Fescue toxicosis is a serious health condition affecting grazing livestock, particularly cattle and horses, across regions where tall fescue grass is the dominant forage. This condition causes significant economic losses in livestock production due to decreased animal performance and reproductive failure. Tall fescue is a resilient and widely planted cool-season grass, especially prevalent throughout the “fescue belt” of the eastern and central United States. The grass’s hardiness leads to a variety of debilitating symptoms in animals consuming it.
The Role of the Endophyte
The toxicity of tall fescue results from a symbiotic relationship with a microscopic fungus, Epichloë coenophiala. This organism is an endophyte, meaning it lives entirely within the intercellular spaces of the plant’s leaf sheaths, stems, and seeds, making it invisible externally. The fungus and the grass share a mutually beneficial relationship: the plant provides nutrients, and the fungus reproduces through infected seeds.
In return, the endophyte produces ergot alkaloids, which act as natural defenses for the plant. These alkaloids benefit the fescue by increasing resistance to drought, insects, and overgrazing, allowing the grass to thrive. The most active toxin is ergovaline, which accounts for up to 97% of the ergopeptide alkaloids present. Ergovaline acts as a potent vasoconstrictor, causing smooth muscle cells in blood vessel walls to contract and significantly reduce blood flow to the body’s extremities and internal organs.
Ergovaline concentrations are highest in the seed heads and stems. Toxicity risk increases when concentrations in the total diet exceed 200 parts per billion (ppb), with severe signs appearing above 400 ppb. While older varieties of tall fescue, such as Kentucky-31, are highly infected, scientists have developed newer cultivars. These include endophyte-free fescue, which lacks the fungus, and novel endophyte fescue, which contains a modified endophyte that provides plant benefits without producing harmful ergot alkaloids.
Identifying Signs in Affected Animals
Fescue toxicosis manifests in livestock through two primary syndromes in cattle, along with unique reproductive issues in horses. The most common presentation is “summer slump,” which occurs during warm weather when animals are unable to regulate their body temperature. The vasoconstrictive effect of ergot alkaloids reduces blood flow to the skin and extremities, limiting the animal’s ability to dissipate heat.
Cattle with summer slump display a higher body temperature, leading them to seek shade or stand in water to cool down. Signs include a failure to shed their winter coat, resulting in a rough, long hair coat that exacerbates heat stress. Affected animals also exhibit decreased feed intake, resulting in poor weight gain and lower weaning weights for calves. Furthermore, the toxins interfere with hormonal balance, causing a decrease in the hormone prolactin, which leads to reduced milk production and poor reproductive performance.
The second syndrome, seen during cold weather, is known as “fescue foot,” caused by the lack of blood circulation to the extremities. The prolonged vasoconstriction leads to necrosis, or tissue death, in peripheral areas. Initial signs include lameness and shifting of weight, often beginning in the hind limbs, along with swelling at the coronary band of the hoof. In severe cases, dry gangrene sets in, leading to the sloughing of the hooves, tail switch, and tips of the ears.
Pregnant mares are sensitive to ergot alkaloids, even at low concentrations, and their symptoms primarily relate to reproduction. Mares consuming toxic fescue can experience prolonged gestation, carrying the foal past the expected 335 to 345 days. This extended pregnancy results in an oversized foal, increasing the difficulty of birth. Additionally, the toxins cause the placenta to become thickened and leathery, leading to agalactia, which is a complete absence of milk production after foaling.
Prevention and Treatment Options
Long-term management of fescue toxicosis involves strategic pasture renovation to reduce or eliminate the source of the toxins. The most effective approach is to destroy the existing toxic tall fescue and reseed the pasture with novel endophyte varieties. These new cultivars maintain the hardiness and yield of the grass but eliminate the production of harmful ergot alkaloids. Another strategy is dilution grazing, which introduces other forages into the toxic fescue stand.
Interseeding with legumes, such as red or white clover, helps dilute the animal’s intake of the toxic fescue and improves animal performance. Grazing management practices are also employed to minimize consumption of the most toxic parts of the plant. Since ergovaline concentrations are highest in the seed heads, keeping the grass clipped or grazed short prevents the plant from forming seed heads and reduces toxin intake.
Animals should be provided with ample shade and access to cool, clean water, especially during the hot summer months, to mitigate the effects of heat intolerance. For pregnant mares, the preventive measure is to remove them from toxic fescue pastures or hay during the final 60 to 90 days of gestation. If the reproductive syndrome has already occurred, a veterinarian may prescribe specific medications, such as domperidone, which can counteract the hormonal effects of the ergot alkaloids and stimulate milk production.