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Ergot: an ancient problem that won’t go away

Ergot occurs when a cool, wet spring and high humidity at flowering favours its spread from native grasses to grain crops.

November 19, 2007
By Helen McMenamin


Every now and again, ergot shows up in grain. It may seem as if there is no
reason for it nor a way to stop it. Although there are solutions for most crop
diseases, or at least strategies to avoid them or recognize them early, ergot
always seems to be a nasty surprise.

"Remember the disease triangle," says Keith Mills, agronomic crop
enhancement specialist with Agricore United in southern Alberta. "For a
disease to occur, we need the pathogen, a susceptible host and a conducive environment
– weather that suits the pathogen. The ergot pathogen is always around.
It's a long-established pathogen of grasses and I've seen it in every area of
Canada where I've worked. In fact, it's been known for thousands of years. The
key part of the disease triangle for ergot is suitable weather."

The overwintering structures, the 'seed' of the fungus, Claviceps purpurea,
are the purple or black ergot bodies sometimes found in cereal seed heads. They
need a cool, wet soil and wet weather to germinate and release ascospores, which
are carried by wind and rain splash to infect the florets of early-flowering


Once established in a floret, the fungus produces secondary spores in honeydew
that oozes from the floret to be carried by insects, wind and rain to other
grass florets. Any open grass florets can be infected. Rye is most commonly
infected because it is open-pollinated and has a relatively long flowering period.
But wheat, barley and rarely oats, are also susceptible. Grasses, with their
wide flowering window, are more susceptible to ergot than cereal crops.

In the infected flower, the ovary is replaced by an ergot body, actually a
sclerotia of the fungus. These fall from the seed head and overwinter in the
field to re-infect another crop, or they may be combined and become a seedborne
infection. The cycle can start over again the following year.

Because ergot is produced in grasses as well as cereals, the part of the disease
triangle that mainly determines whether or not it shows up in grain is the environment.
Wet soil in spring or early summer and wet weather during flowering provide
the environment the fungus needs, so ergot is more common in cool, wet years.
Cool, wet conditions extend cereal flowering, so the crop is susceptible to
infection longer. Poor fertility or herbicide injury can also extend the flowering

"This doesn't mean ergot is outside your control," says Mills. "Varying
seeding dates can reduce the number of crops that are susceptible to damage
during an episode of wet weather."

Mills explains that crops seeded in the fall or early spring tend to escape
damage by flowering before inoculum levels in grasses and neighbouring fields
build up. Sclerotia do not usually remain viable for more than one year, so
rotations can reduce the infection level. Mowing the grass in ditches and around
grain fields can eliminate the source of inoculum.

Some people regard ergot as a symptom of copper deficiency. Others believe
copper deficiency makes cereals more susceptible to ergot. A lack of copper
can lead to sterile flowers, so florets are open and susceptible to fungal disease
for a longer period.

Ergot and copper deficiency can be distinguished by their pattern in the field.
Ergot tends to occur along headlands, field edges and around grassed sloughs,
whereas copper deficiencies are usually in irregular patches throughout fields.
Mills advises testing soil for micronutrients before assuming it is deficient
in copper just because there has been an ergot infection.

If a grower finds ergot in the grain, harvest it gently and bin the outside
round or two separately, advises Mills. It may be worthwhile to clean grain
with ergot before delivery. This is generally less costly than having the grain
companies handle grain contaminated with ergot bodies.

Ergot does not usually affect crop yields, but the ergot body contains alkaloids
that are extremely toxic, so the maximum allowable amount in #1 wheat is 0.01
percent. In #4 wheat the maximum is 0.04 percent. Grain is graded after cleaning,
so only seed-sized ergot pieces are included. The fungus is a particular problem
in durum because semolina is not sifted, as flour is for bread, and ergot shows
up as dark specks in the pasta.

A long history of death, pestilence and empire destruction
Although livestock are occasionally poisoned by ergot in poor quality grain,
inspection generally prevents major ergot poisonings of humans as have occurred
in the past. Penny Le Couteur in her book, Napoleon's Buttons, says, until fairly
recently, ergot was a major killer, after bacteria and viruses. She reports
it caused 40,000 deaths in Germany in the year 994 and many others right up
to 1951. Weakening of their armies by ergot poisoning may have helped dash the
ambitions of Julius Caesar and Napoleon Bonaparte.

One of ergot's alkaloids is used in treating hemorrhage in childbirth, but
it affects circulation to such an extent it can lead to gangrene and loss of
limbs in humans and animals. The symptoms of ergot poisoning include convulsions,
hallucinations, manic behaviour, seizures and death. The hallucinations are
due to ergotamine, a molecule that is very similar to LSD.

In the Middle Ages, ergot poisoning symptoms were called St Vitus dance, after
the mania and convulsions, or St Anthony's fire – due to the burning sensation
in limbs from circulatory problems. When whole communities were affected, the
symptoms were often ascribed to witchcraft.

Today, the only witchcraft going on is usually around Halloween when, hopefully,
a successful harvest means ergot-free cereals. So while there is no magic cure
for ergot, growers should understand that there are cultural and management
solutions to keep from suffering the effects of ergot on their bottom line.


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