B-191. ‘Form Variation’ of the O12 Antigen Is Critical for Persistence of Salmonella enterica serotype Typhimurium in the Murine Intestine

L. Bogomolnaya1, C. Santiviago2, A. Bugbee1, H-J. Yang1, A. J. Baumler3, H. L. Andrews-Polymenis1;
1Texas A&M Univ. System Hlth. Sci. Ctr., College Station, TX, 2Univ. de Chile, Santiago, CHILE, 3Univ. of California, Davis, CA.

S. enterica subspecies I serotypes are responsible for the vast majority of salmonellosis in mammals and birds, yet only a few factors specific to this group that allow them to persist in this niche have been identified. We show that STM0557, a subspecies I specific gene encoding an inner membrane protein, is critical for fecal shedding and persistence of Salmonella enterica serotype Typhimurium ATCC14028 in the intestine of Salmonella-resistant mice (CBA/J). This gene and two others (STM0558 and 0559) are located on a recently described pathogenicity island termed SPI-16, and they resemble genes of the gtr locus (gtrA,B, gtr(type)) in several bacteriophages of Shigella flexneri. In Shigella, these genes are responsible for serotype conversion by addition of a glucose residue to repeating O-antigen subunits. We show by GC-MS that the serotype Typhimurium orthologs of these genes, STM0557-0559, are responsible for ‘form variation’ by glucosylating the galactose residue in the O12 antigen repeat unit at the C4 position to generate the 12-2 O-antigen variant. We further show that form variation occurs upon exposure and during intracellular growth of serotype Typhimurium in J774 macrophages, and is more highly expressed in bacteriologic media in the absence of STM0559.

127/B. Genetic Organization of Pathogens

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