At present, the poultry meat and egg industry has gained a lot of ground, being viewed as a provider of a healthy alternative to red meat and other protein sources. If this trend is to be maintained, solutions must be found to improve resistance of chickens to disease, which often is weakened by stressful conditions. In poultry, stress-induced immunosuppression is manifested by failures in vaccination and increased morbidity and mortality of flocks. Currently, several modern cellular and molecular approaches are being used to explore the status of the immune system during stress and disease. It is likely that these new techniques will lead to the development of new strategies for preventing and controlling immunosuppression in poultry. Using quantitative reverse transcription-PCR assays, a broad spectrum of cytokine, chemokine, and their receptor genes can be quantified in birds and then be used as markers to assess the effects of stress on the immune system. Currently, we are investigating immune and endocrine interactions in the chicken, in particular the cells and molecules that are known to be involved in such interactions in mammals. We have evaluated the effects of corticosterone administration in drinking water on peripheral lymphocyte and heterophil cytokine and chemokine gene profiles. In particular, there seems to be effects on cytokine and chemokine mRNA expression levels in both lymphocytes and heterophils, especially expression of the proinflammatory cytokines interleukin (IL)-1beta, IL-6, and IL-18 and chemokines C-C motif, ligand 1 inflammatory (CCLi1); C-C motif, ligand 2 inflammatory (CCLi2); C-C motif, ligand 5 (CCL5); C-C motif, ligand 16 (CCL16); C-X-C motif ligand 1 inflammatory (CXCLi1); and C-X-C motif ligand 2 inflammatory (CXCLi2), which are initially upregulated and are potentially involved in modulating the adaptive immune response. A chronic treatment with corticosterone downregulates proinflammatory cytokines and chemokines, suggesting that the delayed effects of chronic stress can suppress the immune response. Messenger RNA expression levels of transforming growth factor-beta4 (TGF-beta4) are also upregulated in cortisosterone-treated birds. It appears that the balance between T-helper (Th) 1 and Th2/T regulatory cytokine production is altered in conditions associated with significant changes in plasma corticosterone concentration. Experiments are underway to decipher the cytokine and chemokine responses to vaccination and bacterial challenge on the background of stress-induced immunosuppression.

No abstract

No abstract

Surveys were conducted with cage and alternative layer production systems to assess the prevalence of fatty liver haemorrhagic syndrome (FLHS). Commercial caged laying hens of different ages from three farms in Queensland were monitored for three months. The mortality rate of flocks ranged from 0.8% (the youngest flock) to 11.6% (the oldest flock). Six hundred and fifty-one birds were necropsied, and approximately 40% of hens died due to FLHS. Hens kept in cages in a controlled environment shed, were at a similar risk of developing FLHS to hens kept in naturally controlled sheds, however, the heavier birds in a flock were more likely to have the condition than lighter birds. In another study, layer flocks kept in cage, barn and free-range housing systems at the University of Queensland facility, were monitored for 50 weeks. Data from necropsies and performance records showed no significant differences in mortality rates between the housing systems (6.1%, 6.4% and 5.8%, for cages, barns and free-range, respectively), but the cause of mortality was different. In cages, 74% of necropsied hens died due to FLHS. In the other systems, only 0-5% of dead hens were diagnosed with the condition. These results are in agreement with previous Australian and overseas findings which have shown that FLHS is one of the main causes of hen death in caged flocks. Factors associated with husbandry practices in different production systems, such as restricted movement, increased production and temperature variations, influence hepatic lipid metabolism and predispose hens to FLHS.