Physiological Basis of Fescue Toxicosis

Abstract

Tall 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-fed animals over the past three decades have provided insight concerning the pathophysiological effects of the alkaloids present in tall fescue [Lolium arundinaceum (Schreb.) DarbyshJ infected with the fungal endophyte Neotyphodium coenophialum (Morgan-Jones and Gams) Glenn, Bacon, and Hanlin. To provide the reader a general understanding of the overall problem, we present a detailed discussion of the clinical signs of fescue toxicosis, the proposed toxicants, and projected solutions to this costly disease condition of ungulates. We also explore the physiological mechanisms proposed to be involved in the expression of the syndrome. Finally, we offer our suggestions for future research efforts in this arena and the potential impact of these approaches. T all fescue is an economically important cool-season perennial forage grass covering about 15 million ha in the United States alone (Buckner et al., 1979) and many more in continents outside North America (see Chapter 3, Hannaway et alv 2009, this publication). The vast majority of the tall fescue in the United States is grown within the transition zone of the eastern and central part of the country. With the development of novel nontoxic endophytes, tall fescue is again becoming increasingly popular for pastures in New Zealand and Australia. The wide distribution of tall fescue has been attributed to its symbiotic relationship (see Chapter 14, Christensen and Voisey, 2009, this publication) with the endophytic fungus Neotyphodium coenophialum (Glenn et al., 1996). Although beneficial to

Metabolomics of fescue toxicosis in grazing beef steers

“…AA-5-HT is present in the GI tract of multiple species (Verhoeckx et al, 2011) and it was recently detected in bovine and human brain and thymus tissues, indicating that it becomes systemic (Siller et al, 2014). AA-5-HT is sensitive to dietary fat (Verhoeckx et al, 2011) and decreased uptake of VFA (Dijkstra et al, 1993;Foote et al, 2013;Foote et al, 2014), along with significant increases in putative plasma glycerophospholipid metabolites seen herein, may play a role in decreased nutrient utilization, resulting in lowered weight gains which is a finding consistently reported in chronic E+ grazing (Oliver, 1997;Strickland et al, 2009). It is hypothesized that AA-5-HT increases in tissues with higher levels of serotonin (Verhoeckx et al, 2011);…”

“…Also, phosphocholine, phosphorylcholine, and phosphatidylethanolamine, are intermediates in the synthesis of phosphatidylcholine (DeLong et al, 1999). This significant increase of phosphatidylcholine and PAF precursors involved in the most common PAF biosynthetic pathway could be partially responsible for/reflective of early FT signs, such as smooth muscle cell hyperplasia, endothelial cell damage (Strickland et al, 2009), and enhanced platelet aggregation (Oliver, 1997(Oliver, , 2005, when considered alongside elevated von Willebrand factor, angiotensin converting enzyme (Oliver, 1997), and endothelin (Strickland et al, 1994).…”

Vasoactivity and Vasoconstriction Changes in Cattle Related to Time off Toxic Endophyte-Infected Tall Fescue

“…Ergot alkaloids produced by the endophyte Epichloë coenophiala that is found in tall fescue ( Lolium arundiaceum ) can alter cardiovascular function [1] and induce constriction in vascular tissue of extremities of animals grazing tall fescue [2]. Livestock consuming ergot alkaloids are less able to regulate body temperature, leading to a higher susceptibility to heat stress in warm air temperatures [3,4].…”

Ergovaline, an endophytic alkaloid. 1. Animal physiology and metabolism

“…This, coupled with their ability to assume multiple roles as an agonist, partial agonist and antagonist, may cause several disruptions that manifest as decreases in serum prolactin, vasoconstriction, effects on gastrointestinal activity, and endocrine effects that cause decreases in reproductive performance. The effects of ergot alkaloids are so multifaceted that it is beyond the scope of the present review to cover them all and the reader is referred to Oliver (1997), Pertz and Eckart (1999) and Strickland et al (2009aStrickland et al ( , 2009bStrickland et al ( , 2011 for further detail. The effects discussed below were chosen specifically to represent aspects that could have a direct impact on livestock production in terms of the individual animal.…”

“…The aspect of vasoconstriction as a result of exposure to ergot alkaloid has been reviewed in detail (Strickland et al 2009a(Strickland et al , 2009b in regard to tall fescue consumption. In general, animals that are exposed to high concentrations of ergot alkaloids lose their ability to dissipate heat (excessive panting, spending excessive time in shade and standing in ponds), they lose their ability to maintain peripheral body temperature in cold climates, which can result in frostbite, and the exposure may culminate in complete death of peripheral tissues, which results in loss of hooves, tail switches and ears; all effects are likely to be due to a the resultant decrease in blood flow (Jacobson et al 1963).…”