The time intervals between introduction of penicillin and the emergence of penicillin-resistant Staphylococcus aureus, and between the introduction of methicillin and the emergence of methicillin-resistant S. aureus (MRSA), were very short (3-5 years), and were followed by rapid emergence and spread of the resistant strains. For unclear reasons, the same hasn’t been true for vancomycin-resistant S. aureus (VRSA). Vancomycin was introduced in the 1950s, and use of the drug increased almost exponentially during the advance of MRSA as a hospital pathogen in the 1980s. Yet it wasn’t until 2002 that the first VRSA infection was reported. As soon as it was recognized that plasmid-mediated transfer of the vanA gene to MRSA was responsible, many considered the rapid spread of VRSA to be inevitable.
Interestingly, this spread hasn’t yet happened. Appearance of VRSA strains has remained rare and sporadic, with only 13 confirmed cases in the U.S. since the first report, barely 1 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.