C. Difficile Infection (CDI)

❓What❓

• Spore-forming, toxin-producing, Gram ⊕ anaerobic bacterium that colonizes the GI tract after normal gut flora disrupted 2/2 antibiotic exposure

• While identified in 1978, CDI became more frequent, more severe, & more refractory to standard treatments from 2003-2006 due to emergence of a more virulent strain linked to quinolone resistance

• Colitis is a result of toxin secretion by toxinogenic strain. (In other words, non-toxinogenic strain do not cause CDI.)

• Toxin A secretion mediates GI fluid secretion & mucosal injury, as well as neutrophil activation, with both Toxin A/B promoting neutrophil chemotaxis to resultant pseudomembranes

❓Epidemiology❓

• C. difficile carriage occurs in up to 10% of adults residing in hospitals or LTC facilities, which is problematic as they are capable of shedding spores into the healthcare environment

• Patients previously colonized are more likely to remain asymptomatic during hospitalization, whereas new exposure is more likely to lead to CDI, & this risk is amplified by antibiotic-associated risk factors (↑ spectrum, ↑ duration, ↑ number of agents)

• While classically & most commonly seen after antibiotic exposure, CDI can occur in healthy patients living in the community (i.e. no risk factors), & is thought to be a product of exposure to contaminated food & domestic animals

• Regarding recurrent CDI, up to ~25% experience this within 30 days of treatment. Risk factors for recurrent CDI include age > 65, IBD, need for concurrent non-CDI antibiotics, renal failure, & deficient humoral immunity

❓Presentation❓

• Symptoms can begin during or after completion of antibiotics
• Most cases occur within 2 weeks of antibiotics

• Watery diarrhea (≥ 3 loose stools / 24 hours)
• Neutrophilic leukocytosis → Leukemoid reaction
• Fever (~15%)

⚪ Colonoscopy findings: normal → patchy mild erythema → pseudomembranous colitis:

Obvious = “Fulminant colitis”

• Hypovolemic + distributive hTN
• Ileus vs. Megacolon → perforation

Occult = Dx Atypia

• Colitis without diarrhea (image ⊖) → “unexplained” leukocytosis/delirium
• Ileus without diarrhea (image ⊕) → “explained” leukocytosis/delirium
• Chronic colonic pseudoobstruction (”image ⊖”) → “unexplained” shock
• Protein-losing enteropathy
• Extracolonic (enteritis in colectomy patients, SSTI, reactive arthritis)

• While colonic bowel wall thickening is the most sensitive CT finding for CDI, only ~60% of CDI cases demonstrate this. Those who do have it show the following anatomic distribution:
• ~15-40% pancolonic
• ~15% sigmoid + rectum
• ~5-10% rectum
• ~5% transverse → rectum
• ~1-5% transverse → right colon
• ~1% right colon

• If colonic bowel wall thickening is identified, the presence of pericolonic fat stranding, ascites, & colonic nodularity increase the specificity for CDI:

❓Diagnosis❓

• Institutional specific, but commonly consists of a sensitive screen (e.g. NAAT for detection of C. difficile DNA), followed by reflex test for specific toxin (establishes CDI if ⊕, but imperfect sensitivity if low toxin production)

❓Treatment❓

📚 References 📚

• Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology

• Clostridioides difficile infection in adults: Clinical manifestations and diagnosis

• Pseudomembranous Colitis in Four Ethiopian Patients: A Case Series

• Antibiotic-induced diarrhea: specificity of abdominal CT for the diagnosis of Clostridium difficile disease

• Evaluating the CT Diagnosis of Clostridium difficile Colitis

• A difficult diagnosis: Clostridioides difficile infection without diarrhea

• The Pharmacist's Primer on Clostridioides Difficile Associated Diarrhea (Stephanie Kujawski)

• C. Difficile ⊕ Leukocytosis (The Blood Project)

• Visible mucosal changes of pseudomembranous colitis in a sigmoid colostomy

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