The application of the full assay described by Zhang et al. [12] confirmed these results. The 4mecA +strains that could not be typed on the basis of theirccrB restriction pattern remained Selleckchem Buparlisib non typeable with the full Zhang et al. assay. Discussion S. epidermidisis a normal inhabitant of the skin and mucosal surfaces in healthy hosts and its ubiquitous prevalence as a commensal species makes difficult for a clinician to decide if an isolate represents the etiological agent or a culture contamination [11]. Therefore, isolation of this bacterial species is generally regarded as non-related to a

mastitis case, even when it is the only species present in a milk sample [4]. S. epidermidiswas the dominant or unique staphylococcal species in breast milk of women suffering mastitis, a finding described previously [4], which indicates that this bacterial species could be an etiological agent of human lactational mastitis. Similarly, several studies have shown the implication of this bacterial species as an agent of mastitis in different animal species [13–15]. The genotyping of theS. epidermidisisolates by PFGE revealed a low diversity within this species in the breast milk of women with mastitis, with a mean of 2 different profiles per sample. A lost in the microbial diversity present in milk of women

with mastitis has been previously pointed [4]. Comparison by PFGE dendogram analysis of these

strains with those obtained from breast milk of healthy women showed the existence of two main clusters and, within these two groups, the strains generally IDO inhibitor matched with the origin about (mastitis and healthy women). However, a few strains from healthy women grouped together with the mastitis cluster reflecting a similar genetic background. The fact that their presence in milk of healthy women does not constitute a health problem could indicate that a predisposal host is also need forS. epidermidisto develop an infection [16]. Among theS. epidermidisstrains analyzed, the presence of adhesion-related genes was high independently of the condition of the women from which they were isolated. The presence of genes encoding cell surface proteins may explain, at least partially, the high prevalence ofS. epidermidisin breast milk, mammary areola and ducts of both healthy and mastitis-suffering women. In contrast, the percentage of strains carrying the biofilm-relatedicaoperon was higher in strains from mastitis milk than in that obtained from healthy women. A potential relationship betweenS. epidermidisinfection and the presence of such operon has been reported [8]. In fact, biofilm formation has been described in many cases of staphylococcal mastitis and this is the reason why such property is considered as a potential virulence factor [17,18].