🧭 When to suspect
Suspect Clostridioides difficile (C. diff) infection in any patient with new, unexplained diarrhoea – characteristically watery, frequent and offensive, often with crampy lower abdominal pain – particularly when there has been recent antibiotic exposure. The decisive clinical reflex is simple: new diarrhoea + recent antibiotics = think C. diff.
The pathology is toxin-mediated, not overgrowth alone. Antibiotics disrupt the protective gut flora, allowing toxigenic C. difficile to flourish; it is the toxins (A and B) that injure the colonic mucosa and produce disease ranging from mild diarrhoea to pseudomembranous colitis, toxic megacolon, perforation and death. This matters for diagnosis: detecting the organism is not the same as detecting active toxin.
CDI is no longer a hospital-only problem – community-onset cases have been rising in England, so the diagnosis belongs firmly in the primary-care differential. Management hinges on two skills: stratify by severity, and recognise life-threatening disease early.
| Severity | Defining features |
|---|---|
| Mild | Normal white cell count (WCC); typically fewer than 3 loose stools per day. |
| Moderate | Raised WCC but below 15 × 10⁹/L; typically 3–5 loose stools per day. |
| Severe | WCC above 15 × 10⁹/L, or creatinine risen > 50% above baseline, or temperature > 38.5°C, or evidence of severe colitis. Stool frequency is a less reliable marker here. |
| Life-threatening | Hypotension, partial or complete ileus, toxic megacolon, or CT evidence of severe disease. |
Raise suspicion especially after the "4 Cs" – clindamycin, co-amoxiclav, cephalosporins and ciprofloxacin (and other fluoroquinolones) – though broad-spectrum penicillins and carbapenems also contribute. Other key risks are age 65 and over, recent hospital or care-home stay, proton pump inhibitor (PPI) use, frailty and immunosuppression.
Source: NICE NG199 · UKHSA
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