多药耐受
金黄色葡萄球菌
微生物学
抗生素
生物
抗毒素
细菌
病菌
大肠杆菌
毒素
基因
生物膜
遗传学
作者
Brian P. Conlon,Sarah E. Rowe,Autumn Brown Gandt,Austin S. Nuxoll,Niles P. Donegan,Eliza A. Zalis,Gérémy Clair,Joshua Adkins,Ambrose L. Cheung,Kim Lewis
出处
期刊:Nature microbiology
日期:2016-04-18
卷期号:1 (5)
被引量:568
标识
DOI:10.1038/nmicrobiol.2016.51
摘要
Persisters are dormant phenotypic variants of bacterial cells that are tolerant to killing by antibiotics(1). Persisters are associated with chronic infections and antibiotic treatment failure(1-3). In Escherichia coli, toxin-antitoxin modules have been linked to persister formation(4-6). The mechanism of persister formation in Gram-positive bacteria is unknown. Staphylococcus aureus is a major human pathogen, responsible for a variety of chronic and relapsing infections such as osteomyelitis, endocarditis and infections of implanted devices. Deleting toxin-antitoxin modules in S. aureus did not affect the level of persisters. Here, we show that S. aureus persisters are produced due to a stochastic entrance into the stationary phase accompanied by a drop in intracellular adenosine triphosphate. Cells expressing stationary-state markers are present throughout the growth phase, and increase in frequency with cell density. Cell sorting revealed that the expression of stationary markers is associated with a 100-1,000-fold increase in the likelihood of survival to antibiotic challenge. The adenosine triphosphate level of the cell is predictive of bactericidal antibiotic efficacy and explains bacterial tolerance to antibiotics.
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