{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T09:11:14Z","timestamp":1791277874033,"version":"4.1.0"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2007,2,1]],"date-time":"2007-02-01T00:00:00Z","timestamp":1170288000000},"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":[[2007,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The mechanisms involved in fluoroquinolone resistance in\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            include target alterations and overexpression of efflux pumps. The present study evaluated the role of known and putative multidrug resistance efflux pumps and mutations in topoisomerase genes among laboratory-selected and naturally occurring fluoroquinolone-resistant\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            serovar Typhimurium strains. Strains with ciprofloxacin MICs of 0.25, 4, 32, and 256 \u03bcg\/ml were derived in vitro using serovar Typhimurium S21. These mutants also showed decreased susceptibility or resistance to many nonfluoroquinolone antimicrobials, including tetracycline, chloramphenicol, and several \u03b2-lactams. The expression of efflux pump genes\n            <jats:italic>acrA<\/jats:italic>\n            ,\n            <jats:italic>acrB<\/jats:italic>\n            ,\n            <jats:italic>acrE<\/jats:italic>\n            ,\n            <jats:italic>acrF<\/jats:italic>\n            ,\n            <jats:italic>emrB<\/jats:italic>\n            ,\n            <jats:italic>emrD<\/jats:italic>\n            , and\n            <jats:italic>mdlB<\/jats:italic>\n            were substantially increased (\u22652-fold) among the fluoroquinolone-resistant mutants. Increased expression was also observed, but to a lesser extent, with three other putative efflux pumps:\n            <jats:italic>mdtB<\/jats:italic>\n            (\n            <jats:italic>yegN<\/jats:italic>\n            ),\n            <jats:italic>mdtC<\/jats:italic>\n            (\n            <jats:italic>yegO<\/jats:italic>\n            ), and\n            <jats:italic>emrA<\/jats:italic>\n            among mutants with ciprofloxacin MICs of \u226532 \u03bcg\/ml. Deletion of\n            <jats:italic>acrAB<\/jats:italic>\n            or\n            <jats:italic>tolC<\/jats:italic>\n            in S21 and its fluoroquinolone-resistant mutants resulted in increased susceptibility to fluoroquinolones and other tested antimicrobials. In naturally occurring fluoroquinolone-resistant serovar Typhimurium strains, deletion of\n            <jats:italic>acrAB<\/jats:italic>\n            or\n            <jats:italic>tolC<\/jats:italic>\n            increased fluoroquinolone susceptibility 4-fold, whereas replacement of\n            <jats:italic>gyrA<\/jats:italic>\n            double mutations (S83F D87N) with wild-type\n            <jats:italic>gyrA<\/jats:italic>\n            increased susceptibility &gt;500-fold. These results indicate that a combination of topoisomerase gene mutations, as well as enhanced antimicrobial efflux, plays a critical role in the development of fluoroquinolone resistance in both laboratory-derived and naturally occurring quinolone-resistant serovar Typhimurium strains.\n          <\/jats:p>","DOI":"10.1128\/aac.00600-06","type":"journal-article","created":{"date-parts":[[2007,1,19]],"date-time":"2007-01-19T19:34:53Z","timestamp":1169235293000},"page":"535-542","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":129,"title":["Contribution of Target Gene Mutations and Efflux to Decreased Susceptibility of\n            <i>Salmonella enterica<\/i>\n            Serovar Typhimurium to Fluoroquinolones and Other Antimicrobials"],"prefix":"10.1128","volume":"51","author":[{"given":"Sheng","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Nutrition and Food Science, University of Maryland, College Park, Maryland 20742"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenghui","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Nutrition and Food Science, University of Maryland, College Park, Maryland 20742"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick F.","family":"McDermott","sequence":"additional","affiliation":[{"name":"Division of Animal and Food Microbiology, Office of Research, Center for Veterinary Medicine, the U.S. Food and Drug Administration, Laurel, Maryland 20708"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaohua","family":"Zhao","sequence":"additional","affiliation":[{"name":"Division of Animal and Food Microbiology, Office of Research, Center for Veterinary Medicine, the U.S. Food and Drug Administration, Laurel, Maryland 20708"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David G.","family":"White","sequence":"additional","affiliation":[{"name":"Division of Animal and Food Microbiology, Office of Research, Center for Veterinary Medicine, the U.S. Food and Drug Administration, Laurel, Maryland 20708"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Paulsen","sequence":"additional","affiliation":[{"name":"The Institute for Genomic Research, Rockville, Maryland 20860"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianghong","family":"Meng","sequence":"additional","affiliation":[{"name":"Department of Nutrition and Food Science, University of Maryland, College Park, Maryland 20742"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.41.10.2067"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.43.4.868"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/dkh122"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.48.10.3729-3735.2004"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1101\/gr.186501"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa012261"},{"key":"e_1_3_2_8_2","unstructured":"CLSI. 2002. 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