Mutations in Ribosomal Protein L3 Are Associated with Oxazolidinone Resistance in Staphylococci of Clinical Origin

被引：105

作者：

Locke, Jeffrey B. ^{[1
]}

Hilgers, Mark ^{[1
]}

Shaw, Karen Joy ^{[1
]}

机构：

[1] Trius Therapeut Inc, San Diego, CA 92121 USA

来源：

ANTIMICROBIAL AGENTS AND CHEMOTHERAPY | 2009年 / 53卷 / 12期

关键词：

IN-VITRO ACTIVITY; PEPTIDYL-TRANSFERASE CENTER; LINEZOLID RESISTANCE; CROSS-RESISTANCE; PRODRUG TR-701; AUREUS; RNA; TIAMULIN; SUSCEPTIBILITY; CHLORAMPHENICOL;

D O I：

10.1128/AAC.01032-09

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Following recent reports of ribosomal protein L3 mutations in laboratory-derived linezolid-resistant (LZDr) Staphylococcus aureus, we investigated whether similar mutations were present in LZDr staphylococci of clinical origin. Sequence analysis of a variety of LZDr isolates revealed two L3 mutations, Delta Ser145 (S. aureus NRS127) and Ala157Arg (Staphylococcus epidermidis 1653059), both occurring proximal to the oxazolidinone binding site in the peptidyl transferase center. The oxazolidinone torezolid maintained a >= 8-fold potency advantage over linezolid for both strains.

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页码：5275 / 5278

页数：4

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