Post-Travel Dermatologic Conditions | Yellow Book

Introduction

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 insect bite reactions, superficial bacterial infections (often superimposed on insect bites), and non-specific “itchy rashes” are consistently among the most common skin problems identified at post-travel medical visits (Table 10.5.1).

Table 10.5.1: Most common causes of skin lesions in returned travelers

Healthcare professionals generally use several approaches concurrently when examining a returned traveler with a new onset skin condition (Box 10.5.1). Few travelers’ dermatoses constitute a medical emergency. Any skin condition accompanied by fever, obtunded mental status, petechiae/purpura, or other signs of systemic illness needs a prompt, if not urgent, and thorough diagnostic evaluation. Travel destinations, types (and duration) of exposure, and safety precautions (e.g., vaccinations, use of bed nets, sanitary conditions, etc.) are the next echelon of inquiry. Next, the healthcare professional should consider the morphology of skin lesions noted on physical examination. Primary lesions (i.e., those that are unaltered by time, scratching, crusting, or medical treatment) are most useful. The clinical diagnosis may be straightforward or may require laboratory confirmation using cultures, serologies, skin biopsy, or microscopy.

Box 10.5.1

Many dermatologic problems in returned travelers represent a flare of an existing condition, sometimes because the usual treatment regimen was interrupted while away from home. Other skin disorders might coincide with travel or appear shortly thereafter but are unrelated to travel itself, such as the appearance of actinic keratoses (sun-induced cutaneous precancers) in older travelers with extensive sun exposure history.

Fever and rash

Many illnesses fall into the category of fever with a rash. In returned travelers, fever and rash are most often, but not always, due to viral infections. Nevertheless, bacterial infections, parasitic infections, systemic fungal infections, and some noninfectious conditions can also cause fever and rash. If the rash is characterized by petechiae/purpura or by abundant vesicles, pustules, or widespread blisters, the evaluation should be prompt and thorough.

Systemic viral infections and illnesses

The first 3 conditions discussed—dengue, chikungunya, and Zika—are viral diseases transmitted by Aedes spp. mosquitoes and often present as undifferentiated fevers. Rashes, particularly widespread petechial eruptions, provide important diagnostic information. Viral illnesses often occur in small outbreaks, so epidemiologic clues are significant.

Dengue

Dengue is characterized by an abrupt onset of high fever, frontal headache (often accompanied by retro-orbital pain), and myalgia (see Dengue chapter). A widespread but faint macular rash, interrupted by islands of uninvolved pallid skin, may appear 2–4 days after illness onset. A petechial rash may occur in classic and severe dengue (Figure 10.5.1).

Figure 10.5.1

Chikungunya

The rash associated with chikungunya resembles that of dengue, but hemorrhage, shock, and death are rare (see Chikungunya chapter). A major distinguishing feature of chikungunya is its associated arthritis, arthralgia, or tenosynovitis that can persist for months, particularly in older adults.

Zika

The course of Zika is generally subclinical or mild, characterized by arthralgia, conjunctivitis, fever, lymphadenopathy, and a morbilliform (“maculopapular”) rash (see Zika chapter).

Other hemorrhagic fever viruses

Many viruses that are naturally present in rodents, bats, or non-human primates have the potential to spill over into human populations. Ebola and Marburg viruses are examples. Such viruses might cause serious, hemorrhagic, or otherwise deadly diseases. Subsequently, if the virus is easily transmitted from person to person, then clusters, outbreaks, or even an epidemic might ensue.

Healthcare professionals concerned that a returned traveler may have a possible viral hemorrhagic fever should notify public health authorities and initiate precautions to protect the patient and others. Features of a viral hemorrhagic fever include morbilliform eruptions, bleeding in the skin such as petechiae (pinpoint bleeding) and ecchymoses (bruises), gingival bleeding, epistaxis, and other features such as jaundice.

Morbilliform eruptions

Measles

Measles typically presents with a prodrome that includes fever, cough, runny nose (coryza), and red watery eyes (bilateral conjunctivitis). Koplik spots (small red spots with bluish/white center on the buccal mucosa) begin 2–3 days after symptoms first appear. Within another few days, the typical rash begins, usually first on the head and neck, then spreading downward to the trunk and extremities. The measles rash consists of innumerable small pink-to-red macules and slightly elevated papules, referred to as a morbilliform or maculopapular eruption. Measles can be spread easily (see Measles [Rubeola] chapter).

COVID-19

During the course of acute COVID-19 infection, many people develop cutaneous findings (see COVID-19 chapter). The data are imperfect but seem to show that rashes fall into 2 large groups:

• Morbilliform and urticarial eruptions that resemble common non-specific viral exanthems
• Eruptions associated with hypercoagulability; these are areas of net-like erythema (livedo reticularis, presumably due to altered vascular perfusion) or pathologic hypercoagulability (retiform purpura)

Non-specific acute morbilliform eruptions are widely reported as the most common skin finding in COVID-19. Many other types of eruptions have been attributed to COVID-19. Understanding of the clinical significance, pathophysiology, and epidemiology continues to evolve.

Children and young adults may develop a condition known as “COVID toes,” characterized by sudden onset of painful, dusky red macules and patches, typically on the plantar aspect of the distal phalanges of one or more toes. The clinical and histological appearance of COVID toes resembles a condition known as chilblains (a type of cold exposure injury).

Acute HIV infection

Acute retroviral syndrome is the initial presentation of newly acquired HIV infection (see Sex and Travel chapter). It presents as an influenza-like syndrome that includes fever, generalized lymphadenopathy, and malaise, often accompanied by a generalized skin eruption. In acute HIV infection, associated skin lesions present as pink to deeply red macules or papules, or as a morbilliform eruption. Urticarial and pustular lesions also have been described. Oral ulcers might be present. The clinical appearance is not diagnostic and resembles rashes seen in many acute viral syndromes.

Acute, febrile, vesiculopustular eruptions

This section includes diseases caused by true poxviruses (family: Orthopoxviridae) and a much more common condition, chickenpox or varicella, caused by the varicella-zoster virus (family: Herpesviridae). These viral infections can cause an acute illness with fever and vesiculopustules that can spread easily from person to person.

Early presentations of a poxvirus infection and a case of chickenpox may resemble each other, even though they are virologically, clinically, and epidemiologically dissimilar. The clinical appearance of each type of infection resembles the other, superficially.

Poxvirus diseases

Orthopoxvirus infections present similarly with fever, headache, malaise, and characteristic deep-seated, firm, well-circumscribed lesions that evolve through various stages (including papules, vesicles, and pustules). After 2–4 weeks (longer in immunocompromised people), lesions mature into crusts that resolve in most individuals.

The most significant orthopoxvirus disease is smallpox, caused by variola virus. The virus and the disease have been eradicated in nature, largely due to the global campaign using smallpox vaccine, made from a related orthopoxvirus, vaccinia virus. In 2022, another orthopoxvirus disease, mpox, which was once considered a geographically focal zoonosis, emerged worldwide. During the global outbreak, mpox virus infected mostly men who have sex with men. Most cases were transmitted through skin-to-skin contact. Consequently, the lesions on many patients with mpox appeared mainly or exclusively on anogenital surfaces. In patients with advanced HIV disease or other immunocompromised states, the disease can be particularly virulent and can cause death.

Several other poxviruses cause mild disease with relatively few lesions, often 1–5. In northern Europe, cowpox is present and tends to cause disease when people have direct contact with an infected domestic cat that acquired the disease from a recently caught, infected rodent.

Orf and milker’s nodule are caused by closely related parapoxviruses. Most people acquire these zoonoses occupationally, usually by handling or feeding infected sheep, cattle, or goats. Although less common, there have been parapoxvirus infections in individuals with recent exposure to white-tail deer through handling of carcasses in the United States. A localized lesion at the site of inoculation (often through a skin break) presents after 3–7 days of exposure and can evolve through multiple clinical stages; resolution usually happens after approximately 4–6 weeks. Fever, malaise, or lymphadenopathy may occur but are uncommon.

Varicella (chickenpox)

Varicella (chickenpox) can be mild in children and more severe in adults or immunocompromised patients. It presents with 1–2 days of fever, followed by a generalized pruritic rash consisting of macules that evolve through the papular stage (red bumps) to form vesicles (small, clear, fluid-filled blisters) and pustules (pus-filled blisters) on an erythematous base, which resolve by crusting. Lesions often occur in crops, and various stages of evolution are often present simultaneously, so papules, vesicles, pustules, and crusts may all occur at the same time.

Systemic bacterial infections and illnesses

Meningococcemia

Invasive Neisseria meningitidis disease occurs worldwide and is often associated with outbreaks, especially in the meningitis belt of Sub-Saharan Africa (see Meningococcal Disease chapter). Meningococcemia is often characterized by acute onset of fever and a petechial or purpuric rash, commonly accompanied by hypotension, mental status changes, or multiorgan failure. Rapid diagnosis and immediate treatment (often started empirically before laboratory confirmation is obtained) can be lifesaving.

Rickettsioses

Most rickettsial infections have distinctive geographic and epidemiologic features based on the ecological preferences and behavioral habits of reservoir animals, arthropod vectors, and pathogens. Many of these “geographic rickettsioses” induce a spotted fever that characteristically starts with the bite of an infected tick or mite. After a several-day incubation period, the first cutaneous finding is often an eschar at the bite site. Often called a tache noire (black stain), these are mildly painful, dark brown or black, necrotic lesions with a red rim. The systemic illness begins over the next few days, usually accompanied by a maculopapular, petechial, or vesicular rash.

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.; Figure 10.5.2). Travelers who hike or camp outdoors or are on safari are particularly at risk for this disease, a frequent cause of fever and rash in southern Africa (see Rickettsial Diseases chapter).

Figure 10.5.2

The disease is characterized by fever and an eschar at the site of the tick bite. The eschar, or tache noire, is a mildly painful, dark brown or black, necrotic lesion with a red rim. Several lesions might be present because exposed individuals often suffer multiple tick bites. Within a few days, patients develop a fine petechial or papular rash, associated with regional lymphadenopathy near the bite.

Rocky mountain spotted fever

Rocky Mountain spotted fever (RMSF) is a tick-borne rickettsial disease that is more severe than other spotted fevers. RMSF occurs in North America (U.S. and Mexico) and parts of Central and South America. Because of its potential severity and lethality 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 starts as a blanching maculopapular eruption. Cutaneous blood vessels become inflamed and leaky, sometimes resulting in necrosis. Red blood cells leak from inflamed blood vessels, leading to non-blanching petechiae that are especially prominent on the ankles and wrists. It usually spreads to palms and soles, then becomes generalized. Patients with RMSF are usually very ill with high fever and severe headaches.

Bacterial infections localized to skin and soft tissues

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

Impetigo

Impetigo is a common, highly contagious, superficial bacterial skin infection. S. aureus and S. pyogenes are the most common pathogens. Streptococcal impetigo classically presents in children with golden or “honey-colored” crusts formed from dried serum. Staphylococcal impetigo often appears in body folds, especially the axillae, and might present as fragile pustules.

In temperate climates, most impetigo is caused by S. aureus, either alone or mixed with S. pyogenes. In many tropical areas, however, streptococcal impetigo remains especially common in children. It often arises as a secondary skin infection after the epidermal barrier is disrupted by insect bites, scabies, or scratches. Treatment for impetigo varies based on the severity or extent of the infection and by the suspected pathogen. Mupirocin, a topical antibiotic, is an excellent treatment for mild, localized impetigo caused by either pathogen. More extensive infections may require oral antibiotics, but the regimen differs by pathogen.

Folliculitis (hair follicle infections) and furunculosis (boils or abscesses)

People whose skin or nasal mucosa is colonized with S. aureus are at risk for recurrent folliculitis or furunculosis. By its very nature, folliculitis occurs only on hair-bearing surfaces. People can easily but unintentionally spread the infection (autoinoculation) when they shave the hair from various body surfaces.

Furuncles may continue occurring weeks or months after a traveler’s return. If staphylococcal boils recur frequently, treatment may require 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. However, outside a few endemic areas (mainly the south-central U.S.), 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.

Cellulitis and erysipelas

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

Treatment

Use soap and water for local cleansing of bacterial skin infections. A topical antibiotic, preferably mupirocin, can also be used; bacitracin zinc and polymyxin sulfate (often in combination) are alternatives. Topical antibiotic ointments are widely available in other countries and may contain neomycin (a well-recognized cause of acute allergic contact dermatitis), fusidic acid, or gentamicin.

In low- and middle-income countries, “triple cream” products may be available over the counter. These often contain ultrapotent corticosteroids 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 needing 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 lead to infections with anaerobic bacteria or unusual gram-negative organisms. Appropriate treatment might require care from specialists who can obtain bacterial cultures, prescribe focused antibiotic therapy, and perform surgical debridement, as needed (see Zoonotic Exposures: Bites, Scratches, and Other Hazards chapter).

Skin lesion morphology

Linear lesions

Cutaneous larva migrans

Cutaneous larva migrans, a condition in which the skin is infested with zoonotic hookworms (often Ancyclostoma spp.), presents as an extremely itchy, linear, or serpiginous lesion (Figure 10.5.3). The migrating larvae advance slowly in the skin’s uppermost layers. Cutaneous larva migrans is usually self-limiting after 4–6 weeks. Albendazole and ivermectin are both effective therapies, and topical corticosteroids can be used to relieve severe pruritus, which is often present. Infrequently, more serious disease can result from invasion of deeper organs.

Figure 10.5.3

A deeper lesion that resembles urticarial patches and that progresses rapidly might be due to larva currens (“running larvae”), caused by cutaneous migration of filariform larva of Strongyloides stercoralis. Call or email the CDC for recommendations on diagnosis and treatment of cutaneous larva migrans or larva currens (404-718-4745; parasites@cdc.gov).

Lymphocutaneous or sporotrichoid spread of infection

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

Phytophotodermatitis and other noninfectious exposures

Phytophotodermatitis is a noninfectious condition resulting from the interaction of natural psoralens, most common in the juice of limes, and solar ultraviolet A radiation. This often occurs on tropical vacations after travelers are outside, preparing food or drinks with locally purchased limes. Several days later, the involved surfaces may develop painful streaks of blisters, essentially the equivalent of an exaggerated sunburn. The area heals slowly, evolving into asymptomatic hyperpigmented lines that may take weeks or months to resolve. Because of the several-day delay between the exposure to lime juice and sunlight, people rarely self-identify the cause of this painful rash.

Long linear lesions caused by cnidarian envenomation (e.g., stings from the tentacles of jellyfish or Portuguese man o’ war [Physalia physalis]), often resemble phytophotodermatitis (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter). Another common but self-evident cause of an itchy, often blistering eruption is acute contact dermatitis due to black henna. In places where henna is commonly used, the compound paraphenylenediamine is often 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 more traditional red or brown henna) are at risk for severe, often blistering, acute allergic contact dermatitis due to paraphenylenediamine.

Macular lesions

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

Leprosy/Hansen’s disease

Leprosy frequently presents with hypopigmented or erythematous patches that are hypoesthetic to pinprick 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 (nhdped@hrsa.gov; 800-642-2477).

Lyme disease

Lyme disease is caused by the spirochete Borrelia burgdorferi sensu lato. Endemic to temperate latitudes in North America, Asia, and Europe, the bacterium that causes Lyme disease is transmitted through the bite of infected hard ticks, genus Ixodes.

Infected travelers present with ≥1 large erythematous patches (erythema migrans). If ≥1 lesions are present, the first lesion appears 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 many cases lack central clearing or red-and-white bands. 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 (dermatophyte infections)

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

When a returned traveler has a recalcitrant fungal infection, consider obtaining culture for species identification. A longer course of high-dose oral antifungals might be needed to treat severe or recurrent infections caused by emerging drug-resistant Trichophyton species, such as Trichophyton indotineae, that have been detected in travelers returning from South and Southeast Asia.

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 (Figure 10.5.4).

Figure 10.5.4

Tinea versicolor (also called pityriasis versicolor)

Caused by several species of the fungus Malassezia (e.g., Malassezia furfur [previously Pityrosporum ovale], Malassezia 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 the lesions on any one individual have a uniform color (Figure 10.5.5).

Figure 10.5.5

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. The fungi that cause tinea versicolor are difficult to grow in standard culture media.

Topical azole products (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 to treat severe, relapsing infections, or those 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, topical nystatin, and both oral and topical terbinafine are ineffective against Malassezia.

Nodular and subcutaneous lesions

Gnathostomiasis

Gnathostomiasis is a nematode infec­tion that occurs mainly in Southeast Asia, along the Pacific coast of Ecuador and Peru, in parts of Mexico, and Sub-Saharan Africa. People acquire gnathostomiasis by eating raw or undercooked, infected freshwater fish, amphibians, or reptiles. Infected individuals experience transient, migratory, subcutaneous nodules often described as both itchy and painful. Several reports suggest that initial symptoms can occur weeks or even years after exposure. Symptoms are due to nematode larvae migrating through cutaneous and subcutaneous soft tissues. Humans are accidental, dead-end hosts for gnathostomes. Tissue (skin) and peripheral eosinophilia is common. Reliable serologic tests are not widely available but could be used for diagnosis. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).

Loiasis

Loiasis is caused by Loa loa, a filarial nematode transmitted by day-biting African deer flies (Chrysops spp.). Among travelers, the disease is seen mostly in people who have lived or worked in endemic areas for several months or longer. Clinical manifestations vary among patients; many people develop edematous subcutaneous nodules, often painful or pruritic and located around large joints. These nodules are known as Calabar swellings, named for the Nigeria-Cameroon coastal area where the disease is prevalent. Some people with loiasis have generalized itchy skin with no other cutaneous findings. Adult worms are occasionally observed crossing the bulbar conjunctivae or the soft eyelid tissues, leading to another name for loiasis, African eyeworm disease. Peripheral eosinophilia is common in travelers.

Loiasis is diagnosed using conventional light microscopy to find microfilariae (larvae of the worm) on a blood smear. The blood should be collected during midday hours (i.e., between 10 a.m. and 2 p.m.). In travelers who have crossed time zones, blood should be collected during midday hours of the location where the infection was acquired. Nevertheless, microfilaremia might be undetectable; such cases require serologic testing, although infection with other nematodes may produce a false positive test result.

The drug of choice for the treatment of loiasis is diethylcarbamazine (DEC). Most patients will achieve cure, defined as resolution of symptoms, resolution of eosinophilia, and decreasing antifilarial antibody titers, with 1 or 2 courses of DEC. Some will require additional courses of DEC or a trial of albendazole. DEC is the treatment of choice because there is solid evidence that it kills both the microfilariae and the adult worms, resulting in quicker resolution of the infection. The risk of fatal encephalopathy or other severe adverse neurologic events is related to the microfilarial load. Quantitative blood smears are required before initiating treatment. Prophylactic DEC (300 mg once a week) can be used to prevent infection in long-term travelers to endemic areas. DEC, which is not Food and Drug Administration (FDA)-approved in the United States, can be obtained through consultation with the Parasitic Diseases Branch at CDC (parasites@cdc.gov; 404-718-4745). Albendazole may play a role in the treatment of loiasis in cases of failed DEC treatment or in order to try to lower microfilarial loads so that DEC may be used safely. Ivermectin may play a role in lowering microfilarial loads so that DEC may be safely used in certain circumstances.

Furuncular myiasis

In Sub-Saharan Africa, furuncular myiasis is caused by a skin infestation with larvae of the tumbu fly, also known as the mango or mputsi fly (Cordylobia anthropophaga and related species; Figure 10.5.6). In the Western Hemisphere, larvae of the botfly (Dermatobia hominis) cause similar-appearing furuncular myiasis. The botfly’s range extends from central Mexico to the northern half of South America. Typical lesions are solitary; there can also be multiple painful nodules that resemble furuncles (boils). Each nodule holds only a single larva. The center of a lesion has a small punctum through which the larva both breathes and expels waste.

Figure 10.5.6

More mature larvae sometimes exit on their own, or they can be gently compressed out of nodules. Extracting larvae can be difficult and may take several methods. Start with obstructing the breathing punctum by applying an occlusive substance or dressing (such as petroleum jelly) for several hours. Larvae may emerge from their dermal domicile in search of air to breathe. Removal may require a small, superficial incision that permits gentle extraction of the larvae. The process should be performed carefully to avoid puncturing the larval body, which could result in residual parts retained in the skin. Once a larva has been extracted, the newly vacant cavity should be flushed with sterile water. Additional lesions are often hidden in the scalp, particularly in the case of infestation with Dermatobia. The patient may require treatment for secondary bacterial infection and appropriate prophylaxis for tetanus. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).

Tungiasis

Tungiasis is a skin infestation caused by adult female sand fleas (Tunga penetrans) and is endemic to parts of the Caribbean, South America, and Sub-Saharan Africa. Typically, 1 or more gravid female fleas burrow into the thick skin on a person’s sole 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 her eggs. Clustered lesions can appear as crusty, dirty, or draining plaques. The lesions, which are itchy and painful, continue to expand as the uterus of the sand flea fills with eggs.

Treatment includes extracting the burrowed fleas, consideration of antibiotics for secondary bacterial infection, and prophylaxis for tetanus, if required. Extraction performed in endemic areas using non-sterile procedures has been associated with significant complications. Promising emerging topical therapies include dimeticones (silicone oils) and a neem/coconut oil mixture. Call or email CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).

Papular lesions

Bites by insects and other arthropods

Insect bites are probably the most common cause of papular lesions. Biting insects include bed bugs, fleas, head lice, midges, mosquitoes, and sand flies. Most bites are itchy because of hypersensitivity reactions to proteins and other components in the insect’s 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 is generally limited to the elevated part of the lesion and is surrounded by a subtly pale hypovascular rim.

Lesions are often pruritic, thereby inducing patients to scratch their bites. Scratching often excoriates or erodes the skin’s surface, putting the site at risk for secondary bacterial infections, usually with Staphylococcus spp. or Streptococcus spp. Many arthropods produce bite reactions that have characteristic shapes, patterns, and distributions. For example, bites from bed bugs and fleas often appear as clusters of discrete red papules on unclothed surfaces of the body (Figure 10.5.7).

Figure 10.5.7a

Figure 10.5.7b

Scabies

Scabies infestation usually manifests as a generalized or regional pruritic papular rash with erythema, abundant excoriations, and secondarily infected pustules. Scabies generally presents in a regionally symmetric manner (Figure 10.5.8). For example, 2 of the most commonly involved sites are the volar wrists and finger web spaces; the left and right sides are usually involved in a nearly identical fashion. Also, boys and men with scabies often develop nodular lesions on the scrotum and penis. When considering scabies in any male older than 2 years, a genital examination can be extremely helpful. Scabies burrows are short, delicate, linear lesions that involve the most superficial part of the epidermis; burrows are pathognomonic but are challenging to detect. See treatment information.

Figure 10.5.8a

Figure 10.5.8b

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, sulfonamides). Onchocerciasis (specifically onchocercal dermatitis due to the inflammatory reaction to dying microfilaria in the skin) can occur in expatriates living in endemic areas in Sub-Saharan Africa. Onchocercal dermatitis manifests as a generalized pruritic, finely papular dermatitis, a rare finding in travelers that occurs years after exposure. Swimmer’s itch (cercarial dermatitis) and hookworm folliculitis are extremely itchy eruptions composed of papules on skin surfaces exposed to freshwater and fecally-contaminated soils, respectively.

Skin ulcers

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 Staphylococcus and Streptococcus. Infection with these organisms creates well-demarcated, shallow ulcers with sharp “punched out” borders known as bacterial or common ecthyma. Treatment for ecthyma is described earlier in this chapter.

Ulcers seen in some conditions, such as the chancre of primary syphilis, are ulcerated when they first appear. However, most skin ulcers start as an elevated lesion, typically a papule or vesicle (or perhaps a larger plaque, nodule, or bulla), with an intact surface. As the epidermal surface breaks down, the lesion evolves into an erosion or an ulcer. This is the case with the next conditions to be discussed, anthrax and cutaneous leishmaniasis, along with many other diseases.

Anthrax

Cutaneous anthrax starts as a large, edematous swelling. Within a few days, the skin surface develops a shallow ulcer that progresses into a necrotic black eschar. In all stages, anthrax lesions are surprisingly painless. Most cases of travel-associated anthrax are cutaneous (rather than inhalational or gastrointestinal) and are acquired via exposure to live ruminants (hoofed mammals that chew their cud, such as cattle, goats, and sheep) or from handling unprocessed products made from animal hides or wool.

Any case of human anthrax should be reported immediately to public health authorities. Anthrax spores can be used as a bioweapon (in warfare or in bioterrorism). Therefore, cases of anthrax, which are extremely rare in the developed world, will raise concern for a bioterror or biowarfare attack.

Anthrax treatment requires antibiotics to kill the pathogen, Bacillus anthracis, and antitoxins to neutralize the toxins that the pathogen produces. An FDA-approved vaccine is available to people in certain occupations (veterinarians and other animal handlers; ground soldiers).

Buruli ulcer (Mycobacterium ulcerans infection)

Buruli ulcer is rare in travelers. It is caused by a toxin produced by Mycobacterium ulcerans, a freshwater bacterium found most commonly in equatorial Africa (mainly 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 and form expanding invasive wounds. Despite extensive wounds, Buruli ulcers often lack signs of inflammation; in other words, they are surprisingly painless and do not generate a pustular response.

A condition known as tropical ulcer has a similar appearance, but it is exceptionally painful. Like Buruli ulcer, it commonly appears on the shins. Unlike Buruli ulcer, tropical ulcer is felt to be caused by a polymicrobial bacterial infection, possibly including some mycobacteria.

Cutaneous leishmaniasis

The main areas of risk for cutaneous leishmaniasis (CL) are Africa’s northeastern quadrant, Latin America, South Asia, Central Asia, Mediterranean coastal areas, and the Middle East (see Leishmaniasis chapter). The bite of an infected sand fly transmits the Leishmania parasite, and CL lesions start as localized, typical insect bite reactions that are papules or nodules. Over several weeks, the lesions evolve slowly into shallow ulcers with raised margins. This resembles a broad, shallow, volcanic caldera. The ulcer’s surface is often covered by a dried crust or a raw, fibrinous coat. In the absence of secondary bacterial infection, leishmanial ulcers are generally painless. Lesions may remain as nodules or papules without ulceration, which is more commonly seen in Old World Disease (Figure 10.5.9; Figure 10.5.10).

Figure 10.5.9

Figure 10.5.10

Special techniques are necessary to confirm a diagnosis of CL. The simplest (and office-based) technique is a modified skin scraping with material placed on a glass slide and examined by a dermatopathologist. In travelers, pathogen speciation is often necessary to determine whether the lesion will remain strictly cutaneous and self-healing or if it will require treatment with medication (i.e., oral, topical, or intravenous) or possibly cryotherapy or heat therapy. Refer to the CDC webpage or contact CDC for recommendations on diagnosis and treatment (404-718-4745; parasites@cdc.gov).

Spider bites

An important consideration when evaluating a patient who reports a spider bite is that most alleged spider bites are simply not spider bites (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter). The sudden appearance of a warm, tender lesion with a necrotic center is often diagnosed (by patients, family members, and emergency medical staff) as a spider bite. However, few purported spider bites involve a spider observed to either bite the patient or to merely be present. Indeed, a painful necrotic lesion in this context is more likely to be a bacterial skin infection that likely requires antibiotics.

Nevertheless, necrotizing spider bites can occur and are most often caused by recluse spiders (Loxosceles spp.). In the United States, the most common culprit is the brown recluse (or fiddleback) spider (Loxosceles reclusa), found in the south-central United States. The Mediterranean recluse spider (Loxosceles rufescens) resembles the brown recluse. It is native to the Mediterranean basin and the Near East. This species has become widespread, leading to a large, nearly worldwide distribution. It rarely bites people, and its venom has low toxicity, but it has been implicated in true spider bites. In contrast, many studies show 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), which creates a shallow ulcer on the skin. Just as in oropharyngeal diphtheria, the involved surface typically has a gray membranous surface.

Haemophilus ducreyi causes chancroid, a sexually transmitted infection, but on several island groups in the southwestern Pacific, H. ducreyi causes nonvenereal cutaneous ulcers. Another sexually transmitted infection, syphilis (Treponema pallidum), can also ulcerate the skin.

Trypanosoma brucei rhodesiense, the protozoal pathogen that causes African trypanosomiasis, can produce a chancre at the bite site of the transmitting tsetse fly (Glossina spp.).

Miscellaneous skin infections

Bite-associated infections

Wound infections after cat and dog bites are caused by a variety of microorganisms (see Zoonotic Exposures: Bites, Scratches, and Other Hazards chapter). This includes S. aureus, alpha, beta, and gamma hemolytic streptococci, several genera of gram-negative organisms, and several anaerobes. Pasteurella multocida infection classically occurs after cat bites but can also occur after dog bites; lesions caused by this organism develop quickly and are often painful. Patients lacking spleens are at particular risk for severe cellulitis and sepsis due to Capnocytophaga canimorsus infection after dog bites. Management of cat and dog bites includes consideration of rabies post-exposure prophylaxis (see Rabies chapter), as well as tetanus immunization and antibiotic treatment. Avoid primary closure of dog bites to the hand or puncture wounds anywhere on the body.

Monkey bite management includes wound care, tetanus immunization, rabies post-exposure prophylaxis, and consideration of antimicrobial prophylaxis. Bites and scratches from Old World macaque monkeys, even those that appear healthy, have been associated with fatal encephalomyelitis due to B virus infection in humans; valacyclovir is the recommended post-exposure prophylaxis after high-risk macaque exposure.

Water-associated infections

Skin and soft tissue infections (SSTI) can occur after exposure to fresh, brackish, or salt water, particularly if the skin’s surface is compromised. Infections with water-associated organisms can follow from a variety of types of skin trauma, including: abrasions or lacerations sustained during swimming or wading; bites or stings from marine or aquatic creatures (see Poisonings, Envenomations, and Toxic Exposures During Travel chapter); and punctures from fishhooks.

The most virulent SSTI associated with marine and estuarine exposures are due to Vibrio vulnificus and related non-cholera Vibrio spp. For freshwater exposures, Aeromonas hydrophila is the most dangerous pathogen. Various skin and soft tissue manifestations can occur in association with either infection, 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 infection

Mycobacterium marinum is a free-living environmental bacterium found worldwide in warm, preferably brackish, water. The usual onset of infection is when the bacteria enter the skin after a minor abrasion or shallow puncture injury occurs in or around open water. Typical locations for M. marinum infection include knees, shins, and the dorsal surfaces of hands and feet, where water-associated minor trauma occurs most commonly.is rarely painful, warm, or purulent.

Patients describe a variety of healing patterns after minor water-associated injury—areas that were injured but not infected heal quickly. In contrast, injured areas that were infected with M. marinum will 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, the infection extends proximally along superficial lymphatics, a process known as lymphocutaneous or sporotrichoid spread.

Pseudomonas aeruginosa infection

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 a low-grade fever. The condition is self-limited to 2–12 days; antibiotic therapy is rarely required.

Vibrio vulnificus infection

Necrotizing Vibrio vulnificus infections can be acquired in 2 ways: (1) when open skin surfaces are exposed to contaminated brackish or saltwater; and (2) when people eat Vibrio-contaminated raw or undercooked shellfish, resulting in severe systemic infection. The illness is especially severe in people with underlying liver disease, often from alcoholism or conditions such as hemochromatosis. V. vulnificus skin infections usually start as dramatic cellulitis with hemorrhagic bullae, leading to necrotizing fasciitis and fulminant sepsis. In general, infections caused by these organisms can be more severe in immunocompromised people (see Immunocompromised Travelers chapter).

Shewanella infection

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. Small outbreaks of Shewanella infections have been reported among people who cross the Mediterranean Sea in crowded, unsound boats. Under such conditions, travelers who have had prolonged exposure of their feet and legs to contaminated seawater are at high risk for Shewanella infection.