History and Biology of VRE
To become vancomycin-resistant, vancomycin-sensitive enterococci typically obtain new DNA in the form of plasmids or transposons which encode genes that confer vancomycin resistance. This acquired vancomycin resistance is distinguished from the lower-level, natural vancomycin resistance of certain enterococcal species including E. gallinarum and E. casseliflavus.
High-level vancomycin-resistant E. faecalis and E. faecium clinical isolates were first documented in Europe in the late 1980s. Since then, VRE have been associated with outbreaks of hospital-acquired (nosocomial) infections around the world. In the United States, vancomycin-resistant E. faecium was associated with 4% of healthcare-associated infections reported to the Centers for Disease Control and Prevention National Healthcare Safety Network from January 2006 to October 2007.
VRE can be carried by healthy people who have come into contact with the bacteria. The most likely place where such contact can occur is in a hospital (nosocomial infection), although it is thought that a significant percentage of intensively-farmed chicken also carry VRE.
Read more about this topic: Vancomycin-resistant Enterococcus
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