Prevalence of an inflammation and necrosis syndrome in suckling piglets

Abstract

The current study describes the results obtained from clinical examination of over 4700 suckling piglets from 19 individual herds in Germany. In this cohort the prevalence of inflammation and necrosis in the tails, ears, claw coronary bands, heels and teats was determined using a pre-defined scoring system. Results show that already in the 1st days of life, piglets were affected by inflammation and necrosis of the heels (80%), claw coronary bands (50%) and tail base (20%). The praevalences of these alterations in piglets were influenced by genetics (P <0.001) and age, decreasing gradually in the 2nd week of life (P <0.001). Moreover, a correlation between tail length after tail docking and the prevalence of tail necrosis (P⩽0.04) was found. Tail and ear biting as a behavioural trait was not detected during this study. The early onset, appearance and multiple locations of clinical signs of inflammation and the positive correlation with the genetic background of the piglets may suggest an impairment of the innate immune system by infectious and non-infectious agents. This is in contrast to previously described behavioural abnormalities seen in fattening pigs. Considering the obvious reduction of animal welfare due to the described lesions, there is a need to create awareness among pig farmers and to understand the multifactorial causality involved in this inflammation and necrosis syndrome in piglets.

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

“…Inflammation and necrosis were clinically assessed as described by Reiner et al [ 51 ]. Due to time constraints and to minimize the animal load, clinical signs were recorded using a digital camera (Lumix, Panasonic Corporation) according to a standardized scheme for later detailed evaluation of the images (Windows Media Player, Version 12, Microsoft GmbH, Germany).…”

“…The tail base and tip, ears, teats and navel, coronary bands, wall horn, balls and soles of the feet along with the face were all initially assessed individually. However, the scoring was more detailed than in Reiner et al [ 51 ]. The following clinical characteristics were considered and scored with 0 if the sign was not visible or 1 if the sign was visible.…”

“…Our research on SINS has shown that piglets with inflammation and necrosis around tails and ears may be affected in even more organ systems, in particular the heels, claw coronary bands, teats, umbilicus, vulva and face [ 50 , 51 ].…”

“…Due to the diversity of the organ systems involved and because clinical inflammation and necrosis can occur within the first days of life [ 51 ], the probability that biting or technopathies such as unfavourable floor conditions are the sole aetiologies is reduced, even if such effects are likely to play a decisive role in the final expression of the signs. However, several body parts might be affected simultaneously due to the transfer of bacterial degradation products (e.g., LPS [lipopolysaccharides]) and mycotoxins (e.g., DON [deoxynivalenol]) into the bloodstream, and LPS and mycotoxins from sow’s milk might be directly associated with necrosis of tails, ears and coronary bands in suckling piglets [ 8 , 18 , 23 , 50 , 51 , 54 , 63 , 66 ].…”

“…Due to the diversity of the organ systems involved and because clinical inflammation and necrosis can occur within the first days of life [ 51 ], the probability that biting or technopathies such as unfavourable floor conditions are the sole aetiologies is reduced, even if such effects are likely to play a decisive role in the final expression of the signs. However, several body parts might be affected simultaneously due to the transfer of bacterial degradation products (e.g., LPS [lipopolysaccharides]) and mycotoxins (e.g., DON [deoxynivalenol]) into the bloodstream, and LPS and mycotoxins from sow’s milk might be directly associated with necrosis of tails, ears and coronary bands in suckling piglets [ 8 , 18 , 23 , 50 , 51 , 54 , 63 , 66 ]. The central point of attack for mycotoxins and particularly for DON are posited to be tight junctions [ 12 , 27 , 45 , 46 ], which can be further disintegrated by oxygen deficiency as a result of reduced intestinal perfusion in latent fluid deficiency and LPS-induced systemic inflammation [ 27 , 48 , 53 ], by heat stress [ 39 – 41 ], by intestinal diseases and by high-protein, low-fibre diets [ 25 ], whereupon LPS transfer is supposed to increase from mucosal to basolateral transfer [ 45 ].…”