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Interaction between ascites susceptibility and CO(2) during the second half of incubation of two broiler lines: the effect on post-hatch development and ascites mortality

1. The aim of this study was to investigate if genetic predisposition to ascites interacts with changed incubation conditions, and how this might affect the post-hatch performance and ascites susceptibility. 2. An ascites sensitive (A) and resistant (E) broiler line were incubated under standard or...

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Bibliographic Details
Published in:British poultry science 2012, Vol.53 (2), p.262-269
Main Authors: Everaert, N, Willemsen, H, Debonne, M, Witters, A, Kamers, B, Darras, V M, de Baerdemaeker, J, Decuypere, E, Bruggeman, V
Format: Article
Language:English
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Summary:1. The aim of this study was to investigate if genetic predisposition to ascites interacts with changed incubation conditions, and how this might affect the post-hatch performance and ascites susceptibility. 2. An ascites sensitive (A) and resistant (E) broiler line were incubated under standard or high CO(2) conditions (up to 4%) from embryonic d 10 onwards. After hatch, chicks were exposed to cold from the 15th day of the rearing period to increase the incidence of ascites. 3. The A line had a higher post-hatch body weight from week three, higher blood pCO(2) from d 21, higher haematocrit at d 35 and d 42, and higher plasma corticosterone concentration from d 21 onwards, compared with the E line, regardless of incubation conditions, supporting the given selection criteria. Ascites mortality did not, however, differ between lines. 4. Incubation under high CO(2) conditions during the second half of incubation increased the ascites mortality, decreased body weight from week 4 onwards, affected venous blood pCO(2), decreased blood pO(2) from d 31, increased haematocrit at d 35 and d 42, and lowered the thyroxine and triiodothyronine concentrations at most sampling days. These effects were observed in both lines. The results suggested a metabolic programming of CO(2) incubated chickens which affected ascites susceptibility.
ISSN:1466-1799
DOI:10.1080/00071668.2012.669467