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Clostridium (Clostridioides) difficile - Infection

Clostridium (Clostridioides) difficile - Infection

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Clostridium difficile
Note: this bacterium has been renamed Clostridioides difficile
  • Transmitted via the fecal-oral route
  • Common colonizer of the human colon.
  • Historically associated with hospitalized patients, we’ve seen a rise in community-acquired cases.
A major cause of C. difficile infection is antibiotics that suppress the non-pathogenic colonic flora, which allows the opportunistic C. difficile* to flourish.
Virulence factors include potent toxins:
  • Toxin A is an enterotoxin that attracts neutrophils, which release cytokines.
– Toxin A also increases intestinal wall permeability by attacking colonic epithelial tight junctions.
  • Toxin B is a cytotoxin that acts on enterocyte actin to destroy cytoskeletal integrity.
Binary toxin: Some strains of C. difficile produce Binary toxin, aka, C. difficile* transferase (CDT). – The role of Binary toxin in C. difficile infection is uncertain: Some studies suggest that Binary toxin increases bacterial adherence to host cells and promotes cell death; others report that the toxin suppresses eosinophil activity. It is possible that the toxin has multiple virulence effects.
Infection:
C. difficile infection acts on the colon, where it induces a range of gastrointestinal issues, from mild diarrhea to severe colitis.* – Pseudomembranous colitis is the most serious form of C. difficile infection; characterized by yellowish-white exudate on the mucosal surface of the colon. The pseudomembrane comprises fibrin and inflammatory cells in mucus.
Treatment & Prevention:
  • Withdrawal of the associated antibiotic often suffices to treat diarrheal symptoms.
  • Metronidazole or vancomycin can be administered in more serious cases.
  • Colitis relapse is common. Patients with multiple relapses may benefit from fecal microbiota transfer from a healthy donor, which replenishes the healthy bacteria in the colon.
References
Pseudomembranous colitis (Wikipedia; Author Ed Uthman).

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