Hosoya M, Sato M, Honzumi K, Katayose M, Kawasaki Y, Sakuma H, Kato K, Shimada Y, Ishiko H, Suzuki H
Department of Pediatrics, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Pediatrics. 2001 Jan;107(1):E12. doi: 10.1542/peds.107.1.e12.
To clarify the relationship between enteroviral infection and febrile seizures.
Cerebrospinal fluid (CSF), serum, throat swab, and rectal swab samples were collected for virologic examination from 67 children with febrile seizures from April 1997 to March 1999. Those samples were examined for the presence of enterovirus using cell culture and 2 polymerase chain reaction (PCR) methods.
No enterovirus was isolated from cell culture of CSF, throat swab, or rectal swab samples. All samples were screened for the presence of enteroviral sequences using a sensitive PCR method (PCR-Fukushima). We obtained positive results from 14 of 67 CSF samples, 10 of 62 serum samples, 12 of 64 throat swab samples, and 13 of 64 rectal swab samples. Of 21 patients in whom febrile seizures had developed during the summer months (June through August), 13 (61.9%) had positive PCR results in the CSF. Forty-seven of the 49 samples with a positive result using PCR-Fukushima were reexamined independently for the presence of the enteroviral genome using another PCR method (PCR-Mitsubishi). PCR-Mitsubishi had slightly lower sensitivity than PCR-Fukushima but identified genotypes of enterovirus by subsequent sequence analysis of the PCR products. The presence of the enteroviral genome was confirmed in 39 of the samples (83.0%). In 8 of the 9 enteroviruses detected in the CSF and/or serum samples using PCR-Mitsubishi, the genotypes were identified as coxsackieviruses group A, which are usually difficult to isolate using cell culture methods.
These findings proved that the causative agents of febrile illness associated with seizures in summer were primarily enteroviruses, especially coxsackieviruses group A, and that febrile seizures might be caused by enteroviral infection in the central nervous system.
阐明肠道病毒感染与热性惊厥之间的关系。
1997年4月至1999年3月，收集了67例热性惊厥患儿的脑脊液（CSF）、血清、咽拭子和直肠拭子样本进行病毒学检查。使用细胞培养和两种聚合酶链反应（PCR）方法检测这些样本中是否存在肠道病毒。
脑脊液、咽拭子或直肠拭子样本的细胞培养均未分离出肠道病毒。使用灵敏的PCR方法（福岛PCR）对所有样本进行肠道病毒序列筛查。67例脑脊液样本中有14例、62例血清样本中有10例、64例咽拭子样本中有12例、64例直肠拭子样本中有13例结果呈阳性。在夏季（6月至8月）发生热性惊厥的21例患者中，13例（61.9%）脑脊液PCR结果呈阳性。对49例使用福岛PCR结果呈阳性的样本中的47例，使用另一种PCR方法（三菱PCR）独立重新检测肠道病毒基因组的存在情况。三菱PCR的灵敏度略低于福岛PCR，但通过对PCR产物的后续序列分析鉴定肠道病毒的基因型。39例样本（83.0%）中证实存在肠道病毒基因组。在使用三菱PCR在脑脊液和/或血清样本中检测到的9种肠道病毒中的8种中，基因型被鉴定为A组柯萨奇病毒，通常使用细胞培养方法难以分离。
这些发现证明，夏季与惊厥相关的发热性疾病的病原体主要是肠道病毒，尤其是A组柯萨奇病毒，热性惊厥可能由中枢神经系统的肠道病毒感染引起。
