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  • Enteroviruses are so named because of their ability to multiply in the GI tract, but they do not typically cause gastroenteritis.

  • Enteroviruses are members of the family Picornaviridae and encompass >115 human serotypes: 3 serotypes of poliovirus, 21 serotypes of coxsackievirus A, 6 serotypes of coxsackievirus B, 28 serotypes of echovirus, enteroviruses 68–71, and multiple enteroviruses (beginning with enterovirus 73) recently identified by molecular techniques. In the United States, 58% of all enterovirus infections are caused by coxsackieviruses A6, A9, and B4; echoviruses 6, 11, 18, and 30; and human parechovirus 3.


  • Studies of poliovirus infection form the basis of our understanding of enteroviral pathogenesis.

  • After ingestion, poliovirus infects GI-tract mucosal epithelial cells, spreads to regional lymph nodes, causes viremia, and replicates in the reticuloendothelial system; in some cases, a second round of viremia occurs.

  • Virus gains access to the CNS either via the bloodstream or via direct spread from neural pathways.

  • Virus is present in blood for 3–5 days. It is shed from the oropharynx for up to 3 weeks and from the GI tract for up to 12 weeks after infection. Hypogammaglobulinemic pts can shed virus for >20 years.

  • Infection is controlled by humoral and secretory immunity in the GI tract.


  • Enteroviruses cause disease worldwide, especially in areas with crowded conditions and poor hygiene.

  • Infants and young children are most often infected and are the most frequent shedders.

  • Transmission takes place mainly by the fecal–oral route, but airborne transmission and placental transmission have been described.

  • The incubation period ranges from 2 to 14 days but usually is <1 week in duration. Pts are most infectious shortly before and after the onset of symptoms.



After an incubation period of 3–6 days, ∼5% of pts present with a minor illness (abortive poliomyelitis) that is characterized by fever, malaise, sore throat, myalgias, and headache and that usually resolves within 3 days.

  • Asymptomatic infection: >90% of all infections

  • Aseptic meningitis (nonparalytic poliomyelitis): occurs in ∼1% of pts. Examination of CSF reveals normal glucose and protein concentrations and lymphocytic pleocytosis (with PMNs sometimes predominating early).

  • Paralytic disease: the least common form, presenting ≥1 day after aseptic meningitis as severe back, neck, and muscle pain as well as gradually developing motor weakness

    • – The weakness is usually asymmetric and proximal and is most common in the legs. The arms and the abdominal, thoracic, and bulbar muscles are also frequently involved.

    • – Paralysis generally occurs only during the febrile phase.

    • – Physical examination reveals weakness, fasciculations, decreased muscle tone, and reduced or absent reflexes in affected areas; hyperreflexia may precede the loss of reflexes. Bulbar paralysis is associated with dysphagia, difficulty handling secretions, or dysphonia.

    • – Respiratory insufficiency due to aspiration or neurologic involvement may develop. Severe medullary infection ...

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