{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T16:31:25Z","timestamp":1789403485890,"version":"build-2803163510"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2013,6,1]],"date-time":"2013-06-01T00:00:00Z","timestamp":1370044800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2013,6]]},"abstract":"ABSTRACT<\/jats:title>\n \n We studied a collection of 105 clinical enterobacteria with unusual phenotypes of quinolone susceptibility to analyze the occurrence of plasmid-mediated quinolone resistance (PMQR) and\n oqx<\/jats:italic>\n genes and their implications for quinolone susceptibility. The\n oqxA<\/jats:italic>\n and\n oqxB<\/jats:italic>\n genes were found in 31\/34 (91%)\n Klebsiella pneumoniae<\/jats:named-content>\n and 1\/3\n Klebsiella oxytoca<\/jats:named-content>\n isolates. However, the\n oqxA<\/jats:italic>\n - and\n oqxB<\/jats:italic>\n -harboring isolates lacking other known quinolone resistance determinants showed wide ranges of susceptibility to nalidixic acid and ciprofloxacin. Sixty of the 105 isolates (57%) harbored at least one PMQR gene [\n qnrB19<\/jats:italic>\n ,\n qnrB10<\/jats:italic>\n ,\n qnrB2<\/jats:italic>\n ,\n qnrB1<\/jats:italic>\n ,\n qnrS1<\/jats:italic>\n , or\n aac<\/jats:italic>\n (\n 6<\/jats:italic>\n \u2032)\n -Ib-cr<\/jats:italic>\n )], belong to 8 enterobacterial species, and were disseminated throughout the country, and most of them were categorized as susceptible by the current clinical quinolone susceptibility breakpoints. We developed a disk diffusion-based method to improve the phenotypic detection of\n aac<\/jats:italic>\n (\n 6<\/jats:italic>\n \u2032)\n -Ib-cr<\/jats:italic>\n . The most common PMQR genes in our collection [\n qnrB19<\/jats:italic>\n ,\n qnrB10<\/jats:italic>\n , and\n aac<\/jats:italic>\n (\n 6<\/jats:italic>\n \u2032)\n -Ib-cr<\/jats:italic>\n ] were differentially distributed among enterobacterial species, and two different epidemiological settings were evident. First, the species associated with community-acquired infections (\n Salmonella<\/jats:named-content>\n spp. and\n Escherichia coli<\/jats:named-content>\n ) mainly harbored\n qnrB19<\/jats:italic>\n (a unique PMQR gene) located in small ColE1-type plasmids that might constitute its natural reservoirs.\n qnrB19<\/jats:italic>\n was not associated with an extended-spectrum \u03b2-lactamase phenotype. Second, the species associated with hospital-acquired infections (\n Enterobacter<\/jats:named-content>\n spp.,\n Klebsiella<\/jats:named-content>\n spp., and\n Serratia marcescens<\/jats:named-content>\n ) mainly harbored\n qnrB10<\/jats:italic>\n in IS\n CR1<\/jats:italic>\n -containing class 1 integrons that may also have\n aac<\/jats:italic>\n (\n 6<\/jats:italic>\n \u2032)\n -Ib-cr<\/jats:italic>\n as a cassette within the variable region. These two PMQR genes were strongly associated with an extended-spectrum \u03b2-lactamase phenotype. Therefore, this differential distribution of PMQR genes is strongly influenced by their linkage or lack of linkage to integrons.\n <\/jats:p>","DOI":"10.1128\/aac.01615-12","type":"journal-article","created":{"date-parts":[[2013,3,12]],"date-time":"2013-03-12T01:07:32Z","timestamp":1363050452000},"page":"2467-2475","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":49,"title":["Differential Distribution of Plasmid-Mediated Quinolone Resistance Genes in Clinical Enterobacteria with Unusual Phenotypes of Quinolone Susceptibility from Argentina"],"prefix":"10.1128","volume":"57","author":[{"given":"Patricia","family":"Andres","sequence":"first","affiliation":[{"name":"Servicio Antimicrobianos, Departamento de Bacteriolog\u00eda, Instituto Nacional de Enfermedades Infecciosas-ANLIS Dr. Carlos G. 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