The identification of C. difficile carriers who have the potential to produce toxin can take up to four days, delaying patient isolation and increasing the chance of nosocomial spread of infection. Here, Laura Nottle considers the performance and benefits of a tcdB gene detection assay.
Toxigenic Clostridium difficile was identified as a cause of pseudomembranous colitis associated with antimicrobial therapy in the late 1970s.1,2 Since then, the incidence and severity of C. difficile-associated-disease (CDAD) has grown, and is one of the major causes of nosocomial infection in the UK.
C. difficile is an anaerobic spore-forming rod that is part of the normal intestinal flora of approximately 3% of healthy adults. It produces two large toxins, called toxin A (tcdA) and toxin B (tcdB), which act in the bowel to produce local tissue damage.3 Strains that produce only tcdB have been associated with CDAD, whereas strains that produce neither toxin are thought to be non-pathogenic.4
People may carry toxigenic C. difficile asymptomatically; however, serious sequelae can occur following overgrowth of C. difficile resulting from antimicrobial therapy. Institutional outbreaks of CDAD are frequently caused by ingestion of alcohol-resistant spores that are difficult to eradicate in the environment.
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