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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12917-021-03107-1.