Journal
APPLIED ANIMAL BEHAVIOUR SCIENCE
Volume 246, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.applanim.2021.105514
Keywords
Damaging behaviour; Dietary fibre; Tryptophan metabolism; Short-chain fatty acids; Gut health; Feed competition
Funding
- Ministry of Food, Agriculture and Fisheries of Denmark
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Tail biting is a major challenge in pig production and can be influenced by diet. The communication between gut microbiota, intestinal health, and the brain through the microbiota-gut-brain axis is important in understanding the development of tail biting. This review connects the current research on the microbiota-gut-brain axis with dietary risk factors for tail biting and suggests the potential pathways involved. It also suggests that an imbalance in the microbiota-gut-brain axis influenced by diet could be considered as a pathway for the development of tail biting.
Tail biting (TB) is a major health and welfare challenge in commercial pig production. Diet is one of the six major risk factors proposed by the European commission (Commission, 2016). Research during the last decade has revealed a complex, bidirectional communication between gut microbiota, intestinal health and the brain, affecting mood and behaviour via the so-called microbiota-gut-brain axis (MGBA). This axis is affected by various factors of which diet plays a major role and thus may provide insight in the complex aetiology of TB. Individual differences in the balance of the MGBA may explain why certain risk factors lead to TB in some farms/pens but not in others. This review aims to connect the current research on the MGBA with known and proposed dietary risk factors for TB. The links are still largely unproven but can provide basis for future studies aiming for dietary interventions to mitigate TB. This review suggests that diet-related risk factors for TB are under-and oversupply of protein (incl. tryptophan), lack of satiation, fine feed particle size, low dietary fibre content and a limited number of feeder spaces. We hypothesise that these factors can cause social stress, gastric ulcers, dysbiosis of the gut microbiota, disruption of the intestinal epithelium and affect the animal's stress sensitivity via the MGBA, which might cumulatively lead to TB. Major suggested pathways are via gut microbial metabolites inducing cytokine-induced sickness behaviour (i.e. immune activation) or shifting of the tryptophan-serotonin metabolism (associated with anxiety and depression). We further hypothesise that adequate amino acid levels incl. trypto-phan and the inclusion of certain dietary fibres in the diet exceeding levels in standard diets, may stimulate establishment of a beneficial gut microbiota (e.g. microbial diversity and short-chain fatty acid producing bac-teria) that protect against inflammation and increase stress resilience. While treatment with antibiotics is a useful tool to combat the presence of potential specific bacteria that pose a risk of TB, it can at the same time disturb the gut microbial balance, which in turn increases the risk of TB. In conclusion, while TB is multifactorial, we suggest that an imbalance in the MGBA, modulated via the diet, should be considered as a pathway for the development of TB, but needs more research. We suggest a whole-animal approach, including considerations on gut health, satiety, a beneficial gut microbiota and an adequate feed supply avoiding social stress to mitigate TB.
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