A liaF Codon Deletion Abolishes Daptomycin Bactericidal Activity against Vancomycin-Resistant Enterococcus faecalis

被引:42
作者
Munita, Jose M. [1 ,2 ]
Tran, Truc T. [1 ,5 ]
Diaz, Lorena [1 ,4 ]
Panesso, Diana [1 ,4 ]
Reyes, Jinnethe [1 ,4 ]
Murray, Barbara E. [3 ,6 ,7 ]
Arias, Cesar A. [1 ,3 ,4 ]
机构
[1] Univ Texas Med Sch Houston, Lab Antimicrobial Res, Houston, TX USA
[2] Univ Desarrollo, Sch Med, Clin Alemana, Clin Alemana Santiago, Santiago, Chile
[3] Ctr Study Emerging & Reemerging Pathogens, Div Infect Dis, Dept Internal Med, Houston, TX USA
[4] Univ El Bosque, Mol Genet & Antimicrobial Resistance Unit, Bogota, Colombia
[5] Univ Houston, Coll Pharm, Houston, TX 77030 USA
[6] Univ Texas Med Sch Houston, Lab Enterococcal Res, Houston, TX USA
[7] Univ Texas Med Sch Houston, Dept Microbiol & Mol Genet, Houston, TX USA
关键词
FAECIUM; ENDOCARDITIS; FAILURE;
D O I
10.1128/AAC.00021-13
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The genetic bases for antibiotic tolerance are obscure. Daptomycin (DAP) is a lipopeptide antibiotic with bactericidal activity against enterococci. Using time-kill assays, we provide evidence for the first time that a deletion of isoleucine in position 177 of LiaF, a member of the three-component regulatory system LiaFSR involved in the cell envelope response to antimicrobials, is directly responsible for a DAP-tolerant phenotype and is likely to negatively affect response to DAP therapy.
引用
收藏
页码:2831 / 2833
页数:3
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