{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,17]],"date-time":"2025-12-17T17:57:05Z","timestamp":1765994225267},"reference-count":57,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2014,12,1]],"date-time":"2014-12-01T00:00:00Z","timestamp":1417392000000},"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":["Infect Immun"],"published-print":{"date-parts":[[2014,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Shiga toxin (Stx)-producing\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            (STEC) causes hemorrhagic colitis and the hemolytic-uremic syndrome (HUS). STEC strains may produce Stx1a and\/or Stx2a or variants of either toxin. A 2006 spinach-associated outbreak of STEC O157:H7 resulted in higher hospitalization and HUS rates than previous STEC outbreaks. The spinach isolate, strain K3995, contains both\n            <jats:italic>stx<\/jats:italic>\n            <jats:sub>2a<\/jats:sub>\n            and\n            <jats:italic>stx<\/jats:italic>\n            <jats:sub>2c<\/jats:sub>\n            . We hypothesized that the enhanced virulence of K3995 reflects the combination of\n            <jats:italic>stx<\/jats:italic>\n            <jats:sub>2<\/jats:sub>\n            alleles (carried on lysogenic phages) and\/or the amount of Stx2 made by that strain. We compared the virulence of K3995 to those of other O157:H7 isolates and an isogenic Stx2 mutant in rabbits and mice. We also measured the relative levels of Stx2 produced from those strains with or without induction of the\n            <jats:italic>stx<\/jats:italic>\n            -carrying phage. Some rabbits infected with K3995 exhibited intestinal pathology and succumbed to infection, while none of those infected with O157:H7 strain 2812 (Stx1a\n            <jats:sup>+<\/jats:sup>\n            Stx2a\n            <jats:sup>+<\/jats:sup>\n            ) died or showed pathological signs. Rabbits infected with the isogenic Stx2a mutant K3995\n            <jats:italic>stx<\/jats:italic>\n            <jats:sub>2a<\/jats:sub>\n            ::\n            <jats:italic>cat<\/jats:italic>\n            were not colonized as well as those infected with K3995 and exhibited no signs of disease. In the streptomycin-treated mouse model, more animals infected with K3995 died than did those infected with O157:H7 strain 86-24 (Stx2a\n            <jats:sup>+<\/jats:sup>\n            ). Additionally, K3995 produced higher levels of total Stx2 and toxin phage DNA in cultures after phage induction than did 86-24. Our results demonstrate the greater virulence of K3995 compared to other O157:H7 strains in rabbits and mice. We conclude that this enhanced virulence is linked to higher levels of Stx2 expression as a consequence of increased phage induction.\n          <\/jats:p>","DOI":"10.1128\/iai.02361-14","type":"journal-article","created":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T05:57:57Z","timestamp":1410847077000},"page":"4968-4977","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":23,"title":["Enhanced Virulence of the Escherichia coli O157:H7 Spinach-Associated Outbreak Strain in Two Animal Models Is Associated with Higher Levels of Stx2 Production after Induction with Ciprofloxacin"],"prefix":"10.1128","volume":"82","author":[{"given":"T.","family":"Zangari","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. R.","family":"Melton-Celsa","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Panda","sequence":"additional","affiliation":[{"name":"Program of Comparative Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA"},{"name":"Departments of Pathology, Epidemiology, and Preventive Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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