Cases reported "Histoplasmosis"

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1/53. Disseminated histoplasmosis in a non-immunocompromised child.

    We describe a 2 year-old non-immunocompromised girl with disseminated histoplasmosis who presented with a 2-month history of fever and bloody diarrhoea. On presentation, she was severely wasted and anaemic. There were gross hepatosplenomegaly and multiple lymphadenopathy. A septic screen was negative. A subsequent stool culture isolated salmonella enteriditis. Serial Widal-Weil Felix (WWF) titres showed serological response after 2 weeks of ceftriaxone. However, she continued to have spiking fever, bloody diarrhoea and weight loss. She developed pancytopaenia and disseminated intravascular coagulation. A bone marrow aspirate and trephine, and lymph node biopsy showed the presence of histoplasma capsulatum, confirmed by Gomori-methenamine silver staining. She responded to intravenous amphotericin b followed by fluconazole (intravenous then oral) for 6 months after discharge. Human Immunodeficiency Virus screening tests were negative. Complement and immunoglobulin levels were normal. T and B enumeration tests showed gross leucopaenia with very low T cell function with defective phagocytic function. A repeat T and B cell enumeration test and phagocytic function tests done 3 months later were normal.
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2/53. Disseminated histoplasmosis with reactive hemophagocytosis: aspiration cytology findings in two cases.

    Two cases of disseminated histoplasmosis associated with reactive hemophagocytic syndrome are described. The clinical presentation was with prolonged unexplained fever and hepatosplenomegaly. On a strong clinical possibility of tuberculosis, antitubercular treatment was initiated in both patients. Lymph node (case 1), splenic (case 2), and bone marrow aspiration, however, showed sheets of proliferating histiocytes, and intracellular and extracellular histoplasma organisms. Aspiration cytology was thus valuable in establishing the final diagnosis. The patients had a fulminant clinical course and died of hemorrhagic shock within 48 hr of hospital admission before specific therapy could be initiated. histoplasmosis can mimic tuberculosis clinically. There is a need for an increased awareness of the clinicopathological spectrum of histoplasmosis, especially its rarer manifestations as hemophagocytic syndrome. In suspected cases, aspirations from the lymph node, liver, and spleen can be performed safely and should be utilized for early diagnosis.
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3/53. meningoencephalitis caused by histoplasma capsulatum: occurrence in a renal transplant recipient and a review of the literature.

    A case of meningoencephalitis caused by histoplasmosis in a renal transplant patient is described. The diagnosis was made postmortem. The clinicopathological features of 39 additional cases of central nervous system (CNS) invasion by histoplasmosis were reviewed. In the great majority of instances (92.1%), CNS involvement occurred in the disseminated form of the disease. Diagnosis was proved by culturing the fungus from bone marrow, blood, lymph nodes, or liver. Neurological symptoms and signs and cerebrospinal fluid (CSF) changes did not occur until extensive brain damage had resulted. Difficulty in culturing the organism in the (CSF) caused a further delay in making an early diagnosis of CNS involvement. The use of meningeal and brain biopsy specimens in conjunction with the electroencephalogram (EEG) may help in making an earlier diagnosis of CNS involvement.
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4/53. Prosthetic valve fungal endocarditis due to histoplasmosis.

    Fungal endocarditis is associated with severe patient morbidity and mortality. Unfortunately, fungal endocarditis is difficult to diagnose because fungal pathogens are uncommonly isolated from routine blood cultures. Histopathological examination of surgically excised cardiac valves, peripheral emboli and systemic ulcers may be useful in identifying pathogens as etiological agents of culture-negative endocarditis. The authors describe a 63-year-old man who had culture-negative endocarditis. Multiple echocardiograms showed progression of the vegetations with valve stenosis despite treatment with multiple antimicrobials. He had multiple peripheral emboli before surgery. Disseminated histoplasmosis was diagnosed by bone marrow culture. Yeast organisms consistent with histoplasma were shown in the vegetations of his excised mitral valve prosthesis. The patient was treated with amphotericin and has been doing well in the two years since his surgery. The diagnosis and management of fungal endocarditis are emphasized.
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5/53. Hemophagocytosis in a patient with chronic lymphocytic leukemia and histoplasmosis.

    We present a case of hemophagocytosis in the setting of a disseminated histoplasma infection in a patient with B-cell chronic lymphocytic leukemia (CLL). A 68-year-old man with CLL presented with progressive pancytopenia and fevers after therapy with cyclophosphamide and fludarabine phosphate. Extensive evaluation for a source of infection revealed a pulmonary nodule. A biopsy specimen taken from the nodule showed granulomas containing histoplasma organisms. A bone marrow biopsy specimen demonstrated disseminated histoplasmosis and intense hemophagocytosis. Antifungal therapy with amphotericin b was initiated, and the fevers and cytopenias resolved. Hemophagocytic syndrome is an uncommon condition with many origins. It is characterized by a proliferation of histiocytes with phagocytosis of formed elements of blood. Clinical manifestations include signs and symptoms of immune activation and decreased peripheral blood cell counts. This condition is often underdiagnosed because clinicians are unfamiliar with it.
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6/53. Disseminated histoplasmosis due to histoplasma capsulatum in two Nigerian children.

    Two cases of disseminated histoplasmosis caused by H. capsulatum in Nigerian children are reported. This is a rare infection in this part of the world. The main clinical features were fever, weight loss, lassitude, lymphadenopathy, hepatosplenomegaly and severe anaemia, features indistinguishable from those of tuberculosis, Hodgkins and other reticuloses. Recognition of this infection in this environment is possible if it is considered in the differential diagnosis of pyrexia of undetermined origin and appropriate laboratory tests carried out on suitable specimens such as bone marrow, splenic aspirate or biopsy material. Treatment of choice is amphotericin b given intravenously, starting with 0-25 mg/kg. and increasing slowly to 1 mg/kg. Other useful drugs are Septrin and rifampicin which can be given concurrently. Subcutaneous abscesses and multiple bone lesions occurred in both our cases presumably as a result of blood stream infection, or embolisation from endocarditis.
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7/53. Rapid PCR-based diagnosis of disseminated histoplasmosis in an AIDS patient.

    Disseminated histoplasmosis is an unusual opportunistic infection in patients with advanced hiv infection living outside endemic areas. Diagnosis usually is made on the basis of isolation of histoplasma capsulatum from clinical specimens or histologic examination. Reported is the case of an hiv-infected Columbian individual in whom the diagnosis of histoplasmosis was established within 24 h of collection of an adequate bronchoalveolar lavage specimen. The diagnosis was made by detection of specific fungal dna and confirmed by isolation of histoplasma capsulatum from blood, bone marrow and respiratory specimens 10 days later. The patient recovered under antifungal treatment and remained asymptomatic up to the last follow-up visit 6 months later. The polymerase chain reaction assay might be a powerful and rapid diagnostic tool for the diagnosis of non-European invasive fungal infections and should be further evaluated.
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8/53. histoplasmosis after treatment with anti-tumor necrosis factor-alpha therapy.

    Anti-tumor necrosis factor-alpha (TNF-alpha) antibodies are frequently used to treat inflammatory diseases. However, these drugs also have immunosuppressive effects. We report on three patients who developed disseminated histoplasmosis on therapy with TNF-alpha inhibitors. in vitro assays were used to characterize the role of these agents in host defense against histoplasma capsulatum. Intracellular proliferation of H. capsulatum was measured in alveolar macrophages and peripheral monocytes of normal volunteers in the presence and absence of the TNF-alpha antibody, infliximab. Both infliximab and control antibody enhanced fungal growth in monocytes and alveolar macrophages, suggesting this was a nonspecific antibody response. Despite similar intracellular fungal loads in the presence of both antibodies, lymphocyte proliferation in response to blood monocytes and alveolar macrophages infected with H. capsulatum was inhibited by the addition of physiologic doses of infliximab, whereas control antibody had no effect. The production of H. capsulatum-induced interferon-gamma and TNF-alpha was assessed in 5-day cultures containing lymphocytes and alveolar macrophages or monocytes. interferon-gamma secretion was significantly reduced in the presence of infliximab. In summary, patients receiving anti-TNF-alpha therapy are at risk for developing disseminated histoplasmosis. This may be due to a defect in the TH1 arm of cellular immunity.
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9/53. histoplasmosis of the liver: a rare case.

    A 39 year old male presented with history of fever and jaundice for 3 months. A liver biopsy showed numerous ovoid fungal bodies around 5 mm in size in the macrophages and kupffer cells. A diagnosis of hepatic histoplasmosis was made which is an uncommon entity in our country.
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10/53. Disseminated histoplasmosis in an AIDS patient diagnosed on bone marrow.

    A 29 year old male drug addict, who was hiv positive presented with fever and hepatosplenomegaly. bone marrow examination revealed histoplasma capsulatum confirmed by PAS & GMS stains. However patient had a rapid downhill course with multiorgan failure and died before specific treatment could be instituted.
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