VanA-mediated high level glycopeptide resistance in MRSA

B González-Zorn, P Courvalin - The Lancet infectious diseases, 2003 - thelancet.com
B González-Zorn, P Courvalin
The Lancet infectious diseases, 2003thelancet.com
Acquisition of resistance is most likely due to in-vivo transfer of the vanA operon from
enterococcus to S aureus. 3 Since the first reports of vancomycin-resistant enterococcus in
1988, 4, 5 the VanA-type resistance is seen in the majority of glycopeptideresistant
enterococci isolated worldwide. 6 The vanA operon is located in transposable elements
closely related to Tn1546 that are generally carried by self transferable plasmids. These
plasmids are not specific to enterococci, but are promiscuous genetic elements that can be …
Acquisition of resistance is most likely due to in-vivo transfer of the vanA operon from enterococcus to S aureus. 3 Since the first reports of vancomycin-resistant enterococcus in 1988, 4, 5 the VanA-type resistance is seen in the majority of glycopeptideresistant enterococci isolated worldwide. 6 The vanA operon is located in transposable elements closely related to
Tn1546 that are generally carried by self transferable plasmids. These plasmids are not specific to enterococci, but are promiscuous genetic elements that can be transferred to a wide range of Grampositive bacteria where they confer a high degree of vancomycin resistance. 7 Therefore, when glycopeptides are used for therapy, especially orally, they exert a selective pressure against the normal flora that may become a reservoir of glycopeptide resistance genes potentially transferable to human pathogens.
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