leishmaniasis

The main areas of risk for cutaneous leishmaniasis (CL) are Africa’s northeastern quadrant, Latin America, south and central Asia, the Mediterranean coastal areas, and the Middle East (see Sec. 5, Part 3, Ch. 14, Cutaneous Leishmaniasis). The Leishmania parasite is transmitted by the bite of an infected sandfly, and CL lesions start as localized, typical insect bite reactions. Lesions then evolve slowly over several weeks into shallow ulcers with raised margins, resembling a broad, shallow, volcanic caldera; the ulcer’s surface can be covered by a dried crust or a raw, fibrinous coat. In the absence of secondary bacterial infection, ulcers are generally painless.

Special techniques are necessary to confirm CL diagnosis. In travelers, pathogen speciation often is necessary to determine whether the lesion is strictly cutaneous and self-healing or will require treatment with medication (oral, topical, or intravenous) or possibly cryotherapy or heat therapy. Refer to the Centers for Disease Control and Prevention (CDC) webpage or call or email the CDC for recommendations on diagnosis and treatment (404-718-4745;

Spider Bites

Necrotizing spider bites are usually caused by recluse spiders, the most common culprit being Loxosceles reclusa, the brown recluse, found in the south-central United States. The Mediterranean recluse spider (Loxosceles rufescens), native to regions around the Mediterranean Sea and the Near East, resembles the brown recluse. L. rufescens has become a widespread “tramp” species giving it a large, nearly worldwide distribution; it bites only rarely and has venom of low toxicity. Many studies have shown that outside a few endemic areas, most alleged spider bites are, in fact, methicillin-resistant S. aureus infections and should be treated accordingly.

Uncommon Causes

A less common cause of skin ulcers is cutaneous diphtheria (Corynebacterium diphtheriae). On several island groups in the southwestern Pacific, Haemophilus ducreyi causes nonvenereal cutaneous ulcers. Trypanosoma brucei rhodesiense, the causative agent of African trypanosomiasis, can produce a chancre at the bite site of the transmitting tsetse fly (Glossina spp.). Several sexually transmitted infections (e.g., syphilis [Treponema pallidum], chancroid [H. ducreyi]), also can ulcerate the skin.

Miscellaneous Skin Infections


Wound infections after cat and dog bites are caused by a variety of microorganisms including S. aureus, α-, β-, and γ-hemolytic streptococci, several genera of gram-negative organisms, and several anaerobes. Pasteurella multocida infection classically occurs after cat bites but also can occur after dog bites. Patients lacking spleens are at particular risk for severe cellulitis and sepsis due to Capnocytophaga canimorsus after dog bites. Management of cat and dog bites includes consideration of rabies postexposure prophylaxis (see Sec. 5, Part 2, Ch. 18, Rabies), as well as tetanus immunization and antibiotic prophylaxis. Avoid primary closure of puncture wounds and dog bites to the hand.

Antibiotic prophylaxis after dog bites is controversial, although most experts treat patients lacking spleens prophylactically with amoxicillin-clavulanate. Consider antibiotic prophylaxis of cat bites (P. multocida) with amoxicillin-clavulanate or a fluoroquinolone for 3–5 days.

Monkey bite management includes wound care, tetanus immunization, rabies postexposure prophylaxis, and consideration of antimicrobial prophylaxis. Bites and scratches from Old World macaque monkeys showing no signs of illness have been associated with fatal encephalomyelitis due to B virus infection in humans (see Sec. 5, Part 2, Ch. 1, B Virus); valacyclovir is the recommended postexposure prophylaxis for high-risk macaque exposure.


Skin and soft tissue infections (SSTI) can occur after exposure to fresh, brackish, or salt water, particularly if the skin’s surface is compromised. Skin trauma (e.g., abrasions or lacerations sustained during swimming or wading, bites or stings from marine or aquatic creatures, puncture wounds from fishhooks) can result in waterborne infections.

The most virulent SSTIs associated with marine and estuarine exposures are due to Vibrio vulnificus and related non-cholera Vibrio. For freshwater exposures, Aeromonas hydrophila is the most dangerous pathogen. A variety of skin and soft tissue manifestations can occur in association with these infections, including abscess formation, cellulitis, ecthyma gangrenosum, and necrotizing fasciitis.

Pending identification of a specific organism, treat acute infections related to aquatic injury with an antibiotic that provides both gram-positive and gram-negative coverage (e.g., fluoroquinolone or third-generation cephalosporin).

Mycobacterium Marinum

M. marinum lives in brackish water. Infection can occur on skin surfaces injured by minor abrasions or shallow puncture wounds; typical locations include knees, shins, and the dorsal surfaces of hands and feet where water-associated minor trauma occurs most commonly.

Patients often describe divergent healing patterns after minor water-associated injury—areas that were injured but not infected heal quickly, whereas areas that were injured and infected with M. marinum go on to develop the irregularly bordered, expanding, multinodular violaceous plaques characteristic of this infection. Treatment with antimycobacterial agents for weeks to months is required because lesions do not resolve spontaneously. Occasionally, lymphocutaneous or sporotrichoid spread of infection (see the discussion earlier in this chapter) can occur, resulting in proximal movement of lesions along superficial lymphatics.

Pseudomonas Aeruginosa

So-called “hot tub folliculitis” can occur after using inadequately disinfected swimming pools or hot tubs. Folliculitis (tender or pruritic folliculocentric red papules, papulopustules, or nodules) typically develops 8–48 hours after exposure to water contaminated with Pseudomonas aeruginosa. Usually, several dozen discrete lesions occur on skin surfaces submerged in the infectious water. Most patients have malaise, some have low-grade fever. The condition is self-limited to 2–12 days; typically, no antibiotic therapy is required.


Shewanella, a genus of motile gram-negative bacilli found in warm marine waters worldwide, causes SSTIs that clinically and epidemiologically resemble V. vulnificus infections. Patients, often those with chronic liver disease, can develop sepsis and multiple organ failure. Migrants crossing the Mediterranean with prolonged exposure of their feet and legs to contaminated seawater have developed Shewanella infection.


Necrotizing Vibrio vulnificus skin infections can occur when contaminated brackish or saltwater, or the juices or drippings from contaminated raw or undercooked seafood, contact open wounds. Infections also happen from consuming Vibrio-contaminated shellfish. The illness is especially severe in people with underlying liver disease and can manifest as a dramatic cellulitis with hemorrhagic bullae and severe sepsis. In general, infections caused by these organisms can be more severe in immunosuppressed people.

The following authors contributed to the previous version of this chapter: Karolyn A. Wanat, Scott A. Norton

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