Some Smuts and Rusts of Corn

Arnold J. Ullstrup.

Corn is susceptible to two smuts. Common smut, or boil smut, is widely distributed. Head smut occurs in the far West and rarely east of the Great Plains. It is known to occur in eastern Europe, Asia, Africa, and Australia.

Common smut of corn was identified in Europe in 1754. It was first recorded in the United States in 1822. Since corn is native to the Western Hemisphere, it is probable that common smut has existed along with the culture of its host. Teosinte is the only other host susceptible to the disease.

The prevalence of common smut varies from year to year and from one area to another. In the Corn Belt estimates of loss due to the disease have ranged from a trace to 6 percent. It is doubtful if losses exceed 2 percent for field corn over very wide areas. In sweet corn local losses may be considerably higher and reductions in the yield of sweet corn up to 60 percent have been known.

The size, location, and number of galls on a plant determine the amount of damage. Large galls are more detrimental to a plant than small galls are. Galls above the ear are generally more destructive than those below the ear. Galls on young plants cause more damage than do those that develop later.

Common smut is perhaps the most conspicuous and easily recognized of all corn diseases. Galls or tumors ranging in size from beadlike structures to6 inches or more in diameter are the distinguishing symptom. All above ground parts of the plant are attacked tassels, leaves, ears, stalks, and brace roots.

The galls are at first covered with a glistening, whitish-green membrane. As the gall enlarges, the membrane ruptures, exposing a powdery black mass of spores. Galls may occur wherever young, rapidly growing tissue is exposed to infection. Galls on leaves seldom develop beyond the size of a pea. They usually dry up and become hard and warty. Only a few spores are formed inside them. Ears are especially vulnerable to infection. The largest galls are formed in the ears because they have so much embryonic tissue.

Ustilago maydis is the fungus causing common smut of corn. The spores, called chlamydospores, are brownish black, thick-walled, heavily spined, and oval to spherical in shape. Chlamydospores, which are resistant to extremes of exposure, germinate in the presence of moisture, and within a temperature range of 46 to 97 F., to form small, single-celled, thin-walled, colorless spores, called sporidia. The sporidia germinate and may penetrate the host tissue, but infections arising from single sporidia are not typical; galls and chlamydospores usually are not formed and the life cycle of the fungus is not completed. Typical invasion of the corn plant, with subsequent formation of galls and chlamydospores, takes place following fusion of sporidia of opposite mating type. This fusion process is similar in many respects to the sexual process fertilization that precedes seed formation in higher plants. Each sporidium has a single nucleus and when fusion takes place, nuclei of the opposite types are associated in pairs in the infection hyphae and mycelium of the fungus. These paired nuclei in the mycelium eventually fuse after chlamydospore formation.

The mycelium develops between the host cells and stimulates them to increase in size and number until galls are formed. Galls continue growth until chlamydospores are again formed in the mycelium of the fungus. When the gall is mature it breaks open and releases chlamydospores which may be carried to other plants where they germinate and continue the disease cycle. Thus local infections may continue throughout the growing season because of successive generation of chlamydospores. Infection of young plants may result in infection throughout the plant; galls form as the host tissues develop during the growing season.

The factors determining the incidence of common smut are not fully understood. Dry weather in late spring and early summer seems to favor its spread and development. Corn grown on heavily manured soils often shows a lot of smut. Plants on such soils make a succulent growth, which probably provides for easy penetration of the infection hyphae of the fungus. Such soils may also provide a good medium for overwintering and germination of the chlamydospores. Hail damage and injuries from cultivating machinery increase the prevalence of smut by exposing the host tissue to infection by the smut fungus. Detasseling corn in seed fields often increases smut because the tissues are exposed at the break in the upper stalk where the tassels are removed. Failure of pollination, which sometimes occurs in seed fields, stimulates the plants to produce several small ear shoots, which are susceptible to Smut infection.

Planting resistant hybrids is the most effective means of controlling the common smut. No hybrid is completely immune, but most of the popular hybrids are reasonably resistant. In selecting a hybrid, consideration must be given to desirable agronomic characters, resistance to other diseases, and resistance to smut. Most smut-susceptible inbred lines are usually discarded before they reach commercial production. Breeding for smut resistance has been somewhat complicated by the occurrence of physiologic races of the pathogen and by lack of a completely satisfactory method of artificial inoculation that could be used as a tool to distinguish resistant from susceptible plants. An inbred line may appear resistant in one location and susceptible in another because of the presence of different physiologic races of the smut fungus. Inheritance of resistance to common smut is determined by a relatively large number of genes.

Seed treatment is not effective in reducing the incidence of smut, but may kill smut spores carried on the outside of seed and thus prevent their introduction into places where the disease is not present.

Rotation and sanitation are ineffective in controlling smut where corn is extensively grown. In small garden plantings of sweet corn, destruction of smut galls before spores are produced may help reduce prevalence of the disease in following years.

Head smut of corn was first found in the United States in 1895. The disease is of minor importance in this country and only in localized areas of some of the Western States has it caused any appreciable damage. It is more common in Asia, Africa, Australia, and eastern Europe.

The first symptoms become evident when the tassels and ears appear. Those organs may be completely or partly converted into smut galls. Occasionally the tip of the stalk is involved. Smut galls are at first covered with a delicate membrane that soon breaks open and exposes a mass of reddish-brown to black chlamydospores and strands of conductive tissue. The strands, or fibers, in the galls help to distinguish this disease from common smut. Little or no stunting occurs in infected plants.

Sphacelotheca reiliana is the fungus that causes head smut of corn. Chlamydospores, produced in large numbers in the galls, are reddish brown to black, thick-walled, finely spined, and spherical or else slightly irregular in shape. Chlamydospores, which can withstand periods of unfavorable weather, live over from one growing season to the next in soil or on the seed. They germinate to form small, oval, secondary spores the sporidia.

Penetration of young seedlings is effected by binucleate mycelium that arises following fusion of uninucleate sporidia of compatible mating types. The parasitic mycelium develops in the tissues of the young corn plant and chlamydospores are formed following gall development in the tassels and ears. In head smut, the parasitic fungus is entirely systemic (growing within the plant), and successive local infections do not occur throughout the growing season as in common smut. Sorghum is susceptible to head smut, but the physiologic races attacking it do not parasitize corn; those that attack corn cannot cause the disease in sorghum.