Resistance determinants and clonal diversity in group A streptococci collected during a period of increasing macrolide resistance
Resistance determinants and clonal diversity in group A streptococci collected during a period of increasing macrolide resistance
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DOI：
10.1128/aac.46.6.1816-1822.2002
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发表时间：
2002-06-01
影响因子：
4.9
通讯作者：
Rossolini, GM
中科院分区：
文献类型：
--
作者：
Cresti, S;Lattanzi, M;Rossolini, GM
从意大利中部地区连续6年(1992~1997年)收集299株无重复的化脓性链球菌临床分离株，研究其对大环内酯类和林可酰胺类药物的敏感性。在此期间，大环内酯类药物耐药率稳步上升(从1992年的9%上升到1997年的53%；P<；0.001)。这一增加是由大环内酯类-林科酰胺-链球菌素B耐药表型的菌株引起的，这些菌株主要携带erm(B)但也携带erm(Tr)基因，这些基因在前2年没有被检测到，但在接下来的4年中随着患病率的增加(分别为8，5，26和37%)而被检测到。在同一时期，携带mcf(A)决定基因的大环内酯耐药菌株的流行率没有显著变化；平均为13%，不同年份的比率波动不大，没有明确的趋势。分子分型结果表明，感病菌株和抗病菌株之间存在明显的克隆多样性，抗性基因的遗传环境具有明显的异质性。对与耐药表型和基因类型相关的克隆多样性的分析表明，大环内酯类抗生素耐药率的增加是由于不同机制的复杂相互作用所致，相关的贡献是携带erm(B)基因的遗传元件在循环链球菌种群中的“流行病”传播。
Susceptibility to macrolides and lincosamides was investigated with 299 consecutive nonduplicate Streptococcus pyogenes clinical isolates collected over a 6-year period (1992 to 1997) from an area of central Italy. During this period, macrolide resistance rates steadily increased (from 9% in 1992 to 53% in 1997; P < 0.001). The increase was caused by isolates with a macrolide-lincosamide-streptogramin B resistance phenotype, carrying mostly erm(B) but also erm(TR) genes, that were not detected in the first 2 years and were detected with increasing prevalence (8, 5, 26, and 37%, respectively) during the following 4 years. During the same period, the prevalence of isolates with a macrolide resistance phenotype, carrying mcf(A) determinants, did not vary significantly; on average it was 13%, with modest rate fluctuations in different years and no definite trend. Molecular typing revealed a remarkable clonal diversity among susceptible and resistant isolates and a notable heterogeneity of the genetic environment of the resistance genes. The analysis of clonal diversity in relation with resistance phenotypes and genotypes revealed that increased macrolide resistance rates were due to a complex interplay of different mechanisms, with a relevant contribution played by, an "epidemic" spread of genetic elements carrying the erm(B) gene among the circulating streptococcal population.