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.
“Fescue foot” or dry gangrene of the extremities (hooves, ear tips, tail switches) occurs due to persistent vasoconstriction and damage to the blood vessels supplying oxygenated blood to these distant areas. Only small subsets of cattle develop this condition after an acute exposure to ergot alkaloids during environmental temperature changes towards cooler weather. Vasoconstriction typically affects the hind limbs first, appearing as swelling and redness at the coronary band and progressing to hind limb lameness. The tail may also become discolored. Later signs include “sloughing” or loss of affected portions of the hooves, ear tips, and/or the tail switch.
A third syndrome, fat necrosis or “abdominal lipomatosis” is the least studied manifestation of chronic fescue toxicosis. It has been associated with grazing tall fescue pastures receiving high nitrogen fertilization, particularly with poultry litter. Development of hard masses of necrotic fat causes a variety of symptoms depending on their location. Masses in the pelvic cavity can obstruct the birth canal and contribute to dystocia (difficult birth). Hard fat masses in the abdomen may impinge on abdominal organs and cause outflow obstructions and intestinal blockages with outward signs that may include chronic diarrhea and weight loss, trouble urinating, and loss of appetite. Fat necrosis is occasionally diagnosed by rectal palpation but is most often found at necropsy.
The diagnosis of ergot alkaloid-associated problems in cattle is based on clinical signs as well as knowledge of the geographical area, weather conditions, and testing forage for ergovaline from the pasture of the affected animals. Ergovaline testing can be performed by the University of Kentucky Veterinary Diagnostic Laboratory Toxicology section. Please see the UKVDL website http://vdl.uky.edu/ for submission forms and shipping information. Full sample collection instructions are available at http://vdl.uky.edu/sample-collection-guidelines-ergovaline-testing. Guidelines for how much ergovaline can be safely ingested by cattle are not well established. Some suggest that 100-300 ppb ergovaline on a dry matter basis in the total diet for cattle could result in clinical signs while other studies found that higher concentrations, up to 750 ppb dry matter, are required before clinical signs occur. With high heat and other environmental stressors, the lower-level guidelines are considered more appropriate. It is important to determine the percentage of tall fescue present in the pasture so the overall risk can be calculated. Currently, there are no tests commercially available to confirm fescue toxicosis in cattle from blood or tissue samples.
In summary, tall fescue toxicosis is one of the costliest livestock disorders in the southeastern United States but its impacts often go undetected on many livestock operations. Fescue toxicosis is due to a fungal endophyte within the tall fescue plant that produces ergot alkaloids, primarily ergovaline, a compound that causes profound constriction of blood vessels in cattle. The most common and economically damaging manifestation of fescue toxicosis is “summer slump”, a syndrome resulting in decreased grazing time and decreased liveweight gain, lower calf weaning weights and poor reproductive performance including failure to conceive and early embryonic loss. The first step in managing tall fescue toxicosis is to assess the levels of endophyte in pastures. Once the level of endophyte infection is known, an appropriate management strategy can be developed. However, the only way to completely eliminate the harmful effects of endophyte on livestock is to replace infected stands with other forages or novel endophyte tall fescue.
Source : osu.edu