History and biology
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 natural vancomycin resistance of certain enterococcal species including E. gallinarum and E. casseliflavus.
High-level vancomycin-resistant E. faecalis and E. faecium are clinical isolates first documented in the 1980s. 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, usually in a hospital (nosocomial infection), although it is thought that a significant percentage of intensively farmed chicken also carry VRE. Other regions have noted a similar distribution, but with increased incidence of VRE. For example, a 2006 study of nosocomial VRE revealed a rapid spread of resistance among enterococci along with an emerging shift in VRE distribution in the Middle East region, such as Iran. Treatment failures in enterococcal infections result from inadequate information regarding glycopeptide resistance of endemic enterococci due to factors such as the presence of VanA and VanB. The study from Iran reported the first case of VRE isolates that carried VanB gene in enterococcal strains from Iran. This study also noted the first documented isolation of nosocomial E. raffinosus and E. mundtii in the Middle East region.
Mechanism of acquired resistance
Six different types of vancomycin resistance are shown by enterococcus: Van-A, Van-B, Van-C, Van-D, Van-E and Van-G. The significance is that Van-A VRE is resistant to both vancomycin and teicoplanin, Van-B VRE is resistant to vancomycin but susceptible to teicoplanin, and Van-C is only partly resistant to vancomycin, and susceptible to teicoplanin.
The mechanism of resistance to vancomycin found in enterococcus involves the alteration of the peptidoglycan synthesis pathway. The D-alanyl-D-lactate variation results in the loss of one hydrogen-bonding interaction (four, as opposed to five for D-alanyl-D-alanine) being possible between vancomycin and the peptide. The D-alanyl-D-serine variation causes a six-fold loss of affinity between vancomycin and the peptide, likely due to steric hindrance.
Treatment of infection
Cephalosporin use is a risk factor for colonization and infection by VRE, and restriction of cephalosporin usage has been associated with decreased VRE infection and transmission in hospitals. Lactobacillus rhamnosus GG (LGG), a strain of L. rhamnosus, was used successfully for the first time to treat gastrointestinal carriage of VRE. In the US, linezolid is commonly used to treat VRE.
- Antibiotic resistance
- Drug resistance
- Methicillin-resistant Staphylococcus aureus (MRSA)
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