Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/49959
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dc.contributor.authorTavío, María M.
dc.contributor.authorAquili, Virginia D.
dc.contributor.authorVila, Jordi
dc.contributor.authorPoveda, Jose B.
dc.contributor.otherVila, Jordi
dc.contributor.otherPoveda, Jose
dc.date.accessioned2018-11-24T12:07:36Z-
dc.date.available2018-11-24T12:07:36Z-
dc.date.issued2014
dc.identifier.issn0022-2615
dc.identifier.urihttp://hdl.handle.net/10553/49959-
dc.description.abstractThe mechanisms responsible for the increase in ceftazidime MIC in two Escherichia coli in vitro selected mutants, Caz/20-1 and Caz/20-2, were studied. OmpF loss and overexpression of acrB, acrD and acrF that were associated with acrR and marR mutations and sdiA overexpression, together with mutations A233T and I332V in FtSI (PBP3) resulted in ceftazidime resistance in Caz/20-2, multiplying by 128-fold the ceftazidime MIC in the parental clinical isolate PS/20. Absence of detectable beta-lactamase hydrolytic activity in the crude extract of Caz/20-2 was observed, and coincided with Q191K and P209S mutations in AmpC and a nucleotide substitution at -28 in the ampC promoter, whereas beta-lactamase hydrolytic activity in crude extracts of PS/20 and Caz/20-1 strains was detected. Nevertheless, a fourfold increase in ceftazidime MIC in Caz/20-1 compared with that in PS/20 was due to the increased transcript level of acrB derived from acrR mutation. The two Caz mutants and PS/20 showed the same mutations in AmpG and ParE.
dc.publisher0022-2615
dc.relation.ispartofJournal of Medical Microbiology
dc.sourceJournal Of Medical Microbiology[ISSN 0022-2615],v. 63, p. 56-65
dc.subject.otherAmpc Beta-Lactamase
dc.subject.otherMultiple Antibiotic-Resistance
dc.subject.otherPenicillin-Binding Proteins
dc.subject.otherOrganic-Solvent Tolerance
dc.subject.otherClinical Isolate
dc.subject.otherPseudomonas-Aeruginosa
dc.subject.otherIn-Vivo
dc.subject.otherFluoroquinolone Resistance
dc.subject.otherDecreased Susceptibility
dc.subject.otherAntibacterial Activity
dc.titleResistance to ceftazidime in Escherichia coli associated with AcrR, MarR and PBP3 mutations and overexpression of sdiA
dc.typeinfo:eu-repo/semantics/Articlees
dc.typeArticlees
dc.identifier.doi10.1099/jmm.0.063727-0
dc.identifier.scopus84890741666
dc.identifier.isi000338478100008
dcterms.isPartOfJournal Of Medical Microbiology
dcterms.sourceJournal Of Medical Microbiology[ISSN 0022-2615],v. 63, p. 56-65
dc.contributor.authorscopusid6701659492
dc.contributor.authorscopusid15135115800
dc.contributor.authorscopusid7202012753
dc.contributor.authorscopusid7005736558
dc.description.lastpage65
dc.description.firstpage56
dc.relation.volume63
dc.type2Artículoes
dc.identifier.wosWOS:000338478100008
dc.contributor.daisngid2590173
dc.contributor.daisngid2734488
dc.contributor.daisngid24031
dc.contributor.daisngid498394
dc.identifier.investigatorRIDP-3613-2016
dc.identifier.investigatorRIDL-5987-2014
dc.contributor.wosstandardWOS:Tavio, MM
dc.contributor.wosstandardWOS:Aquili, VD
dc.contributor.wosstandardWOS:Vila, J
dc.contributor.wosstandardWOS:Poveda, JB
dc.date.coverdateDiciembre 2013
dc.identifier.ulpgces
dc.description.sjr1,038
dc.description.jcr2,248
dc.description.sjrqQ2
dc.description.jcrqQ3
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR Investigación Básica y Aplicada en Ciencias de la Salud-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUSA-ONEHEALTH1: Epidemiología, Medicina Preventiva Veterinaria y Zoonosis-
crisitem.author.deptIU de Sanidad Animal y Seguridad Alimentaria-
crisitem.author.deptDepartamento de Patología Animal, Producción Animal, Bromatología y Tecnología de Los Alimentos-
crisitem.author.orcid0000-0002-1808-7461-
crisitem.author.orcid0000-0002-9846-2427-
crisitem.author.parentorgDepartamento de Ciencias Clínicas-
crisitem.author.parentorgIU de Sanidad Animal y Seguridad Alimentaria-
crisitem.author.fullNameTavío Pérez, María Del Mar-
crisitem.author.fullNamePoveda Guerrero, José Bismarck-
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