“Fescue Toxicosis” continues to be a major problem in temperate climates, especially within the “Fescue Belt” of the Eastern half of the USA. This syndrome has been estimated to cost the USA cattle industry nearly one billion dollars annually. The equine and small ruminant industries also suffer significant production and profit losses. Symptoms include: “Fescue Foot” (i.e., dry gangrene of the extremities), “Summer Slump” (i.e., reduced growth and productivity), reduced reproductive performance (especially severe in mares – “Equine Fescue Toxicosis”) and milk production, fat necrosis, rough hair coats, elevated body temperatures and respiration rates, and excessive salivation. Afflicted animals seek shade and wallows during the hotter months to decrease the effects of heat stress. Although, there are direct effects on the production of certain hormones and glands (e.g., prolactin, pituitary gland) as well as the nervous system, many of the aforementioned effects have been connected to a compromised cardiovascular function. This compromised function has been linked to the presence of ergot alkaloids produced by the wild type endophyte, Neotyphodium coenophialum, of tall fescue. A number of these alkaloids (e.g., ergovaline) have been shown to produce direct vasoconstriction of veins and arteries resulting in reduced blood flow to the animal's extremities and skin. This leads to reduced heat transfer from core body tissues (e.g., gastrointestinal tract) to the surface of the animal for cooling during hot months and warming of extremities in the cold months. The objectives of this presentation are 1) to review the alkaloids produced in wild type endophyte-infected tall fescue and their relationship to compounds produced within the animal, 2) to present evidence as to the identity of the causative agents of intoxication, and 3) provide insight into mechanisms by which the causative agents exert their toxic effects.