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Professional Version

Fescue Poisoning in Animals

By

Michelle S. Mostrom

, DVM, MS, PhD, DABVT, DABT, NDSU Veterinary Diagnostic Laboratory Toxicology

Last full review/revision Nov 2021 | Content last modified Mar 2022

Fescue Lameness

Fescue lameness, which resembles ergot toxicosis Ergotism in Animals Ergotism in animals generally presents as lameness; necrosis of the tip of the tail, ears, and hoof tissue; and decay of the wattle, comb, beak, and feet in birds. Additional adverse effects... read more Ergotism in Animals , is believed to be caused by ergot alkaloids, especially ergovaline, produced by the endophyte fungus Neotyphodium coenophialum in tall fescue grass (Lolium arundinaceum, formerly Festuca arundinacea). It begins with lameness in one or both hindfeet and may progress to necrosis of the distal part of the affected limbs. The tail and ears also may be affected independently of the lameness. In addition to gangrene of these extremities, animals may show loss of body mass, an arched back, and a rough coat. Outbreaks have been confirmed in cattle, and similar lesions have been reported in sheep.

Tall fescue is a cool-season perennial grass adapted to a wide range of soil and climatic conditions; it is used in Australia and New Zealand for stabilizing the banks of watercourses. It is the predominant pasture grass in the transition zone in the eastern and central US. Fescue lameness has been reported in Kentucky, Tennessee, Florida, California, Colorado, and Missouri, as well as in New Zealand, Australia, and Italy.

The causative toxic substance, ergovaline, has actions similar to those produced by sclerotia of Claviceps purpurea. However, ergot toxicosis Ergotism in Animals Ergotism in animals generally presents as lameness; necrosis of the tip of the tail, ears, and hoof tissue; and decay of the wattle, comb, beak, and feet in birds. Additional adverse effects... read more Ergotism in Animals is not the cause of fescue lameness. Ergotism is most prevalent in late summer when the seed heads of grass mature. Fescue lameness is most common in late fall and winter and has been reproduced in cattle by feeding dried fescue free of seed heads and ergot. However, occasionally, ergotized fescue seed produced in early summer may inadvertently be baled and result in ergot toxicosis instead of or in addition to fescue toxicosis.

The endophyte fungus N coenophialum growing within the fescue plant can synthesize ergot alkaloids. The ergot alkaloid ergovaline has been detected in toxic fescue and constitutes ~90% of the ergopeptide alkaloids produced. Ergovaline content of infected tall fescue often ranges from 100 to 500 ppb, and >200 ppb is considered a toxic concentration. Susceptible species from most to least sensitive are horses, cattle, and sheep. Endophyte-infected fescue that does not produce ergovaline has not caused fescue toxicosis. In cattle, >90% of ergovaline metabolites are found in urine. Removal of animals from infected fescue pasture reduces urinary ergovaline below detectable concentrations within 48 hours.

Ergovaline is an agonist for dopamine D2 receptors, which initiate several physiologic abnormalities. First, inhibition of prolactin secretion causes agalactia in horses and swine and reduced lactation in cattle. The dopaminergic effect also causes imbalances of progesterone and estrogen, associated with early parturition for cattle and prolonged gestation with oversized fetuses in mares. Finally, inadequate prolactin disturbs the hypothalamic thermoregulatory center, leading to temperature intolerance when environmental temperature exceeds 31°C (88°F).

Some reports indicate an increased incidence of fescue lameness as plants age and after severe droughts. Strains of tall fescue vary in their toxicity (eg, Kentucky-31 is more toxic than Fawn) because of variation in infection level with the fungus and to high variability within a strain. In some Kentucky-31 fescues, infection levels cannot be detected. High nitrogen applications appear to enhance toxicity. Susceptibility of cattle is subject to individual variation.

Low environmental temperature may exacerbate the lesions of fescue lameness; however, high temperatures increase the severity of a toxic problem known as epidemic hyperthermia or summer syndrome, in which a high proportion of a herd of cattle exhibits hypersalivation and hyperthermia. The toxin appears to be a vasoconstrictor acting as an alpha2 adrenergic agonist on blood vessels; this promotes hyperthermia in hot weather and results in cold extremities during cold weather. Another cause of this is poisoning with C purpurea (ergot alkaloids).

Erythema and swelling of the coronary region occur, and cattle are alert but lose weight and may paddle or weight-shift. The back is slightly arched, and knuckling of a hind pastern may be an initial sign. There is progressive lameness, anorexia, depression, and later, dry gangrene of the distal limbs (hind limbs first). Signs usually develop within 10–21 days after turnout into a fescue-contaminated pasture in fall. A period of frost tends to increase the incidence.

For control, all infected forage should be removed.

Summer Fescue Toxicosis

Summer fescue toxicosis is a warm season condition characterized by reduced feed intake and weight gains or milk production. The toxins affects cattle, sheep, and horses during the summer when they are grazing or being fed tall fescue forage or seed contaminated with the endophytic fungus Neotyphodium coenophialum. The severity of the condition varies from field to field and year to year.

Signs other than reduced performance, which may appear within 1–2 weeks after fescue feeding begins, include fever, tachypnea, rough coat, lower serum prolactin concentrations, and excessive salivation. The animals seek wet spots or shade. Lowered reproductive performance also has been reported. Agalactia has been reported for horses and cattle. Thickened placentas, delayed parturition, and birth of weak foals have been reported in horses. The severity increases when environmental temperatures are >75°–80°F (24°–27°C) and if high nitrogen fertilizer has been applied to the grass.

Medical treatment for equine agalactia or reproductive syndrome is domperidone (1.1 mg/kg, PO, every 12 hours for 10–14 days). For control and prevention, toxic tall fescue pastures must either be destroyed and reseeded with seed that does not contain endophytic fungus, or infected fields must be managed to avoid the high risk factor. Transfer of the fungus from plant to plant is primarily, if not solely, via infected seed. Not using pastures during hot weather, diluting tall fescue pastures with interseeded legumes, clipping or close grazing of pastures to reduce seed formation, or offering other feedstuffs help reduce severity. Removing pregnant horses or cattle 1 month before parturition will usually prevent parturition- and lactation-related problems. Specific feed additives may provide some protection against contaminated hay. Yeast cell derivatives known as glucomannans are reported to improve performance by preventing toxin absorption in cattle; a seaweed product is reported to lessen the immunosuppressive effects of toxic tall fescue. (Also see Abdominal Fat Necrosis Abdominal Fat Necrosis .)

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