Etiology

The PIVs are members of the Paramyxoviridae family. Four PIVs cause illness in humans, classified as types 1-4, with diverse manifestations of infection. Type 4 is divided into 2 antigenic subgroups, A and B. PIVs have a nonsegmented, single-stranded RNA genome with a lipid-containing envelope derived from budding through the cell membrane. The major antigenic moieties are the HN and F envelope spike glycoproteins, which exhibit hemagglutinin-neuraminidase and fusion functions, respectively.

Epidemiology

By 5 yr of age, most children have experienced primary infection with PIV types 1, 2, and 3 (Table 251-1). PIV-3 infections often occur in the first 6 mo of life, whereas PIV-1 and PIV-2 are more common after infancy. In the USA and temperate climates, PIV-1 and PIV-2 have biennial epidemics in the fall, usually alternating years in which their serotype is most prevalent. PIV-3 is endemic throughout the year but typically peaks in late spring. In years with less PIV-1 activity, the PIV-3 season may extend longer or have a second peak in the fall. The epidemiology of PIV-4 is less well defined, because it is difficult to grow in tissue culture and was often excluded from early studies.

PIVs are spread primarily from the respiratory tract by inhalation of large respiratory droplets or contact with infected secretions. PIVs are notable for causing outbreaks of respiratory infections in hospital wards, clinics, neonatal nurseries, and other institutional settings. The incubation period from exposure to symptom onset is 2-6 days. Children are likely to excrete virus from the oropharynx for 2-3 wk, but excretion can be more prolonged even in immunocompetent children; in immunocompromised patients, excretion may persist for months. Primary infection does not confer permanent immunity, and re-infections are common throughout life. Re-infections are generally mild and self limited.

Pathogenesis

PIVs replicate in the respiratory epithelium. The propensity to cause illness in the upper large airways is presumably related to preferential replication in the larynx, trachea, and bronchi in comparison with other viruses. Some PIVs induce cell-to-cell fusion. During the budding process, cell membrane integrity is lost, and viruses can induce cell death through the process of apoptosis. In children, the most severe illness coincides with the time of maximal viral shedding. However, disease severity is likely related to the inflammatory response as much as to direct cytopathic effects of the virus.