Cases reported "Leishmaniasis, Visceral"

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1/33. Kala-azar in zambia: first report of two cases.

    Two autochthonous cases of kala-azar, the first such report of the disease from Central and Southern africa, are described. Both patients presented with generalized macules, papules and nodules without ulceration and both also had tuberculosis. Amastigotes were cultured from blood and identified in skin, bone marrow, liver and spleen.
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2/33. Visceral and cutaneous leishmaniasis (report of 2 cases).

    leishmaniasis is an endemic, sporadic infection in many parts of the world. turkey is geographically unique in linking asia and europe. Of special interest is leishmaniasis, as various forms of this disease have long been reported in the surrounding regions. Visceral and cutaneous leishmaniasis are endemic in the western and southeastern parts of turkey, respectively. Here, we report a cutaneous and a visceral leishmaniasis case, to draw attention to the increase in the incidence of leishmaniasis in turkey. In the patient with cutaneous leishmaniasis, the ulcerative lesion on the cheek had persisted for two months before admittance to the hospital. Direct smears prepared from this lesion were negative for leishmania amastigotes whereas the promastigote forms were maintained in NNN (Novy-MacNeal-Nicolle) medium. The second patient was hospitalized with a prediagnosis of haematological malignancy, but the smears prepared from the bone marrow aspirates revealed leishmania amastigotes and promastigotes were seen on the smears from NNN cultures. These two reports mark the importance of inoculation of the specimens to NNN medium for the recovery of the promastigote forms. Cutaneous and visceral leishmaniasis have become endemic in considerable number of foci in turkey, possibly due to the cessation of vector control programmes and increase in the agricultural and irrigation areas. These two reports also point out the increased prevalence of leishmaniasis in turkey after 1980's.
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3/33. 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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4/33. 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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5/33. Visceral leishmaniasis masquerading as tuberculosis in a patient with AIDS.

    We report a case of visceral leishmaniasis presenting as significant lymphadenopathy in a patient with acquired immune deficiency syndrome. The lymphadenopathy was initially suspected to be tubercular in nature on pathological examination. This report highlights the increasing incidence of acquired immune deficiency syndrome and Leishmania co-infection in india, and the importance of demonstrating tubercle bacilli on culture before suggesting a diagnosis of tuberculosis.
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6/33. Visceral leishmaniasis in human immunodeficiency virus (hiv)-infected and non-hiv-infected patients. A comparative study.

    Visceral leishmaniasis is an endemic infection in Mediterranean countries, where it has become a frequent complication of acquired immunodeficiency syndrome (AIDS). The incidence of visceral leishmaniasis is increasing in spain due to human immunodeficiency virus (hiv)-related cases, but some aspects of its epidemiology, clinical features, and management remain unknown. In addition, no comparative clinical studies about the disease in hiv-infected and non-hiv-infected patients have been reported. During a 24-year period, 120 cases of visceral leishmaniasis were diagnosed at our institution and 80 (66%) were associated with hiv infection. The mean age at diagnosis was higher in hiv-infected that in non-hiv-infected patients (33.2 versus 23.2 yr; p = 0.002), but the male/female ratio was similar in both groups. The main risk factor for hiv infection was intravenous drug abuse (78.7%). The clinical presentation of leishmaniasis was similar in both groups, but hiv-infected patients had a lower frequency of splenomegaly than hiv-negative individuals (80.8% versus 97.4%; p = 0.02). hiv-infected patients had a greater frequency and degree of leukopenia, lymphocytopenia, and thrombocytopenia. Most of them were profoundly immunosuppressed (mean CD4 lymphocyte count, 90 cells/mm3) at the time of diagnosis of leishmaniasis, and 53.7% had AIDS. The sensitivity of serologic studies for Leishmania was significantly lower in hiv-infected than in non-hiv-infected patients (50% versus 80%; p < 0.001), but the diagnostic yield of bone marrow aspirate (67.1% versus 79.4%) and bone marrow culture (62.9% versus 66.6%) was similar in both groups. After initial treatment, the response rate was significantly lower in hiv-infected than in non-hiv-infected individuals (54.8% versus 89.7%; p = 0.001). The relapse rate was 46.2% and 7.5%, respectively (p < 0.001). Secondary prophylaxis with antimonial compounds or amphotericin b seems to be useful in preventing relapses in hiv-infected patients. The mortality rate was higher (53.7% versus 7.5%; p < 0.001) and the median survival time shorter (25 versus > 160 mo; p < 0.001) in AIDS patients than in hiv-negative individuals. Although leishmaniasis could contribute to death in a significant number of hiv-infected patients, it was the main cause of death in only a few of them. The CD4 lymphocyte count and the use of highly active antiretroviral therapy and secondary prophylaxis for leishmaniasis were the most significant prognostic factors for survival in AIDS patients. Visceral leishmaniasis behaves as an opportunistic infection in hiv-infected individuals and should be considered as an AIDS-defining disease.
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7/33. Visceral leishmaniasis caused by Leishmania (Viannia) braziliensis in a patient infected with human immunodeficiency virus.

    The current article reports the case of a 19-month-old-girl, from the state of Minas Gerais, brazil, with visceral leishmaniasis, by Leishmania (Viannia) braziliensis, and Human Immunodeficiency Virus (hiv) co-infection. The child's mother and father, aged 22 and 27 years old, respectively, were both hiv positive. The child was admitted to the General Pediatric Center, in Belo Horizonte, presenting high fever, fatigue, weight loss and enlargement of liver and spleen. Indirect immunofluorescent test revealed a titer of 1:320 for Leishmania. Such result was confirmed by the presence of amastigotes in bone marrow aspirate samples and culture of promastigote forms. parasites were identified as being Leishmania (Viannia) braziliensis through PCR, using a L. braziliensis complex primer and a generic primer, followed by hibridization. Specific leishmaniasis therapy (Glucantime register mark or target antimonial) was intravenously administered.
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8/33. Visceral leshmaniasis diagnosed on duodenal biopsy in a child.

    Visceral leishmaniasis is usually easy to recognize when clinical presentation is complete: splenomegaly, fever and palor associated to pancytopenia, hypoalbuminaemia and hypergamma globulinemia. bone marrow smears, culture and serology confirm the diagnosis. We report the case of an infant in whom clinical and biological findings are suggestive of leishmaniasis and the diagnosis confirmed only by duodenal biopsy.
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9/33. Visceral leishmaniasis in a soldier returning from Operation Enduring freedom.

    This report presents a case of visceral leishmaniasis in a soldier returning from Operation Enduring freedom. During the united states' last major military conflict, Operation Desert Storm, the diagnosis of multiple cases of visceral leishmaniasis led to policy changes, including a temporary ban on troop blood donation. This case demonstrates the applicability of recently developed Leishmania polymerase chain reaction and serological assays when conventional methods of diagnosis, such as tissue microscopy and culture, fail.
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10/33. Atypical American visceral leishmaniasis caused by disseminated Leishmania amazonensis infection presenting with hepatitis and adenopathy.

    Leishmania amazonensis is widely recognised as a cause of cutaneous leishmaniasis in latin america, but it can also disseminate to produce atypical visceral leishmaniasis with hepatitis and lymphadenopathy. The patient, an 8-year-old Brazilian boy, presented with a febrile illness and hepatosplenomegaly, elevated liver enzymes and generalised adenopathy. Serological tests using antigens of L. chagasi, the typical cause of visceral leishmaniasis in latin america, were inconclusive. Leishmania amazonensis was eventually isolated in a culture of a lymph node. The patient recovered fully after treatment with meglumine antimoniate. As this case illustrates, L. amazonensis produces a spectrum of disease that includes atypical American visceral leishmaniasis with evidence of hepatocellular injury and generalised lymphadenopathy.
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