{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T17:17:19Z","timestamp":1788542239742,"version":"build-2803163510"},"reference-count":32,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[1999,11,1]],"date-time":"1999-11-01T00:00:00Z","timestamp":941414400000},"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":[[1999,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    We found that NCTC11637, the type strain of\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    , the causative agent of peptic ulcer disease and an early risk factor for gastric cancer, is metronidazole resistant. DNA transformation, PCR-based restriction analysis, and DNA sequencing collectively showed that the metronidazole resistance of this strain was due to mutation in\n                    <jats:italic>rdxA<\/jats:italic>\n                    (gene HP0954 in the full genome sequence of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    26695) and that resistance did not depend on mutation in any of the other genes that had previously been suggested: catalase (\n                    <jats:italic>katA<\/jats:italic>\n                    ), ferredoxin (\n                    <jats:italic>fdx<\/jats:italic>\n                    ), flavodoxin (\n                    <jats:italic>fldA<\/jats:italic>\n                    ), pyruvate:flavodoxin oxidoreductase (\n                    <jats:italic>por<\/jats:italic>\n                    \u03b3\u03b4\u03b1\u03b2), RecA (\n                    <jats:italic>recA<\/jats:italic>\n                    ), or superoxide dismutase (\n                    <jats:italic>sodB<\/jats:italic>\n                    ). This is in accord with another recent study that attributed metronidazole resistance to point mutations in\n                    <jats:italic>rdxA<\/jats:italic>\n                    . However, the mechanism of\n                    <jats:italic>rdxA<\/jats:italic>\n                    inactivation that we found in NCTC11637 is itself also novel: insertion of mini-IS\n                    <jats:italic>605<\/jats:italic>\n                    , one of the endogenous transposable elements of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    , and deletion of adjacent DNA sequences including 462 bp of the 851-bp-long\n                    <jats:italic>rdxA<\/jats:italic>\n                    gene.\n                  <\/jats:p>","DOI":"10.1128\/aac.43.11.2657","type":"journal-article","created":{"date-parts":[[2018,10,8]],"date-time":"2018-10-08T20:33:39Z","timestamp":1539030819000},"page":"2657-2662","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":66,"title":["Insertion of Mini-IS\n                    <i>605<\/i>\n                    and Deletion of Adjacent Sequences in the Nitroreductase (\n                    <i>rdxA<\/i>\n                    ) Gene Cause Metronidazole Resistance in\n                    <i>Helicobacter pylori<\/i>\n                    NCTC11637"],"prefix":"10.1128","volume":"43","author":[{"given":"Yvette J.","family":"Debets-Ossenkopp","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Medical Microbiology and Infection Control, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands1;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond G. J.","family":"Pot","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Medical Microbiology and Infection Control, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands1;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J.","family":"van Westerloo","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Medical Microbiology and Infection Control, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands1;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Avery","family":"Goodwin","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, Canada2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina M. J. E.","family":"Vandenbroucke-Grauls","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Medical Microbiology and Infection Control, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands1;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas E.","family":"Berg","sequence":"additional","affiliation":[{"name":"<!--label omitted: 3-->Department of Molecular Microbiology, Washington University, St. Louis, Missouri3; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul S.","family":"Hoffman","sequence":"additional","affiliation":[{"name":"<!--label omitted: 2-->Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, Canada2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes G.","family":"Kusters","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Medical Microbiology and Infection Control, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands1;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"6221","DOI":"10.1093\/nar\/20.23.6221","article-title":"PCR-based RFLP analysis of DNA sequence diversity in the gastric pathogen Helicobacter pylori.","volume":"20","author":"Akopyants N.","year":"1992","unstructured":"Akopyants N. 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