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K R Parsons

Publications and source records attributed to K R Parsons.

61 records · Page 4Linked to original sources

Plasma enteroglucagon and neurotensin levels in gnotobiotic calves infected with enteropathogenic and non-enteropathogenic viruses.

Five gnotobiotic calves were each infected with five viruses. Each calf was inoculated with coronavirus at seven days old, followed by astrovirus, Newbury agent, parainfluenzavirus type 3 and rotavirus at intervals of two weeks. Three of the viruses were enteropathogenic (bovine coronavirus, bovine calici-like virus and bovine rotavirus) and two were not (bovine astrovirus and parainfluenzavirus type 3). Plasma levels of the peptide hormones enteroglucagon and neurotensin and faecal output were measured daily and xylose absorption was studied before and after each infection. A close correlation was found between a rise in plasma enteroglucagon and neurotensin and infection with enteropathogenic viruses. The three enteropathogenic viruses caused increased daily faecal output, and elevated plasma levels of enteroglucagon and neurotensin, while the non-enteropathogens did not. The calici-like virus and rotavirus but not the coronavirus caused xylose malabsorption.

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Localisation of enteropathogens in paraffin embedded tissue by immunoperoxidase.

An indirect immunoperoxidase technique has been used to identify enteropathogens in formol-sublimate fixed paraffin embedded sections of calf intestine. Infections with bovine rotavirus, bovine coronavirus, Newbury agent SRV -1, and K99+ Escherichia coli have been detected in the intestines from experimentally infected and conventially reared diarrhoeic or normal calves. The ability to visualize enteropathogenic agents in histological sections resulted in the demonstration of virus infected cells at sites not previously shown to be infected using the immunofluorescence technique.

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Lesions of gnotobiotic calves experimentally infected with a calicivirus-like (Newbury) agent.

Fourteen gnotobiotic calves were killed 0.5 to ten days after infection with Newbury agent SRV-1 and the changes in small intestinal structure and function were assessed, qualitatively and quantitatively, by light microscopy, scanning and transmission electron microscopy, enzymology and xylose absorption. The first enterocytes detected as infected by immunoperoxidase were those on the sides of villi at the base. Subsequently exfoliation of degenerate enterocytes resulted in stunted villi; mucosal beta-galactosidase activity fell and there was xylose malabsorption. Small intestinal damage, first detected at 12 hours after infection but almost repaired by ten days, was restricted to the anterior half of the small intestine. In the distal small intestine, where no virus-induced damage occurred, villi lengthened--possibly due to increased mitosis of crypt cells stimulated by enteroglucagon release.

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Quantitation of small intestinal structure and function in unthrifty piglets.

Litters of piglets were weighed at birth, weaning and five weeks later; pairs of thrifty and unthrifty weaned pigs were identified. Small intestinal structure and function were studied in 28 eight-week-old age-matched littermate pairs and in 16 weight-matched littermates. A comparison of age-matched piglets showed changes in mucosal structure in unthrifty piglets, a slight reduction in absorptive function but no biochemical evidence of small intestinal disease. Morphometric studies of weight-matched piglets revealed no differences between thrifty and unthrifty piglets, suggesting that the differences in the age-matched groups may have been an effect of body-weight. If unthrifty pigs grew slowly as a result of small intestinal damage and malfunction immediately after weaning no evidence of it remained when they were studied five weeks later.

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