{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T15:29:09Z","timestamp":1788535749305,"version":"build-2803163510"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2024,8,10]],"date-time":"2024-08-10T00:00:00Z","timestamp":1723248000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Increasing antibiotic resistance in Helicobacter pylori necessitates research on new active molecules. In 2017, delafloxacin, a new fluoroquinolone with chemical properties of activity under acidic conditions, was approved for treatment of community-acquired bacterial pneumonia and acute bacterial skin and soft-tissue infections. Mutations in gyrA are responsible for fluoroquinolone resistance, but certain clinical isolates of H. pylori appear to display a dual phenotype: resistance to levofloxacin associated with very low delafloxacin MICs.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objectives<\/jats:title>\n                  <jats:p>To estimate epidemiological cut-off (ECOFF) values and to identify mutations in the gyrA gene, specific to FQ resistance, without increasing the MICs of delafloxacin.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Clinical strains (n\u200a=\u200a231) were collected in the bacteriology laboratory of Poitiers University Hospital over a 2 year period to determine the ECOFF of delafloxacin. Retrospectively, 101 clinical strains with an levofloxacin-resistant phenotype (MIC\u200a&amp;gt;\u200a1 mg\/L) were selected from 2018 to 2022 for delafloxacin MIC determination and QRDR (gyrA) sequencing.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The estimated ECOFF of delafloxacin was \u22640.125 mg\/L. No H. pylori isolate showed a levofloxacin-sensitive phenotype with a delafloxacin MIC of &amp;gt;0.125 mg\/L. Among the levofloxacin-resistant H. pylori isolates, 53.5% had delafloxacin MICs of \u22640.125 mg\/L. The N87I mutation was associated with dual levofloxacin\/delafloxacin resistance (P\u200a&amp;lt;\u200a0.001) in contrast to the N87K and D91N mutations (P\u200a&amp;gt;\u200a0.05). Mutations D91G and D91Y were not associated with a delafloxacin resistance phenotype (P\u200a&amp;gt;\u200a0.05).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Delafloxacin seems to be a therapeutic alternative for levofloxacin-resistant strains with greater in vitro activity. However, further clinical\/biological investigations are required to determine its efficacy in H. pylori eradication.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/jac\/dkae269","type":"journal-article","created":{"date-parts":[[2024,8,10]],"date-time":"2024-08-10T13:55:23Z","timestamp":1723298123000},"page":"2633-2639","source":"Crossref","is-referenced-by-count":8,"title":["<i>In vitro<\/i> activity of delafloxacin against clinical levofloxacin-resistant <i>Helicobacter pylori<\/i> isolates"],"prefix":"10.1093","volume":"79","author":[{"given":"Victor","family":"Luzarraga","sequence":"first","affiliation":[{"name":"Bacteriology Laboratory, Infectious Agents Department, CHU de Poitiers , 2 rue de la Mil\u00e9trie, 86021 Poitiers ,","place":["France"]},{"name":"PHAR2 Pharmacology of Antimicrobial Agents and Antibiotic Resistance, INSERM U1070, Universit\u00e9 de Poitiers , Poitiers 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