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.
Mechanism of acquired vancomycin resistance
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Six different types of vancomycin resistance are shown by enterococcus : Van-A, Van-B, Van-C, Van-D, Van-E and Van-F. Of these, only Van-A, Van-B and Van-C have been seen in general clinical practice, so far. 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. In the US, linezolid is commonly used to treat VRE, as teicoplanin
The mechanism of resistance to vancomycin found in enterococcus involves the alteration to the terminal amino acid residues of the NAM/NAG-peptide subunits, under normal conditions, D-alanyl-D-alanine, to which vancomycin binds. 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. This loss of just one point of interaction results in a 1000-fold decrease in affinity. The D-alanyl-D-serine variation causes a six-fold loss of affinity between vancomycin and the peptide, likely due to steric hindrance.
Some VREs respond to the presence of vancomycin rather than just its effect on the cell wall.
Prevention and treatment of VRE infection
- Animal Drug Availability Act 1996
- Antibiotic resistance
- Drug resistance
- Methicillin-resistant Staphylococcus aureus (MRSA)
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