Abstract
The occurrence of sustained bacteremia is a critical determinant in the pathogenesis of experimental Hib meningitis. We studied the potential role of (1) extravascular and (2) intravascular replication of Hib in the initiation of bacteremia. To identify tissues, in addition to nasopharynx (np), where Hib might replicate prior to seeding the bloodstream, rats (age 20 d.) were sacrificed 6-24 h. after intranasal (i.n.) inoculation with 105 Hib and whole organs (liver, spleen, etc.) and body fluids (CSF, joint fluid, etc.) were cultured to recover Hib. We were unable to recover Hib from any putative extravascular focus (other than np) prior to the development of bacteremia. To evaluate the potential contribution of intravascular replication in initiation of Hib bacteremia, rats were injected i.v. with a small inoculum (<100 Hib). Serial blood cultures showed a prompt (negligible lag) and exponential increase in bacterial counts in the blood in the ensuing 6 h. (mean doubling time ∼47 min.). We noted a similar exponential increase in bacterial counts when serial blood cultures were performed 12-18 h. after intranasal inoculation with Hib. Thus, a few surviving Hib that enter the bloodstream from the np may undergo intravascular replication to initiate a sustained, high level (≥103 Hib per ml) bacteremia.
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