Molecular basis of foodborne disease risk of variants of Salmonella Typhimurium DT193 and U288

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The considerable economic and health impact of pathogens of the genus Salmonella is the result of their presence in livestock and poultry, entry into and survival within the food chain, and their ability to cause intestinal or systemic disease. However, not all variants of Salmonella are equally likely to cause disease in man and an understanding of the molecular basis of the likelihood that a particular variant will enter the food chain and cause disease in man is critical to food safety. Some variants of Salmonella are prevalent in food animals yet are not a predominant cause of human clinical infections. This research proposal seeks to address these questions using a molecular epidemiology and comparative whole genome sequence approach combined with classical molecular biology and infection models to compare two highly related variants of S. Typhimurium (DT193 and U288) that exhibit distinct risk profiles for foodborne disease in man, despite similar epidemiology in livestock. Little is known about the variation in genotype and phenotype of closely related variants of bacterial pathogens circulating in zoonotic reservoirs and the environment. Crucially, genotypic polymorphisms are not only potential candidate targets for intervention strategies aimed at decreasing the likelihood that these pathogens enter the food chain but also targets for distinguishing variants of pathogens that differ in their risk to food safety, useful for surveillance. This study will define the molecular epidemiology of common variants of Salmonella Typhimurium in the UK pig herds and those entering the food chain via abattoirs by analysis of whole genome sequence variation. Genotypic, transcriptomic and phenotypic variation will be determined and important genotypic differences understood in the context of their associated phenotype by whole genome recombination and mutagenesis approaches.

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