Fescue Toxicosis: Causes, Signs, and How to Manage It

Fescue toxicosis is a common ailment affecting livestock that graze on tall fescue grass, a cool-season perennial found extensively across the United States. This condition results in significant economic losses for livestock producers, particularly in beef cow-calf operations, with annual impacts estimated in billions of dollars annually. The problems arise from a fungal endophyte living within the tall fescue plant, which produces compounds toxic to grazing animals. Understanding this issue helps livestock owners address challenges to animal health and productivity.

The Cause of Fescue Toxicosis

Fescue toxicosis is caused by a symbiotic relationship between tall fescue (Lolium arundinaceum) and an endophytic fungus, Epichloƫ coenophiala. This fungus lives within plant tissues. The relationship is mutually beneficial: the fungus gains nutrients, while the plant receives vigor, pest resistance, and drought tolerance.

Despite these benefits, the fungus produces toxic ergot alkaloids. The primary alkaloid responsible for fescue toxicosis is ergovaline. Ergovaline concentrations vary, with highest levels typically found in the stem and seedhead. Signs of fescue toxicosis generally appear when ergovaline levels in the total diet reach 200-800 ppb or higher.

The ergot alkaloids, particularly ergovaline, cause profound blood vessel constriction in animals. This vasoconstriction reduces blood flow to various body systems. Ergovaline also mimics dopamine, inhibiting prolactin synthesis, a hormone for milk production and reproduction. These changes lead to diverse clinical signs in affected livestock.

Clinical Signs in Livestock

Fescue toxicosis manifests depending on animal species, environmental conditions, and toxin exposure. Symptoms relate to ergot alkaloids’ impact on circulation and hormone regulation.

Cattle

Cattle frequently exhibit “summer slump” during hot, humid weather, due to increased heat stress sensitivity. Affected cattle may show a rough hair coat, often retaining their winter coat, and spend less time grazing, seeking shade or water. Decreased feed intake, reduced weight gain, and lower milk production are common, resulting in lighter calf weaning weights.

In colder weather, cattle can develop “fescue foot” due to severe vasoconstriction. This begins with swelling and redness around the coronary band of the hooves, progressing to lameness, and in severe cases, dry gangrene of the distal limbs, ears, or tail. Affected portions may eventually slough off. Reproductive performance can also be negatively impacted, with reduced conception rates and early embryonic loss.

Horses

Horses are sensitive to ergot alkaloids; fescue toxicosis primarily affects mare reproduction. Pregnant mares grazing infected fescue may experience prolonged gestation, leading to difficult births (dystocia).

Mares may also develop thickened placentas, which can prematurely separate from the uterine wall, a condition known as “red bag” delivery. A lack of milk production (agalactia) is another serious concern, preventing foals from receiving colostrum. Foals born to affected mares can be weak, oversized with poor muscle mass, and more susceptible to infections, sometimes resulting in stillbirths or high mortality rates.

Sheep and Goats

Sheep and goats can also be affected by fescue toxicosis, displaying symptoms similar to cattle. These include reduced feed intake, weight loss, and signs of heat stress. Poor wool production, fever, excessive salivation, and rapid breathing may occur.

Reproductive issues, such as low conception rates and early abortions, can occur in sheep and goats. They may also develop lameness in the hind feet, progressing to tissue death in the extremities (fescue foot). Producers should monitor for these signs.

Diagnosing the Problem

Fescue toxicosis is confirmed by observing clinical signs and laboratory testing of forage. Diagnosis often begins with a producer noticing symptoms in their animals that align with known effects, such as “summer slump” or “fescue foot” in cattle, or mare reproductive issues.

A definitive diagnosis requires testing pasture or hay for the presence and concentration of the endophyte and its toxic alkaloids. Samples of tall fescue are collected and sent to a specialized laboratory. These labs can test for the Epichloƫ coenophiala endophyte and for ergovaline concentration. Forage testing confirms the toxic source and helps determine the level of risk to grazing animals.

Pasture Management and Mitigation

Management of fescue toxicosis involves reducing livestock’s intake of toxic alkaloids and improving pasture health. One common strategy is pasture dilution, which involves interseeding existing toxic fescue pastures with other forages like clover or non-toxic grasses. This practice reduces toxic fescue in the animals’ diet, lowering ergot alkaloid exposure and improving animal performance.

Providing supplemental feed can dilute the effects of ingested alkaloids. Feeding hay, especially during periods of high toxicity, can reduce reliance on infected pastures. Certain feed additives may offer some protection by preventing toxin absorption or supporting animal health.

Rotational grazing can manage exposure by moving animals off fescue pastures when toxin levels are higher. Keeping fescue grasses in a vegetative stage through timely grazing, clipping, or mowing helps, as ergovaline concentrations are higher in seed heads than in leaves. If seed heads are removed before drying or pelleting, the toxicity of stored hay can also be reduced.

For a long-term solution, pasture replacement is highly effective. This involves eliminating existing toxic fescue stands, then replanting with novel-endophyte fescue varieties. These varieties contain a beneficial endophyte strain that provides agronomic advantages without producing harmful ergot alkaloids. While initial costs for renovation and novel-endophyte seed can be higher, improved animal performance often offsets these expenses.

In specific cases, such as pregnant mares, veterinary intervention with medications like domperidone can be used as a mitigation tool. Domperidone acts as a dopamine receptor antagonist, blocking the effects of ergot alkaloids that inhibit prolactin release and interfere with reproductive hormones. Administering domperidone to mares consuming infected fescue can help prevent prolonged gestation, dystocia, and agalactia.

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