Nutrition and enteric diseases in calves

Enteric diseases are of considerable economic importance in calves (a) during the first 2-3 weeks of life, when Escherichia coli is the main organism involved; (b) in the slightly older pre-ruminant calf and also in the young ruminant calf when salmonellosis, particularly that associated with Salmonella dublin and S. typhimurium, may cause severe losses ; (c) in the ruminant calf at pasture when a sufficiently heavy burden of internal parasites may cause clinical disease.T h e discussion in this paper will be limited to enteric disease during the early neonatal period, many aspects of which have been discussed at a recent conference in the USA (Tennant, 1971).T h e manifestation of this disease is considered to depend on the interactions of the immunological, nutritional and microbiological environments of the calf, with its genotypic resistance. The microbiological environmentIn the normal healthy calf, E. coli is one of the first organisms to become established in the alimentary tract after birth, followed by the lactobacilli which become the commonest organism in the stomach and small intestine (Smith, 1965).T h e temporary dominance of the first organisms to colonize the tract has been attributed to the high p H of the abomasal contents in the neonate and the subsequent decline of these organisms has been associated with the increased secretion of abomasal acid.A strain of E. coli is only likely to be pathogenic either if it manages to enter the tissues during the first few days of life, resulting in a septicaemia, or if the strain, although restricted to the alimentary tract, has the ability to proliferate in the anterior region of the smail intestine and to produce an enterotoxin.An E. coli septicaemia is usually associated with deprivation of colostrum or with the feeding of inadequate amounts, although a virulent serotype such as o78:K (?) B will regularly cause a septicaemia in calves given colostrum.T h e proliferation of an enteropathogenic strain of E. coli, which as long ago as 1925 was shown by Smith & Orcutt (1925) to adhere to the epithelial cells of the mucosa, results in profuse diarrhoea, dehydration and death from an E. coli localized intestinal infection associated with a metabolic acidosis.