James G. Dickson.
Leaf blights reduce the green leaf surface that a plant needs to produce its carbohydrates. If that happens early in the life of a cereal plant, it has fewer numbers of heads and kernels in a head. Later leaf blighting reduces the size and weight of kernels.
Head blights kill the head or many of the young kernels when the attack occurs early. When the attack occurs after the kernels are partly developed, the grain is shriveled and may be lost in threshing. Blight late in the season may cause discolored and shrunken grain. Kernels blighted by scab disease will sicken hogs. The fungus bodies (sclerotia) produced on crops blighted by ergot are poisonous. The presence of blighted grains also increases the cost of cleaning and processing grain.
Often one organism or a similar one may incite the same or a similar disease on several of the grain crops. So I group the leaf blights and head blights according to the micro-organism that incites the disease: Bacterial leaf and head blights; fusarium head blights, or scab; ergot of grains and grasses; helminthosporium leaf blights and kernel blights; septoria leaf and culm blights; and rhynchosporium leaf and head blights.
Many of the bacterial leaf and kernel blights occur on cereals and grasses but are generally unimportant. They produce water-soaked stripes or halo-surrounded spots on the leaves. Leaf lesions frequently are abundant for short periods during the growing season, but they cause only minor damage unless they persist into the heading period. Then the bacterial blights produce a sticky mass of bacteria around the spike. The result is a poor set of seed.
Blasted heads are common when moist weather and bacterial blight occur during heading. Later kernel infection is marked by black or brown areas on the chaff and brown, sunken lesions near the germ end of the kernel. The bacteria also may be carried on the kernels without external evidence of their presence.
The bacteria that cause these diseases are minute, short, rod-shaped cells of various species and races. Some species are restricted to a single cereal or grass. Others comprise races, each of which may attack a given grain crop and its closely related grasses.
Seed-borne bacteria are controlled by the use of organic mercury, but the bacteria that spread to grainfields from crop residues and grasses are not affected by seed treatments. Most of the adapted varieties of wheat, oats, and barley are not damaged greatly by bacterial blights. Very susceptible varieties, however, are unsuited to humid areas.
FUSARIUM HEAD BLIGHT, or scab, a disease of wheat, barley, rye, and some grasses, sometimes causes extensive losses. It also damages corn and sorghum. Heavy losses are most frequent in the eastern and central Corn Belt and in similar humid or subhumid areas in this and other countries.
The head blight develops during warm, humid weather at any stage from kernal formation to ripening of the grain. Infection occurs in the flowers and then spreads up and down the spike. The diseased part of the head soon turns a straw color in wheat and rye and light brown in barley. Frequently pink mold growth develops around the base of the flower and cements the chaff to the grain. The kernels of wheat and rye are shriveled, white or gray, and show a rough, scabby surface. In barley the kernels are light in weight and grayish brown; with the hulls removed, they look like scabbed kernels of wheat and rye.
The fungus grows into the kernels and makes the starch floury, discolored, and partly changed to sugars. The proteins are partly broken down into soluble nitrogen compounds. Some of the fats become rancid because of the formation of fatty acids. New compounds are produced that cause acute vomiting in dogs, pigs, and man, but do not affect sheep, cattle, or mature poultry. Grain containing 5 percent or more of badly scabbed kernels, fed to pigs, causes vomiting, loss of appetite, and arrested growth. Scabbed kernels in grain therefore should not be processed into human food or used to feed swine. Scabbed kernels can be separated readily from the sound wheat, rye, or corn. Because it is hard to separate scabbed from healthy barley grain, scabby barley should be fed to cattle, sheep, or poultry.
Several species of Fusarium incite the disease on cereals and grasses. The most common species, F. graminearum, produces the sexual stage (perithecia) on old corn stalks and straw.
The sexual stage is known as Gibberella zeae. The minute, blue-black spore cases (perithecia) of this stage are abundant on the surface of stalks and straw from April through June. The spores that incite head blight or ear rot are carried to the young heads of the small grains and to corn silks by the wind. Two other species, F. culmorum and F. avenaceum, are common north of the Corn Belt and in Canada. All of them also cause seedling blight and root and stalk rot in the cereals.
These pathogens are carried over on crop residues. Spores are not produced or dispersed if all crop residues are covered by a thin layer of soil. All straw and stalks should be plowed under and left below the soil surface to control the diseases. Surface mulching with straw and stalks invites head blight in small grains where wet, warm weather occurs after small grains are headed.
No highly resistant varieties of wheat, rye, or barley have been produced, but some varieties are more susceptible than others. All known varieties will be scabbed if spores are present and the weather is favorable from the heading period to maturity. Two barleys, Chevron (C. I. 1111) and Peatland (C. I. 5267), and three wheats, Haynes Blue-stem (C. I. 2874), Progress (C. I. 6902), and Rival (C. I. 11708), are among the least susceptible varieties. Investigations at the Minnesota and Wisconsin Agricultural Experiment Stations indicate that the inheritance of resistance is complicated.
Seed treatment of well-cleaned grain with organic mercury compounds will control the seed-borne infections.
ERGOT OF GRAINS and grasses is not strictly a head blight, although loss in yield from sterility is always associated with the disease. Resting bodies (sclerotia) of the fungus replace some of the kernels, and the adjacent kernels do not develop. The disease is common and destructive on grasses, rye, barley, durum wheat, and some varieties of hard spring wheat. The damage from it occurs in the humid sections and extends into the subhumid regions, notably in the spring grain areas of Nebraska, the Dakotas, and Montana.
The disease is recognized first by the sticky fluid (honeydew stage) on parts of the spikes soon after heading and later by the purplish-black sclerotia in the ripening heads. The honeydew attracts flies and other insects to the diseased heads. The sclerotia are shaped somewhat like a rye kernel. They usually are longer than a grain and thus protrude from the chaff. The sclerotia thresh out with the grain. The presence of ergot in flour or other grain products can be determined by standard color tests.
The ergot sclerotia contain several chemical compounds, some of which cause acute injury to animals and man. One group of similar compounds has special medicinal value. Bright, hard ergot sclerotia free from molds command a high price for medicinal use. Ergot sclerotia invaded by Fusarium contain compounds affecting the respiratory and other automatic muscular action. Because most of the ergot sclerotia produced in the humid, central area are attacked by Fusarium and are unsuitable for medical extracts, supplies usually are obtained from the drier west central areas or imported. Ergot samples are tested before they are purchased by pharmaceutical companies. The ergot sclerotia contain compounds that cause contraction of the fine blood vessels. Investigations at the Montana Agricultural Experiment Station have confirmed early reports that milk flow in livestock is reduced greatly by continuous feeding of small quantities of ergot sclerotia. Relatively small quantities of ergot may cause serious losses among animals.
Any grain containing more than 0.3 percent ergot sclerotia by weight is graded as ergoty and is discounted on the markets. The ergot content of milled products is limited by law. Although most of the sclerotia can be removed with modern cleaning machinery, it is difficult and expensive to bring the percentage down to the content permitted.
The life cycle of the fungus, Claviceps purpurea, is well synchronized with that of the grain or grass host. The sclerotia falling on the soil or planted with the seed germinate when the grains and grasses are flowering.
The sexual spores are wind-borne to the flowers of the grain or grass, where they invade the young kernel and replace it with fungus growth. The first fungus growth forms a folded mat, which bears millions of spores in a sticky, sweet, honeydew-like mass. The minute spores are carried by insects or are spattered by rain to infect numerous other kernels. The sclerotia develop following this spreading stage.
Some grasses are infected regularly from sclerotia dropped from the previous year's growth. The ergot spreads from the grasses to cereal crops, which are related to them botanically. Therefore, neither crop rotation nor ergot-free seed controls the disease.
Destroying grasses in the grainfields, particularly quackgrass, bromegrass, and wheatgrasses, and mowing grasses near grainfields before they head helps in control. Heavy pasturing, or mowing of grass pastures before heading, also reduces the danger of ergot poisoning of livestock.
No varieties of barley, rye, or wheat resistant to ergot have been found. The Mississippi Agricultural Experiment Station has produced a paspalum grass resistant to the ergot that is common and destructive on this southern pasture grass.
HELMINTHOSPORIUM LEAF BLIGHTS and kernel blights on cereals and grasses are caused by several species of Helminthosporium. Some of the diseases have been so damaging as to necessitate changes in varieties to maintain profitable grain production. Helminthosporium blight, for example, forced much of the susceptible Wisconsin Barbless (Wis. 38) barley out of production in the North Central States not long ago. Another helminthosporium blight forced oats growers to drop varieties with Victoria parentage from production in the Central States. Such diseases are devastating when susceptible varieties are used throughout large areas.
This group of disease-producing fungi attacks seedlings, roots, crowns, leaves, and kernels.
Spores, however, spread from the diseased seedlings to the leaves of healthy plants and from diseased kernels cause blighted seedlings. The spores, produced abundantly on crop residues, further spread the disease to the leaves and heads of growing grain. Seed treatment with organic mercury compounds, crop rotation, plowing under crop residues, and the use of resistant varieties are generally applicable control measures for this large group of cereal diseases.
