Interestingly, this spread hasn’t yet happened—appearance of VRSA strains has remained rare and sporadic, with only 13 confirmed cases in the US since the first report, barely one per year. Furthermore, person-to-person spread hasn’t been demonstrated to be a problem. The first 12 cases were all in the similar genetic background (clonal complex 5, most of which were t002, the most common healthcare-associated MRSA spa type). Furthermore, vancomycin pressure seemed a prerequisite, suggesting that a high fitness cost is associated with maintaining vanA in S. aureus.
In this context, two recent publications should raise new concern about the potential for further emergence of VRSA. As documented in a CDC report of the 13th VRSA case in the US, and in last week’s NEJM report of a VRSA case from Brazil, VRSA has now emerged in the genetic background of community-associated MRSA strains (USA1100 and USA300). USA300 (clonal complex 8) has been particularly successful at rapidly spreading and replacing other MRSA lineages, so stable carriage of vanA in a USA300 background would be a major public health problem.
The above image of the pBRZ01 plasmid harboring vancomycin resistance genes and found in the Brazilian bloodstream infection case is from the NEJM report.