To me, VRE is an old love that never let me down. In 1995 (!) I studied its epidemiology in Chicago (using PFGE), and we described it as the “triple-threat bug”: a gut colonizer like Gram-negatives, a skin colonizer like MRSA and an environmental contaminator like C. diff. A new study in CID, using WGS, illustrates its complex epidemiology. After 20 years, that complexity seems explained, and now we can no longer avoid the question what to do with VRE. Keep on cherishing its “feared pathogen status” like MRSA, or accept that it is just something like MRSE, and stop bothering.
Soon after the rise of VRE, it was obvious that E. faecium (much more than E. faecalis) was the bad bug and sequence-based technology allowed further characterization of the E. faecium species, identifying, what is now called “clade A”, as the clonal lineage associated with almost all invasive infections and hospital outbreaks. This “clade A” is phenotypically recognizable as ampicillin-resistant E. faecium, nicknamed ARE. This is the ugly sister of VRE, and therefore usually ignored. Yet, ARE=”VRE lacking a plasmid/transposon with vanA or vanB”, and ARE, therefore, has exactly the same triple-threat capabilities as VRE. And if you would start looking for ARE in your hospital, you should not be surprised to find many carriers and contaminated surfaces. In fact, I dare to say that almost all hospitals have an “ARE veneer”, aka “a fecal veneer”.
So, we have paved our hospitals with an acceptor population of ARE, sitting there waiting to accept a vanA or vanB containing transposon, and then we wake up as we recognize the VRE. Naturally this VRE can then spread from patient to patient and even to other hospitals, so we implement the necessary measures to control spread (but still ignoring ARE). In the Netherlands, this has been practiced now, almost continuously, since about 5 years and only few hospitals have escaped so far. If we learned anything it is that controlling VRE is difficult and costly.
The question then is: what is the benefit of costly measures to prevent spread and infections caused by VRE? That is the difference in patient outcome for those developing VRE infections compared to those developing ARE infections (not those not developing (enterococcal) infections, or VR E. feacalis infections!). Because if we stop controlling VRE, a proportion of current ARE infections will be VRE infections in the future. That comparison has not yet been made, but it should be done properly, in distinguishing the prognostic aspect (both ARE and VRE infections are a signal of severe underlying disease with a grim prognosis, irrespective of the ARE/VRE infection) from the attributable disease burden caused by the sole aspect of vancomycin resistance. For methicillin-resistance we accept MRSE, but not MRSA. The question to answer for “clade 1 E. faecium” is whether its effects on patients resembles that of coagulase-negative staphylococci (as suggested in this 2015 CID paper) or S. aureus.