**3. Conclusions**

The massive use of glycopeptides (vancomycin and teicoplanin) and nonglycopeptide agents such as extended-spectrum cephalosporins in clinical settings have been implicated in the emergence of VREfm. Delayed effective antimicrobial therapy more than 48 h after the beginning of VRE bacteremia is associated with higher mortality rates.

The core genes bring a phylogenomic reconstruction of the *E. faecium* population structure; the main contribution of accessory genes includes the adaptation of this species to nosocomial environments. It was observed that the plasmid component drives host specificity, while their whole genome and chromosome share a common evolutionary history.

The clinical isolates' mobilome are quite different from the other hosts. In VREfm the plasmid component of the pan-genome plays an important role in adaptation and its emergence as a nosocomial pathogen.
