{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T22:05:52Z","timestamp":1778709952215,"version":"3.51.4"},"reference-count":30,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2008,4,1]],"date-time":"2008-04-01T00:00:00Z","timestamp":1207008000000},"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":[[2008,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We report on a novel CTX-M extended-spectrum \u03b2-lactamase (ESBL), designated CTX-M-42, with enhanced activity toward ceftazidime. CTX-M-42 was identified in a hypermutable\n            <jats:italic>Escherichia coli<\/jats:italic>\n            nosocomial isolate (isolate Irk2320) and is a Pro167Thr amino acid substitution variant of CTX-M-3. By molecular typing of ESBL-producing\n            <jats:italic>E. coli<\/jats:italic>\n            strains previously isolated in the same hospital ward, we were able to identify a putative progenitor (strain Irk1224) of Irk2320, which had a mutator phenotype and harbored the CTX-M-3 \u03b2-lactamase. To reproduce the natural evolution of CTX-M-3, we selected for ceftazidime resistance mutations in\n            <jats:italic>bla<\/jats:italic>\n            <jats:sub>CTX-M-3<\/jats:sub>\n            gene in vitro both in clinical isolate Irk1224 and in laboratory-derived hypermutable (\n            <jats:italic>mutD5<\/jats:italic>\n            ) strain GM2995. These experiments yielded CTX-M-3\n            <jats:sup>Pro167Ser<\/jats:sup>\n            and CTX-M-3\n            <jats:sup>Asn136Lys<\/jats:sup>\n            mutants which conferred higher levels of resistance to ceftazidime than to cefotaxime. CTX-M-3\n            <jats:sup>Asn136Lys<\/jats:sup>\n            had a level of low activity toward ampicillin, which may explain its absence from clinical isolates. We conclude that the selection of CTX-M-42 could have occurred in vivo following treatment with ceftazidime and was likely facilitated by the hypermutable background.\n          <\/jats:p>","DOI":"10.1128\/aac.01060-07","type":"journal-article","created":{"date-parts":[[2008,1,23]],"date-time":"2008-01-23T01:45:33Z","timestamp":1201052733000},"page":"1297-1301","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Convergent In Vivo and In Vitro Selection of Ceftazidime Resistance Mutations at Position 167 of CTX-M-3 \u03b2-Lactamase in Hypermutable\n            <i>Escherichia coli<\/i>\n            Strains"],"prefix":"10.1128","volume":"52","author":[{"given":"Marina N.","family":"Stepanova","sequence":"first","affiliation":[{"name":"Institute of Antimicrobial Chemotherapy, Smolensk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maxim","family":"Pimkin","sequence":"additional","affiliation":[{"name":"Institute of Antimicrobial Chemotherapy, Smolensk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anatoly A.","family":"Nikulin","sequence":"additional","affiliation":[{"name":"Institute of Antimicrobial Chemotherapy, Smolensk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Varvara K.","family":"Kozyreva","sequence":"additional","affiliation":[{"name":"Institute of Antimicrobial Chemotherapy, Smolensk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elena D.","family":"Agapova","sequence":"additional","affiliation":[{"name":"Regional Children's Hospital, Irkutsk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mikhail V.","family":"Edelstein","sequence":"additional","affiliation":[{"name":"Institute of Antimicrobial Chemotherapy, Smolensk, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj2760269"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/dkl252"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/dkf151"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.48.1.1-14.2004"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/dkg256"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2006.08.011"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mimet.2005.03.018"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.48.6.2308-2313.2004"},{"key":"e_1_3_2_10_2","unstructured":"Performance standards for antimicrobial susceptibility testing; 16th informational supplement M100-S16. 2006"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.50.2.731-738.2006"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.48.8.2808-2815.2004"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.47.12.3724-3732.2003"},{"key":"e_1_3_2_14_2","doi-asserted-by":"crossref","first-page":"800","DOI":"10.1111\/j.1469-0691.2006.01424.x","volume":"12","year":"2006","unstructured":"Ellington, M. 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