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Swine Inflammation and Necrosis Syndrome (SINS) is an increasingly recognised condition in pigs characterised by inflammatory and necrotic alterations at multiple anatomical sites, including the tail, ears, teats, coronary bands, heels and claws. Its simultaneous occurrence at anatomically distant body regions, its presence at birth and the histopathological evidence of vascular inflammation and thrombosis support the concept that SINS is not primarily a local or mechanically induced disorder, but reflects a systemic endogenous process. This review integrates clinical, pathological, transcriptomic, metabolomic, genetic and field evidence to propose SINS as a systemic vascular-inflammatory syndrome centred on the gut–liver–vascular axis. A proposed pathophysiological model links dysbiosis, impaired intestinal barrier function and translocation of microbe-associated molecular patterns to hepatic inflammatory activation, oxidative stress, endothelial dysfunction, coagulation disturbances and microcirculatory impairment. Transcriptomic findings support this model by revealing alterations in genes associated with acute-phase responses, inflammation, oxidative stress, vascular regulation and metabolism in the liver. Genetic studies further indicate moderate heritability, breed and sire effects, and a complex polygenic architecture involving immune, metabolic and vascular pathways. Recent European field studies support the reproducibility of SINS under commercial conditions and show that early-life SINS is associated with later tail integrity and tail lesions. The available evidence supports a phase-based model describing age-related changes in clinical expression and associated systemic alterations, while the precise temporal relationships between inflammatory, metabolic and vascular processes remain incompletely resolved. Practical implications include the need for integrated prevention strategies targeting genetics, feeding, water supply, thermoregulation, transition management and early detection. Overall, SINS may represent a previously under-recognised biological contributor to impaired tissue integrity and welfare problems in modern pig production.
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Becker et al. (2026) studied this question.
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