{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T15:03:39Z","timestamp":1785769419460,"version":"3.56.0"},"reference-count":59,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T00:00:00Z","timestamp":1771286400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T00:00:00Z","timestamp":1771286400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000030","name":"Centers for Disease Control and Prevention","doi-asserted-by":"publisher","award":["U54CK000609-05"],"award-info":[{"award-number":["U54CK000609-05"]}],"id":[{"id":"10.13039\/100000030","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000051","name":"National Human Genome Research Institute","doi-asserted-by":"publisher","award":["T32 HG000045"],"award-info":[{"award-number":["T32 HG000045"]}],"id":[{"id":"10.13039\/100000051","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000030","name":"Centers for Disease Control and Prevention","doi-asserted-by":"publisher","award":["U01CK000587"],"award-info":[{"award-number":["U01CK000587"]}],"id":[{"id":"10.13039\/100000030","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"published-print":{"date-parts":[[2026,2,17]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                      is a public health threat capable of causing multiple types of infection, carrying a variety of antimicrobial resistance genes (ARGs), and disseminating ARGs to other microbes. Since ARG-carrying\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      can exist as a commensal gut microbe, intestinal\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      in community-associated (CA) members presents an under-appreciated reservoir of ARGs. We cultured 75 CA\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      isolates from stool of 64 patients lacking inpatient healthcare exposures &gt;24 hours in the previous 12 weeks. Remnant stool submitted to the Barnes-Jewish Hospital (BJH) microbiology laboratory for\n                      <jats:italic toggle=\"yes\">Clostridioides difficile<\/jats:italic>\n                      testing was plated to MacConkey agar with ciprofloxacin and extended-spectrum beta-lactamase (ESBL) Chrome Agar to isolate resistant\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      colonies, which were whole-genome sequenced. Isolates were compared to ESBL\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      genomes published by Mahmud et al. (B. Mahmud, M. A. Wallace, K. A. Reske, K. Alvarado, et al., mSystems 7:e00519-22, 2022,\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1128\/msystems.00519-22\" xlink:type=\"simple\">https:\/\/doi.org\/10.1128\/msystems.00519-22<\/jats:ext-link>\n                      ), which were collected from bloodstream and urinary tract infections. We identified ESBL genes and quinolone resistance elements in\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      isolates from all patients, 32 (50%) of whom had no recent antibiotic exposure. Sequence type (ST) 131 isolates carried more quinolone resistance elements but fewer ESBL genes than other STs. Eleven patients carried two distinct\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      lineages simultaneously. CA ESBL\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      displayed a lower diversity of beta-lactamase genes but similar rates of antibiotic resistance genes compared to ESBL\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      reported by Mahmud et al. (\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1128\/msystems.00519-22\" xlink:type=\"simple\">https:\/\/doi.org\/10.1128\/msystems.00519-22<\/jats:ext-link>\n                      ). Carriage of resistance elements without recent antimicrobial exposure suggests the presence of circulating, resistant\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      . Our results show the continually evolving resistance profile of CA\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                      , demonstrating the importance of characterizing antimicrobial resistance in the community.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Antimicrobial-resistant\n                        <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                        presents a substantial threat to public health, limiting treatment options and potentially horizontally transferring its resistance to other members of the gut microbiome. Resistance to quinolones and beta-lactams, specifically, hinders treatment of urinary tract and gastrointestinal infections, both commonly caused by\n                        <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                        . Tracking successful lineages, such as ST131, within the healthcare setting can inform clinicians about resistance patterns among their patients, but this work shows that other STs present an even higher antimicrobial resistance burden than ST131. In addition to monitoring multiple lineages of antimicrobial-resistant\n                        <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                        , it is necessary to identify and understand community-associated carriage of this organism, as evidenced by the increasing prevalence of community-associated ESBL\n                        <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                        carriage and our specific results showing similar resistance burdens within the clinic and community. This work presents insight into antimicrobial-resistant\n                        <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                        among those without significant healthcare exposures, providing important community-focused surveillance that is currently lacking.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msystems.01591-25","type":"journal-article","created":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T14:01:13Z","timestamp":1768226473000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["Community-associated quinolone-resistant and extended-spectrum beta-lactamase-producing\n                    <i>Escherichia coli<\/i>\n                    isolates are similar to clinical infection isolates by sequence type and resistome"],"prefix":"10.1128","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3243-3874","authenticated-orcid":true,"given":"Emily E.","family":"Benedict","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01yc7t268","id-type":"ROR","asserted-by":"publisher"}],"name":"The Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wesley","family":"Agee","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01yc7t268","id-type":"ROR","asserted-by":"publisher"}],"name":"The Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiffany","family":"Hink","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katelyn L.","family":"Parrish","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberly A.","family":"Reske","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate","family":"Peacock","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Washington University School of Medicine","place":["St. Louis, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel 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