Over the past eight years, a Wistar rat model for intraabdominal sepsis has been developed and used to document the role of obligate anaerobes in this infections. The ability of Bacteroides fragilis alone to provoke abscesses in this model system is due to a species-specific capsular polysaccharide. It has been shown that active immunization of rats with capsular polysaccharide of B. fragilis protects these animals against the development of abscesses after intraperitoneal challenge with this species. Passive transfer of hyperimmune globulin provided protection against B. fragilis bacteremia in nonimmune, challenged animals but did not confer protection against abscess development. Adoptive transfer of spleen cells from immunized to nonimmunized animals resulted in protection against abscess following challenge with B. fragilis, a finding suggesting that a T cell-dependent immune response was involved in protection. It has also been shown that inbred, congenitally athymic OLA/Rnu rats that were actively immunized developed abscesses despite the presence of capsular antibody, as did 100% of unimmunized athymic control rats. However, no phenotypically normal, littermate control rats that were actively immunized developed abscesses. These data suggest that a T cell-dependent immune response is an important part of immunity to B. fragilis. Additional experiments are being performed to better define the immunologic and chemical basis for the protection afforded by immunization.