Mechanism of potentiation of experimental Haemophilus influenzae type B disease in infant rats by influenza A virus.

Intranasal infection of infant rats by virulent influenza A virus increases the frequency and magnitude of bacteremia induced by subsequent atraumatic intranasal inoculation of Haemophilus influenzae type b (HIb). The mechanism of the "potentiating" effect was studied by histology, by measurement of the frequency and kinetics of bacteremia in rats preinoculated with virus, or a chemical irritant (0.1 N HCl), by comparison of the latter with physically "traumatic" bacterial inoculation, and correlation of these data with nasal HIb titers. Both virus and acid induced significant nasal inflammation which progressed following bacterial inoculation. A period of intranasal proliferation of HIb preceded bacteremia in rats preinoculated with either virus or acid. In contrast, bacteremia occurred almost immediately following physically traumatic bacterial inoculation suggesting that direct intravascular invasion had occurred under those circumstances. Repeated atraumatic inoculation of HIb or HIb followed by growth medium both produced a significantly increased frequently of bacteremia compared to a single inoculation, suggesting that the prolonged presence of large numbers of intranasal HIb was a factor in producing bacteremia and that virus or acid-induced mucosal inflammation may lead to elaboration of growth factors for HIb in nasal tissues.