Bacteria Genomes - BACTEROIDES FRAGILIS

Bacteroides fragilis, a Gram-negative rod and obligate anaerobe, constitutes a large component, 1% to 2% of the normal colonic bacterial microflora in humans.The human colon contains the largest, most complex bacterial population of any colonised area of the human body. The colonic contents contain in excess of 1011 organisms per gram of wet weight, representing over 400 species.

B. fragilis is an opportunistic pathogen with the potential to severely limit the success of gastro-intestinal surgery, and is frequently associated with extraintestinal infections such as abscesses and soft tissue infections, as well as diarrheal diseases in animals and humans. Enterotoxigenic B. fragilis (ETBF) is an emerging enteric pathogen associated with diarrheal diseases in children, adults, and animals.

The Bacteroides genus comprise the majority of microorganisms that inhabit the digestive tract. 50% of most fecal matter is actually Bacteroides fragilis cells. Bacteroides organisms are the anaerobic counterpart of E. coli except they are somewhat smaller. They grow well on blood agar, and under the microscope, they may contain large vacuoles that are similar in appearance to spores. Members of Bacteroides species are not spore-forming, but they do produce a very large capsule. Their pathogenicity is limited, however, because they possess no endotoxin in their cell membrane.

Bacteroides fragilis is primarily associated with infections of the peritoneal cavity. B. fragilis is not overtly invasive, but is capable of participating in intraabdominal infections in the event the mucosal wall of the intestine being disrupted. Incidences during which Bacteroides infections may be initiated include gastrointestinal surgery, perforated or gangrenous appendicitis, perforated ulcer, diverticulitis, trauma, and inflammatory bowel disease. After disruption of the intestinal wall, members of the normal flora infiltrate the normally sterile peritoneal cavity, and during the early, acute stage of infection (approximately 20 hours), the aerobes, such as E. coli, are the most active members of infection , establishing preliminary tissue destruction and reducing the oxidation-reduction potential of the oxygenated tissue. Once sufficient oxygen has been removed to allow the anaerobic Bacteroides to replicate, these bacteria begin to predominate during the second, chronic stage of infection

The Bacteroides contribute to develop infection in three ways: stimulation of abscess formation, reduced phagocytosis by polymorphonuclear leukocytes (PMN's), and inactivation of antibiotics by b lactamase production. Abscess formation is a major complication of intestinal infections, and results in the formation of a fibrous membrane surrounding a mass of cellular debris, dead PMN's, and a mixed population of bacteria. If not removed, the abscess will expand, possibly causing intestinal obstruction, erosion of resident blood vessels, and ultimately fistula formation. Abscesses may also metastasize, resulting in bacteremia and disseminated infection. Formation of the abscess is a pathological response of the immune system to the presence of the Bacteroides capsular polysaccharide. B. fragilis is the only bacterium that has been shown to induce abscess formation as the sole infecting organism. B. fragilis is the most common anaerobic organism isolated from clinical infections, the percentage being put as high as 81%, and untreated has a mortality rate of 60%.

Bacteroides fragilis is a rare cause of septic arthritis. Most patients with B. fragilis septic arthritis have a chronic joint disease, particularly rheumatoid arthritis, and sources of infection are lesions of the gastrointestinal tract and the skin.

Antibiotic treatment usually consists of metronidazole or clindamycin.

References:

http://www.sanger.ac.uk/Projects/B_fragilis/
http://www.cdc.gov/ncidod/eid/vol6no2/prindiville.htm
http://medic.med.uth.tmc.edu/path/00001490.htm
http://jac.oupjournals.org/cgi/content/full/45/5/691
http://borg.med.ecu.edu/~webpage/about.html
Clin. Rheumatol. 16(6):632-4 (1997)
Science 307:1463-1465(2005).