Endogenous factors and mechanisms that confer resistance to Salmonella enteritidis infectivity in the intestinal tract of Leghorn chickens

Abstract

Four experiments are reported to explain some of the endogenous factors and mechanisms which confer resistance to Salmonella enteritidis (SE) infectivity in the intestinal tract of Leghorn chicks: (A) The effects of 14 or 19 days of 10% dietary lactose administration on SE infection, and pH, histological, morphometric and organic acid changes of the ceca. In both trials, the observed lactose-induced resistance to SE organ invasion following 14 days (P < 0.001) or 19 days (P < 0.005) was associated not only which an increase in organic acid concentration and acidic cecal pH (P < 0.05), but with measurable morphologic changes of the cecal mucosa as well (P < 0.05). (B) The effects of 14 or 19 days of 18 ppm dietary capsaicin administration on SE infection, and histological, morphometric and pH changes of the ceca. In both trials, the observed capsaicin-induced resistance to SE organ invasion (P < 0.05) was associated with measurable pH and morphometric changes of the cecal mucosa (P < 0.05) due to the presence of inflammatory cells in lamina propria. (C) The effect of prophylactic treatment of chickens with the soluble products from Con A-stimulated SE-immune T-cells on SE infection, histological and morphometric changes. In these experiments, the resistance to SE organ infectivity was associated with a significant increase in lamina propria thickness based on morphometric analysis (P < 0.05). This increase appears to be due to a marked infiltration of inflammatory cells, indicating that the protective effect of prophylactic administration of lymphokines, prepared from Con A-activated SE-immune T-cells, against a challenge infection with SE is associated with measurable and morphometric changes of the cecal mucosa. (D) Comparable measurable and morphometric changes were associated with the significant decrease in SE organ infectivity (P < 0.05) following the administration of either low doses of Eimeria tenella (ET) or high doses of the heterologous Eimeria adenoeides (EA). In both trials, a significant correlation, (r = -0.98) for ET or (r = -0.99) for EA, between organ invasion and lamina propria thickness was observed, suggesting that the thicker the lamina propria is, due to the presence of inflammatory cells, the less SE organ invasion occurs.