Navigating fluoroquinolone resistance in Gram-negative bacteria: a comprehensive evaluation.

IF 3.7 Q2 INFECTIOUS DISEASES
JAC-Antimicrobial Resistance Pub Date : 2024-08-14 eCollection Date: 2024-08-01 DOI:10.1093/jacamr/dlae127
Linda Kherroubi, Joanna Bacon, Khondaker Miraz Rahman
{"title":"Navigating fluoroquinolone resistance in Gram-negative bacteria: a comprehensive evaluation.","authors":"Linda Kherroubi, Joanna Bacon, Khondaker Miraz Rahman","doi":"10.1093/jacamr/dlae127","DOIUrl":null,"url":null,"abstract":"<p><p>Since the introduction of quinolone and fluoroquinolone antibiotics to treat bacterial infections in the 1960s, there has been a pronounced increase in the number of bacterial species that have developed resistance to fluoroquinolone treatment. In 2017, the World Health Organization established a priority list of the most critical Gram-negative resistant pathogens. These included <i>Klebsiella pneumoniae</i>, <i>Acinetobacter baumannii</i>, <i>Pseudomonas aeruginosa</i>, and <i>Escherichia coli</i>. In the last three decades, investigations into the mechanisms of fluoroquinolone resistance have revealed that mutations in the target enzymes of fluoroquinolones, DNA gyrase or topoisomerase IV, are the most prevalent mechanism conferring high levels of resistance. Alterations to porins and efflux pumps that facilitate fluoroquinolone permeation and extrusion across the bacterial cell membrane also contribute to the development of resistance. However, there is a growing observation of novel mutants with newer generations of fluoroquinolones, highlighting the need for novel treatments. Currently, steady progress has been made in the development of novel antimicrobial agents that target DNA gyrase or topoisomerase IV through different avenues than current fluoroquinolones to prevent target-mediated resistance. Therefore, an updated review of the current understanding of fluoroquinolone resistance within the literature is imperative to aid in future investigations.</p>","PeriodicalId":14594,"journal":{"name":"JAC-Antimicrobial Resistance","volume":null,"pages":null},"PeriodicalIF":3.7000,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11323783/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JAC-Antimicrobial Resistance","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/jacamr/dlae127","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
引用次数: 0

Abstract

Since the introduction of quinolone and fluoroquinolone antibiotics to treat bacterial infections in the 1960s, there has been a pronounced increase in the number of bacterial species that have developed resistance to fluoroquinolone treatment. In 2017, the World Health Organization established a priority list of the most critical Gram-negative resistant pathogens. These included Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Escherichia coli. In the last three decades, investigations into the mechanisms of fluoroquinolone resistance have revealed that mutations in the target enzymes of fluoroquinolones, DNA gyrase or topoisomerase IV, are the most prevalent mechanism conferring high levels of resistance. Alterations to porins and efflux pumps that facilitate fluoroquinolone permeation and extrusion across the bacterial cell membrane also contribute to the development of resistance. However, there is a growing observation of novel mutants with newer generations of fluoroquinolones, highlighting the need for novel treatments. Currently, steady progress has been made in the development of novel antimicrobial agents that target DNA gyrase or topoisomerase IV through different avenues than current fluoroquinolones to prevent target-mediated resistance. Therefore, an updated review of the current understanding of fluoroquinolone resistance within the literature is imperative to aid in future investigations.

引导革兰氏阴性菌对氟喹诺酮类药物产生耐药性:全面评估。
自 20 世纪 60 年代引入喹诺酮类和氟喹诺酮类抗生素治疗细菌感染以来,对氟喹诺酮治疗产生耐药性的细菌种类明显增多。2017 年,世界卫生组织制定了一份最关键的革兰氏阴性耐药病原体优先名单。其中包括肺炎克雷伯菌、鲍曼不动杆菌、铜绿假单胞菌和大肠埃希菌。在过去 30 年中,对氟喹诺酮类药物耐药性机制的研究表明,氟喹诺酮类药物的靶酶 DNA 回旋酶或拓扑异构酶 IV 发生突变是产生高水平耐药性的最普遍机制。促进氟喹诺酮渗透和挤出细菌细胞膜的孔蛋白和外排泵的改变也会导致耐药性的产生。然而,在新一代氟喹诺酮类药物中发现的新型突变体越来越多,这凸显了对新型疗法的需求。目前,针对 DNA 回旋酶或拓扑异构酶 IV 的新型抗菌剂的开发取得了稳步进展,这些抗菌剂通过与现有氟喹诺酮类药物不同的途径来防止靶向介导的耐药性。因此,当务之急是对文献中关于氟喹诺酮类药物耐药性的现有认识进行最新回顾,以帮助未来的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
5.30
自引率
0.00%
发文量
0
审稿时长
16 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信