Chapter 11 Posttravel Evaluation
Skin & Soft Tissue Infections
Skin problems are among the most frequent medical problems in returned travelers. A large case series of dermatologic problems in returned travelers showed that cutaneous larva migrans, insect bites, and bacterial infections were the most frequent skin problems in ill travelers seeking medical care, making up 30% of the 4,742 diagnoses (Table 11-07).
There are several ways to approach the diagnosis and management of skin conditions in returned travelers. A useful approach is to consider whether the skin condition is accompanied by fever. Skin eruptions and cutaneous lesions that are accompanied by fever constitute a minority of travelers’ dermatoses, but fever may indicate a systemic infection, usually viral or bacterial, which may require prompt attention. A second consideration should focus on the geographic and exposure aspects of the travel history. A third consideration should focus on the morphology of the lesions as noted on physical examination. The most successful approach combines all of these considerations and may be supported by laboratory confirmation (skin biopsy, serology, cultures, microscopy) if required or indicated.
Diagnosis of skin problems in returned travelers should involve the following elements of the medical history and physical examination:
- Systemic diseases: cancer, allergy to penicillin
- Location and duration of travel
- Exposure history: freshwater, ocean, insects, animals, plant contact, human contact, occupational and recreational exposures, sexual contact
- Time of onset of lesions during or after travel
- Whether other travelers have similar findings
- Associated symptoms: fever, pain, pruritus
- Vaccination status and adherence to standard travel precautions (food, water, personal protection from insects)
- Medications taken during travel (that may have side effects or may provide adequate prophylaxis for certain conditions)
- Existing skin conditions
- Shape of lesions, such as papules, plaques, nodules, macular lesions, or ulcerated lesions
- Number, pattern, and distribution of lesions
- Location of lesions: exposed versus unexposed skin surfaces
It is important to recognize that skin conditions in returned travelers may not have a travel-related cause or may represent worsening of a preexisting condition.
Table 11-07. Ten most common skin lesions in returned travelers, by cause
|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.
Arthropod bites are probably the most common cause of papular lesions. Biting flies (such as mosquitoes, midges, and sandflies), bed bugs, headlice, and fleas are among the most common and universal biting arthropods. Itching associated with arthropod bites is due to hypersensitivity reactions to proteins and other components in the 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 broke the surface. The pink-to-red color generally does not extend beyond the elevated part of the lesion. The 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 clustered papules (see Box 3-02, Bed bugs and international travel).
By contrast, scabies infestation usually manifests as a generalized or regional pruritic papular rash amidst erythema, abundant excoriations, and secondarily infected pustules. Scabies generally has regional symmetry, involving 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 linear lesions involving just the most superficial part of the epidermis and are pathognomonic but can be difficult to detect.
Other causes of widespread, extremely pruritic eruptions include allergic contact dermatitis (perhaps due to plants) and photosensitive dermatitis (often due to photosensitizing medications, such as doxycycline). Onchocerciasis (specifically onchocercal dermatitis due to microfilaria migrating through the skin) may occur in long-stay travelers living in endemic areas in sub-Saharan Africa and manifests as a generalized pruritic, papular dermatitis. Swimmer’s itch and hookworm folliculitis are extremely itchy eruptions composed of papules on skin surfaces exposed to fresh water and contaminated soils, respectively.
NODULAR OR SUBCUTANEOUS LESIONS, INCLUDING BACTERIAL SKIN INFECTIONS
Bacterial skin infections may occur more frequently after bites, minor scratches, or abrasions, particularly when maintaining good hygiene is difficult. Common organisms responsible are Staphylococcus aureus or Streptococcus pyogenes. Resulting infections are collectively called pyodermas (“pus skin”) and can present as impetigo, folliculitis, ecthyma (ulcers or open sores), boils (also called furuncles and abscesses), cellulitis and erysipelas, lymphangitis, or ulceration. People whose skin or nasal mucosa is colonized with S. aureus are at risk for recurrent folliculitis or furunculosis. Boils may continue to occur weeks or months after a traveler returns, and, if associated with S. aureus, treatment usually involves a decolonization regimen with nasal mupirocin, a skin wash with an antimicrobial skin cleanser, and oral antibiotics. Many travelers who develop boils when abroad mistakenly attribute the tender lesions to spider bites; however, outside a few endemic areas, 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 manifest as warm, red, edematous areas. They may 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, and is more likely to be associated with fever. Cellulitis and erysipelas are usually caused by group A β-hemolytic streptococci. 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 “honey-colored” or golden crusting formed from dried serum. Streptococcal impetigo is usually the causative agent for the classic “honey-colored crust” seen in the mid-face of children. Staphylococcal impetigo often appears in body folds, especially the axillae, and may present with delicate pustules.
Soap and water should be used for local cleansing of skin infections. A topical antibiotic, such as bacitracin zinc and polymyxin sulfate, or mupirocin, may be used. In many developing countries gentian violet is the treatment of choice for impetigo. If the skin infection is extensive, expanding, or associated with systemic symptoms such as fever, parenteral antibiotics may be required. Antibiotic resistance among many bacterial species should be considered if the condition does not respond to therapy. Unusual gram-negative organisms and anaerobes may be involved in bites and scratches from animals, including domestic animals, and may require a specialist’s care and debridement. See below and Chapter 3, Mosquitoes, Ticks & Other Arthropods, for more information.
Myiasis presents as a painful lesion, resembling a furuncle or boil, which is most often caused by infestation with larvae of the African tumbu fly (Cordylobia anthropophaga, found in much of sub-Saharan Africa) or the New World botfly (Dermatobia hominis, found from central Mexico to the northern half of South America). There can be single or multiple lesions; each lesion holds only 1 larva. The center of the lesion has a small punctum through which the larva can breathe. Extraction of the fly larva can be difficult and may be facilitated by first obstructing the breathing punctum with an occlusive dressing or covering (such as a bottle cap filled with petroleum jelly) for several hours. Larvae may exit on their own or can be gently squeezed out. Treatment for secondary infection and updating tetanus vaccination may be required.
Tungiasis is caused by infestation by a sand flea (Tunga penetrans). A gestating female burrows into the usually thick skin on the 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, there is a central minute opening, often black in color, through which the embedded flea breathes and eventually extrudes her eggs. Clustered lesions may appear as a dirty, crusty, draining plaque. Lesions are typically itchy, painful, and continue to expand as the female produces eggs in her uterus. Treatment involves flea extraction, treatment for secondary bacterial infection, and updating tetanus vaccination, if required. In many countries, extraction is performed at home by using a heat-sterilized needle to pluck out the mature flea and her eggs.
Loiasis, caused by Loa loa, a deerfly-transmitted nematode, occurs rarely in long-term travelers living in rural sub-Saharan Africa. The traveler may present with transient, migratory, subcutaneous, painful, or pruritic nodules (Calabar swelling) produced by adult nematode migration through the skin. Rarely, the worm can be visualized crossing the conjunctiva or eyelid. Peripheral eosinophilia is common. Loiasis can be diagnosed by finding microfilariae in blood collected during daytime; however, since microfilaremia may be absent, serologic tests may be helpful. Treatment of choice is diethylcarbamazine, but special consideration is warranted for areas endemic with both loiasis and onchocerciasis due to the relative contraindication for using diethylcarbamazine in onchocerciasis. Use of ivermectin to treat loiasis may cause neurological problems. Consultation with an expert is required for these cases (see Chapter 4, Filariasis, Lymphatic).
Gnathostomiasis is a nematode infection found primarily in Southeast Asia, the Pacific coast of Peru and Ecuador, parts of Mexico, and equatorial Africa. Infection results from eating undercooked or raw freshwater fish, amphibians, or reptiles. Infected travelers may experience transient, migratory, subcutaneous, pruritic and painful nodules 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 serologic tests may be available for diagnosis. Treatment of cutaneous gnathostomiasis includes albendazole or ivermectin.
Macules and patches (flat lesions) are common and often nonspecific and are often due to drug reactions or viral exanthems. Purpura is typically macular—and any purpuric lesion associated with fever may indicate a life-threatening emergency such as meningococcemia.
Tinea versicolor, due to several species of fungi, Malassezia (for instance M. furfur, previously Pityrosporum ovale), is characterized by abundant, asymptomatic, hypopigmented or hyperpigmented oval skin patches. Individual lesions are often 1–3 cm in diameter, but dozens of lesions may coalesce to form a “maplike” appearance on the upper chest and back. The skin surface typically has a dry or dusty surface. The lesions may be skin colored, slightly hypopigmented, or slightly hyperpigmented (versicolor means “changed color”), but all lesions on a person have a uniform color.
Clinicians can make this diagnosis in various ways. Under the light of a Wood ultraviolet lamp, tinea versicolor produces a subtle yellowish-orange hue. Examination under a microscope can also identify tinea versicolor. Briefly apply a piece of clear cellophane tape to skin lesions to pick up superficial scales. Then place the tape (sticky side down) onto a glass slide. Next, put a drop of methylene blue at the edge of the tape allowing it to run between the tape and the slide. Detection of hyphae (“spaghetti”) and spores (“meatballs”) suggest the diagnosis. Often, however, a clinical diagnosis is made based on the appearance of the lesions.
Treatment with topical azoles (such as clotrimazole cream or ketoconazole shampoo used as a body wash), systemic azoles (such as fluconazole), or selenium sulfide shampoo is recommended. In many countries, the most common treatment is Whitfield ointment (salicylic acid 3% and benzoic acid 6%, mixed in a vehicle such as petrolatum). Antifungal agents such as griseofulvin and nystatin are ineffective.
Tinea corporis (ringworm) may be caused by a number of different superficial fungi. The lesion is often an expanding red, raised ring, with an area of central clearing. Treatment is usually several weeks’ application of a topical antifungal agent or a short course of an oral antifungal agent (terbinafine, fluconazole, or griseofulvin).
Lyme disease, a tickborne infection with the spirochete 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 (erythema migrans). Lyme disease is transmitted by the bites of the hard tick, genus Ixodes, found mostly in temperate latitudes. If there are several lesions, the first to appear is where the tick bite occurred; subsequent lesions are due to a secondary, probably hematogenous, spread of Borrelia, not to multiple tick bites. Erythema migrans is often described as targetoid, but central clearing or red-and-white bands do not occur with every case. The lesions are generally asymptomatic; if a patient reports pruritus, it is usually intermittent and very mild.
Leprosy (Hansen disease) frequently presents with hypopigmented or erythematous patches frequently hypoesthetic to pin prick and associated with peripheral nerve enlargement. This condition is found almost exclusively in immigrants from developing countries. Diagnosis is made by biopsy of the lesions. The national Hansen disease clinical center in Baton Rouge, Louisiana, makes themselves available for consultations (e-mail firstname.lastname@example.org; phone 800-642-2477).
Cutaneous larva migrans, a skin infestation 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 4, Cutaneous Larva Migrans). A deeper lesion that resembles urticarial patches and that progresses rapidly may be due to larva currens (“running larva”) caused by cutaneous migration of filariform larvae of Strongyloides stercoralis.
Lymphocutaneous or sporotrichoid spread of infection occurs when organisms ascend proximally along superficial cutaneous lymphatics, producing raised, linear, cordlike lesions. This is also called nodular lymphangitis. Another presentation is an ascending chain of discontinuous, sometimes ulcerated, nodules, after primary percutaneous inoculation of certain pathogens. Examples include sporotrichosis, atypical Mycobacterium (such as infection with M. marinum after exposure to brackish water or with rapidly growing Mycobacteria after pedicure footbaths), cutaneous leishmaniasis (particularly New World leishmaniasis), nocardiosis, tularemia, and coccidioidomycosis.
Phytophotodermatitis is a noninfectious condition resulting from interaction of natural psoralens, most commonly found in the juice of limes, and ultraviolet A radiation from the sun. The result is an exaggerated sunburn that creates a painful line of blisters, followed by asymptomatic hyperpigmented lines that may take weeks or months to resolve. Linear lesions caused by cnidarian envenomations, such as jellyfish stings, often resemble phytophotodermatitis.
A skin ulcer forms when the epidermis, the skin’s superficial layer, is damaged or absent, and the damaging process has entered the dermis, the skin’s deeper, more leathery layer. The most common cutaneous ulcers are caused by the common pyogenic bacteria, staphylococci and streptococci, creating well-demarcated, shallow ulcers with sharp borders. These lesions are called bacterial or common ecthyma, and their treatment is described earlier in this chapter.
Cutaneous leishmaniasis (CL) can resemble bacterial ecthyma by forming shallow, although usually painless, ulcers. The surface of leishmanial ulcers can have a dried crust or a raw, fibrinous coat. The main areas of risk for CL are Latin America, the Mediterranean coastal areas, the Middle East, south and central Asia, and Africa’s northeastern quadrant. Typically, CL forms a painless ulcer unless superinfected. It has heaped-up margins on exposed skin surfaces and is slow growing. Special diagnostic techniques are necessary to confirm the diagnosis. Both topical and systemic treatments may be effective; it is often necessary to speciate the pathogen to determine the proper treatment. When CL is suspected, clinicians may go to the CDC’s web page, www.cdc.gov/parasites/leishmaniasis/index.html, or contact the CDC at 404-718-4745 or email@example.com for recommendations on diagnosis and treatment (see Chapter 3, Cutaneous Leishmaniasis).
Cutaneous anthrax produces a large edematous swelling that, surprisingly, is painless. The surface develops a shallow ulcer that progresses into a necrotic black eschar. Nearly all cases of travel-associated anthrax will come from exposure to live cattle, sheep, or goats, or from handling unprocessed products made from their hides or wool (see Chapter 4, Anthrax).
Less common causes of ulcers include cutaneous diphtheria (Corynebacterium diphtheriae), Buruli ulcer (Mycobacterium ulcerans), and sexually transmitted infections of syphilis (Treponema pallidum) and chancroid (Haemophilus ducreyi). On several island groups in the southwestern Pacific, H. ducreyi causes nonvenereal cutaneous ulcers. Rarely, a painless destructive ulcer with undermined edges may arise from infection with M. ulcerans (Buruli ulcer), a freshwater bacterium found most commonly in equatorial Africa and in the Australian state of Victoria. The central African form of human African trypanosomiasis (due to Trypanosoma brucei rhodesiense) can produce a trypanosomal chancre at the bite site of the transmitting tsetse fly (Glossina spp.).
Necrotizing spider bites are usually caused by recluse spiders, of which the most common culprit is Loxosceles reclusa, the brown recluse found in the south-central part of the United States. Many studies have shown that outside a few endemic areas, most alleged spider bites are, in fact, infections with methicillin-resistant S. aureus and should be treated accordingly.
MISCELLANEOUS SKIN INFECTIONS
Skin Infections Associated with Water
Skin and soft tissue infections (SSTI) can occur after exposure to fresh, brackish, or saltwater, particularly if the skin’s surface is compromised. Abrasions or lacerations from submerged objects during wading and swimming, puncture wounds from fishhooks, and bites or stings from marine or aquatic creatures may be the source of the trauma leading to waterborne infections. The most virulent SSTIs associated with marine and estuarine exposures are due to Vibrio vulnificus (and related non-cholera Vibrio); for freshwater exposure, Aeromonas hydrophila is the most dangerous pathogen. 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 infections may be acquired directly through the skin or by consumption of contaminated shellfish. The illness is 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 to contaminated water and consists of tender or pruritic, folliculocentric red papules, papulopustules, or nodules. There are usually several dozen discrete lesions that occur only on skin surfaces submerged in the infectious waters. 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. Pasteurella multocida infection classically occurs after cat bites and may also occur after dog bites. 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 postexposure prophylaxis, 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 would treat splenectomized patients with amoxicillin-clavulanate prophylactically. Since P. multocida is a common accompaniment of cat bites, consider prophylaxis with amoxicillin-clavulanate or a fluoroquinolone for 3–5 days. 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 4, 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 4, Dengue). The disease is transmitted by Aedes spp. mosquitoes 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 widespread but faint macular rash interrupted by islands of uninvolved pallid skin that becomes evident on the second to fourth day of illness. A petechial rash may be found in classic dengue as well as in severe dengue. Diagnostic modalities include antigen and antibody detection tests, as well as PCR assays; detecting IgM in the appropriate clinical scenario supports the diagnosis. Treatment is supportive; avoid using nonsteroidal anti-inflammatory drugs (NSAIDs) which may increase the risk of bleeding in patients with dengue.
Chikungunya, a virus also transmitted by Aedes spp. mosquitoes, has caused major outbreaks of illness in southeast Africa, South Asia, the Americas, and the Caribbean (see Chapter 3, Chikungunya). Chikungunya resembles dengue clinically, including the rash, although hemorrhage, shock, and death are not typical of chikungunya. A major distinguishing feature of chikungunya is its associated arthritis or arthralgia that may persist for months, whereas in dengue, myalgia is the major clinical feature. Similar to dengue, serologic tests are available. Chikungunya may resolve with persistent arthritis or tenosynovitis. After ruling out dengue, treatment of the arthritis is with NSAIDs.
Zika, a flavivirus also transmitted by Aedes spp. mosquitoes, caused major outbreaks in the Western Hemisphere beginning in 2015 (see Chapter 4, Zika). Sexual transmission has been documented up to several months after acquisition of the disease. Zika infection is generally subclinical or mild, characterized by fever, arthralgia, lymphadenopathy, morbilliform (“maculopapular”) rash, and conjunctivitis. Infection of pregnant women can cause fetal loss or fetal microcephaly and neurological damage. Zika-associated Guillain-Barré syndrome has also been reported after infection. Zika virus infection is usually diagnosed by using molecular diagnostics and serologic testing. Treatment is supportive.
Acute HIV (acute retroviral syndrome) can present with a flulike syndrome including fever, malaise, generalized lymphadenopathy, and generalized skin eruption. Acute HIV infection associated skin findings are often nonspecific and present as pink to deeply red macules or papules, but urticarial and pustular eruptions have also been described. Oral ulcerations may be present.
African tick-bite fever or South African tick typhus, caused by Rickettsia africae, is a frequent cause of fever and rash in southern Africa. Travelers participating in safaris or who hike and camp outdoors are particularly at risk. Transmitted by ticks, the disease is characterized by fever and an eschar, called a tache noire (a mildly painful black necrotic lesion with a red rim), at the site of the tick bite. Within a few days, patients develop a fine petechial or papular rash, associated with localized lymphadenopathy. Several taches noires may be present, as people often suffer multiple tick bites. Diagnosis is usually through clinical recognition and is confirmed by serologic testing. Treatment is with doxycycline. Other rickettsial infections such as Mediterranean spotted fever, 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 third and fifth 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 starts as a blanching maculopapular eruption that becomes petechial, although in some patients it begins with petechiae. Doxycycline is the treatment of choice.
Meningococcemia represents invasive Neisseria meningitidis disease, occurs worldwide and is often associated with outbreaks, especially in the “meningitis belt” of sub-Saharan Africa. Meningococcemia is characterized by acute onset of fever and purpuric macules and patches, which can continue to spread, and is often associated with hypotension and multiorgan failure. Immediate treatment can be life-saving.
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; histoplasmosis; and syphilis.
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