Effects of fescue toxicosis on reproduction in livestock.

Abstract

Fescue toxicosis in livestock is due to ingestion of endophyte (Acremonium coenophialum) -infected tall fescue. Understanding mechanisms responsible for decreased calving and growth rates, delayed onset of puberty, and impaired function of corpora lutea in heifers at puberty consuming endophyte-infected fescue is an emerging field in reproductive toxicology. The condition decreases overall productivity through a reduction in reproductive efficiency, reduced weight gains, and lowered milk production. Reproduction in cattle may be further compromised by winter coat retention, increased susceptibility to high environmental temperatures, and light intolerance. Endocrine effects in steers associated with infected tall fescue include reduced prolactin and melatonin secretions and altered neurotransmitter metabolism in the hypothalamus, the pituitary, and pineal glands. Ewes have decreased prolactin and lengthened intervals from introduction of the ram until conception. The endophyte induces prolonged gestation, thickened placentas, large, weak foals, dystocia, and agalactia in pregnant mares. Ergot peptide alkaloids, produced by the endophyte, are suggested as the primary cause of fescue toxicosis. These compounds reduce prolactin, increase body temperatures, and have powerful vasoconstrictive effects. Neurohormonal imbalances of prolactin and melatonin, with restricted blood flow to internal organs, may be the principal causes of aberrant reproduction, growth, and maturation in livestock consuming endophyte-infected tall fescue.