Impact of Yersinia enterocolitica enteritis on disaccharidase activity and small intestinal morphology in colostrum-deprived newborn piglets

Shu, D.; Simpson, H.V.; Xu, R.J.; Mellor, D.J.; Reynolds, G.W.; Marshall, R.B.

New Zealand Veterinary Journal 45(1): 27-36

1997


ISSN/ISBN: 0048-0169
PMID: 16031944
DOI: 10.1080/00480169.1997.35984
Accession: 002865278

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Abstract
Newborn, colostrum-deprived piglets were infected with a human isolate of Y. enterocolitica (serotype O:3, biotype 4). The piglets were killed 3 days (n=6) or 5 days (n=8) after infection, or antibiotic therapy was commenced on day 5 and the animals killed on day 14 (n=5). Compared with the non-infected controls, infected animals had reduced mucosal lactase and sucrase, but not maltase activity, while after antibiotic therapy, previously infected piglets had a lower lactase and a higher maltase and sucrase activity. Lactase activity was significantly reduced in the duodenum and jejunum, and mean values were lower in the ileum, but the difference did not reach significance; maltase activity was greater at all ages from the distal jejunum to the mid-ileum; sucrase activity was reduced in all segments up to day 5 but after antibiotic therapy was increased in the jejunum and appeared early in the ileum. Enzyme profiles were more mature along the crypt-villus axis in some segments of the intestine in previously infected piglets. Sodium-potassium-ATPase activity was unchanged. There was a reduced villus height:crypt depth ratio, crypt hyperplasia and increased crypt cell proliferation. Morphological maturation, indicated by loss of vacuoles and location of the nucleus at the base of the enterocyte, proceeded distally from the duodenum to ileum from 3 to 14 days of age when only the ileum remained immature. In infected piglets, there was reduced vacuolation and earlier location of the nucleus at the base of the cell in the distal intestine. It is concluded that accelerated maturity of specific disaccharidases and enterocyte morphology in infected piglets appears to be due to physical damage to the mucosa resulting in faster proliferation of crypt cells and migration of enterocytes. It is suggested that this may reduce macromolecular internalization and impair the ability to utilize dietary carbohydrate and may have long-term effects on growth and immunological responses of the gut.