ABSTRACT
From a comparison of the effects produced by injecting different strains of Staphylococcus aureus either subcutaneously or intraperitoneally into normal, complement-deficient, or complement-depleted mice, it was possible to assess the pathogenic significance of various staphylococcal virulence factors and the defensive role of complement components in the two sites of infection. In skin lesions the inflammation-suppressing factor found in the cell walls of strain PS80 played a major role. In contrast, in intraperitoneal infection the antiphagocytic capsule of the Smith diffuse and M strains was more important. All strains used produced alpha-hemolysin, which is the ultimate lethal agent in intraperitoneal infection but is only one factor in the production of dermonecrosis. The severity of the skin lesions was inversely related to the amount of early fluid exudate rather than to the rate of bacterial growth, whereas in the peritoneum increased bacterial growth was associated with increased mortality. Both C3 and C5 were needed in the production of fluid exudate in response to staphylococcal skin infection. C3 appeared to be more important in the increased exudate formed in immune mice. In the peritoneum the opsonic and chemotactic actions for complement were important as shown by the results in cobra venom-treated normal mice and in C5-deficient B10D2 old-line mice.
