Abstract
Pulmonary virus infections predispose to bacterial infections in the lung. The mechanism of this effect was studied by quantitative comparison of the effects of airborne acute viral infection on pulmonary transport vs. in situ bactericidal mechanisms in mice. Animals infected by aerosol with 104 TCID50 of Sendai virus developed pathologic pulmonary changes of interstitial pneumonitis, bronchial epithelial desquamation, and peribronchial mononuclear cell infiltration 7 days later. At that time, the mice were challenged with an aerosol of viable 32P-labeled Staphylococcus aureus. Pulmonary bactericidal activity and physical transport by the lung were determined by the determination of viable staphylococcal and 32P radiotracer counts respectively at 4, 24, 48, and 72 hr after bacterial challenge. Infected mice showed a significant decrease from normal in the rate of reduction of viable bacterial counts in the first 4 hr after challenge followed by a proliferation of the staphylococci. By contrast, radiotracer removal rates at 4 and 24 hr were similar in infected and noninfected mice. There was a small but significant retention of 32P in the lungs of the infected animals at the later periods. These data demonstrate that bacterial multiplication associated with virus infection of lungs is related to defects in in situ bactericidal (phagocytic) mechanisms rather than transport mechanisms of the lung, despite histologic evidence of extensive destruction of bronchial-ciliated epithelium.
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