Selection for increased resistance to Salmonella carrier-state (defined as the persistency of the bacteria 4 wk after inoculation) could reduce the risk for the consumer of food toxi-infections. The effects of two genomic regions on chromosomes 7 and 17 harboring two genes, NRAMP1 (SLC11A1) and TLR4, known to be involved in the level of chicken infection 3 d after inoculation by Salmonella were thus tested on a total of 331 hens orally inoculated at the peak of lay with 10(9) bacteria. The animals and their parents were genotyped for a total of 10 microsatellite markers mapped on chromosomes 7 and 17. Using maximum likelihood analysis and interval mapping, it was found that the SLC11A1 region was significantly involved in the control of the probability of spleen contamination 4 wk after inoculation. Single nucleotide polymorphisms (SNP) within the SLC11A1 and TLR4 gene were tested on those animals as well as on a second batch of 279 hens whose resistance was assessed in the same conditions. As the former was significantly associated with the risk of spleen contamination and the number of contaminated organs, SLC11A1 appears to be involved in the control of resistance to Salmonella carrier state. The involvement of the TLR4 gene was also highly suspected as a significant association between SNP within the gene, and the number of contaminated organs was detected.
1. Four groups of hens, each of a different line, were inoculated at peak of lay, per os in the crop with 1 ml of a suspension containing 10(9) cfu/ml Salmonella enteritidis PT4 (SE). The kinetics of SE contamination in the environment, egg shell and yolk were studied during the first 28 d post inoculation. On the day of slaughter, intestines, caeca, spleen, liver, ovary, oviduct and content were investigated for SE contamination. 2. The commercial egg-type line L2 was found to be the most susceptible to SE. It laid many SE-positive yolks (13.8%) and internal and faecal organs were frequently infected. 3. Certain lines are found to exhibit a degree of resistance to SE; the cause of which is unknown and might be attributed to major genes.
The heritability of resistance of poultry to Salmonella enteritidis (SE) was investigated. Three m easurem ents of resistance were m ade: survival after intram uscular inoculation of 419 day-ol d chicks, absence versus presence of Salm onella in spleens and caeca 4 weeks after oral inoculation of 304 hens at peak of laying, and antibody response of 228 hens following two inoculations of an aroA m utant of this serotype. In the ® rst two models of infection, resistance appeared to be heritable. The heritability was estim ated from the sire and dam com ponents, respectively, at 0.14 6 0.10 and 0.62 6 0.16 for chick m ortality, 0.47 6 0.21 and 0.13 6 0.26 for resistance to spleen contam ination, and 0.24 6 0.15 and 0.53 6 0.26 for resistance to caecal contam ination in laying hens. By contrast the estim ated heritability of antibody response was very low (0.03 6 0.08 and 0.10 6 0.08 when estim ated from the sire and dam com ponents, respectively). These results suggest that a selection for increased resistance to SE m ay be ef® cient.
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