Mechanism of Acquired Vancomycin Resistance
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 sensitive to teicoplanin, and Van-C is only partly resistant to vancomycin, and sensitive to teicoplanin. In the US, linezolid is commonly used to treat VRE, as teicoplanin is not available.
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.
Read more about this topic: Vancomycin-resistant Enterococcus
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