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Background

Clostridium difficile is an anaerobic spore-forming bacillus that can be found in a wide range of habitats, from soil and water to intestines of animals, including humans. The bacterium was identified as the most important infectious cause of antibioticassociated diarrhea in the 1970s [1]. C. difficile infection (CDI) is transmitted via the fecal-oral route. It has been associated mainly with hospitals, where it occurs both endemically and epidemically. However, since the beginning of the new millennium, the epidemiology of CDI appears to be changing. Higher incidence rates of CDI were recorded and large outbreaks with relatively high morbidity and mortality were noticed, first in Canada, followed by the US, the UK and the European mainland [2]. These outbreaks were found to be caused by a specific strain of C. difficile, typed as North American pulse field gel electrophoresis type I and PCR ribotype 027 [3]. This change in epidemiology renewed scientific interest in CDI, which led to more advanced understanding of the disease.

Pathogenesis Much has been learnt about how C. difficile causes disease. This has been helped by molecular techniques, such as the construction of C. difficile mutants, and the availability of improved animal models. C. difficile spores, which are resistant to various physical and chemical attacks, may survive for years. Once they have been ingested and have passed the stomach, they germinate in the intestinal lumen under the influence of the binding of the primary bile acids cholic acid and cheodeoxycholic acid [4] to the receptor CspC [5]. The vegetative forms of the bacterium have to colonize the mucosa, a …