ABSTRACT
Abstract This study was undertaken to investígate the resistance phenotypes to macrolide-lincosamide-streptogramin B (MLSb) antibiotics and their associated genotypes in isolates of Staphylococcus aureus. We analyzed one hundred, consecutive, non-duplicate isolates (methicillin-susceptible MSSA, n = 53 and methicillin-resistant MRSA, n =47) obtained from var-ious clinical samples between July 2012 to December 2013. The resistance profile to MLSb antibiotics was determined by phenotypic methods and the resistance genes were detected by PCR assays. All of the isolates were subjected to pulsed-field gel electrophoresis (SmaI-PFGE). The overall prevalence of resistance to MLSb antibiotics was 38% and the resistance phenotype distribution was as follows: cMLSb, 22%; iMLSB, 10%; MSb, 5% and L, 1%. We detected ermA, ermC, ermB and mrsA/B genes in these resistant isolates. The single ermA gene was commonly observed mainly in those with a cMLSb R phenotype, whereas the combination ermA and ermC was more commonly observed in isolates with inducible expression. The patterns of SmaI-PFGE suggest a great genetic diversity in both MRSA and MSSA resistant to MLSb antibiotics. The results demonstrate the local presence of S. aureus resistant to MLSb antibiotics and its most frequently described responsible genes. Some of these isolates, especially those with the iMLSB phenotype, may be associated with therapeutic failure. Therefore, efforts should be directed to the correct detection of all MLSb resistant isolates using appropriate laboratory tests. PFGE results reveal a wide spread of resistance genes rather than the circulation of S. aureus clones resistant to MLSb antibiotics.
Resumen Los objetivos de este estudio fueron investigar en Staphylococcus aureus la presencia de fenotipos resistentes a los antibióticos macrólidos, lincosamidas y estreptograminas tipoB (MLSb) y conocer sus genotipos responsables. Analizamos 100 aislamientos consecutivos, no duplicados (53 sensibles a meticilina [MSSA] y 47 resistentes a meticilina [MRSA]), obtenidos entre 2012 y 2013 a partir de diferentes muestras clínicas. El perfil de resistencia a los antibióticos MLSb fue determinado por métodos fenotípicos y los genes de resistencia se detectaron por PCR. Todos los aislamientos fueron comparados por SmaI-PFGE. La prevalencia global de resistencia a los antibióticos MLSB fue del 38% y la distribución de los fenotipos de resistencia fue la siguiente: cMLSB, 22%; iMLSB, 10%; MSB, 5%; L, 1%. Se detectaron los genes ermA, ermC y mrsA/B en los aislamientos resistentes. El gen ermA se observó, sobre todo, en aislamientos con fenotipo resistente constitutivo R (cMLSB), mientras que la combinación ermA y ermC se detectó principalmente en aislamientos con resistencia inducible (iMLSB). Los patrones de Smal-PFGE sugieren una gran diversidad genética en los aislamientos resistentes a los antibióticos MLSb, tanto MRSA como MSSA. Los resultados demuestran la presencia local de S. aureus resistentes a los antibióticos MLSB y de sus genes responsables más frecuentemente descritos. Estos cultivos, especialmente aquellos con fenotipo resistente iMLSB, pueden asociarse con fallas terapéuticas. Por lo tanto, los esfuerzos deben dirigirse a la correcta detección de todos los cultivos resistentes a MLSB utilizando pruebas de laboratorio adecuadas. Los resultados de Smal-PFGE sugieren una amplia diseminación de genes de resistencia, más que la circulación de clones resistentes a los antibióticos MLSB.
Subject(s)
Humans , Staphylococcal Infections , Drug Resistance, Multiple, Bacterial , Methicillin-Resistant Staphylococcus aureus , Phenotype , Staphylococcal Infections/epidemiology , Staphylococcus aureus/genetics , Uruguay , Microbial Sensitivity Tests , Macrolides/pharmacology , Streptogramin B/pharmacology , Drug Resistance, Multiple, Bacterial/genetics , Methicillin-Resistant Staphylococcus aureus/genetics , Lincosamides/pharmacology , Tertiary Care Centers , Genotype , Hospitals, Public , Anti-Bacterial Agents/pharmacologyABSTRACT
BACKGROUND: Macrolide resistance in beta-hemolytic streptococci has increased during the 1990s, and the proportion of MLS (Macrolide-lincosamide-streptogramin) resistance phenotypes and genotypes of beta-hemolytic streptococci are quite different by geographical variation and study period. The aim of the present study was to determine the distribution of MLS resistance phenotypes and genotypes in beta-hemolytic streptococci isolated from Wonju Christian Hospital. METHODS: The minimal inhibitory concentrations of erythromycin and clindamycin of 426 beta- hemolytic streptococci isolated from clinical specimens between 1990 to 1999 were determined by agar dilution method. MLS resistance phenotypes were determined by double disk diffusion method using erythromycin and clindamycin disk, and genotypes were determined by polymerase chain reaction (PCR). The PCR primers for erm(A), erm(B), erm(C), erm(TR), and mef(A) were used in these study. RESULTS: The proportion of MLS resistance phenotypes of 80 erythromycin-resistant beta-hemolytic streptococci were 60.0% for constitutive phenotype, 23.8% for M phenotype, and 16.2% for inducible phenotype. The proportion of three MLS resistance phenotypes of group A streptococci were nearly equal. About three-fourths of group B streptococci had the constitutive phenotypes, whereas three-fourths (75%) of group G streptococci had the M phenotypes. All MLS resistant strains carried the erm(B) genes in constitutive phenotypes, erm(TR) genes in inducible phenotypes, and mef(A) genes in M phenotypes, respectively. CONCLUSIONS: Mechanisms and phenotype proportions of MLS resistance are different by species in beta-hemolytic streptococci. It is possible that MLS resistance genes have transferred among beta- hemolytic streptococci because the erythromycin resistance genes are the same in beta-hemolytic streptococci.