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A genetic basis for resistance to enteric disease caused by E. coli

Abstract

THE K88 antigen on the surface strains of E. coli which cause neonatal diarrhoea in piglets1,2 is an essential virulence determinant3,4 because its adhesive properties enable K88-positive strains to attach to piglet intestinal mucosa4–7 and establish in the small intestine4. These bacteria multiply to reach abnormally large numbers in the gut8 and synthesise enterotoxins that cause diarrhoea and death of infected piglets9,10. K88-positive bacteria, however, do not attach to intestinal tissue from all piglets, and at least two pig phenotypes occur6,7, which we have designated ‘adhesive’ (signifying that K88-positive bacteria attach to their brush borders) or ‘non-adhesive’ (K88-positive bacteria do not attach to their brush-borders). Phenotypes are the products of two alleles at a single locus which are inherited in a simple Mendelian manner7, and the phenotypes of progeny from selected matings support the conclusion that the product of the ‘adhesive’ allele is dominant over the product of the ‘non-adhesive’ allele (R. A. G., R. S. and J. M. R., unpublished).

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RUTTER, J., BURROWS, M., SELLWOOD, R. et al. A genetic basis for resistance to enteric disease caused by E. coli. Nature 257, 135–136 (1975). https://doi.org/10.1038/257135a0

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