Cutaneous leishmaniasis (CL), caused by a variety of geographically restricted protozoan parasites within the genus Leishmania, is rarely seen in the United States and diagnosed mainly in travelers, with most autochthonous cases occurring in Texas.1–4 Infection usually begins as a papule or pustule appearing 2 to 8 weeks after a sand fly bite, which progresses to form a painless ulcer over the following weeks. Such ulcers may spontaneously heal or progress caused by a combination of factors including sand fly vector-mediated immunomodulation, intrinsic human host immunity, and parasite virulence factors that depend on the species of the infecting parasite.5 Old World Leishmania species that cause CL are found in the Mediterranean basin, sub-Saharan Africa, and South Asia.5 In contrast, New World CL occurs throughout Central and South America, and is caused by 14 recognized species of Leishmania divided between the subgenera Leishmania and Viannia.6 Although most commonly seen with Leishmania (Viannia) braziliensis, other members of the Viannia subgenus are known to cause mucocutaneous leishmaniasis, either concurrently or after resolution of the cutaneous lesion.6,7 Treatment of the initial skin lesions may reduce the risk of subsequent mucosal disease.8
Here, we describe a cluster of five cases of CL secondary to Leishmania (Viannia) panamensis (L. panamensis) among men attempting emigration from East Africa, who acquired New World CL while traveling from Central America to the United States. Species identification of the infecting parasite revealed important information about what appears to be a well-trodden human smuggling route with potential public health and political consequences.
We thank Leslie Martin, Remus Popa, Robin Ryder, and Daniel Synkowski for their assistance in the care of these patients. We thank Ramona Popa (Northwest Medical Specialties) and Peter K. Marsh, the physicians for the cases in Tacoma, WA. We also thank Frank Steurer and Marcos de Almeida of the Centers for Disease Control and Prevention for performing the PCR and isoenzyme species characterization and identification of the parasites.
Chen LH, Wilson ME, Davis X, Loutan L, Schwartz E, Keystone J, Hale D, Lim PL, McCarthy A, Gkrania-Klotsas E, Schlagenhauf P, 2009. Illness in long-term travelers visiting GeoSentinel clinics. Emerg Infect Dis 15: 1773–1782.
McHugh CP, Melby PC, LaFon SG, 1996. Leishmaniasis in Texas: epidemiology and clinical aspects of human cases. Am J Trop Med Hyg 55: 547–555.
Wright NA, Davis LE, Aftergut KS, Parrish CA, Cockerell CJ, 2008. Cutaneous leishmaniasis in Texas: a northern spread of endemic areas. J Am Acad Dermatol 58: 650–652.
Silveira FT, Lainson R, Corbett CE, 2004. Clinical and immunopathological spectrum of American cutaneous leishmaniasis with special reference to the disease in Amazonian Brazil: a review. Mem Inst Oswaldo Cruz 99: 239–251.
Osorio LE, Castillo CM, Ochoa MT, 1998. Mucosal leishmaniasis due to Leishmania (Viannia) panamensis in Colombia: clinical characteristics. Am J Trop Med Hyg 59: 49–52.
Chen DQ, Lu H, Chang KP, 1999. Replacement of Leishmania N-acetylglucosamine-1-phosphate transferase gene requires episomal rescue. Mol Biochem Parasitol 100: 223–227.
Kreutzer RD, Christensen HA, 1980. Characterization of Leishmania spp. by isozyme electrophoresis. Am J Trop Med Hyg 29: 199–208.
Perez-Ayala A, Norman F, Perez-Molina JA, Herrero JM, Monge B, Lopez-Velez R, 2009. Imported leishmaniasis: a heterogeneous group of diseases. J Travel Med 16: 395–401.
Amato VS, Tuon FF, Bacha HA, Neto VA, Nicodemo AC, 2008. Mucosal leishmaniasis. Current scenario and prospects for treatment. Acta Trop 105: 1–9.
Castro R, Scott K, Jordan T, Evans B, Craig J, Peters EL, Swier K, 2006. The ultrastructure of the parasitophorous vacuole formed by Leishmania major. J Parasitol 92: 1162–1170.
Miranda A, Carrasco R, Paz H, Pascale JM, Samudio F, Saldana A, Santamaria G, Mendoza Y, Calzada JE, 2009. Molecular epidemiology of American tegumentary leishmaniasis in Panama. Am J Trop Med Hyg 81: 565–571.
Christensen HA, de Vasquez AM, Petersen JL, 1999. Short report epidemiologic studies on cutaneous leishmaniasis in eastern Panama. Am J Trop Med Hyg 60: 54–57.
Brown M, Noursadeghi M, Boyle J, Davidson RN, 2005. Successful liposomal amphotericin B treatment of Leishmania braziliensis cutaneous leishmaniasis. Br J Dermatol 153: 203–205.
Nonata R, Sampaio R, Marsden PD, 1997. Mucosal leishmaniasis unresponsive to glucantime therapy successfully treated with AmBisome. Trans R Soc Trop Med Hyg 91: 77.
Solomon M, Baum S, Barzilai A, Scope A, Trau H, Schwartz E, 2007. Liposomal amphotericin B in comparison to sodium stibogluconate for cutaneous infection due to Leishmania braziliensis. J Am Acad Dermatol 56: 612–616.
Sampaio SA, Godoy JT, Paiva L, Dillon NL, da Lacaz CS, 1960. The treatment of American (mucocutaneous) leishmaniasis with amphotericin B. Arch Dermatol 82: 627–635.