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Skin Lesions in Returning Travelers
154 Skin Lesions in Returning Travelers Eric Caumes
KEY FEATURES • Skin diseases are one of the three most common health problems in returning travelers. • Travel-related dermatoses include infectious and environmental diseases of exotic or cosmopolitan origin. • Insect bites, localized cutaneous eruption, and pruritic rashes are the most frequent reasons for consultation. • Common skin infections are bacterial diseases (pyoderma, cellulitis), dermatophytosis, and scabies. • The main parasitic dermatoses are hookworm-related cutaneous larva migrans, localized cutaneous leishmaniasis, tungiasis, and furuncular myiasis. • Environmental skin diseases include sunburns, arthropod-related reactions, contact dermatitis, marine-life dermatitis, and superficial injuries.
INTRODUCTION Dermatoses are a leading cause of health problems in returning travelers and are reported in approximately 20% of ill patients. The most common dermatologic problems are skin and soft tissue infections (pyoderma, cellulitis), hookworm-related cutaneous larva migrans (HrCLM), and reactions to arthropod bite or sting (with or without secondary infection).1–3 Among skin disease in returned travelers, tropical parasitic disease accounts for about 20% of cases. Approximately 10% of these patients are ill enough to be hospitalized.4
APPROACH TO A TRAVELER WITH A SKIN LESION The patient’s history should evaluate the type of travel, use of preventive measures, risk exposure, and history of similar signs and symptoms in fellow travelers. The dermatologic history will focus on the initial presentation and onset relative to potential exposures, the progression of lesions, and their duration. Clinical examination will focus on the morphologic characteristics of the lesions (papule, nodule, vesicle, bullous, plaque, ulcer, creeping dermatitis) (Fig. 154.1), together with their anatomic distribution (i.e., localized, generalized, or limited to a specific anatomic location) and the presence of pruritus. Any associated local and systemic signs and symptoms should be noted. Further diagnostic procedures are warranted depending on the clinical findings.
LOCALIZED SKIN DISEASES Skin and Soft Tissue Infection Bacterial infections are the most common skin diseases in returned travelers.4 The spectrum ranges from impetigo and abscess to erysipelas and necrotizing cellulitis.1,4,5 Infections are usually due to Streptococcus pyogenes (group A Streptococcus [GAS]) and/or Staphylococcus aureus. Arthropod bites or stings can become superinfected, with the bite acting as a portal of entry (Fig. 154.2) or becoming infected secondary to scratching.
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The clinical presentation provides clues toward a specific microbial agent. Impetigo (Fig. 154.3) (presenting as bullae, pustules, or post-bullous erosions) is more often due to S. aureus than to Streptococcus spp.1,5 Ecthyma (Fig. 154.4) (presenting as a crusted lesion) is more likely secondary to S. pyogenes.5 Folliculitis, carbuncles, and abscesses (Fig. 154.5) are almost exclusively due to S. aureus.5 Erysipelas and cellulitis (Fig. 154.6) are more likely due to S. pyogenes, but other bacteria (S. aureus, anaerobes, Aeromonas hydrophila, Vibrio vulnificus, Pasteurella spp.) should be considered in the case of dog bite or marine envenomation, as examples.6 S. aureus can be either methicillin-resistant (MRSA) or methicillin-sensitive (MSSA).7 Both can carry the gene for the Panton–Valentine leukocidin (PVL), a cytotoxin that confers higher morbidity. PVL-positive S. aureus strains acquired abroad can be transmitted after arrival home.4 S. pyogenes remains sensitive to penicillins.5
Creeping Dermatitis Creeping eruption is defined as a linear or serpiginous cutaneous track that is slightly elevated, erythematous, and migrating (Fig. 154.7). The characteristics of the cutaneous trail (length, width, speed of migration, location, duration) help to differentiate between causes.8 HrCLM caused by non-human (cat, dog) hookworm larvae is the most common cause of creeping dermatitis.9 HrCLM is widely distributed in tropical and sub-tropical countries worldwide and is usually acquired while lying or walking on the beaches in hot seaside areas, particularly in Southeast Asia or the Caribbean. The striking symptom of HrCLM is pruritus localized at the site of the eruption, and the clinical sign is creeping dermatitis. Edema or local swelling and vesiculobullous lesions along the course of the larva are reported in approximately 10% of patients. Hookworm folliculitis is a particular form of HrCLM (Fig. 154.8). The most frequent anatomic locations of HrCLM are the feet, followed by the buttocks and thighs. Without treatment, the eruption usually lasts weeks. Creeping eruptions may also be seen in diseases involving non-hookworm larvae (e.g., “larva currens” of strongyloidiasis), maggots, adult nematodes, trematode larvae, and mites (Box 154.1). Oral ivermectin (200 µg/kg, single dose) and albendazole (400–800 mg/day, according to weight, for 3 days) are the treatments of HrCLM.10,11 Ivermectin in a single dose is well tolerated and highly efficacious with cure rates of 94% to 100% in all but one of the series.9
Cutaneous Ulcer Beside pyodermas, the main cause of cutaneous ulcer is cutaneous leishmaniasis (CL) (Fig. 154.9). Old World CL (primarily Leishmania major and L. tropica) usually occurs in travelers to sub-Saharan and North Africa, the Mediterranean basin, and the Middle East. New World CL (primarily species of L. braziliensis and L. mexicana complexes) usually occurs in travelers to the forested areas of South and Central America. The clinical forms of CL also include papules, nodules, plaques, and nodular lymphangitis.4 The average number of cutaneous lesions varies from 1 to 3 and rarely exceeds 10 per patient. Usual features of CL are return from an endemic country in the New or Old World, anatomic location on exposed skin (face, arms, legs), absence of pain, chronicity (more than 1
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Cyst
Fissure
Macule
Nodule
Papule
Polyp
Pustule
Vesicle
Wheal
Fig. 154.1 Skin lesion morphology.
month duration), and failure of antibiotic treatment (often prescribed to treat “pyoderma”). Other causes of cutaneous ulcer in returned travelers include inoculation eschars seen during rickettsioses (e.g., African tick bite fever [ATBF]) (Fig. 154.10), the early stage of African trypanosomiasis (trypanosomal chancre) (Fig. 154.11), and less commonly, cutaneous anthrax. Sporotrichosis and Buruli ulcer (Mycobacterium ulcerans infection) more often present as chronic lesions (Box 154.2).
Fixed Localized Papules and Nodules Myiasis and tungiasis are among the most common causes of fixed papules and nodules (Box 154.3).12,13 Myiasis is infestation of human
tissue by larvae or maggots of flies (Diptera). Furuncular myiasis (caused by Cordylobia anthropophaga in sub-Saharan Africa and Dermatobia hominis in Central and South America) gives rise to a papule then a nodule with a central punctum; the patient typically complains of a crawling sensation inside the lesion.4,12 Cases due to Cochliomyia hominivorax, Oestrus ovis, C. ruandae, and C. rodhani also occur.4 Tungiasis is caused by penetration of the gravid female sand flea Tunga penetrans, which burrows into the skin of its host, usually on the feet or a toe, where it appears as a slowly growing nodule. The infection is acquired via direct contact (e.g., bare feet) with infested soil or beach sand. 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.4,13
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Fig. 154.2 Bullous bacterial cellulitis complicating an insect bite (return from Central Africa).
Fig. 154.5 Abscess of the leg due to a methicillin-susceptible but Panton–Valentine-producing strain of Staphylococcus aureus after return from the Ivory Coast.
Fig. 154.3 Large superficial crusted cutaneous lesion of the thigh (impetigo).
Fig. 154.6 Cellulitis of the calf associated with a cutaneous trail of lymphangitis.
Fig. 154.4 Limited deep post-bullous erosion of the leg (ecthyma).
Fig. 154.7 Creeping dermatitis of the buttocks after return from the French West Indies (hookworm-related cutaneous larva migrans).
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Fig. 154.8 Creeping dermatitis and folliculitis due to hookwormrelated cutaneous larva migrans (return from Thailand).
Fig. 154.9 Chronic cutaneous ulcer due to cutaneous leishmaniasis (return from French Guyana) and febrile exanthem associated with an adverse cutaneous drug reaction secondary to amoxicillin.
Fig. 154.10 Eschar of African tick bite fever acquired on a walking safari in South Africa.
Fig. 154.11 Acute cutaneous ulcer of West African trypanosomiasis due to T. brucei gambiense (trypanosomal chancre) (evacuation from Gabon).
BOX 154.1 Causes of Creeping Eruption in Travelers
BOX 154.2 Causes of Cutaneous Ulcer in Travelers
• Nematode larvae • Animal hookworms (HrCLM)*, Pelodera strongyloides, zoonotic Strongyloides spp. • Gnathostomiasis (Gnathostoma spp.) • Larva currens (Strongyloides stercoralis)
• Non-infectious causes: spider bite, cupping • Bacterial infection: ecthyma*, tick eschar* (rickettsiosis), anthrax, mycobacterial infection (M. ulcerans), melioidosis, glanders, tularemia, cutaneous diphtheria, plague • Parasitic infection: leishmaniasis*, trypanosomal chancre (African trypanosomiasis), chagoma (American trypanosomiasis), cutaneous amebiasis • Fungal infection: sporotrichosis, mycetomas, West African histoplasmosis, North American blastomycosis, paracoccidioidomycosis, chromomycosis • Viral infection: herpes simplex infection
• Adult nematodes • Loiasis (Loa loa) • Dracunculiasis (Dracunculus medinensis) • Dirofilariasis (Dirofilaria immitis) • Trematode larvae • Fascioliasis (Fasciola gigantica) • Fly maggots • Migratory myiasis (Gasterophilus spp.) • Mite • Scabies (Sarcoptes scabiei)* • Pyemotes dermatitis (Pyemotes ventricosus) HrCLM, Hookworm-related cutaneous larva migrans. * Common cause.
* Common cause.
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BOX 154.3 Causes of Fixed Localized Papules and Nodules in Travelers • Non-infectious: arthropod bites*, sea urchin granuloma, tick granuloma, acne exacerbation • Bacterial infection: mycobacterial infection (leprosy, tuberculosis) • Parasitic infection: leishmaniasis*, tungiasis*, myiasis*, scabies*, 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
BOX 154.4 Causes of Febrile Exanthem in Travelers • Non-infectious causes: adverse drug reaction* • Viral infection: dengue*; chikungunya*; Zika, other arboviral infections; measles; rubella; HIV, EBV, and cytomegalovirus primary infection; viral hemorrhagic fever • Bacterial infection: rickettsial infections*, typhoid, meningococcemia (purpura), syphilis, rat bite fever, leptospirosis, brucellosis • Parasitic infection: African trypanosomiasis, trichinellosis, toxoplasmosis EBV, Epstein–Barr virus; HIV, human immunodeficiency virus. * Common cause.
* Common cause.
OTHER LOCALIZED DERMATOLOGIC SYNDROMES
Fixed and Localized Pruritic Eruption Arthropod-Related Dermatitis Arthropod-related dermatitis is caused by fleas, sandflies, chiggers, bedbugs, and, less commonly, mosquitoes and mites. The bites can result in vesiculobullous lesions, cellulitis-like reactions, papular urticaria, and prurigo. Identification of the implicated arthropod can be difficult; however, treatment is the same. Corticosteroidbased ointments are indicated in mild to moderate cases, whereas systemic corticosteroids can be suggested in more severe cases. Oral antihistamines can improve the symptoms. An antibiotic is usually indicated if secondarily infected.
Contact Dermatitis Allergic contact dermatitis has been widely reported after contacts with plants such as cashew nut tree, poison ivy/oak (poison ivy dermatitis), mango, and pistachio. Irritant contact dermatitis can occur after contacts with moths as well as nocturnal beetles of the genus Paederus. Paederus dermatitis, also called blister beetle dermatitis, occurs when nocturnal beetles of the genus Paederus (rove beetles) are crushed on the skin. One or 2 days after crushing the insect and release of paederin, linear, erythematous plaques with a “burnt” aspect and the appearance of vesicles or pustules occur.14 The lesions are usually on the neck, face, or arms. Contact with the conjunctiva and/or cornea can induce severe eye disease (“Nairobi eye”). In the case of irritant dermatitis, the irritant should be removed by washing. Phytophotodermatitis is a cutaneous phototoxic reaction that occurs after contact with a variety of plant substances (e.g., limes, lemons) followed by sunlight exposure. The acute presentation is similar to sunburn but with well-delimited and circumscribed erythema and vesicles. Secondarily, the involved skin has marked hyperpigmentation.15
Dermatophytosis Dermatophytes have a higher incidence in the tropics. They rank among the most common skin diseases observed after travel abroad.4 They can present as tinea corporis (infection of the non-hairy glabrous skin), tinea cruris and axillaris (infection of the groin or axillae), tinea of the feet (the most common dermatophytic infection), and tinea capitis (often in children returning from visiting friends and relatives or adopted in Africa).4
The most frequent cause of nodular lymphangitis (defined by nodular and/or ulcerative lesions distributed along the line of lymphatic drainage) is leishmaniasis and bacterial lymphangitis. Localized erythematous edema can be due to a cellulitis-like reaction after an insect bite or a bacterial cellulitis.4 Marine dermatitis or envenomation can be traced to contact with jellyfish, fire coral, stone fish, sea anemones, urchins, or other sea creatures.
DISSEMINATED SKIN DISEASES Febrile Exanthem A febrile exanthem can be a symptom of potentially life-threatening disease (Box 154.4). The main etiologies are arboviruses, usually dengue fever, and rickettsioses, often ATBF.16 Chikungunya, Zika, and dengue rashes are difficult to differentiate; all have diffuse (potentially pruritic) macular or maculopapular exanthems in which small islands of skin are spared. Arthralgia is more frequent with chikungunya, and leukopenia and thrombocytopenia are more frequent in dengue.16 Other less common arboviral diseases presenting with fever and rash are West Nile and O’Nyong Nyong. ATBF is the most common rickettsiosis in travelers, usually in those returning from rural sub-equatorial Africa.4 ATBF can occur in clusters of travelers exposed to Amblyomma ticks during game hunting, safaris, adventure races, and military exercises. Clinical presentation includes fever, headache, neck myalgia, one to several inoculation eschars (see Fig. 154.10), maculopapular or vesicular cutaneous rash, and regional adenopathy. It is usually mild. Other rickettsioses that may be observed in travelers are Rocky Mountain spotted fever (in Americas), Mediterranean spotted fever (in Mediterranean Europe, Africa, and Asia), scrub typhus (in rural south and southeastern Asia and the western Pacific), and murine typhus (in tropical and sub-tropical regions). Life-threatening infections include meningococcal disease, toxic staphylococcal and streptococcal infection, leptospirosis, and other rickettsioses.4,16 Although rare, viral hemorrhagic fevers (VHFs), such as Lassa, Marburg and Ebola, Rift Valley fever, and CrimeanCongo hemorrhagic fever, have been reported in travelers.4,17 Yellow fever should be suspected in non-vaccinated travelers returning from areas of endemicity.18 Hypersensitivity reaction to drugs must be considered in the diagnosis of fever and exanthem (see Fig. 154.9).
Urticaria Acute schistosomiasis (Katayama fever) is a leading cause of urticaria in travelers with freshwater exposure, usually in Africa.4 Acute
CHAPTER 154 Skin Lesions in Returning Travelers
BOX 154.5 Causes of Urticaria in Travelers • Non-infectious causes: adverse drug reaction* • Viral infection: hepatitis A infection • Parasitic infection: invasive phase of helminthic diseases (ascariasis, hookworm, strongyloidiasis, anisakiasis, gnathostomiasis, schistosomiasis*, fascioliasis), chronic helminthic infections where humans are dead-end host (trichinellosis, toxocariasis), and rupture of cyst during hydatid disease * Common cause.
urticaria can also be seen during the invasive phase of other helminths such as ascariasis, strongyloidiasis, or fascioliasis, whereas chronic urticaria is more often related to toxocariasis and trichinosis (Box 154.5). Hypersensitivity reaction to drugs and, less commonly, viral hepatitis A can be considered in the differential diagnosis of acute urticaria.
Disseminated Pruritus With or Without Rash Scabies is the most common cause of diffuse pruritic skin disease.4 The patient complains of generalized and intense itching, worsening at night, usually sparing the face and head. Specific skin findings include 5- to 10-mm burrows and papulonodular genital lesions. The classic distribution of lesions are the interdigital web spaces; flexor surfaces of the wrists, the elbows, axillae, buttocks, and genitalia; and on the breasts of women. Other skin changes are secondary to pruritus and include excoriation and lichenification. Ciguatera is a cause of localized pruritic neurosensory manifestations (perioral and distal extremity paresthesias) without cutaneous manifestations. There should be a history of fish consumption, other cases among travelers sharing the same meal, a short incubation period (2–30 hours), and the association of gastrointestinal and neurologic signs. The latter can last for months after the initial event. This fish poisoning is acquired by the ingestion of fish containing the toxins produced by the dinoflagellate Gambierdiscus toxicus, which is found in damaged coral reef systems in tropical and sub-tropical regions. Seabather’s eruption (also called sea lice) is a highly pruritic maculopapular eruption that occurs after swimming in the ocean and is generally confined to the skin under swimwear. It is caused by larval forms of sea anemones (e.g., Edwardsiella lineata) and jellyfish (e.g., Linuche unguiculata) that become trapped under swimwear. Cercarial dermatitis (swimmer’s itch) is also a pruritic maculopapular eruption but is predominantly distributed on uncovered body areas. It results from penetration of the skin by cercariae of non-human schistosomes while swimming in freshwater. It can last for several days.
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Prevention From the “skin” point of view, travelers must be instructed to avoid arthropod bites, sun overexposure, walking barefoot, and scratching in the case of pruritus.19 They should be up-to-date against tetanus. Travel first aid kits should include insect repellents, sunscreen, corticosteroid ointments, and appropriate dressings and bandages. Travelers can consider carrying antibiotics to treat streptococcal and staphylococcal skin infection. Upon return they should seek medical care upon the appearance of new skin lesions. REFERENCES
1. Monsel G, Caumes E. What’s new in travel-associated dermatology. J Travel Med 2015;22:221–4. 2. 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;12:593–602. 3. Leder K, Torresi J, Libman MD, et al. GeoSentinel surveillance network. GeoSentinel surveillance of illness in returned travelers, 2007-2011. Ann Intern Med 2013;158:456–68. 4. Hochedez P, Caumes E. Common skin infections in travelers. J Travel Med 2008;15:223–33. 5. Hochedez P, Canestri A, Lecso M, et al. Skin and soft tissue infections in returning travelers. Am J Trop Med Hyg 2009;80:431–4. 6. Diaz JH. Skin and soft tissue infections following marine injuries and exposures in travelers. J Travel Med 2014;21:207–13. 7. Zanger P. Methicillin-resistant Staphylococcus aureus and intercontinental travel—bad bugs on the move! J Travel Med 2014;21:225–7. 8. Vanhaecke C, Perignon A, Monsel G, et al. Aetiologies of creeping eruption: 78 cases. Br J Dermatol 2014;170:1166–9. 9. Hochedez P, Caumes E. Hookworm-related cutaneous larva migrans. J Travel Med 2007;14:339–46. 10. Vanhaecke C, Perignon A, Monsel G, et al. The efficacy of single dose ivermectin in the treatment of hookworm related cutaneous larva migrans varies depending on the clinical presentation. J Eur Acad Dermatol Venereol 2014;28:655–7. 11. Veraldi S, Bottini S, Rizzitelli G, Persico MC. One-week therapy with oral albendazole in hookworm-related cutaneous larva migrans: a retrospective study on 78 patients. J Dermatolog Treat 2012;23:189–91. 12. Lachish T, Marhoom E, Mumcuoglu K, et al. Myiasis in travelers. J Travel Med 2015;22:232–6. 13. Belaz S, Gay E, Beaucournu JC, Guiguen C. Tungiasis outbreak in travelers from Madagascar. J Travel Med 2015;22:263–6. 14. Dursteler BB, Nyquist RA. Outbreak of rove beetle (Staphylinid) pustular contact dermatitis in Pakistan among deployed U.S. personnel. Mil Med 2004;169:57–60. 15. Weber IC, Davis CP, Greeson DM. Phytophotodermatitis: the other “lime” disease. J Emerg Med 1999;17:235–7. 16. Hochedez P, Canestri A, Guihot A, et al. Management of travelers with fever and exanthema, notably dengue and chikungunya infections. Am J Trop Med Hyg 2008;78:710–13. 17. Beeching NJ, Fletcher TE, Hill DR, Thomson GL. Travellers and viral haemorrhagic fevers: what are the risks? Int J Antimicrob Agents 2010;36:S26–35. 18. Hamer DH, Angelo K, Caumes E, et al. Fatal yellow fever in travelers to Brazil, 2018. MMWR Morb Mortal Wkly Rep 2018;67:340–1. 19. Diaz JH, Nesbitt LT Jr. Sun exposure behavior and protection: recommendations for travelers. J Travel Med 2013;20:108–18.
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KEY FEATURES • Skin diseases are one of the three most common health problems in returning travelers. • Travel-related dermatoses include infectious and environmental diseases of exotic or cosmopolitan origin. • Insect bites, localized cutaneous eruption, and pruritic rashes are the most frequent reasons for consultation. • Common skin infections are bacterial diseases (pyoderma, cellulitis), dermatophytosis, and scabies. • The main parasitic dermatoses are hookworm-related cutaneous larva migrans, localized cutaneous leishmaniasis, tungiasis, and furuncular myiasis. • Environmental skin diseases include sunburns, arthropod-related reactions, contact dermatitis, marine-life dermatitis, and superficial injuries.
INTRODUCTION Dermatoses are a leading cause of health problems in returning travelers and are reported in approximately 20% of ill patients. The most common dermatologic problems are skin and soft tissue infections (pyoderma, cellulitis), hookworm-related cutaneous larva migrans (HrCLM), and reactions to arthropod bite or sting (with or without secondary infection).1–3 Among skin disease in returned travelers, tropical parasitic disease accounts for about 20% of cases. Approximately 10% of these patients are ill enough to be hospitalized.4
APPROACH TO A TRAVELER WITH A SKIN LESION The patient’s history should evaluate the type of travel, use of preventive measures, risk exposure, and history of similar signs and symptoms in fellow travelers. The dermatologic history will focus on the initial presentation and onset relative to potential exposures, the progression of lesions, and their duration. Clinical examination will focus on the morphologic characteristics of the lesions (papule, nodule, vesicle, bullous, plaque, ulcer, creeping dermatitis) (Fig. 154.1), together with their anatomic distribution (i.e., localized, generalized, or limited to a specific anatomic location) and the presence of pruritus. Any associated local and systemic signs and symptoms should be noted. Further diagnostic procedures are warranted depending on the clinical findings.
LOCALIZED SKIN DISEASES Skin and Soft Tissue Infection Bacterial infections are the most common skin diseases in returned travelers.4 The spectrum ranges from impetigo and abscess to erysipelas and necrotizing cellulitis.1,4,5 Infections are usually due to Streptococcus pyogenes (group A Streptococcus [GAS]) and/or Staphylococcus aureus. Arthropod bites or stings can become superinfected, with the bite acting as a portal of entry (Fig. 154.2) or becoming infected secondary to scratching.
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The clinical presentation provides clues toward a specific microbial agent. Impetigo (Fig. 154.3) (presenting as bullae, pustules, or post-bullous erosions) is more often due to S. aureus than to Streptococcus spp.1,5 Ecthyma (Fig. 154.4) (presenting as a crusted lesion) is more likely secondary to S. pyogenes.5 Folliculitis, carbuncles, and abscesses (Fig. 154.5) are almost exclusively due to S. aureus.5 Erysipelas and cellulitis (Fig. 154.6) are more likely due to S. pyogenes, but other bacteria (S. aureus, anaerobes, Aeromonas hydrophila, Vibrio vulnificus, Pasteurella spp.) should be considered in the case of dog bite or marine envenomation, as examples.6 S. aureus can be either methicillin-resistant (MRSA) or methicillin-sensitive (MSSA).7 Both can carry the gene for the Panton–Valentine leukocidin (PVL), a cytotoxin that confers higher morbidity. PVL-positive S. aureus strains acquired abroad can be transmitted after arrival home.4 S. pyogenes remains sensitive to penicillins.5
Creeping Dermatitis Creeping eruption is defined as a linear or serpiginous cutaneous track that is slightly elevated, erythematous, and migrating (Fig. 154.7). The characteristics of the cutaneous trail (length, width, speed of migration, location, duration) help to differentiate between causes.8 HrCLM caused by non-human (cat, dog) hookworm larvae is the most common cause of creeping dermatitis.9 HrCLM is widely distributed in tropical and sub-tropical countries worldwide and is usually acquired while lying or walking on the beaches in hot seaside areas, particularly in Southeast Asia or the Caribbean. The striking symptom of HrCLM is pruritus localized at the site of the eruption, and the clinical sign is creeping dermatitis. Edema or local swelling and vesiculobullous lesions along the course of the larva are reported in approximately 10% of patients. Hookworm folliculitis is a particular form of HrCLM (Fig. 154.8). The most frequent anatomic locations of HrCLM are the feet, followed by the buttocks and thighs. Without treatment, the eruption usually lasts weeks. Creeping eruptions may also be seen in diseases involving non-hookworm larvae (e.g., “larva currens” of strongyloidiasis), maggots, adult nematodes, trematode larvae, and mites (Box 154.1). Oral ivermectin (200 µg/kg, single dose) and albendazole (400–800 mg/day, according to weight, for 3 days) are the treatments of HrCLM.10,11 Ivermectin in a single dose is well tolerated and highly efficacious with cure rates of 94% to 100% in all but one of the series.9
Cutaneous Ulcer Beside pyodermas, the main cause of cutaneous ulcer is cutaneous leishmaniasis (CL) (Fig. 154.9). Old World CL (primarily Leishmania major and L. tropica) usually occurs in travelers to sub-Saharan and North Africa, the Mediterranean basin, and the Middle East. New World CL (primarily species of L. braziliensis and L. mexicana complexes) usually occurs in travelers to the forested areas of South and Central America. The clinical forms of CL also include papules, nodules, plaques, and nodular lymphangitis.4 The average number of cutaneous lesions varies from 1 to 3 and rarely exceeds 10 per patient. Usual features of CL are return from an endemic country in the New or Old World, anatomic location on exposed skin (face, arms, legs), absence of pain, chronicity (more than 1
CHAPTER 154 Skin Lesions in Returning Travelers
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Cyst
Fissure
Macule
Nodule
Papule
Polyp
Pustule
Vesicle
Wheal
Fig. 154.1 Skin lesion morphology.
month duration), and failure of antibiotic treatment (often prescribed to treat “pyoderma”). Other causes of cutaneous ulcer in returned travelers include inoculation eschars seen during rickettsioses (e.g., African tick bite fever [ATBF]) (Fig. 154.10), the early stage of African trypanosomiasis (trypanosomal chancre) (Fig. 154.11), and less commonly, cutaneous anthrax. Sporotrichosis and Buruli ulcer (Mycobacterium ulcerans infection) more often present as chronic lesions (Box 154.2).
Fixed Localized Papules and Nodules Myiasis and tungiasis are among the most common causes of fixed papules and nodules (Box 154.3).12,13 Myiasis is infestation of human
tissue by larvae or maggots of flies (Diptera). Furuncular myiasis (caused by Cordylobia anthropophaga in sub-Saharan Africa and Dermatobia hominis in Central and South America) gives rise to a papule then a nodule with a central punctum; the patient typically complains of a crawling sensation inside the lesion.4,12 Cases due to Cochliomyia hominivorax, Oestrus ovis, C. ruandae, and C. rodhani also occur.4 Tungiasis is caused by penetration of the gravid female sand flea Tunga penetrans, which burrows into the skin of its host, usually on the feet or a toe, where it appears as a slowly growing nodule. The infection is acquired via direct contact (e.g., bare feet) with infested soil or beach sand. 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.4,13
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Fig. 154.2 Bullous bacterial cellulitis complicating an insect bite (return from Central Africa).
Fig. 154.5 Abscess of the leg due to a methicillin-susceptible but Panton–Valentine-producing strain of Staphylococcus aureus after return from the Ivory Coast.
Fig. 154.3 Large superficial crusted cutaneous lesion of the thigh (impetigo).
Fig. 154.6 Cellulitis of the calf associated with a cutaneous trail of lymphangitis.
Fig. 154.4 Limited deep post-bullous erosion of the leg (ecthyma).
Fig. 154.7 Creeping dermatitis of the buttocks after return from the French West Indies (hookworm-related cutaneous larva migrans).
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Fig. 154.8 Creeping dermatitis and folliculitis due to hookwormrelated cutaneous larva migrans (return from Thailand).
Fig. 154.9 Chronic cutaneous ulcer due to cutaneous leishmaniasis (return from French Guyana) and febrile exanthem associated with an adverse cutaneous drug reaction secondary to amoxicillin.
Fig. 154.10 Eschar of African tick bite fever acquired on a walking safari in South Africa.
Fig. 154.11 Acute cutaneous ulcer of West African trypanosomiasis due to T. brucei gambiense (trypanosomal chancre) (evacuation from Gabon).
BOX 154.1 Causes of Creeping Eruption in Travelers
BOX 154.2 Causes of Cutaneous Ulcer in Travelers
• Nematode larvae • Animal hookworms (HrCLM)*, Pelodera strongyloides, zoonotic Strongyloides spp. • Gnathostomiasis (Gnathostoma spp.) • Larva currens (Strongyloides stercoralis)
• Non-infectious causes: spider bite, cupping • Bacterial infection: ecthyma*, tick eschar* (rickettsiosis), anthrax, mycobacterial infection (M. ulcerans), melioidosis, glanders, tularemia, cutaneous diphtheria, plague • Parasitic infection: leishmaniasis*, trypanosomal chancre (African trypanosomiasis), chagoma (American trypanosomiasis), cutaneous amebiasis • Fungal infection: sporotrichosis, mycetomas, West African histoplasmosis, North American blastomycosis, paracoccidioidomycosis, chromomycosis • Viral infection: herpes simplex infection
• Adult nematodes • Loiasis (Loa loa) • Dracunculiasis (Dracunculus medinensis) • Dirofilariasis (Dirofilaria immitis) • Trematode larvae • Fascioliasis (Fasciola gigantica) • Fly maggots • Migratory myiasis (Gasterophilus spp.) • Mite • Scabies (Sarcoptes scabiei)* • Pyemotes dermatitis (Pyemotes ventricosus) HrCLM, Hookworm-related cutaneous larva migrans. * Common cause.
* Common cause.
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PART 10 The Sick Returning Traveler
BOX 154.3 Causes of Fixed Localized Papules and Nodules in Travelers • Non-infectious: arthropod bites*, sea urchin granuloma, tick granuloma, acne exacerbation • Bacterial infection: mycobacterial infection (leprosy, tuberculosis) • Parasitic infection: leishmaniasis*, tungiasis*, myiasis*, scabies*, 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
BOX 154.4 Causes of Febrile Exanthem in Travelers • Non-infectious causes: adverse drug reaction* • Viral infection: dengue*; chikungunya*; Zika, other arboviral infections; measles; rubella; HIV, EBV, and cytomegalovirus primary infection; viral hemorrhagic fever • Bacterial infection: rickettsial infections*, typhoid, meningococcemia (purpura), syphilis, rat bite fever, leptospirosis, brucellosis • Parasitic infection: African trypanosomiasis, trichinellosis, toxoplasmosis EBV, Epstein–Barr virus; HIV, human immunodeficiency virus. * Common cause.
* Common cause.
OTHER LOCALIZED DERMATOLOGIC SYNDROMES
Fixed and Localized Pruritic Eruption Arthropod-Related Dermatitis Arthropod-related dermatitis is caused by fleas, sandflies, chiggers, bedbugs, and, less commonly, mosquitoes and mites. The bites can result in vesiculobullous lesions, cellulitis-like reactions, papular urticaria, and prurigo. Identification of the implicated arthropod can be difficult; however, treatment is the same. Corticosteroidbased ointments are indicated in mild to moderate cases, whereas systemic corticosteroids can be suggested in more severe cases. Oral antihistamines can improve the symptoms. An antibiotic is usually indicated if secondarily infected.
Contact Dermatitis Allergic contact dermatitis has been widely reported after contacts with plants such as cashew nut tree, poison ivy/oak (poison ivy dermatitis), mango, and pistachio. Irritant contact dermatitis can occur after contacts with moths as well as nocturnal beetles of the genus Paederus. Paederus dermatitis, also called blister beetle dermatitis, occurs when nocturnal beetles of the genus Paederus (rove beetles) are crushed on the skin. One or 2 days after crushing the insect and release of paederin, linear, erythematous plaques with a “burnt” aspect and the appearance of vesicles or pustules occur.14 The lesions are usually on the neck, face, or arms. Contact with the conjunctiva and/or cornea can induce severe eye disease (“Nairobi eye”). In the case of irritant dermatitis, the irritant should be removed by washing. Phytophotodermatitis is a cutaneous phototoxic reaction that occurs after contact with a variety of plant substances (e.g., limes, lemons) followed by sunlight exposure. The acute presentation is similar to sunburn but with well-delimited and circumscribed erythema and vesicles. Secondarily, the involved skin has marked hyperpigmentation.15
Dermatophytosis Dermatophytes have a higher incidence in the tropics. They rank among the most common skin diseases observed after travel abroad.4 They can present as tinea corporis (infection of the non-hairy glabrous skin), tinea cruris and axillaris (infection of the groin or axillae), tinea of the feet (the most common dermatophytic infection), and tinea capitis (often in children returning from visiting friends and relatives or adopted in Africa).4
The most frequent cause of nodular lymphangitis (defined by nodular and/or ulcerative lesions distributed along the line of lymphatic drainage) is leishmaniasis and bacterial lymphangitis. Localized erythematous edema can be due to a cellulitis-like reaction after an insect bite or a bacterial cellulitis.4 Marine dermatitis or envenomation can be traced to contact with jellyfish, fire coral, stone fish, sea anemones, urchins, or other sea creatures.
DISSEMINATED SKIN DISEASES Febrile Exanthem A febrile exanthem can be a symptom of potentially life-threatening disease (Box 154.4). The main etiologies are arboviruses, usually dengue fever, and rickettsioses, often ATBF.16 Chikungunya, Zika, and dengue rashes are difficult to differentiate; all have diffuse (potentially pruritic) macular or maculopapular exanthems in which small islands of skin are spared. Arthralgia is more frequent with chikungunya, and leukopenia and thrombocytopenia are more frequent in dengue.16 Other less common arboviral diseases presenting with fever and rash are West Nile and O’Nyong Nyong. ATBF is the most common rickettsiosis in travelers, usually in those returning from rural sub-equatorial Africa.4 ATBF can occur in clusters of travelers exposed to Amblyomma ticks during game hunting, safaris, adventure races, and military exercises. Clinical presentation includes fever, headache, neck myalgia, one to several inoculation eschars (see Fig. 154.10), maculopapular or vesicular cutaneous rash, and regional adenopathy. It is usually mild. Other rickettsioses that may be observed in travelers are Rocky Mountain spotted fever (in Americas), Mediterranean spotted fever (in Mediterranean Europe, Africa, and Asia), scrub typhus (in rural south and southeastern Asia and the western Pacific), and murine typhus (in tropical and sub-tropical regions). Life-threatening infections include meningococcal disease, toxic staphylococcal and streptococcal infection, leptospirosis, and other rickettsioses.4,16 Although rare, viral hemorrhagic fevers (VHFs), such as Lassa, Marburg and Ebola, Rift Valley fever, and CrimeanCongo hemorrhagic fever, have been reported in travelers.4,17 Yellow fever should be suspected in non-vaccinated travelers returning from areas of endemicity.18 Hypersensitivity reaction to drugs must be considered in the diagnosis of fever and exanthem (see Fig. 154.9).
Urticaria Acute schistosomiasis (Katayama fever) is a leading cause of urticaria in travelers with freshwater exposure, usually in Africa.4 Acute
CHAPTER 154 Skin Lesions in Returning Travelers
BOX 154.5 Causes of Urticaria in Travelers • Non-infectious causes: adverse drug reaction* • Viral infection: hepatitis A infection • Parasitic infection: invasive phase of helminthic diseases (ascariasis, hookworm, strongyloidiasis, anisakiasis, gnathostomiasis, schistosomiasis*, fascioliasis), chronic helminthic infections where humans are dead-end host (trichinellosis, toxocariasis), and rupture of cyst during hydatid disease * Common cause.
urticaria can also be seen during the invasive phase of other helminths such as ascariasis, strongyloidiasis, or fascioliasis, whereas chronic urticaria is more often related to toxocariasis and trichinosis (Box 154.5). Hypersensitivity reaction to drugs and, less commonly, viral hepatitis A can be considered in the differential diagnosis of acute urticaria.
Disseminated Pruritus With or Without Rash Scabies is the most common cause of diffuse pruritic skin disease.4 The patient complains of generalized and intense itching, worsening at night, usually sparing the face and head. Specific skin findings include 5- to 10-mm burrows and papulonodular genital lesions. The classic distribution of lesions are the interdigital web spaces; flexor surfaces of the wrists, the elbows, axillae, buttocks, and genitalia; and on the breasts of women. Other skin changes are secondary to pruritus and include excoriation and lichenification. Ciguatera is a cause of localized pruritic neurosensory manifestations (perioral and distal extremity paresthesias) without cutaneous manifestations. There should be a history of fish consumption, other cases among travelers sharing the same meal, a short incubation period (2–30 hours), and the association of gastrointestinal and neurologic signs. The latter can last for months after the initial event. This fish poisoning is acquired by the ingestion of fish containing the toxins produced by the dinoflagellate Gambierdiscus toxicus, which is found in damaged coral reef systems in tropical and sub-tropical regions. Seabather’s eruption (also called sea lice) is a highly pruritic maculopapular eruption that occurs after swimming in the ocean and is generally confined to the skin under swimwear. It is caused by larval forms of sea anemones (e.g., Edwardsiella lineata) and jellyfish (e.g., Linuche unguiculata) that become trapped under swimwear. Cercarial dermatitis (swimmer’s itch) is also a pruritic maculopapular eruption but is predominantly distributed on uncovered body areas. It results from penetration of the skin by cercariae of non-human schistosomes while swimming in freshwater. It can last for several days.
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Prevention From the “skin” point of view, travelers must be instructed to avoid arthropod bites, sun overexposure, walking barefoot, and scratching in the case of pruritus.19 They should be up-to-date against tetanus. Travel first aid kits should include insect repellents, sunscreen, corticosteroid ointments, and appropriate dressings and bandages. Travelers can consider carrying antibiotics to treat streptococcal and staphylococcal skin infection. Upon return they should seek medical care upon the appearance of new skin lesions. REFERENCES
1. Monsel G, Caumes E. What’s new in travel-associated dermatology. J Travel Med 2015;22:221–4. 2. 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;12:593–602. 3. Leder K, Torresi J, Libman MD, et al. GeoSentinel surveillance network. GeoSentinel surveillance of illness in returned travelers, 2007-2011. Ann Intern Med 2013;158:456–68. 4. Hochedez P, Caumes E. Common skin infections in travelers. J Travel Med 2008;15:223–33. 5. Hochedez P, Canestri A, Lecso M, et al. Skin and soft tissue infections in returning travelers. Am J Trop Med Hyg 2009;80:431–4. 6. Diaz JH. Skin and soft tissue infections following marine injuries and exposures in travelers. J Travel Med 2014;21:207–13. 7. Zanger P. Methicillin-resistant Staphylococcus aureus and intercontinental travel—bad bugs on the move! J Travel Med 2014;21:225–7. 8. Vanhaecke C, Perignon A, Monsel G, et al. Aetiologies of creeping eruption: 78 cases. Br J Dermatol 2014;170:1166–9. 9. Hochedez P, Caumes E. Hookworm-related cutaneous larva migrans. J Travel Med 2007;14:339–46. 10. Vanhaecke C, Perignon A, Monsel G, et al. The efficacy of single dose ivermectin in the treatment of hookworm related cutaneous larva migrans varies depending on the clinical presentation. J Eur Acad Dermatol Venereol 2014;28:655–7. 11. Veraldi S, Bottini S, Rizzitelli G, Persico MC. One-week therapy with oral albendazole in hookworm-related cutaneous larva migrans: a retrospective study on 78 patients. J Dermatolog Treat 2012;23:189–91. 12. Lachish T, Marhoom E, Mumcuoglu K, et al. Myiasis in travelers. J Travel Med 2015;22:232–6. 13. Belaz S, Gay E, Beaucournu JC, Guiguen C. Tungiasis outbreak in travelers from Madagascar. J Travel Med 2015;22:263–6. 14. Dursteler BB, Nyquist RA. Outbreak of rove beetle (Staphylinid) pustular contact dermatitis in Pakistan among deployed U.S. personnel. Mil Med 2004;169:57–60. 15. Weber IC, Davis CP, Greeson DM. Phytophotodermatitis: the other “lime” disease. J Emerg Med 1999;17:235–7. 16. Hochedez P, Canestri A, Guihot A, et al. Management of travelers with fever and exanthema, notably dengue and chikungunya infections. Am J Trop Med Hyg 2008;78:710–13. 17. Beeching NJ, Fletcher TE, Hill DR, Thomson GL. Travellers and viral haemorrhagic fevers: what are the risks? Int J Antimicrob Agents 2010;36:S26–35. 18. Hamer DH, Angelo K, Caumes E, et al. Fatal yellow fever in travelers to Brazil, 2018. MMWR Morb Mortal Wkly Rep 2018;67:340–1. 19. Diaz JH, Nesbitt LT Jr. Sun exposure behavior and protection: recommendations for travelers. J Travel Med 2013;20:108–18.
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