Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 11/11/2009
Publication Date: 12/6/2009
Citation: Eicher, S.D., Lay Jr, D.C., Rostagno, M.H. 2009. Feed Withdrawal and Transport Interactions with Intestinal and Peripheral Immunity. Research Workers in Animal Diseases Conference Proceedings. p. 107.
Technical Abstract: Multiple stressors associated with transporting finishing pigs to slaughter can result in increased shedding of pathogens. Previously we found feed withdrawal by itself or followed by transportation increased Salmonella concentrations in ileal contents. However, no difference was found among treatments in frequency of Salmonella-positive samples, and rectal contents consistently contained very low concentrations of Salmonella regardless of treatment. The objective of this study was to evaluate the effects of transport and feed withdrawal on intestinal and peripheral immunity of transported finishing pigs. Finishing pigs (n=60) were assigned to one of four treatments: control (C), 12-h feed withdrawal (FW), 2-h transport (T), or feed withdrawal and transport (FWT). Blood was collected for differential counts and cortisol concentrations. Lung, spleen, and mesenteric lymph nodes were collected for RNA expression of IL-1ß, IL-1 receptor antagonist (Ra), TNF-a, and anti-microbial peptide PR-39. Total WBC and eosinophil counts were greatest (P<0.01) for T compared with other treatments. Transport treatments had greater neutrophil counts and fewer lymphocyte and monocyte counts compared to non-transported pigs (P<0.01). Hematocrit percentages and plasma cortisol concentrations did not differ among the treatments. Lung and mesenteric lymph node tissues did not differ in RNA expression of IL-1ß, IL-1Ra, TNF-a, or PR-39. Although spleen tissue did not differ for IL-1ß and TNF-a expression, IL-1Ra tended to be greater for T compared with FWT (P= 0.07) and T pigs tended to have more PR-39 than FWT (P=0.06) and C (P=0.09). These data imply that although immunity is activated, opportunity for innate immune modulation of a pathogen in this time frame is very limited.