Resistance to these and other antibiotics in pathogenicS. epidermidisisolates has been reported previously [10,19]. The resistance of these strains could be partly due to the increasing use of broad-spectrum antibiotics, which encourage selection of multirresistant strains [11].

Improper antibiotherapy may explain why staphylococcal mastitis frequently becomes a chronic and/or recurrent infection. In this study, the presence ofmecA gene accompanied with resistance to oxacillin (MIC > 2 μg mL-1) was observed in 62% of the strains from mastitis, but only in 33% from the healthy group. ThemecA gene was not detected in four oxacillin-resistant strains. These strains may represent cases of borderline resistance which is characterized by an oxacillin MIC at or just above the susceptibly breakpoint (4 to 8 μg mL-1). In contrast, themecA gene was detected selleck kinase inhibitor in five oxacillin-susceptible strains, a fact that has been previously described [20] and that may be due to gene deletions. Methicillin-resistantStaphylococcus

aureus(MRSA) are being reported with increasing frequency in EPZ5676 the community and they have been called community-acquired (CA)-MRSA, which are associated with skin and soft tissue infection [21] but are also frequently isolated from healthy hosts [22]. Most of themecA+strains used in this study could be ascribed to type IV SCCmec. InS. epidermidis, some studies Farnesyltransferase have reported that SCCmectype IV is generally carried by CA-MRS [23,24] but this type seems to be predominant among clinically relevantS. epidermidisisolates [9]. The fact that theccrB gene was not amplified from fourmecA+strains may be due to the presence of different alleles for this gene [25]. In the last years, a renewed medical and research interest has been focused onS. epidermidissince it has become the most important

cause of nosocomial infections [6]. The complete Lenvatinib research buy Genome analysis of some methicillin-resistantS. aureusandS. epidermidisstrains of human origin have revealed the propensity ofS. aureusto cause fulminant and sometimes life-threatening infections, as opposed to the predisposition ofS. epidermidisfor chronic and recurrent infections [26]. Identification ofS. epidermidisas etiological agents of infection is sometimes hindered by the fact that infections associated with this microorganims are characterized by subtle, non-specific clinical manifestations [5]. Precisely, these characteristics occur in most cases of lactational mastitis. Genome flexibility inS. epidermidismay contribute to the acquisition of some transferable virulence and resistant traits [6,27] and to the evolution of this species from a commensal to a pathogenic microorganism in susceptible hosts [28].