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Enterovirus infections 

Enterovirus infections

Enterovirus infections

Philip Minor

and Ulrich Desselberger


July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Viruses—newly recognised genera and updated classification.

Clinical presentation—revised table of clinical symptoms related to specific viruses.

Prevention of polio—expanded discussion of vaccination strategies and description of the present situation in various countries.

Updated on 28 Aug 2014. The previous version of this content can be found here.
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date: 28 April 2017

Enteroviruses are single-stranded, positive sense RNA viruses comprising poliomyelitis viruses (3 types), Coxsackie A viruses (23 types), Coxsackie B viruses (6 types), and echoviruses (33 types). They have recently been reclassified into 4 human enterovirus species (A–D) on the basis of sequence comparisons. Transmission is by the faeco-oral route, with marked seasonal peaks of infection in areas of temperate climate, but infections occurring all year round in tropical regions.

Pathogenesis—following transmission, enteroviruses undergo a first round of replication in cells of the mucosal surfaces of the gastrointestinal tract and in gut-associated lymphoid cells, followed by viraemia, which leads to infection of distant organs (brain, spinal cord, meninges, myocardium, muscle, skin, etc.), where lesions may be produced. Shedding of virus occurs from throat and faeces for many weeks.

Clinical manifestations and diagnosis

Most enterovirus infections are silent or only produce minor illness, but severe major illness can develop in a few of the infected.

Poliomyelitis—infection with poliovirus is normally inapparent, but a few of the infected (1% or less) develop neurological symptoms comprising aseptic meningitis, or paralytic poliomyelitis. Five to ten days after a mild upper respiratory tract infection the disease presents is with flaccid paralysis resulting from motor neuron destruction; this may affect the limbs (spinal form) or muscles supplied by the medulla oblongata or bulb (bulbar form), with potentially life-threatening respiratory muscle involvement. Treatment is supportive; mortality is 2 to 5% in children and 15 to 30% in adults, and there is residual paralysis in 90% of survivors.

Other clinical syndromes include: (1) aseptic meningitis, the most frequent clinical presentation of enterovirus infection, caused by Coxsackie viruses and echoviruses; (2) encephalitis, a rare event, possibly following aseptic meningitis; (3) pleurodynia (Bornholm disease), presenting abruptly with fever and chest pain and usually caused by Coxsackie B viruses; (4) myopericarditis; (5) herpangina; (6) exanthema, rubella-like or hand-foot-and-mouth disease; and (7) conjunctivitis.

Diagnosis is by virus isolation in cell culture or by viral genome detection using RT-PCR.


Paralytic poliomyelitis has been eradicated in most countries of the world following universal mass vaccination with formaldehyde-inactivated poliovirus (Salk vaccine) and/or live-attenuated viral vaccine (Sabin vaccine). However, it persists in a few countries (e.g. Pakistan, Afghanistan, Nigeria) from which it has been exported to otherwise polio-free states. For example, strains from Nigeria have caused disease in other countries of Western Africa, Indian strains have been repeatedely isolated in Angola, there was a major outbreak in Tajikistan caused by strains from Northern India, and in 2011 there were at least 18 cases in China caused by strains from Pakistan. The incident in China was particularly unexpected as the immunization programme has been well executed and was effective for many years. As long as there are pockets of infection, the world remains at risk of re-emergence of the disease. At present there are three countries that have never eradicated polio; namely Nigeria, Pakistan and Afghanistan. India was declared polio free in 2014 after three years without a case caused by wild type virus. No case attributable to a naturally occurring wild type 2 virus has been reported since October 1999 and there has been no case attributable to a wild type 3 virus since November 2012. Progress is striking but as long as there are pockets of infection, the world remains at risk of re-emergence of the disease.

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