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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #141954
Title: THE ROLE OF DIETARY VITAMIN E IN EXPERIMENTAL LISTERIA MONOCYTOGENES INFECTIONS IN TURKEYS

Author
item ZHU, M - IOWA STATE UNIVERSITY
item Wesley, Irene
item NANNAPANENI, R - UNIVERSITY OF ARKANSAS
item COX, M - UNIVERSITY OF ARKANSAS
item MENDONCA, A - IOWA STATE UNIVERSITY
item JOHNSON, M - UNIVERSITY OF ARKANSAS
item AHN, D - IOWA STATE UNIVERSITY

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/21/2003
Publication Date: 10/20/2003
Citation: ZHU, M., WESLEY, I.V., NANNAPANENI, R., COX, M., MENDONCA, A., JOHNSON, M.G., AHN, D. THE ROLE OF DIETARY VITAMIN E IN EXPERIMENTAL LISTERIA MONOCYTOGENES INFECTIONS IN TURKEYS. POULTRY SCIENCE. 2003. v. 82. p. 1559-1564.

Interpretive Summary: L. monocytogenes is a major human bacterial foodborne pathogen which annually accounts for ~ 2,500 cases with a mortality rate of nearly 20%. The goal of this study was to determine if vitamin E, which is known to boost the immune response, protected turkeys against experimental infection. No statistically significant differences were seen in the gut clearance of turkeys on control versus vitamin E diets. However, CD4**+ and CD8**+ lymphocytes, which are required to eliminate infection, were augmented. Therefore, as a general immune stimulant, vitamin E may be an attractive alternative to the on-farm use of antimicrobials and may ultimately contribute to the reduction of Listeria contamination of the final poultry product. This information is of value to both turkey producers and processors.

Technical Abstract: Two experiments were conducted to evaluate the effect of dietary vitamin E in turkeys experimentally infected with Listeria monocytogenes. In Experiment 1, 1-d-old turkeys (n = 90) were assigned to one of three dietary treatments (0, 100 or 200 IU vitamin E). In Experiment 2, 1-d-old turkeys (n = 70) were fed diets containing either 0 or 200 IU vitamin E. In both Experiments 1 and 2, after 6 wk on the experimental diet, turkeys were orally inoculated with L. monocytogenes (~ 109 CFU). To monitor infection status, cloacal swabs were taken on selected days post inoculation (DPI). At necropsy, samples of viscera, including liver, spleen, caecum, proximal and distal small intestine, and large intestine, were collected and cultured for L. monocytogenes. In both Experiments 1 and 2, the recovery of L. monocytogenes from cloacal swabs, tissues, and intestines of turkeys fed vitamin E was generally lower than that of turkeys fed the control diet, although these differences were not statistically significant. In Experiment 1, L. monocytogenes was detected more frequently in cloacal swabs of control diet turkeys than in turkeys assigned to the vitamin E diet groups. In Experiment 2, L. monocytogenes was not recovered in cloacal swabs of birds fed 200 IU vitamin E at 6 DPI, yet was cultured in control birds at 8 DPI. There were no changes in virulence characteristics of L. monocytogenes cells, as measured by in vitro killing of Ped-2E9 cells, recovered from either cloacal swabs or tissues of experimentally infected turkeys fed either control or vitamin E treatment diets. Flow cytometric analysis indicated that CD4+ and CD8+ lymphocytes were elevated at 6- and 8-DPI in infected turkeys given 200 IU vitamin E. Taken together, these data suggest that vitamin E may stimulate host defenses, which may augment clearance of L. monocytogenes.