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 are possible, such as poor reproduction in animals and agalactia in swine and horses. The disease occurs after the consumption of sclerotia produced by Claviceps purpurea invading the grain or seed of cereal grains (rye, wheat, barley, oats) and of grasses (brome, timothy, fescues, and quack grasses).
Extreme weather conditions (cold or heat) can exacerbate clinical signs. Diagnosis is based on typical clinical presentation and gangrenous clinical signs in animals, and observation of sclerotia with chemical analysis and detection of ergot alkaloids in feed by laboratory methods, generally liquid chromatography-mass spectrometry. Treatment involves stopping the exposure of ergot in feed, providing moderate environmental conditions for animals, and supportive treatment, including good bedding, for clinical signs. If necrosis of the distal part of the limbs has progressed to gangrene and significant tissue damage, the terminal appendages can be lost. In some cases of severe (multiple) distal limb necrosis, the animal must be euthanized.
Ergotism is a worldwide disease of farm animals that results from ingestion of sclerotia of the parasitic fungus Claviceps purpurea, which replaces the grain or seed of rye and other small grains or forage plants, such as the bromes, bluegrasses, fescues, and ryegrasses. The hard, black, elongated sclerotia may contain varying quantities of ergot alkaloids, of which ergotamine and ergonovine (ergometrine) are pharmacologically most important. Cattle, pigs, sheep, and poultry are involved in sporadic outbreaks, and most other species are susceptible. Toxicosis can result from ingesting seed heads, infected grains in concentrate rations, or infected seed heads in hay.
Etiology of Ergotism in Animals
Ergot causes vasoconstriction by direct action on the muscles of the arterioles, and repeated doses injure the vascular endothelium. These actions initially reduce blood flow and eventually lead to complete stasis with terminal necrosis of the extremities due to thrombosis. A cold environment predisposes the extremities to gangrene. In addition, ergot also causes stimulation of the CNS, followed by depression. Ergot alkaloids inhibit pituitary release of prolactin in many mammalian species, with failure of both mammary development in late gestation and delayed initiation of milk secretion, resulting in agalactia at parturition. Ergot alkaloid ingestion during hot weather has also been associated with heat intolerance, dyspnea, and reduced milk production in dairy cattle, similar to the summer syndrome described for fescue toxicosis.
Clinical Findings and Lesions of Ergotism in Animals
Cattle may be affected by eating ergotized hay or grain or occasionally by grazing seeded pastures infested with ergot. Lameness, the first sign, may appear 2–6 weeks or more after initial ingestion, depending on the concentration of alkaloids in the ergot and the quantity of ergot in the feed. Hind limbs can be affected before forelimbs; however, the extent of involvement of a limb and the number of limbs affected depends on the daily intake of ergot. Body temperature and pulse and respiration rates are increased. Epidemic hyperthermia and hypersalivation may also occur in cattle poisoned with C purpurea (Also see Fescue Poisoning in Animals). Ergot alkaloids may interfere with embryonic development in pregnant females. Animals can exhibit rough coats, poor production, and weight loss.
Associated with the lameness are swelling and tenderness of the fetlock joint and pastern. Within ~1 week, sensation is lost in the affected part, an indented line appears at the limit of normal tissue, and dry gangrene affects the distal part. Eventually, one or both claws or any part of the limbs up to the hock or knee may be sloughed. In a similar way, the tip of the tail or ears may become necrotic and slough. Exposed skin areas, such as teats and udder, appear unusually pale. Abortion does not occur.
Courtesy of Dr. Michelle Mostrom.
The most consistent lesions at postmortem examination are in the skin and subcutaneous parts of the extremities. The skin is normal to the indented line, but beyond, it is cyanotic, and hardened in advanced cases. Subcutaneous hemorrhage and some edema occur proximal to the necrotic area.
In pigs, ingestion of ergot-infested grains may result in reduced feed intake and reduced weight gain. Occasionally, swine may show necrosis of the tips of ears or tail. If fed to pregnant sows, ergotized grains result in lack of udder development with agalactia at parturition, and the piglets born may be smaller than normal. Most of the litter die within a few days because of starvation. No other clinical signs or lesions are evident.
Clinical signs in sheep are similar to those in cattle. Additionally, the mouth may be ulcerated, and marked intestinal inflammation may be evident at postmortem examination. A convulsive syndrome has been associated with ergotism in sheep.
Diagnosis of Ergotism in Animals
Observation of causative fungus
Confirmation by analytical identification of suspect feed samples
Courtesy of Dr. Michelle Mostrom.
Courtesy of Dr. Michelle Mostrom.
Identical signs and lesions of lameness, and sloughing of the hooves and tips of ears and tail, occur in fescue foot in cattle grazing in winter on tall fescue grass infected with an endophyte fungus, in which the ergot alkaloid ergovaline is considered a major toxic principle. In gilts and sows, lactation failure not associated with ergot alkaloids must be differentiated from prolactin inhibition due to ergot.
Treatment of Ergotism in Animals
Cessation of exposure
Temperate environment (shade and cooling in hot weather or warmth in cold weather); good bedding for animals with lameness and distal limb lesions
Supportive treatment, including the use of antimicrobials if the distal limb lesions are infected; adequate and easily accessible food and water
Animals with only moderate lameness and little separation of tissue above the hoof can gradually recover over the next 3 to 6 weeks. However, animals with severe and usually multiple distal limb gangrene and sloughing should be euthanized.
In horses, parenteral use of the dopamine receptor D2-antagonist domperidone (1.1 mg/kg, PO, every 12 hours for 10–14 days) is effective in prevention of agalactia from ergot alkaloids in fescue. Use against the same alkaloids produced by C purpurea could be medically logical.
Control of Ergotism in Animals
Depending on the weather, animal species, animal physiological status and susceptibility (horses are very sensitive), the concentration of ergot alkaloids (-ines and the epimer -inines) in the total diet should be < 1 ppm for cattle, weaned piglets, sheep, and horses and < 2 ppm for finishing pigs and poultry. Ergotism can be controlled by an immediate change to an ergot-free diet. In pregnant sows, however, removal of ergot in late gestation (< 1 week before parturition) may not correct the agalactia syndrome, and animals with clinical peripheral gangrene will not likely recover. Under pasture feeding conditions, frequent grazing or topping of pastures prone to ergot infestation during the summer months reduces flower-head production and helps control the disease. Grain that contains even small amounts of ergot should not be fed to pregnant or lactating sows.
Key Points
Ergot sclerotia or hard, dark bodies develop after Claviceps purpurea invasion of the ovary or seed of grains (rye, wheat, barley, oats, and others) and grasses (timothy, brome, fescues, ryegrasses, and others) and contain varying concentrations of ergot alkaloids and other compounds that can exert toxic effects.
Low dietary ergot alkaloid concentrations, as low as 200 ppb or mcg/kg (0.2 ppm), can have adverse health and performance impact across all livestock groups, resulting in production losses.
Ergot toxicosis in animals can result in lameness and gangrenous loss of lower limbs, tails, ears; agalactia; poor thermoregulation; rough coat, weight loss and poor production; and poor reproduction.
No specific antidote is available; exposure to the contaminated feed must be halted, and supportive care with adequate bedding should be provided.
For More Information
Evans TJ, Rottinghaus GE, Casteel SW. Ergot. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis: Mosby, 2004;239-243.
Strickland JR, Looper ML, Matthews JC et al. St. Anthony’s fire in livestock: Causes, mechanisms, and potential solution. J Anim Sci 2011;89:1603-1626.
Also see pet health content regarding fungal poisoning in animals.
