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Features of intensive farming can seriously threaten pig homeostasis, well-being and productivity. Disease tolerance of an organism is the adaptive ability in preserving homeostasis and at the same time limiting the detrimental impact that infection can inflict on its health and performance without affecting pathogen burden per se. While disease resistance (DRs) can be assessed measuring appropriately the pathogen burden within the host, the tolerance cannot be quantified easily. Indeed, it requires the assessment of the changes in performance as well as the changes in pathogen burden. In this paper, special attention is given to criteria required to standardize methodologies for assessing disease tolerance (DT) in respect of infectious diseases in pigs. The concept is applied to different areas of expertise and specific examples are given. The basic physiological mechanisms of DT are reviewed. Disease tolerance pathways, genetics of the tolerance-related traits, stress and disease tolerance, and role of metabolic stress in DT are described. In addition, methodologies based on monitoring of growth and reproductive performance, welfare, emotional affective states, sickness behavior for assessment of disease tolerance, and methodologies based on the relationship between environmental challenges and disease tolerance are considered. Automated Precision Livestock Farming technologies available for monitoring performance, health and welfare-related measures in pig farms, and their limitations regarding DT in pigs are also presented. Since defining standardized methodologies for assessing DT is a serious challenge for biologists, animal scientists and veterinarians, this work should contribute to improvement of health, welfare and production in pigs.

We profiled individual differences in alcohol consumption upon initial exposure and during 5 weeks of voluntary alcohol intake in female mice from 39 BXD recombinant inbred strains and parents using the drinking in the dark (DID) method. In this paradigm, a single bottle of 20% (v/v) alcohol was presented as the sole liquid source for 2 or 4 h starting 3 h into the dark cycle. For 3 consecutive days mice had access to alcohol for 2 h followed by a 4th day of 4 h access and 3 intervening days where alcohol was not offered. We followed this regime for 5 weeks. For most strains, 2 or 4 h alcohol intake increased over the 5-week period, with some strains demonstrating greatly increased intake. There was considerable and heritable genetic variation in alcohol consumption upon initial early and sustained weekly exposure. Two different mapping algorithms were used to identify QTLs associated with alcohol intake and only QTLs detected by both methods were considered further. Multiple suggestive QTLs for alcohol intake on chromosomes (Chrs) 2, 6, and 12 were identified for the first 4 h exposure. Suggestive QTLs for sustained intake during later weeks were identified on Chrs 4 and 8. Thirty high priority candidate genes, including Entpd2, Per3, and Fto were nominated for early and sustained alcohol intake QTLs. In addition, a suggestive QTL on Chr 15 was detected for change in 2 h alcohol intake over the duration of the study and Adcy8 was identified as a strong candidate gene. Bioinformatic analyses revealed that early and sustained alcohol intake is likely driven by genes and pathways involved in signaling, and/or immune and metabolic function, while a combination of epigenetic factors related to alcohol experience and genetic factors likely drives progressive alcohol intake.