Role of mycotoxins in herds with and without problems with tail necrosis in neonatal pigs

Abstract

This study aimed to investigate a possible involvement of mycotoxins in neonatal tail necrosis in piglets. Ten affected and 10 non-affected farms were selected. Sow feed samples were analysed for the presence of 23 mycotoxins by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Blood plasma samples of sows and their piglets were analysed for the presence of deoxynivalenol (DON), de-epoxydeoxynivalenol, T-2 and HT-2 toxin, zearalenone, alfa-zearalenol, and beta-zearalenol, using LC-MS/MS. Additionally, high-resolution mass spectrometry (HRMS) was performed to detect DON-glucuronide (DON-Glca). There was a significant difference between case herds and control herds for mean DON concentrations in feed and sow plasma. For piglet samples, concentrations of DON were above the limit of quantification of 0.1 ng/ml in only 12 samples. Positive correlations were found between DON concentrations in sow feed and plasma of sows; DON concentration in sow feed and DON-Glca concentration in plasma of sows; and between DON and DON-Glca concentration in sow-plasma. In conclusion, high prevalence of DON in feed samples was found, with significantly higher concentrations in case herds, as well as the presence of DON and DON-Glca in sow plasma. Additional research is needed to identify risk factors, including within-herd factors, associated with neonatal tail necrosis in piglets.

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

“…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 ].…”

Minimal Concentrations of Deoxynivalenol Reduce Cytokine Production in Individual Lymphocyte Populations in Pigs

“…However, the concentration of DON in the serum of pigs after consumption of contaminated feed is usually much lower. Piglets fed a DON-contaminated diet with concentrations under the limit recommended by the EU (0.9 mg/kg) [20] exhibited DON serum concentrations 1-10 ng/mL [21,22]. Even though the oral route is the most frequent way of mycotoxin entry into the organism, it is very complicated to study the cellular impact of very small doses of mycotoxin via nutritional studies.…”

Occurrence of Mycotoxins in Swine Feeding from Spain

“…Especially abundant are the number of studies about the pathological effects of Fusarium toxins on pig reproduction [11]; these include abortion, embryonic and foetal death, increased number of oestrus repetitions, failure of induction programs with PGF2α and increased number of stillbirths and splaylegged piglets. What is more, ZEA can produce hyperestrogenism [12] and tail necrosis in suckling piglets [13]. The effects of DON on gut function [14,15], and DON and ZEA on colon microbiota, have also been reported [16].…”