An outbreak of vancomycin resistant MRSA, or VMRSA, would be the ‘perfect microbiological storm’, even worse than vancomycin resistant Staphylococcus aureus (VRSA). The only currently available antibiotics that would be effective against it would have to be used off-label, and are not very effective against sepsis (bloodstream) infections. Fortunately, VRSA is observed only anecdotally: a single patient, usually on long-term vancomycin therapy, is infected with it, and it is not spread to other patients or healthy people.
One reason is that most patients with VRSA are already in hospitals, usually in isolation. We’re fortunate that these infections evolve in these settings (and that vancomycin is administered intravenously, making it hard for fucking morons who don’t know medicine to misuse this drug–Got Cipro?).
A second reason is described in a recent article: it’s very hard to evolve vancomycin resistance in a methicillin resistant S. aureus. When MRSA is evolved in a vancomycin-containing medium, it loses the methicillin resistance genes. And when the researchers knocked out the methicillin genes, they found that these S. aureus grew faster. The reason appears to be that these resistance genes are very poorly regulated; they’re never turned completely off, even when they’re not needed (i.e., there’s no vancomycin around). While the mechanism is unclear, these genes do appear to lower growth rates.
So the good news is that it appears very difficult to evolve a VMRSA.
At some point, with all of the MRSA strains out there, one (or more) of them is going to evolve a better regulated methicillin resistance gene.
Cited article: Noto MJ, Fox PM, Archer GL. 2008. Spontaneous Deletion of the Methicillin Resistance Determinant, mecA, Partially Compensates for the Fitness Cost Associated with High-Level Vancomycin Resistance in Staphylococcus aureus. Antimicrob Agents Chemother. 52(4):1221-9. doi: 10.1128/AAC.01164-07.