Fescue lameness, which resembles ergot poisoning, 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 limb(s). 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 USA. 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 poisoning (see Ergotism) 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 hr.
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
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
α2-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
Erythema and swelling of the coronary region occur, and
cattle are alert but lose weight and may be seen “paddling” or weight-shifting.
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 (hindlimbs 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
toxin(s) affects cattle, sheep, and horses during the summer when they are
grazing or being fed tall fescue forage or seed contaminated with the endophytic
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 wk after fescue feeding is started, include fever, tachypnea, rough
coat, lower serum prolactin levels, and excessive salivation. The animals seek
wet spots or shade. Lowered reproductive performance also has been reported.
Agalactia has been reported for both 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/reproductive
syndrome is domperidone administered at 1.1 mg/kg, PO, bid 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, through 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 mo
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.)
Last full review/revision December 2014 by Gary D. Osweiler, DVM, MS, PhD