The negative impacts of ergot contamination in food were recognized as early as the fifth century AD. Ergot, a plant parasite, commonly affects rye grass, but wheat, rye, barley, oats, brome, fescue, blue, timothy, western and intermediate wheatgrass and other grasses can also be infected. Environmental conditions associated with a cool wet spring followed by hot early summer temperatures are ideal for the ergot fungus to proliferate. Delayed harvesting of grass hay because of rain also means that late-cut hay may also be at risk of ergotism. The fungus invades plant flowers when young and induces cells to divide abnormally, creating large brown, hard sclerotia that allow the fungus to survive adverse conditions like winter and desiccation. The sclerotia fall to the ground, overwinter, and germinate in the spring, producing spores to continue the life cycle. Extended periods of increased moisture and cold during flowering promote the development of ergot in cereal crops. When the sclerotia inadvertently get mixed with grains and incorporated into food, they cause ergotism in humans and livestock. Although ergotism is now rare in humans, cleaning contaminated grain concentrates ergot bodies in screenings used as livestock feed.
Ergot is found worldwide. Ergot alkaloids (toxic components) are produced by a group of fungi of the genus Claviceps. Even low concentrations of alkaloids in the diet (<100 ppb total) can reduce feed efficiency. Allowable limits for ergot in livestock feed, often determined by the number of ergot bodies or total levels of alkaloids, are confusing and often fail to reflect the true degree of toxicity. Current recommendations on safe levels of ergot in feeds are unreliable. Increasing concentrations of ergot in feed grains pose a challenge.
In 2011, an estimated 20 per cent of the wheat produced in Western Canada showed some degree of ergot infestation. Climate change models predict increased concentrations of ergot in Canadian cereal grains in the future. Susceptibility of grains to ergot (from most to least) include rye, wheat, triticale, barley, and oats. Though ergot reduces yields by five to 10 per cent, the reduction in quality grade accounts for the majority of economic loss.
Unlike other mycotoxins formed post-harvest as a result of spoilage during storage, ergot only forms pre-harvest, with concentrations of alkaloids remaining relatively constant during storage. Toxic principles do not appear to degrade over time. Distiller processes used for ethanol production retain and concentrate ergot alkaloids.
Clinical symptoms are highly variable and can appear in as little as a few hours, or may require months to develop. Differences in physiological response to the type and concentration of alkaloids account for the variability and frequent misdiagnosis of ergot toxicity. Symptoms of ergot toxicosis often resemble other conditions, like foot rot, frostbite, and respiratory disease. Toxic levels of ergot in growing and finishing livestock rations affect performance, which may not become apparent for six to eight weeks after contaminated grain is introduced.
Classic signs of ergot poisoning are produced by the effect alkaloids have on peripheral circulation. Sustained intake of ergot causes vasoconstriction, or shutting down of blood supply to the extremities. Over time, poor blood supply to peripheral areas causes gangrene and sloughing of the tail, ear tips and hooves. Blood-starved extremities freeze in cold weather. Gangrenous signs can also appear in hot weather when thermoregulation to extremities is impaired.
Other clinical symptoms may include:
- Altered endocrine function.
- Staggering, convulsions and muscle spasms.
- Lack of rigor mortis at slaughter.
- Decreased reproductive performance.
- Feed refusal.
Outside the classic signs of vasoconstriction, symptoms caused by ergot can be vague. Things like heat stress, reduced growth, and feed refusal are a challenge to diagnose. With no universal standard for the safe concentration of ergot in feed, producers must exercise caution with potentially contaminated feed sources, especially grain screenings into feeding programs.
While some livestock tolerate greater concentrations of ergot in feed, potential tissue residues could become an issue. With the prevalence of ergot increasing from 0.01 per cent in 2002 to 0.025 per cent in 2014 (Western Canada), it is evident that monitoring ergot will become more essential for the safety of both livestock and humans.
There seems to be no clear answer to how much is too much. In the view of some nutritionists, the ergot limit for pigs is zero. For all other species, the maximum limit is one kernel per 1,000 or 0.1 per cent by weight (10 ergot bodies per litre of grain). Some feed mills will not accept grain deliveries with ergot levels above 0.04 to 0.06 per cent (four to six ergot-infected kernels per litre of grain). The risk associated with selling contaminated complete feeds and pelleted rations is high.
If swath grazing, there is no easy way to assess the degree of ergot infestation. Producers need to evaluate swaths on a case-by-case, field-by-field basis, pulling swaths apart, calculating how much ergot is present and making a judgment call. If swaths look like they contain borderline toxic levels of ergot, dilute the feed with ergot-free forage.
Unfortunately, there is no silver bullet.Things that help include:
- Use of certified seed with low levels of ergot.
- Cleaning grain.
- Control of grasses growing along headlands or roadways adjacent to fields.
- Blending feeds.
- Harvest and bin headlands separately.
- Harvesting grain as soon as practically possible, especially when ergot is visually detected.
- Areas highly susceptible to ergot should be harvested as forage prior to heading.
- Crop rotations between cereals and broadleaf crops like canola.
- Understanding risk and discussing options with a veterinarian.
- Feed testing (Ergovaline assays — Oregon State University).
Minimizing the economic losses caused by ergot contamination is complex. Climate change favours ergot-producing fungi and as regulations for human food become stricter, managing ergot-contaminated grain will get more complicated.