{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T13:13:40Z","timestamp":1791465220824,"version":"4.3.4"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2017,5,1]],"date-time":"2017-05-01T00:00:00Z","timestamp":1493596800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"Centre hospitalier d'Amiens"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    In this study, an ertapenem-nonsusceptible\n                    <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n                    isolate was investigated to determine the genetic basis for its carbapenem resistance phenotype. This clinical strain was recovered from a patient that received, 1 year previously, ertapenem to treat a cholangitis due to a carbapenem-susceptible extended-spectrum-\u03b2-lactamase (ESBL)-producing\n                    <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n                    isolate. Whole-genome sequencing of these strains was performed using Illumina and single-molecule real-time sequencing technologies. It revealed that they belonged to the ST131 clonal group, had the predicted O25b:H4 serotype, and produced the CTX-M-15 and TEM-1 \u03b2-lactamases. One nucleotide substitution was identified between these strains. It affected the\n                    <jats:italic>ompR<\/jats:italic>\n                    gene, which codes for a regulatory protein involved in the control of OmpC\/OmpF porin expression, creating a Gly-63-Val substitution. The role of OmpR alteration was confirmed by a complementation experiment that fully restored the susceptibility to ertapenem of the clinical isolate. A modeling study showed that the Gly-63-Val change displaced the histidine-kinase phosphorylation site. SDS-PAGE analysis revealed that the ertapenem-nonsusceptible\n                    <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n                    strain had a decreased expression of OmpC\/OmpF porins. No significant defect in the growth rate or in the resistance to\n                    <jats:named-content content-type=\"genus-species\">Dictyostelium discoideum<\/jats:named-content>\n                    amoeba phagocytosis was found in the ertapenem-nonsusceptible\n                    <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n                    isolate compared to its susceptible parental strain. Our report demonstrates for the first time that ertapenem resistance may emerge clinically from ESBL-producing\n                    <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n                    due to mutations that modulate the OmpR activity.\n                  <\/jats:p>","DOI":"10.1128\/aac.00014-17","type":"journal-article","created":{"date-parts":[[2017,3,6]],"date-time":"2017-03-06T20:40:36Z","timestamp":1488832836000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":32,"title":["Structural Alteration of OmpR as a Source of Ertapenem Resistance in a CTX-M-15-Producing Escherichia coli O25b:H4 Sequence Type 131 Clinical Isolate"],"prefix":"10.1128","volume":"61","author":[{"given":"Herv\u00e9","family":"Dupont","sequence":"first","affiliation":[{"name":"D\u00e9partement d'Anesth\u00e9sie-R\u00e9animation, CHU Amiens-Picardie, and INSERM U1088, Universit\u00e9 de Picardie 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