Reproductive effects have been noted in several species consuming E+ tall fescue, including mice, rabbits, horses, sheep, and cattle (Daniels et al., 1984; Boling, 1985; Zavos et al., 1987; Bond et al., 1988; Monroe et al., 1988; Porter and Thompson, 1992; Jones et al., 2003; Schuenemann et al., 2005). Ruminants typically have reduced conception rates and, thus, reduced reproductive efficiency. However, monogastrics and hindgut fermenters generally appear to be more susceptible to serious manifestations (e.g., dystocia, abortion) of reproductive maladies than ruminants (Strickland et al., 1993). At present, the cause of this apparent differential effect is not entirely clear. As with digestibilities and intakes, a number of physiological differences among species could account for the differential effect, including blood flow and placental barriers, heterogeneity of receptors and transport systems, microbial and/or gastrointestinal and hepatic biotransformation of reproductive toxicants (not as of yet identified but suspected to be ergot alkaloids), presumably produced by E+ tall fescue.

By far, the animal most affected to date by E+ tall fescue consumption is the late-term mare. Hoveland (1993) estimated that nearly 680,000 horses were kept on tall fescue pastures in the United States. For many years managers and veterinarians reported reproductive problems in mares consuming tall fescue. However, it was not until 1988 (Monroe et al., 1988) that a conclusive link between E+ tall fescue and the reproductive problems was established. Equine reproductive fescue toxicosis is a particularly severe reproductive consequence to pregnant mares consuming wild-type E+ tall fescue, especially late in gestation. They exhibit prolonged gestation, dystocia, retained and thickened placentas, poor milk production, or agalactia (Monroe et al., 1988). They often deliver large, emaciated, and immature-appearing foals, with loss of both the foal and mare common (Cross et al., 1995). Ireland et al. (1991) reported that the administration of bromocryptine (a synthetic ergopeptine) to pregnant pony mares induced a reproductive syndrome that was similar to that observed with E+ tall fescue. These studies, taken together with the identification of ergot alkaloids (especially the presence of ergopeptines like ergovaline) in E+ tall fescue (Lyons et al., 1986), provided strong evidence that ergot alkaloids were the causative agents of the equine reproductive fescue toxicosis. Attempts to curtail toxicity using a biogenic amine receptor antagonist (e.g., domperidone), reported targets of the ergot alkaloids in cattle and horses, have had varying success (Oliver, 1997). Additionally, removal from toxic pasture 30 d before expected due date has had some success (Cross et al., 1995). However, there is an almost total lack of information concerning potential developmental toxicology (either in utero or postpartum) associated with the ergot alkaloids (i.e., presumed toxicants of E+ tall fescue) in grazers.


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