By Dr. Michelle Arnold
Tall fescue (Schedonorus arundinaceus (Schreb.) Dumort., nom. cons.) is the most important cool-season grass in the transition area between the temperate northern and subtropical southern United States. In most unimproved pastures, tall fescue is infected with the fungal endophyte Epichloë coenophiala, that imparts tolerance to abiotic and biotic stresses. An “endophyte” is a fungus or bacteria that lives entirely within the intercellular spaces of the leaf sheaths, stems, and seeds and is only visible microscopically. The grass and fungus enjoy a mutually beneficial relationship; the plant provides nutrients and a means for the endophyte to reproduce through infected seeds. The fungus, in turn, produces chemicals known as “ergot alkaloids” that function as chemical defenses, making the grass more vigorous, pest-resistant, drought-resistant, and tolerant of many adverse soil and environmental conditions. Often KY 31 tall fescue is the only grass that can survive and thrive in poor conditions or with poor grazing management. Importantly, the ergot alkaloids cause cattle to eat less, protecting tall fescue from overgrazing during its vulnerable decline in summer growth. Of the alkaloids produced by the endophyte, ergovaline is the predominant ergot alkaloid mycotoxin that significantly impacts livestock health and productivity. Ergovaline accounts for approximately 90% of the ergot alkaloids in tall fescue with the highest concentrations found within the seed head. “Fescue toxicosis” is the broad term used for the variety of clinical disorders that can affect cattle grazing endophyte-infected (E+) tall fescue. The most common and economically damaging manifestation of fescue toxicosis is “summer slump”, a syndrome characterized by an increased sensitivity to heat stress due to hyperthermia (elevated core body temperature). External signs include rough hair coats during the summer, decreased grazing time and decreased liveweight gain, less milk production, lower calf weaning weights and poor reproductive performance. Two additional syndromes resulting from fescue toxicosis, “fescue foot” and “fat necrosis”, are less commonly recognized and underdiagnosed so disease incidences and economic impacts from these two disorders are largely unknown.
Ergot alkaloids are structurally similar to the neurotransmitters serotonin, dopamine, and norepinephrine, allowing the alkaloids to bind to neurotransmitter receptors and thus interrupt biological processes. Symptoms observed in cattle depend on the type and location of these receptors, the quantity of alkaloids bound to the receptors, the level and duration of alkaloid exposure, the environmental conditions (temperature and humidity), and the individual animal’s susceptibility to ergot alkaloids. Ergovaline strongly binds to receptors on blood vessels, resulting in vasoconstriction that reduces blood flow to peripheral tissues including the skin and extremities, to the digestive system, and to reproductive tissues, resulting in the wide variety of symptoms observed. Cattle may initiate the vasoconstrictive response to ergot alkaloids in as little as 1-2 days after exposure and accumulation of the alkaloids in the tissues may cause the
vessels to stay constricted for up to 6-7 weeks after removal of the animal from infected pasture. Early clinical signs are sometimes reversible if promptly removed from contaminated pastures or hay. The severity of observed symptoms may increase if tall fescue becomes infected (ergotized) with the fungus Claviceps purpurea which also produces alkaloids such as ergotamine and ergocristine that contribute to vasoconstriction.
The visible signs of “summer slump” are due to the cattle’s increased sensitivity to heat stress experienced during hot and humid weather. Ergovaline increases core body temperature (hyperthermia) by reducing blood flow from the body core to the skin surface, limiting the body’s ability to dissipate heat and cool itself. Affected cattle fail to shed the winter hair coat, worsening the heat’s effect. Cattle spend more time idling in shade, mudholes, ponds, and streams and less time grazing during the day. Those most severely affected exhibit rapid and labored respirations, open mouth breathing or panting, and excessive salivation. Simply stated, affected cattle graze less, eat less and therefore gain less weight, resulting in lower average daily gain (ADG) in stocker cattle, and lower calf weaning weights. Beyond the visible increase in heat stress from ergot alkaloids, grazing E+ tall fescue disrupts the release of the hormones prolactin and progesterone, decreases milk production, and negatively affects reproductive performance. Prolactin, a hormone linked to lactation and mammary gland development, is consistently low in livestock due to ergot alkaloids inhibiting the hormone’s secretion from the anterior pituitary. Dams produce less milk, further contributing to lower calf weaning weights. Decreased reproductive performance is caused by the combined effects of less blood flow to reproductive tissues, less dry matter intake and the increase in core body temperature. In addition to lowered prolactin, females also have a lower level of the hormone progesterone that is necessary for establishment and maintenance of pregnancy. One study measured a 41% lower conception rate in cows grazing E+ infected pastures versus E- pastures. Bulls may have altered sperm motility parameters and reduced fertilization potential. Recent studies indicate embryo quality and subsequent embryo development are negatively affected as well. Economically, cow-calf producers can expect reduced pregnancy rates, longer breed back intervals and lighter calves at weaning when cattle graze E+ fescue pastures.