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Experiments were desinged to test the hypothesis that structural and chemical changes in the small intestine associated with total parenteral nutrition (TPN) alter relationships between hosts and enteric parasites. Parenteral feeding of rats immunized to Trichinella spiralis (nematoda) led to a decrease in gut mass. This was reflected by a significant drop in gut wet weight and reductions in mucosal dry weight, DNA, protein, carbohydrate and lipid. These changes were accompanied also by lowered brush border enzyme activity. When challenged orally with 8 X 10(3) T. spiralis larvae and switched immediately to oral feeding, more worms became established in the small intestines of these rats than in rats given similar doses of larvae, but maintained by oral feeding throughout the experiment. Despite the significant difference in initial worm burden, both enterally fed and parenterally fed rats completely expelled their parasites by 7 and 8 days postinfection, respectively. Results indicated that factors involved in preventing establishment of T. spiralis in immunized rats were suppressed by the prolonged absence of food from the GI tract, whereas factors responsible for expelling worms that were able to gain residence in the mucosa appeared to be unaltered or at least functionally reversible.

Experiments were designed to test the hypothesis that alterations of intestinal motility accompany enteric helminth infections. Motility was measured in rats during the intestinal phase of infection with the nematode Trichinella spiralis by following the transit of radioactive chromium through the gut. Intraduodenal catheters were surgically implanted in rats. One week after the operation one group of animals was infected with 8 x 10(3) T. spiralis larvae and a second group was infected with 16 x10(3) larvae. A third group of uninfected rats served as controls. Three, four, or five days postinfection, Na2 51CrO4 was injected through the catheter into the duodenum or fasted animals and its propulsion through the small bowel was allowed to progress for 15 min. The distribution of radioactivity throughout the small intestine and cecum was then plotted as a function of gut length. Intestinal transit was increased significantly by infection. The leading edge of radioactivity transversed 100% of the gut length in infected rats and 70% in controls. The amount of injected radioactivity transversing the midpoint of the small intestine was estimated by regression equations to be 38% of the injected dose for control rats and 59 and 57% for infected groups. Increased propulsive activity in parasitized rats was associated with inflammatory changes and a significant reduction in disaccharidase levels in the gut mucosa. The latter conditions were most marked in the proximal small bowel where the majority of worms resided.

The importance of the presence of food in the gastointestinal (GI) tract in maintaining normal enzyme activity in the small intestine was investigated in rats that were kept from eating for as long as 2 weeks. During this time animals were sustained on a nutrient solution administered intravenously. Enzyme activity and small bowel mass in these animals and similiar parameters in rats that were administered the same solution orally were compared with control groups fed an essentially isoenergetic diet of stock rat food and water. Disaccharidase and peroxidase levels in mucosal scrapings expressed as activity/milligram protein, activity/intestine, and activity/100 g body weight, were significantly reduced in intravenously nourished rats but not in rats receiving the solution orally. In addition to changes in enzyme activities, parenteral feeding was accompanied by a significant reduction in the small bowel weight:body weight ratio as compared with that of rats fed the stock diet or nutrient solution orally. Results support the conclusion that normal activity of intestinal enzymes spatially distributed with regard to depth within the mucosa depends on the presence of food in theGI tract and cannot be maintained at normal levels by total intravenous nutrition.