Skip to main content
ARS Home » Midwest Area » Lexington, Kentucky » Forage-animal Production Research » Research » Research Project #433380

Research Project: Optimizing the Biology of the Animal-Plant Interface for Improved Sustainability of Forage-Based Animal Enterprises

Location: Forage-animal Production Research

Project Number: 5042-32630-003-000-D
Project Type: In-House Appropriated

Start Date: Aug 30, 2017
End Date: Aug 29, 2022

Objective 1: Determine relationships of ergot alkaloids to receptors in animal tissues and subsequent effects on animal physiology, and the implications of these relationships on clearance from animal tissues. Subobjective 1.A. Evaluate the effect of ergot alkaloid exposure on vascular biogenic amine receptors. Subobjective 1.B. Characterize the interaction of isoflavones and their metabolites with ergot alkaloids on vasoactivity. Subobjective 1.C. Determine if there is ergovaline in bovine portal blood and determine site of absorption. Subobjective 1.D. Develop an oral endotoxin challenge model to determine the effects of fescue-derived alkaloid consumption on intestinal barrier function and innate immunity in cattle. Objective 2: Develop cost-effective management approaches to alleviate or mitigate the adverse effects of fescue toxicosis on animal physiology and well-being. Subobjective 2.A. Determine the impact of combining feeding soybean hulls (SBH) and red clover on weight gain performance of steers grazing toxic E+ tall fescue and mitigation of fescue toxicosis. Subobjective 2.B. Compare vasorelaxation between different sources of isoflavones for goats exhibiting ergot alkaloid-induced vasoconstriction. Subobjective 2.C. Determine if rumen tryptophan-utilizing bacteria will degrade ergot alkaloids in vivo. Subobjective 2.D. Assess phenotypic variation of cattle in their susceptibility to fescue toxicosis. Subobjective 2.E. Evaluate management approaches to cost effectively add value to cull cows and enhance ground beef quality. Subobjective 2.F. Comparison of supplemental selenium form to ameliorate physiological and gene expression stress response parameters in white blood cell (WBC), pituitary, adrenal, kidney, and liver of growing steers consuming E+ or E- tall fescue seed. Subobjective 2.G. Assess effects of animal temperament on fescue toxicosis-induced changes in animal growth and immunological responses. Objective 3: Determine the biological mechanisms used by certain plant secondary metabolites to function as antimicrobials in ruminants and non-ruminants, and assess their impact on animal health, performance, and well-being. Subobjective 3.A. Elucidate the antimicrobial mechanism of action of the red clover isoflavone, biochanin A, and determine antagonistic, additive or synergistic activity with other antimicrobials. Subobjective 3.B. Determine the effect of biochanin A on the rates of antibiotic resistance in ruminants. Subobjective 3.C. Determine the effect of clover phenolic compounds on nitrogen efficiency and weight gain in lambs. Subobjective 3.D. Evaluate spent brewer’s yeast as a carrier for hops secondary metabolites (prenylated phloroglucinols) in ruminant production.

Experiments will be conducted to determine mechanisms by which ergot alkaloids interact with receptors in animal tissues and affect their physiology. Saphenous veins collected from cattle at a local abattoir will be used to determine in vitro if inhibition of the phospholipase C and protein kinase C enzymes will alleviate ergot alkaloid induced vasoconstriction of smooth muscle. An in vitro experiment will ascertain if plant secondary metabolites, isoflavones, can mitigate the vasoactivity caused by ergot alkaloids. Endothelium cells from saphenous cells will also be exposed to ergot alkaloids to assess their effects on receptor signaling by ß-arrestin and G proteins. Catheters will be inserted in in the hepatic, portal and mesenteric veins of six rumen-fistulated steers to determine if rumen infused ergovaline is absorbed by the rumen and small intestines, or if the ergopeptine is degraded by rumen microbes. Field experiments will be conducted to evaluate management approaches to mitigate fescue toxicosis. Rumens will be infused with ergot alkaloids at a diet concentration of 0.8 ppm ergovaline and combined with either ground soybean meal, red clover, white clover, or a no isoflavone control. Cross sectional luminal areas of the right carotid artery of each goat will be measured by color Doppler ultrasonography. A grazing experiment with steers will evaluate the effects of feeding soybean hulls and overseeding toxic endophyte-infected tall fescue with red clover on animal weight gain and well-being. Four combinations of with and without the two treatments will be used as treatments to determine cost effectiveness of the treatments and mitigation of fescue toxicosis. Ear notches and phenotype data will be collected from multiple cow herds to detect polymorphisms of certain genes associated with fescue toxicosis and determine if these polymorphisms can be used to predict genetic tolerance to toxic ergot alkaloids. Three management approaches (soybean hulls, chemical seed head suppression, and red clover) to mitigate fescue toxicosis will be compared for adding body condition and weight to cull cows that graze toxic endophyte-infected tall fescue in either the spring or fall. To assess if selenium can ameliorate fescue toxicosis and if ergot alkaloids suppress immune response and alter gene expression in the liver, steers will be fed selenium depleted diets for 28 days and then switched to either inorganic selenium or an inorganic and organically bound selenium treatments for the remaining 98 days of the trial. The steers will also be fed either endophyte-infected or endophyte-free seed for the final 42 days. Jugular blood will be periodically collected and there will be staggered euthanasia of the steers for tissue collection. Effects of biochanin A on rate of antibiotic resistance will be determined by feeding rumen fistulated steers with either 0, 3 or 6 g biochanin A/day/steer and collecting rumen and fecal samples and using metagenomic DNA for quantitative PCR screening for antibiotic resistant genes.