Abstract
Clostridium difficile is a major cause of hospital-associated diarrhoea, and in severe cases leads to pseudomembranous colitis and toxic megacolon. The frequency of C. difficile infection (CDI) has increased in recent decades, with 453 000 cases identified in 2011 in the USA. This is related to antibiotic-selection pressure, disruption of normal host intestinal microbiota and emergence of antibiotic-resistant C. difficile strains. The burden of community-acquired CDI has been increasingly appreciated, with disease identified in patients previously considered low-risk, such as young women or patients with no prior antibiotic exposure. C. difficile has been identified in livestock animals, meat products, seafood and salads. It has been postulated that the pool of C. difficile in the agricultural industry may contribute to human CDI. There is widespread environmental dispersal of C. difficile spores. Domestic households, turf lawns and public spaces are extensively contaminated, providing a potential reservoir for community-acquired CDI. In Australia, this is particularly associated with porcine-derived C. difficile UK PCR ribotype 014/020. In this article, the epidemiological differences between hospital- and community-acquired CDI are discussed, including some emerging evidence for community-acquired CDI being a possible zoonosis.
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