Genetic architecture of swine inflammation and necrosis syndrome and its genetic correlation with repeated skin damage scores.

Lesions and injuries to the extremities of the pig's body parts, like the tail and ears, are often associated with biting. However, lesion signs observed at birth and in 3-d-old piglets suggest that injuries may also result from swine inflammation and necrosis syndrome (SINS), which occurs without animal interaction. We aimed to investigate whether 1) there is a direct and maternal genetic effect on SINS; 2) we can use a proxy for different body parts for SINS and skin damage; 3) there is a genetic correlation between SINS and skin damage recorded in multiple time points; 4) there are genetic variants and important genes associated with both traits. We analyzed 7k female pigs born from February 2022 to June 2023 on three farms in the Netherlands. At birth, we scored SINS (no SINS = 0, and SINS = 1) on the ears, tail, and teats. Tail docking occurred after SINS phenotyping. We defined the Total_sins as the number of affected parts by SINS. The same animals were scored for skin damage (DMG on the ears, tail, and flank on average three times during the rearing phase (no DMG = 0, slight DMG = 1, severe DMG = 2, and very severe DMG = 3), resulting in 20k DMG records. We defined Sum_dmg as the sum of scores for DMG in the three body parts. Single and two-trait animal models were used to estimate heritabilities and genetic correlations. Direct (maternal) heritabilities for SINS ranged from 0.03 ± 0.01 (0.01 ± 0.00) to 0.08 ± 0.01 (0.06 ± 0.05); DMG ranged from 0.04 ± 0.01 to 0.09 ± 0.01. Although maternal heritability estimates were low and had high standard errors, likely reflecting limitations in separating direct and maternal effects, rather than the biological absence of maternal influence. Total_sins and Sum_dmg were highly genetically correlated (0.76). Our findings suggest that selection for reduced skin damage may be initiated earlier in life, based on SINS, and that piglets genetically less susceptible to SINS are more likely to experience improved welfare throughout the production system. Genomically, SINS was genetically associated with the genes DLL1, PHF10, WDR27, and THBS2, which are mainly related to embryonic and tissue formation, and warrant further investigation.