Molecular epidemiology of coagulase-negative bloodstream isolates: detection of Staphylococcus epidermidis ST2, ST7 and linezolid-resistant ST23

Abstract

The mechanisms contributing to persistence of coagulase-negative staphylococci are diverse; to better understanding of their dynamics, the characterization of nosocomial isolates is needed. Our aim was to characterize phenotypic and molecular characteristics of Staphylococcus epidermidis and Staphylococcus haemolyticus human blood isolates from two tertiary care hospitals in Mexico, the Hospital Universitario in Monterrey and the Hospital Civil in Guadalajara. Antimicrobial susceptibility was determined. Biofilm formation was assessed by crystal violet staining. Detection of the ica operon and Staphylococcal Cassette Chromosome mec typing were performed by PCR. Clonal relatedness was determined by Pulsed-fiel gel electrophoresis and Multi locus sequence typing. Methicillin-resistance was 85.5% and 93.2% for S. epidermidis and S. haemolyticus, respectively. Both species showed resistance >70% to norfloxacin, clindamycin, levofloxacin, trimethoprim/sulfamethoxazole, and erythromycin. Three S. epidermidis and two S. haemolyticus isolates were linezolid-resistant (one isolate of each species was cfr+). Most isolates of both species were strong biofilm producers (92.8% of S. epidermidis and 72.9% of S. haemolyticus). The ica operon was amplified in 36 (43.4%) S. epidermidis isolates. SCCmec type IV was found in 47.2% of the S. epidermidis isolates and SCCmec type V in 14.5% of S. haemolyticus isolates. No clonal relatedness was found in either species. Resistance to clindamycin, levofloxacin, erythromycin, oxacillin, and cefoxitin was associated with biofilm production for both species (p<0.05). A G2576T mutation in 23S rRNA gene was detected in an S. haemolyticus linezolid-resistant isolate. All linezolid-resistant S. epidermidis isolates belonged to ST23; isolate with SCCmec type IV belonged to ST7, and isolate with SCCmec type III belonged to ST2. This is the first report of ST7 in Mexico. There was a high genetic diversity in both species, though both species shared characteristics that may contibute to virulence.

Emergence of Staphylococcus epidermidis Clinical Isolates with Resistance to Both Mupirocin and Fusidic Acid

“…The monitor for presence of FA resistance genes among S. epidermidis should be helpful for preventing the dissemination of fusidic acid resis- clone. ST23 was found among linezolid-resistant S. epidermidis isolates (32,33). In the present study, ST23 was identified in two S. epidermidis isolates with resistance to both mupirocin and FA.…”

Methicillin resistance and virulence genes in invasive and nasal Staphylococcus epidermidis isolates from neonates

“…However, the high frequency of the SCC mec IV in clinical isolates of S. epidermidis was already observed previously [47–49], demonstrating that this SCC mec type has become a common occurrence among hospital isolates. In addition, it was observed in our study that the ccr2 complex that comprises the SCC mec type IV was also associated with BSI isolates.…”

Peer Review #3 of "Genomic diversity of prevalent Staphylococcus epidermidis multidrug-resistant strains isolated from a Children’s Hospital in México City in an eight-years survey (v0.4)"

“…Multidrug resistance is a significant concern in most health care settings worldwide because of the difficulties associated with clinical treatment and the potential of dissemination. It has been reported that the prevalent SE clonal lineages ST5, ST12, and ST23 often display high resistance toward most of the antibiotic classes (Martinez-Melendez et al 2016;Widerstrom et al 2012). Furthermore, there is evidence of increasing of rifampicin resistance over time in clinical SE isolates that belong to ST2 and ST23 from the USA, Australia, and some European countries (Lee et al 2018).…”

“…Furthermore, there is evidence of increasing of rifampicin resistance over time in clinical SE isolates that belong to ST2 and ST23 from the USA, Australia, and some European countries (Lee et al 2018). Mutations in the rpoB gene conferring rifampicin resistance have emerged independently, suggesting the view that a limited number, well adapted multi-resistant clonal SE lineages, prevail in clinical settings (Lee et al 2018;Martinez-Melendez et al 2016). Reports of the profiles of antibiotic multi-resistance changes over time are scarce (Lee et al 2018).…”