In mammals, it has become increasingly clear that the gut microbiota influences not only gastrointestinal physiology but also modulates behavior. In domestic birds, ceca have the greatest gastrointestinal microbial population. Feather-pecking (FP) behavior in laying hens is one of the most important unsolved behavioral issues in modern agriculture. The aim of the present study was to assess the cecal microbial community of divergently selected high (HFP; n = 20) and low (LFP; n = 20) feather-pecking birds at 60 wk of age. The cecal samples were subjected to community profiling of 16S rRNA and in silico metagenomics using a modified bar-coded Illumina sequencing method on a MiSeq Illumina sequencer. Our results revealed that compared to HFP birds, LFP birds are characterized by an increased overall microbial diversity (beta diversity) shown by a difference in the Bray–Curtis index (R2 = 0.171, P < 0.05). Furthermore, operational taxonomic unit comparisons showed an increased presence of Clostridiae and decreased presence of Lactobaccillacae in HFP birds when compared to LFP birds (False Discovery Rate < 0.05, Mann–Whitney comparisons). Our data indicate that there may be differences in the cecal profile between these 2 lines of laying hens. More research, building on this first study using sequencing technology for profiling the chicken cecal microbiome, will be needed in order to reveal if and how there exists a functional link between the performance of FP and the cecal microbial community.

Research into the role of tryptophan (TRP) breakdown away from the serotonergic to the kynurenine (KYN) pathway by stimulating the brain-endocrine-immune axis system interaction has brought new insight into potential etiologies of certain human behavioral and mental disorders. TRP is involved in inappropriate social interactions, such as feather-destructive pecking behavior (FP) in birds selected for egg laying. Therefore, our goal was to determine the effect of social disruption stress on FP and the metabolism of the amino acids TRP, phenylalanine (PHE), tyrosine (TYR), their relevant ratios, and on large neutral amino acids which are competitors with regard to their transport across the blood-brain barriers, at least in the human system, in adolescent birds selected for and against FP behavior. We used 160 laying hens selected for high (HFP) or low (LFP) FP activity and an unselected control line (UC). Ten pens with 16 individuals each (4 HFP birds; 3 LFP birds; 9 UC birds) were used. At 16 weeks of age, we disrupted the groups twice in 5 pens by mixing individuals with unfamiliar birds to induce social stress. Blood plasma was collected before and after social disruption treatments, to measure amino acid concentrations. Birds FP behavior was recorded before and after social disruption treatments. HFP birds performed significantly more FP and had lower KYN/TRP ratios. We detected significantly higher FP activity and significantly lower plasma PHE/TYR ratios and a trend to lower KYN/TRP ratios in socially disrupted compared to control pens. This might indicate that activating insults for TRP catabolism along the KYN axis in laying hens differs compared to humans and points toward the need for a more detailed analysis of regulatory mechanisms to understand the role of TRP metabolism for laying hen immune system and brain function.

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Antibiotic use in animal farming is one of the main drivers of antibiotic resistance both in animals and in humans. In this paper we propose that one feasible and fair way to address this problem is to tax animal products obtained with the use of antibiotics. We argue that such tax is supported both by (a) deontological arguments, which are based on the duty individuals have to compensate society for the antibiotic resistance to which they are contributing through consumption of animal products obtained with the use of antibiotics; and (b) a cost-benefit analysis of taxing such animal products and of using revenue from the tax to fund alternatives to use of antibiotics in animal farming. Finally, we argue that such a tax would be fair because individuals who consume animal products obtained with the use of antibiotics can be held morally responsible, i.e. blameworthy, for their contribution to antibiotic resistance, in spite of the fact that each individual contribution is imperceptible.

Acute tryptophan depletion (ATD) is a valuable non-invasive nutritional tool in human and rodent research to study dysfunctions of the serotonergic system and related behavioral disorders. Serotonergic dysfunction is thought to be involved in the pathology of feather pecking behavior of laying hens, one of the most relevant welfare and production issues in modern intensive egg-production systems. ATD temporarily compromises the influx of tryptophan (TRP) across the blood brain barrier which reduces central availability of TRP, the substrate for serotonin (5-HT) synthesis. However, ATD has never before been developed and evaluated in birds. We hereby report that ATD in laying hens effectively depletes plasma levels of TRP to 50% of the baseline concentration, 4 hours after administration. Furthermore, ATD reduces the ratios of TRP towards aromatic amino acids (AAA) by 60% and the ratio of TRP towards large neutral amino acids (LNAA) by 70%, three hours after administration. Further studies will be needed to determine the effects of peripheral depletion on brain TRP and 5-HT levels in birds. However, our study showed for the first time in an avian species that ATD causes lowering of plasma TRP and the ratio in plasma of TRP towards other AAA or LNAA.