Clostridium difficile infection

An antibiotic-associated infection of the colon by the spore-forming bacterium Clostridioides difficile (formerly *Clostridium*) that releases toxins causing colonic inflammation and pseudomembranous colitis (diarrhea with pseudomembranes).

• Common cause of healthcare-associated diarrhea and can be life-threatening (e.g., toxic megacolon, sepsis). U.S. burden ~500k cases/year with ~15k deaths. Frequent culprit in outbreaks linked to antibiotic overuse, making antibiotic stewardship and infection control critical. Often tested on exams due to its classic presentation of post-antibiotic colitis with pseudomembranes.

• Usually occurs after recent antibiotic use (classically clindamycin, fluoroquinolones, cephalosporins) or prolonged healthcare exposure (hospitalization or nursing home stay). Other risk factors include older age (>65), proton pump inhibitors use, serious underlying illness (e.g., ICU patients), and immunosuppression.
• Watery diarrhea with a distinct foul odor is the hallmark (ranging from ≥3 loose stools/day to severe diarrhea 10–15×/day) accompanied by lower abdominal cramping and sometimes fever. Stool is usually not grossly bloody in C. diff (blood suggests very severe colitis or alternative diagnosis). Severe cases may cause dehydration, ileus (↓ or no diarrhea due to bowel paralysis), or even shock.
• Severe/fulminant infection leads to pseudomembranous colitis – colonoscopy would show yellow-white pseudomembranes (plaque-like fibrinous exudates). Patients often have high leukocytosis (WBC >15,000; can exceed 30k) and rising creatinine from acute kidney injury. Fulminant CDI can progress to toxic megacolon (distended colon with loss of motility), perforation, and peritonitis if not promptly treated.

1. Confirm the diagnosis with stool tests for C. diff toxin or genes. Most labs use a multistep algorithm (GDH antigen + toxin immunoassay, with PCR for toxin genes if results are discordant) for accuracy. Only test unexplained new-onset diarrhea – avoid testing formed stool or asymptomatic patients (common colonizer).
2. If C. diff is suspected in a patient (especially if severe), initiate empiric therapy without delay. Isolate the patient under contact precautions (gown and gloves) as soon as CDI is considered. Do NOT give anti-diarrheal medications (risk of toxin retention and toxic megacolon). Remove any inciting antibiotic if still ongoing, and provide supportive fluids/electrolytes.
3. Assess severity: check WBC and creatinine. Severe CDI is defined by WBC ≥15k or Cr ≥1.5× baseline, whereas fulminant CDI includes hypotension, shock, ileus, or megacolon. Obtain abdominal imaging (X-ray or CT) if ileus or toxic megacolon is suspected to evaluate for colonic dilatation.
4. Once confirmed, treat according to severity (see treatment). Monitor closely for any signs of deterioration (increasing abdominal distension, mental status changes). Avoid repeat stool tests to "test for cure" – C. diff toxin may remain positive even after successful treatment, so rely on clinical improvement.

1. Initial infection (non-severe or severe): First-line therapy is oral vancomycin (125 mg QID) or fidaxomicin (200 mg BID) for 10 days. These are superior to metronidazole (which is now reserved for mild cases if vanco/fidaxo are unavailable).
2. Fulminant (hypotension, ileus, or megacolon): Use high-dose oral vancomycin (e.g., 500 mg QID), plus IV metronidazole 500 mg q8h. If ileus prevents oral intake, give vancomycin via rectal enema. Surgical consultation for urgent subtotal colectomy is indicated if there's no improvement or if toxic megacolon is present.
3. Recurrences: For a first recurrence, avoid repeating the same regimen – options include fidaxomicin (if not used initially) or a tapered and pulsed vancomycin course. For >1 recurrence, consider fecal microbiota transplantation (FMT) after antibiotic therapy. Also, bezlotoxumab (monoclonal antibody against C. diff toxin B) can be given during treatment to reduce future recurrences.

• Classic association: Clindamycin is famously linked to C. diff in exams (though any broad-spectrum antibiotic can precipitate it).
• Hand sanitizer won't kill C. diff – spores require soap-and-water handwashing and bleach-based disinfectants for environmental cleaning.
• C. diff stool often has a characteristic odor (described as a sharp, sickly sweet smell) that can hint at the diagnosis.

• Signs of impending toxic megacolon – e.g., severe abdominal distension, absent bowel sounds (ileus), peritoneal signs, or WBC >30k – require emergent surgical evaluation (this is life-threatening).
• Never use anti-motility drugs (loperamide, etc.) in C. diff colitis, as they can precipitate toxin retention and fulminant colitis.

1. Patient on antibiotics or in healthcare setting with new-onset diarrhea → Suspect C. diff infection.
2. Place patient on contact isolation and send stool for C. diff testing (toxin EIA and/or PCR); if severe symptoms, start empirical treatment pending results.
3. If positive, determine severity: non-severe (WBC ≤15k and Cr <1.5) vs severe (WBC >15k or Cr ≥1.5) vs fulminant (hypotension, shock, ileus, or megacolon).
4. Begin appropriate therapy: oral vancomycin or fidaxomicin for 10 days (add IV metronidazole + consider surgery for fulminant cases).
5. Ensure infection control measures: continue isolation, strict hand hygiene (soap and water), and environmental disinfection with bleach. For recurrent cases, use alternative therapy (fidaxomicin, vancomycin taper) or FMT as needed.

• Hospitalized 68‑year‑old on clindamycin for pneumonia develops foul-smelling watery diarrhea (~10+ stools/day) with abdominal cramps and low-grade fever → C. diff colitis (antibiotic-associated diarrhea).
• Nursing home patient on prolonged antibiotics becomes lethargic with a distended abdomen and no bowel movements; WBC 30k, hypotension, and fever are noted → Fulminant C. diff infection with toxic megacolon.