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INTRODUCTION

MICROBIOLOGY

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

  • Enteroviruses encompass 96 human serotypes: 3 serotypes of poliovirus, 21 serotypes of coxsackievirus A, 6 serotypes of coxsackievirus B, 28 serotypes of echovirus, enteroviruses 68–71, and 34 new enteroviruses (beginning with enterovirus 73) that have been identified by molecular techniques. In the United States, coxsackievirus B1 and echoviruses 18, 9, and 6 account for ∼50% of all enteroviral infections.

PATHOGENESIS

  • 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 up to 20 years.

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

EPIDEMIOLOGY

  • 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.

CLINICAL MANIFESTATIONS

Poliovirus

After an incubation period of 3–6 days, ∼5% of pts present with a minor illness (abortive poliomyelitis) characterized by fever, malaise, sore throat, myalgias, and headache 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; presents ≥1 day after aseptic meningitis as severe back, neck, and muscle pain as well as a gradual development of 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 other frequently involved sites.

    • – 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 may lead to circulatory collapse.

    • – Most pts recover some function, but around two-thirds have residual neurologic sequelae.

  • Vaccine-associated poliomyelitis: The risk ...

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