Introduction neonatal infections (2). The genus Enterococcus is composed

Enterococci are gram positive, facultatively anaerobic cocci that form chains of various lengths. They are robust and versatile, with a remarkable propensity to survive under harsh conditions (1) . Enterococci have been known for more than a century as a common cause of endocarditis, a disease that is fatal without effective antimicrobial therapy. Since then, they have been shown to cause a range of infections including pelvic infections, wound infections, meningitis, intra-abdominal and pelvic infections, urinary tract infections (UTI) and neonatal infections (2). The genus Enterococcus is composed of 38 species, the most important of which are Enterococcus faecalis and Enterococcus faecium—both human gastro-intestinal (GI) colonisers. The clinical importance of the genus Enterococcus is directly related to its antibiotic resistance, which contributes to the risk of colonisation and infection. The tremendous progress of medical care in the last hundred years towards more intensive care and invasive medical procedures has undoubtedly contributed to the increased prevalence of these opportunistic pathogens (3).
Over the past twenty years infections due to multi-drug resistant organisms (MDRO) have escalated worldwide, affecting patient morbidity, mortality and healthcare costs. Among these bacteria Enterococcus faecium and Enterococcus faecalis represent opportunistic nosocomial pathogens that have been known to cause infections for decades (4). With ampicillin resistance in E. faecium being almost ubiquitous, treatment of infections caused by this isolate relies heavily on vancomycin (5-7). 
First encountered in 1986, vancomycin resistance in Enterococcus species has increased in prevalence (8), with Ireland having the highest rate of vancomycin resistant Enterococcus (VRE) compared to any other European country. This has become a serious issue for nosocomial infection control, with increased pathogenicity seen in E. faecium due to an expansion of hospital-adapted genetic lineages showing more resistance and virulence traits. A staggering  44.4%  of all E. faecium from bloodstream infections (BSI) in Ireland were resistant to vancomycin in 2016 (9). Resistance to glycopeptides in Enterococcus spp. is mediated by the vancomycin resistance (Van) operon, which may be carried chromosomally or on on a plasmid. This Van operon contains a variable ligase gene, which is central in determining the level of vancomycin resistance – the most commonly identified genes being vanA, vanB and vanC (8).

Typically, vanA-mediated vancomycin resistance is plasmid-borne and is found predominantly in E. faecium. Vancomycin resistance in vanA-bearing isolates is mediated by the group of genes vanR, vanS, vanH, vanA and vanX, which are usually carried on the Tn1546 transposon. The expression of these genes leads to replacement of the C-terminal D-Ala residue with D-Lac during cell wall synthesis, thus modifying the vancomycin-binding target. The transposon is often contained on plasmids, making it easy to transfer among enterococcal strains. Historically, there has been little sequence variation in this gene cluster (10). In recent years, vancomycin sensitive E. faecium with ‘silent’ vanA genotypes have been reported, further supporting the need for genotypic testing (11-15). These so-called vancomycin-variable vanA+ enterococci (VVE) have the ability to switch into vancomycin resistance during therapy through the constitutive expression of the vancomycin resistance cassette thus escaping phenotypic detection. By definition, the term VVE should be restricted to vancomycin-susceptible enterococci containing vanA and capable of reverting to a glycopeptide-resistant phenotype. Accordingly, enterococci containing remnants of the vanA cluster that are not able to revert to a resistant phenotype or enterococci with vanB showing an MIC below the clinical breakpoint are not VVE (11). Due to the majority of the detection of VRE being via phenotypic methods, the overall prevalence for VVE cannot be accounted for, with the possibility of unrestricted transmission of these strains occurring in health care facilities (13). In one case, these VVE isolates have been shown to grow (poorly) on chromogenic VRE agar, such as Brilliance Agar (Oxoid, Canada) – then when tested for vancomycin resistance, demonstrated a vancomycin MIC of

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