Maria Rosario Amezaga1, Hamish McKenzie. 1. Department of Medical Microbiology, University of Aberdeen School of Medicine, Polwarth Buildings, Foresterhill, Aberdeen AB25 2ZD, UK.
Abstract
OBJECTIVES: To study the molecular mechanisms of erythromycin resistance in beta-haemolytic streptococci of Lancefield groups A, B, C and G. METHODS: Erythromycin-resistant clinical isolates from North East Scotland were collected over 2 years. Resistance phenotypes were determined by disc diffusion and MICs by Etest. Resistance genes mef, msr(D), erm(B) and erm(TR) were identified by PCR and mef and msr(D) were sequenced. RESULTS: Erythromycin resistance prevalence was 1.9% in group A streptococci (31 of 1625), 4.3% in group B (53 of 1233), 3.8% in group C (18 of 479) and 6.2% in group G (64 of 1034). The numbers of resistant isolates available were 26, 42, 9 and 52 in each group respectively. The majority of resistant isolates in groups A (57.7%, 15 of 26), B (88.1%, 37 of 42) and G (90.4%, 47 of 52) were MLS(B). The contribution of M phenotype was significant in groups C (77.8%, 7 of 9) and A (42.3%, 11 of 26). Group A isolates carried mef(A) and group B carried mef(E) exclusively. A mef sequence distinct from mef(A) and mef(E) was identified in group G and was associated with a new msr(D) sequence. These sequence variants appear to be part of a new genetic element that is inserted in the comEC gene. A bimodal distribution of erythromycin MICs was noted in erm(TR) isolates. CONCLUSIONS: The results demonstrate significant differences in the mechanisms of macrolide resistance amongst different Lancefield groups in the same geographical area. New sequences show that resistance mechanisms are still evolving.
OBJECTIVES: To study the molecular mechanisms of erythromycin resistance in beta-haemolytic streptococci of Lancefield groups A, B, C and G. METHODS:Erythromycin-resistant clinical isolates from North East Scotland were collected over 2 years. Resistance phenotypes were determined by disc diffusion and MICs by Etest. Resistance genes mef, msr(D), erm(B) and erm(TR) were identified by PCR and mef and msr(D) were sequenced. RESULTS:Erythromycin resistance prevalence was 1.9% in group A streptococci (31 of 1625), 4.3% in group B (53 of 1233), 3.8% in group C (18 of 479) and 6.2% in group G (64 of 1034). The numbers of resistant isolates available were 26, 42, 9 and 52 in each group respectively. The majority of resistant isolates in groups A (57.7%, 15 of 26), B (88.1%, 37 of 42) and G (90.4%, 47 of 52) were MLS(B). The contribution of M phenotype was significant in groups C (77.8%, 7 of 9) and A (42.3%, 11 of 26). Group A isolates carried mef(A) and group B carried mef(E) exclusively. A mef sequence distinct from mef(A) and mef(E) was identified in group G and was associated with a new msr(D) sequence. These sequence variants appear to be part of a new genetic element that is inserted in the comEC gene. A bimodal distribution of erythromycin MICs was noted in erm(TR) isolates. CONCLUSIONS: The results demonstrate significant differences in the mechanisms of macrolide resistance amongst different Lancefield groups in the same geographical area. New sequences show that resistance mechanisms are still evolving.
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