机构：[1]Division of Laboratory Management, Chinese Centre for Disease Control and Prevention, Beijing,[2]Department of Pathology, Hong Kong University, Hong Kong Special Administrative Region, China,[3]Division of Infectious Disease, Key Laboratory of Surveillance and Early-warning on Infectious Disease, Chinese Centre for Disease Control and Prevention, Beijing,[4]Office of the Director, Chinese Centre for Disease Control and Prevention, Beijing,[5]Pathology Department, Beijing Hospital, Beijing,[6]Pathology Department, Beijing Capital Medical University Affiliated Xuanwu Hospital, Beijing,病理科首都医科大学宣武医院[7]Beijing IPE Center for Clinical Laboratory, Beijing,[8]Pathology Department, Affiliated Hospital of Guilin Medical University,[9]Institution for Infectious Disease Control and Prevention, Guangxi Provincial Centre for Disease Control and Prevention, Nanning, Guangxi,[10]Institution for Infectious Disease Control and Prevention, Hebei Provincial Centre for Disease Control and Prevention, Shijiazhuang, Hebei,[11]Institution for Infectious Disease Control and Prevention, Henan Provincial Centre for Disease Control and Prevention, Zhengzhou, Henan,[12]Division of Infectious Disease Control and Prevention, Changping District Centre for Disease Control and Prevention, Beijing,[13]School of Public Health, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong Special Administrative Region, China
In the past 17 years, neurological disease associated with enterovirus A71 (EV-A71) has increased dramatically in the Asia-Pacific region with a high fatality rate in young infants, often due to pulmonary oedema, however the mechanism of this oedema remains obscure. We analysed the brainstem, heart and lungs of 15 fatal cases of confirmed EV-A71 infection in order to understand the pathophysiological mechanism of death and pulmonary oedema. In keeping with other case studies, the main cause of death was neurogenic pulmonary oedema. In the brainstem, 11 cases showed inflammation and all cases showed parenchymal inflammation with seven cases showing moderate or severe clasmatodendrosis. No viral antigen was detected in sections of the brainstem in any of the cases. All fatal cases showed evidence of pulmonary oedema; however, there was absence of direct pulmonary viral damage or myocarditis-induced damage and EV-A71 viral antigen staining was negative. Though there was no increase in staining for Na/K-ATPase, 11 of the 15 cases showed a marked reduction in aquaporin-4 staining in the lung, and this reduction may contribute to the development of fatal pulmonary oedema.
基金：
Area of Excellence Scheme of the University Grants Committee (grant AoE/M-12/96) by Government of Hong Kong Special Administrative Region, China.
National Science Fund for Distinguished Young Scholars (No. 81525023),
National Natural Science Foundation of China (No. 81473031)
Li Ka Shing Oxford Global Health Programme (No. B9RST00-B900.57).
第一作者机构：[1]Division of Laboratory Management, Chinese Centre for Disease Control and Prevention, Beijing,
共同第一作者：
通讯作者：
通讯机构：[*1]Chinese Centre for Disease Control and Prevention, No. 155 Chang Bai Road, Chang Ping District, Beijing, 102206, People’s Republic of China.
推荐引用方式(GB/T 7714)：
ZIJUN WANG,JOHN M. NICHOLLS,FENGFENG LIU,et al.Pulmonary and central nervous system pathology in fatal cases of hand foot and mouth disease caused by enterovirus A71 infection[J].PATHOLOGY.2016,48(3):267-274.doi:10.1016/j.pathol.2015.12.450.
APA：
ZIJUN WANG,JOHN M. NICHOLLS,FENGFENG LIU,JOSHUA WANG,ZIJIAN FENG...&YU WANG.(2016).Pulmonary and central nervous system pathology in fatal cases of hand foot and mouth disease caused by enterovirus A71 infection.PATHOLOGY,48,(3)
MLA：
ZIJUN WANG,et al."Pulmonary and central nervous system pathology in fatal cases of hand foot and mouth disease caused by enterovirus A71 infection".PATHOLOGY 48..3(2016):267-274
