Bacteroides fragilis

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,[1][2] but can cause infection if displaced into the bloodstream or surrounding tissue following surgery, disease, or trauma.[3]

Epidemiology and pathogenesis[edit]

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.[4]

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.[5] 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[6] and stimulates abscess formation.[7]

B. fragilis is involved in 90% of anaerobic peritoneal infections.[8] It also causes bacteremia[9] associated with intraabdominal infections, peritonitis and abscesses following rupture of viscus, and subcutaneous abscesses or burns near the anus.[10]Though it is gram negative, it has an altered LPS and does not cause endotoxic shock.

Bacteroides fragilis
Classification and external resources


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 cephamycin 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.[11] Clindamycin is no longer recommended as the first-line agent for B. fragilis due to emerging high-level resistance (>30% in some reports).[12][13]

Medical research[edit]


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.[14] 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[edit]

Preliminary in vivo studies with mice suggest that probiotic therapy with B. fragilis may alleviate some of the behavioral and gastrointestinal symptoms associated with Autism Spectrum Disorder. [15]

Immune system[edit]

Preliminary in vivo studies indicate that B. fragilis polysaccharide A (PSA) protects mice against experimental colitis induced by Helicobacter hepaticus.[16] 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.[16][17][18] 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.[19]

Environmental research[edit]

B. fragilis bacteriophages are commonly used as tracers of human faecal material.[20]


  1. ^ Kuwahara T, Yamashita A, Hirakawa H et al. (October 2004). "Genomic analysis of Bacteroides fragilis reveals extensive DNA inversions regulating cell surface adaptation". Proc. Natl. Acad. Sci. U.S.A. 101 (41): 14919–24. doi:10.1073/pnas.0404172101. PMC 522005. PMID 15466707. 
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  3. ^ Levinson, W. (2010). Review of Medical Microbiology and Immunology (11th ed.). 
  4. ^ Snydman DR, Jacobus NV, McDermott LA et al. (January 2010). "Lessons learned from the anaerobe survey: historical perspective and review of the most recent data (2005–2007)". Clin. Infect. Dis. 50 (Suppl 1): S26–33. doi:10.1086/647940. PMID 20067390. 
  5. ^ Baron EJ, Allen SD (June 1993). "Should clinical laboratories adopt new taxonomic changes? If so, when?". Clin. Infect. Dis. 16 (Suppl 4): S449–50. doi:10.1093/clinids/16.Supplement_4.S449. PMID 8324167. 
  6. ^ Wexler HM (October 2007). "Bacteroides: the good, the bad, and the nitty-gritty". Clin. Microbiol. Rev. 20 (4): 593–621. doi:10.1128/CMR.00008-07. PMC 2176045. PMID 17934076. 
  7. ^ Levinson, W. (2010). Review of Medical Microbiology and Immunology (11th ed.). 
  8. ^ Bacteroides infections at eMedicine
  9. ^ Brook I (June 2010). "The role of anaerobic bacteria in bacteremia". Anaerobe 16 (3): 183–9. doi:10.1016/j.anaerobe.2009.12.001. PMID 20025984. 
  10. ^ Brook I (October 2008). "Microbiology and management of abdominal infections". Dig. Dis. Sci. 53 (10): 2585–91. doi:10.1007/s10620-007-0194-6. PMID 18288616. 
  11. ^ Ayala, J.; Quesada, A.; Vadillo, S.; Criado, J.�n.; Píriz, S. (2005). "Penicillin-binding proteins of Bacteroides fragilis and their role in the resistance to imipenem of clinical isolates". Journal of Medical Microbiology 54 (11): 1055. doi:10.1099/jmm.0.45930-0.  edit
  12. ^ Mandell GL, Bennett JE, Dolin R (2004). Principles and Practice of Infectious Diseases (6th ed.). Churchill Livingstone. ISBN 0-443-06643-4. 
  13. ^ Brook I (December 2007). "Treatment of anaerobic infection". Expert Rev Anti Infect Ther 5 (6): 991–1006. doi:10.1586/14787210.5.6.991. PMID 18039083. 
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  15. ^ Hsiao, Elaine Y.; McBride, Sara W.; Hsien, Sophia; Sharon, Gil; Hyde, Embriette R.; McCue, Tyler; Codelli, Julian A.; Chow, Janet; Reisman, Sarah E.; Petrosino, Joseph F.; Patterson, Paul H.; Mazmanian, Sarkis K. (December 2013). "Microbiota Modulate Behavioral and Physiological Abnormalities Associated with Neurodevelopmental Disorders". Cell 155 (7): 1451–1463. doi:10.1016/j.cell.2013.11.024. 
  16. ^ a b Mazmanian SK, Round JL, Kasper DL (May 2008). "A microbial symbiosis factor prevents intestinal inflammatory disease". Nature 453 (7195): 620–5. doi:10.1038/nature07008. PMID 18509436. 
  17. ^ Mazmanian SK. "The Microbial Health Factor: Just one molecule can make the difference in mediating a healthy immune response. Surprisingly, it comes from bacteria". The Scientist 23 (8): 34. 
  18. ^ Mazmanian SK, Liu CH, Tzianabos AO, Kasper DL (July 2005). "An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system". Cell 122 (1): 107–18. doi:10.1016/j.cell.2005.05.007. PMID 16009137. 
  19. ^ Daniels G, Withers SG (April 2007). "Towards universal red blood cells". Nat. Biotechnol. 25 (4): 427–8. doi:10.1038/nbt0407-427. PMID 17420747. 
  20. ^[dead link]
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