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.

In rats, it has been observed that treatment with activators of peroxisome proliferator-activated receptor α (PPARα) disturbs metabolic adaptations during lactation, which in turn lead to a reduction of milk fat content and gains of litters during the suckling period. It has not yet been investigated whether agonists of PPARα are impairing milk production of lactating sows in a similar manner as in rats. Therefore, the present study aimed to investigate the effect of treatment with clofibrate, a strong synthetic agonist of PPARα, on milk composition and litter gains in lactating sows. Twenty lactating sows received either a basal diet (control group) or the same diet with supplementation of 2 g of clofibrate per kg of diet (clofibrate group). In the clofibrate group, mRNA concentrations of various PPARα target genes involved in fatty acid utilization in liver and skeletal muscle were moderately up-regulated. Fat and energy content of the milk and gains of litters during the suckling period were not different between the control group and the clofibrate group. It is shown that treatment with clofibrate induces only a moderate up-regulation of PPARα target genes in liver and muscle of lactating sows and in turn might have limited effect on whole body fatty acid utilization. This may be the reason why clofibrate treatment did not influence milk fat content and gains of litters during the suckling period. Thus, the present study indicates that activation of PPARα induced either by native agonists such as dietary polyunsaturated fatty acids or a by negative energy balance might be largely uncritical in lactating sows with respect to milk production and litter gains in lactating sows.

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.

Swine Inflammation and Necrosis Syndrome (SINS) is a simple and non-invasive animal-based health and welfare indicator that combines the clinical observation of bristle loss, swelling, redness, exudation, necrosis and haemorrhage in various parts of the body. It provides a point-of-care measure with direct intervention capability. Several studies from different countries demonstrate its considerable prevalence, particularly among newborn, suckling and weaned piglets. The syndrome has been demonstrated to be endogenous, as evidenced by clinical, pathohistological, clinical chemical, metabolomic, transcriptomic and genomic analysis. It has been established that the first and fourth weeks of life represent suitable time points for examination. However, longitudinal follow-up of individual animals has hitherto been lacking. In order to address this issue, a total of 1080 complete SINS examinations were conducted on 59 piglets at days 1 to 14, 19, 22, 26 and 41 of life. The findings substantiate the bimodal progression and evince a robust correlation between signs in disparate anatomical regions, including body temperature. Two peaks with significantly increased SINS signs were observed, the first around the fourth day of life and the second around day 26. The majority of indications of SINS in the second peak manifested prior to the initiation of the weaning process. The development of SINS signs in the piglets as a group followed a clear pattern. However, it was not feasible to predict the subsequent course of SINS based on individual animals. It is recommended that SINS, as an animal-based health and welfare indicator, be screened on days three to four and/or in the fourth week of life. It is imperative that the day of life is specified with the greatest possible precision, given the propensity for considerable deviations to occur within a time frame of one to three days, especially during the initial week of life. The implementation of these findings has the potential to make a decisive contribution to improving inventory herd analyses and studies on SINS, thereby improving the welfare and health of piglets.

Animal-based measures, such as detecting inflammation in areas like the tail, ears, teats, coronary band, heels and claws (Swine Inflammation and Necrosis Syndrome, SINS), are used to monitor animal health and welfare. When parameters deviate from the established range, these measures enable prompt action to adjust husbandry practices, feeding regimens and management strategies. In addition to environmental factors, genetics have been shown to play a key role in inflammation and necrosis processes, and selection can reduce the severity of the disease. This study examined whether different breeds of AI boar exhibit different signs of SINS and how these signs are associated with SINS in their offspring when they are suckling piglets and weaners. Initially, 286 AI boars of 7 breeds from a German artificial insemination center were evaluated for SINS. The following parameters were assessed: tail base, tail tip, ears, skin, scrotum, coronary bands, heels and claws. Subsequently, 23 Pietrain and Duroc boars were used in combination with a Topigs DL sow line. The progeny of the AI boars was evaluated as suckling and weaned piglets, with the assessment framework encompassing SINS traits. The results revealed significant differences between the breeds and lines, as well as a strong correlation between the SINS phenotypes of the AI boars and the SINS scores of their offspring. The offspring of the 25% most extreme boars exhibited a 17% variation in SINS scores. This association was particularly evident when comparing the boars’ tail base. However, the development of the boars’ heels and claws was found to be significantly influenced by mechanical environmental factors and not associated with the piglets’ scores. These findings imply that heritable, endogenous processes, as proposed for SINS, also visibly impact the phenotype of the AI boar. This study’s fundamental premise suggests that pre-selecting AI boars could mitigate the occurrence of SINS and enhance piglet health and welfare.