Thomas V Riley1,2,3
1School of Medical & Health Sciences, Edith Cowan University, Joondalup, Western Australia, 2School of Life & Veterinary Sciences, Murdoch University, Murdoch, Western Australia, 3Department of Microbiology, PathWest Laboratory Medicine, Nedlands, Western Australia
Clostridium difficile, a Gram positive, spore-forming, anaerobe, is the primary aetiological agent of pseudomembranous colitis and a leading cause of antibiotic-associated diarrhoea. C. difficile virulence is classically attributed to two large glucosylating toxins: toxin A and toxin B. With an estimated 500,000 cases annually in the USA and medical costs totalling up to $3 billion USD, C. difficile infection (CDI) is a significant economic and medical burden across the globe. Epidemic strains of C. difficile have emerged in several parts of the world, notably North America, but the reasons for this are poorly understood. Diagnosis and surveillance of CDI rely on having available a sufficiently sensitive and specific laboratory test suitable for both purposes. Currently such a test does not exist, leading to much confusion about what to do. In the UK, the English Department of Health has mandated that a test to detect free toxin in faeces should be used for the laboratory diagnosis of disease. In the USA, molecular tests to detect toxin genes have been implemented widely leading to suggestions of over-reporting of CDI cases.