Vancomycin-resistant enterococci (VRE) initially emerged as a relevant Public Health threat due to the use GS-9973 in the past of the glycopeptide avoparcin as growth promoter in animal feed. Once avoparcin was banned, the persistence of VRE was associated to co-selection of van genes and genes conferring MK0683 purchase resistance to other antibiotics (such as erythromycin) due to the intensive use of other antibiotics, such as tylosin [56]. After the ban of antibiotics as growth promoters in all European

Union countries (July 1999), Aarestrup [57] speculated that occurrence of VRE among pigs would decrease in the following years. In this study, none of the strains was resistant to vancomycin, an antibiotic commonly used for infections caused by multidrug-resistant bacteria, although most of the E. faecalis strains isolated from porcine milk were resistant to erythromycin. All our E. faecalis, E. faecium and E. hirae strains of food animals (porcine and ovine) were resistant to tetracycline, which has been widely used for therapy in food animals in many countries, including Spain; this usage also could have contributed HSP inhibitor clinical trial to the successful persistence of tet genes. A comparison between antibiotic resistance among enterococci isolated from pigs in Sweden, Denmark and Spain showed that tet (L) and tet (S) genes were more frequently found among isolates from Spain [55]. Globally, frequent occurrences of antibiotic-resistant enterococci have

been observed among food animals, and it has been suggested that these animals may be a reservoir of resistant enterococci and resistance genes capable of transferring to humans

through the food chain [58]. Antimicrobial resistance genes appear to spread freely between enterococci from different reservoirs, irrespective of their apparent host association [58]. Therefore, continuous surveillance of antimicrobial resistance in enterococci from humans, animals and foods of animal origin is essential to detect emerging resistance and new infections [26]. As an example, an outbreak of infective mastitis due to E. faecalis was recently reported in Elongation factor 2 kinase an intensive sheep farm in Italy. Forty-five out of the 48 E. faecalis isolates showed the same multi-drug resistance pattern and had a clonal origin. This was the first reported case of ewe’s mastitis caused by E. faecalis[59]. Such strains could arrive to the human food chain through the consumption of cheeses elaborated with raw ewe’s milk. Pets can also be a source of enterococci and enterococcal resistance genes to humans and other animals and vice versa. Recent results suggest that direct and frequent contact with dogs may significantly shape the composition of our microbial communities [60]. The widespread occurrence of ampicillin-resistant clones in dogs is worrying since these animals may spread such clones among humans due to the close relationships that are usually established between dogs and humans [61, 62].