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Vancomycin-resistant Staphylococcus aureus
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==Mechanism of acquired resistance== Vancomycin-resistant ''Staphylococcus aureus'' was first reported in the United States in 2002.<ref name=":0" /> To date, documented cases of VRSA have acquired resistance through uptake of a [[vancomycin]] resistance gene cluster from ''Enterococcus'' (i.e. [[Vancomycin-resistant Enterococcus|VRE]]).<ref>{{cite journal |last1=Chang |first1=Soju |last2=Sievert |first2=Dawn M. |last3=Hageman |first3=Jeffrey C. |last4=Boulton |first4=Matthew L. |last5=Tenover |first5=Fred C. |last6=Downes |first6=Frances Pouch |last7=Shah |first7=Sandip |last8=Rudrik |first8=James T. |last9=Pupp |first9=Guy R. |date=2003-04-03 |title=Infection with Vancomycin-Resistant Staphylococcus aureus Containing the vanA Resistance Gene |journal=New England Journal of Medicine |volume=348 |issue=14 |pages=1342β1347 |doi=10.1056/NEJMoa025025 |issn=0028-4793 |pmid=12672861|doi-access=free }}</ref> The acquired mechanism is typically the ''vanA'' gene and operon from a plasmid in ''Enterococcus faecium'' or ''Enterococcus faecalis''.<ref name=":0" /> This mechanism differs from strains of [[#vancomycin-intermediate Staphylococcus aureus|vancomycin-intermediate ''Staphylococcus aureus'']] (VISA), which appear to develop elevated MICs to vancomycin through sequential mutations resulting in a thicker cell wall and the synthesis of excess amounts of [[D-Ala-D-Ala dipeptidase|<small>D</small>-ala-<small>D</small>-ala]] residues.<ref>{{cite journal|last1=Howden|first1=Benjamin P.|last2=Davies|first2=John K.|last3=Johnson|first3=Paul D. R.|last4=Stinear|first4=Timothy P.|last5=Grayson|first5=M. Lindsay|date=2010-01-01|title=Reduced Vancomycin Susceptibility in Staphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications|journal=Clinical Microbiology Reviews|volume=23|issue=1|pages=99β139|doi=10.1128/CMR.00042-09|issn=0893-8512|pmc=2806658|pmid=20065327}}</ref>
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