GWAS reveals genomic associations with swine inflammation and necrosis syndrome.

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.

Inflammation and necrosis syndrome is associated with alterations in blood and metabolism in pigs.

BACKGROUND: Swine inflammation and necrosis syndrome (SINS) can lead to significant clinical alterations at tail, ears, claws and other parts of the body in suckling piglets, weaners and fatteners. Clinical findings are associated with vasculitis, intima proliferation and thrombosis. The syndrome can be found in newborns, indicating a primarily endogenous aetiology. It has been hypothesized that SINS is triggered by gut-derived microbial-associated molecular patterns, causing derangements in liver metabolism and activity of peripheral white blood cells involving inflammation and blood haemostasis. In order to characterize these metabolic derangements of SINS for the first time, red and white blood counts, parameters of blood haemostasis, serum metabolites and acute phase proteins in the serum were analysed in 360 piglets, weaners and fatteners, each with significantly different SINS scores. RESULTS: SINS scores and haematological/clinical chemical parameters were significantly associated (P < 0.05), especially in weaners and fatteners. Higher degrees of clinical SINS were associated with increased numbers of monocytes and neutrophils. Blood coagulation was altered in weaners and a thrombocytopenia was found in fatteners. Additionally, acute phase proteins, especially C-reactive protein and fibrinogen were increased in serum. Serum metabolites and serum liver enzymes were slightly altered. Aspartate transaminase levels overall exceeded physiological limit and increased in parallel with SINS scores in fatteners. CONCLUSION: Clinical inflammation and necrosis at tail, ears, claws and other parts of the body were significantly associated with haematology and serum clinical chemistry, especially in weaners and fatteners. The involvement of inflammatory cells, blood coagulation, acute phase proteins and certain serum metabolites support the inflammatory-necrotising character of the syndrome and provide starting points for further studies to decipher its exact pathogenesis. The low to moderate variations seem less suitable for diagnostic use.

Swine Inflammation and Necrosis Syndrome (SINS).

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 Is Associated with Plasma Metabolites and Liver Transcriptome in Affected Piglets.

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 effects of boar on susceptibility to swine inflammation and necrosis syndrome in piglets.

Inflammation and necrosis can appear in pigs in several parts of the body simultaneously. The signs can affect newborns, suckling piglets and older pigs, and recent studies suggest that the syndrome is primarily endogenous. Inflammation and necrosis indicate impaired animal welfare, and thus should be controlled in pig production. This can be achieved by improving husbandry conditions. However, the variation in signs also appears to have a genetic component. The aim of the present study was therefore to test the effects of different boars from the Duroc and Pietrain breeds on the prevalence of swine inflammation and necrosis syndrome in their offspring. For this purpose, 646 suckling pigs from 39 sows (two herds) and 19 boars were made available. On the third day of life, the piglets were examined for clinical signs of inflammation and necrosis at tail base, tail tip, ears, face, teats, navel and claws. For the evaluation, we included the boar within the breed and the breed as fixed effects and the sow within the herd as random effects. More than 70% of the piglets were affected at the tail base, ears, coronary bands and heels. Bristle loss, swelling, redness, venous congestion and claw wall bleeding occurred most frequently. Exudation and necrosis affected fewer piglets. None of the piglets was completely free from signs of SINS. Offspring from Duroc boars had significantly lower SINS scores (4.87 ± 0.44) than offspring from Pietrain boars (10.13 ± 0.12). Within the Pietrain breed, significant effects of the boar were observed on inflammation and necrosis levels. Under the present study conditions, using Duroc boars instead of Pietrain boars resulted in a 59% reduction in the SINS scores of their offspring. The SINS score in the offspring of the most favourable Pietrain boar was almost 40% lower than that of offspring in the least favourable. These findings confirm considerable genetic effects on the outcome of SINS under a given husbandry. Further studies are necessary to characterise the genetic effects in detail and to make them useful to combat the syndrome.

Swine inflammation and necrosis syndrome is influenced by husbandry and quality of sow in suckling piglets, weaners and fattening pigs.

BACKGROUND: Swine inflammation and necrosis syndrome (SINS) is a newly identified syndrome in swine that can affect different parts of the extremities in suckling piglets. This study investigates the hypotheses that the clinical signs of SINS have histological equivalents, that SINS can also be observed in weaners and fatteners, that improving sow quality and husbandry (here the supply of water and fibre) can reduce the signs, and that coprostasis in sows is significantly associated with SINS in their offspring. From a cohort of 123 hybrid sows, the twenty sows exhibiting the best conditions and the twenty exhibiting the worst conditions were selected based on detailed scores from coronary bands, soles, heels, claws and teats. Half of the sows in each group, along with their offspring, were kept under conventional conditions, while the environment for the remaining sows in each group was improved with drinking bowls, water disinfection and additional feeding with hay and straw. In total, 115 suckling piglets, 113 weaners and 103 fatteners were scored for the degree of inflammation and necrosis of their tails, ears, teats, coronary bands, soles, heels and claws. RESULTS: The clinical signs of SINS are associated with inflammatory signs at the histological level. SINS scores in suckling piglets, weaners and fatteners derived from low-quality sows under standard husbandry conditions were high, but they decreased significantly when husbandry was improved (water consumption and additional fibre). Sow quality had significant effects on suckling piglets and weaners under standard husbandry conditions. Coprostasis in sows led to significantly higher SINS scores in their offspring at any age. Improved husbandry conditions were associated with a reduced prevalence of coprostasis (R2 = 0.74). Taking all factors together, husbandry improvements, sow quality and coprostasis explained 57, 67 and 45% of SINS score variance in suckling piglets, weaners and fatteners, respectively. CONCLUSION: The present study shows that SINS is not limited to suckling piglets but can also be found in weaners and fatteners. Coprostasis in sows is significantly correlated with SINS in their offspring and adds a good prognostic tool. Water supply and fibre could play a crucial role in combatting the syndrome.