Field and experimental investigations were conducted to study the fatty liver haemorrhagic syndrome (FLHS) in caged laying hens. The main goal of the research was to gain a greater understanding of the aetiology and pathogenesis of this non-infectious disease. The disease is characterized by excessive accumulation of fat in the liver and abdominal cavity, subsequent liver rupture, haemorrhage and sudden death of hens. It has been shown that the balance between hepatic synthesis and secretion of lipids is the key point that regulates hepatic and extrahepatic fat deposition in hens. Liver fat accumulation can be increased by many factors, especially nutrition, housing conditions, and inflammatory challenges. A description of normal and abnormal lipid metabolism in the hen, and consequences for hen health and disease (including FLHS) is given in the literature review (Chapter 2).
The initial study examined mortality of layer flocks kept in three different housing systems (cage, barn and free range) on the Gatton Campus, University of Queensland (Chapter 4). It was shown that there were no significant differences in mortality rates of hens (6.1%, 6.4% and 5.8%, for cages, barns and free range, respectively) between the housing systems but the causes of death were different. The most common cause of death in hens kept in cages was FLHS with 74% of dead hens dying from the condition. In contrast, FLHS only accounted for 0 to 5% of hen mortality in the other systems. Post-mortem of dead hens and body weight monitoring of flocks throughout the laying cycle were recommended as tools to predict FLHS.
An epidemiological survey (Chapter 5) of caged flocks in South-Eastern Queensland was undertaken to explore the prevalence of FLHS in commercial layer flocks. From necropsies of dead birds from 7 flocks of different ages, it was found that approximately 40% of hens died due to FLHS. This result indicated that FLHS continues to be the major cause of mortality in commercial caged laying hens kept in either controlled environment sheds or naturally ventilated sheds. As part of the epidemiological study, a questionnaire was circulated among farms and the responses revealed that there is a general lack of knowledge of FLHS in the industry.
The study of the pathogenesis of FLHS is very difficult as it occurs sporadically and over an extended period of time in the field. In the studies in Chapter 6, an oestradiol (E2) hen model was used to study the condition. The administration of exogenous E2 reproduced the disease in 30 wk old laying hens, and was associated with significant changes in E2 plasma levels and metabolic profiles, increased liver weights, and macroscopic (fat depositions, haemorrhages and haematomas) and microscopic alterations. Hens exposed to E2 and fed ad libitum diet experienced severe FLHS and had a higher incidence of FLHS than hens that had their feed intake restricted by 10%. One interesting observation from this study (not reported from other investigators) was the alteration of total leukocyte numbers and plasma fibrinogen concentrations after E2 exposure, suggesting that inflammation (as a part of the acute phase response) contributed to the development of FLHS. Further investigations were conducted using E2 hens injected with lipopolysaccharide (LPS) to simulate an immunological challenge in Chapter 7. This challenge increased the incidence of FLHS. Gene expression levels of important inflammatory cytokines (IL-1β, IL-6, and IL-18 involved in the generation of systemic and local responses to infection and injury) were evaluated. The mRNA expression of both IL-1β, IL-6 was greatly up-regulated in E2 and LPS treated hens, with IL-6 giving the greatest increase in the acute phase response (3 h post-treatments), while IL-1β gave the greatest response in a later stages (at 24 h) of the response. It was confirmed that the stimulation of fibrinogen synthesis during acute-phase response was mediated by leukocytes and cytokines, and the IL-6 had a prominent role.
Studies conducted in this thesis indicate that FLHS is a significant disease of caged layer hens and impacts on hen health and welfare. The finding of the role of inflammation during elevated circulating levels of oestradiol in inducing FLHS is a useful step in understanding the pathogenesis of this condition. Further studies of these factors and the pathogenesis of FLHS are required. Finally, it will not be possible to develop strategies to reduce the incidence of FLHS until the factors that predispose birds to the condition are fully understood.