Cutaneous and Presumed Visceral Leishmaniasis in a Soldier Deployed to Afghanistan

James P. Woodrow, MD; Joshua D. Hartzell, MD; Jim Czarnik, MD; David M. Brett-Major, MD; Glenn Wortmann, MD


November 30, 2006

Case Report

A 35-year-old man presented to his local hospital, complaining of persistent fevers, testicular pain, night sweats, and weight loss. His symptoms began 1 week prior to presentation. He also noted a nonhealing lesion on his right forearm, which had been present for 3 months. An active-duty US Army soldier, he had recently returned from an 8-month deployment to Afghanistan near the Pakistani border. From the perspective of his health, he reported that his duty there had been uneventful except for numerous insect bites, which occurred despite the use of insect repellant, and 2 or 3 mild, self-limited bouts of diarrhea. While deployed he routinely ate food from the local economy and was exposed to local livestock. He reported complete adherence to his mefloquine malaria prophylaxis regimen, though he took only 3 doses of his primaquine for terminal prophylaxis. He stopped taking this medication due to perceived side effects. He began to feel ill 7 days after his return to the United States, and it was at this time that he sought medical attention.

On initial presentation to an outlying hospital, the patient had normal vital signs. His physical exam was notable for a 1x1-cm dry ulcer on the volar surface of his right forearm. His spleen was not palpable and he had no notable lymphadenopathy. His only recent medication was primaquine, which had been discontinued a few days earlier. Laboratory workup was significant for a mild normocytic anemia, a mild leukopenia, and a slight elevation of liver-associated enzymes (Hgb 12.4g/dL, MCV 87 fl, WBC 2800 cells/mm3, PLT 252x103/mL, AST 186 U/L, ALT 372 U/L). A thick and thin smear for malarial parasites was negative. Radiographic data included a normal chest radiograph. A shave biopsy of his forearm lesion was subsequently performed and amastigotes were directly visualized, confirming a diagnosis of cutaneous leishmaniasis. PCR analysis of the tissue biopsy identified L donovani complex as the causative organism. At this time the patient was transferred to Walter Reed Army Medical Center (WRAMC) for further evaluation.

Upon arrival to WRAMC, the patient continued to complain of fevers, weight loss, night sweats, and testicular pain. He had developed diarrhea, consisting of 3 to 4 loose watery bowel movements per day. His temperature was 102 degrees F with otherwise normal vital signs. Initial laboratory studies revealed a persistence of his leukopenia, anemia, and elevated liver-associated enzymes, but a normal platelet count. Blood and urine cultures, as well as 3 additional thick and thin blood smears for malaria, were negative. Serum HIV enzyme-linked immunoadsorbent assay (ELISA) was negative. An elevated lactate dehydrogenase (LDH) and an undetectable haptoglobin were consistent with hemolysis. He had a negative stool culture, negative ova and parasite screen, negative occult blood, and negative fecal leukocytes. A computed tomography scan of his abdomen and pelvis revealed splenomegaly and thickening of the sigmoid colon.

The differential diagnosis at that point included visceral leishmaniasis vs other endemic and troop-common illnesses including lymphoma, brucellosis, tuberculosis, typhoid fever, and Q fever. A serum Kalazar Detect Assay (InBios, Seattle, Washington) was positive, consistent with a diagnosis of visceral leishmaniasis (VL). A bone marrow biopsy and aspirate was performed and revealed a normal marrow histopathology, and cultures for mycobacteria, fungi, Leishmania, Brucella, and routine pathogens were negative. A PCR assay of the bone marrow tissue for Leishmania was also negative. Given his exposure history, clinical syndrome, multiple negative malaria smears, and a positive rK39 assay, a presumed diagnosis of VL was made and treatment was initiated.

The patient received liposomal amphotericin B (Ambisome, Astellas Pharma US, Inc., Deerfield, Illinois) at an intravenous dose of 3 mg/kg per day. He was dosed on Days 1 through 5, then again on Days 14 and 21 without any significant drug toxicity. The patient became afebrile, and laboratory studies demonstrated normalization of his liver-associated enzymes and improvement in his leukopenia and anemia. The patient was discharged from the hospital and returned home. However, after several weeks of clinical normalcy he became acutely ill and was diagnosed with malaria (P vivax), which was successfully treated with chloroquine and primaquine.


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