Common Skin Infections in Travelers

Authors


Eric Caumes, MD, Département des Maladies Infectieuses et Tropicales, Hôpital Pitié-Salpêtrière, 45-83 Bld de l’hôpital, F-75013 Paris, France. E-mail: eric.caumes@psl.aphp.fr

Dermatoses are a leading cause of health problems in travelers. They cover a large spectrum of diseases, which includes infectious skin diseases of exotic or cosmopolitan origin as well as environmental skin diseases. The purposes of this review were to identify the most common travel-related skin infections and to familiarize health providers with their epidemiology, clinical features, prevention, diagnosis, and treatment.

Epidemiologic data

During travel, dermatoses have been reported by 8% of 784 American travelers worldwide in a questionnaire-based survey published in 2000. Of the 63 dermatoses reported in this cohort, 14 were related to insect bites or stings, 10 to sun exposure, 7 to dermatophytes, 7 to contact allergy, 5 to infectious cellulites, 4 to miscellaneous causes, and 16 were from unknown causes.1

Similarly, on-site studies of health impairment described dermatoses as being one of the three main reasons for consultation in travelers abroad. In Nepal, three studies showed that dermatoses were the third to the fourth most frequent presenting illness among tourists: skin diseases accounted for 12% of health impairments among 838 French tourists in 1984, 8.7% of consultations among 276 French tourists in 2001, and 10% of 19,616 presentations of patients of all nationalities at a private clinic in the 1980s.2,3 In two of these three Nepalese studies, bacterial and fungal skin infections as well as scabies infestation were the most common travel-associated dermatoses reported.2 Considering a different environment in the Maldives and Fiji, dermatoses were the most frequent presenting illnesses in tourists, with sunburns, superficial injuries (including those due to contact with marine creatures), and skin infections documented most often.4,5 In Burkina Faso, among 100 Westerners with 106 dermatoses diagnosed through teledermatology, the most frequently observed skin diseases were bacterial (21%), viral (12%), and fungal (17%) infections; arthropod-induced dermatitis (8%); and dermatoses of another origin (29%). Fungal diseases were only observed in expatriates but not in tourists.6 Taken together, these six on-site studies from different regions of the world illustrate that the leading dermatoses observed during travel are skin infections and environmental skin diseases (arthropod-induced pruritic dermatitis, sunburns, marine-associated dermatitis, and superficial injuries).

In an international study concerning 17,353 returning travelers, dermatologic disorders were the third most common cause of health problems after systemic febrile illness and acute diarrhea. The most common causes of dermatologic problems were insect bites (with or without secondary infection), cutaneous larva migrans, allergic reactions, and skin abscesses.7 In a prospective study of 269 short-term travelers (tourists and business) who presented to a tropical disease clinic in Paris with dermatoses, similar skin diseases were diagnosed (Table 1). Of the 269 cases, 137 (53%) involved an imported tropical disease.8 In a prospective study made 10 years later in the same hospital unit among a broader spectrum of travelers (immigrants returning from visiting their home countries, expatriates, business travelers, and tourists), the part of imported dermatoses declined to 33.9% (Table 1).9

Table 1.  The top 10 leading dermatoses in three series of returning travelers
Year199520062007
  1. HrCLM = hookworm-related cutaneous larva migrans.

First authorCaumes8Freedman7Ansart9
Study typeObservational monocentric studyObservational multicentric studyObservational monocentric study
Study siteFrance30 GeoSentinel sites worldwideFrance
Study period1991–1993 (2 y)1996–2004 (8 y)2002–2003 (6 mo)
Number of patients2692,947165
Top 10 diagnosesHrCLM (24.9%)Insect bite, with or without superinfection (18.7%)Infectious cellulitis (13%)
Pyoderma (17.8%)HrCLM (12.9%)Scabies (10%)
Arthropods-related pruritic dermatitis (9.7%)Allergic rash or reaction (11.3%)Pruritus of unknown origin (9%)
Myiasis (9.3%)Skin abscess (9.7%)Pyoderma (8%)
Tungiasis (6.3%)Rash of unknown cause (6.6%)Myiasis (7%)
Urticaria (5.9%)Superficial mycosis (5.6%)Dermatophytosis (6%)
Rash with fever (4.1%)Animal bite requiring rabies postexposure prophylaxis (4.7%)Filariasis (5%)
Cutaneous leishmaniasis (3%)Leishmaniasis (3.8%)HrCLM (4.8%)
Scabies (2.2%)Myiasis (3.5%)Urticaria (4.8%)
Injuries (1.9%)Swimmer’s itch (2.8%)Tungiasis (4%)
Diagnosis related to imported tropical diseases53%33.9%

Common localized skin infections and infestations

Bacterial skin infections

Bacterial skin infections are one of the most common dermatoses in travelers. The clinical spectrum ranges from impetigo and ecthyma to erysipelas, abscess, and necrotizing cellulitis. Lesions usually appear while the patient is still abroad but are also a leading cause of consultation in returning travelers.7–9 Pyodermas were the second cause (18%) of dermatoses after cutaneous larva migrans (25%) in a prospective study of travel-associated dermatoses conducted in Paris.8 Among the 48 patients with bacterial cutaneous infections, 75% were diagnosed as impetigo, erysipelas, or ecthyma. Among the 19 patients with impetigo, Staphylococcus aureus and Streptococcus sp. were identified in 80% of the 15 available swab samples, and 63% were secondary to an insect bite. Fifteen years later in the same center, bacterial skin infections were the leading cause of dermatoses in 165 returning travelers (21%) and were secondary to insect bites in 6 (28.6%) of the 21 cases of cellulitis.9 Insect bite, with or without superinfection, was also the first etiologic diagnosis in 2,947 travelers with dermatologic disorder within wide clinician-based surveillance data for 17,353 ill-returned travelers.7 Therefore, insect bites probably act as a frequent portal of entry of bacterial skin infections in travelers. Beyond the area of travel-related dermatosis, the association between impetigo and insect bites has been suggested in a community-based study conducted in England and Wales.10

Bacterial analysis and susceptibility testing should be widely recommended considering the risk of antibiotic resistance and the possibility of highly pathogenic S aureus strains exhibiting Panton–Valentine leukocidin.11 Otherwise, these cutaneous infections are mainly due to S aureus and Streptococcus pyogenes and therefore should be initially treated according to published guidelines after systematic bacterial skin sample, without taking into consideration the area visited.12 Nonetheless, in case of a marine portal of entry, the spectrum of culprit agents must also include Gram-negative bacilli such as Vibrio vulnificus. Finally, the antibiotics recommended in this setting should cover S aureus and Streptococcus sp. and thus include penicillinase-resistant penicillins, first-generation cephalosporins, clindamycin, or vancomycin for patients with life-threatening penicillin allergies.12

Considering that rupture of the cutaneous barrier, whatever is its cause, has been shown to be a common factor associated with cellulitis,13 travelers should avoid skin injuries and should increase their self-protection against insect bites.

Hookworm-related cutaneous larva migrans

Hookworm-related cutaneous larva migrans (HrCLM) is the most frequent travel-associated skin disease of tropical origin and has been recently reviewed in the Journal.7,8,14

HrCLM is caused by the penetration of the skin by cat or dog nematode larvae usually while landing or walking on contaminated lake and ocean beaches or soils of tropical and subtropical countries worldwide.

The incubation period of HrCLM is usually a few days and rarely goes beyond 1 month. In three series, cutaneous lesions appeared after return in 51% to 55% of the travelers, and the mean time of onset after return ranged from 5 to 16 days.8,15,16 In a German study, the time of onset ranged from 16 weeks before return to 28 weeks after return (mean 1.5 d after return).17 In two clusters of HrCLM, the median time from the start of the trip to the development of the eruption ranged from 10 to 15 days.18,19 However, some extremely long incubation periods have been reported, up to 7 months.14

The striking symptom of HrCLM is pruritus localized at the site of the eruption. It is reported in 98% to 100% of patients.15,16 The most frequent and characteristic sign of HrCLM is “creeping dermatitis,” a clinical sign defined as an erythematous, linear, or serpiginous track that is approximately 3 mm wide and may be up to 15 to 20 mm in length, which may extend a few millimeters to a few centimeters daily15 (Figure 1). The mean number of lesions per person varies from one to three.8,15,16 Two other major clinical signs are edema and vesiculobullous lesions along the course of the larva. Local swelling is reported in 6% to 17% and vesiculobullous lesions in 4% to 40% of patients, respectively.8,15,19,20 Potentially, all unprotected parts of the skin in contact with contaminated soil may be involved. However, the most frequent anatomic locations of HrCLM lesions are the feet in more than 50%, followed by the buttocks and thighs.8,15,17,19 Without any treatment, the eruption usually lasts between 2 and 8 weeks.14 Hookworm folliculitis is a particular form of HrCLM, consisting of folliculitis-like lesions associated with numerous relatively short tracks, generally arising from follicular lesions.21

Figure 1.

Creeping eruption due to hookworm-related cutaneous larva migrans.

Local complications of HrCLM are led by secondary bacterial infection of the involved skin area, which may occur in up to 8% of cases.16 Systemic complications have been rarely reported.14

HrCLM is usually a clinical diagnosis based on the typical clinical presentation in the context of recent travel to a tropical country and beach exposure. The differential diagnoses include the other dermatoses that give rise to creeping dermatitis22 (Table 2).

Table 2.  Causes of creeping eruption in travelers*
  • *

    Adapted from Caumes.22

Nematode’s larvae
 Animal hookworms (hookworm-related cutaneous larva migrans), Pelodera strongyloides, zoonotic Strongyloides spp.
 Gnathostomiasis (Gnathostoma spp.)
 Spirurina spp.
 Larva currens (Strongyloides stercoralis)
Adult nematodes
 Loiasis (Loa loa)
 Dracunculiasis (Dracunculus medinensis)
Trematode’s larvae
 Fascioliasis (Fasciola gigantica)
Fly’s maggot
 Migratory myiasis (Gasterophilus spp.)
Arthropod
 Scabies (Sarcoptes scabiei)

Oral ivermectin and albendazole are the first-line treatments. Taken in a single dose, ivermectin is well tolerated and highly efficacious with cure rates of 94% to 100% in all but one of the largest series.14 In the case of hookworm folliculitis, treatment may necessitate repeated courses of oral anthelmintic agents.21 When oral ivermectin and albendazole are contraindicated (eg, very young children), then the application of a 10% albendazole ointment, twice a day for 10 days, is a safe and effective alternative treatment.14 Where available, thiabendazole ointment remains the first-choice treatment.14

Localized cutaneous leishmaniasis

Localized cutaneous leishmaniasis (LCL) occurs in tropical and warm temperate countries and is transmitted by sandflies. Old World LCL (caused primarily by Leishmania major and Leishmania tropica) mainly occurs in travelers to the sub-Saharan and North Africa, the Mediterranean basin, and the Middle East. New World LCL (caused primarily by the species of Leishmania braziliensis and Leishmania mexicana complexes) mainly occurs in travelers to the Amazon Forest of South America.

The main clinical form of cutaneous leishmaniasis among travelers is LCL. Of the 59 cases of cutaneous leishmaniasis reported to the National Institutes of Health from 1973 to 1991, there were 42 cases of LCL (23 Old World and 19 New World), 4 cases of recurrent cutaneous leishmaniasis, 2 cases of mucosal leishmaniasis, and 10 cases of diffuse cutaneous leishmaniasis.23 Similarly, in Germany, 23 cases of LCL and 3 cases of mucocutaneous forms of imported leishmaniasis were reported to the German surveillance network for imported infectious diseases from January 2001 to June 2004. The median time to a definitive diagnosis was 61 days in cases of cutaneous/mucocutaneous leishmaniasis, reflecting the unfamiliarity of physicians working in industrialized countries with leishmanial infections.24 This is also illustrated by a study of cutaneous leishmaniasis in the United States where the median time interval from when the lesions were first noticed to when treatment was instituted was 112 days (range 0–1,032 d).25

The incubation period varies from a few days to a few months. The median time interval between return from the tropics and the onset of cutaneous lesions has been estimated to be 15 (range 7–30 d) to 22 days (range 1–150 d).23,26 The clinical forms of LCL include papule, nodule, ulcer, and nodular lymphangitis (Figure 2). The average number of cutaneous lesions varies from 1 to 3 and rarely exceeds 10 per patient. Usual features of LCL include the anatomic location on exposed skin (face, arms, and legs), absence of pain, chronicity (more than 15 d duration), and failure of antibiotics (which are often prescribed, given that it often looks like pyoderma). Old World LCL is often benign and self-limiting cutaneous disease.27 Meanwhile, in travelers returning from South America, the clinical spectrum is larger, ranging from ulcerative skin lesions to destructive mucosal inflammation, the latter usually being a rarely described complication of L (Viannia) braziliensis infection in travelers.28

Figure 2.

Ulcer due to Old World localized cutaneous leishmaniasis.

The differential diagnosis of LCL includes all diseases that give rise to localized macular, papular, nodular lesion or cutaneous ulcer (Table 3). New World LCL may present with sporotrichoid lesions mimicking sporotrichosis (Table 4).29

Table 3.  Causes of localized skin diseases in travelers according to the primary cutaneous lesion
Papules and nodules
 Noninfectious causes: arthropod bites, sea urchin granuloma, tick granuloma, acne exacerbation
 Bacterial infection: pyodermas, mycobacterial infection (leprosy, tuberculosis, etc.)
 Parasitic infection: scabies, leishmaniasis, tungiasis, myiasis, onchocerciasis, gnathostomiasis, cysticercosis, late cutaneous schistosomiasis, dirofilariasis, paragonimiasis, sparganosis, trypanosomiasis
 Fungal infection: lobomycosis, mycetoma, paracoccidioidomycosis, chromomycosis, sporotrichosis, West African histoplasmosis
 Viral infection: Orf, milker’s nodules
Erythematous plaque
 Bacterial infection: cellulitis, pyoderma, Lyme disease
 Parasitic infection: African trypanosomiasis, leishmaniasis
 Fungal infection: dermatophytosis
Vesicles and bullae
 Noninfectious causes: sunburn, blister beetle dermatitis, contact dermatitis, irritant dermatitis, phytophotodermatitis, arthropod bites, fixed drug eruption
 Bacterial infection: bullous impetigo
 Parasitic infection: hookworm-related cutaneous larva migrans
 Viral infection: herpes simplex infection, herpes zoster, varicella, pox virus
Ulcers
 Noninfectious causes: spider bite, cupping
 Bacterial infection: ecthyma, pyodermas, tick eschar, syphilis, anthrax, mycobacterial infection (Mycobacterium ulcerans), melioidosis, glanders, tularemia, cutaneous diphtheria, plague
 Parasitic infection: leishmaniasis, sporotrichosis, cutaneous amebiasis, dracunculiasis
 Fungal infection: mycetomas, West African histoplasmosis, North American blastomycosis, paracoccidioidomycosis, chromomycosis
 Viral infection: herpes simplex infection
Table 4.  Causes of nodular lymphangitis in travelers*
  • Nodular lymphangitis: nodular and/or ulcerative lesions along the line of lymphatic drainage distributed as in a sporotrichosis.

  • *

    Adapted from Kostman and colleagues.29

Parasitic infection: cutaneous leishmaniasis
Mycose: sporotrichosis
Bacterial infection: tularemia, cat-scratch disease, pyogenic or mycobacterial (Mycobacterium marinum) infection

Diagnosis is based on direct examination of a slit-skin smear of the cutaneous lesion stained with Giemsa under light microscopy and/or culture with identification of subsequent subspecies.30 Skin biopsy from the edge of the ulcer may reveal the characteristic amastigotes within macrophages but is less sensitive than culture. The recently developed polymerase chain reaction (PCR) technology allows a rapid and high-sensitivity diagnosis with determination of most species.28

The response to treatment varies according to the species. Therefore, identification techniques that, like PCR, allow a species-orientated treatment are particularly useful.28 In cases of Old World LCL, absence of treatment may be considered, given that the cutaneous lesions heal spontaneously in nearly all the patients within 1 year. Topical treatment with paromomycin ointment could also be an attractive alternative.31 Otherwise, the mainstay of treatment is pentavalent antimonial agents given intralesionally. Fluconazole is more questionable even in those with L major infections.32 In contrast, treatment is strongly recommended for New World leishmaniasis, at least because it is supposed to prevent mucosal invasion. If pentavalent antimonial drugs are still the drug of choice for New World leishmaniasis, liposomal amphotericin B, pentamidine isethionate, and miltefosine could be attractive alternatives according to the culprit species.28

Myiasis

Myiasis is defined as the infestation of human tissues by larvae or maggots of flies (Diptera). The most common form of human myiasis reported in travelers is furuncular myiasis, which is often caused by Cordylobia anthropophaga (tumbu fly) in sub-Saharan Africa and Dermatobia hominis (human botfly) in Central and South America.33 However, according to the results of series of imported cases in Western countries, a wide variety of clinical presentations of myiasis are observed in travelers.8,34,35 In a series of 25 imported cases seen in France, 20 were due to C anthropophaga, 4 to D hominis, and 1 to Cochliomyia hominivorax.8 In a series of 18 cases imported in England, 9 were due to C anthropophaga, 4 to D hominis, 2 to Oestrus ovis (sheep nasal botfly), 1 to Cordylobia rodhaini, 1 to C hominivorax, and 1 to unidentified Oestrid larva.34 The genus Cordylobia also contains two less common species, Cordylobia ruandae and Cordylobia rodhani. The usual hosts of C rodhani are mainly mammals like rodents, but travelers can be accidentally infested as reported in two Israeli travelers returning from Ghana.36 The most common form of myiasis after travel to Central and South America is due to D hominis. It was reported in a series of 14 Israeli travelers returning from South America.37

Depending on which fly is involved, the presentation of myiasis differs by the method of infestation, place of acquisition, duration of maturation, number of cutaneous lesions, anatomic location, and the ability to manually extract the larvae. Cordylobia anthropophaga larvae penetrate the skin after hatching from eggs deposited on moist soil or clothing and bed linens hung to dry outdoors and that have not been ironed. The infestation by D hominis larvae develops from fly eggs carried to the human by a biting mosquito.33,38 In both cases, the larvae develop by successive molts. The incubation period varies from 7 days to 3 weeks (7–10 d for the tumbu fly and 15–45 d for the botfly).8 The mean time from exposure to diagnosis was 1.5 months in 12 Israeli travelers with D hominis myiasis after return from the Amazon River basin of Bolivia.39

The cutaneous lesion is a 1 to 2 cm furuncle-like lesion with a central punctum through which serosanguineous or purulent fluid discharges. Importantly, the patient complains of a crawling sensation within the lesion, and movements of the larvae may be seen within the central punctum. Cordylobia anthropophaga lesions are more commonly multiple, whereas D hominis lesions usually number from one to three.35Cordylobia anthropophaga lesions are usually located on areas of the body covered by clothing (such as the trunk), whereas D hominis lesions are commonly located on exposed areas of the body (such as the scalp, face, forearms, and legs). The largest number of lesions ever reported was 94 in a child from Ghana infected by C anthropophaga.40

The diagnosis of myiasis is made by the identification of the larva from the lesion. The treatment is the removal of the larvae. No oral antiparasitic medication is usually recommended for myiasis, but ivermectin has been showed to be efficient. It is important to avoid breaking the larvae in that incomplete removal may result in a hypersensitivity or foreign body reaction to the larvae. In the case of C anthropophaga, manual pressure to the lateral aspects of the lesion easily allows the expression of the maggot. With D hominis, extraction is facilitated by placing an occlusive agent (eg, paraffin, petrolatum, pork fat, toothpaste cap) onto the lesion that may cause the larva to migrate to the skin surface.41 Unsuccessful occlusive therapy may necessitate sterile surgical extraction and debridement.33 Although rarely reported, bacterial superinfection is the main complication. Myiasis wounds should be disinfected in addition to the provision of tetanus prophylaxis and antibiotic treatment for secondary bacterial infections.33 In Brazil and Colombia, oral use of ivermectin has been reported as a useful surgery-associated treatment in case of severe orbital myiasis due to C hominivorax.42

Tungiasis

Tungiasis is caused by penetration of the gravid female sand flea Tunga penetrans that burrows into the skin of its host, usually on the feet to feed on blood while producing and extruding eggs.33 The infection is usually acquired via direct contact (eg, bare feet) with infested soil or beaches where adult fleas live. Tungiasis (also called chigoe flea, jigger flea) is widely distributed throughout Latin America, the Caribbean, Africa, and Asia up to the west coast of India.33,43 Humans and animals (eg, dogs, pigs) can be affected. In the largest study of 17 imported cases, tungiasis manifested after return in eight cases (47%), and the median lag time between return and onset was 5 days (range 2–10 d). For all 17 cases, the median lag time between return and presentation was 12 days (range 5–40 d), and all lesions were located at the extremity of a toe.8

The acute cutaneous lesion is a papule with a central black dot at the site of penetration that develops into a wart-like nodule through which eggs of the flea are expelled. There is a limited number of nodules (most commonly one), which are usually located on the feet (subungual, soles, tips or toes, and web spaces) and lower extremities.8,43

The diagnosis relies on clinical findings and is confirmed by the morphology of the flea after its extraction. The differential diagnosis includes myiasis, pyoderma, and foreign body reaction.

Treatment consists of complete sterile excision of all embedded fleas with needles or curettes, administration of tetanus prophylaxis, and oral antibiotherapy if there are signs of secondary bacterial infection.33

Scabies

Scabies is the commonest cause of diffuse pruritic skin disease diagnosed in travelers returning from the tropics.7,9 Scabies is an infestation by the mite Sarcoptes scabiei and is acquired by skin-to-skin contact. Clinically, a patient complains of generalized and intense itching, worsening at night, usually sparing the face and head. Pruritus occurs within 3 weeks of contact in case of primary exposure and within a few days in patients with a history of previous scabies exposure. The most specific skin findings include 5 to 10 mm burrows and papulonodular genital lesions. The classic distributions of lesions are the interdigital web spaces, flexor surfaces of the wrists, the elbows, the axillae, the buttocks and genitalia, and on the breasts of women. Other skin changes are secondary to pruritus and include excoriation, lichenification, and impetiginization.

A family history of pruritus is a classical clue to the diagnosis. Diagnosis is confirmed by the microscopic identification of the female mite, eggs, or fecal pellets on skin scrapings of a cutaneous lesion. Treatment includes permethrin cream 5%, lindane 1% (gamma-benzene hexachloride), benzyl benzoate (in Europe), and ivermectin. For oral ivermectin, which is a simple and well-tolerated alternative, a second dose 2 weeks later should be recommended.44 Bedding and clothing must be laundered or removed from contact for at least 3 days. Personal and household contacts must also be treated.

Common systemic febrile illnesses with skin involvement

Arboviral infections

The most frequent arboviral infections that give rise to a cutaneous eruption in travelers are caused by dengue and chikungunya viruses. Both infections are transmitted to humans by arthropods, and both are responsible for febrile exanthema (Table 5). Dengue is the most common cause of arboviral disease in the world, one of the most frequent specific causes of systemic febrile illness among travelers and the most frequent arbovirus reported after travel to tropical and subtropical countries.7,45 Dengue virus belongs to the family Flaviviridae and is transmitted by mosquitoes Aedes aegypti and Aedes albopictus. Dengue is widely reported in tropical and subtropical countries, and dengue hemorrhagic fever is reported in travelers returning from Southeast Asia, South Pacific Islands, Caribbean, and Latin America.

Table 5.  Causes of febrile rash in travelers
Noninfectious causes: adverse drug reaction
Viral infection: dengue, chikungunya, other arboviral infections, measles, rubella, human immunodeficiency virus, Epstein–Barr Virus and cytomegalovirus primary infection, viral hemorrhagic fever
Bacterial infection: rickettsial infections, typhoid fever, meningococcemia (purpura), syphilis, rat-bite fever, leptospirosis, trench fever, brucellosis
Parasitic infection: African trypanosomiasis, trichinellosis, toxoplasmosis

Typical presentation of classic dengue fever includes the sudden onset of fever, headache, retroorbital pain, fatigue, musculoskeletal symptoms (arthralgia and myalgia), and a exanthema that usually appears when the fever decreases. The exanthema is typically macular or maculopapular, confluent with the sparing of small islands of normal skin. Other dermatologic signs include pruritus, flushed facies, and hemorrhagic manifestations such as petechiae and purpura.46 Most patients present with classic dengue fever and have benign febrile illness, but dengue hemorrhagic fever and dengue shock syndrome must be systematically evaluated.

Typical lab abnormalities include thrombocytopenia, leukopenia, lymphopenia, and elevations of hepatic aminotransferases. A usual fall in the platelet count and a rise in hematocrit must be monitored to promptly diagnose dengue hemorrhagic fever. Diagnosis of dengue virus infection is often based on serology or PCR. Diagnosis of dengue hemorrhagic fever is made on the basis of the association of hemorrhagic manifestations, a platelet count of less than 100,000/μL, and objective evidence of plasma leakage (eg, pleural effusion, ascites, or hypoproteinemia).45

Chikungunya virus was first isolated in Tanzania in 1953; since then, chikungunya outbreaks have been reported in Africa and Asia and more recently in the Indian Ocean. Transmission to humans occurs through bites of Aedes (mainly A aegypti and A albopictus) mosquitoes. Since 2005, chikungunya has emerged in the islands of the southwestern Indian Ocean (Comoros, Mauritius, Seychelles, and Reunion) and has later reemerged in India. Since 2005, chikungunya cases have been reported in travelers returning from known outbreak areas to Europe (especially in France), Canada, and the United States.47–49

Skin manifestations of chikungunya infection in travelers seem to be very similar to those described for classic dengue fever infection, with a pruritic, macular, or a maculopapular exanthema in which small islands of normal skin are spared48 (Figure 3). Diagnosis confirmation is based on serology or PCR, and treatment of the acute phase is only symptomatic (eg, antipyretic agents such as paracetamol and bed rest). Chikungunya and dengue skin manifestations are difficult to differentiate.50 Moreover, the viruses are transmitted by the same mosquito species, and disease-endemic areas are nearly the same in Asia, Africa, and the Indian Ocean. Finally, it is important to differentiate between the two illnesses because shock and gastrointestinal hemorrhages are complications associated with dengue fever,50 whereas long-lasting arthralgia is a complication specifically associated with chikungunya.49

Figure 3.

Exanthema attributed to chikungunya infection.

Other arboviruses presenting with fever and rash should be considered: West Nile virus in North America, Africa, and southern Europe; the Ross River and Barmah Forest viruses in the South Pacific; O’nyong-nyong and Sindbis viruses in tropical Africa; and Mayaro virus in South America.51

Rickettsioses and scrub typhus

Rickettsioses are zoonotic bacterial infections transmitted to humans by arthropods and are considered as emerging diseases in travelers. Regardless of the causative agent, most patients usually present with a benign febrile illness accompanied by headache, myalgia, and cutaneous eruptions (diffuse skin rash and sometimes a cutaneous eschar, the portal of entry). Severe complications such as multiorgan failure and fatalities are occasionally seen.52

African tick bite fever (ATBF) is currently the leading rickettsiosis reported in travelers.52 It is caused by Rickettsia africae and transmitted by cattle ticks of the Amblyomma genus. ATBF is endemic in large parts of rural sub-Saharan Africa and the eastern Caribbean. ATBF frequently occurs in clusters of travelers exposed to Amblyomma ticks during game hunting, safaris, adventure races, and military exercises.53

ATBF is usually a mild disease, and typical clinical presentation usually includes one or several inoculation eschars with a maculopapular or vesicular cutaneous rash accompanied by fever, headache, and neck myalgia (Figure 4).52 In 38 travelers with confirmed ATBF returning from rural sub-Equatorial Africa, more than 80% of patients had fever, headache, and/or myalgia, whereas less than 50% of patients had inoculation eschars, lymphadenitis, cutaneous rash, and aphthous stomatitis.54 In this study, risk factors included game hunting, travel to southern Africa, and seasonal travel from November to April.54 Long-lasting subacute neuropathy has been reported following ATBF contracted during safari trips to southern Africa.55

Figure 4.

African tick bite fever: eschar associated with a few cutaneous lesions.

Other rickettsioses reported in the travelers include:

  • • Mediterranean spotted fever, caused by Rickettsia conorii, transmitted by dog ticks and endemic in Mediterranean Europe, Africa, and Asia.
  • • Murine typhus, a flea-borne infection, caused by Rickettsia typhi, and widely distributed in tropical and subtropical regions.
  • • Rocky Mountain spotted fever, caused by Rickettsia rickettsii, transmitted by dog ticks and endemic in the Americas.
  • • Scrub typhus, caused by Orientia tsutsugamushi, transmitted by the bite of larval trombiculid mites (chiggers) and endemic in rural south and southeastern Asia and the western Pacific.52

Diagnosis of rickettsiosis is often made on clinical grounds. Serological analysis mainly provides a retrospective confirmation of the clinical diagnosis. However, an early diagnosis may be possible using PCR testing of skin biopsies performed on the eschar. Presumptive therapy with doxycycline is recommended whenever a case of rickettsiosis is suspected allowing for rapid recovery and prevention of complications.52 The usual dosage of doxycycline is 200 mg/d, and the antibiotic is contraindicated for children. Symptoms usually resolve within 24 to 48 hours after the onset of treatment, which may also help with the diagnosis of rickettsiosis.

There are many other travel-related skin infections beyond the scope of this review. Tables 2 to 8 are provided to help clinicians considering morphologic characteristics of cutaneous lesions.

Table 6.  Causes of pruritus in travelers
Localized pruritusGeneralized pruritus
Noninfectious causes: contact dermatitis, irritant dermatitis, phytophotodermatitis, arthropod bite, lice, seabather’s eruptionNoninfectious causes: adverse drug reactions, ciguatera fish poisoning, atopic dermatitis exacerbation
Arthropods: arthropod bite, liceViral infection: varicella (in adult), dengue, chikungunya
Parasitic infections: enterobiasis (perianal), hookworm-related cutaneous larva migrans and other causes of creeping eruption (see Table 2).Parasitic infections: cercarial dermatitis, scabies, loiasis, onchocerciasis, African trypanosomiasis and invasive phase of other helminthic diseases in association with urticarial rash (see Table 7).
Table 7.  Causes of urticaria in travelers
Noninfectious causes: adverse drug reaction
Viral infection: hepatitis A infection
Parasitic infection: invasive phase of schistosomiasis, ascariasis, hookworm, anisakiasis, trichinellosis, strongyloidiasis, fascioliasis, toxocariasis, and rupture of cyst during hydatid disease
Table 8.  Causes of localized edema in travelers
Noninfectious causes: reaction to arthropod
Bacterial infection: infectious cellulitis
Parasitic infection: acute lymphatic filariasis, lymphedema of onchocerciasis, Calabar swelling of loiasis, gnathostomiasis, American trypanosomiasis, trichinellosis (located on the face)

Conclusion

Skin diseases as a whole are a common cause of morbitidy among international travelers and are a reason for presenting to a doctor after travel. It is important for travel medicine providers to understand the epidemiology, clinical features, preventive measures, diagnostic testing, and treatment options for their patients. The pretravel consultation provides an opportunity to review some of these commonly encountered skin infections and provide travelers with strategies to prevent or self-treat them as they may arise during their travels. When seeing a patient following travel, it is important to recognize important conditions that may require prompt therapy and/or further evaluation with an infectious disease specialist or dermatologist.

Declaration of interests

The authors state that they have no conflicts of interest.

Ancillary