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Untersuchungen zur genetischen Prädisposition im Zusammenhang mit dem Entzündungs- und Nekrosesyndrom beim Schwein

Erscheinungsjahr: 2024
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ISBN/EAN: 9783835972018
Sprache: Deutsch
Umfang: 174
Format (T/L/B): 21.0 x 14.0 cm

Beschreibung

Episodes of tail and ear biting can lead to considerable economic burdens and massively restrict animal welfare. For this reason 95% of suckling piglets in the EU have their tails docked to prevent tail biting. However, routine tail docking is prohibited by EU Directive 2008/120/EC. Society and the EU are calling for measures to prevent tail biting and for an end to routine tail docking. However, necrosis and inflammatory changes can also occur without the involvement of other pigs. In most cases, these occur not only in the tail, but also in other organs at the same time. The ears, tail, claws, pads, coronet band, face, teats and vulva are susceptible. The "Swine Inflammation and Necrosis Syndrome" (SINS) was derived from the parallel occurrence of necrosis and inflammation in several parts of the body and the occurrence in neonatal suckling piglets. The main cause is thought to be a massive flooding of endotoxins from the intestine via the liver into the systemic circulation, which leads to an activation of the immune system. Numerous studies based on clinical, histological, metabolomic and transcriptomic results show that systemic and local inflammatory processes are ultimately set in motion and blood vessels are clogged in the acres. This results in inflammatory symptoms and even necrosis in the tissues to be supplied. Based on these findings, the aim of this study was to generate insights into the pathogenesis of SINS by searching for the genes involved. For this purpose, boars with different susceptibility of their offspring to SINS were first identified and mated to a total of 27 sows of a Danzucht cross via mixed semen to reduce environmental effects in order to investigate the segregation of the associated genes by means of a genome-wide association study. A total of 8 boars from two different lines were included. The sows were also photographed and scored for inflammation in the claws, teats, skin, ears and tails on the 50th day of gestation and on the 3rd day post partum. 477 piglets were born from 27 sows, of which 402 suckling piglets were photographed and later scored on day 3 of life, 382 rearing piglets on day 39 of life, 366 pre-fattening pigs on day 81 of life and 347 finishing pigs on the last day of life. In order to avoid excessive tail-biting episodes, the suckling piglets had their tails docked on the third day of life. The piglets' DNA was later isolated from the docked tail tips and the paternity test and genome-wide association study (GWAS) (Illumina PorcineSNP60 chip) were carried out. For the genetic predisposition test, at least 3 offspring of both boars had to be present in each litter. In the end, 260 suckling piglets, 243 rearing piglets, 233 pre-fattening pigs and 233 finishing pigs were available. The first part of the research question was based on the hypothesis that SINS-associated changes occur simultaneously in several organs. On average, 4.78 ± 1.21 (MW ± SD) of the 8 organs examined were affected simultaneously in suckling piglets and 4.14 ± 1.21 (MW ± SD) in weaned piglets, which confirms the hypothesis. Hypotheses two and three assumed that SINS-associated changes occur at different ages, sometimes with high prevalence. In fact, inflammatory changes in the ears, base and tip of the tail occurred in more than half of the suckling piglets. SINS-associated symptoms on the teats were found in up to 39.6% of the suckling piglets. Changes to the claws, such as bale bleeding and inflammation of the coronet band, were found in between 33.6 and 86.1 % of suckling piglets. Changes to the ears and the tip of the tail were observed in almost three quarters of the weaned piglets. Teat lesions were observed in up to 33.2 % of the rearing piglets. Changes in the claws were detected in up to 73.8 % of the piglets. More than half of the pre-fattening pigs showed symptoms on the ears and the tip of the tail. In the finishing pigs, more than half of the animals showed lesions on the ears and the tip of the tail. Hypothesis four investigated the influence of the mother sow on the prevalence and intensity of SINS in her offspring. This effect was only slightly pronounced in the present study. Hypothesis five regarding a significant role of boars on the quantitative expression of SINS in their offspring was also confirmed: Thus, the offspring of boar 2 were significantly (p < 0.05) less sensitive to the syndrome than offspring of boars 1, 3, 4, 5, 6 and 8. Unfavorable and favorable boars occurred in both lines. Nevertheless, there were also significant line effects. Hypothesis six dealt with the genetic basis of the boar effects found and resulted in 38 gene markers distributed over the entire genome with association to the SINS phenotypes. Potential candidate genes were deduced from the location of the markers. However, no functional markers could be mapped for which a functional change in the gene product was known, either qualitatively or quantitatively. The associated markers were in the range of the candidate genes TLR7 (Toll-Like Receptor 7), TLR8 (Toll-Like Receptor 8), TMSB4X (Thymosin Beta 4 X-Linked), MOSPD2 (Motile Sperm Domain Containing 2), ACE2 (Angiotensin Converting Enzyme 2), F2 (Thrombin Gene), F9 (Coagulation Factor IX), LOX (Lysyl Oxidase), TNFAIP 8 (TNF Alpha Inuced Protein 8), BCLxL (Apoptosis Regulator Bcl-X), RAB9A (RAB9A, Member RAS Oncogene Family) and DDX3X (DEAD-Box Helicase 3 X-Linked). The markers prove the genetic basis of the known different sensitivities to SINS in the offspring of different boars. They could be used as non-functional markers in selection against the syndrome. However, it remains for further studies to identify the functional gene variants. Overall, it can be concluded from the present study that the intact tail together with intact conditions of ears, face, coronet band, pads and claws, navel and teats can be regarded as meaningful signs for animal welfare in pigs, and that in addition to the known factors from husbandry, feeding and management, genetics can also contribute to combating the syndrome.

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