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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Poultry Microbiological Safety & Processing Research » Research » Publications at this Location » Publication #347440

Research Project: Production and Processing Intervention Strategies for Poultry Associated Foodborne Pathogens

Location: Poultry Microbiological Safety & Processing Research

Title: Effect of dietary fructooligosaccharide supplementation on internal organs Salmonella colonization, immune response, ileal morphology and ileal immunohistochemistry in laying hens challenged with Salmonella Enteritidis

Author
item ADHIKARI, PRATIMA - University Of Georgia
item Cosby, Douglas
item Cox, Nelson - Nac
item FRANCA, M - University Of Georgia
item WILLIAMS, S - University Of Georgia
item GOGAL JR, R - University Of Georgia
item RITZ, CASEY - University Of Georgia
item KIM, WOO - University Of Georgia

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/8/2018
Publication Date: 6/22/2018
Citation: Adhikari, P., Cosby, D.E., Cox Jr, N.A., Franca, M.S., Williams, S.M., Gogal Jr, R.M., Ritz, C.W., Kim, W.K. 2018. Effect of dietary fructooligosaccharide supplementation on internal organs Salmonella colonization, immune response, ileal morphology and ileal immunohistochemistry in laying hens challenged with Salmonella Enteritidis. Poultry Science. 97:2525-2533. https://doi.org/10.3382/ps/pey101.
DOI: https://doi.org/10.3382/ps/pey101

Interpretive Summary: Controlling Salmonella Enteritidis contamination of laying hens is an ongoing issue in the poultry industry and the food industry. Use of feed additives to alter the intestinal microflora has been proposed as a way to control the Salmonella Enteritidis contamination. This research demonstrates that the use of fructoligosaccharides reduces the levels of cecal and fecal contamination, impairs Salmonella Enteritidis pathogenesis and modulates humoral immunity within the gut associated lymphoid tissue.

Technical Abstract: A study was conducted to evaluate the efficacy of fructoligosaccharides (FOS) in controlling the infection of Salmonella Enteritidis (SE) in White Leghorns. Thirty laying hens/experiment x 2 experiments were challenged both orally (OR) and intracloacally (IC) with approximately 108 colony forming units (cfu) of nalidxic acid resistant SE (SENAR) and divided into 3 treatments: 1) SENAR challenged + 0.0 % FOS 2) SENAR challenged + 0.5% FOS (Nutraflora®); and 3) SENAR challenged + 1.0% FOS. SENAR recovery via fecal shedding was measured at 3 and 6-day post-infection (dpi) whereas in the ceca and internal organs, SENAR recovery was measured at 7 dpi. In the first experiment, there was a 1.0 log10 and a 1.3 log10 reduction in cecal SENAR by supplementation of FOS at 0.5 and 1.0%, respectively. In the second experiment, there was a 0.6 log10 and a 0.8 log10 reduction in cecal SENAR by supplementation of FOS at 0.5 and 1.0%, respectively. Fecal shedding was significantly lower in 1.0% FOS supplemented groups compared to SENAR challenge 0.0% FOS. There was no significant difference among the three treatments on SENAR recovery in liver with gall bladder (L/GB) and ovaries. However, the frequency of positive SENAR in the ovaries (10 to 40%) in SENAR challenge 0.0 % FOS was significantly lower than L/GB (60 to 80%) in both experiments. There was a significant upregulation of toll-like receptor (TLR)-4 in 1.0% FOS and interferon gamma (IFN- ') in both 0.5 and 1.0% FOS. Histologic measurements of ileal villi height (VH) and crypt depth (CD) were similar across all treatments. Immunohistochemistry analyses of ileal samples showed that immunoglobulin A (IgA) positive cells increased as FOS concentration increased reaching significance at 1.0% as well as altered cytokine gene expression in the ileum. Further, FOS supplementation also reduced cecal SENAR and feces SENAR levels. Collectively, the results suggest that dietary supplementation with FOS may impair SE pathogenesis while modulating humoral immunity within the gut associated lymphoid tissue (GALT).