Biology:Bacteroides fragilis

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Short description: Species of bacterium

Bacteroides fragilis is an anaerobic, Gram-negative, pleomorphic to rod-shaped bacterium. 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.[3]

Bacteroides fragilis
BacteroidesFragilis Gram.jpg
Scientific classification edit
Domain: Bacteria
Phylum: Bacteroidota
Class: Bacteroidia
Order: Bacteroidales
Family: Bacteroidaceae
Genus: Bacteroides
Species:
B. fragilis
Binomial name
Bacteroides fragilis
(Veillon and Zuber 1898) Castellani and Chalmers 1919 (Approved Lists 1980)

Habitat

Bacteroides fragilis resides in the human gastrointestinal tract and is essential to healthy gastrointestinal function such as mucosal immunity and host nutrition.[4] As a mesophile, optimal growth occurs at 37 °C and a pH around 7.[5][4]

Morphology

Cells of B. fragilis are rod-shaped to pleomorphic with a cell size range of 0.5-1.5 x 1.0-6.0 μm.[4]B. fragilis is a Gram-negative bacterium and does not possess flagella or cilia making it immotile. However, it does utilize peritrichous fimbriae for adhesion to other molecular structures. 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]

Metabolism & mutualism in the gut microbiome

B. fragilis is an aerotolerant, anaerobic chemoorganotroph capable of fermenting a wide variety of glycans available in the human gut microenvironment including glucose, sucrose, & fructose. B. fragilis can also catabolize a variety of biopolymers, polysaccharides, and glycoproteins into smaller molecules which can then be used and further broken down by other microbes. Fatty acids produced by the fermentation of carbohydrates can serve as a source of energy for the host.[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.[7][6] Animals lacking gut bacteria require 30% more caloric intake to maintain body mass.[6]

Environment-sensing systems

The complex environmental-sensory system allows B. fragilis to survive/adapt in the ever-changing human gut microbiome. This system is composed of/designed to effectively handle:

Bacteriocins: B. fragilis intestinal isolates secrete high levels of bacteriocin proteins and are resistant to other bacteriocins secreted by other closely related isolates. This mechanism is believed to reduce the level of intra-specific competition.[4]

Bile salt resistance: Utilizes enzymes such as bile salt hydrolase to resist the degrading effects of bile salts. Detergent activity of bile salts can permeabilize bacterial membranes which can eventually lead to membrane collapse and/or cell damage.[4]

Oxidative Stress Response: Proteins such as catalase, superoxide dismutase, & alkyl hydroperoxide reductase protect the organism from harmful oxygen radicals. This permits growth in the presence of nanomolar concentrations of O2.[4]

Antibiotic resistance

Member of the genus Bacteroides are characterized with having the highest numbers of antibiotic resistance mechanisms accompanied by the highest resistance rates amongst anaerobic bacteria. The high resistance to antibiotics of B.fragilis is mainly attributed to genetic plasticity.[8] Species of the Bacteroidaceae have displayed increasing resistance to antimicrobial agents such as cefoxitin, clindamycin, metronidazole, carbapenems, & fluoroquinolones.[6][4]

Resistance Reservoirs: Bacteroides species accumulate a variety of antibiotic/antimicrobial resistance genes as they reside in the gastrointestinal tract. 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. This is exacerbated by the tendency of resistance genes to be relatively stable even without the presence of the antibiotic.[6]

Epidemiology and pathogenesis

The B. fragilis group is the most commonly isolated Bacteroidaceae in anaerobic infections, especially those that originate from the gastrointestinal microbiota. 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.[9]

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.[10] B. fragilis (formerly known as B. f. ssp. fragilis) is often recovered from blood, pleural fluid, peritoneal fluid, wounds, and brain abscesses.[citation needed]

Although the B. fragilis group is the most common species found in clinical specimens, it is the least common Bacteroides present in fecal microbiota, 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.[3]

Bacteroides fragilis is involved in 90% of anaerobic peritoneal infections.[11] It also causes bacteremia[12] associated with intra-abdominal infections, peritonitis and abscesses following rupture of viscus, and subcutaneous abscesses or burns near the anus.[13] Though it is gram negative, it has an altered LPS and does not cause endotoxic shock. Untreated B. fragilis infections have a 60% mortality rate.[6]

Anti-inflammatory effects

B. fragilis polysaccharide A (PSA) has been shown to protect animals from experimental diseases like colitis, asthma, or pulmonary inflammation.[14] B. fragilis mutants lacking surface polysaccharides cannot easily colonize the intestine.[8] PSA colonization of B. fragilis in the gut mucosa induces regulatory T cells and suppresses pro-inflammatory T helper 17 cells.[14]

See also

References

  1. ↑ "Genomic analysis of Bacteroides fragilis reveals extensive DNA inversions regulating cell surface adaptation". Proceedings of the National Academy of Sciences of the United States of America 101 (41): 14919–14924. October 2004. doi:10.1073/pnas.0404172101. PMID 15466707. Bibcode: 2004PNAS..10114919K. 
  2. ↑ "Bacteroides fragilis". Johns Hopkins ABX Guide. https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_ABX_Guide/540052/all/Bacteroides_fragilis. 
  3. ↑ 3.0 3.1 Review of Medical Microbiology and Immunology (11th ed.). 2010. 
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 "The Genus Bacteroides" (in en). The Prokaryotes. Berlin, Heidelberg: Springer. 2014. pp. 459–484. doi:10.1007/978-3-642-38954-2_129. ISBN 978-3-642-38954-2. 
  5. ↑ "BacMap". http://bacmap.wishartlab.com/organisms/92. 
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 "Bacteroides: the good, the bad, and the nitty-gritty". Clinical Microbiology Reviews 20 (4): 593–621. October 2007. doi:10.1128/CMR.00008-07. PMID 17934076. 
  7. ↑ "The strict anaerobe Bacteroides fragilis grows in and benefits from nanomolar concentrations of oxygen". Nature 427 (6973): 441–444. January 2004. doi:10.1038/nature02285. PMID 14749831. Bibcode: 2004Natur.427..441B. 
  8. ↑ 8.0 8.1 "A potential species of next-generation probiotics? The dark and light sides of Bacteroides fragilis in health". Food Research International 126: 108590. 2019. doi:10.1016/j.foodres.2019.108590. PMID 31732047. 
  9. ↑ "Lessons learned from the anaerobe survey: historical perspective and review of the most recent data (2005-2007)". Clinical Infectious Diseases 50 (Suppl 1): S26–S33. January 2010. doi:10.1086/647940. PMID 20067390. 
  10. ↑ "Should clinical laboratories adopt new taxonomic changes? If so, when?". Clinical Infectious Diseases 16 (Suppl 4): S449–S450. June 1993. doi:10.1093/clinids/16.Supplement_4.S449. PMID 8324167. 
  11. ↑ Bacteroides infections at eMedicine
  12. ↑ "The role of anaerobic bacteria in bacteremia". Anaerobe 16 (3): 183–189. June 2010. doi:10.1016/j.anaerobe.2009.12.001. PMID 20025984. 
  13. ↑ "Microbiology and management of abdominal infections". Digestive Diseases and Sciences 53 (10): 2585–2591. October 2008. doi:10.1007/s10620-007-0194-6. PMID 18288616. 
  14. ↑ 14.0 14.1 "Exploring the Gut-Brain Axis for the Control of CNS Inflammatory Demyelination: Immunomodulation by Bacteroides fragilis' Polysaccharide A". Frontiers in Immunology 12: 662807. 2021. doi:10.3389/fimmu.2021.662807. PMID 34025663. 

External links

Wikidata ☰ Q221817 entry



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