Abstract

Pseudomembranous colitis has been recognized as a complication of antimicrobial therapy since 1952. Most recently, evidence has been accumulated showing that a heat labile toxin is involved. Though little is known so far about the normal ecology of C. difficile and the host factors of potential importance in the development of colitis by this anaerobe, antimicrobial agent-induced suppression of the normal gut flora seems to be a major factor leading to the intestinal proliferation of resistant toxinogenic C. difficile. Factors independent of susceptibility are, however, probably responsible for cases of pseudomembranous colitis associated with penicillin, ampicillin, and other antibiotics active against C. difficile. In monitoring antibiotic therapy, the application of selective media for the isolation of C. difficile from faecal specimens and proper tools for the demonstration of toxin and the study of immunity might prove to be fruitful from both a diagnostic and therapeutic viewpoint. In established pseudomembranous colitis treatment consists of oral vancomycin (2 g/day), cholestyramine and, if necessary, intensive intravenous regimen.