Influenza virus-induced encephalopathy. Clinicopathologic study of an autopsied case.
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Accession number;00A0435945
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| Title;Influenza virus-induced encephalopathy. Clinicopathologic study of an autopsied case. |
| Author;
TAKAHASHI M
(Fukuoka Univ., Fukuoka, Jpn)
YAMADA T
(Fukuoka Univ., Fukuoka, Jpn)
NAKASHITA Y
(Sasebo Municipal General Hospital,sasebo, Jpn)
SAIKUSA H
(Saikusa Pediatric Clinic, Sasebo, Jpn)
DEGUCHI M
(Deguchi Pediatric Clinic, Nagasaki, Jpn)
KIDA H
(Hokkaido Univ., Hokkaido, Jpn)
TASHIRO M
(National Inst. Infectious Disease, Tokyo, Jpn)
TOYODA T
(Kurume Univ., Fukuoka, Jpn)
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Journal Title;Pediatr Int
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Journal Code:Z0373B
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ISSN:1328-8067
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VOL.42;NO.2;PAGE.204-214(2000)
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| Figure&Table&Reference;FIG.5, TBL.2, REF.37 |
| Pub. Country;Japan |
| Language;English |
| Abstract;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. (author abst.) |
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