Physiological responses of the small intestine to nutritional factors and rotavirus infection afflicting young pigs

Life of the young pig is influenced by nutritional, immunological, environmental, and behavioral factors. In this thesis, four experiments are described that concern positive and negative factors that influence the physiology of the small intestine in young pigs. Experiment 1: After early-weaning, pig performance is decreased mainly by a reduction in feed intake, which impacts swine production negatively. Feeding a milk replacer the first week after weining more than doubled weight gain compared to weaning to starter diet. Weaning to milk replacer might overcome negative effects of early-weaning by increasing feed intake. Experiment 2: Soy proteins are used as protein source for infants with allergies to cow milk protein; however, soy proteins might initiate allergic reactions as well. Partial enzymatic hydrolysis of soy proteins did not result in elevated plasma concentrations of free amino acids, glucose and pancreatic hormones. Therefore, hydrolyzed soy proteins are an acceptable protein source for infants. Removal of trypsin inhibitors and partial enzymatic hydrolysis of soy protein source creates an acceptable protein source for young pigs. Experiment 3: Rotavirus infection causes damage of the mucosa in the small intestine resulting in severe watery diarrhea. Presumably, rotaviral diarrhea is caused by a reduction of enzymatic and absorptive capacity in the small intestine, resulting in a malabsorptive-type diarrhea. Growth factors, e.g. epidemal growth factor (EGF) stimulate cell proliferation in the small intestine. Inclusion of EGF in milk formula stimulated recovery of the mucosa in the small intestine after a rotavirus infection. Addition of EGF to infant formulas might stimulate intestinal recovery of infants after viral gastroenteritis. Experiment 4: Malnutrition retards mucosal development in the small intestine. Therefore, malnutrition in combination with rotavirus infection might be a more chronic stress to the small intestine than rotavirus infection by itself. Malnutrition prolonged diarrhea and delayed recovery of the mucosa in the small intestine after rotavirus infection. Rotavirus caused increased tissue concentration of PGE$\sb2$ and increased expression of major histocompatibility genes. Rotaviral diarrhea causes an inflammatory response in the mucosa in the small intestine, which might stimulate secretory diarrhea. Malnutrition influenced the inflammatory response to rotavirus and might thereby prolong diarrhea.U of I OnlyETDs are only available to UIUC Users without author permissio