Suppression of pulmonary antibacterial activity by virus infection

Resistance to bacterial pneumonia may be impaired by a pre-existing virus infection. It has been proposed that this is due to an effect the virus has on the phagocytic and cytopeptic capacities of the alveolar macrophages. Guinea pigs were exposed to influenza Al virus in a Tri-R airborne infection chamber. The alveolar and peritonea macrophages were harvested and allowed to attach to the flat surfact of Leighton tubes. These macrophages were then challenged with a suspension of Klebsiella pneumoniae for 2 hours. The macrophages were washed free of extracellular bacteria and antibiotics were added to prevent extracellular multiplication. Plate counts were made at various time intervals on disrupted macrophages to determine the number of viable intracellular bacteria remaining. The samples counted immediately after the 2 hour challenge were considered to represent phagocytosis and those counted at various times following removal of extracellular bacteria were considered to be indicators of either cytopepsrs or intracellular multiplication. In vivo virus exposed macrophages ingested the bacteria at a rate significantly greater (p <.05) than that of non-virus exposed, control macrophages. However, virus exposed macrophages exhibited significantly reduced cytopepsis (p <.01) as compared to controls. These effects were observed in both the alveolar and peritoneal macrophages. It seems that virus infection may reduce host resistance to pulmonary bacterial infection by interfering with intracellular digestion of the ingested bacteria.