Chapter 5 Post-Travel Evaluation
Skin & Soft Tissue Infections in Returned Travelers
Skin problems are among the most frequent medical problems in returned travelers. A large case series of dermatologic problems in returned travelers from the GeoSentinel Surveillance Network showed that cutaneous larva migrans, insect bites, and bacterial infections were the most frequent skin problems in ill travelers who sought medical care, making up 30% of the 4,742 diagnoses (Table 5-05). A recent Canadian study of 1,076 returned travelers with dermatologic problems confirmed this finding. However, both of these studies are biased in that they do not include skin problems that were diagnosed and, in many cases, easily managed during travel or that were self-limited.
Skin problems generally fall into either of the following categories: (1) those associated with fever, usually a rash or secondary bacterial infection (cellulitis, lymphangitis, bacteremia, toxin-mediated) and (2) those not associated with fever. Most skin problems are minor and are not accompanied by fever. Diagnosis of skin problems in returned travelers is based on the following:
- Pattern recognition of the lesions: papular, macular, nodular, linear, or ulcerative
- Location of the lesions: exposed versus unexposed skin surfaces
- Exposure history: freshwater, ocean, insects, animals, or human contact
- Associated symptoms: fever, pain, pruritus
- Location and duration of travel
- Time of onset of lesions during or after travel
It is important to recognize that skin conditions in returned travelers may not have a travel-related cause.
Insect bites, the most common cause of papular lesions, may be associated with secondary infection or hypersensitivity reactions. Bed bug and flea bites may produce grouped papules (see Box 2-05 for more information about bed bugs). Flea bites tend to have hemorrhagic centers. Scabies infestation usually manifests as a generalized or regional pruritic, papular rash. Scabies burrows may present as papules or pustules in a short linear pattern on the skin, frequently in the web spaces of the fingers.
Onchocerciasis may occur in long-stay travelers living in rural sub-Saharan Africa and, rarely, Latin America. It usually manifests as a generalized pruritic, papular dermatitis.
NODULAR OR SUBCUTANEOUS LESIONS, INCLUDING BACTERIAL SKIN INFECTIONS
Bacterial skin infections may occur more frequently after bites and other wounds in the tropics, particularly when good hygiene cannot be maintained. Organisms responsible are commonly Staphylococcus aureus or Streptococcus pyogenes. Drug-resistant organisms are frequently acquired in the tropics. The presentations can include pyoderma or impetigo, abscess formation, erysipelas, cellulitis, lymphangitis, or ulceration. Furunculosis, or recurrent pyoderma, may be the result of colonization of the skin and nasal mucosa with S. aureus. Boils may continue to occur weeks or months after a traveler returns and, if associated with S. aureus, definitive treatment usually involves decolonization with nasal mupirocin, a skin wash with an antimicrobial skin cleanser, and less often, an oral antibiotic combination including rifampin.
In addition to pyoderma, cellulitis or erysipelas may complicate excoriated insect bites or any trauma to the skin. Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth in the absence of an underlying suppurative focus. Unlike cellulitis, erysipelas lesions are raised, there is a clear line of demarcation at the edge of the lesion, and the lesions are more likely to be associated with fever. Cellulitis, on the other hand, is more likely to be associated with lymphangitis. Cellulitis and erysipelas are usually caused by β-hemolytic streptococci (such as groups A, B, C, G, and F Streptococcus). S. aureus (including methicillin-resistant strains) and gram-negative aerobic bacteria may also cause cellulitis.
Another common bacterial skin infection, especially in children in the tropics, is impetigo due to S. aureus or S. pyogenes. Impetigo is a highly contagious superficial skin infection that generally appears on the arms, legs, or face as “honeycolored” or golden crusting formed from dried serum. Local care and a topical antibiotic such as mupirocin may be used, although a systemic antibiotic may be required. Emerging antibiotic resistance among staphylococci and streptococci complicates antimicrobial options.
Myiasis presents as a painful lesion similar to a boil. It is caused by infestation with the larval stage of the African tumbu fly (Cordylobia anthropophaga) or the Latin American bot fly (Dermatobia hominis). At the center of the lesion is a small punctum that allows the larva to breathe. Extraction of the fly larva can be difficult, especially of the bot fly; extraction may be facilitated by first asphyxiating the larva, usually with an occlusive dressing or covering (such as a bottle cap filled with petroleum jelly) for several hours and then squeezing the larva out.
Tungiasis is caused by a sand flea (Tunga penetrans). The female burrows into the skin, usually the foot, and produces a nodular, pale, subcutaneous lesion with a central dark spot. The painful or pruritic lesion expands as the female produces eggs in her uterus. Treatment involves extraction.
Loa loa filariasis occurs rarely in long-term travelers living in rural sub-Saharan Africa. The traveler may present with transient, migratory, subcutaneous, painful, or pruritic swellings produced by the adult nematode migration (Calabar swelling). Rarely, the worm can be visualized crossing the conjunctiva of the eye or eyelid. Eosinophilia is common. Loiasis can be diagnosed by finding microfilariae in blood collected during daytime; however, since microfilaremia may be absent, filarial serologic tests may be helpful.
Gnathostomiasis is a nematode infection found primarily in Southeast Asia and less commonly in Africa and Latin America. Infection results from eating undercooked or raw freshwater fish. Infected travelers may experience transient, migratory, subcutaneous, pruritic, or painful swellings that may occur weeks or even years after exposure. The symptoms are due to migration of the worm through the body, and the central nervous system may be involved. Eosinophilia is common, and a definitive diagnosis is often difficult.
Table 5-05. Ten most common skin lesions in returned travelers, by cause1
|SKIN LESION||PERCENTAGE OF ALL DERMATOLOGIC DIAGNOSES (N = 4,742)|
|Cutaneous larvae migrans||9.8|
|Superinfected insect bite||6.8|
|Rash, unknown origin||5.5|
|Superficial fungal infection||4.0|
|Spotted-fever group rickettsiae||1.5|
1Modified from Lederman ER, Weld LH, Elyazar IR, et al. Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance Network. Int J Infect Dis. 2008;12(6):593–602.
Macular lesions are common and often nonspecific and may be due to drug reactions or viral exanthems. Superficial mycoses, such as tinea versicolor and tinea corporis, may also present as macular lesions.
Tinea versicolor, due to Malassezia furfur (previously Pityrosporum ovale), is characterized by asymptomatic hypopigmented or hyperpigmented oval, slightly scaly patches measuring 1–3 cm that are found on the upper chest, neck, and back. Diagnosis may be made by examination with a Wood’s lamp or by placing a drop of methylene blue on a slide onto which clear cellulose acetate tape is placed sticky side down, after it has been touched briefly to the skin lesions to pick up superficial scales. Detection of hyphae (“spaghetti”) and spores (“meatballs”) suggest the diagnosis. Treatment with topical or systemic azoles (ketoconazole, fluconazole), terbinafine, or selenium sulfide (present in some shampoos) is recommended.
Tinea corporis (ringworm) may be caused by a number of different superficial fungi. The lesion is often a single lesion with an expanding red, raised ring, with a central area of clearing in the middle. Treatment is usually several weeks’ application of a topical antifungal agent or a short course of an oral antifungal agent.
Lyme disease, a tickborne infection with Borrelia burgdorferi, is common in North America, Europe, and Russia (see Chapter 3, Lyme Disease). An infected traveler may present with ≥1 large erythematous patches, with or without central clearing, often surrounding a prior tick bite. The patient may not have noticed the tick bite.
Leprosy (Hansen disease) frequently presents with hypopigmented or erythematous patches that are frequently hypoesthetic to pin prick and associated with peripheral nerve enlargement. This condition is almost exclusively found in immigrants from developing countries.
Cutaneous larva migrans, a skin infection with the larval stage of dog or cat hookworm (Ancylostoma spp.), manifests as an extremely pruritic, serpiginous, linear lesion that advances in the epidermis of the skin relatively slowly (see Chapter 3, Cutaneous Larva Migrans). A similar lesion that may be more urticarial and that rapidly progresses may be due to larva currens (running larva) due to cutaneous migration of filariform larvae of Strongyloides stercoralis.
Lymphocutaneous spread of infection occurs when organisms spread along superficial cutaneous lymphatics, producing raised, linear, cord-like lesions; nodules or ulcers may also be found. Examples include sporotrichosis, Mycobacterium marinum infection (associated with exposure to water), leishmaniasis, bartonellosis (cat-scratch disease), Nocardia infection, tularemia, melioidosis, and blastomycosis.
Phytophotodermatitis is a noninfectious condition that results from interaction of natural psoralens, most commonly from spilled lime juice, and ultraviolet radiation from the sun. The result is an exaggerated sunburn that gives rise to a linear, asymptomatic lesion that later develops hyperpigmentation. The hyper-pigmentation may take weeks or months to resolve.
Ulcerated skin lesions may result from Staphylococcus infections or may be the direct result of an unseen spider bite. The necrotic ulcer of anthrax is often surrounded by edema and usually results from handling animal hides or products. Rarely, a painless destructive ulcer with undermining edges may result from infection with Mycobacterium ulcerans (Buruli ulcer). Of particular concern is the ulcer (or less commonly, nodule) caused by cutaneous leishmaniasis. The main areas of risk are Latin America, the Mediterranean, the Middle East, Asia, and parts of Africa. The lesion is a chronic, usually painless ulcer unless superinfected, with heaped-up margins on exposed skin surfaces. Special diagnostic techniques are necessary to confirm the diagnosis. Both topical and systemic treatments may be effective; the species of the infection often determines the treatment modality. If cutaneous leishmaniasis is suspected, clinicians can contact CDC at 404-718-4745 or firstname.lastname@example.org for further advice about diagnosis and treatment (see Chapter 3, Leishmaniasis, Cutaneous).
MISCELLANEOUS SKIN INFECTIONS
Skin Infections Associated with Water
Soft tissue infections can occur after both freshwater and saltwater exposure, particularly if there is associated trauma. Puncture wounds due to fishhooks and fish spines, lacerations from inanimate objects during wading and swimming, and bites or stings from fish or other sea creatures may be the source of the trauma leading to waterborne infections. Soft tissue infections associated with exposure to water or water-related animals include M. marinum, Aeromonas spp., Plesiomonas spp., Edwardsiella tarda, Erysipelothrix rhusiopathiae, and Vibrio spp. A variety of skin and soft tissue manifestations may occur in association with these infections, including cellulitis, abscess formation, ecthyma gangrenosum, and necrotizing fasciitis. Vibriosis infection may be especially severe in those with underlying liver disease and may manifest as a dramatic cellulitis with hemorrhagic bullae and sepsis. In general, infections caused by these organisms may be more severe in those who are immunosuppressed. Acute infections related to aquatic injury should be treated with an antibiotic that provides both gram-positive and gram-negative coverage (such as a fluoroquinolone or third-generation cephalosporin) until a specific organism has been identified. M. marinum lesions are usually indolent and usually appear as solitary nodules or papules on an extremity, especially on the dorsum of feet and hands; subsequent progression to shallow ulceration and scar formation may occur. Occasionally, “sporotrichoid” spread may occur as the lesions spread proximally along superficial lymphatics.
“Hot tub folliculitis” due to Pseudomonas aeruginosa may result from the use of inadequately disinfected swimming pools and hot tubs. Folliculitis typically develops 8–48 hours after exposure in contaminated water and consists of tender, pruritic papules, papulopustules, or nodules. Most patients have malaise, and some have low-grade fever. The condition is self-limited in 2–12 days; typically no antibiotic therapy is required.
Skin Infections Associated with Bites
Wound infections after dog and cat bites are caused by a variety of microorganisms. S. aureus; α-, β-, and γ-hemolytic streptococci; several genera of gram-negative organisms; and a number of anaerobic microorganisms have been isolated. The prevalence of Pasteurella multocida isolates from dog bite wounds is 20%–50%; P. multocida is a major pathogen in cat bite infections. Splenectomized patients are at particular risk of severe cellulitis and sepsis due to Capnocytophaga canimorsus after a dog bite. Management of dog and cat bites includes consideration of rabies post-exposure prophylaxis, tetanus immunization, and antibiotic prophylaxis. Primary closure of puncture wounds and dog bites to the hand should be avoided. Antibiotic prophylaxis for dog bites is controversial, although most experts would treat splenectomized patients with amoxicillinclavulanate prophylactically. Since P. multocida is a common accompaniment of cat bites, prophylaxis with amoxicillin-clavulanate or a fluoroquinolone for 3–5 days should be considered. Management of monkey bites includes wound care, tetanus immunization, rabies postexposure prophylaxis, and consideration of antimicrobial prophylaxis. Bites and scratches from Old World macaque monkeys have also been associated with fatal encephalomyelitis due to B virus infection in humans (see Chapter 3, B virus). Valacyclovir postexposure prophylaxis is recommended after a high-risk macaque exposure.
FEVER AND RASH
Fever and rash in returned travelers are most often due to a viral infection.
Dengue is caused by 1 of 4 strains of dengue viruses (see Chapter 3, Dengue). The disease is transmitted by an Aedes mosquito often found in urban areas, and its incidence continues to increase. The disease is characterized by the abrupt onset of high fever, frontal headache (often accompanied by retro-orbital pain), myalgia, and a faint macular rash (containing islands of pallor) that becomes evident on the second to fourth day of illness. A petechial rash may be found in classical dengue, as well as in severe dengue. Antigen and antibody detection tests, as well as PCR assays, are available to diagnose dengue; detecting IgM in the appropriate clinical scenario would support the diagnosis. Treatment is supportive.
Chikungunya, a virus transmitted by a primarily Aedes mosquito, has caused major outbreaks of illness in southeast Africa, South Asia, the Americas, and the Caribbean (see Chapter 3, Chikungunya). Chikungunya is similar to dengue clinically, including the rash, although hemorrhage, shock, and death are not typical of chikungunya. A major distinguishing feature is that arthritis or arthralgia is common with chikungunya (and may persist for months), whereas in dengue, myalgia is the major clinical feature. Similar to dengue, serologic tests are available. Treatment of the arthritis is with nonsteroidal anti-inflammatory drugs.
Zika, a virus also transmitted by Aedes mosquitoes has caused a major outbreak in the Western Hemisphere since May 2015 (see Chapter 3, Zika). Sexual transmission has been documented as well. The infection is characterized by fever, arthralgia, lymphadenopathy, maculopapular rash, and conjunctivitis. Microcephaly, brain and eye damage, and fetal loss have occurred as a result of fetal infection. An increased risk of Guillain-Barré syndrome has also been documented. Diagnosis is by molecular diagnostics and serologic testing. Treatment is supportive.
South African tick typhus, or African tick-bite fever (Rickettsia africae), is the most frequent cause of fever and rash in southern Africa. Transmitted by ticks, the disease is characterized by fever and a papular or vesicular rash associated with localized lymphadenopathy and the presence of an eschar (a mildly painful 1 to 2 cm black necrotic lesion with an erythematous margin). Satellite lesions may be present. Diagnosis is usually through clinical recognition and is confirmed by serologic testing. Treatment is with doxycycline. Other rickettsial infections such as rickettsialpox and scrub typhus may present with eschars or maculopapular, vesicular, and petechial rashes.
Rocky Mountain spotted fever (RMSF), although uncommon in travelers, is an important cause of fever and rash because of its potential severity and the need for early treatment. This tickborne infection is found in the United States, Mexico, and parts of Central and South America. Most patients with RMSF develop a rash between the 3rd and 5th days of illness. The typical rash of RMSF begins on the ankles and wrists and spreads both centrally and to the palms and soles. The rash commonly begins as a maculopapular eruption and then becomes petechial, although in some patients it begins with petechiae. Doxycycline is the treatment of choice.
The category of fever with rash is large, and providers caring for ill travelers should also consider the following diagnoses: enteroviruses, such as echovirus and coxsackievirus; hepatitis B virus; measles; Epstein-Barr virus; cytomegalovirus; typhus; leptospirosis; syphilis; and HIV.
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