Pathogenesis of bacteremia due to Pseudomonas aeruginosa in cyclophosphamide-treated mice and potentiation of virulence of endogenous streptococci.

Mice treated with cyclophosphamide on day 0 were killed at sequential intervals during subsequent administration of Pseudomonas aeruginosa in drinking water and were examined for sites of bacterial colonization and multiplication with use of peroxidase-labeled antibody and culture techniques. These studies were coordinated with those of clinical and histopathologic changes. Bacterial antigen was first detected on day 4 on the surface of nasal squamocolumnar junctions and the stratum corneum of gingival sulci and crests. Invasion of tissue by P. aeruginosa proceeded rapidly from these sites and led to bacteremia. There was no invasion of the lower alimentary canal. Endogenous group B beta-hemolytic streptococci colonized and penetrated ulcers created by previous pseudomonas invasion. These results suggest that epithelial colonization is the critical event in the pathogenesis of bacteremia due to P. aeruginosa in the immunosuppressed host. The resulting infection may provide a conduit for invasion and enhancement of the virulence of endogenous streptococci.