Cases reported "Leishmaniasis, Visceral"

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1/38. Visceral leishmaniasis in costa rica: first case report.

    We describe a 15-month-old eutrophic immunocompetent male who presented with fever, hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia. Leishmania amastigotes were identified in spleen and bone marrow specimens. In addition, tissue culture, animal inoculation, and isoenzyme analysis identified the parasite as leishmania donovani infantum or leishmania donovani chagasi. The infant was successfully treated with an antimonial drug. These findings represent the first case of visceral leishmaniasis reported in costa rica.
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2/38. Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child.

    In this article, we report the case of a 16-month-old German boy who was admitted to the Children's Hospital of Stuttgart with a 4-week history of intermittent fever, decreased appetite, weakness, fatigue, and difficulty sleeping. He was healthy at birth and remained so for the first 15 months of his life. On admission, physical examination showed enlarged cervical, axillary, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory data revealed pancytopenia, elevated liver function tests, and hypergammaglobulinemia. blood, stool, and urine culture results were negative. Viral infections and rheumatologic and autoimmune disorders were ruled out, but a positive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral leishmaniasis was made by combining the cultures of both the liver and the bone marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degrees C for 5 days. The parasite was identified by Southern blot analysis as leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the patient became afebrile. The side effects of treatment, including erosive gastritis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzymes, pancreatitis, and electrocardiogram abnormalities, necessitated the discontinuation of treatment after 17 days. On discharge 4 weeks later, the patient was stabilized and afebrile with a normal spleen, normal complete blood count, normal gammaglobulins, and decreasing antibody titers to Leishmania. During the next 24 months, the patient experienced intermittent episodes of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia. But at his last examination in January 1998, he was well; all symptoms mentioned above had disappeared. Because the child had never left germany, nonvector transmission was suspected and household contacts were examined. His mother was the only one who had a positive antibody titer against leishmania donovani complex. She had traveled several times to endemic Mediterranean areas (portugal, malta, and Corse) before giving birth to the boy. But she had never been symptomatic for visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy results were within normal limits. culture results and polymerase chain reaction of this material were negative. A montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis showed specific recognition by maternal antibodies of antigens of Leishmania cultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical countries, but also to the mediterranean region. It is transmitted by the sand fly (phlebotomus, Lutzomyia). Occasional nonvector transmissions also have been reported through blood transfusions, sexual intercourse, organ transplants, excrements of dogs, and sporadically outside endemic areas. Only 8 cases of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother must have had a subclinical infection with Leishmania that was reactivated by pregnancy, and then congenitally transmitted to the child. Visceral leishmaniasis has to be considered in children with fever, pancytopenia, and splenomegaly, even if the child has not been to an endemic area and even if there is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.
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3/38. Therapy of visceral leishmaniasis in renal transplant recipients intolerant to pentavalent antimonials.

    Visceral leishmaniasis should be suspected in renal transplant recipients in whom a fever develops of unknown origin. A 53-year-old renal transplant recipient developed pyrexia, hepatosplenomegaly, and pancytopenia 4 years after transplantation. Antileishmaniasis serology was negative, and the diagnosis was confirmed through bone marrow examination. Treatment with glucantine (N-methylglucamine antimoniate) led to acute pancreatitis, and treatment with ketoconazole plus allopurinol for 21 days was effective to eradicate leishmania donovani.
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4/38. Hemophagocytic lymphohistiocytosis associated with visceral leishmaniasis.

    A 2-year-old child presented with fever and hepatosplenomegaly. Laboratory findings showed pancytopenia, hypertriglyceridemia, hyperferritinemia, and high levels of soluble-IL2 receptors. Initial bone marrow aspiration and biopsy revealed mild hemophagocytosis. A diagnosis of hemophagocytic lymphohistiocytosis was made and appropriate treatment was begun. Repeated marrow aspiration performed because of lack of clinical response revealed Leishmania amastigotes in macrophages in addition to active hemophagocytosis. Treatment with liposomal amphotericin resulted with rapid recovery. Visceral leishmaniasis should be considered in the differential diagnosis of hemophagocytic syndrome.
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5/38. Non-typhoid salmonella septicemia and visceral leishmaniasis in a renal transplant patient.

    BACKGROUND: We report on a renal transplant patient with recurrent attacks of fever, in which salmonella septicemia as well as visceral leishmaniasis were diagnosed. PATIENT: The patient was a 62-year-old man with diabetic nephropathy and a living related kidney transplantation. RESULTS: Nearly 2 years after the transplantation, the patient developed recurrent attacks of fever, which were initially diagnosed as non-typhoid salmonellosis and improved after treatment. Three months later, he had relapses of fever. As the patient developed pancytopenia, a bone marrow aspiration was done, showing Leishmania parasites. The patient responded well to treatment with sodium stibogluconate. CONCLUSIONS: A high index of suspicion, together with better diagnostic assays to detect visceral leishmaniasis, is warranted in the diagnostic work-up of any fever of unknown origin in immunocompromised patients, especially in endemic areas.
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6/38. Secondary myelofibrosis in visceral leishmaniasis--case report.

    A 39-year-old woman with a history of travel to the Montenegrin coast presented with a 9-month long history of fever and weakness, and on examination was found to be emaciated with hepatosplenomegaly and pancytopenia. Marrow aspiration showed poor cellularity with abundant Leishman Donovan (LD) bodies in the macrophages. Bone marrow trephine biopsy revealed a marked myelofibrosis (Manoharan classification: grade III) with osteosclerosis. The impression smears of a trephine biopsy stained with Guiemsa also showed LD bodies. The patient did not exhibit evidence of any risk factors for visceral leishmaniasis (VL). She was treated with meglumine antimoniate (Glucantime) without any adverse effect. The spleen returned to a normal volume after 4 months and bone marrow trephine biopsy performed 6 months after initiation of the therapy had returned to normal. A diagnosis was difficult to establish as VL is rarely encountered in the continental parts of yugoslavia, and with the presence of associated myelofibrosis it could easily have been mistaken for chronic idiopathic myelofibrosis. The association of myelofibrosis with visceral leishmaniasis has been reported in the literature only three times; we thus feel that documentation of this case is merited.
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7/38. Hemophagocytic syndrome: a rare life-threatening complication of visceral leishmaniasis in a young boy.

    The authors report a case of hemophagocytic syndrome (HPS) associated with acute visceral leishmaniasis (VL). A 4-year-old boy was admitted with high fever, hepatosplenomegaly, and pancytopenia. Elevated serum ferritin and triglyceride, low fibrinogen levels, and bone-marrow (BM) histiocytic hyperplasia with prominent hemophagocytosis were consistent with a HPS. An initial diagnosis of kala-azar was refuted because of negativity of BM aspiration and serology for this parasite, and the diagnosis HPS was made. Three months after first admission, reevaluation of the BM aspiration revealed many amastigotes of Leishmania parasites. The serology of VL became positive, finally establishing the diagnosis of VL. Although specific therapy for VL was instituted, the patient died 4 weeks after the diagnosis.
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8/38. Visceral leishmaniasis: a rare cause of post-transplant fever and pancytopenia.

    Despite the endemic distribution of visceral leishmaniasis in certain parts of our country, there are only a few reports of this infection in renal transplant recipients. We report one renal transplant recipient from non-endemic area with visceral leishmaniasis and graft dysfunction that responded to treatment with stibogluconate. The infection should be considered in the differential diagnosis of a febrile transplant recipient with pancytopenia and allograft dysfunction.
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9/38. Hemophagocytic syndrome as the presenting manifestation of visceral leishmaniasis.

    Hemophagocytosis in visceral leishmaniasis is rare and usually mild. However, presentation as hemophagocytic syndrome is exceptionally rare. We report the case of a 28 years man who presented with fever, hepatosplenomegaly, pancytopenia, reactive histiocytes and severe hemophagocytosis. Subsequent investigations revealed he had leishmania donovani infection.
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10/38. epiglottis involvement in a visceral leishmaniasis.

    The visceral form of leishmaniasis caused by leishmania infantum is frequently observed in Mediterranean countries, however otorhinolaryngeal involvement has only rarely been reported in the literature. We report here the case of a 23-year-old cameroon man, resident in france since 1991, and presenting with recurrent epistaxis and an epiglottis tumoral lesion. The visceral form of leishmaniasis with hepatosplenomegaly and pancytopenia was diagnosed. culture of the epiglottal lesion revealed L. infantum. Serological test for human immunodeficiency virus was negative and the patient was not on immunosuppressive drugs. Dramatic improvement was observed with antimony.
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