Bacteroides Fragilis Disease

B .  fragilis  DISEASE

Deep pain and tenderness anywhere below the diaphragm is typical of the onset of B. fragilis infection. Depending on the extent and spread of the intra-abdominalabscess, fever and widespread findings of an acute abdomen may also be seen.

EPIDEMIOLOGY

Like the other Gram-negative anaerobes, B. fragilis infections are endogenous, originat- ing in the patient’s own intestinal flora. Although B. fragilis is among the most common of intestinal anaerobes, the frequent presence of this species in clinically significant infections is striking. It is typically mixed with other anaerobes and facultative bacteria. Human-to-human transmission is not known and seems unlikely.

PATHOGENESIS

The relative oxygen tolerance of B. fragilis probably plays a role in its virulence by aid-ing its survival in oxygenated tissues in the period between its displacement from the intestinal flora and the establishment of a reduced local microenvironment. Its pili have adhesive properties, and the polysaccharide capsule confers resistance to phagocytosis and inhibits macrophage migration. The most distinguishing pathogenic feature of the organism is its ability to cause abscess formation. This capsule experimentally stimu-lates abscess formation, even in the absence of live bacteria. This property is not found in the capsular polysaccharides of organisms such asStreptococcus pneumoniae. B.fragilis and other Bacteroides species produce a number of extracellular enzymes (col-lagenase, fibrinolysin, heparinase, hyaluronidase) that may also contribute to the for-mation of the abscess.

Some strains of B. fragilis produce an enterotoxin that causes enteric disease in ani-mals, and in some studies they have been associated a self-limited, watery diarrhea in children. Because these enterotoxin-producing strains are found in up to 10% of healthy individuals, their pathogenic importance is still undetermined.

IMMUNITY

Although it has been demonstrated that antibody to capsular polysaccharide facilitates clas-sical complement pathway killing, there is no evidence that this confers immunity to rein-fection. In contrast, there is some evidence that cell-mediated immunity may be protective.