February 2001: a farmer telephoned and reported that he decided to drench a mob of 15 months old steers (47 head Murray Grey and Angus) he thought weren’t doing well. While he was attempting to move them to the yards, they became very agitated, disorientated, started salivating and grouped under trees and were hard to move. He persevered and got them into the yards where he drenched them. They seemed to get worse; one went down and subsequently died. The remainder were released into a paddock near the yards. Two days later I visited the farm. The cattle appeared clinically normal. I inspected the paddocks where the cattle had been for 3 months prior to drenching. It was a 60 acre pasture/clover paddock. The paddock was previously used to grow wheat and had been let back to pasture the year before. Closer inspection revealed a significant proportion of dry ryegrass. Many of the seed heads were infested with ergot. (Confirmed to be Claviceps purpurea at Orange vet lab).
Based on these observations a diagnosis of ergot poisoning was made. The steers were kept on another paddock until slaughter some months later and showed no further episodes of above described clinical signs. The ergot infested paddock was ploughed and re-sown.
Ergot, or Claviceps purpurea, is a fungal parasite of the seed heads of grasses and cereals. In mid-to late-summer, entire grains are replaced by the dark purple to black, hardened bodies of the fungus, called sclerotia. Sclerotia are 1-2 cm long, longer than the normal grain, and protrude conspicuously from the seed heads. One to a half dozen ergot bodies may develop on one head of grass or cereal plant. The ergot bodies consist of a mass of vegetative strands of the fungus. Ergot is found wherever it’s host plants grow. Rye is the most frequently attacked grain. Other grain, hay, turf and weedy grasses may be affected, including wheat, oats, triticale, fescue and barley. When grain or hay is harvested, ergot bodies may fall to the ground and be left behind to infect the next season’s crop.
The ergot is spread from plant to plant by wind, insects, and rain splash. Wild grasses that grow nearby may contaminate ’clean’ grain. Cool and damp weather seems to favour the development of ergot. The ergot forms spores that may be dropped to the soil so that next year’s crop may also be infected. The spores do not seem to survive for more than one year.
Ergot poisoning in cattle is commonly seen in beef and dairy cattle being fed grain rations that are contaminated with ergot or in late summer on pasture when mature seed head are infested with ergot.
Alkaloids in ergot are responsible for the poisoning that occurs in animals. These alkaloids constrict peripheral blood vessels. The constriction of the blood vessels results in reduced ability to lose body heat, which leads to hyperthermia, in hot weather. Under cold weather conditions, constricted blood vessels result in reduced blood flow to the extremities such as tail, ears and limbs. This results in peripheral gangrene, and affected tissues slough off.
Ergot toxins also affect the function of brain chemical messengers, which causes dysfunction of many body functions controlled by the nervous system. An example is pituitary gland dysfunction, which results in reduced blood prolactin concentration. Prolactin is responsible for milk secretion and reduced prolactin leads to reduced milk production.
Any animal consuming ergot infested feed is susceptible to poisoning. Clinical signs of ergot poisoning include drop in milk production, reduced weight gain, inappetence, depression, reproductive problems (including anoestrous, embryonic death and abortion), lameness, behavioural changes and deaths.
In warm weather, body temperature will be increased and animals seek shade or water, salivate excessively and seem agitated if moved.
In cold weather, peripheral body parts including lower limbs, tail and ears will be cool to touch, animals may be lame commonly in hind legs, and eventually sloughing of affected tissue may occur.
Consumption of large amounts of ergot may lead to convulsions and sudden death. Sudden death may also occur when overheated animals get stressed.
Nervous signs, milk production and reproductive performance may or may not improve after the removal of ergot contaminated feed.
Seed that is planted should be free of ergot sclerotia. Ergot infestations are usually highest at the margins of fields. These areas of a field should be harvested and handled separately when ergot infestations are severe.
Sclerotia will not germinate when they are covered by 2-4cm of soil. Therefore, ploughing infested crops/pasture paddocks to bury sclerotia is a control option after severe ergot outbreaks.
Sclerotia only remain viable for approximately one year under field conditions. Consequently, crop rotation away from susceptible grasses and cereals for a year will reduce the probability of ergot infection.
Keeping the pasture grasses mowed to prevent seed head formation will decrease the presence of the ergot fungus.
If feeding ergot infested grain is unavoidable, the amount of sclerotia should be less than 0.1% by weight of the feed through mixing with ’clean’ grain. Ergot infested grain should not be fed to lactating or breeding females.
Bourke CA, Bailey BD and Kemp JB. The case for solar light radiation being more significant than ambient temperature in producing lethal hyperthermic ergotism in cattle. Australian Veterinary Journal 2000; 78:618-621
Bourke CA, Evidence that enforced sunlight exposure can cause hyperthermia in cattle ingesting low levels of ergot of rye (Claviceps purpurea), when air temperature and humidity conditions are only moderate; Aust Vet J Vol 81;9 2003;553-558