Distribution of macrolide, lincosamide, streptogramin, ketolide and oxazolidinone (MLSKO) resistance genes in Gram-negative bacteria.

Marilyn C Roberts
{"title":"Distribution of macrolide, lincosamide, streptogramin, ketolide and oxazolidinone (MLSKO) resistance genes in Gram-negative bacteria.","authors":"Marilyn C Roberts","doi":"10.2174/1568005043340678","DOIUrl":null,"url":null,"abstract":"<p><p>A number of different mechanisms of macrolide resistance have been described in Gram-negative bacteria. These include 16 acquired genes (esterases, phosphorylases, rRNA methylases, and effluxes) and include those thought to be unique to Gram-negative bacteria (both esterases and two of the phosphorylases) and those shared with Gram-positive bacteria (one phosphorylase) and those primarily of Gram-positive origin (rRNA methylases and efflux genes). In addition, mutations, which modify the 23S rRNA, ribosomal proteins L4 and/or L22, and/or changes in expression of innate efflux systems which occur by missense, deletion and/or insertion events have been described in five Gram-negative groups, while an innate transferase conferring resistance to streptogramin A has been identified in a sixth genus. However, the amount of information on both acquisition and mutations leading to macrolide, lincosamides, streptogramins, ketolides and oxazolidinones (MLSKO) resistance is limited. As a consequence this review likely underestimates the true distribution of acquired genes and mutations in Gram-negative bacteria. As use of these drugs increases, it is likely that interaction between members of the MLSKO antibiotic family and Gram-negative bacteria will continue to change resistance to these antibiotics; by mutations of existing genes as well as by acquisition and perhaps mutations of acquired resistant genes in these organisms and more work needs to be done to get a clearer picture of what is in the Gram-negative population now, such that changes can be monitored.</p>","PeriodicalId":84525,"journal":{"name":"Current drug targets. Infectious disorders","volume":"4 3","pages":"207-15"},"PeriodicalIF":0.0000,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"64","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current drug targets. Infectious disorders","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1568005043340678","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 64

Abstract

A number of different mechanisms of macrolide resistance have been described in Gram-negative bacteria. These include 16 acquired genes (esterases, phosphorylases, rRNA methylases, and effluxes) and include those thought to be unique to Gram-negative bacteria (both esterases and two of the phosphorylases) and those shared with Gram-positive bacteria (one phosphorylase) and those primarily of Gram-positive origin (rRNA methylases and efflux genes). In addition, mutations, which modify the 23S rRNA, ribosomal proteins L4 and/or L22, and/or changes in expression of innate efflux systems which occur by missense, deletion and/or insertion events have been described in five Gram-negative groups, while an innate transferase conferring resistance to streptogramin A has been identified in a sixth genus. However, the amount of information on both acquisition and mutations leading to macrolide, lincosamides, streptogramins, ketolides and oxazolidinones (MLSKO) resistance is limited. As a consequence this review likely underestimates the true distribution of acquired genes and mutations in Gram-negative bacteria. As use of these drugs increases, it is likely that interaction between members of the MLSKO antibiotic family and Gram-negative bacteria will continue to change resistance to these antibiotics; by mutations of existing genes as well as by acquisition and perhaps mutations of acquired resistant genes in these organisms and more work needs to be done to get a clearer picture of what is in the Gram-negative population now, such that changes can be monitored.

革兰氏阴性菌大环内酯类、利可沙胺类、链霉素类、酮类和恶唑烷酮类耐药基因的分布。
革兰氏阴性菌对大环内酯耐药的多种不同机制已被描述。这些基因包括16个获得性基因(酯酶、磷酸化酶、rRNA甲基化酶和外排基因),包括那些被认为是革兰氏阴性菌特有的基因(两种酯酶和两种磷酸化酶)、与革兰氏阳性菌共有的基因(一种磷酸化酶)和那些主要来自革兰氏阳性的基因(rRNA甲基化酶和外排基因)。此外,在5个革兰氏阴性组中已经发现了修饰23S rRNA、核糖体蛋白L4和/或L22的突变,以及/或由错义、缺失和/或插入事件引起的先天外排系统表达的变化,而在第6个属中已经发现了一种赋予链脲蛋白A抗性的先天转移酶。然而,关于获得和突变导致大环内酯类、林肯胺类、链状gramins、酮类和恶唑烷酮类(MLSKO)耐药的信息有限。因此,这篇综述可能低估了革兰氏阴性菌中获得性基因和突变的真实分布。随着这些药物使用的增加,MLSKO抗生素家族成员与革兰氏阴性菌之间的相互作用可能会继续改变对这些抗生素的耐药性;通过现有基因的突变,以及在这些生物体中获得或可能获得的耐药基因的突变,需要做更多的工作来更清楚地了解现在革兰氏阴性菌群中是什么,以便监测变化。
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
自引率
0.00%
发文量
0
×
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:604180095
Book学术官方微信