## 1 Introduction  
The increasing incidence of health care-associated infections (HAI) has been attributed mainly to a group of six pathogenic germs, characterized by multidrug resistance (MDR) and virulence and known by the name ESKAPE: _Enterococcus ficeium_, _Staphylococcus aureus_, _Klebsiella pneumoniae_, _Acinetobacter buannannili_, _Pseudomonas aeruginosa_, and _Enterobacter_ spp. [1]. In the last 20 years, the incidence of enterococcal infections has increased. This pathogen has been reported the second most common pathogen associated with HAI, mainly in catheter-associated urinary infections and central-line associated bloodstream infections, both in Europe and USA [2]. Vancomycin-resistant enterococci (VRE) colonize the gastrointestinal tract and are frequently associated with _Clostridioides difficile_ infection or colonization, implying interactions with the metabolic pathways [3; 4; 5]. Previous studies have identified several risk factors for VRE colonization, such as advanced age; severe underlying disease; inter-hospital transfer; home health care; prolonged hospitalization; central venous catheterization; hematological malignancies; solid organ allograft; chronic hemodialysis; exposure to antibiotics, multiple antibiotics, or high-risk antibiotics (vancomycin, third-generation cephalosporporins, metronidazolezo); and longer duration of antibiotic exposure [6; 7; 8; 9]. The increase in antibiotic resistance among enterococci, especially to vancomycin, has developed due to the selective pressure of antibiotics exposure, either by genetic mutation or horizontal gene transfer [2; 10]. The increasing minimum inhibitory concentration (MIC) and slow tolerance to the \(\beta\)-lactams are genetically coded, but other acquired resistance mechanisms are also used against this antibiotic group, including plasmid production and transfer, antibiotic inactivation by \(\beta\)-lactamase, and point mutations in genes [11]. The MIC for penicillins is usually 2-8 \(\mu\)g/mL for _E. faecalis_ and 8-16 \(\mu\)g/mL for _E. facecium_ and is much higher than the MIC for other related Gram-positive bacteria [12]. Intrinsic resistance to aminoglycos was attributable to enterococci, due to natural cell wall impermeability, while other resistance mechanisms include the plasmid transfer that codes the enzymes inactivating the antibiotic and the occurrence of point mutations in the ribosome [11]. Acquired resistance to glycopeptides (vancomycin), macrolides, tetracyclines, linezolid, and chloramphenicol exists. Enterococci resistance to limcosamides and streptograms is acquired by genes coding a new ion pump, antibiotic inactivation by acetylation, or interference with the binding site on the 50S ribosome. Alteration of the ribosomal binding site is also induced by the acquired gene _cf_, that is related to linezolid resistance [11; 13]. The development of vancomycin resistance is connected to the synthesis of the modified precursors of peptidoglycan that give rise to a cluster of 11 genes that confer VRE. There are described two clusters of genes, van A, B, D, F, I, M and van C, E, G, L, N, depending on the ending sequence of the peptidoglycan precursors [14]. In practice, there are two main phenotypes of glycopeptide resistance. The first one is VanA, with a high level of resistance to vancomycin and a variable level of resistance to teicoplanin, and the second is VanB, with a variable level of resistance, mainly to vancomycin [2]. The reported nosocomial VRE enterococcal isolates range from 19.1 to 25% of the total entercococcal isolates; they are related to increased morbidity and mortality rates in cases of enterococcal bacteremia, with longer hospitalization and increased in-hospital health care costs, compared with vancomycin-susceptible enterococci [15; 16; 17; 18; 19; 20; 21; 22; 23; 24; 25]. HAI are mainly caused by two species: _E. facecium_ (85-90%) and _E. faecalis_ (5-10%) [26]. Most VRE are strains of _E. facecium_. Characteristic of both _E. facecium_ and _E.