Cases reported "Hemorrhagic Fevers, Viral"

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1/3. Fatal hemorrhagic fever caused by west nile virus in the united states.

    BACKGROUND: Most west nile virus (WNV) infections in humans are asymptomatic; severe disease occurs in relatively few patients and typically manifests as encephalitis, meningitis, or acute flaccid paralysis. A few cases of life-threatening disease with diffuse hemorrhagic manifestations have been reported in africa; however, this clinical presentation has not been documented for any of the >16,700 cases of WNV disease reported in the united states during 1999-2004. We describe a case of fulminant WNV infection in a 59-year-old florida man who died following a brief illness that resembled hemorrhagic disease caused by rickettsia reckettsii, dengue virus or yellow fever virus. methods: Traditional and contemporary diagnostic assays, including culture isolation, electron microscopic examination, reverse-transcriptase polymerase chain reaction amplification, and immunohistochemical stains, were used to confirm systemic WNV infection in the patient. RESULTS: WNV was isolated in a cell culture from a skin biopsy specimen obtained from the patient shortly prior to death. Electron microscopic examination identified the isolate as a flavivirus, and reverse-transcriptase polymerase chain reaction amplified specific WNV sequences from the isolate and patient tissue. Quantitative polymerase chain reaction identified approximately 1x10(7) viral copies/mL in the patient's serum. WNV antigens were detected by immunohistochemical stains in intravascular mononuclear cells and endothelium in skin, lung, liver, kidney, spleen, bone marrow, and central nervous system; no viral antigens were identified in neurons or glial cells of the central nervous system. CONCLUSIONS: Although hemorrhagic disease is a rare manifestation of WNV infection, the findings provided by this report may offer new insights regarding the clinical spectrum and pathogenesis of WNV disease in humans.
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2/3. Virologic investigation of a case of suspected haemorrhagic fever.

    After travelling in subSaharan africa, an area known for sporadic cases of Marburg virus infection, a young Swedish man presented with a classical picture of severe viral haemorrhagic fever complicated by disseminated intravascular coagulation and septicaemia. serum samples examined by electron microscopy revealed particles of a size compatible with filovirions. Indirect fluorescent antibody tests indicated transient seroconversion to Marburg virus. In lymphocyte transformation assays of cells isolated from the patient 11 months after the onset of acute disease, Marburg viral antigen was able to stimulate lymphocyte proliferation 3.9-fold; however, exhaustive attempts to isolate virus from acute phase blood cultured in vitro or in vivo from guinea pigs and monkeys failed. Data suggest that this patient may have been infected with a filovirus. This case demonstrates the difficulties that may occur in laboratory diagnosis of viral haemorrhagic fevers.
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3/3. Marburg hemorrhagic fever: report of a case studied by immunohistochemistry and electron microscopy.

    The histologic and ultrastructural findings in a fatal human case of Marburg hemorrhagic fever are reported. Marburg virus was isolated from fluids and tissues and was identified in tissues by immunohistochemistry and electron and immunoelectron microscopy. The distribution of viral antigen by light level immunohistochemistry correlated with histologic lesions and also with the ultrastructural localization of virions. The tissue distribution and lesions of Marburg virus in this patient were consistent with the disease described in other human Marburg infections. Immunocytochemistry and ultrastructural examination revealed several previously unreported findings. A striking predilection for viral infection of the pancreatic islet cells was noted. In other tissues, macrophages were the primary cellular target for Marburg virus infection, with hepatocytes, adrenal cortical and medullary cells, and fibroblast-like cells also serving as important sites of viral replication. This case demonstrates the value of transmission electron microscopy as a tool for assisting in the definitive diagnosis of Marburg or Ebola hemorrhagic fever, as well as providing insight into the pathogenesis of these agents.
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