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On the Trails: Ergot

Posted: December 21, 2012 - 1:00am
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In the second phase of the fungal life cycle, the black spurs emerging from the seed head of beach rye fall to the ground; from the spurs, tiny mushrooms germinate in spring and produce spores that infect more beach rye that summer.            Photo by Bob Armstrong
Photo by Bob Armstrong
In the second phase of the fungal life cycle, the black spurs emerging from the seed head of beach rye fall to the ground; from the spurs, tiny mushrooms germinate in spring and produce spores that infect more beach rye that summer.

This past summer was cool and wet, and that set of conditions is just right for the fungus known as ergot. There are many species of ergot in the world, parasitizing many different grasses, including grains such as wheat, barley, and perhaps especially rye. This summer there was a bumper crop of it on beach rye in Juneau. Cruising around at the upper side of various beaches, we noticed many of the blackish “spurs” sticking out of the seed heads of beach rye. (Reportedly, the name “ergot” comes from the Old French word for spur — as in the spur on the leg of a rooster.)

Although ergot has some pharmaceutical uses, it contains nasty poisonous alkaloids. Not only does the fungus infection decrease the yield of domestic grains, the poisons have serious unpleasant effects when consumed by mammals and at least some birds (domestic poultry). One effect in mammals is constriction of blood vessels, which can cause dry gangrene and often loss of body parts (ears, feet, legs, and so on). Reproduction is often impaired. Another effect in mammals involves the nervous system, including incoherency, hallucinations, convulsions, seizure, unconsciousness, and even death. Severity of the poisoning is dose-dependent but also varies among individuals.

Historically, ergot poisoning has been suspected of having major effects on human populations. Apparently, ergot poisoning was known to the Chinese as early as 1100 B.C. and in parts of the Middle East by 600 B. C. It must have been known in Europe early on, but the earliest documented reports seem to come from the Middle Ages. In Europe in the middle 1300s, the weather was cool and wet, which made good growing conditions for rye crops (and ergot). More bread was then made from rye than from wheat, and there were said to be epidemics of “madness” in England. In France in the Middle Ages, poor folks commonly ate bread made from rye, which was cheaper than wheat bread, and thousands died. Some researchers suggested that the recovery of the European population after the Black Death was slower than expected, because ergot poisoning was common. By the 1600s, scientists were beginning to suspect that ergot poisoning was related to food, specifically ergot fungi on grain, but it took about two hundred years for this knowledge to be confirmed and to begin to percolate into general knowledge.

Many (but not all) historians believe that the Salem witch trials in 1692 were driven by ergot poisoning. Some girls became hysterical, had convulsions, and made wild accusations of witchery against certain older women. The women were probably healers, using herbs to treat various ailments. The “rationale” would have been that those who cure diseases may also cause them! The girls’ convulsions were thought to be due to the “witches,” and the entire town must have been overtaken by hysteria, because eventually twenty people were executed as “witches.” Mind you, the causative agent in ergot was not known for hundreds of years (at least in European cultures), and it was common to assume some kind of supernatural causation.

Ergot’s effects are now well known, but very small percentages of ergoty grain are reportedly allowed in our food sources (wheat, less than 0.05 percent by weight; rye, less than 0.3 percent, and so on). One presumes that such low amounts are thought to do negligible damage. (It is not unusual for tiny amounts of various toxins to be allowed in human food.)

The life cycle of ergot is interesting. A fungal spore lands on the female parts of a grass flower, and sends filaments down into the ovary (where the seed would have developed) and taps into the plant’s circulation. Using the plant’s nutrients, the fungus produces a soft, whitish mass that produces, in turn, a yellowish “honeydew” that often drips off the flowers. The honeydew contains asexual spores, which may be picked up by an insect drawn to sip the honeydew, or by wind, or by animal bodies swishing through the grass, and thus transferred to another grass flower. As the fungus matures, the whitish mass becomes a hard, dry, blackish “spur” that sticks up out of the seed head. The spur eventually falls to the ground. It germinates in the following spring, producing tiny little mushroom-shaped bodies. These produce sexual spores that are dispersed by wind, landing on grass flowers, and beginning the cycle again.

Although ergot is known to affect domestic poultry, its possible effects on wild birds apparently have been little studied. Ergot poisoning, with attendant dry gangrene, has been reported for Canada geese and suspected in mourning doves. So I wonder if the savanna sparrows and snow buntings and other birds that commonly forage near beach rye stands might be subject to ergot poisoning, perhaps especially in years when ergot is abundant.

However, I was interested to find that certain other fungi that live inside the leaves, stems, and seeds of grasses also produce the ergot poisons. One study showed that if juncos happen to eat too many of infected seeds, they are likely to lose weight. But juncos and several species of sparrows tend to avoid seeds from infected plants. So perhaps our wild birds may be able to avoid serious ergot poisoning.

• Mary F. Willson is a retired professor of ecology.

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