Inheritance of resistance to neonatal E. coli diarrhoea in the pig: examination of the genetic system

Gibbons, R. A.; Sellwood, R.; Burrows, M. R.; Hunter, Philip

doi:10.1007/bf00299479

Cited by 116 publications

(69 citation statements)

References 24 publications

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“…These receptors are not present in every pig and their absence causes resistance to F4 ETEC induced diarrhea (Sellwood et al, 1975). Their expression is genetically determined and inherited in a dominant way (Bijlsma and Bouw, 1987;Gibbons et al, 1977). The gene underlying resistance to F4ab/ac ETEC has been assigned by linkage analysis to porcine www.elsevier.com/locate/vetmic Veterinary Microbiology 123 (2007) [249][250][251][252][253] chromosome 13 (Guérin et al, 1993), whereas the F4ad ETEC receptor is localized on another chromosome (Peelman, 1999).…”

Section: Introductionmentioning

confidence: 99%

Screening of pigs resistant to F4 enterotoxigenic Escherichia coli (ETEC) infection

Rasschaert

Verdonck

Goddeeris

et al. 2007

Veterinary Microbiology

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The present study analysed quantitatively the mucin 4 polymorphism for determing the F4ac/ab receptor status of a total of 63 pigs by comparing it with the in vitro villous adhesion assay. The probability of a susceptible genotype for the mucin 4 increases significantly with increasing F4ab or F4ac ETEC adhesion per 250 mm villi (P = 0.029 for F4ab, P = 0.030 for F4ac), with the odds ratio for each unit increase of F4ab or F4ac equal to, respectively, 1.036 (95% CI [1.004-1.069]) and 1.018 (95% CI [1.002-1.034]). In the phenotypic in vitro villous adhesion test, a cut-off value of 5 bacteria was chosen as a criteria for the distinction between an F4R positive and F4R negative pig. The sensitivity and specificity for the in vitro villous adhesion test, with the genotyping test for mucin 4 as golden standard, is 100% and 24%, respectively, for F4ab as well as F4ac. Absence of adhesion of F4ac and F4ab ETEC to the villous brush borders was not associated with genotypic resistance suggesting that there is at least one other receptor for F4ab/ac Escherichia coli. As a consequence, not only mucin 4 gene polymorphism but also expression of these other receptor(s) has to be included in a screening assay for F4ac/ab receptor negative pigs. #

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Section: Introductionmentioning

confidence: 99%

Screening of pigs resistant to F4 enterotoxigenic Escherichia coli (ETEC) infection

Rasschaert

Verdonck

Goddeeris

et al. 2007

Veterinary Microbiology

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“…Gibbons et al (1977) published evidence that susceptibility to E. coli F4ac adhesion is dominantly inherited in the host. This is characterised by the presence or absence of specific receptors on the brush borders of enterocytes in the small intestine; homozygous recessive animals lack the K88 receptor, which enables coliforms to adhere to the gut, causing diarrhoea.…”

Section: Opportunities In Livestock Disease Geneticsmentioning

confidence: 99%

An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

Davies

Genini

Bishop

et al. 2009

Animal

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This paper reviews the evidence for host genetic variation in resistance to infectious diseases for a wide variety of diseases of economic importance in poultry, cattle, pig, sheep and Atlantic salmon. Further, it develops a method of ranking each disease in terms of its overall impact, and combines this ranking with published evidence for host genetic variation and information on the current state of genomic tools in each host species. The outcome is an overall ranking of the amenability of each disease to genomic studies that dissect host genetic variation in resistance. Six disease-based assessment criteria were defined: industry concern, economic impact, public concern, threat to food safety or zoonotic potential, impact on animal welfare and threat to international trade barriers. For each category, a subjective score was assigned to each disease according to the relative strength of evidence, impact, concern or threat posed by that particular disease, and the scores were summed across categories. Evidence for host genetic variation in resistance was determined from available published data, including breed comparison, heritability studies, quantitative trait loci (QTL) studies, evidence of candidate genes with significant effects, data on pathogen sequence and on host gene expression analyses. In total, 16 poultry diseases, 13 cattle diseases, nine pig diseases, 11 sheep diseases and three Atlantic salmon diseases were assessed. The top-ranking diseases or pathogens, i.e. those most amenable to studies dissecting host genetic variation, were Salmonella in poultry, bovine mastitis, Marek’s disease and coccidiosis, both in poultry. The top-ranking diseases or pathogens in pigs, sheep and Atlantic salmon wereEscherichia coli, mastitis and infectious pancreatic necrosis, respectively. These rankings summarise the current state of knowledge for each disease and broadly, although not entirely, reflect current international research efforts. They will alter as more information becomes available and as genome tools become more sophisticated for each species. It is suggested that this approach could be used to rank diseases from other perspectives as well, e.g. in terms of disease control strategies.

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“…Inheritance of gene encoding receptor for F4ab/ac has been characterised and clearly demonstrated to follow a Mendelian dominance model (Gibbons et al, 1977). Moreover, several candidate genes (Joller et al, 2006;Peng et al, 2007;Zhang et al, 2008) for the F4ab/ac and F18 receptors (Meijerink et al, 2000) have been proposed.…”

Section: Introductionmentioning

confidence: 99%

Detection of quantitative trait loci for porcine susceptibility to enterotoxigenic Escherichia coli F41 in a White Duroc × Chinese Erhualian resource population

Yang

Huang

Yan

et al. 2009

Animal

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Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhoea in neonatal and postweaning pigs. F41 is one of ETEC fimbriae that adhere to the small intestinal epithelium and lead to development of diarrhoea. The genetic architecture of susceptibility to ETEC F41 remains elusive in pigs. In this study, we determined the in vitro adhesion phenotypes of ETEC F41 in a total of 835 F 2 animals from a White Duroc 3 Erhualian intercross, and performed a genome scan using both F 2 and half-sib analyses with 183 microsatellite markers to detect quantitative trait loci (QTL) for porcine susceptibility to ETEC F41. The two analyses consistently revealed a 1% genome-wide significant QTL on pig chromosome 4. Moreover, we determined F41 adhesion phenotypes in 14 purebred Erhualian and 14 White Duroc pigs. The results showed that both the founder breeds are segregating for the F41 adhesion phenotype, while less percentage of Erhualian pigs were adhesive to ETEC F41 compared to White Duroc pigs.

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Inheritance of resistance to neonatal E. coli diarrhoea in the pig: examination of the genetic system

Cited by 116 publications

References 24 publications

Screening of pigs resistant to F4 enterotoxigenic Escherichia coli (ETEC) infection

Screening of pigs resistant to F4 enterotoxigenic Escherichia coli (ETEC) infection

An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

Detection of quantitative trait loci for porcine susceptibility to enterotoxigenic Escherichia coli F41 in a White Duroc × Chinese Erhualian resource population

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