The rise of the Enterococcus: beyond vancomycin resistance

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Abstract
Enterococci are some of the most versatile organisms found to infect hospitalized patients. The epidemiology of enterococcal infections has evolved since the emergence of these pathogens and has seen the rise of Enterococcus faecium as a nosocomial pathogen with serious clinical implications. The effect of antibiotics on the microbiota of the gastrointestinal tract and subsequent alterations in the regulation of the gut immune system can favour colonization by multidrug-resistant enterococci. Enterococcal genomes are extremely malleable, with the ability to exchange large fragments of chromosomal DNA. In addition, the lack of CRISPR (clustered regularly interspaced short palindromic repeats) elements has a potential role in the adaptation of hospital-associated enterococci. Specific pathogenicity factors contribute to the ability of enterococci to produce disease and/or survive in the gastrointestinal tract of mammals. The major factors include secreted and cell surface-associated determinants. Antibiotic resistance is widespread for the anti-enterococcal antibiotics that are most commonly used in clinical practice, and the mechanisms of resistance for many of these antibiotics are known. These antibiotics include ampicillin, linezolid, daptomycin and quinupristin–dalfopristin, and there is also high-level resistance to aminoglycosides. Such resistances have important therapeutic implications.