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Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia

Macrolides, lincosamides, and streptogramins (MLS) resistance genes are responsible for resistance to these antibiotics in Staphylococcus infections. The purpose of the study was to analyze the distribution of the MLS resistance genes in community- and hospital-acquired Staphylococcus isolates. The...

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Autores principales: Mišić, Milena, Čukić, Jelena, Vidanović, Dejan, Šekler, Milanko, Matić, Sanja, Vukašinović, Mihailo, Baskić, Dejan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581325/
https://www.ncbi.nlm.nih.gov/pubmed/28894731
http://dx.doi.org/10.3389/fpubh.2017.00200
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author Mišić, Milena
Čukić, Jelena
Vidanović, Dejan
Šekler, Milanko
Matić, Sanja
Vukašinović, Mihailo
Baskić, Dejan
author_facet Mišić, Milena
Čukić, Jelena
Vidanović, Dejan
Šekler, Milanko
Matić, Sanja
Vukašinović, Mihailo
Baskić, Dejan
author_sort Mišić, Milena
collection PubMed
description Macrolides, lincosamides, and streptogramins (MLS) resistance genes are responsible for resistance to these antibiotics in Staphylococcus infections. The purpose of the study was to analyze the distribution of the MLS resistance genes in community- and hospital-acquired Staphylococcus isolates. The MLS resistance phenotypes [constitutive resistance to macrolide–lincosamide–streptogramin B (cMLSb), inducible resistance to macrolide–lincosamide–streptogramin B (iMLSb), resistance to macrolide/macrolide–streptogramin B (M/MSb), and resistance to lincosamide–streptogramin A/streptogramin B (LSa/b)] were determined by double-disc diffusion method. The presence of the MLS resistance genes (ermA, ermB, ermC, msrA/B, lnuA, lnuB, and lsaA) were determined by end-point polymerase chain reaction in 179 isolates of staphylococci collected during 1-year period at the Center for Microbiology of Public Health Institute in Vranje. The most frequent MLS phenotype among staphylococcal isolates, both community-acquired and hospital-acquired, was iMLSb (33.4%). The second most frequent was M/MSb (17.6%) with statistically significantly higher number of hospital-acquired staphylococcal isolates (p < 0.05). MLS resistance was mostly determined by the presence of msrA/B (35.0%) and ermC (20.8%) genes. Examined phenotypes were mostly determined by the presence of one gene, especially by msrA/B (26.3%) and ermC (14.5%), but 15.6% was determined by a combination of two or more genes. M/MSb phenotype was the most frequently encoded by msrA/B (95.6%) gene, LSa/b phenotype by lnuA (56.3%) gene, and iMLSb phenotype by ermC (29.4%) and ermA (25.5%) genes. Although cMLSb phenotype was mostly determined by the presence of ermC (28.9%), combinations of two or more genes have been present too. This pattern was particularly recorded in methicillin-resistant Staphylococcus aureus (MRSA) (58.3%) and methicillin-resistant coagulase-negative staphylococci (MRCNS) (90.9%) isolates with cMLSB phenotype. The msrA/B gene and M/MSb phenotype were statistically significantly higher in hospital-acquired than community-acquired staphylococci strains (p < 0.05). There are no statistically significant differences between staphylococci harboring the rest of MLS resistance genes acquired in community and hospital settings (p > 0.05). The prevalence of iMLSb phenotypes may change over time, so it is necessary to perform periodic survey of MLS resistance phenotypes, particularly where the D-test is not performed routinely.
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spelling pubmed-55813252017-09-11 Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia Mišić, Milena Čukić, Jelena Vidanović, Dejan Šekler, Milanko Matić, Sanja Vukašinović, Mihailo Baskić, Dejan Front Public Health Public Health Macrolides, lincosamides, and streptogramins (MLS) resistance genes are responsible for resistance to these antibiotics in Staphylococcus infections. The purpose of the study was to analyze the distribution of the MLS resistance genes in community- and hospital-acquired Staphylococcus isolates. The MLS resistance phenotypes [constitutive resistance to macrolide–lincosamide–streptogramin B (cMLSb), inducible resistance to macrolide–lincosamide–streptogramin B (iMLSb), resistance to macrolide/macrolide–streptogramin B (M/MSb), and resistance to lincosamide–streptogramin A/streptogramin B (LSa/b)] were determined by double-disc diffusion method. The presence of the MLS resistance genes (ermA, ermB, ermC, msrA/B, lnuA, lnuB, and lsaA) were determined by end-point polymerase chain reaction in 179 isolates of staphylococci collected during 1-year period at the Center for Microbiology of Public Health Institute in Vranje. The most frequent MLS phenotype among staphylococcal isolates, both community-acquired and hospital-acquired, was iMLSb (33.4%). The second most frequent was M/MSb (17.6%) with statistically significantly higher number of hospital-acquired staphylococcal isolates (p < 0.05). MLS resistance was mostly determined by the presence of msrA/B (35.0%) and ermC (20.8%) genes. Examined phenotypes were mostly determined by the presence of one gene, especially by msrA/B (26.3%) and ermC (14.5%), but 15.6% was determined by a combination of two or more genes. M/MSb phenotype was the most frequently encoded by msrA/B (95.6%) gene, LSa/b phenotype by lnuA (56.3%) gene, and iMLSb phenotype by ermC (29.4%) and ermA (25.5%) genes. Although cMLSb phenotype was mostly determined by the presence of ermC (28.9%), combinations of two or more genes have been present too. This pattern was particularly recorded in methicillin-resistant Staphylococcus aureus (MRSA) (58.3%) and methicillin-resistant coagulase-negative staphylococci (MRCNS) (90.9%) isolates with cMLSB phenotype. The msrA/B gene and M/MSb phenotype were statistically significantly higher in hospital-acquired than community-acquired staphylococci strains (p < 0.05). There are no statistically significant differences between staphylococci harboring the rest of MLS resistance genes acquired in community and hospital settings (p > 0.05). The prevalence of iMLSb phenotypes may change over time, so it is necessary to perform periodic survey of MLS resistance phenotypes, particularly where the D-test is not performed routinely. Frontiers Media S.A. 2017-08-28 /pmc/articles/PMC5581325/ /pubmed/28894731 http://dx.doi.org/10.3389/fpubh.2017.00200 Text en Copyright © 2017 Mišić, Čukić, Vidanović, Šekler, Matić, Vukašinović and Baskić. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Public Health
Mišić, Milena
Čukić, Jelena
Vidanović, Dejan
Šekler, Milanko
Matić, Sanja
Vukašinović, Mihailo
Baskić, Dejan
Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title_full Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title_fullStr Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title_full_unstemmed Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title_short Prevalence of Genotypes That Determine Resistance of Staphylococci to Macrolides and Lincosamides in Serbia
title_sort prevalence of genotypes that determine resistance of staphylococci to macrolides and lincosamides in serbia
topic Public Health
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581325/
https://www.ncbi.nlm.nih.gov/pubmed/28894731
http://dx.doi.org/10.3389/fpubh.2017.00200
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