Molecular mechanisms of fluoroquinolone resistance in Klebsiella.

Yun-Liang Yang, Tsai-Ling Lauderdale, Hsiu-Jung Lo
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引用次数: 7

Abstract

Klebsiella are well-recognized community and nosocomial pathogens responsible for septicemias, urinary tract infections, pneumonia, and soft tissue infections. The emergence of multi-drug resistant Klebsiella is becoming a global concern. Since fluoroquinolones are excellent antibiotics for clinical therapy of complicated infections, their consumptions have increased rapidly. Coincidental with the increased usage of fluoroquinolones, the incidences of drug resistance have increased, which highlights the need for understanding the molecular mechanisms of fluoroquinolone resistance. Alterations in targets and reduction of intracellular drug accumulation are two major mechanisms involved in fluoroquinolone resistance. This review focuses on the mechanisms of action of fluoroquinolones and molecular mechanisms of drug resistance, including known and proposed ones, and the discussion on clinical impact of multi-drug resistance in Klebsiella.

克雷伯菌耐氟喹诺酮类药物的分子机制。
克雷伯氏菌是公认的社区和医院病原体,可导致败血症、尿路感染、肺炎和软组织感染。耐多药克雷伯菌的出现正在成为全球关注的问题。由于氟喹诺酮类药物是临床治疗复杂感染的优良抗生素,其用量迅速增加。随着氟喹诺酮类药物使用的增加,耐药的发生率也在增加,这突出表明需要了解氟喹诺酮类药物耐药的分子机制。靶点的改变和细胞内药物积累的减少是氟喹诺酮类药物耐药的两个主要机制。本文综述了氟喹诺酮类药物的作用机制和耐药的分子机制,包括已知的和可能的耐药机制,并对克雷伯菌多重耐药的临床影响进行了讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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