Clostridioides difficile (C. diff) (C. diff)

Clostridioides difficile (formerly Clostridium difficile) is a Gram-positive, anaerobic, spore-forming bacterium that serves as a major enteric pathogen, primarily causing healthcare-associated diarrhea and pseudomembranous colitis [1]. The organism typically colonizes the human colon following the disruption of the normal gut microbiota by broad-spectrum antimicrobial therapy [2]. Its pathogenicity is driven by the secretion of two large protein exotoxins, Toxin A (TcdA) and Toxin B (TcdB), which glucosylate Rho-family GTPases within host cells, leading to actin cytoskeleton collapse, cell death, and profound mucosal inflammation [3]. Therapeutic strategies currently involve the use of specialized antibiotics like vancomycin and fidaxomicin to eliminate the vegetative bacteria, or monoclonal antibodies such as bezlotoxumab to neutralize the toxins directly [4]. A significant clinical challenge is the bacterium's ability to produce highly resilient spores that persist in the environment and facilitate frequent disease recurrence [5].

Other names

Clostridium difficilePeptostreptococcus difficileC. difficile

Antibiotics target Clostridioides difficile through various mechanisms: vancomycin inhibits peptidoglycan cell wall synthesis; fidaxomicin inhibits the bacterial RNA polymerase; and metronidazole causes DNA strand breakage via reductive metabolism. Monoclonal antibodies like bezlotoxumab act by binding and neutralizing the secreted Toxin B, thereby preventing the destruction of the intestinal epithelial barrier.