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ARS Home » Midwest Area » Lexington, Kentucky » Forage-animal Production Research » Research » Publications at this Location » Publication #215835

Title: Physiological basis of fescue toxicosis

item Strickland, James
item Aiken, Glen
item SPIERS, DON - University Of Missouri
item FLETCHER, LESTER - Agresearch

Submitted to: Tall Fescue On-line Monograph
Publication Type: Monograph
Publication Acceptance Date: 4/17/2008
Publication Date: 6/25/2008
Citation: Strickland, J.R., Aiken, G.E., Spiers, D.E., Fletcher, L.R., Oliver, J.W. 2008. Physiological basis of fescue toxicosis. Tall Fescue On-line Monograph. 8:203-227.

Interpretive Summary:

Technical Abstract: “Fescue Toxicosis” continues to be a major syndrome in temperate climates of the world in terms of economic loss to animal producers. Studies with forage-animals over the past three decades have provided insight concerning the pathophysiological effects of the alkaloids present in toxic endophyte-infected tall fescue. Further, gains have been made in the management of Fescue Toxicosis through selection of fescue genotypes which suppress the production of ergot alkaloids (one class of alkaloids in tall fescue) by the wild-type endophyte and by inoculation of elite endophyte-free tall fescue germplasm with selected endophytes which do not produce ergovaline (an ergot alkaloid). Adoption of this technology has been slow to develop, due to the cost and difficulty of renovating existing pasturelands with the improved fescue-endophyte associations. As such, endophyte-infested pasturelands remain widespread. Although limited success has been achieved with alleviator drug treatments and nutritional manipulation, fully successful methods of alleviating this costly syndrome still remain elusive. With this review, we provide a quick survey of the clinical signs of Fescue Toxicosis, proposed toxicants, and proposed solutions to provide the reader a general understanding of the overall problem. Further, we provide an in depth look at the physiological mechanisms proposed to be involved in the expression of the “Fescue Toxicosis” syndrome. Finally, we provide our suggestions for future research efforts in this arena and the potential impact of these approaches.