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Sources: Wortmann GW, et al. Cutaneous leishmaniasis following local trauma: A clinical pearl. Clin Infect Dis. 2000;31:201-202; Bogdan C, et al. Visceral leishmaniasis in a German child who had never entered a known endemic area: Case report and review of the literature. Clin Infect Dis. 2001;32:302-306; Sundar S, et al. Short-course of oral miltefosine for treatment of visceral leishmaniasis. Clin Infect Dis. 2000;31:1110-1113.
After evaluating a patient who developed cutaneous leishmaniasis at the site of a recent tattoo, Wortmann and colleagues summarized Walter Reed Army Medical Center’s experience with cutaneous leishmaniasis apparently precipitated by local trauma. They also reviewed a small series of trauma-induced leishmaniasis cases described by Walton and Valverde consisting of 4 American soldiers in Panama who had a defined history of exposure to leishmaniasis followed by an extended period in a nonendemic location.1 After sustaining minor trauma (puncture wound, eyelid struck by gravel, abraded elbow, and manipulated pimple), each patient developed a leishmanial lesion at the site. Wortmann et al then go on to describe Walter Reed’s 7 cases of local penetrating trauma (eg, tattoos, bee stings, rifle wound, rugby abrasion, shaving cut) precipitating Leishmania panamensis, L braziliensis, and L guyanensis infections at sites of trauma 1-4 months after leaving endemic areas. They describe an animal model where mice subcutaneously infected with L amazonensis develop metastatic lesions at sites of artificial trauma such as ear tags.
Bogdan and associates describe a case of visceral leishmaniasis in a 15-month-old child who had no travel outside of Germany or to any known endemic area. Congenital or blood transfusion-associated leishmaniasis was ruled out. There was no known dog exposure. Potential autochthonous transmission is discussed since the index case and family spent a 3-week vacation camping in a site in southern Germany frequently visited by tourists returning from the Mediterranean. The child presented with hepatosplenomegaly, pancytopenia, and fever. Amastigotes were seen on bone marrow smear and peripheral blood yielded parasites identified as L infantum.
Sundar and colleagues describe a total of 54 Indian patients with visceral leishmaniasis treated with oral miltefosine, 50 mg b.i.d. × 14 days, 21 days, or 28 days. Patients were eligible if they had symptoms of fever, weakness, weight loss, splenomegaly, and characteristic amastigotes on splenic aspirates. No HIV-seropositive patients were included. Adverse reactions were self-limited to mild nausea, vomiting, and/or diarrhea. Asymptomatic increases in serum blood urea nitrogen and creatinine described in higher dosage studies were not seen in these dose ranges. Eleven subjects had asymptomatic transaminitis with the highest serum glutamic-oxaloacetic transaminase ranging from 100-157 IU/mL. Cure was achieved in 89% of the 14-day course, 100% of the 21-day course, and 100% of the 28-day course. All patients considered cured had parasite-free splenic aspirates and resolution of symptoms.
1. Walton BC, Valverde L. Evidence for trauma as a precipitating factor of American Leishmaniasis after occult infection (abstract F6). In: Proceedings of the 3rd International Congress of Parasitology (Munich). Vienna: Facta Publication. 1974;3:1571-1572.