Abstract

The predominant cool-season forage in the southeastern United States is the tall fescue cultivar Kentucky 31 (KY31). Kentucky 31 possesses an endophyte (), which produces a family of toxins called ergot alkaloids. These toxins negatively affect the physiology of animals on consumption and result in the syndrome known as fescue toxicosis. Currently, the United States annually produces approximately 11.4 billion kg of beef, of which 25% originates in the southeastern region of the United States where forage systems frequently are tall fescue based. Cattle within this forage system exhibit reduced gains and reproductive performance. The result is a reduction in the nation's beef supply with annual revenue losses recently estimated at approximately US$1 billion. Our hypothesis is that exposure to these ergot alkaloids in conjunction with limited availability of nutrients decreases bull semen quality and fertility. Although the literature is clear that these toxins affect BW, body temperature, blood flow, hair growth, and female reproduction in cattle, their effect on bull reproduction and the mechanisms through which the toxins act are not well defined. Six studies published from 2004 to 2015 assessed bull growth, body composition, and semen quality of young beef bulls exposed to ergot alkaloids. If semen quality or fertility is altered, the mechanisms involved may be either direct effects of ergot alkaloids through neurotransmitter receptors or indirect effects such as inhibiting the release of prolactin (PRL). The possible effects of ergot alkaloids or PRL require establishing the presence or absence of dopamine, adrenergic, serotonin, or PRL receptors in the testis, epididymis, and sperm cell of the bull. The objective of this review is to relate our findings to the few previous studies conducted that evaluated the impact of fescue toxicosis on bull reproduction and to propose possible mechanisms of action for lowered semen quality.

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