Chapter

Enterovirus infections

Philip Minor and Ulrich Desselberger

in Oxford Textbook of Medicine

Fifth edition

Published on behalf of Oxford University Press

ISBN: 9780199204854
Published online May 2012 | e-ISBN: 9780199570973 | DOI: http://dx.doi.org/10.1093/med/9780199204854.003.070508_update_001

Series: Oxford Textbooks

Enterovirus infections

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Enteroviruses are single-stranded RNA viruses comprising poliomyelitis viruses (3 types), Coxsackie A viruses (23 types), Coxsackie B viruses (6 types), and echoviruses (28 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 with only limited seasonality.

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 (1) aseptic meningitis, or (2) paralytic poliomyelitis—5 to 10 days after a mild upper respiratory tract infection presentation 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.

Prevention

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.

Chapter.  7457 words.  Illustrated.

Subjects: Medical Microbiology and Virology ; Infectious Diseases

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