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. Poisoning can come from grazing seed heads or
from infected grains in concentrate rations.
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.
Clinical Findings and Lesions
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
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
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
Last full review/revision December 2014 by Gary D. Osweiler, DVM, MS, PhD