在临床Staphylococcus aureus分离物中发现了一种与tigecycline耐药性相关的mepR突变
Hongjie Xing1, Likuan Zhang1, Chenglong Li1
1College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, P. R. China.
The Journal of antimicrobial chemotherapy
|February 6, 2025
概括
一种新的mepR变体 (mepRD) 通过增加mepA基因表达来间接赋予Staphylococcus aureus的tigecycline耐药性. 这一发现对于了解临床隔离物中的抗菌素耐药性机制至关重要.
科学领域:
- 微生物学 微生物学
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- 提格环素是治疗多抗药性细菌感染的关键抗生素.
- 了解耐药机制对于有效的抗微生物药物治疗至关重要.
- 黄金葡萄球菌 (Staphylococcus aureus) 是一个具有显著的人类病原体,其抗性越来越强.
研究的目的:
- 在临床中识别和描述mepR变异金黄色葡萄球菌分离物.
- 阐明mepR变异在tigecycline耐药性中的功能作用.
- 研究mepR和mepA在赋予抗性的相互作用.
主要方法:
- 全基因组测序和爆发对齐以识别mepR和mepA变异.
- 删除和补充分析,以评估变异对tigecycline敏感性的影响.
- 用RT-qPCR来确定基因表达水平.
- 抗微生物敏感性测试以确定最小抑制度 (MIC).
主要成果:
- 一种新的mepR变体 (mepRD) 和一种mepA变体 (mepAD) 在一种对tigecycline耐药的金黄色细菌分离物中被发现.
- 单独删除mepA并没有影响tigecycline MIC.
- 同时表达的mepRD和mepAD导致tigecycline MIC增加了4倍.
- mepRD显著上调了mepAD的表达 (增加了6倍).
结论:
- 一种mepR变种 (mepRD) 间接导致tigecycline耐药性.
- 这种抗性是由mepR变体增加mepA表达的能力介导的.
- 这些发现突出了临床S. aureus中tigecycline耐药性的新机制.
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