Version May 2024
INTRODUCTION — Skin lesions are a common reason for returned travelers to seek medical evaluation (table 1). Among more than 17,000 ill returned travelers evaluated at one of the 30 GeoSentinel travel clinics worldwide, dermatologic disorders were the third most common problem (after systemic febrile illness and acute diarrhea) [1]. In another study of GeoSentinel network data including more than 25,000 patients evaluated following travel, a skin-related diagnosis was reported in 18 percent of patients [2].
The causes, manifestations, and diagnosis of skin lesions in the returned traveler will be reviewed here [3].
CAUSES OF SKIN LESIONS IN TRAVELERS — The differential diagnosis for skin lesions that occur during or after travel is broad and includes infections due to pathogenic organisms (viruses, bacteria, fungi, helminths, protozoa), arthropod bites and infestations, allergic and hypersensitivity reactions [4], injury by chemicals and ultraviolet light, and trauma [5,6]. Among 269 patients in France with travel-associated skin problems, the most common diagnoses were [7]:
●Cutaneous larva migrans – 25 percent
●Pyoderma – 18 percent
●Arthropod-reactive dermatitis – 10 percent
●Myiasis – 9 percent
●Tungiasis – 6 percent
●Urticaria – 5 percent
●Fever and rash – 4 percent
●Cutaneous leishmaniasis – 3 percent
Among 4594 returned travelers seen through the GeoSentinel network, the most common dermatologic disorders included cutaneous larva migrans (9.8 percent), insect bites (8.2 percent), skin abscess (7.7 percent), superinfected insect bites (6.8 percent), and allergic rash (5.5 percent). Dengue fever was diagnosed in 3.4 percent and leishmaniasis in 3.3 percent [2].
Many skin lesions associated with exotic travel are caused by the same pathogens that affect patients in non-tropical regions [8,9]. Infected bites, cellulitis, and lymphangitis in travelers returned from tropical travel are common (typically caused by Staphylococcus aureus [often methicillin resistant] [10] and Streptococcus pyogenes). Bacterial skin infections may frequently complicate bites in the tropics where good hygiene is difficult to maintain. Additional skin problems related to travel to tropical and developing areas include sunburn, scabies, and prickly heat. Chronic skin problems such as atopic dermatitis may worsen in a tropical environment. Exposure to tropical plants or plant products may cause immediate or delayed hypersensitivity reactions or phytophotodermatitis [11,12]. Hypersensitivity reactions to drugs taken for treatment or prophylaxis may occur.
History and exposures — Key elements of the history to help define possible diagnoses include:
●Time since travel
●Location and duration of travel
●Exposure history (eg, fresh or sea water, animals, arthropods, plants, breaks in skin including tattoos, sexual activity, occupational activities, and medications including over-the-counter drugs)
●Time of onset of skin lesion(s) and their evolution
●Associated symptoms (eg, itching or pain)
●Accompanying systemic symptoms
SYSTEMIC INFECTIONS — The initial focus should be on infections that are treatable, transmissible, or associated with serious sequelae or death. Dermatologic manifestations may offer a valuable clue for diagnosis of systemic illness. Multiple systemic infections are associated with skin lesions (table 2). In a prospective study of 62 returned travelers to France with fever and widespread rash, the most common diagnoses were chikungunya (35 percent), dengue (26 percent), and African tick bite fever (ATBF; 10 percent) [13]. The high rate of chikungunya infection reflected frequent travel to the Indian Ocean region, where there was an ongoing epidemic.
Viral infections
●Dengue, chikungunya, and Zika virus – Dengue virus, chikungunya virus, and Zika virus can all cause maculopapular rash (table 3). Geographic distributions of dengue, chikungunya, and Zika virus infection overlap [14]. In a study including 346 Nicaraguan patients with suspected viral infection, rash was present in 91 percent of patients with Zika virus infections, 56 percent of patients with chikungunya virus infections, and 50 percent of those with dengue virus infections [15].
•Dengue – Among patients with dengue fever, a diffuse maculopapular rash is observed in 30 to 50 percent of patients (picture 1 and picture 2). Diffuse erythema resembling a sunburn or toxic shock syndrome may be present early in the course of infection. The rash of dengue may become petechial or hemorrhagic. Intense itching may be observed toward the end of the febrile period [16,17]. (See "Dengue virus infection: Clinical manifestations and diagnosis".)
•Chikungunya – Chikungunya infection is characterized by intense polyarthralgia, arthritis, and tenosynovitis; diffuse rash is present in 40 to 56 percent of patients with chikungunya (picture 3) [18,19]. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis".)
•Zika – Zika virus infections commonly cause widespread micropapular rash, often with pruritus, dysesthesias, and conjunctivitis [14]. (See "Zika virus infection: An overview".)
●Measles and rubella – Measles and rubella occasionally occur in travelers who have visited areas where these viruses circulate (picture 4). Unvaccinated travelers with measles have been a source of multiple introductions of measles into the United States.
●Mpox (monkeypox) – Mpox (previously referred to as monkeypox) is a systemic infection and can manifest with fever, lymphadenopathy, and other general symptoms, including generalized rash [20-22]. Skin lesions may be localized or generalized (including hands and feet) and may be confined to a few or a single lesion. In some cases, lesions have been confined to genital, anorectal, and oral areas (picture 5 and picture 6). Skin lesions evolve from macule to papular and become vesicular and then pustular. The pustules scab over and desquamate. Lesions may be painful during the acute stage. (See "Epidemiology, clinical manifestations, and diagnosis of mpox (monkeypox)" and "Treatment and prevention of mpox (monkeypox)".)
Rickettsial infections — Rickettsial infections occur worldwide and are a relatively common, treatable cause of fever and rash in travelers [23-27]. Skin findings vary with the type of rickettsial infection and range from diffuse lesions to a single eschar (picture 7). The appearance of rash due to rickettsial infection may be delayed or absent. The most characteristic rashes for many of the spotted fever rickettsioses are macular, maculopapular, and petechial rashes (picture 8A-B). Vesicular eruptions resembling varicella have been reported in infections due to Rickettsia conorii, R. akari, and R. australis [28-30]. A diffuse rash is observed in 30 to 60 percent of patients with scrub typhus; recognition of an eschar can suggest the diagnosis [31]. (See "Clinical manifestations and diagnosis of Rocky Mountain spotted fever" and "Murine typhus" and "Rickettsialpox" and "Scrub typhus", section on 'Clinical manifestations'.)
Rash is common among travelers with African tick bite fever due to Rickettsia africae. Among 940 Norwegian travelers to rural sub-Equatorial Africa, 4 percent had serologic evidence of infection with R. africae. Among those Norwegian travelers with flu-like symptoms, 26 percent were diagnosed with ATBF [26]. In another series including 119 cases of ATBF, rash occurred in 46 percent of cases [32]. Rashes were most often maculopapular (51 percent); vesicular rashes and purpuric changes were also observed (45 and 4 percent, respectively). An eschar at the site of the tick attachment was noted in 95 percent of patients (picture 9); multiple eschars were observed in 54 percent of cases. Eschars most commonly occurred on the legs (62 percent), followed by chest, abdomen, or groin (18 percent), arms (11 percent), face, neck, or scalp (5 percent), and back or buttocks (4 percent). Regional lymphadenopathy was observed in 43 percent of patients. (See "Other spotted fever group rickettsial infections".)
African trypanosomiasis — African trypanosomiasis (sleeping sickness) is rare in travelers, though an increase in cases has been observed in some areas, including among short-term travelers to Tanzania [33,34]. Early recognition is important since therapy is more complex once central nervous system invasion has occurred [35,36]. A chancre (indurated nodule) appears at the site of the tsetse fly bite in up to 70 to 90 percent of infected patients. A rash characterized by circinate erythematous patches, most prominent on the trunk, may appear later [37].
Fungal infections — Coccidioidomycosis is associated with rash. Among 20 patients with acute symptomatic coccidioidomycosis related to inhalation exposures in Mexico, 62 percent developed a rash [38]. In most patients, the manifestations were papular lesions progressing to maculopapular lesions on the trunk and sometimes on palms, soles, and buccal mucosa. Fever, headache, and chest pain were also prominent findings [38].
Other fungal infections can cause localized findings at the site of skin penetration. (See 'Nodules' below.)
Sexually transmitted infections — Sexual contact with new partners is common during travel. Several sexually transmitted infections can cause systemic infection and nongenital skin lesions, including syphilis, gonorrhea, and acute human immunodeficiency virus (HIV) [39]. In one study, 3 percent of returned travelers with fever and widespread rash had acute HIV [13]. Mpox has emerged as an important sexually transmitted infection globally.
CLINICAL MANIFESTATIONS
Widespread pruritic papules or pustules — Direct penetration of the skin by pathogens may result in diffuse skin lesions. This frequently occurs following immersion in water during recreational or occupational activities.
Swimmer's itch — Cercarial dermatitis, also known as swimmer's itch, is an itchy maculopapular rash that follows skin penetration by cercariae of nonhuman schistosomes (often avian) [40,41]. The distribution of the rash is limited to areas of the body immersed in water. Itchy, red papules that may become vesicular develop hours to a day or so after exposure to water contaminated with schistosomes (picture 10). This infection usually arises from exposure to fresh water, but, occasionally, contact with brackish or salt water can lead to the rash. The nonhuman schistosomes are unable to complete development in the human host though elicit an intense inflammatory response that is more rapid and severe if repeat exposure occurs. Nonhuman schistosomes are widely distributed and found on all continents.
Human schistosomes can also produce a rash (redness, urticaria, itchy papules) after penetration of the skin. Among 28 travelers to Mali, Africa, who developed schistosomiasis after water exposure, 10 (36 percent) had schistosomal dermatitis [42]. (See "Schistosomiasis: Epidemiology and clinical manifestations".)
Seabather's eruption — Seabather's eruption is due to skin penetration by Linuche unguiculata, Edwardsiella lineata, and probably other larvae of the phylum Cnidaria, which are found in oceans (salt water) [43-45]. The tiny jellyfish larvae release nematocysts and inject toxin. The distribution of the lesions matches areas covered by a bathing suit, wet suit, or points of pressure (eg, wristbands of diving suits, flexural areas). Skin lesions are inflammatory papules, often becoming vesicular or pustular (picture 11A-B). Many descriptions have been reported from the Atlantic coast of North America and from the Caribbean.
Hot tub folliculitis — A diffuse folliculitis ("hot tub folliculitis") is usually caused by Pseudomonas aeruginosa that contaminates swimming pools, hot tubs, whirlpools, or water slides. An itchy maculopapular and vesiculopustular eruption develops within 48 hours of exposure and is most common in areas covered by bathing garments (picture 12A-B). (See "Fever and rash in the immunocompetent patient", section on 'Exposure history' and "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Hot tub-associated eruptions'.)
Nodules — Nodules in the skin can occur as a result of a variety of parasitic infections (table 4). Nodular lesions are found in echinococcosis, dirofilariasis, cysticercosis (picture 13), and toxocariasis [46-49]. Cutaneous leishmaniasis lesions can be nodular initially. Following treatment for visceral leishmaniasis, a diffuse nodular eruption can develop (post–kala-azar dermal leishmaniasis). Onchocerciasis is a common cause of nodules among residents of endemic areas but typically causes an itchy rash among travelers who become infected [50-52]. Papular lesions can occur in the setting of schistosomiasis due to ectopic deposition of schistosome eggs years after exposure to schistosomiasis [53].
Disseminated fungal infections can also cause nodular skin lesions. Talaromyces (formerly Penicillium) marneffei has become an important cause of infection in acquired immunodeficiency syndrome (AIDS) patients, especially in Southeast Asia. Several bacterial pathogens, including Mycobacteria, Nocardia, and Bartonella, can also cause nodular skin lesions [54].
Lymphangitis — Lymphangitis may be caused by a variety of pathogens including Nocardia, tularemia, Mycobacterium marinum, Leishmania brasiliensis, and sporotrichosis (picture 14) [55]. Many of these pathogens are broadly distributed. The clear exception is leishmaniasis, which has a focal distribution. (See "Tularemia: Clinical manifestations, diagnosis, treatment, and prevention" and "Clinical features and diagnosis of sporotrichosis" and "Lymphangitis", section on 'Nodular lymphangitis'.)
Lymphangitis with retrograde progression, lymphadenitis, orchitis, and epididymitis are characteristic of bancroftian filariasis [56,57]. Brugia malayi, B. timori, and other filarial parasites cause similar clinical findings. Infections with these filarial parasites are rare in short-term travelers.
Ulcers — Causes of skin ulcers include pyoderma, tularemia, mycobacterial infection, anthrax, mpox, and others (table 5) [58-60]. Several of these pathogens initially induce nodules that progress to ulceration, usually at the site of inoculation of the organism. Cutaneous leishmaniasis typically begins as a papule that enlarges to a nodule with a central crust that drops off to expose an ulcer that is painless, chronic, and may have a raised border (picture 15). Identification of the specific leishmania cause helps to guide treatment [61]. Several sexually transmitted pathogens (such as chancroid) also cause ulcers.
Hemorrhagic lesions — Illnesses associated with petechial rashes and hemorrhage require urgent evaluation. Causes include viral hemorrhagic fevers, including Ebola virus infection, dengue fever, leptospirosis, meningococcemia, and rickettsial infections (table 6).
Outbreaks of leptospirosis have occurred in travelers [62]; manifestations can be protean and have been mistaken for dengue hemorrhagic and other viral hemorrhagic fevers [63,64]. Leptospirosis can also be associated with an erythema nodosum–like rash [65]. (See "Leptospirosis: Treatment and prevention".)
Migratory lesions — Several parasites migrate in human tissues (table 7). Migrating parasites frequently cause eosinophilia. These have a restricted geographic distribution, so knowledge of travel and exposures is important in establishing the differential diagnosis.
Cutaneous larva migrans — Cutaneous larva migrans is the most common migratory skin infection in travelers [1,66-69]. It develops when infective larvae of animal hookworms (usually Ancylostoma braziliense) penetrate the skin and migrate in superficial tissues, producing a characteristic serpiginous eruption (picture 16). Humans become infected after direct skin contact with soil, sand, or other material contaminated with feces from hookworm-infected animals, usually dogs or cats.
Lesions appear within several days of exposure and most often are found on the feet, buttocks, and thighs [70]. Lesions can be itchy or painful and may be papular or vesiculobullous. The lesions can be complicated by secondary staphylococcal or streptococcal infection. Cutaneous larva migrans is typically self-limited, though medical treatment can shorten the clinical course [71]. (See "Hookworm-related cutaneous larva migrans".)
Strongyloidiasis — Chronic strongyloidiasis can be associated with episodic, itchy, urticarial, or serpiginous skin lesions (larva currens). These lesions are most often located on the buttocks, groin, or trunk [72,73].
Gnathostomiasis — Migrating Gnathostoma larvae cause localized swellings that typically last one to two weeks and are associated with edema, pain, itching, and erythema (picture 17) [74,75]. Lesions begin three to four weeks after ingestion of the parasite, although the swellings can continue to appear months to years later. One or multiple parasites may be present and can migrate to tissues throughout the body including the central nervous system, gastrointestinal or genitourinary tracts, lungs, and eye [76]. (See "Eosinophilic meningitis", section on 'Gnathostomiasis'.)
Treatment of cutaneous gnathostomiasis consists of albendazole (400 mg orally with fatty meal twice daily for 21 days) or ivermectin (200 mcg/kg/day orally for 2 days); no controlled trials of these agents have been performed and patients should be monitored closely for relapse [77-79]. In one study including 31 patients with cutaneous gnathostomiasis in Thailand, clinical response to a single dose of ivermectin was observed in only 41 percent of patients [80]. In a study including 13 patients who developed gnathostomiasis following travel in Southeast Asia or Central America (including nine cases of cutaneous disease), neither ivermectin nor albendazole was fully effective [81]. Relapse was observed in 1 patient treated with a single day of ivermectin and in 7 of 12 patients treated with albendazole (400 mg twice a day for 21 days).
Loiasis — Loiasis is characterized by localized areas of angioedema known as Calabar swellings. These are transient, migratory, warm, itchy, or painful swellings that often recur multiple times per year (picture 18) [82-84]. Calabar swellings typically persist for several days to weeks [85]. Worms can survive for more than 10 years and can occasionally be observed crossing the conjunctiva.
Arthropod bites — Arthropod bites induce skin reactions in one of three ways (table 8):
●Transmission of a pathogen [86]
●Localized and systemic hypersensitivity reaction [87]
●Retained arthropod parts, which can cause a localized granulomatous reaction
A few arthropods inhabit human tissues or infest hair and superficial layers of skin.
Myiasis — The most common presentation of myiasis in returning travelers is furuncular myiasis caused by Dermatobia hominis, the botfly (picture 19), and Cordylobia anthropophaga, the tumbu fly [88-90]. In each instance, larvae penetrate skin and develop in subdermal tissue. Typically, one larva is found in each lesion. Multiple lesions (each containing a single larva) may be present, especially with the tumbu fly [91].
Patients typically note an apparent insect bite that slowly enlarges over time to a nodule measuring 1 to 3 cm in diameter (picture 20A-B). Scant serosanguineous fluid may drain from the lesion. Patients may have a sensation of irritation, crawling, or episodic lancinating pain.
Removal of the intact larva is curative, although secondary bacterial infection can complicate the infestation. A range of approaches have been successful, including occluding the opening (eg, with petroleum jelly or strips of bacon) and gentle extraction of the intact larva when it protrudes its abdomen to reach air (picture 21) [89,92].
Tungiasis — The female sand flea (Tunga penetrans), also known as chigger or jigger, can penetrate human skin, usually on the feet and often under toenails and between toes. The flea feeds on blood, enlarges to a spherical form 5 to 8 mm in diameter, and produces eggs that are expelled through the host's skin [93,94]. The flea can live in tissues for up to a month, causing inflammation, itching, and pain. Lesions are nodular and may be single or multiple, often demonstrating a black color centrally (picture 22). The nodules may ulcerate or become secondarily infected.
Removal of the flea with a sterile needle remains the cornerstone of treatment. Preventive application of coconut oil-based lotion and treatment with dimethicone may be beneficial, but supportive evidence is scant; other studied agents include oral niridazole, oral ivermectin, and topical lotions or ointments containing ivermectin, metrifonate, or thiabendazole [95].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Travel medicine".)
SUMMARY
●Skin lesions are a common reason for returned travelers to seek medical evaluation. The differential diagnosis for skin lesions that occur during or after travel is broad and includes infectious and noninfectious causes. The most common causes include cutaneous larva migrans, insect bites, skin abscess, allergic rash, dengue fever, and leishmaniasis. (See 'Causes of skin lesions in travelers' above.)
●Several systemic infections are associated with skin lesions (table 2). The most common include dengue, chikungunya, mpox, and African tick bite fever. (See 'Systemic infections' above.)
●Direct penetration of the skin by pathogens may result in diffuse skin lesions. This frequently occurs following immersion in water during recreational or occupational activities. (See 'Widespread pruritic papules or pustules' above.)
●Nodules in the skin can occur as a result of a variety of parasitic infections (table 4). Fungal infections can also cause nodular skin lesions. Several bacterial pathogens, including Mycobacteria, Nocardia, and Bartonella, can also cause nodular skin lesions. Lymphangitis may be caused by a variety of pathogens including Nocardia, tularemia, Mycobacterium marinum, Leishmania brasiliensis, and sporotrichosis. (See 'Nodules' above and 'Lymphangitis' above.)
●A range of pathogens can cause skin ulcers (table 5). Several of these pathogens initially induce nodules that progress to ulceration, usually at the site of inoculation of the organism. Several sexually transmitted pathogens (such as chancroid and mpox) also cause ulcers. (See 'Ulcers' above.)
●Illnesses associated with petechial rash and hemorrhage require urgent evaluation. Causes include viral hemorrhagic fevers, dengue fever, leptospirosis, meningococcemia, and rickettsial infections (table 6). (See 'Hemorrhagic lesions' above.)
●Causes of migratory lesions include cutaneous larva migrans, strongyloidiasis, gnathostomiasis, and loiasis (table 7). (See 'Migratory lesions' above.)
●Skin lesions due to arthropod bites include myiasis and tungiasis (table 8). (See 'Arthropod bites' above.)
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