The epidemiology of Staphylococcus epidermidis in U.S. hospitals remains limited. This study aimed to address the genetic backgrounds of linezolid-susceptible and -resistant S. epidermidis strains (isolated in 2010), including cfr-carrying strains. In addition, the antimicrobial susceptibility profiles and linezolid resistance mechanisms among clonal lineages were assessed. A total of 71 S. epidermidis isolates were selected, and linezolid-resistant strains were screened for cfr and mutations in 23S rRNA, L3, and L4. All isolates were subjected to multilocus sequence typing (MLST), and the results were analyzed by eBURST. Strains showing a G2576 alteration also had M156 (7/7; 100.0%) and/or H146 (6/7; 85.7%) L3 modifications. This study provides an overview of the S. epidermidis clonal distribution and reports higher resistance rates among CC2-I strains. The results show that cfr may be acquired and expressed by both CC2 main subclusters, while 23S rRNA mutations appeared more often within CC2-I strains. Interestingly, these 23S rRNA mutants also had L3 alterations, which may act synergistically or in a compensatory manner to minimize the fitness cost while providing survival advantages under selective pressure.
Staphylococcus epidermidis is ubiquitous in the human skin and mucosal microflora and causes infections in immunocompetent patients when the integrity of the skin barrier is disturbed (23). However, the vast majority of S. epidermidis infections among hospitalized patients have been associated with indwelling medical devices, such as intravascular and intrathecal catheter systems, pacemaker electrodes, urinary tract catheters, and other polymer and metal implants, which are used as vehicles for entering the host (33). It has been demonstrated that the organism possesses great capability for genetic recombination and gene acquisition, including resistance determinants (20). In fact, the rates of methicillin (oxacillin) resistance among S. epidermidis strains currently exceed 70% in many institutions worldwide (1, 7). However, although antimicrobial resistance can compromise therapy, treatment failure has been primarily associated with the species' ability to form biofilms on medical devices, which is a common feature of many nosocomial pathogens (29).Strains of S. epidermidis resistant to antimicrobial agents other than oxacillin (-lactams) have also been reported. In large surveillance studies, the linezolid resistance rates are still low; however, there seems to be a trend toward increased rates (7). S. epidermidis appears to be prone to accumulate linezolid resistance mechanisms, such as mutations in the 23S rRNA and in the ribosomal proteins L3 and L4 (7,10,13,18,19). In addition to alterations in the target site, a more recent linezolid resistance mechanism, the cfr gene, has been increasingly reported in the literature (6,8,30). cfr encodes a methyltransferase that catalyzes the posttranscriptional methylation of nucleotide A2503 in the 23S rRNA (6). This gene was initially detected in a transferab...