Molecular typing and characterization of macrolide, lincosamide and streptogramin resistance in Staphylococcus epidermidis strains isolated in a Mexican hospital

Abstract

Staphylococcus epidermidis is a normal commensal of skin that has become a serious clinical problem because of the combination of increased use of intravascular devices and an increasing number of hospitalized immunocompromised patients. In addition, there is a lack of information pertaining to resistance to macrolide, lincosamide and streptogramin type B (MLS B ) in developing countries, including Mexico. The aim of this study was to investigate the incidence of resistance to MLS B antibiotics in isolates of S. epidermidis obtained in the General Hospital of Acapulco in Mexico. Susceptibility to erythromycin, clindamycin and quinupristin-dalfopristin was tested by a diffusion test, and MICs to oxacillin, erythromycin and lincomycin were determined. Differentiation between MLS B phenotypes was performed by a double disc diffusion test. A total of 38 of the 47 strains of S. epidermidis isolated from nosocomial infections were resistant to oxacillin [meticillinresistant S. epidermidis (MRSE)]. The phenotypes obtained were: 18 constitutive MLS B , 3 inducible MLS B , 6 macrolide streptogramin and 4 lincosamide; 7 strains were susceptible to MLS B antibiotics. The genes associated with resistance were detected by PCR. Genotyping showed a predominance of the ermA gene followed by genes ermC and msrA. The frequency of the genes detected varied slightly from results that have been reported in isolates from other countries. Clonal types were identified by PFGE and revealed the dissemination of two major clones of MRSE in the Mexican hospital. This is believed to be the first report in Mexico on the genes associated with the MLS B resistance phenotype in S. epidermidis, in addition to observing a wide distribution of clonal types in the General Hospital of Acapulco, Mexico.

Antibiotic resistance, ability to form biofilm and susceptibility to copper alloys of selected staphylococcal strains isolated from touch surfaces in Polish hospital wards

“…The most frequent phenotypically detected mechanism of resistance to macrolide antibiotics, lincosamides and streptogramins B was the constitutive MLSB mechanism (35.8%), which agrees with the study by Lina [ 31 ] (here, it was 36.6%) and is a little less than Castro-Alarcon’s results [ 32 ] (47%) but different from Lenart-Boroń’s findings (where it was present only in 4% of the strains and where the inducible mechanism was predominant) [ 25 ]. The phenotype of resistance to erythromycin and retained sensitivity to clindamycin (MSB) was confirmed in 17 isolates (17.9%), and for Lenart-Boroń, it was 28% [ 25 ].…”

“…The gene associated with resistance to macrolides that was most often detected in our study was the msr A gene encoding a pump responsible for active efflux of the antibiotic from the cell (29.5% of the strains); the erm B gene, one of the genes encoding a methylase, was present in only 1 strain. Castro-Alarcon had contrasting results in which 32% of strains had the erm A gene [ 32 ]. The differences between the genes detected and the phenotypic detection of mechanisms of resistance may stem from testing only several selected genes – we did not look, e.g., at different variants of the msr gene, mph genes (encoding phosphotransferase), or the flax gene (responsible for resistance to lincosamides).…”

Phenotypic and molecular assessment of antimicrobial resistance profile of airborne Staphylococcus spp. isolated from flats in Kraków

“…The results presented by Lina et al (17) show that among coagulase-negative staphylococci the inducible mechanism was detected in 28.7% of strains, while constitutive one—in 36.6%. On the other hand, Castro-Alarcon et al ( 2011 ) reported that 47% of S. epidermidis strains tested in their study showed constitutive mechanism while inducible one was detected in 8% of strains. They also determined that 16% of strains were characterized by the MS B type of resistance, while 11% showed the resistance to lincosamides.…”

“…Lenart-Boroń et al ( 2016 ) detected erm(B1) (55% of isolates) and mph(A) (9% of isolates) genes, whereas they were not observed in our study. These differences could result from different origin of the analyzed strains, since hospital isolates can acquire various genes conferring antimicrobial resistance much more frequently (Murray 2007 ; Castro-Alarcon et al 2011 ). The isolates analyzed in this study had a maximum of 7 resistance-determining genes at the same time, and some of them did not have any of the searched genes.…”

The prevalence of genotypes that determine resistance to macrolides, lincosamides, and streptogramins B compared with spiramycin susceptibility among erythromycin-resistant Staphylococcus epidermidis

“…However, they can be responsible for several serious infections in immunocompromised patients, particularly those associated with biomaterials (e.g., catheters, prosthetics etc. ), leading to bacteraemia and sepsis ( Ziebuhr et al 2006 , Caesy et al 2007 , Schoenfelder et al 2010 , Castro-Alarcón et al 2011 ). On the other hand, as a natural part of the microflora, drug resistant strains may be selected during antibiotic therapy, which is a potential source of the resistance genes for pathogenic strains, e.g., Staphylococcus aureus ( Reyes et al 2007 , Otto 2013 , Vitali et al 2014 ).…”