A genome scan for quantitative trait loci affecting the Salmonella carrier-state in the chicken

Abstract

-Selection for increased resistance to Salmonella colonisation and excretion could reduce the risk of foodborne Salmonella infection. In order to identify potential loci affecting resistance, differences in resistance were identified between the N and 6 1 inbred lines and two QTL research performed. In an F2 cross, the animals were inoculated at one week of age with Salmonella enteritidis and cloacal swabs were carried out 4 and 5 wk post inoculation (thereafter called CSW4F2 and CSW4F2) and caecal contamination (CAECF2) was assessed 1 week later. The animals from the (N × 6 1 ) × N backcross were inoculated at six weeks of age with Salmonella typhimurium and cloacal swabs were studied from wk 1 to 4 (thereafter called CSW1BC to CSW4BC). A total of 33 F 2 and 46 backcross progeny were selectively genotyped for 103 and 135 microsatellite markers respectively. The analysis used least-squares-based and non-parametric interval mapping. Two genome-wise significant QTL were observed on Chromosome 1 for CSW2BC and on Chromosome 2 for CSW4F2, and four suggestive QTL for CSW5F2 on Chromosome 2, for CSW5F2 and CSW2BC on chromosome 5 and for CAECF2 on chromosome 16. These results suggest new regions of interest and the putative role of SAL1.

New QTL for resistance to Salmonella carrier-state identified on fowl microchromosomes

“…ten micro-chromosomes more than in our previous QTL analysis (Tilquin et al 2005). Other microchromosomes could not be covered since no sequence was available.…”

“…P2, although at slightly different positions, while in P2 it spread over the entire chromosome length. Two genome regions on chromosomes 2 and 5 were associated with F variations not significant at the chromosome-wide level ( Table 2) but located at the same position than QTL previously identified (Tilquin et al 2005;Calenge et al 2009). …”

“…As already described for P1 (Tilquin et al 2005), according to the infection model developed previously (Duchet-Suchaux et al 1995), 1-week-old birds were orally inoculated with 5 9 10 4 bacteria from the S. Enteritidis phage type 4 (PT 4) strain 1009, which is a spontaneous nalidixic acid (NA) and streptomycin (SM) resistant mutant strain. In P1, in order to assess the number of bacteria excreted, two cloacal swabs were made at weeks 4 and 5 post infection (pi).…”

“…A first F2 progeny of 185 animals (P1) was derived from the experimental inbred White Leghorn lines N and 6 1 [from USDA Avian Disease and Oncology Laboratory, East Lansing, MI; provided by the Institute for Animal Health (IAH), Compton, UK] and has been studied previously (Tilquin et al 2005;Calenge et al 2009). A second, independent N 9 6 1 F2 progeny of 193 animals (P2) was produced in 2007: 18 F0 males and 20 F0 females were mated to produce the F1 progeny, and 6 F1 males and 18 F1 females (3 females per male) were mated to produce the 193 F2 animals.…”

“…Several QTL for resistance to carrier state were identified in two populations both derived from crosses between the White Leghorn inbred lines N and 6 1 [back-cross (BC) and F2] using a selective genotyping approach (Tilquin et al 2005). In the latter study, carrier state resistance to either S. Enteritidis (F2) or S. Typhimurium (BC) was assessed by bacteria counting from cloacal swabs performed 2 weeks post inoculation (pi) for the BC progeny and 4 and 5 weeks pi for the F2 progeny.…”