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In a single-strain infection model, compared to \u03c77122, the \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain demonstrated reduced colonization of the lungs, liver, and spleen. Complementation of the \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain restored virulence. In a coinfection model, compared to the virulent APEC strain, the \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain demonstrated mean 50-fold, 126-fold, and 25-fold decreases in colonization of the lungs, liver, and spleen, respectively. A \u0394\n            <jats:italic>mntH<\/jats:italic>\n            \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain was further attenuated, demonstrating reduced persistence in blood and mean 1,400-fold, 954-fold, and 83-fold reduced colonization in the lungs, liver, and spleen, respectively. In coinfections, the \u0394\n            <jats:italic>feoB<\/jats:italic>\n            \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain demonstrated reduced persistence in blood but increased colonization of the liver. The \u0394\n            <jats:italic>mntH<\/jats:italic>\n            , \u0394\n            <jats:italic>feoB<\/jats:italic>\n            , and \u0394\n            <jats:italic>feoB<\/jats:italic>\n            \u0394\n            <jats:italic>mntH<\/jats:italic>\n            strains were as virulent as the wild type in either of the infection models. Strains were also tested for sensitivity to oxidative stress-generating agents. The \u0394\n            <jats:italic>mntH<\/jats:italic>\n            \u0394\n            <jats:italic>sit<\/jats:italic>\n            strain was the most sensitive strain and was significantly more sensitive than the other strains to hydrogen peroxide, plumbagin, and paraquat.\n            <jats:italic>sit<\/jats:italic>\n            sequences were highly associated with APEC and human extraintestinal pathogenic\n            <jats:italic>E. coli<\/jats:italic>\n            compared to commensal isolates and diarrheagenic\n            <jats:italic>E. coli<\/jats:italic>\n            . Comparative genomic analyses also demonstrated that\n            <jats:italic>sit<\/jats:italic>\n            sequences are carried on conjugative plasmids or associated with phage elements and were likely acquired by distinct genetic events among pathogenic\n            <jats:italic>E. coli<\/jats:italic>\n            and\n            <jats:italic>Shigella<\/jats:italic>\n            sp. strains. Overall, the results demonstrate that SitABCD contributes to virulence and, together with MntH, to increased resistance to oxidative stress.\n          <\/jats:p>","DOI":"10.1128\/iai.00789-07","type":"journal-article","created":{"date-parts":[[2007,11,20]],"date-time":"2007-11-20T02:08:18Z","timestamp":1195524498000},"page":"601-611","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":105,"title":["Contribution of the SitABCD, MntH, and FeoB Metal Transporters to the Virulence of Avian Pathogenic\n            <i>Escherichia coli<\/i>\n            O78 Strain \u03c77122"],"prefix":"10.1128","volume":"76","author":[{"given":"Mourad","family":"Sabri","sequence":"first","affiliation":[{"name":"INRS-Institut Armand-Frappier, Laval, Que\u0301bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Me\u0301lissa","family":"Caza","sequence":"additional","affiliation":[{"name":"INRS-Institut Armand-Frappier, Laval, Que\u0301bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Proulx","sequence":"additional","affiliation":[{"name":"INRS-Institut Armand-Frappier, Laval, Que\u0301bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria H.","family":"Lymberopoulos","sequence":"additional","affiliation":[{"name":"INRS-Institut Armand-Frappier, Laval, Que\u0301bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annie","family":"Bre\u0301e","sequence":"additional","affiliation":[{"name":"INRA, Centre de Tours, Infectiologie Animale et Sante\u0301 Publique UR1282, 37380 Nouzilly, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maryvonne","family":"Moulin-Schouleur","sequence":"additional","affiliation":[{"name":"INRA, Centre de Tours, Infectiologie Animale et Sante\u0301 Publique UR1282, 37380 Nouzilly, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"III","given":"Roy","family":"Curtiss","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, The Biodesign Institute, Arizona State University, Tempe, Arizona 85287"},{"name":"Department of Biology, Washington University, St. Louis, Missouri 63130"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles M.","family":"Dozois","sequence":"additional","affiliation":[{"name":"INRS-Institut Armand-Frappier, Laval, Que\u0301bec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-6445(03)00055-X"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/msb4100050"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1999.01360.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.70.11.6032-6042.2002"},{"key":"e_1_3_2_6_2","first-page":"210","volume":"12","year":"2005","unstructured":"Braun, V. 2005. 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