Fescue Toxicosis in Horses: Signs, Causes, Treatment & Prevention

Fescue toxicosis in horses results from ingestion of fescue grass contaminated with the fungus Neotyphodium coenophialum. The fungus produces ergot alkaloid toxins which cause changes in hormone concentrations and blood flow in pregnant mares grazing contaminated pastures or hay.

Nearly all fescue grass contains the fungus, making fescue a particularly high-risk feed for pregnant mares. Affected mares most commonly develop agalactia (lack of milk production), premature placental separation, and prolonged gestation.

These conditions have serious effects on the development of the growing foal, and may result in abortion, stillbirth, or weak-born foals. Dystocia is also common, due to the relatively large size of the foal and malpositioning within the uterus, and can be fatal to both the mare and foal.

Domperidone is used to treat fescue toxicosis in mares by counteracting the effects of ergot alkaloids. While it can induce lactation in mares and prevent some symptoms, it does not treat dysmaturity in the foal.

Prevention of toxicosis involves removing late gestation mares from fescue pastures and providing them with fescue-free hay or grain. Some breeders may also opt to manage or re-seed their pastures to decrease fescue grass concentrations.

Fescue Toxicosis in Horses

Fescue grasses are a group of cool-season perennial grasses belonging to the genus Festuca. They are widely used for livestock pasture and hay, especially in temperate regions. ^[1]

One of the most common types of fescue used for pasture is tall fescue (Festuca arundinacea), which is known for its hardiness and ability to tolerate a range of conditions, including drought and poor soil quality.

However, tall fescue grass is commonly infected by Neotyphodium coenophialum, a fungal endophyte that produces toxins called ergot alkaloids. ^[1] Estimates suggest that over 95% of tall fescue pastures have fungal contamination. ^[2]

The fungus has a symbiotic relationship with fescue, allowing the plant to be more resilient to environmental extremes. ^[3] But, this fungus also produces detrimental effects in livestock that consume toxic alkaloids in the grass.

Ergot Alkaloids

Ergot alkaloids are a complex group of chemicals produced by fungi infecting grasses. An alkaloid is a naturally occurring organic compound, often derived from plants, that typically contains nitrogen atoms and has a pharmacological effect.

Horses most commonly consume ergot alkaloids by ingesting contaminated hay, pasture, or seed grains. ^[4] Drought, excessive rain and fertilization all increase the risk of fungal growth and alkaloid contamination on fescue grass. ^[2]

Ergovaline is the most abundant ergot alkaloid in tall fescue and fescue toxicosis is typically associated with this fungal toxin. ^[7]

Ergot alkaloids affect horses by binding to cellular receptors and either increasing or decreasing their function. ^[1] The toxin primarily targets and activates dopamine receptors in horses. This inhibits the release of prolactin, a hormone responsible for milk production in lactating mares.

Alkaloids can also affect blood vessels, restricting blood flow that can lead to damage in affected tissues. ^[1]

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Pathophysiology

Fescue toxicosis results in three main syndromes in pregnant mares:

• Agalactia
• Prolonged gestation
• Premature placental separation

These syndromes primarily arise through reduced levels of prolactin, the main hormone that stimulates milk production after birth. ^[1]

Clinical signs in affected mares include lack of milk production, continuing pregnancy well past their anticipated due date, and difficulty foaling. Foals born to affected mares are dysmature, showing symptoms such as a silky hair coat, floppy ears, and poor muscle tone.

Affected foals have a high risk of “dummy foal syndrome” and failure of passive transfer, due to the toxin’s effect on their dam. Most foals require intensive care or hospitalization and have a very poor prognosis.

Agalactia

Agalactia, or lack of milk production, is a hallmark sign of fescue toxicosis. Approximately 90% of mares with fescue toxicosis develop agalactia. ^[3]

Ergot alkaloids mimic the effects of dopamine on prolactin-secreting cells in the pituitary gland, resulting in decreased prolactin production. ^[4] In mares, prolactin is essential for lactation, and when its levels are low, it leads to agalactia or the inability to produce milk.

Mares with agalactia show few of the typical signs of impending birth, such as “waxing” of the teats or increased calcium concentrations in mammary secretions. ^[4] Because these classic signs are usually absent, there is a high risk of unexpected and unattended delivery of the foal.

Foals born to mares with agalactia have a significantly increased risk of failure of passive transfer, which predisposes them to septicemia and other infections. ^[1]

Prolonged Gestation

The typical gestation length for a horse is approximately 340 days, or about 11 months. In pregnant mares grazing on fescue, the length of gestation increases by an average of 27 days. ^[1]

The exact mechanism for prolonged gestation is unknown. Ergot alkaloids interrupting prolactin production may prevent the normal signaling that stimulates the in utero foal to mature. ^[4]

Under normal circumstances, the foal produces corticotrophin-releasing hormone, which stimulates the release of cortisol from the adrenal gland. ^[3] This increase in fetal cortisol levels signals the broodmare’s body to begin delivery by triggering a cascade of events including re-positioning of the foal and final maturation of the lungs.

Reduced prolactin may prevent the foal from producing corticotrophin-releasing hormone, interrupting the normal signaling that occurs around delivery. This could cause the foal to continue to grow in utero beyond the expected due date.

The foal also receives no stimulus to re-position themselves within the uterus in preparation for delivery. The combined effects of increased foal size and abnormal positioning significantly increases the risk of dystocia (difficulty birthing), which can be fatal for both mare and foal. ^[1][4]

Dysmature foals (immature development despite prolonged gestation) are also likely to have poor lung development, as the stimulus to produce the lung surfactant relies on hormonal activation. ^[1]

Premature Placental Separation

Mares with fescue toxicosis have a higher risk of premature placental separation, or “red bag delivery”.

Ergot alkaloids cause thickening of the chorioallantois, the major placental membrane surrounding the foal. The thickening results from decreased blood flow to the uterus due to ergot alkaloid activity. ^[1]

The foal is unable to break through the thickened membrane as it moves into the pelvic canal during delivery. The foal’s movement pulls the placenta away from the uterus, cutting off the foal’s oxygen supply via the umbilical cord.

Additionally, the membrane over the foal’s head prevents normal breathing, resulting in an emergency situation that requires rapid intervention to remove the membrane and allow the foal to breathe. ^[1]

Foals born from premature placental separation are very likely to develop “dummy foal syndrome” due to oxygen deprivation. ^[1]

Other Effects

Fescue toxicosis can also cause abortion in pregnant mares. Ergot alkaloids can stimulate the muscle within the uterine wall, causing uterine contractions that lead to abortion. Their effects on blood vessels can also prevent proper blood flow within the placenta, resulting in foal death. ^[4]

Fescue toxicosis may also increase the risk of retained placentas in affected mares. ^[3] Retained placentas carry significant risks for the mare including metritis (infection of the uterus) and acute laminitis. ^[2]

Fescue toxicosis also appears to affect fertility rates, with affected mares having lower pregnancy rates, higher embryonic death rates and poor cyclicity. ^[1][3] Research suggests that the effects on fertility are due to the toxin preventing implantation of the egg in the uterine wall, although this has not been confirmed in horses. ^[3]

Mares recovering from fescue toxicosis may also have decreased fertility, particularly if they had a retained placenta or dystocia event during their previous pregnancy that damaged the uterine wall. ^[3]

There are also reports of fescue toxicosis causing laminitis and lameness in some affected horses. ^[1] This is likely due to the vessel constricting effect of fescue alkaloids, resulting in injury and death of tissues in the lower limb. ^[1]

Clinical Signs

Symptoms of fescue toxicosis typically arise during late gestation. If the mare’s expected due date is known, usually the first sign of toxicosis is the mare passing her due date with little evidence of udder development.

Mares with an unknown expected due date have a higher risk of developing symptoms, as it is unlikely that the toxicosis will be recognized before the mare gives birth. ^[3]

Time of Delivery

At the time of delivery, symptoms of fescue toxicosis may include: ^[1][4]

• “Red bag delivery”, with the presence of the chorioallantois at the vulva before the foal
• Dystocia (difficulty birthing) particularly with foals rotated 90° within the uterus
• Little to no production of mammary secretions
• Brown or straw-coloured mammary secretions rather than white milk
• Thick placenta that is difficult to break

Dummy Foal Syndrome

Foals with fescue toxicosis show signs of dysmaturity or “dummy foal syndrome”, including: ^[1][3]

• Weakness and poor muscle tone
• Silky, fine hair coat
• Overgrown hooves
• Floppy ears
• No erupted incisor teeth
• Lack of interest in the mare
• Poor suckling reflex

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Diagnosis

Diagnosis of fescue toxicosis can be challenging, particularly if the pasture or hay composition is unknown.

In pregnant mares, ultrasound of the uterus may show a thickened placenta and abnormally large foal. Measuring blood concentrations of prolactin can also provide evidence of fescue toxicosis. ^[2]

Ultrasound can also be used to measure the diameter of the palmar artery in the mare’s foot. Horses consuming toxic endophyte affected tall fescue often have narrower vessels, due to vasoconstriction. ^[7]

In foals, identification of low serum thyroid hormone levels or cortisol levels can also aid in diagnosis. ^[2]

Confirming a diagnosis of fescue toxicosis requires measurement of ergot alkaloid concentrations in pasture or hay. Hay or pasture should be sampled and submitted to a diagnostic lab for ergot alkaloid testing.

Pasture sampling typically involves collecting 10-15 samples at each end of a “W” shape walked in the middle of the pasture. ^[3] For pregnant mares, 200 ppb (parts per billion) is the maximum allowable level of ergot alkaloids in the diet. ^[5]

Treatment

The primary treatment for fescue toxicosis in pregnant mares is domperidone, a dopamine antagonist. ^[1][4][6] Domperidone blocks the effect of ergot alkaloids on dopamine receptors, preventing the inhibition of prolactin-secreting cells. ^[1][6]

This results in normal prolactin levels within the mare, and appropriate hormonal stimulus of the foal. Mares treated in late gestation produce milk normally, have a normal gestation length, and have normally developed foals. ^[1][2]

Domperidone can also be given as a rescue treatment, to stimulate lactation in mares with agalactia after the foal is born. ^[6]

Foals born in these scenarios typically have failure of passive transfer, due to lack of colostrum production, and require plasma transfusions or supplemental colostrum and bottle feeding until their dam is able to produce milk. ^[6]

Other dopamine receptor antagonists, such as fluphenazine, may also be effective for supporting placental function and hormone levels. ^[8]

Treating Fescue Toxicosis in Foals

Foals born with signs of fescue toxicosis require intensive care due to their dysmaturity and high risk of neonatal hypoxia. Treatments may include:

• Oxygen therapy
• Nasogastric intubation
• Colostrum supplementation
• Plasma transfusions
• Antibiotics ^[2]

Affected foals have a very poor prognosis, even with treatment.

Prevention

Prevention of fescue toxicosis focuses on reducing exposure of pregnant mares to fescue grasses. This is particularly important during late gestation, although endocrine disruptive effects have also been noted with short-term exposure in early gestation. ^[9]

Ergot alkaloid testing on available hay, pasture, and grain sources allows formulation of an appropriate diet for late gestation mares. Total amounts of ergot alkaloids in all feed sources must be below 200 ppb to minimize risk for pregnant mares. ^[5]

Completely removing late gestation mares from pasture and replacing their diet with a nutritionally balanced combination of hay and feed is often the easiest prevention strategy for breeders. Hay and feed sources must be tested for alkaloid concentrations as part of the diet formulation.

Work closely with an equine nutritionist to ensure the diet meets the mare’s nutritional needs.

Pasture Management

Pasture management to reduce ergot alkaloid concentrations is more challenging. Alkaloid levels are influenced by season, rainfall, temperature, and pasture management strategies. ^[5]

The first step is to identify the amount of tall fescue grass present in the pasture. Fescue content of less than 10% is considered safe for late-term mares, and is typically only a risk when grasses are severely stressed, such as during a drought. ^[5]

Pastures with fescue levels between 10% and 50% can be managed to reduce alkaloid levels through specific herbicides or overseeding measures. ^[5]

In pastures with greater than 50% fescue, complete re-establishment of the pasture with safe grass species is recommended. ^[5] Some newer fescue species contain beneficial endophytes that do not produce toxins that affect livestock and offer a safe choice for renewing a contaminated pasture. ^[5][7]

Pasture replanting usually takes around 2 years for the plants to fully establish and can have significant associated costs. ^[3]

Broodmare Management

Mares grazing pastures that are 10% to 50% fescue should be removed from pasture at least 3 – 4 weeks before their expected due date. ^[2][5] If removal of fescue from the mare’s diet is not feasible, administering domperidone in the last 2 weeks of gestation can prevent many symptoms of fescue toxicosis. ^[2]

Finally, careful management of broodmares is an important component of fescue toxicosis prevention. Knowing the expected due date of the mare allows for monitoring for signs of fescue toxicosis, as well as adjusting the diet appropriately to avoid fescue.

Keeping a log of breeding dates, expected due dates, and past reproductive history including average gestational lengths can help breeders identify symptoms early, allowing for early treatment and a better prognosis. ^[1]

Frequently Asked Questions

Here are some frequently asked questions about Fescue Toxicosis in Horses:

Summary

Fescue toxicosis is a reproductive disorder in pregnant mares caused by eating fescue grass infected with the endophyte Neotyphodium coenophialum . The fungus produces ergot alkaloids that disrupt hormones, reduce milk production, and impair blood flow to the placenta, leading to serious foaling complications.

• Nearly all tall fescue pastures contain the toxic endophyte, posing high risk for late-gestation mares.
• Clinical signs include agalactia, prolonged gestation, premature placental separation, and foal dysmaturity.
• Treatment with domperidone restores prolactin levels and can prevent or lessen symptoms if given before birth.
• Prevention involves removing mares from infected pastures, testing hay and feed, and replanting with endophyte-free fescue species.