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Ergot poses potential problem for livestockErgot poses potential problem for livestock
Ergot is a disease of cereal crops and many grasses that is favored by cool wet weather during flowering. These conditions have predominated over much of Montana the past 2 weeks. The ergot fungus, Claviceps purpurea, produces dark purple to black sclerotia and these sclerotia are poisonous to warm blooded animals that consume them. As little as 0.1% ergot in whole rations can have adverse effects on livestock health and performance. While ergot is most common in rye and triticale, it does occur on wheat and occasionally on barley. It is relatively uncommon in oats. Ergot is common in many grasses when cool wet weather during flowering favors infection. Grasses commonly infected include; quackgrass, brome grass, red top, feather grass, foxtail, rye grass, orchard grass, crested wheat grass and timothy. In many cases, sclerotia produced in indigenous and pasture grasses are the major source of inoculum for wheat and other cereal crops since ascospores produced in overwintered sclerotia can be windblown long distances. Pastures should be checked for ergot infections if headed grasses are grazed since the ergot sclerotia are toxic to livestock. If ergot is widespread, the grass heads should be cut and left to dry several weeks before grazing. Ergot infections are easily seen as purple to black sclerotia that have replaced individual seeds in the head. These sclerotia will vary in size from up to 1 inch long on rye to less than ¼ inch on some grasses but in most cases will be similar or slightly larger than healthy seeds. When wet weather predominates during flowering, the sclerotia from previous years infections will produce ascospores which blow in the wind and infect the open flowers of the cereal grain or grass. Soon after infection, a yellowish-white to orange colored stick fluid exudes from infected flowers. This is the “honey-dew” stage of the disease. This sticky fluid contains spores of the ergot fungus which are spread by insects or rain splash to other grass flowers. Infections can take place so long as pollination is occurring. Warm-hot dry weather is unfavorable for infection. Ergot is a problem because the ergot sclerotia contain alkaloids such as ergotamine, ergocornine, ergocryptine, ergocristine, ergoclavine, ergonovine and ergometrine; amide and peptide derivatives of lysergic acid; and tremorgenic alkaloids of the indolediterpene class. Ingestion of these alkaloids can cause a wide variety of symptoms ranging from fatigue, inflammation and blistering of skin, painful burning sensations, muscle spasms, backward arching of the back, convulsions, itching, numbness of extremities, dry gangrene particularly of the nose, ears, tails and limbs, loss of extremities, hallucinations, permanent insanity, abortion, loss of milk production, lack of mammary gland development and even death. Typically, lameness in the hind limbs may appear from 2-6 weeks after first ingesting ergot. Responses of animals vary and are dependent on the alkaloid content of the sclerotia, frequency and quantity of ergot sclerotia ingestion and age and reproductive status of the animal. Diagnosis of ergot poisoning is based on the presence of sclerotia in feed or pasture and whether animals are exhibiting the above symptoms. Note, if a pasture has been grazed such that no headed grasses are available, examine grasses outside of grazing range along fences for ergot sclerotia. The only treatment for ergot poisoning is to remove ergot contaminated feeds or remove animals from contaminated pasture. If advanced symtoms of ergotism are present consult your veterinarian for advice and supplemental therapy. Ergot poisoning can only be prevented by feeding feeds or forage free of ergot sclerotia. Since ergot will likely be common this year, avoid feeding screening as they will likely be contaminated. Commercial grain lots can be screened to remove sclerotia and growers should be aware that grain having more than 0.05% ergot by weight is declared ergoty and cannot be sold for human consumption. Pastures with headed grasses should be checked for ergot infection before grazing, Practical control of ergot should be based on planting seed free of sclerotia. Sclerotia can be removed from seed lots by modern seed cleaning equipment or by brine floatation techniques. Seed treatment triazole fungicides such as Dividend or Raxil applied to seed lots will reduce the viability of sclerotia. Rotations that allow for a one year absence of a gramineous host will markedly reduce the number of viable sclerotia in soil. Tillage that buries sclerotia deeper than 4 cm will prevent the release of ascospores to the aerial environment. Control of grassy weeds in wheat production fields will reduce the number of sclerotia in fields and will reduce spread of the conidial stage from these hosts to wheat. Burning of wheat stubble will also reduce the number of viable sclerotia. Mowing or chemical treatment of headland, roadway and ditch bank grasses to prevent heading will eliminate these grasses as a source of inoculum. Wheat cultivars vary widely in their susceptibility and resistance is available. In general those cultivars with shorter flowering times and more closed florets are less susceptible. Cultivars with only short susceptible times following pollination are also less susceptible. Based on limited data, triticale is more susceptible than durum wheat and soft wheats are the least susceptible. Ergot resistance should be a significant factor in cultivar selection in regions where ergot is endemic.
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