The changing epidemiology of Clostridium difficile infections.

The epidemiology of Clostridium difficile infection (CDI) has changed dramatically during this millennium. Infection rates have increased markedly in most countries with detailed surveillance data. There have been clear changes in the clinical presentation, response to treatment, and outcome of CDI. These changes have been driven to a major degree by the emergence and epidemic spread of a novel strain, known as PCR ribotype 027 (sometimes referred to as BI/NAP1/027). We review the evidence for the changing epidemiology, clinical virulence and outcome of treatment of CDI, and the similarities and differences between data from various countries and continents. Community-acquired CDI has also emerged, although the evidence for this as a distinct new entity is less clear. There are new data on the etiology of and potential risk factors for CDI; controversial issues include specific antimicrobial agents, gastric acid suppressants, potential animal and food sources of C. difficile, and the effect of the use of alcohol-based hand hygiene agents.

Ecological replacement of Enterococcus faecalis by multiresistant clonal complex 17 Enterococcus faecium.

The proportion of enterococcal infections caused by ampicillin-resistant Enterococcus faecium (AREfm) in a European hospital increased from 2% in 1994 to 32% in 2005, with prevalence rates of AREfm endemicity of up to 35% in at least six hospital wards. Diabetes mellitus, three or more admissions in the preceding year, and use of beta-lactams and fluoroquinolones, were all associated with AREfm colonisation. Of 217 AREfm isolates that were genotyped, 97% belonged to clonal complex 17 (CC17). This ecological change mimics events preceding the emergence of vancomycin-resistant E. faecium (VREF) in the USA and may presage the emergence of CC17 VREF in European hospitals.