Tall 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). 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) with the endophytic fungus Neotyphodium coenophialum (Glenn et al., 1996). Although beneficial to the plant, the presence of the wild-type endophyte (i.e., toxic form) in tall fescue forage consumed by ungulates (e.g., cattle, horses, sheep) has induced a toxicity syndrome known collectively as tall fescue toxicosis (often shortened to fescue toxicosis) considered to be the major grass-induced toxicosis in the United States (Cheeke, 1995).
Fescue foot, a malady of fescue toxicosis, is characterized by the following signs or combinations of them: tenderness and/or swelling around the fetlock and hoof region, lameness, dry gangrene (tissue necrosis) of tips of ears and tails and surrounding tissues, and loss of tail switch (Cunningham, 1948). In the most advanced cases, hooves of affected animals may slough off. Such clinical signs are manifestations of the effects of ergot alkaloids on blood vessels, which result in damage to vessel-lining cells, enhanced blood clotting, narrowing (vasoconstriction) of the vessel lumens (Tor-Agbidye et al., 2001), and ultimately lack of blood flow (Strickland et al., 1993; Oliver, 1997, 2005).
Summer slump and fat necrosis, terms less used today than a few years ago, are components of the overall fescue toxicosis syndrome and are characterized by reduced body weight (BW) gain during summer and necrotic fat formation, respectively (Strickland et al., 1993). There are no external signs of fat necrosis apart from poor thrift in cases where necrotic fat is constricting internal organs. In addition to these signs, the majority of afflicted animals express the following conditions in varying degrees: poor growth rate, rough haircoat, elevated body temperature, increased respiration rate, excessive salivation, and reduced milk production by cows or agalactia (cessation of milk production), particularly in horses. Behaviorally, affected animals often seek shade, form wallows around water troughs and in shaded areas, and spend less time grazing than their unaffected counterparts (Schmidt and Osborn, 1993; Strickland et al., 1993; Oliver, 1997, 2005).
Perennial ryegrass (Lolium perenne L.) commonly is infected with a similar endophyte (N. lolii Latch, M.J. Christensen & Samuels) that likewise produces ergot alkaloids. Consumption of infected ryegrass results in a syndrome that is similar to fescue toxicosis, but sometimes milder. Toxicosis signs derived from ergot alkaloids often are included incorrectly in the ryegrass staggers syndrome. In contrast, ryegrass staggers is caused by a tremorgenic mycotoxin, lolitrem B, which is produced also by N. lolii. Although ryegrass staggers is not caused by ergot alkaloids, both staggers and tall fescue toxicosis can be induced by the same ryegrass-endophyte association (Fletcher and Easton, 1997; Fletcher et al., 1999; Fletcher, 2005).
Before association of N. coenophialum with fescue toxicosis, attempts to identify the agent(s) responsible for the intoxication led to identification of several classes of candidate compounds (Yates et al., 1989). These included halostachine, perloline, b-carboline alkaloids, loline alkaloids (i.e., saturated pyrrolizidine alkaloids), and several ergot alkaloid classes (e.g., clavines, lysergic acid derivatives, ergopeptines). Although candidates have been proposed as possible toxicants, the primary agent or set of agents has not been elucidated completely. Relatively recent research findings generally favor the ergot alkaloids as the primary agents of intoxication, with ergovaline and lysergic acid being top candidates (see Chapter 13). Additional research is required to confirm which of these or other compounds are of primary concern for each of the affected physiological systems in grazing animals.
A complete evaluation of these compounds is beyond the scope of this chapter. The reader is directed to the review by Strickland et al. (1993) for information concerning halostachine, perloline, b-carboline, and loline alkaloids, as these have recently become of little concern in relation to fescue toxicosis. The remainder of this discussion will focus on the potential involvement of ergot alkaloids in the physiological dysfunctions associated with fescue toxicosis. It is intended to stimulate discussion of future research directions to clarify our knowledge of the causative agents and physiological mechanisms responsible for the fescue toxicosis syndrome. Broadening our insight into the physiological basis of this costly syndrome will improve our design of management protocols for alleviating toxicosis from tall fescue.
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