Murine resistance to inhaled Neisseria meningitidis after infection with an encephalomyocarditis virus.

A reduction in pulmonary anti-bacterial activity due to a preceding viral illness has been suggested as the mechanism responsible for some meningococcal infections of the lung. We investigated this proposed pathogenesis by infecting mice with airborne encephalomyocarditis virus (EMC) and then challenging them 1, 4, and 7 days later with aerosols of Neisseria meningitidis. Meningococcal clearance was assessed by comparing the numbers of bacteria present immediately after inhaling the aerosols with the numbers present 3 hr later. To insure that EMC virus adequately depressed murine defense mechanisms, we also determined staphylococcal killing rates at 4 hr by using radiophosphorus-labeled staphylococcal aerosols. Viral infection depressed murine pulmonary antimeningococcal activity at 1 and 4 days (P < 0.01) but not at 7 days. Intrapulmonary staphylococcal killing was impaired on day 4 (P < 0.01) but not on days 1 or 7. Pulmonary viral titers decreased rapidly from 10(7) to 10(3) plaque-forming units/ml of lung during the experimental period. According to these data viral disease transiently depresses resistance to meningococcal infection. This impairment in host resistance is present while the viral titer is decreasing and follows a relatively similar pattern to the transient decrease noted for staphylococci.