Search

To define the contribution of exoenzyme S to the pathogenesis of infections with Pseudomonas aeruginosa, we have compared the ability of an exoenzyme S-deficient mutant, 388 exs1::Tn1, and that of its exoenzyme S-producing parent to colonize and disseminate in burned mice infected with this organism. Both the exoenzyme S-deficient mutant and the parent strain proliferated in burned skin, but only the parent strain was able to effectively disseminate to blood and other tissues. The reduced ability of the mutant to disseminate was not due to alterations in serum sensitivity, lipopolysaccharide composition, or motility. The exoenzyme S-deficient mutant was able to disseminate in the presence of the exoenzyme S-producing parent. Antibody to purified exoenzyme S was able to greatly reduce dissemination of the exoenzyme S-producing parent strain but did not prevent colonization in the burned skin. These data suggest that exoenzyme S does not contribute to the initial colonization but does contribute to the establishment of disseminated infection.

Preincubation of human polymorphonuclear leukocytes (PMNLs) with Legionella pneumophila toxin impaired activation of the superoxide-generating complex induced by latex particles and by the Ca++ ionophore A23187. The toxin had no effect, however, on activation of the complex induced by phorbol myristate acetate (PMA), concanavalin A, valinomycin, or bromolasalocid. The toxin prevented PMNL plasma membrane depolarization induced by A23187 but failed to influence the membrane depolarization induced by PMA. These observations indicate that Legionella pneumophila toxin selectively impairs activation of the phagocyte superoxide-generating complex without affecting the functional integrity of components of the complex.

The effect of Legionella pneumophila toxin on selected functions of human polymorphonuclear leukocytes was investigated. Amounts of L. pneumophila toxin that had no effect on leukocyte viability or phagocytosis significantly decreased hexose monophosphate shunt activity and O2 consumption during phagocytosis and bacterial iodination and killing in a dose-dependent fashion. The mechanism of action of this toxin appears to be unique among bacterial products thus far studied.