Understanding underlying mechanisms for feather-pecking behaviour in laying hens

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Modern production systems for egg-laying hens are associated with many serious animal welfare concerns. With global hen numbers of 5 billion, improvements have the potential to positively impact a huge population of animals. One of the most challenging issues is feather pecking (FP), in which individuals peck repetitively other birds, pulling out feathers and often causing significant skin damage. Despite 50+ years of research and efforts to alleviate this major problem, its causes are not fully understood and no practicable solution has yet emerged. A recent epidemiological study showed that FP in laying hens has a prevalence of 60-80%, with mortality rates of up to 20-40% in FP victims. These mortality rates translate to hundreds of millions of bird dying due to FP each year. In general there are two approaches to understanding abnormal repetitive behaviours (ARB) in animals: one, the ethological view, emphasizes the role of the environment and biology of the species in shaping behaviour, while the dysfunctional view emphasizes possible underlying abnormal functioning induced by chronic stress or inappropriate rearing environments. Both approaches may contribute to ARB, but their relative importance and how they interact is unknown. In FP studies to date, these two approaches were always investigated in isolation. My long-term objective is to integrate both: 1. the ethological view that FP reflects sustained motivational frustration of foraging/feeding behaviour in a nutritionally, physically and sensorily deprived environment where highly motivated foraging/feeding behaviours cannot be executed normally; and 2. the dysfunctional view that FP reflects underlying brain/gut dysfunction, testing hypotheses derived from studies of behavioural inhibitory control disorders in humans such as hair pulling disorders where serotonin (5-HT) deficits increase the risk of impaired behavioural control and gastrointestinal (GI) dysfunction. To address this, my specific short-term objectives are to: 1. test whether FP is induced by suboptimal conditions (unnaturalistic diets), which lead to motivational frustration (quantified by measuring motivation to return to an optimal condition using a consumer demand approach) and/or by brain/gut dysfunction (quantified by operant learning tests/GI motility tests, patho-histology); 2. test whether FP is induced by motherless rearing, and if so, whether this leads to behavioural control deficits (quantified by operant learning tests) and/or gut dysfunction (GI motility tests, patho-histology); 3. determine whether motivational frustration, behavioural control deficits and gut dysfunction have additive effects, statistically accounting for more of the variance in FP than each process individually; 4. test whether different aspects of FP are mediated by different underlying causes; specifically, whether motivational frustration more strongly predicts FP’s form and timing, while brain/gut dysfunction more strongly predicts FP’s persistence (resistance to environmental enrichment); 5. assess whether 5-HT is the crucial molecule in dysfunctions of brain and GI that help cause FP. This work will reveal for the first time whether FP indicates brain and/or gut dysfunction; help in identifying environments likely to both reduce FP and prevent motivational feeding/foraging frustration; and determine whether motivational frustration and behavioural disinhibition are complementary. Overall, this research will explain different aspects of FP, be a breakthrough in how FP is conceptualized, and help to provide a completely new approach to address ARB in other species.