Ergotism

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 alkaloids have also been associated with heat intolerance, dyspnea, and reduced milk production in dairy cattle, similar to the “summer syndrome” described for fescue toxicosis.

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 wk or more after initial ingestion, depending on the concentration of alkaloids in the ergot and the quantity of ergot in the feed. Hindlimbs are affected before forelimbs, but 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). Ergot alkaloids may interfere with embryonic development in pregnant females.

Associated with the lameness are swelling and tenderness of the fetlock joint and pastern. Within ~1 wk, 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 or anemic. Abortion is not seen.

The most consistent lesions at necropsy 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 seen.

Clinical signs in sheep are similar to those in cattle. Additionally, the mouth may be ulcerated, and marked intestinal inflammation may be seen at necropsy. A convulsive syndrome has been associated with ergotism in sheep.

Diagnosis is based on finding the causative fungus (ergot sclerotia) in grains, hay, or pastures provided to livestock showing signs of ergotism. Ergot alkaloids may be extracted and detected in suspect ground grain meals. At 200–600 ppb, ergot alkaloids may cause clinical signs and effects; however, this is influenced by the relative amounts of various ergot alkaloids in the grain.

Identical signs and lesions of lameness, and sloughing of the hooves and tips of ears and tail, are seen 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.

In horses, parenteral use of the dopamine D2 antagonist domperidone (1.1 mg/kg, PO, bid 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 (see Fescue Poisoning).

Intake of ergot bodies should be <0.1% of the total diet, and concentrations of ergot alkaloids should be <100 ppm in the total diet. Ergotism can be controlled by an immediate change to an ergot-free diet. In pregnant sows, however, removal of ergot in late gestation (<1 wk 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.