Pulmonary defense mechanisms in consolidated and nonconsolidated regions of lungs infected with Sendai virus

Pulmonary virus infections depress antibacterial defenses in the lung and predispose to bacterial pneumonias. The role of virus-induced edema and consolidation in producing this effect was studied in mice infected intranasally with 10⁵ TCID₅₀ of Sendai virus and challenged aerogenically seven days later with ³²P-labelled Staphylococcus aureus. Clearance of particles and intrapulmonary bactericidal activity were quantified in equal volumes of nonconsolidated and fully consolidated lung tissue. Pulmonary bactericidal activity in nonconsolidated areas of lungs infected with virus was decreased significantly from normal. Rates of removal of labeled organisms (determined by radiotracer) were similar to those observed in uninfected mice. In the consolidated areas of infected lungs, bacterial multiplication was accompanied by an increase in radiotracer activity and extension of the consolidated areas of pneumonia. These data demonstrate that pulmonary virus infections suppress intrapulmonary bactericidal activity in nonconsolidated as well as in consolidated areas of the lung, and that bactericidal multiplication is limited to the consolidated areas. The increase of tracer activity in consolidated areas may reflect either transport of organisms toward these areas or spread of the consolidation into the previously nonconsolidated areas.