Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: A study in gnotobiotic piglets

Abstract

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteri­tis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were innoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar de­creased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thy­midine kinase activities. Also we noted comparable dimi­nution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls. We conclude that small intestinal recovery of the undernourished animal after viral enteritis is prolonged and speculate that impaired mucosal repair is important determinant of the delayed recovery of structural and functional abnormalities in this animal model of a major human disease. © 1985 International Pediatric Research Foundation, Inc.