IMPACT OF CHRONIC PROTEIN-CALORIE MALNUTRITION ON SMALL INTESTINAL REPAIR AFTER ACUTE VIRAL-ENTERITIS - A STUDY IN GNOTOBIOTIC PIGLETS

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, small intestinal structure, enzyme activity, and Na transport were examined 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 inoculated 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, a further decrease in weight gain and an increased mortality were observed only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities were seen. Comparable diminution of glucose-stimulated jejunal Na absorption was seen 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. Small intestinal recovery of the undernourished animal after viral enteritis is prolonged and impaired mucosal repair is an important determinant of the delayed recovery of structural and functional abnormalities in this animal model of a major human disease.