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Ergot is a disease of cereals that has had considerable historical
impact. The fungus produces toxins that cause ergotism in animals,
including humans. Ergotism may cause either gangrenous or convulsive
reactions and has been associated with several great historical
events, such as the Salem witch trials, the invasion of France
by Norsemen, and the failure of Peter the Great to capture the
Dardanelles. Ergot chemicals are widely used in medicine, for
example as a vasoconstricting agent in the treatment of migraine
and in childbirth.
Cause
Ergot is caused by Claviceps purpurea. This fungus, an
ascomycete, forms sclerotia, ascospores and conidia. The sclerotia
vary in size (2-20 millimeters long), depending on the host (the
host's seed size, which the sclerotia replace) and are purple-black,
elongate (spur-like), with white centers. Ascospores are long,
thin, and septate; conidia are small, round and one-celled. |
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Hosts
Ergot has a wide host range of about 60 genera, all in the grass
family. Rye and triticale are particularly susceptible, because
they are open-pollinated, but wheat, barley, and many grasses
(including weed grasses such as quack grass, meadow foxtail,
wild oat, cheatgrass, hair grass, wild barley, annual bluegrass,
and green foxtail) are among the hosts.
Symptoms and Signs
At flowering a cloudy, tan, sticky "honeydew" may appear
on the florets, especially if the weather is humid. The most
noticeable signs of the disease, though, are the sclerotia (Photo
14), which protrude from the glumes and are produced as the host
plant matures. The sclerotia that contaminate harvested grain
are easily seen because they are dark.
Disease Cycle
Sclerotia remain viable for about 1 year. After over-wintering
or being exposed to cold temperatures, they germinate to produce
several small stalked, mushroom-shaped perithecial stroma. Ascospores
from the perithecia comprise the primary inoculum and are spread
by wind and splashing rain to host plant flowers. Ascospores
germinate and invade the flower through the stigma to penetrate
the ovary. A convolute mycelial mat forms over the developing
ovary, and masses of conidia in a sticky matrix (honeydew) appear
in about 5 days. These conidia constitute secondary inoculum.
Honeydew attracts insects visiting the flowers, and the insects
in turn disseminate the conidia. Upon host maturity, fungal mycelium
replaces the ovary tissues to form a sclerotium.
Wet conditions during flowering and open flowers favor the
disease. Susceptibility of different hosts relates to the length
of time the flowers are open; hosts with longer flowering periods
are more susceptible than those with shorter flowering periods.
Control
Cultural. Wheat cultivars whose florets remain
open for short periods of time may escape infection, but sanitation
measures are the most important way of controlling ergot. Remove
sclerotia from seed by screening or by brine flotation. In addition,
seeding deeper than 3 inches buries sclerotia and eliminates
primary inoculum by preventing emergence of perithecial stroma.
Alternate-year rotations allow time for sclerotial disintegration
and reduce the amount of inoculum in the soil. Destroy stands
of ergoted grass near seed or grain fields.
Other Interesting Ergot
sites:
University
of California Statewided Integrated Pest management guidelines
-- pictures and descriptions.
Alberta
Agriculture, Food, and Rural Development -- good description
and great pictures at the bottom of their page.
Wheat
Diseases * Barley
Diseases
WSU
Home Page * Small
Grains Home * Grow Serve
Edited and reviewed by Ed Adams, WSU Extension Plant Pathologist
Comments and questions: adamse@wsu.edu
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