Bacteroides fragilis is an obligately anaerobic, Gram-negative, rod-shaped bacterium. It is part of the normal flora of the human colon and is generally commensal, but can cause infection if displaced into the bloodstream or surrounding tissue following surgery, disease, or trauma.
Epidemiology and pathogenesis
The B. fragilis group is the most commonly isolated Bacteroidaceae in anaerobic infections, especially those that originate from the gastrointestinal flora. B. fragilis is the most prevalent organism in the B. fragilis group, accounting for 41% to 78% of the isolates of the group. These organisms are resistant to penicillin by virtue of production of beta-lactamase, and by other unknown factors.
This group was formerly classified as subspecies of B. fragilis (i.e. B. f. ssp. fragilis, B. f. ssp. distasonis, B. f. ssp. ovatus, B. f. ssp. thetaiotaomicron, and B. f. ssp. vulgatus). They have been reclassified into distinct species on the basis of DNA homology studies. B. fragilis (formerly known as B. f. ssp. fragilis) is often recovered from blood, pleural fluid, peritoneal fluid, wounds, and brain abscesses.
Although the B. fragilis group is the most common species found in clinical specimens, it is the least common Bacteroides present in fecal flora, comprising only 0.5% of the bacteria present in stool. Their pathogenicity partly results from their ability to produce capsular polysaccharide, which is protective against phagocytosis and stimulates abscess formation.
B. fragilis is involved in 90% of anaerobic peritoneal infections. It also causes bacteremia associated with intraabdominal infections, peritonitis and abscesses following rupture of viscus, and subcutaneous abscesses or burns near the anus. Though it is gram negative, it has an altered LPS and does not cause endotoxic shock.
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In general, B. fragilis is susceptible to metronidazole, carbapenems, tigecycline, beta-lactam/beta-lactamase inhibitor combinations (e.g., Unasyn, Zosyn), and certain antimicrobials of the cephalosporin class, including cefoxitin. The bacteria have inherent high-level resistance to penicillin. Production of beta lactamase appears to be the main mechanism of antibiotic resistance in B. fragilis. Clindamycin is no longer recommended as the first-line agent for B. fragilis due to emerging high-level resistance (>30% in some reports).
Working with lab cultures and mice, Johns Hopkins scientists have found a strain of Bacteroides fragilis which causes colon inflammation, and increases activity of a gene for the enzyme spermine oxidase in the intestine. These results suggest some strains of B. fragilis may increase the colon's exposure to hydrogen peroxide, contributing to DNA damage and the formation of tumors. Further research is needed to establish if these findings are generalizable to other strains of B. fragilis, and whether the effects observed in mice also occur in humans.
Autism Spectrum Disorder
Preliminary in vivo studies indicate that B. fragilis polysaccharide A (PSA) protects mice against experimental colitis induced by Helicobacter hepaticus. Additional in vivo research with mice has shown PSA intermediates in several markers of a healthy mammalian immune system: the levels of CD4 T cells, the balance of T-helper cells, the presence of well-defined follicular structures in the spleen, and in the inflammatory gut response to pathogens. Further studies are needed to establish if these beneficial effects also occur in the human gastrointestinal tract and immune system.
B. fragilis-derived glycosidase enzymes are capable of removing the immunodominant sugars from A and B red blood cells. The enzyme GalNAC-ase cleaves A blood cells (the most common non-O blood group) into O type blood cells. Though further studies are needed to establish if this technology is safe, this research raises the possibility that A, B and AB cells could be used to produce universal blood units in times of blood insufficiency.
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