Swine Inflammation and Necrosis Syndrome (SINS) – a new syndrome related to tail biting in pig

The aetiology of tail biting is highly complex and its appearance in a herd can hardly be predicted. Thus, it becomes extremely important to recognise that tail biting is not a singular symptom. Cases of primary cannibalism are rather rare and need differentiation from cases of tail necrosis without support of other pigs, and from cases of secondary cannibalism as a result of primary necrosis of the tail. The aim of the present study was to show that tail necrosis can occur without biting or manipulating the tails and that these signs are part of a syndrome that involves also ears, teats and even claws, heels and coronary band of pigs.

We have developed a scoring system to evaluate the degree of inflammation and necrosis of tails, ears, teats and claws in the field. This system has been applied to a set of 44 weaners, kept under standardised conditions on slatted plastic floor for a detailed evaluation of interactions between inflammation and necrosis at the different tissues. The pigs were observed thoroughly and there were neither cases of tail biting, nor cases of claw lesions directly due to problems with the slatted floor (e.g. panaritium).

Swelling of the heels, layering of the claw wall, exudations from the tail and scabs at the tip of the tail were found in 90 to 100% of the pigs.

Haemorrhages of the claw wall, reddening and bulging of the soles, heel-sole cracks, congestions of veins of the legs and the ears and rhagades of the tail were visible in 60 to 80% of the pigs. Around 40 to 50% of the pigs had tail necrosis, inflammation of the coronary band and swelling and scabs at the teats.

Haemorrhages of the tails and ear necrosis were seen in 30% of the pigs. Ring constrictions of the tails were seen in 5% of the pigs. Tail inflammation and necrosis was significantly correlated with reddening, bulging and haemorrhages of the heels and claw walls, with swelling and scabs at the teats and with venous digestion of the limbs. Claw lesions were found not only in one claw per animal, but in most of the claws; almost all animals were involved.

We conclude that tail necrosis can occur independently (or prior) to tail biting, integrated into a syndrome of correlated lesions at ears, teats and even claws/heels. Facts on the patho-mechanisms of primary necrosis, including aspects of metabolic overload, of endo- and mycotoxins, inadequate feeding, water supply and thermo-regulation are discussed. We point out that the neglection of primary necrosis and the exclusive classification of additional symptoms as traumatic disorders might retard the development of suitable solutions to combat tail biting.

Disclosure of Interest: None Declared.