Four chicken lines, L2, B13, PA12 (egg-type), and Y11 (meat-type), were tested for experimental carrier state of Salmonella enteritidis (SE) in two identical trials. After oral inoculation of SE at 1 wk of age with 5 x 10(4) SE colony-forming units (CFU), 10 chickens per line were necropsied weekly for 6 wk and then every 8 or 15 days until the 12th week postinoculation (PI). Liver, spleen, ovary, and ceca were examined for level of SE colonization. Numbers of positive livers and spleens and levels of the challenge strain in these organs differed little between the four chicken lines. Only three positive ovaries were detected. According to the chicken line, ceca exhibited generally significant (P < 0.05) differences in the number of positive organs during weeks 5-11 PI, in the SE CFU levels (P < 0.05) in the first 5 wk PI and during weeks 8 and 10 PI, and in the duration of colonization. L2 and B13 chickens generally carried SE in their ceca at higher levels, in more animals, and for a longer time than PA12 and Y11 chickens. Y11 chickens were the most resistant to SE cecal colonization.

Quantification of the carrier state of Salmonella enteritidis in chicks (i.e., persistent asymptomatic association of S. enteritidis with the host), should provide an optimized means for further investigations into this problem. We therefore developed an experimental carrier state model by oral inoculation of low doses (10(2)-10(4)) of S. enteritidis in B13 chicks at different ages. Liver, spleen, and ceca colonizations by the challenge strains were measured weekly by enumeration of S. enteritidis colony-forming units (CFU) for 7-12 weeks. High mortality rates, incompatible with the carrier state, were observed in chicks inoculated with 10(2) organisms of either a parental strain of S. enteritidis (5556) or a mutant resistant to streptomycin (Smr) and nalidixic acid (Nalr) (strain 1009) at 1 day old. Both strains colonized organs similarly, allowing us to use subsequently the SmrNalr mutant strain. The selected low doses of S. enteritidis induced no deaths in chicks inoculated at 1 or 3 weeks of age. However, inoculation of 3-week-old chicks did not induce a satisfactory carrier state; organ colonization by S. enteritidis was weak and transient, even after inoculation of 10(8) SE. In contrast, some birds infected at 1 week of age presented the challenge strain in the liver and spleen for 3 weeks after inoculation and in the ceca for 12 weeks postchallenge. Most of these birds were colonized by S. enteritidis in the liver and in the ceca for 3 weeks and 10 weeks, respectively, following inoculation. Generally, CFU levels were highest during the first week(s) after inoculation and then decreased progressively. Levels of S. enteritidis were lower in the liver and spleen than in the ceca. Oral inoculation of 1-week-old birds with 5 x 10(4) S. enteritidis provided the required model, allowing quantification of the carrier state of S. enteritidis in chicks.

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.

Summary. Infant mice from outbred Swiss OF1 and from inbred DBA/2, C57BL/6, BALB/cBy and CBA strains were screened for usefulness in the diarrhoea model with enterotoxigenic Escherichia coli (ETEC) strains of bovine, porcine and human origin. Mouse strains were either weakly susceptible or not susceptible to ETEC strains of porcine or human origin bearing antigen K88, 987P, CFA/I or CFA/II. In contrast, some mouse strains were highly susceptible to bovine and porcine ETEC strains bearing K99 or F41 or both antigens. Swiss OF1 and CBA infant mice were highly susceptible to one bovine ETEC strain bearing antigen K99, whereas DBA/2, BALB/ cBy and C57BL/6 mice exhibited nearly complete resistance to the same ETEC strain. Except DBA/2, all mouse strains were highly susceptible to bovine and porcine ETEC strains bearing antigen F41 alone or in combination with antigen K99. Challenge ETEC strains colonised intestines of all infant mice, but they reached very high levels soon after inoculation in the diarrhoeic ones only.

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 (P < 0.001) 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.