Role of fibrinogen-binding adhesin expression in septic arthritis and septicemia caused by Streptococcus agalactiae.

Abstract

Streptococcus agalactiae (group B streptococcus) is an important human pathogen that causes neonatal pneumonia, sepsis, septic arthritis, and meningitis, as well as severe infections in immunocompromised adult patients. The streptococci produce several molecules important for virulence. We used a murine model of sepsis and septic arthritis to assess the role of FbsA, a fibrinogen-binding adhesin of S. agalactiae as a virulence determinant. NMRI mice were inoculated intravenously with S. agalactiae strains isogenic for the expression of FbsA. Inoculation with wild-type (wt) streptococci resulted in significantly higher mortality, more-pronounced weight decrease, and more-severe arthritis, compared with inoculation with the FbsA mutant isogenic strain. Neither active nor passive immunization with FbsA or FbsA-specific antibodies, respectively, resulted in any protection against subsequent infection with the S. agalactiae wt strain. Our results clearly indicate that the expression of FbsA by Streptococcus agalactiae is a significant virulence determinant in septic arthritis and septicemia. However, because blocking of the fibrinogen binding properties did not protect the host against the action of FbsA-expressing streptococci, we believe that the FbsA molecule has some other presently unknown biological in vivo properties.