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The capacity of four chicken lines (Y11, L2, B13, PA12) to control Salmonella enteritidis (SE) phage type 4 (PT4) systemic colonization was investigated. Thirteen-week-old chickens were intravenously inoculated with 10(6) SE colony-forming units, and the levels of SE colonization were determined at various time intervals after inoculation in liver, spleen, genital organs, and ceca. The course of SE infection showed a rapid contamination of liver, spleen, and genital organs, whereas the ceca were infected later. A significant (P0.001) effect of the chicken line on levels of SE was detected on day 3 postinoculation (PI) in liver and ceca, on day 10 PI in ceca, and on day 15 PI in spleen. Because an early control of systemic Salmonella infection by the Ity/Nramp1 gene has been demonstrated in mice, we aimed to study the early resistance of chickens to SE. As a consequence, we then focused our study on the between- and within-line variabilities of SE levels on day 3 PI. According to the SE levels in liver on day 3 PI, the chicken lines could be classified as susceptible (Y11 and L2) or resistant (PA12 and B13). This early variability was explored in resistant B13 and susceptible L2 lines. Differences between these two lines were confirmed in liver but not in ceca. A large within-line variability was observed in all organs of these two lines. The genetic origin of this variability will have to be determined as a prerequisite to an eventual selection.

Previously, we have shown differences in susceptibility to the cecal carrier state in chicks orally infected with Salmonella enteritidis (SE) at 1 wk of age for four outbred lines: L2, B13, PA12, and Y11. The egg-type line L2 was one of the most susceptible lines and presented a large variability in cecal SE colonization. The heritability (h2) of the resistance to SE colonization in ceca was estimated in L2 chickens to determine whether genetic factors might be involved in its control. In three independent trials, a total of 819 L2 chicks produced from 88 sires and 232 dams were challenged orally with SE at 1 wk of age. Each week after inoculation, the frequency of cecal colonization was estimated. When this value had fallen to 50%, all the remaining animals were killed. The extent of cecal colonization by SE was estimated directly by counting the viable organisms in organs and determining the numbers of positive ceca. Enrichment culture was used in Trials 2 and 3. The effects of trial, of room within trial, and of cage within room on the frequency of SE contaminated ceca were often significant. No significant effect of sex was observed. Estimation of h2 using the frequency of SE positive ceca was low, 0.06 +/- 0.07, when results of direct culture were considered. In contrast, when considering the frequency obtained after enrichment, the h2 was estimated at 0.20 +/- 0.12. This result suggests a genetic basis for the expression of the resistance to colonization. An experiment of selection for resistance to SE carrier state in the chicken ceca should definitively confirm the genetic origin of the resistance.

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373 thirteen-week-old chicks issued from a commercial cross and 312 chickens from the L2 line were intravenously inoculated with 106 Salmonella enteritidis and the numbers of Salmonella in the spleen, liver and genital organs were assessed 3 days later. Heritabilities of the number of Salmonella were estimated at 0.02 ± 0.04 and 0.05 ± 0.05 in the liver; at 0.29 ± 0.07 and 0.10 ± 0.06 in the spleen; and at 0.16 ± 0.05 and 0.11 ± 0.08 in the genital organs, in the first and second experiments, respectively. The difference between the two experiments could result from sampling variations and from differences in the genetic structure of the two populations possibly including both heterosis and additive effects as well as their interaction in the first experiment. Genetic correlations between the number of bacteria in the genital organs and liver (0.56 ± 0.58 and 0.76 ± 0.32 in the first and second experiments, respectively) and spleen (0.37 ± 0.24 and 0.79 ± 0.23) were positive. Moreover a significant within-sire effect of VIL1, a marker gene for NRAMP1, was observed in 117 progeny resulting from 25 informative matings. These results indicate that there are genetic differences in the resistance to visceral infection by S. enteritidis in these commercial egg-laying flocks, and suggest that these differences are at least partly due to genetic polymorphism in the NRAMP1 region.