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.  


2 thoughts on “VRE: MRSA or MRSE?

  1. I would love to see experts thoughts on this subject. After 20 + years as a microbiology medical lab technologist, I wonder the same thing. I recently learned that there are strain of ARE that test vancomycin sensitive, but harbour the van A or van B gene?


  2. This is the part of the article that most caught my attention:

    “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””

    For me this raises the question of the role of biofilm, especially in surface contamination of problematic pathogens such as ARE.

    Just as biofilm is known to play a role inhibition of antibiotics against certain pathogens (most recently detailed in a specific case study on Candida albican – http://www.mdpi.com/2309-608X/3/1/14/htm ) that same biofilm appears to be preventing much of the surface cleaners (quats, bleaches and oxidizers) from addressing the presence of pathogens such as ARE.

    If biofilm on surfaces is an active participant in the presence and protection of such pathogens on surfaces, then is one of the means of addressing such pathogen presence, (with a view to reducing the risks their presence pose), lie in the dismantling of biofilm on such surfaces?

    This is a crucial question. Over the decades we have seen the spread of antibiotic resistant pathogens spread from hospitals to a host of other public places, such as schools, public transport and sports and fitness centers to name a few.

    That we are now on 6th generation quaternary ammonium cleaners is an indication that there is a likely adaptation of pathogens to the cleaning chemistry that we use, just as these same pathogens have developed resistance to much of the antibiotics used against them in health care protocols.

    It is increasingly understood that quats, bleaches and oxidizers do not remove biofilm. Here, in recognition of this understanding, in the US EPA notes that the most effective means of addressing biofilm on surfaces is abrasion. Use of abrasion in combination with such cleaning chemistry is effective, but only to a limited extent.

    Abrasion (for example scrubbing, or wiping with microfibre) in conjunction with such cleaning agents such as quats, can adress the presence of a lot of biofilm, but given that such a combination often doesn’t get into every “nook and cranny”, such as tight corners and joins, or microscopic cracks, there is still a residual presence of some of the pathogen biofilm.

    Given pathogens and the biofilms they create can replicate in the right environments as rapidly as every 20 minutes, such residual biofilm and the pathogens they house pose a critical risk.

    The introduction of a biological component to the cleaning of these surfaces, to better address the “veneer” referred to in this article is one such solution.

    Introducing probiotics into the cleaning equation, delivering an abundance of beneficial bacteria that via the concept of Competitive Exclusion effectively starve the pathogens to death, (a method to which there is no mutuation risk), which trough that same process also break down the biofilm in which such pathogens hide, could prove an important component to reducing the presence and risk of dangerous pathogens.

    Such an approach (the use of proibiotic based cleaners) also fits into the expanding awareness of the need for a healthy, balanced indoor microbiome; (Research by the likes of Jessica Greene at u of Oregon and Jack Gilbert at U of Chicago being two leaders in this field). Conventional Physics (scrubbing, wiping) and Chemistry (quats, bleaches and oxidizers) seek to “kill everything”, both the unwanted pathogens, and the much needed beneficial bacteria.

    Introducing a Biological component to the cleaning equation, to address what is a biological problem represents a completely different approach. The biosurfactants excreted by the probiotics in their process of out consuming the available food source help breakdown the very biofilm that is not addressed by conventional chemistry cleaners alone, nor completely dealt with such chemistry is used in conjunction with some form of abrasive physics.

    As such probiotic cleaners better address the contaminated surface “veneer” referred to in this article, and in doing reduce the risk of the spread of problematic pathogens such as ARE, VRE and many others.


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