An animal model of foodborne Listeria monocytogenes virulence: effect of alterations in local and systemic immunity on invasive infection.

Development of foodborne listeriosis is dependent on an interplay between organism-specific virulence factors and host susceptibility. Gastric inoculation of Sprague-Dawley rats was used as a model to explore Listeria-specific virulence and host susceptibility. Gastric inoculation leads to invasive infection with "smooth" hemolytic Listeria monocytogenes but not with "rough" L. monocytogenes or other Listeria species. Infection is dose-dependent with an ID50 of 10(6) virulent Listeria monocytogenes. In these experiments, the ID50 was not altered by pregnancy but invasive infection led to abnormal reproductive outcomes including stillbirth and reabsorption of fetuses. Immunosuppression by cyclosporin A led to more prolonged infection but did not alter the ID50. Manipulation of intestinal flora with antibiotics suggested increased rates of infection with antibiotics that decreased anaerobic flora. Growth of virulent Listeria in milk at varying temperatures did not enhance virulence. No differences in invasive potential of flagellated vs. non-flagellated L. monocytogenes were found. Oral models of invasive Listeria monocytogenes infection provide a useful tool for studying organism virulence and host susceptibility.