An Outbreak of Coxsackievirus A16 Infection: Comparison With Other Enteroviruses in a Preschool in Taipei

Wu, Pei-Chieh; Huang, Li‐Min; Kao, Chuan-Liang; Fan, Tsui-Yen; Cheng, Ai-Ling; Chang, Luan‐Yin

doi:10.1016/s1684-1182(10)60043-6

Cited by 28 publications

(29 citation statements)

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“…3,59 Evidence available from other countries has derived mostly from community surveillance or outbreaks among wider population age-groups, without laboratory confirmation of EV71 as the causative strain, and were therefore excluded from this review. 7,44,58,[60][61][62][63][64][65] Recommendations for future outbreaks…”

Section: Limitations Of This Studymentioning

confidence: 99%

Best practices to prevent transmission and control outbreaks of hand, foot, and mouth disease in childcare facilities: a systematic review

et al. 2017

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Section: Limitations Of This Studymentioning

confidence: 99%

Best practices to prevent transmission and control outbreaks of hand, foot, and mouth disease in childcare facilities: a systematic review

et al. 2017

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“…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).…”

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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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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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“…9 Good sanitation and hygiene, as well as health education, are important aspects in preventing the further spread of enteroviruses during outbreaks. 5 This case highlights an uncomplicated course of HFMD caused by CVA6 in a patient who was on HIV treatment. This is the first reported case in South Africa in which CVA6 was identified in a patient with HFMD.…”

Section: Discussionmentioning

confidence: 89%

“…4 Enteroviruses are mainly transmitted via the faeco-oral route, through consumption of contaminated food and water, direct contact with infected persons, and vertical spread during the intrapartum period. 5,6 These viruses are shed in high quantities in stools, and can have prolonged shedding of up to 11 weeks in some settings, such as preschool environments. 5 Immunosuppressive conditions, such as agammaglobulinaemia, can lead to considerably prolonged shedding and disseminated enteroviral infection.…”

Section: Discussionmentioning

confidence: 99%

“…5,6 These viruses are shed in high quantities in stools, and can have prolonged shedding of up to 11 weeks in some settings, such as preschool environments. 5 Immunosuppressive conditions, such as agammaglobulinaemia, can lead to considerably prolonged shedding and disseminated enteroviral infection. 6 However, this prolonged shedding or increased disease severity has not been noticed in patients infected with HIV.…”

Section: Discussionmentioning

confidence: 99%

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Hand-foot-and-mouth disease caused by coxsackievirus A6 in a patient infected with HIV

Mayaphi

Zyl

Sono

et al. 2015

Southern African Journal of Infectious Diseases

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Case studyIn August 2013, a 12-year-old boy infected with human immunodeficiency virus (HIV), who has been on antiretroviral therapy for more than two years, presented to the Tshwane District Hospital HIV clinic with fever and a rash. His symptoms had started two days ago. The rash was mainly on the palms and soles, and was sometimes itchy. His antiretroviral (ARV) drug regimen consisted of zidovudine, lamivudine and nevirapine. He was no longer receiving prophylaxis for pneumocystis pneumonia at the time of consultation.On examination, he was clinically stable and pyrexial (37.6 °C). The boy had a macular rash on his palms and soles (Figure 1), and a vesicular rash at the right corner of his mouth. There were dark streaks on his palate, and no other lesions. In addition to his ARV drugs, he was also prescribed mupirocin ointment and oral acyclovir. A blood sample for syphilis tests was taken on the day of consultation, and a stool sample was submitted a day later for enterovirus testing.Blood taken a month before this consultation revealed that the patient's HIV viral load was undetectable, and the CD4 count was 929 cells/µl (30.9%). The syphilis tests, rapid plasma reagin and the Treponema pallidum haemagglutination assay were all negative. Enterovirus realtime reverse transcription polymerase chain reaction (RT-PCR), carried out on a stool sample, tested positive. A leftover serum sample (after the syphilis testing) tested negative on enterovirus real-time RT-PCR.However, this sample was slightly haemolysed and was tested five days after collection. Nucleotide sequence analysis of the nested enterovirus RT-PCR products from the stool sample showed that the patient was infected with the coxsackievirus A6 (CVA6) strain. At the follow-up visit, the patient and his guardian reported that the rash had disappeared completely without any complications, roughly a week after the consultation. MethodEthical approval for this investigation was obtained from the University A 12-year-old boy on treatment for human immunodeficiency virus (HIV) presented to an HIV clinic with fever and a rash on the palms and soles. The syphilis test were negative. Enterovirus was identified from a stool sample by PCR and characterised as as coxsackievirus A6(CVA6). The patient completely recovered a week later. CVA6 has recently been associated with HFMD. This case highlights the significance of the laboratory confirmation of suspected HFMD cases aand phylogenetic analysis of the identified virus.Peer reviewed.

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An Outbreak of Coxsackievirus A16 Infection: Comparison With Other Enteroviruses in a Preschool in Taipei

Abstract: Compared with CA2 and CA4, CA16 infections resulted in more cases of HFMD and had significantly higher transmission rates in preschoolers.

Cited by 28 publications

References 10 publications

Best practices to prevent transmission and control outbreaks of hand, foot, and mouth disease in childcare facilities: a systematic review

Best practices to prevent transmission and control outbreaks of hand, foot, and mouth disease in childcare facilities: a systematic review

A Neonatal Mouse Model of Coxsackievirus A16 for Vaccine Evaluation

Hand-foot-and-mouth disease caused by coxsackievirus A6 in a patient infected with HIV

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