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在Enterobacterales中对tigecycline耐药性的分子机制

Lukasz Korczak¹, Piotr Majewski¹, Dominika Iwaniuk¹

¹Department of Microbiological Diagnostics and Infectious Immunology, Medical University of Bialystok, Bialystok, Poland.

Frontiers in cellular and infection microbiology

|April 24, 2024

概括

抗微生物药物耐药性是一个日益增长的全球威胁,特别是在阴性细菌. 本综述详细介绍了肠道细菌中tigecycline耐药性机制,这对于最后手段治疗至关重要.

科学领域:

微生物学微生物学
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

格拉姆阴性细菌的抗微生物耐药性 (AMR) 是一个重大的公共卫生问题.
作为最后一种抗生素,tigecycline对于治疗由多药耐药 (MDR),广泛耐药 (XDR) 和泛耐药 (PDR) 细菌引起的感染至关重要.
了解耐药性机制至关重要,因为耐卡巴和素等最后手段治疗的病原体的传播越来越大.

研究的目的:

审查和阐明肠道细菌对tigecycline耐药性的分子机制.
提供关于新兴抗生素对最后手段抗生素耐药性所带来的挑战的见解.
突出在全球AMR的背景下研究tigecycline耐药性的重要性.

主要方法:

文献综述侧重于对tigecycline耐药性的分子机制.
对详细介绍肠道细菌耐药性的研究进行分析.
综合了关于排泄,基因和外膜毛孔的信息.

主要成果:

排泄的过度表达是tigecycline耐药性的主要机制,将抗生素驱逐到亚毒水平.
获取特定的基因,如tet基因,有助于tigecycline耐药性.
外膜毛孔的变化也起到了降低对tigecycline敏感性的作用.

结论:

肠道细菌中对tigecycline的耐药性是由明确的分子机制介导的,包括排泄,酶失活和目标修改.
耐药性传播需要持续监测和研究有效的治疗策略.
解决tigecycline耐药性对于全球打击严重细菌感染至关重要.

关键词:

进入细菌体中的细菌.排放的排放.糖基环环林是一种.多药性耐药性 (MDR) 是一种多药性耐药性.这种药物是tigecycline.

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