Cases reported "Leishmaniasis, Visceral"

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1/9. 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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2/9. 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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3/9. Visceral leishmaniasis and Coombs' positive hemolytic anemia: a rare association in an infant treated with liposomal amphotericin b.

    Visceral leishmaniasis is a worldwide, disseminated intracellular protozoal infection that usually manifests by fever, hepatosplenomegaly, anemia, thrombocytopenia, leukopenia and hypergammaglobulinemia. Although anemia is a usual finding, Coombs' positive hemolytic anemia has rarely been reported in association with this disease. Pentavalent antimonials have been the preferred treatment for this disease for decades, but increasing numbers of treatment failure with antimony are being reported. Liposomal amphotericin b is a new drug which is highly efficacious in the treatment of visceral leishmaniasis and produces minimal toxicity. Here we report an infant with visceral leishmaniasis associated with Coombs' positive hemolytic anemia who was successfully treated with liposomal amphotericin b.
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4/9. Visceral leishmaniasis in a patient treated for polyarteritis nodosa.

    We report a case of visceral leishmaniasis in a patient receiving steroids and cyclophosphamide for polyarteritis nodosa. The clinical presentation of leishmaniasis, with fever, pancitopenia and hypergammaglobulinemia may be confused with a reactivation of vasculitis or with other non-infectious conditions such as haematologic diseases. In endemic areas, the case of latent leishmaniasis must be considered and serology for Leishmania should be performed before starting immunosuppressive treatment.
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5/9. Kala-azar associated with coombs-positive autoimmune hemolytic anemia in the patients coming from the endemic area of this disease and successful treatment of these patients with liposomal amphotericin b.

    Kala-azar is an intracellular parasitic infection that infects and multiplies in the macrophages of the liver, the spleen, and the bone marrow. It is characterized by intermittent fever, hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia. Although anemia is a usual finding, Coombs-positive autoimmune hemolytic anemia (AIHA) has rarely been reported with this disease. Pentavalent antimonial compounds remain the mainstay of treatment worldwide. Liposomal amphotericin b (L-AmB) is currently preferred in the treatment of kala-azar because of the resistance to pentavalent antimonals. The authors diagnosed kala-azar associated with Coombs-positive AIHA in 3 patients and treated them with L-AmB (1-5 mg/kg/day) for 30-36 days. Now, all of these patients are healthy following up at the outpatient base for 18-34 months. Kala-azar must be considered in patients with Coombs-positive AIHA and living in and coming from the endemic region for this disease, and it can be successfully treated with L-AmB.
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6/9. Visceral leishmaniasis in an hiv-infected patient: clinical features and response to treatment.

    We report the case of 43-year-old homosexual patient with hiv infection and a history of travel to the far east in whom visceral leishmaniasis was the first infectious complication. Symptoms were fever, malaise, weight loss, hepatosplenomegaly, generalized lymphadenopathy, and oral thrush. Laboratory abnormalities included a slight elevation of liver enzymes, impairment of liver function tests, leukocytopenia, anemia, hypergammaglobulinemia, and markedly depressed CD4( )-cell counts. Despite initially successful treatment with pentavalent antimony, a relapse of leishmaniasis occurred after 7 months. Eradication of the infection was not achieved. Treatment was continued as a palliative chronic suppressive treatment with fortnightly pentamidine infusions. The clinical course was complicated by legionella pneumonia and the development of rapidly progressing Kaposi's sarcoma. The case is presented in detail, and the influence of hiv infection on the course of leishmaniasis is discussed.
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7/9. Leishmania in SLE mimicking an exacerbation.

    Systemic lupus erythematosus is a protean disease which may present manifestations that resemble other diseases posing serious problems of differential diagnosis. Visceral leishmaniasis is a parasitic infection, endemic in 88 countries, whose hallmarks may mimic a lupus flare. fever, pancytopenia, splenomegaly, hypergammaglobulinemia, production of autoantibodies and complement consumption are some of the overlapping features between the two diseases. Thus, extra attention must be paid to patients with lupus who present with the mentioned symptoms. diagnosis of visceral leishmaniasis relies on the detection of leishmania antibodies, on the presence of amastigotes in bone marrow aspirates, biopsies and cultures of the parasite. Treatment is based on the use of i.v. liposomal amphotericin b. The missed recognition of a leishmania infection in a lupus patient may lead to death, since both the omission of a specific anti-parasite treatment and the increase of the immunosuppressive therapy, in the conviction of a lupus flare, accelerate a fatal outcome. In this paper we present a case of visceral leishmaniasis occurring in a lupus patient. The clinical and laboratory features that overlap in the two diseases and the current literature on the topic were discussed.
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8/9. Visceral leishmaniasis misdiagnosed as malignant lymphoma.

    Visceral leishmaniasis is a chronic infectious disease caused by a protozoan parasite of the genus Leishmania, characterized by intermittent fever, monocytosis, hepatosplenomegaly and hypergammaglobulinemia. This morbid condition is rather difficult to diagnose correctly, especially at its early stage, because it is rarely encountered in japan. Recently we treated a case of visceral leishmaniasis in which the patient was misdiagnosed as malignant lymphoma, and went through splenectomy and steroid administration, which made the diagnosis more difficult.
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9/9. Diffuse necrotic hepatic lesions due to visceral leishmaniasis in AIDS.

    A rare case of an AIDS patient who developed scattered necrotic involvement of the liver caused by leishmania infantum is described. Of interest, marked splenomegaly, hypergammaglobulinemia and serum anti-Leishmania antibodies were absent and an incomplete response to therapy was observed. diagnosis of visceral leishmaniasis (VL) was achieved by the demonstration of numerous amastigotes in both hepatocytes and macrophages on liver biopsy. Hepatic necrotic lesions, which when extensive could lead to acute hepatic failure, possibly reflect an atypical manifestation of liver involvement caused by L. infantum and depend on the immunological impairment which characterizes AIDS patients, thus preventing the formation of granulomas. Our observation confirms that VL can manifest atypical aspects in hiv-positive patients depending on the degree of the immunodeficiency. The frequency and severity of this pathology accounts for the need to list VL among AIDS-defining conditions.
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