[Frontiers in Bioscience 2, d471-481, September 15, 1997]

Table of Conents
 Previous Section   Next Section


Guillermo G. Gomez

Department of Animal Science, North Carolina State University, Raleigh, NC 27695-7626 and Center for Gastrointestinal Biology and Diseases, Chapel Hill and Raleigh, NC

Received 9/5/97 Accepted 9/10/97


Young conventional pigs infected with human rotavirus have shown viral invasion of villous epithelium, lesions on jejunal mucosa and depression in mucosal disaccharidase activity (13). Viral induced histopathological changes have been restricted to the small intestine and were more pronounced within the jejunum and the ileum (12). Severe stunting of villi has been reported in studies with gnotobiotic pigs infected with either porcine rotavirus (12, 17) or neonatal calf rotavirus (9), as well as with conventional pigs infected with human rotavirus (13) and colostrum-deprived pigs infected with porcine rotavirus (20 - 22). As a consequence of these changes, villi surface area was significantly reduced (21).

Villous atrophy in pigs with clinical signs of rotaviral enteritis appeared to be more severe between 24 and 48 hours after the onset of diarrhea (12). In addition, crypt hyperplasia has been found in most studies (12, 13, 17, 22) but crypt depth was not affected in infected pigs studied by Rhoads et al. (21).

Table 2 presents data on villi height, crypt depth and lactase activity at the mid-jejunum and mid-ileum of non-infected and rotavirus-infected pigs at different infective stages (Gomez et al., unpublished results). Jejunal and ileal villi height in infected pigs at 7 days post-inoculation were reduced (p < .05) to ~70% and 42%, respectively, while jejunal crypt depth was 60% higher than that of non-infected control pigs of similar age. By the end of the trial or 13 days after inoculation, jejunal and ileal villi were still shorter (p < .05) than villi of non-infected pigs as well as of villi of pigs before rotavirus inoculation. Our results indicate that the shortening of ileal villi was more pronounced than that observed in jejunal villi, in part due to the fact that ileal villi in non-infected pigs grew taller than jejunal villi from 6 to 13 or 19 days of age. Neonatal pigs inoculated at 8 days of age with a higher dose of rotavirus inoculum (8.4 x 108 particles per pig) than that used in this study (7.8 x 104 particles administered at 6 days of age) and evaluated at 4 rather than 7 days post-inoculation had a more dramatic reduction of both jejunal and ileal villi height (22).

Table 2. Jejunal and ileal villi height (VH in micrometers), crypt depth (CD in micrometers) and lactase activity1 in non-infected and rotavirus-infected neonatal pigs at different infective stages.





Infective stage








6 days of age - before rotavirus inoculation



563 79

129 4

94 8

597 50

157 18

86 14

13 days of age or 7 days post-inoculation



637 70a

136 17b

77 8a

1029 128a

173 18

109 14a



442 41b

218 22a

46 8b

437 11b

172 21

37 4b

19 days of age or 13 days post-inoculation



625 50a

148 9b

56 5a

1169 134a

148 9b

52 3a



498 32b

210 16a

39 3b

533 54b

190 8a

34 3b

1:Expressed as micromoles of lactose hydrolyzed per minute per g of protein. 2:Values are means SE. Values in a column, within each infective stage, with unlike superscripts are different (p < .05).

Rotaviral-induced villous atrophy appears to be due to a rapid and extensive infection of the differentiated epithelial cells that subsequently leads to their accelerated desquamation from the villi (12) and the resulting diarrhea in rotavirus-infected animals seems to be caused by the repopulation of the damaged mucosa with immature cells that cannot absorb nutrients (13). The decrease or loss in body weight following rotavirus infection and the mortality of pigs presumably are the result of gut damage as evidenced by the depression in the activity of intestinal enzymes and the subsequent impaired or abnormal villous-digestive processes. Lactase has been extensively studied as the main marker enzyme in rotavirus gastroenteritis because it is localized on the brush border of differentiated epithelial cells and not in the crypts or the lower portions of the villi of the small intestine, it occurs at maximum concentrations in neonatal mammals and gradually decreases with age (67), and it appears to function as a combined receptor and uncoating enzyme for rotaviruses (68).

Rotavirus infection depressed lactase-specific activity in the duodenal mucosa of children (69) as well as in the jejunal and ileal mucosa of pigs (13, 16, 20 - 22, 66). The decrease in jejunal and ileal lactase-specific activity at 7 and even 13 days post-inoculation found in our recent study (Table 2, Gomez et al., unpublished results) confirms these reports. The magnitude in the depression of lactase-specific activity appears to be associated, at least to some extent, with the dose of rotavirus used as evidenced by a larger reduction of lactase activity in pigs infected with inoculum containing a high concentration of rotavirus (22). Our data on jejunal and ileal lactase activity (21, 22; Gomez, unpublished results) clearly indicate that even when pigs have recovered from diarrhea induced by rotaviral infection, their gut is still not fully recovered as evidenced by shorter villi and lower lactase activity than that found in non-infected pigs of similar age (Table 2).

Activities of other intestinal enzymes such as sucrase (66), alkaline phosphatase (16, 20, 66), leucine aminopeptidase (16) and Na+,K+-ATPase (20, 66) have also been depressed by rotavirus infection in pigs. Absorption of Na+ and water in jejunum and ileum (66) as well as active glucose transport in the mid-jejunum (Gomez & Black, unpublished data) have been significantly decreased in rotavirus-infected pigs. On the other hand, activity of thymidine kinase, a crypt cell enzyme involved in mucosal regeneration, has been shown to increase threefold in rotavirus-infected pigs as compared to values of control, non-infected pigs (20).