Lipopolysaccharides (LPS) modulate the metabolism of deoxynivalenol (DON) in the pig.

Pigs might be exposed to lipopolysaccharides (LPS) and deoxynivalenol (DON) at the same time, and both toxins are thought to interactively affect the intestinal barrier, the innate immune system, and the xenobiotics metabolism. Hence, we aimed at examining the single and combined effects of both toxins on nutrient digestibility and DON metabolism. For this purpose, barrows (26 ± 4 kg) were fed restrictedly either a control diet (CON) or a diet contaminated with 3.1 mg DON/kg (DON) for 37 days. At day 37 of the experiment, pigs were infused intravenously for 60 min either with 100 µg DON/kg body weight (BW) (CON-DON), 7.5 µg LPS/kg BW (CON-LPS, DON-LPS) or a combination of both substances (CON-DON + LPS), or physiological saline (CON-CON, DON-CON). Blood samples were collected frequently until 3.25 h before the pigs were sacrificed for bile, liver, and kidney collection. The apparent digestibility of N-free extractives was significantly increased by 1 % when the DON-contaminated diet was fed. The total DON content in blood was significantly higher in endotoxemic pigs (34.8 ng/mL; CON-DON + LPS) when compared to the pigs infused with DON alone (18.8 ng/mL; CON-DON) while bile concentrations were not influenced by LPS. DON residue levels in liver and kidney closely reflected the treatment effects as described for blood. In contrast to DON infusion, the LPS challenge resulted in a significantly lower total DON concentration (13.2 vs. 7.5 ng/mL in groups DON-CON and DON-LPS, respectively) when the pigs were exposed to DON through the diet. The conjugation degree for DON in blood and bile was not influenced by treatments. In conclusion, endotoxemic pigs are characterized by higher DON residue levels in blood, liver, and kidney, probably by a compromised elimination.

Difference method for analysing infrared images in pigs with elevated body temperatures.

Infrared imaging proves to be a quick and simple method for measuring temperature distribution on the pig's head. The study showed that infrared imaging and analysis with a difference ROI (region of interest) method may be used for early detection of elevated body temperature in pigs (> 39.5°C). A high specificity of approx. 85% and a high sensitivity of 86% existed. The only prerequisite is that there are at least 2 anatomical regions which can be recognised as reproducible in the IR image. Noise suppression is guaranteed by averaging the temperature value within both of these ROI. The subsequent difference imaging extensively reduces the off-set error which varies in every thermal IR-image.

The Fusarium toxin deoxynivalenol (DON) modulates the LPS induced acute phase reaction in pigs.

The systemic effects of the Fusarium toxin deoxynivalenol (DON) and of bacterial lipopolysaccharides (LPS) were studied in male castrated pigs (40.4 ± 3.7 kg) infused intravenously with either DON or LPS alone (100 µg DON/kg/h, 7.5 µg/LPS/kg/h), or together (100 µg DON plus 7.5 µg/LPS/kg/h). The Control group received a saline infusion (n=6/treatment, 24h observation period). An additional DON infusion did not exacerbate the clinical signs observed in LPS-infused pigs. For example, rectal temperature climaxed after 4h (40.4 ± 0.2°C) and 5h (40.1 ± 0.3°C), in the LPS and LPS+DON group, respectively. Saline and DON alone did not induce an acute phase reaction as indicated by unaltered plasma levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) while LPS caused a significant rise of both cytokines. TNF-alpha plasma peak concentrations were significantly higher in the LPS compared to the DON+LPS group (94.3 ± 17.2 ng/mL vs. 79.2 ± 15.7 ng/mL) while IL-6 climaxed earlier in the latter group (3h p.i. vs. 2h p.i.). From the tested clinical-chemical plasma characteristics the total bilirubin concentration and the ASAT activity were strongly elevated by the LPS infusion and additionally increased and decreased by DON, respectively. In conclusion, the LPS-induced effects were only marginally modified by DON.

A chronic oral exposure of pigs with deoxynivalenol partially prevents the acute effects of lipopolysaccharides on hepatic histopathology and blood clinical chemistry.

Lipopolysaccharides (LPS), a cell wall component of gram-negative bacteria, and deoxynivalenol (DON), a prevalent Fusarium-derived contaminant of cereal grains, are each reported to have detrimental effects on the liver. A potentiating toxic effect of the combined exposure was reported previously in a mouse model and hepatocytes in vitro, but not in swine as the most DON-susceptible species. Thus, pigs were fed either a control diet (CON) or a Fusarium contaminated diet (DON, 3.1mg DON/kg diet) for 37 days. At day 37 control pigs were infused for 1h either with physiological saline (CON_CON), 100µg/kg BW DON (CON_DON), 7.5µg/kg BW LPS (CON_LPS), or both toxins (CON_DON/LPS) and Fusarium-pigs with saline (DON_CON) or 7.5µg/kg BW LPS (DON_LPS). Blood samples were taken before and after infusion (-30, +30, +60, +120, and +180min) for clinical blood chemistry. Pigs were sacrificed at +195min and liver histopathology was performed. LPS resulted in higher relative liver weight (p<0.05), portal, periportal and acinar inflammation (p<0.05), haemorrhage (p<0.01) and pathological bilirubin levels (CON_CON 1.0µmol/L vs. CON_LPS 5.4µmol/L, CON_DON/LPS 8.3µmol/L; p<0.001). DON feeding alleviated effects of LPS infusion on histopathology and blood chemistry to control levels, whereas DON infusion alone had no impact.

The plasma clearance of the Fusarium toxin deoxynivalenol (DON) is decreased in endotoxemic pigs.

The plasma elimination kinetics of the Fusarium toxin deoxynivalenol (DON) was investigated in male castrated pigs (40.4±3.7 kg) when infused intravenously either alone (100 µg/kg/h, n=6) or together with lipopolysaccharides (LPS, 7.5 µg/kg/h, n=6). The maximum DON concentration after one hour of infusion was significantly higher by 61% in the DON+LPS Group compared to pigs infused with DON alone. The area under the plasma DON concentration vs. time curve of the DON+LPS Group was approximately twice as high as that of the DON Group after 24h while the initial (0.63 vs. 0.6 h) and terminal half-lifes (2.97 vs. 2.30 h) remained uninfluenced. The apparent volume of distribution and the plasma clearance were significantly lower for the DON+LPS Group compared to the DON Group (2.14 vs. 1.45 L/kg and 11.9 vs. 5.87 mL/kg/min). Glucuronidated DON seemed to persist longer in the DON+LPS Group. In conclusion, clearance of DON was decreased during an LPS induced acute phase reaction in pigs. Whether the higher plasma DON concentrations in endotoxemic pigs are due to a hemodynamically associated longer persistence of the DON glucuronide or because of an altered glucuronidation activity needs to be examined further.

Systemic and local effects of the Fusarium toxin deoxynivalenol (DON) are not alleviated by dietary supplementation of humic substances (HS).

The aim of this study was to examine the effects of a control diet (CON) or a Fusarium toxin contaminated diet (FUS) with and without HS (CON-HS and FUS-HS, respectively) on pigs during a 10-week growth trial starting at 35.1±3.2 kg live weight (n=12/group). Moreover, 2 additional choice feeding groups were included to test the ability of the pigs to differentiate between the CON and FUS diet. Feeding the FUS diets (∼3 mg DON/kg) did not depress feed intake irrespective of HS addition. However, the pigs of the choice feeding groups recognised the FUS diets and acquired an ability to avoid these diets. DON residues were detected exclusively in the blood of pigs exposed to the FUS diets (7-21 ng/mL) but their levels were not affected by HS, suggesting their inefficiency in preventing DON absorption. While zonula occludens-1 protein expression and villus height in jejunum and ileum were not compromised by FUS feeding, the jejunal crypts were significantly deepened at 31% compared to the CON group. These changes had no consequences for nutrient digestibility or LPS levels in systemic blood (0.02-0.08 EU/mL). As portal LPS levels were not measured, FUS effects on intestinal LPS translocation cannot be excluded.