Ergot of Cereals and Grasses

Ergot is a plant disease caused by the fungus Claviceps purpurea, which infects the developing grains of cereals and grasses. Ergot symptoms become evident during kernel formation, when ergot bodies are formed in place of kernels.

The ergot bodies, which are also called sclerotia, are formed from a hard mass of fungal mycelium, and are the over-wintering structures in the disease cycle. The ergot bodies have a hard protective rind on the outside, which is black to dark purple in colour, and a white to grey coloured interior. They are often elongated and protrude from the glumes of maturing heads, and may be up to 10 times larger than the seed it has replaced.

In some cereals, ergot bodies may reach up to two cm in length, but in forage grasses they remain small and slender. Heads may contain one to several ergot bodies. Ergot can easily be identified in unclean grain.

Host Crops and Grasses

Crops, such as rye and some grasses, are more susceptible to ergot infection because they are open-pollinated, allowing easy access of the fungus into the flowering head. Ergot may also be a concern in forage grasses grown for seed production. Grains such as wheat and barley are less likely to become infected because they are self-pollinated, but may still develop levels that result in downgrading. Oats are seldom affected. Plants are less susceptible once the fertilization process has occurred. Broadleaf crops are not susceptible to ergot, which makes them an effective crop rotation choice.

The Disease Cycle of Ergot

There are two stages to the ergot disease cycle. The first stage occurs in the spring when ergot bodies germinate to produce tiny drumstick-shaped fruiting structures. Ergot bodies may be present in a field from a previous cereal crop, or from grasses along roadsides or neighbouring pastures. Ergot bodies may also be introduced into a field with planted seed.

The conditions required for the germination of ergot bodies are a cold stratification period (winter), followed by prolonged wet soils in the spring.

The drumstick-type structures (stromata) produce spores called ascospores that become wind-borne. Ascospores land on florets and penetrate the ovaries of early flowering plants such as wild grasses, fall-sown cereals, or early-sown spring crops. Within five days of the floret being infected by an ascospore, the second stage in the disease cycle occurs. This stage is known as the "honeydew stage."

During the honeydew stage, the florets exude a sticky ooze of spores (conidia). Conidia are spread by insects and rain-splash to other florets. These spores can be disseminated for as long as flowering occurs. The honeydew stage declines once the infected ovary enlarges and becomes replaced by the hardened ergot body.

Ergot bodies fall from the head to the soil before or during harvest, or may be harvested with the seed. Ergot bodies rarely survive for more than one year in the soil.

Conditions That Favour Ergot

Ergot is most prevalent in years when continuous moist conditions prevail during both stages of the disease cycle. First, moisture is needed at the soil surface during spring and early summer to promote germination of ergot bodies. Second, wet, cloudy and cool weather extends the period of flowering and increases the window of infection for spores to enter the florets. These weather conditions may also favour insect populations of aphids, thrips, midge and leaf hoppers, which serve as potential vectors of sticky spores.

Agronomic conditions, such as poor fertility, may delay maturity and create a more open floret physiology that is susceptible to infection. Ergot has also been linked to copper deficiency. Copper deficiency can delay flowering and triggers male sterility, causing the floret to remain open longer. Sandy or light loam soils are most likely to be copper deficient. Crops with a high proportion of tillers will flower unevenly, and also be exposed to infection for a longer period of time. Furthermore, herbicide injury can also delay maturity and cause sterility.

Past Occurrences of Ergot

Only occasionally will the right environmental conditions and plant development stages coincide to result in widespread ergot problems. The last widespread outbreaks of ergot in Saskatchewan were in 1999 and 2008. In 2008, cool soils caused poor emergence, resulting in crops with uneven growth stages, lengthening the period of time crops were flowering and susceptible to ergot. Cool, moist weather in late spring and early summer promoted ergot germination and initial infections, which continued to spread from plant to plant through rain splash and insects. Similarly, in 1999 early spring rains provided ideal conditions for germination of ergot bodies, and cool, wet summer conditions extended cereal flowering.

Canadian Western Red Spring (CWRS) wheat was one of the main crops affected during these outbreaks. An average of 17 per cent of CWRS samples from the province had ergot infection in both 1999 and 2008, with an average infection level of 0.02 per cent ergot bodies by weight in 1999 and 0.04 percent ergot bodies by weight in 2008 (Canadian Grain Commission). These levels resulted in substantial downgrading of many samples. Prior to 1999, ergot had not been reported at significant levels since the early 1980s.

There were sporadic appearances of ergot in 2000 and 2001 due to the increased ergot load to the soil from 1999. Ergot was also observed in pockets across Saskatchewan in 2005, particularly in the south eastern region in forage grasses for seed production.

The Importance of Ergot

Ergot alone does not typically cause significant yield loss, but economic losses may result due to rejection of grain or downgrading at the elevator (Table 1). The reason for low tolerance is that ergot bodies contain numerous alkaloids, or toxic chemicals, that remain active even after processing for food (e.g. flour) or feed has been completed. These alkaloids are toxic to humans and animals.

Ergotism is the symptom that develops in humans and animals after eating food or feed with ergot contamination. Ergotism in humans is now rare because of the strict guidelines for allowable ergot bodies in grain. Ergot poisoning from eating contaminated rye flour led to deaths in the Middle Ages. Symptoms include impaired blood circulation, causing alternating burning and freezing sensations, followed by gangrene of extremities. This symptom was referred to as St. Anthony's Fire. Nervous convulsions can also occur and lead to eventual death. Commercially produced flour and grain products are at very little risk of contamination, but home-grown grain should not be used unless checked thoroughly to ensure it is free of ergot.

Ergotism can still be common in livestock when fed contaminated grain at the farm level. Symptoms may include lameness, loss of body parts from gangrene, abortions in pregnant animals, seizures, and eventually death. Consumption of contaminated feeds with sub-lethal doses may still lead to problems of poor growth and performance, loss of milk production in lactating animals, and animals going "off feed." Animals will recover from these milder symptoms when contaminated feed is removed. Animals differ in their susceptibility to ergot poisoning. Young or pregnant animals are considered highly susceptible. For beef cattle, current recommendations indicate that ergot may be present at levels up to 0.1 per cent (by weight) of their daily dry matter intake.

At one time, pharmaceutical companies developed some of the chemical compounds found in ergot into medicines to aid in child birth, and for the control of migraines and bleeding. Now these derivatives are made from synthetic forms of the alkaloids. The alkaloid compounds found in ergot are also similar to those found in the drug LSD.

Ergot Management

Unfortunately, there is not much a farmer can do to control ergot in the field. Prevention is the best management strategy, but it is too late to practice once ergot symptoms have been observed.

• Harvesting techniques - Ergot levels are typically higher around the edge of the field, as this is where the spores come in from roadside grasses, and where insects are most active. Prior to harvest, farmers may scout their field to determine where ergot development is the worst, such as the headlands, and harvest those areas separately. The heavily infected seed should then be binned and taken to the elevator separately, or even destroyed by burning or burial if it has a very high infestation. In some cases, delaying harvest of a standing crop may allow more time for ergot bodies to fall out of the head.
• Tillage - For farmers using conventional tillage, burying the crop residue and ergot bodies to a depth of approximately four centimetres can impede their germination the following spring.
• Seed cleaning - Ergot bodies are relatively easy to clean from the seed lot, but cleaning can be expensive, especially if a gravity separator is used. However, if the farmer has access to cleaning equipment, it is likely worth the cost to save a grade at the elevator. For small or expensive seed lots such as forage grasses, a flotation method can be used. Soak the seed in a 20 per cent salt solution and stir. The ergot bodies will rise to the top and can be skimmed off. Then thoroughly rinse and dry the remaining seed.
• Plant clean seed - Planting seed infested with ergot bodies can spread disease to previously clean fields. There are no seed treatments effective against ergot. If you use two-year old seed, the viability of the ergot should be greatly reduced. However, even non-viable ergot bodies still contain alkaloids and should not be fed to livestock.
• Crop rotation - Ergot bodies survive in the soil for approximately one year, so crop rotation away from cereals for one to two years is recommended. Avoid planting spring cereals next to winter cereals.
• Crop choice - Although cereal varieties may differ in their susceptibility to ergot infection, there are no truly resistant varieties. In Saskatchewan in 1999, regional cereal variety trials were assessed to compare susceptibility to ergot (Fernandez 2000). They found that average ergot levels were similar in Canadian Western Red Spring and Canadian Western Amber Durum (CWAD) tests, and slightly lower in Canadian Prairie Spring (CPS) tests. Overall, disease levels were too variable to be able to draw any conclusions regarding varietal differences. In a more recent study conducted in a controlled environment, both CPS and CWAD classes of wheat developed fewer and smaller ergot bodies (Menzies 2004).
• Ensure uniform stands - Use seed with good germination, seed at a consistent depth, and use a balanced fertilizer program so that the cereal crop is uniform in development. The addition of copper will also help control ergot infection, but only in copper deficient soils. Planting cereal crops at the same time within a region, so they flower over a narrower time period, will prevent the spread of the disease from one field to another. Apply herbicides at the correct rate and timing to prevent floret sterility.
• Sanitation - Mow around headlands or roadways to remove grasses before they flower so they do not serve as a host for the first stage of the disease cycle. Also, cut or graze hay at the heading stage if a severe ergot infestation is expected.

Allowable Levels of Ergot in Grain

Guidelines are set by the Canadian Grain Commission (CGC). For cereals, ergot is assessed in a minimum sample size of 500 grams to an optimum/export sample size of 1,000 grams. If kernel count is excessive, the weight of ergot as a per cent of the net weight of the sample is determined. For further explanation, please contact an elevator agent or CGC representative.

* number of kernel sized pieces in 500 g

¹ Canadian Western Red Spring (CWRS)
² Canadian Western Hard White Spring (CWHWS)
³ Canadian Western Soft White Spring (CWSWS)
⁴ Canadian Western Amber Durum (CWAD)
⁵ Canadian Western Red Winter (CWRW)
⁶ Canadian Western Extra Strong (CWES)
⁷ Canadian Prairie Spring White (CPSW)
⁸ Canadian Prairie Spring Red (CPSR)
⁹ Canadian Western General Purpose (CWGP)

Bailey, K.L, Gossen, B.D., Gugel, R.K., and Morrall, R.A.A. 2003, Diseases of Field Crops in Canada , Canadian Phytopathological Society, Saskatoon , SK. pages 89-92.
Canadian Grain Commission: http://www.grainscanada.gc.ca/
Fernandez, M.R., DePauw, R.M., and Dunbar, B. 2000, Ergot in common and durum wheat in Saskatchewan in 1999, Canadian Plant Disease Survey, Volume 80: 54-55.
Menzies, J.G. 2004, The reactions of Canadian spring wheat genotypes to inoculation with Claviceps purpurea, the causal agent of ergot, Canadian Journal of Plant Science, Volume 84: 625-629.
Seaman, W.L. 1980, Ergot of grains and grasses, Information Services, Agriculture and Agri-Food Canada , Ottawa . Publication No. 1438.