Some event that displaces B. fragilis along with other members of the intestinal flora is required to initiate infection; there is no evidence the organism is invasive on its own. This mucosal break may be the result of trauma or other disease states such as diverticulitis.
The local effects of the developing abscess include abdominal pain and tenderness, often with a low-grade fever. The subsequent course depends on whether the abscess re-mains localized or ruptures through to other sites such as the peritoneal cavity. This may cause several other abscesses or peritonitis. The course of illness is strongly influenced by the other bacteria in the abscess, particularly members of the Enterobacteriaceae. Spread to the bloodstream is more common with B. fragilis than any other anaerobe.
Drainage of abscesses and debridement of necrotic tissue are the mainstays of the treat-ment of B. fragilis infections, as with anaerobic infections in general. The accompany-ing antimicrobial therapy is complicated by the fact that abdominal B. fragilis isolates almost always produce a β-lactamase, which not only inactivates penicillin but other β-lactams, including many cephalosporins. Resistance to tetracycline is also common, but most strains are susceptible to chloramphenicol, clindamycin, and metronidazole. Among the β-lactams, cefoxitin and imipenem have been used effectively, as have combinations of a β-lactamase inhibitor (clavulanate, sulbactam) and a β-lactam (ampicillin, ticarcillin).
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