Source: OHIO STATE UNIVERSITY - VET MED submitted to NRP
GASTRIC MICROBES AND THE DEVELOPMENT OF GASTRIC ULCER DISEASE IN SWINE: POTENTIATION OF DISEASE BY MANIPULATION OF DIET
Sponsoring Institution
National Institute of Food and Agriculture
Project Status
COMPLETE
Funding Source
ANIMAL HEALTH
Reporting Frequency
Annual
Accession No.
0200911
Grant No.
(N/A)
Cumulative Award Amt.
(N/A)
Proposal No.
(N/A)
Multistate No.
(N/A)
Project Start Date
Apr 1, 2004
Project End Date
Sep 30, 2004
Grant Year
(N/A)
Program Code
[(N/A)]- (N/A)
Recipient Organization
OHIO STATE UNIVERSITY - VET MED
1900 COFFEY ROAD, 127L VMAB
COLUMBUS,OH 43210
Performing Department
PATHOBIOLOGY
Non Technical Summary
Gasroesophageal ulceration (GEU) of the pars esophagea, gastric inflammation (equivalent to type B gastritis in humans) are responsible for 3% annual mortality in swine. A further 10% of hogs (roughly 60 million in the USA) develop anemia adn unthriftiness attributable to gastric disease. Economic losses are substantial. Data obtained from these studies will provide the rationale for implementation of additional measures (specifically, parenteral vaccinations) for the prevention of gastric disease in conventional swine
Animal Health Component
80%
Research Effort Categories
Basic
20%
Applied
80%
Developmental
(N/A)
Classification

Knowledge Area (KA)Subject of Investigation (SOI)Field of Science (FOS)Percent
31135101100100%
Knowledge Area
311 - Animal Diseases;

Subject Of Investigation
3510 - Swine, live animal;

Field Of Science
1100 - Bacteriology;
Goals / Objectives
We wish to determine if dual colonization of gnotobiotic swine with both microbial species (Helicobacter and Lactobacillus) potentiates gastric mucosal inflammation, GEU and gastric mucosal ulceration. The microbial hypothesis of porcine gastric disease predicts that: 1. The gastric mucosal inflammatory response, a prerequisite for mucosal ulcers and GEU,is potentiated in H heilmannii and L fermentum-colonized gnotobiotic piglets fed sow replacement diet; and 2. Gastric mucosal inflammation, mucosal ulcers and GEU are further potentiated and becomes clinically evident in H heilmannii and L fermentum-colonized gnotobiotic piglets fed a liquid sow milk replacement diet containing fermentable carbohydrate.
Project Methods
1.Experiment 1 will determine if gastric co-colonization of gnotobiotic swine with both H heilmannii and L fermentum results in gastritis, ulcers and GEU greater than that observed by gastric colonization with either agent alone. Experiment 2 will determine if gastric co-colonization of gnotobiotic swine with both H heilmannii and L fermentum and supplemented with 5-15% liquid corn syrup ulcerogen in the diet in gastritis, ulcers and GEU greater than that observed by gastric colonization with both agents together

Progress 04/01/04 to 09/30/04

Outputs
In these experiments, we report induction of erosions and gastroesophageal ulcers (GEU) in the pars esophagea of young gnotobiotic swine fed a carbohydrate-enriched liquid diet and infected with two different fermentative commensal bacteria, Lactobacillus, Bacillus ssp., and a newly identified swine gastric Helicobacter pylori-like species. In contrast, piglets, fed a similar diet and inoculated with Helicobacter heilmannii, a helicobacter species which colonizes the gastric mucosa as a commensal, did not develop GEU.

Impacts
Experimental GEU likely develops secondary to epithelial damage mediated by microbial acidic products of carbohydrate metabolism and parietal cell origin hydrochloric acids whose production is potentiated by dietary carbohydrate.

Publications

  • Krakowka, S., Eaton, K. A., Rings, D. M. and Agrenzio, R. A. 1998. Production of Gastroesophageal Erosions and Ulcers (GEU) in Gnotobiotic Swine Monoinfected with Fermentative Commensal Bacteria and Fed High Carbohydrate Diet. Vet. Pathol, 35:274 282.