Colitis due to Clostridium difficile toxins: underdiagnosed, highly virulent, and nosocomial

Clostridium difficile colitis is a major complication of antibiotic therapy. Antibiotics cause a reduction in bacteria that normally reside in the colon. If an antibiotic-treated patient ingests C. difficile bacteria, this organism may proliferate in the colon because it is resistant to most antibiotics and because it does not have to compete with the normal bacteria for nutrients. If the C. difficile organism has the gene for toxin production, the toxin can produce a colitis. In addition to antibiotics, other proposed risk factors for development of C. difficile colitis include advanced age, contact with infected patients and with their health care providers, impaired immune function, suppression of gastric acid secretion by a proton pump inhibitor, and postpyloric tube feeding. Many of the risk factors become simultaneously focused on patients admitted to the hospital. The incidence of C. difficile disease has been rising, and strains have become more virulent. In some forms of the disease, the patient doesn't have diarrhea, and in such patients C. difficile can be deadly but difficult to diagnose. The standard treatment, with metronidazole or vancomycin, fails to work in up to 25% of patients with the fulminant form of colitis. Since C. difficile causes only 20% of cases of antibiotic-associated diarrhea, a specific test is needed to diagnose this organism. Toxigenic cultureis highly specific but not available at most institutions. The tests that are available--enzyme-linked immunosorbent assay and fecal cytotoxicity assay--have high false-negative rates, even in patients with severe clinical disease, creating a diagnostic dilemma. The only proven way to reduce the risk of C. difficile disease is implementation of an antibiotic management program in conjunction with enhanced infection control procedures.