Fatal Infection in an Infant Associated with Coxsackie Virus Group A, Type 16

Wright, Harry T.; Landing, Benjamin H.; Lennette, Edwin H.; McAllister, Robert M.

doi:10.1056/nejm196305092681904

Cited by 89 publications

(32 citation statements)

References 8 publications

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“…Clinical symptoms and disease caused by CA16 infection are usually mild, such as HFMD, fever, and herpangina. However, some reports indicate that CA16 infection also can cause severe complications, such as aseptic meningitis, rhombencephalitis, pulmonary complications, cardiac and pericardial disease, and even fatal myocarditis and pneumonitis (14,21,34,40,(44)(45)(46)50). The disease process caused by the CA16 infection progressed very quickly when severe complications occurred.…”

Section: Discussionmentioning

confidence: 99%

“…While most CA16-associated HFMD infections present only mild symptoms, many recent reports show that CA16 infections might lead to severe health issues, such as aseptic meningitis, rhombencephalitis, cardiac and pericardial disease, pulmonary complications, spontaneous abortion, and even lethal myocarditis and pneumonia (14,21,23,40,(44)(45)(46)50). The coinfection of EV71 and CA16 makes it more complex and difficult to control epidemic HFMD (54).…”

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confidence: 99%

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A Neonatal Mouse Model of Coxsackievirus A16 for Vaccine Evaluation

Mao

Wang

Gao

et al. 2012

J Virol

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cTo evaluate vaccine efficacy in protecting against coxsackievirus A16 (CA16), which causes human hand, foot, and mouth disease (HFMD), we established the first neonatal mouse model. In this article, we report data concerning CA16-induced pathological changes, and we demonstrate that anti-CA16 antibody can protect mice against lethal challenge and that the neonatal mouse model could be used to evaluate vaccine efficacy. To establish a mouse model, a BJCA08/CA16 strain (at 260 50% lethal doses [LD 50 ]) was isolated from a patient and used to intracerebrally (i.c.) inoculate neonatal mice. The infection resulted in wasting, hind-limb paralysis, and even death. Pathological examination and immunohistochemistry (IHC) staining indicated that BJCA08 had a strong tropism to muscle and caused severe necrosis in skeletal and cardiac muscles. We then found that BJCA08 pretreated with goat anti-G10/CA16 serum could significantly lose its lethal effect in neonatal mice. When the anti-G10 serum was intraperitoneally (i.p.) injected into the neonatal mice and, within 1 h, the same mice were intracerebrally inoculated with BJCA08, there was significant passive immunization protection. In a separate experiment, female mice were immunized with formaldehyde-inactivated G10/CA16 and BJCA08/CA16 and then allowed to mate 1 h after the first immunization. We found that there was significant protection against BJCA08 for neonatal mice born to the immunized dams. These data demonstrated that anti-CA16 antibody may block virus invasion and protect mice against lethal challenge, and that the neonatal mouse model was a viable tool for evaluating vaccine efficacy. C oxsackievirus A16 (CA16) belongs to the Enterovirus genus of the Picornaviridae family and is one of the major pathogens associated with human hand, foot, and mouth disease (HFMD) (4,16,19). CA16 was first isolated in 1951 (43). It is a single positive-stranded RNA virus and has an icosahedral symmetry structure. Its genome has approximately 7,410 nucleotides with one predominant serotype. Based on the VP4 nucleotide sequences, CA16 is classified into three distinct genetic lineages: A, B, and C. Before the 1990s, lineages A and B were the major epidemic strains in Asia (predominantly the B strain). After that, the CA16 gene gradually mutated to form lineage C, which replaced the B strain as the predominant epidemic strain (22).Epidemics of HFMD have been reported in England, Australia, Japan, Germany, Malaysia, Singapore, mainland China, and Taiwan (2,4,11,19,23,27,32,38,41,48). Recently, HFMD was highly epidemical in the west Pacific region, resulting in severe illness and fatalities (15, 23). The HFMD epidemics were mainly caused by CA16 and human enterovirus 71 (EV71), which circulated alternatively or together in the epidemic area (19,22,23,25,37). Because the most severe or fatal cases were caused by EV71, studies have mainly focused on EV71 but not CA16. However, in England, the largest HFMD outbreak (in 1994) was caused by CA16 (2). Similarly, in Taiwan the leading cau...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

A Neonatal Mouse Model of Coxsackievirus A16 for Vaccine Evaluation

Mao

Wang

Gao

et al. 2012

J Virol

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“…Treatment is symptomatic, and the disease resolves spontaneously without complications within 7 to 10 days. However, there have been rare reports of severe complications such as pneumonia, cardiomyositis 10 , and aseptic meningitis 11 . Since HFM disease is highly contagious, and elderly people, pregnant women, and immunocompromised adults may develop severe complications, early diagnosis and isolation are necessary.…”

Section: Discussionmentioning

confidence: 99%

A Case of Hand-foot-mouth Disease in an Immunocompetent Adult

Shin

Lee

2010

Ann Dermatol

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“…In a comparative study of 177 EV-A71 and 64 CV-A16 patients in Taiwan, only 6.3 % of CV-A16 infections developed into aseptic meningitis, but 32 % of EVA-71 cases resulted in aseptic meningitis, encephalitis, polio-like syndrome, encephalomyelitis and fatal pulmonary oedema; 7.9 % of EV-A71 infections were lethal [62]. Occasional severe and fatal CV-A16 cases have been reported in the USA [63], Taiwan [64], France [65], Japan [66] and China [67].…”

Section: Enterovirus 71 and Coxsackievirus A16mentioning

confidence: 99%

Human picornaviruses associated with neurological diseases and their neutralization by antibodies

Anastasina

Domanska

Palm

et al. 2017

Journal of General Virology

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Picornaviruses are the most commonly encountered infectious agents in mankind. They typically cause mild infections of the gastrointestinal or respiratory tract, but sometimes also invade the central nervous system. There, they can cause severe diseases with long-term sequelae and even be lethal. The most infamous picornavirus is poliovirus, for which significant epidemics of poliomyelitis were reported from the end of the nineteenth century. A successful vaccination campaign has brought poliovirus close to eradication, but neurological diseases caused by other picornaviruses have increasingly been reported since the late 1990s. In this review we focus on enterovirus 71, coxsackievirus A16, enterovirus 68 and human parechovirus 3, which have recently drawn attention because of their links to severe neurological diseases. We discuss the clinical relevance of these viruses and the primary role of humoral immunity in controlling them, and summarize current knowledge on the neutralization of such viruses by antibodies.

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Fatal Infection in an Infant Associated with Coxsackie Virus Group A, Type 16

Cited by 89 publications

References 8 publications

A Neonatal Mouse Model of Coxsackievirus A16 for Vaccine Evaluation

A Neonatal Mouse Model of Coxsackievirus A16 for Vaccine Evaluation

A Case of Hand-foot-mouth Disease in an Immunocompetent Adult

Human picornaviruses associated with neurological diseases and their neutralization by antibodies

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