The other piece of infectious disease-related news in the Straits Times today was on parechovirus infections. In an (as far as I can tell) unpublished study, follow-up of 80 babies infected with human parechovirus (HPeV) type 3 in Sydney showed that developmental delays had occurred in more than half of them after a year. About a fifth had “significant neurological problems”. Yet another virus associated with neurological complications in very young children, after Zika (which technically causes the damage in utero).
What on earth are parechoviruses? There is a helpful entry on Wikipedia. Essentially, these are viruses that belong to the Picornaviridae (small RNA viruses) family – Parechovirus A are human parechoviruses while Parechovirus B affects rodents like bank voles. There are 6 types of human parechoviruses. HPeV type 1 and type 2 are associated with respiratory and gastrointestinal infections (almost always mild) in young children, and were isolated way back in 1956. HPeV types 3-6 were all discovered in the 21st century between 1999 and 2007. HPeV types 4-6 are also associated with relatively mild gastrointestinal and respiratory infections for the most part.
The particular genotype of interest, HPeV-3, was first isolated in Japan in 1999 from an infant girl with transient paralysis, high fever and diarrhoea. Since then, it had been sporadically linked with more severe infections in neonates and infants, including sepsis, sudden unsuspected infant death, and meningoencephalitis. A smaller Australian study published in February this year also described a strong association (5 of 8 cases) with neurodevelopmental delay. There have been a small number of outbreaks described in U.S.and Australia, with the largest outbreak occurring in New South Wales, Australia, between 2013 and 2014, affecting 183 infants. 30% of the 183 infants aged below 3 months had to be admitted to the intensive care unit, as opposed to 14% of older infants. The presence of low titres of maternal antibodies to HPeV-3 appears to be correlated with severe disease in the children, and the source of infection for the neonates and infants – at least in Japan – may be their older siblings.
Does HPeV-3 only cause infections in children? The Japanese have described HPeV-3 as being associated with epidemic myalgia in adults, with 22 cases occurring in an outbreak in Yonezawa, Japan, in 2008. All presented with severe proximal myalgia followed by weakness and fever, and 4 of 15 men also had orchiodynia (i.e. testicular pain). One patient had seizures and encephalopathy, but all survived the infection. An immunocompromised teenager in Denmark presented with subacute myocarditis and encephalitis.
Given the global spread of HPeV, including HPeV-3, it is likely that these viruses are already present in Singapore. It will be interesting – perhaps even necessary – to understand the local situation better.
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