Escherichia coli and salmonella in pigs

Diarrhoea due to bacterial infections is a problem mainly in the young growing animal, including the pig. Among the bacteria that cause diarrhoea in pigs are various strains of Escherichia coli and Salmonella. Considerable genetic variation in resistance/susceptibility has been found for both neonatal and post-weaning diarrhoea caused by E. coli carrying F4 fimbriae and post-weaning diarrhoea and oedema disease due to E. coli strains with F18 fimbriae. The loci for the receptors of both types of fimbriae have been mapped: the F4 receptor(s) to chromosome 13 (SSC13) and the F18 receptor to chromosome 6 (SSC6). Several candidate genes have been suggested for the F4 receptor, among them different mucine genes (MUC4, MUC13), and a very close association between a single-nucleotide polymorphism (SNP) in an alpha (1, 2) fucosyltransferase gene (FUT1) and the F18 receptor has been identified. Resistance to Salmonella infections in mice is associated with the antimicrobial activity of macrophages, and some studies have suggested that it is linked with polymorphism in the Nramp1 gene. The gene has been identified in several species including the pig, but data are so far lacking concerning association between polymorphism in the porcine gene and resistance-susceptibility to Salmonella infection. Using transcriptome profiles, several porcine genes that are differentially up or downregulated during Salmonella infection have been identified. Further studies of associations between polymorphisms in these genes and the outcome of Salmonella infection may facilitate the development of tools to identify carrier pigs, and lead towards identification of markers that can be used to select for resistant pigs. Breeding for increased disease resistance can be potentially performed in several ways; excluding susceptible breeding of animals after exposure, marker-assisted selection (MAS) based on closely linked loci or direct selection based on polymorphism in the causative gene. The rapid development in molecular genetics has provided dense genome maps and the tools to identify and study individual genes, both at the deoxyribonuclease acid (DNA) and the expression level. Overall use of genetic markers influencing disease traits is expected to increase significantly in the coming years. This number will grow as large-scale accurate disease phenotypes are collected in pedigreed populations. It is likely that many disease markers will contribute additively to the selection criteria and will be used as part of complex selection indices that will balance other economically significant traits.