It is part of the normal microbiota of the human colon and is generally commensal,[1][2] but can cause infection if displaced into the bloodstream or surrounding tissue following surgery, disease, or trauma.

B. fragilis also utilizes a complex series of surface proteins, lipopolysaccharide chains, and outer membrane vesicles to help survive the volatile intestinal micro-environment.

[6] B. fragilis is an aerotolerant, anaerobic chemoorganotroph capable of fermenting a wide variety of glycans available in the human gut microenvironment including glucose, sucrose, and fructose.

[6][4] Cytochrome bd oxidase is essential for oxygen consumption in B. fragilis and can allow other obligate anaerobes to survive in the now oxygen-reduced microenvironment.

[4] Proteins such as catalase, superoxide dismutase, and alkyl hydroperoxide reductase protect the organism from harmful oxygen radicals.

[8] Species of the Bacteroidaceae have displayed increasing resistance to antimicrobial agents such as cefoxitin, clindamycin, metronidazole, carbapenems, and fluoroquinolones.

This allows the genetic transfer of these genes to other Bacteroides species and possibly other more virulent bacteria leading to an overall increase in multi-drug resistance.

Their pathogenicity partly results from their ability to produce capsular polysaccharide, which is protective against phagocytosis[6] and stimulates abscess formation.

[6] B. fragilis polysaccharide A (PSA) has been shown to protect animals from experimental diseases like colitis, asthma, or pulmonary inflammation.