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[喹诺酮耐药性产生的机制]

[Mechanisms for the development of quinolone resistance].

作者信息

Kojima M

机构信息

Department of Pharmacy, Mie University Hospital, School of Medicine.

出版信息

Nihon Rinsho. 1997 May;55(5):1252-60.

PMID:9155183
Abstract

New fluoroquinolones have potent and broad antimicrobial activity and spectra, respectively, against gram-positive and -negative bacteria including P. aeruginosa. As a result of their frequent use, bacterial resistance to the quinolones has gradually developed and limited their therapeutic efficacy in infections, especially, with P. aeruginosa, S. pneumoniae, S. aureus (especially MRSA), and N. gonorrhoeae. Bacterial resistance to the quinolones probably results from : 1) mutations with chromosomal genes of DNA gyrase or DNA topoisomerase in E. coli and S. aureus, 2) decreased permeability of the cell envelope through OmpF, porin-forming protein, in gram-negative bacteria, and 3) activation of active efflux-mediated permeability through the cell membrane protein, either NorA in S. aureus or Opr in P. aeruginosa. Proper use of the quinolones is also proposed to prevent emergence of the bacterial resistance.

摘要

新型氟喹诺酮类药物分别对包括铜绿假单胞菌在内的革兰氏阳性菌和阴性菌具有强大且广泛的抗菌活性和抗菌谱。由于它们的频繁使用,细菌对喹诺酮类药物的耐药性逐渐产生,限制了它们在感染治疗中的疗效,尤其是在治疗铜绿假单胞菌、肺炎链球菌、金黄色葡萄球菌(尤其是耐甲氧西林金黄色葡萄球菌)和淋病奈瑟菌感染时。细菌对喹诺酮类药物的耐药性可能源于:1)大肠杆菌和金黄色葡萄球菌中DNA回旋酶或DNA拓扑异构酶的染色体基因突变;2)革兰氏阴性菌中通过孔蛋白形成蛋白OmpF导致细胞包膜通透性降低;3)通过细胞膜蛋白(金黄色葡萄球菌中的NorA或铜绿假单胞菌中的Opr)激活主动外排介导的通透性。还建议合理使用喹诺酮类药物以防止细菌耐药性的出现。

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