Cases reported "Hantavirus Infections"

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11/17. Fatal illness associated with a new hantavirus in louisiana.

    A fatal case of hantaviral illness occurred in louisiana, outside of the range of P. maniculatus, the rodent reservoir for sin nombre virus. Hantavirus rna and antigens were detected in patient autopsy tissues, and nucleotide sequence analysis of amplified polymerase chain reaction (PCR) products identified a newly recognized unique hantavirus, provisionally named Bayou virus. Prominent features of the clinical illness are compatible with hantavirus pulmonary syndrome (HPS), but several features such as renal insufficiency and intraalveolar hemorrhage are more compatible with hemorrhagic fever with renal syndrome (HFRS), a disease associated with Eurasian hantaviruses.
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12/17. Short report: isolation and partial characterization of a puumala virus from a human case of nephropathia epidemica in france.

    Puumala (PUU) virus (bunyaviridae: Hantavirus), the etiologic agent of nephropathia epidemica (NE), the mid form of hemorrhagic fever with renal syndrome, is enzootic in europe and has been known to occur in france since 1983. We report the first isolation of PUU virus in france and western europe from a case of NE acquired in france. The virus was isolated from a serum collected in the acute phase of the clinical course by successive blind passages in Vero E6 cells. Serologic typing using monoclonal antibodies confirmed the identity of the virus as PUU. The sequence of an 832-nucleotide fragment of the virus medium rna segment obtained by the polymerase chain reaction (PCR) also classified it as a PUU virus. The sequence of this isolate from a human case in france is closely related to the sequence of a PUU virus obtained by the PCR from a German patient.
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13/17. Four fatal cases of nephropathia epidemica.

    Four serologically confirmed fatal cases of nephropathia epidemica (NE), the mild form of hemorrhagic fever with renal syndrome (HFRS) are described. All the patients had disseminated intravascular coagulation. Autopsies revealed hemorrhage and necrotic areas of their pituitary glands, myocarditis, venous congestion and hemorrhage of the kidneys as well as pulmonary edema and hemorrhage of the lungs in all patients. This report provides new evidence that NE can be a fatal disease.
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14/17. Analysis of fatal pulmonary hantaviral infection in new york by reverse transcriptase in situ polymerase chain reaction.

    The purpose of this study was to analyze the histological distribution of polymerase chain reaction (PCR)-amplified hantaviral cDNA in three cases of fatal hantaviral infection that occurred 2 years ago in Long Island, NY. The three otherwise healthy patients had a rapid death characterized by fever and pulmonary failure and were identified from the autopsy files at University Hospital, Stony Brook. Six autopsy controls with either no pulmonary disease (three) or fatal pneumonitis of known etiology (three) were also studied. PCR-amplified hantaviral cDNA was detected in the lung tissue of the three cases and none of the six controls using the reverse transcriptase in situ PCR technique. In the positive cases, viral rna was detected in approximately 20% of pneumocytes and alveolar endothelial cells as determined with a consensus and Four Corners-specific primer pair. Infected endothelial cells were identified in a wide variety of other sites, but at rates much lower than in the lungs. The selective localization of the viral rna in many pneumocytes and pulmonary endothelial cells using a highly sensitive PCR-based test demonstrates a correlation between direct viral infection in the lung and the disease process.
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15/17. hantavirus pulmonary syndrome in wisconsin.

    In the spring of 1993 an outbreak of a new illness caused by a new pathogen was identified in the southwestern united states. This infection struck relatively young, healthy individuals, was characterized by fever, myalgias, respiratory failure, and a high mortality rate. This illness was caused by a new hantavirus and has been termed hantavirus pulmonary syndrome (HPS). The virus is carried by rodents, shed in saliva, urine, and feces. Human infection occurs through inhalation of aerosolized virus. The clinical syndrome has many non-specific signs and symptoms, but does follow a typical course with characteristic laboratory and radiographic findings. Early recognition of this infection is important so maximal supportive care can be initiated. We report the first documented case of hantavirus pulmonary syndrome in wisconsin and illinois.
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16/17. Severe thrombocytopenia and response to corticosteroids in a case of nephropathia epidemica.

    Nine days after working in the woods, a previously healthy 32-year-old man fell seriously ill. His symptoms included high fever, chills, diffuse myalgia, severe headache, and back pain. On the fifth day of onset of symptoms, blood tests showed creatinine levels of 5.4 mg/dL accompanied by marked proteinuria. After admission to the hospital, a diagnosis of nephropathia epidemica (NE) caused by puumala virus was made using solid-phase enzyme-linked immunosorbent assay (ELISA). The patient gradually recovered renal function without requiring dialysis. However, he surprisingly experienced a sharp decline in platelet count to a minimum of 2,000/microL with concomitant occurrence of petechiae and conjunctival hemorrhage. prednisolone was initiated, resulting in a swift rise in platelets. Six days later, when the medication was withdrawn, a sharp decrease in platelets recurred. The steroids were then readministered for the next 3 months, thus reestablishing a stable platelet count. The immediate rise of platelets after administration of prednisolone supports the pathophysiological view of hantavirus infection as an immunologically mediated disease. Corticosteroids in the treatment of hantavirus-associated thrombocytopenia might need further systematic evaluation.
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17/17. Acute exacerbation of autoimmune liver disease associated with hantaviral infection.

    Hantavirus is known to cause haemorrhagic fever with renal syndrome (HFRS). Although liver dysfunction has been reported in HFRS, hepatic manifestations of hantaviral infection have not been well described. We describe a case of autoimmune cholangitis in which an exacerbation of hepatitis was associated with hantaviral infection. Seroconversion of both IgG- and IgM-class antibodies to hantavirus was noted coincident with acute exacerbation of hepatitis, which was resolved promptly by treatment with corticosteroid. No extrahepatic manifestations were noted. This case suggests that hantavirus may trigger acute exacerbation of autoimmune liver disease without extrahepatic manifestations and that it may cause community-acquired hepatitis.
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keywords = haemorrhagic fever, fever
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