By plasmid manipulation and by other techniques, forms of non-pathogenic and of enteropathogenic strains were obtained that possessed different combinations of the genes that control the production of enterotoxin (Ent) and of 88, 99, 987P, polysaccharide K and O antigens and the utilisation of raffinose and lactose. Mixtures of forms derived from the same strain, each resistant to a different antibiotic, together with much larger numbers of non-pathogenic organisms and lactobacilli were then given orally to colostrum-deprived calves and lambs and to colostrum-deprived piglets that were genetically resistant (R) or genetically susceptible (S) to infection with 88 strains of The concentrations that each form subsequently attained in different parts of the alimentary tract of these animals was then determined by performing bacterial counts on culture media containing appropriate antibiotics. By this procedure it was possible to compare the part played by the different bacterial components in colonising the alimentary tract.

A non-pathogenic 09:K36:H19 strain, but not K12, was rendered enteropathogenic for 88S piglets by implanting an 88 and an Ent plasmid in it and for calves and lambs by implanting a 99 and an Ent plasmid in it. The 88 form of this strain and of wild enteropathogenic strains proliferated throughout the small intestine of 88S piglets, but the concentrations they attained in the small intestine of 88R piglets, calves and lambs were, if anything, less than those attained by their 88 counterparts; the small intestines of 88S and 88R piglets appeared equally susceptible to other colonising factors. 0149:K91,88 strains that had been isolated from sick calves produced neither small-intestinal colonisation nor diarrhoea in calves. The 99 form of the 09:K36:H19 strain and of all the wild enteropathogenic strains examined proliferated in the small intestine of calves, but only some of them proliferated in the small intestine of piglets. The enteropathogenicity for piglets of a wild 99 enteropathogenic strain of calf origin was confirmed by producing small-intestinal colonisation and diarrhoea with it in two colostrum-fed conventionally reared piglets. Forms of some wild enteropathogenic strains from which the 99 plasmid had been removed proliferated in the small intestine of calves and piglets to an extent sufficient to cause diarrhoea, but they did not proliferate to the extent shown by the corresponding 99 form in mixed infections.

The 987P antigen was a potent factor in the colonisation of the small intestine in piglets but not in calves. In piglets and in calves, the polysaccharide K and O antigens enhanced colonisation. The 88 forms usually proliferated to a similar degree throughout the small intestine, but forms possessing the other colonising factors either proliferated only in the posterior small intestine or to a much greater degree in the posterior than in the anterior small intestine. Forms possessing both the 987P and 88 antigens proliferated throughout the small intestine of 88S piglets; they proliferated only in the posterior small intestine of 88R piglets and to a lesser degree than the corresponding 987P88 forms. Neither the Ent plasmid, the Raf (raifinose) plasmid nor the ability to utilise lactose influenced small intestinal colonisation. Wild 8899987P strains that were enteropathogenic for weaned pigs did not proliferate in the small intestines of piglets.


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