Mechanisms of resistance and decreased susceptibility to azithromycin in Shigella

IF 1 Q4 GENETICS & HEREDITY

Gene Reports Pub Date : 2024-08-10 DOI:10.1016/j.genrep.2024.102011

Zohreh Ghalavand , Parisa Behruznia , Mansoor Kodori , Hamed Afkhami , Elham Isaei , Foroogh Neamati , Solmaz Mahmoodzadeh Poornaki

引用次数: 0

Abstract

Azithromycin (AZM) is a primary treatment for shigellosis in children and a secondary option for adults. However, Shigella spp., has increasingly developed resistance to multiple antibiotics, including AZM. This rise in AZM-induced resistance complicates treatment, particularly with the emergence of multi-drug resistant (MDR) strains and the inappropriate and excessive use of antibiotics. Moreover, various mechanisms contribute to the decreased susceptibility to azithromycin (DSA) in Shigella spp., often involving antimicrobial resistance genes harboring on mobile genetic elements. These mechanisms hinder efforts to control the spread of DSA-Shigella strains. Therefore, this review aims to discuss the mechanisms of AZM resistance in Shigella infections and shed light on the important mechanisms underlying DSA in Shigella.

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志贺氏菌对阿奇霉素耐药和易感性降低的机制

阿奇霉素（AZM）是治疗儿童志贺氏杆菌病的主要药物，也是成人志贺氏杆菌病的辅助药物。然而，志贺菌属对包括 AZM 在内的多种抗生素产生了越来越多的耐药性。AZM 引起的耐药性增加使治疗变得更加复杂，尤其是耐多药（MDR）菌株的出现以及抗生素的不当和过度使用。此外，导致志贺菌属对阿奇霉素（DSA）的敏感性降低的机制多种多样，通常涉及移动遗传因子上携带的抗菌药耐药基因。这些机制阻碍了控制 DSA 志贺菌菌株传播的努力。因此，本综述旨在讨论志贺菌感染对 AZM 产生耐药性的机制，并阐明志贺菌产生 DSA 的重要机制。

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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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.