Influenza virus-induced encephalopathy: Clinicopathologic study of an autopsied case
Influenza virus-induced encephalopathy: Clinicopathologic study of an autopsied case
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DOI：
10.1046/j.1442-200x.2000.01203.x
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发表时间：
2000-04-01
影响因子：
1.4
通讯作者：
Toyoda, T
中科院分区：
文献类型：
--
作者：
Takahashi, M;Yamada, T;Toyoda, T
背景：自 1995 年以来，日本流感大流行期间，偶有报道儿童出现快速进行性脑病，伴有高烧、意识丧失和反复抽搐。我们检查了一名患有失血性休克和与急性甲型流感病毒感染相关的脑病综合征（A/Nagasaki/76/98；H3N2）的 2 岁女孩，以回答几个没有组织学或病毒学数据的问题。方法：临床病理学研究对该病例进行免疫组化染色和逆转录聚合酶链反应（RT-PCR）病毒基因组检测。结果：肺和脾CD8（+）T淋巴细胞病毒抗原阳性。该病毒感染了大脑的非常有限的部分，特别是小脑中的浦肯野细胞和脑桥中的许多神经元，但没有引起宿主明显的免疫反应。用于检测血凝素基因的RT-PCR显示，在尸检时采集的所有冰冻组织和脑脊液中均呈阳性条带，而在入院时获得的样本中未见阳性条带。 结论：直接病毒侵入引起的病理变化不能解释所有症状，特别是在最初呼吸道症状后24-48小时内疾病迅速而严重的临床过程。随着多种炎症细胞因子的快速产生，血脑屏障的破坏可能引起严重的脑水肿，并且可能是该疾病的主要病理变化。任何控制疾病多步进展的治疗策略都可能是有效的。
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.