Tail biting is a prevalent and undesirable behaviour in pigs and a major source of significant reduction in well-being. However, focusing on biting considers only one part of the solution, because tail damage can be found with a high prevalence without any action by other pigs. The lesions are not limited to the tail but can also be found in the ears, heels, soles, claw coronary bands, teats, navel, vulva, and face. Environmental improvement alone often fails to overcome the problem. This review addresses a new inflammation and necrosis syndrome in swine (SINS). It shows the clinical signs and the frequencies of occurrence in different age groups. It compiles scientific evidence from clinical and histopathological studies in newborn piglets that argue for a primary endogenous aetiology of the disease. Bringing together the findings of a broad body of research, the possible mechanisms leading to the disease are identified and then discussed. This part will especially focus on microbe-associated molecular patterns in the circulation and their role in activating defence mechanisms and inflammation. Finally, the methods are identified to ameliorate the problem by optimizing husbandry and selecting a suitable breeding stock.

Swine Inflammation and Necrosis Syndrome can lead to severe clinical signs, especially in tails, ears, teats, and claws in pigs. Clinical and histopathological findings in newborn piglets with intact epidermis indicate a primarily endogenous etiology, and microbial-associated molecular patterns (MAMPs), such as lipopolysaccharide (LPS) are assumed to play a central role in the development of the syndrome. We hypothesized that swine inflammation and necrosis syndrome (SINS) is indirectly triggered by gut-derived MAMPs entering the circulatory system via the liver and thereby causing derangements on liver metabolism. To test this hypothesis, metabolomes, candidate genes of the liver and liver transcriptomes of 6 piglets with high-grade clinical signs of SINS (SINS high) were examined and compared with 6 piglets without significant signs of SINS (SINS low). Several hepatic pro-inflammatory genes and genes involved in stress response were induced in piglets of the SINS high group. The most striking finding from hepatic transcript profiling and bioinformatic enrichment was that the most enriched biological processes associated with the approximately 220 genes induced in the liver of the SINS high group were exclusively related to metabolic pathways, such as fatty acid metabolic process. Within the genes (≈390) repressed in the liver of the SINS high group, enriched pathways were ribosome biogenesis, RNA processing, RNA splicing, spliceosome, and RNA transport. The transcriptomic findings were supported by the results of the metabolome analyses. These results provide the first evidence for the induction of an inflammatory process in the liver of piglets suffering from SINS, accompanied by lipid metabolic derangement.

The recently identified swine inflammation and necrosis syndrome (SINS) occurs in high prevalence from newborn piglets to fattening pigs and resembles an important concern for animal welfare. The primary endogenous syndrome affects the tail, ears, teats, coronary bands, claws and heels. The basis of clinical inflammation and necrosis has been substantiated by histopathology, metabolomic and liver transcriptomic. Considerable variation in SINS scores is evident in offspring of different boars under the same husbandry conditions. The high complexity of metabolic alterations and the influence of the boar led to the hypothesis of a polygenic architecture of SINS. This should be investigated by a genome-wide association study. For this purpose, 27 sows were simultaneously inseminated with mixed semen from two extreme boars. The mixed semen always contained ejaculate from a Pietrain boar classified as extremely SINS susceptible and additionally either the ejaculate from a Pietrain boar classified as SINS stable or from a Duroc boar classified as SINS stable. The 234 piglets were phenotyped on day 3 of life, sampled and genetically assigned to the respective boar. The piglets showed the expected genetic differentiation with respect to SINS susceptibility. The suspected genetic complexity was confirmed both in the number and genome-wide distribution of 221 significantly associated SNPs, and led to 49 candidate genes. As the SNPs were almost exclusively located in noncoding regions, functional nucleotides have not yet been identified. The results suggest that the susceptibility of piglets to SINS depends not only on environmental conditions but also on genomic variation.

Ensuring animal health and well-being requires animal-based measures for early and direct intervention at the point of care. Insight into the pathophysiology of Swine Inflammation and Necrosis Syndrome (SINS) has led to a non-invasive, clinical scoring system that can be used in daily practice. This provides information on the cause of observed lesions for direct intervention in affected herds. The aim of the current study was to re-evaluate the practicality of the SINS scoring system under field conditions. In addition, this is the first study to provide insight into the prevalence of SINS on Dutch farms. This study involved the scoring of 5958 piglets from 20 visits on 13 farms randomly selected by a veterinary practice in the Netherlands. The results showed that up to 64.1% of the piglets had visible inflammatory alterations in different body parts within the first seven days of life. Sow rectal temperature, signs of coprostasis and water intake during pregnancy were significantly (p ≤ 0.05) correlated with the prevalence of SINS in piglets. In conclusion, the SINS scoring system is an easy-to-use, non-invasive diagnostic tool that summarises animal-based observations at the point of care, providing a valuable communication tool between farmers, nutritionists and veterinarians in their efforts to improve animal health and welfare.

Tail biting is a widespread problem in pig production worldwide and a major cause of reduced welfare in pigs. To prevent this harmful behavior, it is a common practice to optimize husbandry and enrich the environment with organic materials. Fiber-rich materials such as straw, hay, or alfalfa reduce tail biting. These observations were also made for swine inflammation and necrosis syndrome (SINS), which causes acral necrosis and increase the risk for tail biting. A supplementation of the diet with straw and hay significantly reduced systemic inflammation in pigs. Organic materials and feed components play an important role in preventing tail biting and SINS. Gut health in particular is influenced by diet and its components. Different effects of nutritional ingredients could disrupt the balance of the gut microbiota, damage the intestinal barrier and results in leaky gut and systemic inflammation. This inflammatory response can induce SINS and behavioral changes. The aim of this literature review is to summarize current knowledge on the effects of feeding and gut health on the occurrence of tail biting and SINS in pigs and to derive possible measures for prevention.

Swine inflammation and necrosis syndrome (SINS) is a widespread disease in pigs, causing pain, suffering, and damage. Inflammation is documented at different levels based on clinical signs, histopathology, clinical chemistry, metabolomics and transcriptomics. The influence of sow and boar, as well as a heritability of around 0.3, suggest a genetic component to the disease. The aim of the present study was to identify functional single nucleotide polymorphisms (SNPs) in the vicinity of gene markers previously mapped using GWAS. DNA samples were available from 234 already phenotyped piglets. These animals were re-sequenced with additional prior enrichment. The nine selected chromosomal regions cover a total length of 22 Mbp. The genome-wide association study (GWAS) revealed two series with a total of 15 significant missense polymorphisms on chromosomes 11, 14, and 15. The homozygous genotypes of the most discriminating SNPs in series 1 resulted in SINS scores of 3.5 and 17.9, respectively. Despite the partial linkage of the SNPs, interesting candidate genes were defined. The results allow a significant narrowing of the possible candidate genes for understanding the pathogenesis of SINS and for future use in selection breeding to overcome the syndrome. Further studies should be carried out on larger animal populations.