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在实验室中对Mycobacterium abscessus中对Linezolid的耐药性的表征

Dereje A Negatu^1,2, Wassihun Wedajo Aragaw¹, Véronique Dartois^1,3

¹Center for Discovery and Innovation, Hackensack Meridian Health, Nutley, New Jersey, USA.

Microbiology spectrum

|July 17, 2023

概括

在Mycobacterium abscessus中,高水平的linezolid耐药性源于核糖体突变,而低水平的耐药性则涉及药物排泄. 核糖体突变意外地赋予了对其他抗生素的交叉耐药性,揭示了新的多药耐药性机制.

科学领域:

微生物学微生物学
分子生物学分子生物学
抗微生物耐药性抗微生物耐药性

背景情况:

利尼佐利德是治疗Mycobacterium的肺部感染的关键抗生素.
许多M. abscessus菌株对linezolid的敏感性或耐药性较差.
在M. abscessus中,非核糖体线类抗性背后的机制在很大程度上是未知的.

研究的目的:

为了研究Mycobacterium abscessus.linezolid耐药性发展的机制.
识别与高水平和低水平线化物耐药性相关的遗传突变.
为了探索被识别的突变所赋予的潜在的交叉抵抗模式.

主要方法:

在实验室中选择了对线化物耐药的Mycobacterium abscessus突变菌.
基因组分析以确定23SrRNA,核糖体蛋白L3和调节基因中的突变.
现型测试用于评估抗生素敏感性和交叉耐药性.

主要成果:

高水平的linezolid耐药性与23SrRNA或核糖体蛋白L3的突变有关,发生在低频率.
低水平的线化物耐药性与转录调节器MAB_4384的功能丧失突变有关,影响MmpL5-MmpS5药物排泄.
一个rRNA突变的子集赋予了对多种无关抗生素的交叉耐药性,表明了一个新的多药耐药性机制.

结论:

在M. abscessus中,线化物耐药性可以来自基于标 (核糖体) 或非基于标 (药物排放) 的机制.
鉴定药物外流作为抗药机制,为临床linezolid耐药性提供了洞察力.
通过核糖体突变调解的交叉耐药性的发现突显出一个重要的,以前未被识别的多药耐药性途径.

关键词:

在MAB_4384中,我们可以看到MAB_4384.在MmpL5-MmpS5中使用MmpL5-MmpS5.在NTM中,NTM是NTM.这就是TETR的意思.交叉电阻交叉电阻交叉电阻没有结核的真菌菌.一个Oxazolidinones是一个Oxazolidinones.rplCC 的时间.这是一个很棒的时刻.

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