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Clostridium difficile

Cell Wall: Gram Positive Shape: Spore-forming Rod
Metabolism: Obligate Anaerobe
  • C. difficile spores are found widely in many environments but especially in hospitals where they often seed the GI system of hospitalized patients. However, extensive growth and release of exotoxin is normally held in check by the presence of the normal GI flora. However, treatment of broad-spectrum antibiotics such as clindamycin, ampicillin, as well as second and third generation cephalosporins often result in disruption of the normal GI flora allowing C. difficile over-growth, exotoxin release, and thus resulting in diarrheal disease.
Virulence Factors
  • C. difficile produces two potent exotoxins
    • Toxin A: An enterotoxin that disrupts enterocyte junctions, resulting in backleak of fluid into into the intestinal lumen
    • Toxin B: A Cytotoxin that causes enterocyte death.
Clinical Consequences
  • The characteristic infectious diarrhea caused by C. difficile is termed "Pseudomembranous Colitis". Diarrhea is usually loose to watery and almost never contains blood. Endoscopic evaluation will reveal expanding colonic "Pseudomembranes" which are appear as whitish/yellowish plaques composed of necrotic cellular debris that overly colonic mucosal erosions. Pseudomembranes begin as small, millimeter-wide plaques of the colonic mucosa but expand and often coalesce to cover the entire large intestine.
  • Infection can be confirmed using stool analysis for C. difficile enterotoxin.
  • If possible, discontinuation of broad-spectrum antibiotics resolves a large fraction of cases. Otherwise, metronidazole or vancomycin are administered orally since systemic administration of these normally IV-delivered antibiotics is not necessary for this purely GI infection.