Publications by authors named "Heidi Elisabeth Schwartz-Zimmermann"

Aim: This study aimed to characterize the critical points for determining the development of dysbiosis associated with feed intolerances and ruminal acidosis.

Methods And Results: A metabologenomics approach was used to characterize dynamic microbial and metabolomics shifts using the rumen simulation technique (RUSITEC) by feeding native cornstarch (ST), chemically modified cornstarch (CMS), or sucrose (SU). SU and CMS elicited the most drastic changes as rapidly as 4 h after feeding.

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Starch-rich diets are a commonly adopted strategy in order to sustain high milk yields in dairy cows. However, these diets are known to increase the risk of gut dysbiosis and related systemic health disorders. This study aimed to evaluate the effects of supplementing a clay mineral-based feed additive (CM; Mycofix® Plus, BIOMIN) on fecal microbiota structure, fecal short-chain fatty acid (SCFA) fermentation, serum metabolome, and liver health in primiparous (PP, = 8) and multiparous (MP, = 16) early-lactation Simmental cows (737 ± 90 kg of live body weight).

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The objective of the present study was to demonstrate the efficiency of the decontamination process applied to deoxynivalenol (DON)-contaminated maize by sodium sulphite (NaSO) treatment in vivo. Additionally, in vitro characterisation of the toxicity of the DON sulphonates (DONS 1, 2 and 3 denote structurally different forms), the resulting DON metabolites, on peripheral blood mononuclear cells (PBMC) should substantiate the inactivation of DON. In a piglet experiment, both DON-contaminated maize and -uncontaminated control maize either untreated (DON-, CON-) or NaSO-treated (DON+, CON+) were mixed into feed and fed for 42 d starting from weaning.

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The mycotoxin fumonisin B₁ (FB₁) is a frequent contaminant of feed and causes various adverse health effects in domestic animals. Hence, effective strategies are needed to prevent the impact of fumonisins on livestock productivity. Here we evaluated the capability of the fumonisin carboxylesterase FumD to degrade FB₁ to its less toxic metabolite hydrolyzed FB₁ (HFB₁) in the gastrointestinal tract of turkeys and pigs.

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Deoxynivalenol (DON) exposure of pigs might cause serious problems when critical dietary toxin concentrations are exceeded. As DON contamination of agricultural crops cannot be completely prevented, detoxification measures are needed. Wet preservation with sodium sulfite resulted in a significant DON reduction of naturally-contaminated maize in previous experiments.

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Background: Ergopeptines are a predominant class of ergot alkaloids produced by tall fescue grass endophyte Neotyphodium coenophialum or cereal pathogen Claviceps purpurea. The vasoconstrictive activity of ergopeptines makes them toxic for mammals, and they can be a problem in animal husbandry.

Results: We isolated an ergopeptine degrading bacterial strain, MTHt3, and classified it, based on its 16S rDNA sequence, as a strain of Rhodococcus erythropolis (Nocardiaceae, Actinobacteria).

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Under moderate climatic conditions, deoxynivalenol (DON) contamination occurs frequently on cereals. Detoxification measures are required to avoid adverse effects on farm animals. In the present study, a wet preservation method with sodium sulfite (Na2SO3) and propionic acid was tested to titrate the optimum Na2SO3-dose for maximum DON reduction of contaminated maize kernels and meal and to examine the interaction between dose and moisture content in dependence on the preservation duration.

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Fumonisin B1 (FB1) is a Fusarium mycotoxin frequently occurring in maize-based food and feed. Alkaline processing like nixtamalisation of maize generates partially and fully hydrolysed FB1 (pHFB1 and HFB1) and thermal treatment in the presence of reducing sugars leads to formation of N-(1-deoxy-D-fructos-1-yl) fumonisin B1 (NDF). The toxicity of these metabolites, in particular their effect on the sphingolipid metabolism, is either unknown or discussed controversially.

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Plants can metabolize the Fusarium mycotoxin deoxynivalenol (DON) by forming the masked mycotoxin deoxynivalenol-3-β-D-glucoside (D3G). D3G might be cleaved during digestion, thus increasing the total DON burden of an individual. Due to a lack of in vivo data, D3G has not been included in the various regulatory limits established for DON so far.

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