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Trends in Helicobacter pylori resistance to clarithromycin: from phenotypic to genomic approaches

dc.contributor.authorMarques, Andreia T.
dc.contributor.authorVítor, Jorge M.B.
dc.contributor.authorSantos, Andrea
dc.contributor.authorOleastro, Mónica
dc.contributor.authorVale, Filipa F.
dc.date.accessioned2021-03-31T15:07:58Z
dc.date.available2021-03-31T15:07:58Z
dc.date.issued2020-03-02
dc.description.abstractFor a long time Helicobacter pylori infections have been treated using the macrolide antibiotic, clarithromycin. Clarithromycin resistance is increasing worldwide and is the most common cause of H. pylori treatment failure. Here we review the mechanisms of antibiotic resistance to clarithromycin, detailing the individual and combinations of point mutations found in the 23S rRNA gene associated with resistance. Additionally, we consider the methods used to detect clarithromycin resistance, emphasizing the use of high-throughput next-generation sequencing methods, which were applied to 17 newly sequenced pairs of H. pylori strains isolated from the antrum and corpus of a recent colonized paediatric population. This set of isolates was composed of six pairs of resistant strains whose phenotype was associated with two point mutations found in the 23S rRNA gene: A2142C and A2143G. Other point mutations were found simultaneously in the same gene, but, according to our results, it is unlikely that they contribute to resistance. Further, among susceptible isolates, genomic variations compatible with mutations previously associated with clarithromycin resistance were detected. Exposure to clarithromycin may select low-frequency variants, resulting in a progressive increase in the resistance rate due to selection pressure.pt_PT
dc.description.sponsorshipF. F. V. is the recipient of a project grant (PTDC/BTM-SAL/28978/2017) from the Fundação para a Ciência e a Tecnologia (FCT), which supported this work. J. V.’s research group was financed by New England Biolabs, Inc. (USA).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMicrob Genom. 2020 Mar;6(3):e000344. doi: 10.1099/mgen.0.000344pt_PT
dc.identifier.doi10.1099/mgen.0.000344pt_PT
dc.identifier.issn2057-5858
dc.identifier.urihttp://hdl.handle.net/10400.18/7609
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMicrobiology Societypt_PT
dc.relationPhage-Enzybiotic: dealing with critical pathogenic antibiotic-resistant bacteria
dc.relation.publisherversionhttps://www.microbiologyresearch.org/content/journal/mgen/10.1099/mgen.0.000344#tab2pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAnti-Bacterial Agentspt_PT
dc.subjectClarithromycinpt_PT
dc.subjectDrug Resistance, Bacterialpt_PT
dc.subjectGenome, Bacterialpt_PT
dc.subjectGenomicspt_PT
dc.subjectHelicobacter Infectionspt_PT
dc.subjectHelicobacter pyloript_PT
dc.subjectHigh-Throughput Nucleotide Sequencingpt_PT
dc.subjectPhenotypept_PT
dc.subjectRNA, Ribosomal, 23Spt_PT
dc.subjectInfecções Gastrointestinaispt_PT
dc.titleTrends in Helicobacter pylori resistance to clarithromycin: from phenotypic to genomic approachespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitlePhage-Enzybiotic: dealing with critical pathogenic antibiotic-resistant bacteria
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FBTM-SAL%2F28978%2F2017/PT
oaire.citation.issue3pt_PT
oaire.citation.startPagee000344pt_PT
oaire.citation.titleMicrobial Genomicspt_PT
oaire.citation.volume6pt_PT
oaire.fundingStream3599-PPCDT
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.embargofctAcesso de acordo com política editorial da revista.pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublicatione76f78dc-058d-47bd-a8e4-b555d358bb14
relation.isProjectOfPublication.latestForDiscoverye76f78dc-058d-47bd-a8e4-b555d358bb14

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