The swine inflammation and necrosis syndrome (SINS) is a syndrome visually characterized by the presence of inflamed and necrotic skin at extreme body parts, such as the teats, tail, ears, and claw coronary bands. This syndrome is associated with several environmental causes, but knowledge of the role of genetics is still limited. Moreover, piglets affected by SINS are believed to be phenotypically more susceptible to chewing and biting behaviors from pen mates, which could cause a chronic reduction in their welfare throughout the production process. Our objectives were to 1) investigate the genetic basis of SINS expressed on piglets' different body parts and 2) estimate SINS genetic relationship with post-weaning skin damage and pre and post-weaning production traits. A total of 5,960 two to three-day-old piglets were scored for SINS on the teats, claws, tails, and ears as a binary phenotype. Later, those binary records were combined into a trait defined as TOTAL_SINS. For TOTAL_SINS, animals presenting no signs of SINS were scored as 1, whereas animals showing at least one affected part were scored as 2. Apart from SINS traits, piglets had their birth weight (BW) and weaning weight (WW) recorded, and up to 4,132 piglets were later evaluated for combined skin damage (CSD), carcass backfat (BF), and loin depth (LOD). In the first set of analyses, the heritability of SINS on different body parts was estimated with single-trait animal-maternal models, and pairwise genetic correlations between body parts were obtained from two-trait models. Later, we used four three-trait animal models with TOTAL_SINS, CSD, and an alternative production trait (i.e., BW, WW, LOD, BF) to access trait heritabilities and genetic correlations between SINS and production traits. The maternal effect was included in the BW, WW, and TOTAL_SINS models. The direct heritability of SINS on different body parts ranged from 0.08 to 0.34, indicating that reducing SINS incidence through genetic selection is feasible. The direct genetic correlation between TOTAL_SINS and pre-weaning growth traits (BW and WW) was favorable and negative (from -0.40 to -0.30), indicating that selection for animals genetically less prone to present signs of SINS will positively affect the piglet's genetics for heavier weight at birth and weaning. The genetic correlations between TOTAL_SINS and BF and between TOTAL_SINS and LOD were weak or not significant (-0.16 to 0.05). However, the selection against SINS was shown to be genetically correlated with CSD, with estimates ranging from 0.19 to 0.50. That means that piglets genetically less likely to present SINS signs are also more unlikely to suffer CSD after weaning, having a long-term increase in their welfare throughout the production system.
Keywords: behavior; genetic correlation; heritability; pig; tail-biting; welfare.
The swine inflammation and necrosis syndrome (SINS) is visually characterized by the presence of inflamed and necrotic skin at extreme body parts, such as the teats, tail, ears, and claw coronary bands. Piglets affected by this syndrome are considered phenotypically more susceptible to chewing and biting behaviors from pen mates. However, the genetic relationship between SINS and post-weaning skin damage is still unclear. In this study, we aimed to investigate the genetic basis of SINS expressed on piglets’ different body parts and to estimate the SINS genetic relationship with skin damage and pre and post-weaning production traits. We showed that SINS on different body parts is heritable and that the direct selection against a combined score of SINS in different body parts (TOTAL_SINS) will favor the piglet’s genetics for heavier weight at birth and weaning. However, TOTAL_SINS is not significantly correlated with carcass backfat thickness and loin depth at the piglet genetic level. The direct selection against SINS is genetically correlated with skin damage after weaning, meaning that piglets genetically more prone to present signs of SINS are more likely to receive skin damage later in life.
© The Author(s) 2023. Published by Oxford University Press on behalf of the American Society of Animal Science.