**1. Introduction**

*Enterococcus faecium* is a main bacterial agent of healthcare-associated infections in immunocompromised as well as severely ill patients, with a worldwide distribution [1, 2].

In 1988, vancomycin-resistant *E. faecium* (VREfm) was reported for the first time. Along the 1990s, a fast increase of infectious diseases due to this bacterium was detected in the United Kingdom hospitals, linking its emergence with the employment of the glycopeptide avoparcin in animal husbandry for food industry. In addition, at U.S hospitals it was observed the emergence of VREfm, but with not proved association to the use of avoparcin in animals [3–5].

The World Health Organization's global priority pathogens list of antibioticresistant bacteria has categorized VREfm as of high priority. For infectious diseases produced by VREfm, it has been reported that the therapeutic options are more limited, altogether with higher mortality rates and financial costs for the Health system when compared with vancomycin-susceptible enterococci [6, 7].

Food chain can be considered as one possible way of VREfm spread or for the transfer of its antimicrobial resistance genes to humans, as it has been reported for cattle, pork and poultry meat [5, 8].

In the European Union, despite the avoparcin ban 18 years ago, VREfm circulation in the environment has continued. A likely cause of vancomycin-resistance

plasmid genes persistence is the co-selection of other antimicrobials used in animals, such as macrolides or narasin, as it has been suggested by the presence of *ermB* type transporter genes (macrolide-lincosamide-streptogramin B resistance), as well as ABC type transporter genes and the presence of a toxin/anti-toxin system. Other possibilities which can relate with VREfm spread is their persistence in food farms, slaughterhouses or their environments due to poor hygienic conditions or through avian transmission [9–11].

It is important to highlight that, enterococci, as part of human and animal intestinal microbiota, are able to acquire resistance genes from other commensal bacteria, which can be spread as well to other pathogenic bacteria [12, 13].

Evolution of *E. faecium* from intestinal commensal bacteria to opportunistic pathogen is a complex and sequential process, in which seem to have been involved different factors, such as resistance and virulence determinants acquisition and persistence. Their expression is assumed to give an adaptive advantage since these factors facilitate the colonization of different epithelial cells (urinary, oral or intestinal), and at the same time, the bacterial adhesion to a wide variety of extracellular matrix proteins.
