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Infect. Immun. doi:10.1128/IAI.00789-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of an avian pathogenic Escherichia coli (APEC) O78 strain

INRS-Institut Armand-Frappier, Laval, Québec, CANADA; INRA - Centre de Tours - Infectiologie Animale et Santé Publique UR1282, 37380 Nouzilly, France; Center for Infectious Diseases, The Biodesign Institute. Arizona State University, Tempe, AZ, 85287 U. S. A.; Department of Biology, Washington University, St. Louis, MO, U.S.A. 63130

^* To whom correspondence should be addressed. Email: charles.dozois{at}iaf.inrs.ca.

	Abstract

The roles of SitABCD, MntH, and FeoB metal transporters for virulence of APEC O78 strain 7122 were assessed using isogenic mutants in chicken infection models. In a single-strain infection model, compared to 7122, the sit strain demonstrated reduced colonization of the lungs, liver, and spleen. Complementation of the sit strain restored virulence. In a co-infection model, compared to the virulent APEC strain, the sit strain demonstrated a mean 50-fold, 126-fold, and 25-fold decrease in colonization of the lungs, liver, and spleen respectively. A mntHsit strain was further attenuated, demonstrating reduced persistence in blood, and a mean 1400-fold, 954-fold, and 83-fold reduced colonization in lungs, liver, and spleen respectively. In co-infections, the feoBsit strain demonstrated reduced persistence in blood, but increased colonization of the liver. The mntH, feoB, and feoBmntH 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 mntHsit strain was the most sensitive strain and was significantly more sensitive to hydrogen peroxide, plumbagin and paraquat. sit sequences were highly associated with APEC and human ExPEC compared to commensal isolates and diarrheagenic E. coli. Comparative genomic analyses also demonstrated that sit sequences are encoded on conjugative plasmids or associated with phage elements, and have likely been acquired by distinct genetic events among pathogenic E. coli and Shigella spp. Overall, results demonstrate that SitABCD contributes to virulence and, together with MntH, to increased resistance to oxidative stress.