Intoxication caused by metabolites produced by members of the Claviceps genus is the oldest known mycotoxicosis. The species usually involved are C. purpurea, the ergot of rye and other grain crops and grasses, and C. paspali, the ergot of Paspalum spp.
Fescue foot or tall fescue lameness of cattle has been reported in NZ, Australia and North America for many years. Its occurrence has been most prevalent in the autumn and winter period and it has been reported in both cattle and sheep grazing tall fescue, Festuca arundinacea. The disease is now known more correctly as fescue toxicity and it is caused by ergovaline produced by the fescue endophyte (Neotyphodium coenophialum).
As a result of Claviceps infection of the seed head the ovary is destroyed and replaced by a compacted mass of hyphae known as a sclerotium. This projects from the ear as a small, dark, horn like or rounded structure. Grazing stock become affected when they consume pasture heavily infested with this stage of the parasite.
Similarly, Neotyphodium coenophialum is eaten with tall fescue. The plants offer the fungus a substrate, protection and a means of dispersal via the seed. In return, the fungus offers the fescue resistance to insect attack and protection from overgrazing by herbivores.
Many features of fescue endophyte infection, its mode of spread and toxin production are similar to those of the ryegrass endophyte. These include the location of the endophyte in the plant, its transmission by seed and the effect of storage time on the viability of the fungus in the fescue seed. Vasoconstrictive peptide and clavine ergot alkaloids have been demonstrated in the aerial portions of tall fescue grass. Higher concentrations were found in the sheath than the leaf. In particular, the more active vasoconstrictive compound ergovaline was found to be the most common peptide present. Drought and high nitrogen levels in the soil increase the risk of poisoning.
Cultivated tall fescue in NZ is either endophyte free or contains a "safe" endophyte. Problems only arise with wild tall fescue.
There are four main classes of ergot alkaloids: clavine alkaloids, lysergic acids, lysergic acid amides and peptide alkaloids. The last group contains most of the substances which affect smooth muscle.
| fungus | plant | toxin | effect |
| Claviceps purpurea | many grasses, including ryegrass | ergotamine ergometrine (ergonovine) |
vasoconstriction uterine contraction |
| Claviceps paspali | Paspalum spp. | paspalitrems A & B | tremors |
| Neotyphodium coenophialum | tall fescue | ergovaline | vasoconstriction |
The main alkaloids of ergot are amides and polypeptide derivatives of lysergic and isolysergic acids, known as ergotamine, ergometrine and ergotoxine. Ergotaminestimulates and then depresses the central nervous system, but its main action is a stimulant effect on constrictor adrenergic nerves supplying arteriolar smooth musculature and on uterine musculature. It is also a powerful blocker of alpha adrenergic receptors. Ergometrineand ergotoxineare similar in their effects except that they do not stimulate sympathetic nerve endings so strongly, if at all. Together with constrictor activity, capillary damage leads to thrombosis of arterioles, vascular stasis, ischaemia and gangrene of the affected part the so called gangrenous ergotism. Crude ergots may also be irritant to the alimentary tract, causing diarrhoea.
Convulsive ergotism (paspalum staggers) resembles tetanus and occurs rapidly in animals when the daily intake of toxin in affected pasture is substantially higher. The toxins producing paspalum staggers are thought to be paspalitrems A & B. These have similar properties to lolitrem, which produces ryegrass staggers.
The vasoconstrictor compound associated with the fescue endophyte has its most serious effect on the extremities of cattle and sheep during cooler weather, hence the higher incidence of this syndrome (fescue lameness) at these times. However, it is somewhat of a paradox to find that ergovaline is also associated with bovine hyperthermia, a summer time disease, which is not seen in sheep. While cattle dilate their peripheral vessels to dissipate heat, sheep do not. They rely more on the respiratory passages and the protective effect of wool to prevent overheating. This may explain why sheep do not suffer "summer hyperthermia" in the same way that cattle do when exposed to ergots or endophyte infected fescue in the summer.
Fescue lameness
Signs may appear within 10 to 14 days after animals begin grazing tall fescue and new cases may appear for up to a week after animals have been removed from affected pasture.
Animals show severe lameness with the hindlimbs in particular being affected, but all four legs may become involved. Animals lose weight and initially there is a drying of the skin near the hoof. Moist gangrene with loss of hair or wool of the lower extremities takes place. In some cases the lower limb will actually drop off. Radiographs of affected limbs show a complete cessation of blood circulation. In severe cases, the tips of the tail and the ears of cattle may also be affected.
Summer hyperthermia
This can be a serious disease of cattle in NZ. In 1985 it was estimated to have occurred in 445 North Auckland dairy herds.
It is characterised by a rough coat and the animal develops a rapid panting respiration, with protrusion of the tongue and excessive salivation. Affected cattle seek shade, hilltop breezes and will stand in water in an effort to reduce the high body temperature. Milk production is reduced.
In Australia hyperthermia in cattle grazing annual ryegrass has been reported. The syndrome of hyperthermia appeared identical to summer hyperthermia. The ryegrass was heavily contaminated with Claviceps purpurea.
Infertility
Ergovaline found in endophyte infected pastures has been shown to decrease ewe live weight, ovulation rates, number of fetuses at 90 days of pregnancy and serum prolactin levels.
Growth rates
Average daily weight gain in beef steers decreased by 0.45 kg/day for each 10% increase in infestation of endophyte on the pasture.
Equine Fescue Toxicity
Pregnant mares that ingest fescue containing ergovaline have prolonged gestation, dystocia, and decreased milk production or agalactia.
Two other conditions which have been associated with toxic fescue are fat necrosis in cattle and deer, and agalactia in cattle and horses.
The clinical signs of gangrenous ergotism are similar to those of fescue toxicity. However it is believed that ergotism characterised by ataxia and tremors is the more common disease.The disease is similar in all species, requiring several kilograms of seed heads containing sclerotia, consumed over 2 - 6 days for animals to become affected.
Initially animals become nervous and hypersensitive. This is followed by tremors of the muscles of the limbs and body, seen particularly after exercise. This may become so severe that animals are unable to feed. There is marked incoordination of gait with swaying hindquarters, staggering and difficulty in posturing. Excess salivation and a rapid heart rate are also features.
Once the signs of fescue lameness are advanced there is no treatment possible. Some veterinarians have reported success in treating early cases in cattle by providing shelter from cold weather and applying warmth to the affected extremities. Such measures, however, are unsatisfactory.
Treatment of affected animals involves removing them from toxic paddocks where ergotised seedheads are present, to safe paddocks where the pasture is non toxic and the risk of misadventure is minimal. Animals should be moved as gently as possible and where possible left undisturbed until recovered.
Ergotism may be prevented by restricting access to ergotised paspalum or other ergotised grasses. Animals can be protected by making sure that the flower head is not allowed to remain standing long enough for the sclerotia to develop. Paddocks with ergotised seedheads can be made safer by topping the pasture to remove the heads.
Domperidone, a dopamine receptor antagonist, can be used for the prevention and treatment of fescue toxicity in the pregnant mare.
The control measures for the diseases caused by endophyte infected fescue are similar to those suggested for ryegrass staggers and are mainly a matter of planting grass seed infected with a safe endophyte. Short term measures include the dilution of endophyte infected pasture with other feed sources and the avoidance of overstocking and overgrazing of pastures. When there is a choice, avoid utilizing endophyte infected fescue during the hottest and coldest times of the years.
Animals will recover from ergot poisoning if removed from affected pasture carefully. In this respect the condition is very similar to perennial ryegrass staggers. Ischaemia of the feet in fescue toxicity means the animal will have to be killed.
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