Effect of prolonged heat stress in single-comb white leghorn hens on progeny resistance to Salmonella enteritidis organ invasion.
In our laboratory, we have often had difficulty infecting neonatal chickens with invasive salmonellae when ambient temperatures exceed 30 C. We hypothesized that this increased resistance in chicks during warmer months may be associated with heat stress-associated maternal factors. Presently, single-comb white leghorn hens were separated into a non-heat-stressed group, reared under temperatures from approximately 10 to 24 C, and a heat-stressed group, in which environmental temperature was incrementally elevated to near 37 C and maintained for the duration of the 13-wk study. For Expt. 1, eggs from heat-stressed or control hens, collected on days 8-14 of the study, were pooled respective to treatment and incubated. At the time of egg collection, mean hen-day egg production was 51.83% or 65% for heat-stressed or control hens, respectively. On day of hatch, progeny from hens in each group were orally challenged with 0.9 x 10(4) colony-forming units (CFU) Salmonella enteritidis (SE). Rates of SE organ invasion of 97.3% or 94.4% were obtained in progeny from heat-stressed or control hens, respectively. In Expt. 2, eggs from heat-stressed or control hens from days 30-42 of the study were collected and pooled by treatment for incubation. Mean hen-day egg production was 46.5% or 72.85% for heat-stressed or control hens, respectively. On day of hatch, progeny were orally challenged with either 2.2 x 10(3) or 2.2 x 10(4) CFU SE. A 100% incidence in SE organ invasion was observed in all groups. In Expt. 3, eggs were collected from days 43 through 56 of the study. Mean hen-day egg production was 19.8% or 76.8% for heat-stressed or control hens, respectively. On day of hatch, progeny were orally challenged with 2 x 10(3) CFU SE. Rates of SE organ invasion of 95.8% or 95.6% were obtained in progeny from heat-stressed or control hens, respectively. These data suggest that factors other than elevated temperature may be responsible for seasonal resistance to invasive salmonellae infection in neonatal chickens observed in our laboratory during warmer months in Texas.
Farnell
M B
MB
Department of Poultry Science and Veterinary Pathology, Texas Agricultural Experiment Station, Texas A&M University, College Station 77843, USA.
Moore
R W
RW
McElroy
A P
AP
Hargis
B M
BM
Caldwell
D J
DJ
D000818:Animals; D016022:Case-Control Studies; D002645:Chickens; D015169:Colony Count, Microbial; D004198:Disease Susceptibility / Q000662:veterinary; D005260:Female; D018882:Heat Stress Disorders / Q000150:complications / Q000503:physiopathology / Q000662:veterinary*; D010058:Oviposition; D011201:Poultry Diseases / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D011897:Random Allocation; D012481:Salmonella Infections, Animal / Q000276:immunology* / Q000503:physiopathology; D012477:Salmonella enteritidis / Q000276:immunology / Q000472:pathogenicity*; D012621:Seasons; D013997:Time Factors