Submitted to: Meeting Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 5/28/2009
Publication Date: 9/30/2009
Citation: Bearson, B.L., Bearson, S.M. 2009. Differences in Pathogenesis for Salmonella enterica serovar Typhimurium in the Mouse Versus the Swine Model Identify Bacterial Gene Products Required for Systemic but not Gastrointestinal Disease. International Symposium on the Epidemiology and Control of Foodborne Pathogens in Pork, September 30-October 2, 2009, Quebec City, Canada. p. 88. Interpretive Summary:
Technical Abstract: Over the last several decades, the mouse model of Typhoid fever has been an extremely productive model to investigate Salmonella enterica serovar Typhimurium pathogenesis. The mouse is the paradigm for investigating systemic disease due to infection by Salmonella; however, the swine model of gastrointestinal colonization and enteric disease due to Salmonella is better suited to address food safety. Although certain Salmonella mutants may be attenuated for colonization and disease in both the mouse and swine model, others may only be attenuated in one of the models depending on whether the gene product is required for gastrointestinal or systemic disease. Recent research performed on the swine model in our laboratories with comparison to the literature on the mouse model, illustrates the discrepancy between these two models. The fepA iroN and cirA gene products of S. Typhimurium are required for iron acquisition by uptake of enterochelin, salmochelin, and their breakdown products. In the mouse model, a S. Typhimurium mutant with deletions in the fepA iroN and cirA genes is attenuated for disease. In contrast, no significant difference in gastrointestinal colonization or fecal shedding was found comparing a S. Typhimurium fepA iroN cirA mutant to wild-type in the swine model. Furthermore, investigation of a two-component system for sensing the bacterial environment has demonstrated that inactivation of the qseBC (preAB) genes has a two-day delay in mouse mortality and a competitive defect in the liver and spleen compared to wild-type S. Typhimurium. However, in the pig no significant difference was observed in fecal shedding or gastrointestinal colonization between the qseBC mutant and the wild-type strain. The difference between these two models suggests roles in systemic but not gastrointestinal disease for these S. Typhimurium gene products and highlights the importance of utilizing the swine model for the development of Salmonella interventions to enhance pork safety.