{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T19:39:11Z","timestamp":1781638751361,"version":"3.54.5"},"reference-count":155,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2023,12,21]],"date-time":"2023-12-21T00:00:00Z","timestamp":1703116800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,12,21]],"date-time":"2023-12-21T00:00:00Z","timestamp":1703116800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"crossref","award":["U01AI123394, R01AI155893"],"award-info":[{"award-number":["U01AI123394, R01AI155893"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"crossref"}]},{"name":"HHS | PHS | Agency for Healthcare Research and Quality","award":["R01HS027621"],"award-info":[{"award-number":["R01HS027621"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"published-print":{"date-parts":[[2023,12,21]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Staphylococcus saprophyticus<\/jats:italic>\n            is the leading Gram-positive cause of uncomplicated urinary tract infections. Recent reports of increasing antimicrobial resistance (AMR) in\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            warrant investigation of its understudied resistance patterns. Here, we characterized a diverse collection of\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            (\n            <jats:italic>n<\/jats:italic>\n            = 275) using comparative whole genome sequencing. We performed a phylogenetic analysis of core genes (1,646) to group our\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            and investigated the distributions of antibiotic resistance genes (ARGs).\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            isolates belonged to two previously characterized lineages, and 14.91% (41\/275) demonstrated multidrug resistance. We compared antimicrobial susceptibility phenotypes of our\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            with the presence of different ARGs and gene alleles. 29.8% (82\/275) carried staphylococcal cassette chromosome mobile elements, among which 25.6% (21\/82) were\n            <jats:italic>mecA<\/jats:italic>\n            <jats:sup>+<\/jats:sup>\n            . Penicillin resistance was associated with the presence of\n            <jats:italic>mecA<\/jats:italic>\n            or\n            <jats:italic>blaZ<\/jats:italic>\n            . The\n            <jats:italic>mecA<\/jats:italic>\n            gene could serve as a marker to infer cefoxitin and oxacillin resistance of\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            , but the absence of this gene is not predictive of susceptibility. Utilizing computational modeling, we found several genes were associated with cefoxitin and oxacillin resistance in\n            <jats:italic>\n              mecA\n              <jats:sup>\u2212<\/jats:sup>\n            <\/jats:italic>\n            isolates, some of which have predicted functions in stress response and cell wall synthesis. Furthermore, phenotype association analysis indicates ARGs against non-\u03b2-lactams reported in other staphylococci may serve as resistance determinants of\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            . Lastly, we observed that two ARGs [\n            <jats:italic>erm<\/jats:italic>\n            and\n            <jats:italic>erm (44)v<\/jats:italic>\n            ], carried by bacteriophages, were correlated with high phenotypic non-susceptibility against erythromycin (11\/11 and 10\/10) and clindamycin (11\/11 and 10\/10). The AMR-correlated genetic elements identified in this work can help to refine resistance prediction of\n            <jats:italic>S. saprophyticus<\/jats:italic>\n            during antibiotic treatment.\n          <\/jats:p>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              <jats:italic>Staphylococcus saprophyticus<\/jats:italic>\n              is the second most common bacteria associated with urinary tract infections (UTIs) in women. The antimicrobial treatment regimen for uncomplicated UTI is normally nitrofurantoin, trimethoprim-sulfamethoxazole (TMP-SMX), or a fluoroquinolone without routine susceptibility testing of\n              <jats:italic>S. saprophyticus<\/jats:italic>\n              recovered from urine specimens. However, TMP-SMX-resistant\n              <jats:italic>S. saprophyticus<\/jats:italic>\n              has been detected recently in UTI patients, as well as in our cohort. Herein, we investigated the understudied resistance patterns of this pathogenic species by linking genomic antibiotic resistance gene (ARG) content to susceptibility phenotypes. We describe ARG associations with known and novel SCC\n              <jats:italic>mec<\/jats:italic>\n              configurations as well as phage elements in\n              <jats:italic>S. saprophyticus<\/jats:italic>\n              , which may serve as intervention or diagnostic targets to limit resistance transmission. Our analyses yielded a comprehensive database of phenotypic data associated with the ARG sequence in clinical\n              <jats:italic>S. saprophyticus<\/jats:italic>\n              isolates, which will be crucial for resistance surveillance and prediction to enable precise diagnosis and effective treatment of\n              <jats:italic>S. saprophyticus<\/jats:italic>\n              UTIs.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/msystems.00697-23","type":"journal-article","created":{"date-parts":[[2023,12,5]],"date-time":"2023-12-05T14:00:31Z","timestamp":1701784831000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":10,"title":["Comparative genomics reveals the correlations of stress response genes and bacteriophages in developing antibiotic resistance of\n            <i>Staphylococcus saprophyticus<\/i>"],"prefix":"10.1128","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6994-9033","authenticated-orcid":false,"given":"Kailun","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pathology and Immunology, Division of Laboratory and Genomic Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA"},{"name":"The Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert F.","family":"Potter","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Division of Laboratory and Genomic Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie","family":"Marino","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol E.","family":"Muenks","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Division of Laboratory and Genomic Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew G.","family":"Lammers","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Division of Laboratory and Genomic Medicine, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0524-9473","authenticated-orcid":false,"given":"Jennifer","family":"Dien Bard","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Children\u2019s Hospital Los Angeles, Los Angeles, California, USA"},{"name":"Keck School of Medicine, University of Southern California, Los Angeles, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanis C.","family":"Dingle","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of Calgary, Calgary, Alberta, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6568-156X","authenticated-orcid":false,"given":"Romney","family":"Humphries","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars F.","family":"Westblade","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, 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Disclosure: Stephen Leslie declares no relevant financial relationships with ineligible companies, Wanda Reygaert declares no relevant financial relationships with ineligible companies. Urinary tract infection. 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