In experimental animals, influenza prediposes the lung to superinfection by reducing the antibacterial efficiency of the alveolar macrophage system. Because such defects may represent abnormalities in ingestion or inactivation of inhaled bacteria, these subcomponents of phagocytosis were tested in mice infected 5 days previously with influenza A virus (NWS or WSN). The mice were exposed to aerosols of Staphylococcus epidermidis and then the rates of bacterial inactivation and percentages of intracellularly located staphylococci were measured. Rates of bacterial inactivation were determined for the left lung by pour-plate enumeration methods. The percentage of ingested bacteria was determined in the in situ perfused right lung by histologically determining the intra- or extracellular location of 100 or more staphylococci. Rates of inactivation of S. epidermidis at 4 hours after bacterial challenge were: control, 90.1 per cent; WSN, 73.0 per cent; NWS, 68.6 per cent, P less than 0.01. The percentage of intracellular staphylococci at 4 hours were: control, 90.9 per cent; WSN, 69.9 per cent; and NWS, 73.8 per cent, P less than 0.01. Microcolonies of proliferating staphylococci were also observed within macrophages of mice infected with each strain of influenza. These experiments demonstrated that in this experimental model, influenzal infection impairs the inactivation of inhaled bacteria by retarding the ingestion of bacteria and by allowing bacteria to proliferate within macrophages.