Clostridium difficile

Clostridium difficile — reclassified as Clostridioides difficile and universally known as C. diff — is a gram-positive, spore-forming, obligate anaerobic bacillus. It is the leading cause of healthcare-associated diarrhea. In a healthy colon, normal bacterial flora keep C. diff in check; when broad-spectrum antibiotics such as clindamycin, fluoroquinolones, and cephalosporins wipe out that competing flora, C. diff can overgrow and cause disease.

The organism damages the colon through two exotoxins. Toxin A (an enterotoxin) and toxin B (a cytotoxin) disrupt the cytoskeleton of intestinal epithelial cells, causing inflammation, fluid secretion, and cell death. Severe cases produce pseudomembranous colitis — yellow-white plaques of fibrin, mucus, and inflammatory debris coating the colonic mucosa — and can progress to toxic megacolon. Clinically, infection ranges from watery diarrhea and cramping to fever, leukocytosis, and life-threatening colitis.

C. diff spreads by the fecal-oral route via hardy spores that persist on surfaces and resist alcohol-based hand sanitizers — a key infection-control point: handwashing with soap and water and contact precautions are required. Diagnosis relies on stool testing for the toxins or their genes. First-line therapy centers on oral vancomycin or fidaxomicin, with recurrence common enough that fecal microbiota transplantation is used for refractory cases.

C. diff is high-yield across health exams. The USMLE Step 1 tests its toxins, risk factors, and pseudomembranous colitis; the CCMA touches on it in gastroenterology and infection control; and the PTCE connects it to the antibiotics that trigger it and the drugs that treat it.