Cases reported "Influenza, Human"

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1/146. Human infection with influenza H9N2.

    We report the clinical features of two cases of human infection with influenza A virus subtype H9N2 in hong kong, and show that serum samples from blood donors in hong kong had neutralising antibody suggestive of prior infection with influenza H9N2.
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2/146. rhabdomyolysis and acute renal failure associated with influenza virus type A.

    Two patients with rhabdomyolysis-induced acute renal failure due to influenza a virus infection are presented. Both had influenza symptoms, with high fever and severe muscular pain leading to walking problems. In addition, they were dehydrated due to vomiting and diarrhoea. Both had evidence of an ongoing influenza infection according to serological tests. Muscle injury due to the viral infection gave rise to rhabdomyolysis with efflux of myoglobin from the muscles, causing renal failure. In conclusion, influenza a virus infection can cause rhabdomyolysis accompanied by reversible acute renal failure.
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3/146. Hepatic decompensation in patients with cirrhosis during infection with influenza A.

    BACKGROUND: patients with chronic liver disease can develop hepatic decompensation during systemic infections. Although gram-negative and gram-positive bacteria are well recognized as causes of decompensation, the effect of influenza virus infection on patients with chronic liver disease is poorly documented. methods: Retrospective analysis of patients with positive viral cultures who were seen at a liver transplantation clinic in a tertiary care referral center during the 1997-1998 influenza A (H3N2) epidemic in San Diego, Calif. RESULTS: Three patients with end-stage liver disease (1 with Wilson disease and 2 with alcoholic liver disease) developed hepatic decompensation and required hospitalization during infection with influenza A. Two patients had biochemical and clinical evidence of hepatic decompensation, including ascites, hepatic encephalopathy, and peripheral edema, and the third had acute hepatocellular damage, with elevated levels of aminotransferases. Viral hepatitis serologic test results, acetaminophen levels, drug and alcohol screening findings, and bacterial and fungal cultures were negative in all 3 patients. Hepatic decompensation resolved without the need for transplantation in the 2 patients with liver failure, and all patients recovered to their baseline liver function levels within 1 month of onset of acute illness. CONCLUSIONS: Influenza A infection can cause hepatic decompensation and hospitalization in patients having cirrhosis or who are awaiting liver transplantation. Effective prevention with vaccination and early recognition and treatment of influenza are strongly recommended in these individuals.
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4/146. Two cases of acute myositis associated with influenza a virus infection in the elderly.

    During the influenza epidemic of 1998-1999, we observed two elderly patients with influenza-like symptoms who had evidence of acute myositis with elevated serum enzymes. Influenza A infection was confirmed serologically in either case. The present cases suggest that it is important to distinguish influenzal myositis from other forms of myopathy in the elderly patients.
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5/146. Reversible frontal lobe syndrome associated with influenza virus infection in children.

    Two patients, a 3-year-old female and a 1-year-old female, both with a focal encephalopathic process associated with influenza a virus infection, are reported. Both children had neuropsychologic signs suggesting frontal and limbic dysfunction, without disturbances of consciousness or motor function, and had good recoveries. The results of single-photon emission computed tomography and electroencephalography support the finding of reversible impairment of the frontal and limbic areas. Focal reversible encephalopathy has rarely been reported in association with influenza virus infection, although it often provokes diffuse encephalopathies, with a poor prognosis.
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6/146. Hypothetical pathophysiology of acute encephalopathy and encephalitis related to influenza virus infection and hypothermia therapy.

    BACKGROUND: To establish a treatment strategy for acute encephalopathy and encephalitis associated with influenza virus infection, the pathophysiology of the disease was investigated through manifestations and laboratory findings of patients. patients AND methods: A child with central nervous system (CNS) complications during the course of influenza virus infection was analyzed in view of immunologic abnormalities. In addition, four children with acute encephalopathy and encephalitis were enrolled in the hypothermia treatment for the purpose of stabilizing the cytokine storm in the CNS. RESULTS: The CNS symptoms preceded the systemic progression to the failure of multiple organs (MOF) and disseminated intravascular coagulopathy (DIC). The mild hypothermia suppressed the brain edema on computed tomography (CT) scanning and protected the brain from the subsequent irreversible neural cell damage. CONCLUSION: The replicated viruses at the nasopharyngeal epithelium may disrupt the olfactory mucosa and gain access to the brain via the olfactory nerve system. The direct virus-glial cell interaction or viral stimulation of the glial cells induces the production and accumulation of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-alpha, in the CNS. The cytokine storm results in neural cell damage as well as the apoptosis of astrocytes, due to the TNF-alpha-induced mitochondrial respiratory failure. The disruption of the blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF. Mild hypothermia appears promising in stabilizing the immune activation and the brain edema to protect the brain from ongoing functional, apoptotic neural and glial damage and the systemic expansion of the cytokine storm.
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7/146. Influenza virus-induced encephalopathy: clinicopathologic study of an autopsied case.

    BACKGROUND: Rapid progressive encephalopathy with a high fever, consciousness loss and recurrent convulsions has been occasionally reported in children during influenza pandemics in japan since 1995. We examined a 2-year old girl with hemorrhagic shock and encephalopathy syndrome associated with acute influenza a virus infection (A/Nagasaki/76/98; H3N2), to answer several questions for which no histologic or virologic data exist. methods: A clinicopathologic study using immunohistochemical staining and viral genome detection by reverse transcriptase polymerase chain reaction (RT-PCR) was performed with this autopsied case. RESULTS: The virus antigen was positive in CD8 T lymphocytes from the lung and spleen. The virus infected a very limited part of the brain, especially Purkinje cells in the cerebellum and many neurons in the pons, without inducing an overt immunologic reaction from the host. The RT-PCR used for detecting the hemagglutinin gene demonstrated positive bands in all frozen tissues and cerebrospinal fluid taken at autopsy and not in samples obtained on admission. CONCLUSIONS: The pathologic change induced by the direct viral invasion cannot be responsible for all of the symptoms, especially for the rapid and severe clinical course of the disease within 24-48 h after the initial respiratory symptoms. Together with the rapid production of several inflammatory cytokines, the breakdown of the blood-brain barrier may induce severe brain edema and can be a major pathologic change for the disease. Any therapeutic strategy to control this multistep progression of the disease could be effective.
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8/146. Influenza-associated encephalopathy in japan: pathogenesis and treatment.

    It is estimated that more than 100 children die of influenza-associated encephalopathy (influenza encephalopathy) every year in japan. Influenza encephalopathy is distinct from Reye's syndrome. Specifically, 20% of influenza encephalopathy patients exhibit bilateral thalamic necrosis on neuroimaging, a lesion referred to as acute necrotizing encephalopathy (ANE). Influenza encephalopathy may develop by the same pathogenetic mechanisms as ANE, possibly via vasoactive substances or a process leading to vasoconstriction in the central nervous system (CNS). A novel substitution at the receptor-binding site (Tyr 137 to Phe) was reported to be found exclusively in influenza type A (H3N2) viruses isolated from patients with influenza encephalopathy, suggesting that encephalopathy may be caused by a variant influenza type A (H3N2) virus. Recently, it has been reported that cytokines may mediate the disease and that a high plasma concentration of interleukin-6 could be an indicator of progression to encephalopathy. Although it is unknown whether influenza virus invades the CNS, amantadine therapy for influenza encephalopathy has been tried in japan, in patients in whom influenza type A infection has been demonstrated by rapid antigen detection tests.
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9/146. influenza b virus encephalitis.

    Acute encephalitis and postinfectious encephalopathy have been reported infrequently in association with influenza A and B virus infections. We report herein a case of a 6-year-old girl with acute influenza b virus encephalitis resulting in neurological sequelae. The diagnosis was made by isolation of influenza b virus from the nasopharynx, seroconversion to influenza B, and reverse transcription polymerase chain reaction (RT-PCR) identification of the virus from the patient's cerebrospinal fluid. Direct sequencing of viral rna from the patient's nasopharynx and cerebrospinal fluid revealed identical nucleotide sequences in the HA1 region of the hemagglutinin gene. This is the first report of influenza b virus encephalitis diagnosed by use of RT-PCR and illustrates the need for increased awareness of influenza virus as a cause of acute encephalitis. PCR may be a useful tool for diagnosing future cases.
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10/146. High incidence of acute myositis with type A influenza virus infection in the elderly.

    We describe six elderly cases of acute myositis with type A influenza virus infection (Sydney) during the 1998-1999 outbreak. All six cases suffered from myalgia or muscle weakness especially in the lower extremities and the serum creatine kinase (CK) values were elevated above 1,000 IU/l without MB isoenzymes or electrocardiogram abnormalities. There have been a few case reports of acute myositis associated with influenza virus infection in the elderly. However, we noticed a high incidence of acute myositis among elderly patients with type A influenza virus infection. This complication may occur more commonly in elderly patients than has previously been thought.
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ranking = 7
keywords = virus
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