Submitted to: Meeting Abstract
Publication Type: Proceedings
Publication Acceptance Date: 2/1/2003
Publication Date: 8/1/2003
Citation: Czuprynski, C.J., Faith, N.G., Tamplin, M.L., Uhlich, G.A., Wonderling, L.D., Bayles, D.O., Luchansky, J.B. 2003. Environmental, host, and bacterial factors that influence the pathogenesis of gastrointestinal listeriosis. Meeting Abstract. Part 8,Section 15, No.3. Interpretive Summary:
Technical Abstract: Listeria monocytogenes is an intracellular pathogen whose site of residence in the human body during the early stages of infection is not known. To better understand the pathogenesis of this bacterium, it is important to develop suitable models for studying listeriosis. We have identified the A/J mouse as a suitable model for investigating gastrointestinal (GI) listeriosis. This particular strain of mouse is not immune deficient, but it does possess an innate susceptibility to infection with L. monocytogenes via various routes, including the GI tract. Prefatory experiments suggested that the severity of infection may be greater in A/J mice inoculated with L. monocytogenes previously grown on slices of turkey meat rather than in microbiological media. Studies are ongoing to confirm this with other types of food and to investigate if growth on turkey meats affects the ability of L. monocytogenes to invade or multiply in intestinal epithelial cells (Caco-2 cells) or fibroblasts (HeLa or 3T3 eclls).These experiments also demonstrated that a serotype 4b strain was more virulent by intragastric inoculation than a serotype 1/2a and a serotype 1/2b strain. In related studies, we made the novel observation that anesthesia with sodium pentobarbital results in a dramatic, but transient, increase in the susceptibility of mice to intragastric inoculation. Collectively, these efforts will increase our understanding of how different strains of L. monocytogenes vary in their ability to cause illness, how innate defense mechanisms combat infection, and how growth on different food products might alter the virulence of this bacterium in the GI tract.