This diarrhoeal illness, of variable severity, is caused by Clostridium difficile. The condition derives its name from yellowish-white plaques which are found throughout the colon and rectum in its severe form.

Pseudomembranous colitis is caused by a cytotoxin produced by C. difficile, a Gram-positive, anaerobic, spore-forming bacillus. The bacterium is not normally present in the colon and infection only occurs in individuals with diminished resistance to colonization. Although pseudomembranous colitis has been reported in patients with chronic obstruction and in association with cancer chemotherapy, it most commonly occurs as a complication of antibiotic treatment, especially in patients with diminished host resistance. All antibiotics in common medical use have been reported to precipitate pseudomembranous colitis; the link is strongest with lincomycin, clindamycin, ampicillin, amoxycillin, and cephalosporins.

This is an acute, exudative, inflammatory process. If present, plaques are multiple but not confluent, 2 to 5 mm in diameter, and they adhere to the underlying mucosa. Microscopically, they consist of fibrin, mucous, polymorphs, and epithelial debris (Fig. 1) 1063.

The most common presenting features are watery diarrhoea of variable severity and a low grade fever. These can occur from 2 days to 3 weeks after antibiotic treatment, including antibiotic chemoprophylaxis before surgical procedures. Colicky abdominal pain, bloody diarrhoea, and toxic megacolon are recognized but infrequent complications. Sigmoidoscopy usually discloses rectal plaques in severely affected patients. The mucosa between plaques appears normal.

Diagnosis is established by demonstrating the presence of C. difficile toxin in the stools of symptomatic individuals. The organism can be cultured and its presence may be demonstrated in the absence of measurable toxin production. Under these circumstances, alternative diagnoses should be considered and these are outlined in Table 1 333.

Fluid and electrolyte resuscitation should be instituted if necessary, and urgent surgical opinion sought in patients with toxic megacolon in whom perforation is imminent or has actually occurred. Otherwise, pseudomembranous colitis is managed conservatively. Symptomatic patients whose stools contain C. difficile toxin, should be treated with oral metronidazole 250 mg or vancomycin 125 mg every 6 h. If possible, other antibiotics should be withdrawn. In addition, barrier nursing is required to prevent spread of the organism to other patients, as it is highly contagious. Clinical improvement should be noted within 48 h, but relapse may occur, due to either reinfection or the failure of initial treatment to eradicate the bacteria completely.

Treatment is not recommended if toxin production cannot be demonstrated, despite positive C. difficile cultures. Antibiotic therapy may be instituted in spite of this if a patient is symptomatic and other causes of diarrhoea have been excluded.

Burdon DW. Bacterial infections: Clostridia and gastrointestinal disease. Curr Opin Gastroenterol 1987; 3: 127–9.

Keighley MRB, Burdon DW. Pseudomembranous colitis. In: Marston A, ed. Vascular Disease of the Gut. London: Edward Arnold, 1986; 86–102.