Abstract

The scale of the problem now posed by Clostridium difficile infection (CDI) is becoming frighteningly clear. Since 2001, a dramatic increase in the incidence and severity of CDI has occurred, particularly, in North America, the United Kingdom and Europe, associated with the emergence of a fluoroquinolone-resistant clone known as restriction endonuclease type BI, pulsed field type NAP1 or PCR ribotype 027 (RT027) Clostridium difficile (CD)1–3. CD is now the most commonly identified nosocomial pathogen in the USA4–6 and in 2011 there were approximately 450 000 incident cases of CDI in the USA and 29 300 deaths at day 30 post diagnosis6. Using an estimated attributable mortality rate of 50%, approximately 15 000 deaths due to CDI occurred in the USA in 2011.

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