Humans are the only natural host of nonpolio enteroviruses that infect people. Spread is from person to person and by the fecal-oral and, possibly, oral-oral (respiratory spread) routes. Transmission of infection by fomites and the contaminated hands of health care personnel has been documented in the hospital setting. Contaminated swimming and wading pools may serve as a means of spreading of enteroviruses during summer. Children are the main susceptible cohort; therefore, primary spread is from child to child. Secondary spread occurs to susceptible contacts in family groups. The incidence of infection and disease is related inversely to age, and the prevalence of specific antibodies is related directly to age. Epidemics and outbreaks depend on new susceptible individuals in the population; reinfection with clinical disease with a particular serotype is not thought to occur routinely. In temperate climates, enteroviral infections occur primarily in the summer and fall; in the tropics, infections regularly occur throughout the year.

Although 65 nonpolio enteroviral and parechoviral types exist, usually only a few viral types circulate in a community during any one season. From the early 1960s to 1990, echovirus type 9 was the most prevalent of the nonpolio enteroviruses. Other common types in widespread circulation were as follows: echoviruses 4, 6, 11, and 30; all coxsackie B viruses except B6; and coxsackieviruses A9 and A16. Since 1990, echoviruses 30 and 11 have been the most common circulating types. Recently, major epidemic disease caused by enterovirus 71 has occurred in Taiwan, Malaysia, Australia, and Japan.

After an individual is exposed, an enterovirus becomes implanted in the pharynx and the lower alimentary tract. The infection quickly spreads to the regional lymph nodes, the virus multiplies, and minor viremia occurs on approximately the third day. This viremia results in involvement in many secondary infection sites, and viral multiplication in these sites coincides with the onset of clinical symptoms 4 to 6 days after exposure. As the virus multiplies at the secondary infection sites, major viremia begins during days 3 to 7 of infection. Involvement of the central nervous system may occur as a result of the initial minor viremia, or it may be delayed and be the result of major viremia. Major viremia usually lasts for 3 to 7 days. Cessation of viremia correlates with the appearance of antibody and the beginning of clinical recovery. Infection may continue, however, in the lower intestinal tract for prolonged periods.

Enteroviral illnesses vary from clinically unrecognized to severe fatal illnesses. Pathologic findings are described only in the more severe illnesses. The most striking findings in severe cases are in the heart (myocarditis), brain and spinal cord (meningitis and encephalitis), lungs (pneumonitis), adrenals (cortical necrosis), and liver (hepatic necrosis).

Nonpolio enteroviral infections are exceedingly common findings in the United States. Virtually all children have one or more infections each summer and fall. Although few specific enteroviral diseases exist, a variety of interrelated syndromes and anatomically associated illnesses can occur. Table 194.1 presents the protean clinical spectrum of disease. Many illnesses and syndromes can be caused by different coxsackieviral, echoviral, and enteroviral types, and most types can produce a variety of clinical syndromes. In a few instances, clinical characteristics indicate one or two specific enteroviral types.