JMI Laboratories, North Liberty, Iowa, USA.
Antimicrob Agents Chemother. 2012 Sep;56(9):4656-61. doi: 10.1128/AAC.00279-12. Epub 2012 Jun 11.
The epidemiology of Staphylococcus epidermidis in U.S. hospitals remains limited. This study aimed to address the genetic backgrounds of linezolid-susceptible and -resistant S. epidermidis strains (isolated in 2010), including cfr-carrying strains. In addition, the antimicrobial susceptibility profiles and linezolid resistance mechanisms among clonal lineages were assessed. A total of 71 S. epidermidis isolates were selected, and linezolid-resistant strains were screened for cfr and mutations in 23S rRNA, L3, and L4. All isolates were subjected to multilocus sequence typing (MLST), and the results were analyzed by eBURST. Overall, 27 sequence types (STs) were detected, and ST5 (21.1%) and ST2 (16.9%) predominated. The majority (62/71; 87.3%) of STs belonged to clonal complex 2 (CC2), which was mostly comprised of subclusters CC2-II (41/62; 66.1%) and CC2-I (21/62; 33.9%). Other STs were grouped within CC23 or CC32 or were singletons. CC2-I strains were more likely to display a methicillin (95.2% versus 33.3 to 70.7%), a linezolid (47.6% versus 0.0 to 7.3%), or a multidrug (81.0% versus 33.3 to 36.6%) resistance phenotype. Among linezolid-resistant isolates, cfr was noted only within CC2 strains, and it was detected equally in the CC2-I (3/10; 30.0%) and CC2-II (1/3; 33.3%) subclusters. 23S rRNA mutations (G2576 [seven strains] and C2534 [one strain]) were observed only among CC2-I (8/10; 80.0%) isolates. Strains showing a G2576 alteration also had M156 (7/7; 100.0%) and/or H146 (6/7; 85.7%) L3 modifications. This study provides an overview of the S. epidermidis clonal distribution and reports higher resistance rates among CC2-I strains. The results show that cfr may be acquired and expressed by both CC2 main subclusters, while 23S rRNA mutations appeared more often within CC2-I strains. Interestingly, these 23S rRNA mutants also had L3 alterations, which may act synergistically or in a compensatory manner to minimize the fitness cost while providing survival advantages under selective pressure.
美国医院中表皮葡萄球菌的流行病学仍然有限。本研究旨在探讨利奈唑胺敏感和耐药表皮葡萄球菌(2010 年分离)的遗传背景,包括携带 cfr 的菌株。此外,还评估了克隆谱系中的抗菌药物敏感性谱和利奈唑胺耐药机制。共选择了 71 株表皮葡萄球菌分离株,筛选了利奈唑胺耐药株中 cfr 和 23S rRNA、L3 和 L4 中的突变。所有分离株均进行多位点序列分型(MLST),并通过 eBURST 进行分析。总体而言,检测到 27 种序列类型(ST),ST5(21.1%)和 ST2(16.9%)占主导地位。大多数 ST(71/71;87.3%)属于克隆复合体 2(CC2),其中主要由亚群 CC2-II(41/62;66.1%)和 CC2-I(21/62;33.9%)组成。其他 ST 属于 CC23 或 CC32 或为单克隆。CC2-I 菌株更可能表现出耐甲氧西林(95.2%比 33.3%至 70.7%)、利奈唑胺(47.6%比 0.0%至 7.3%)或多药耐药(81.0%比 33.3%至 36.6%)表型。在耐利奈唑胺的分离株中,仅在 CC2 菌株中发现 cfr,在 CC2-I(3/10;30.0%)和 CC2-II(1/3;33.3%)亚群中检测到的 cfr 数量相等。仅在 CC2-I(8/10;80.0%)分离株中观察到 23S rRNA 突变(G2576[7 株]和 C2534[1 株])。表现出 G2576 改变的菌株也具有 M156(7/7;100.0%)和/或 H146(6/7;85.7%)L3 修饰。本研究概述了表皮葡萄球菌的克隆分布,并报告了 CC2-I 菌株更高的耐药率。结果表明,cfr 可能由 CC2 的两个主要亚群获得和表达,而 23S rRNA 突变在 CC2-I 菌株中更为常见。有趣的是,这些 23S rRNA 突变体也具有 L3 改变,这可能以协同或补偿的方式发挥作用,以在选择性压力下最小化适应性成本,同时提供生存优势。