Nonparasitic Disorders of Cotton

W. Hardy Tharp.

Potash hunger of cotton was known as rust or black rust before 1892, when George F. Atkinson demonstrated that it could be controlled by additions of potash to the soil. He called the disease yellow leaf blight, but the name rust has remained in common usage.

Scientists frequently use the term "rust or potash hunger" because it describes both the symptoms and the cause.

Rust occurs commonly on the lighter soils of the Coastal Plain areas of the Cotton Belt and in many other soils of several mid-South States, including Alabama, Arkansas, Louisiana, and Mississippi. W. W. Gilbert estimated the average damage for the entire Cotton Belt at 4 or 5 percent in 1920, but greater use of balanced fertilizers in the affected areas undoubtedly has reduced the loss in recent years.

Affected plants are usually stunted and fail to develop a normal green color. The lower or older leaves are first to show the typical mottled appearance; the areas between the veins turn yellow. Toward midseason the symptoms are visible over the entire plant. The yellowish spots on the leaves enlarge and become reddish brown or bronzed. Later the entire leaf may become blackened, curled downward, and ragged. Brown or black circular or irregular spots are often produced on many affected leaves by the growth of Alternaria and perhaps other secondary invaders. Leaves usually are shed prematurely and often the stalk is left bare. The number and the size of bolls are reduced. Yields are severely lowered. Affected bolls do not flare open properly, and so the cotton is hard to pick. Lint and seed from affected plants are inferior.

The primary cause of rust is insufficient potash to meet the nutritional requirements of the plant. The condition usually is found on potash-deficient soils, but not necessarily so. Excessive applications of nitrogen or phosphorus, or both, often may accentuate severity. Over-liming or a scarcity of sodium, which substitutes to some extent for potash, likewise tend to increase rust. Lack of humus in the soil and improper drainage have also been listed as conditions responsible for or contributing to severity of the disease.

The application of fertilizers that contain ample potash to furnish the needs of the plant throughout the season is considered the standard method of control. The exact amount needed to correct the condition depends on the supply of other soil nutrients. A common practice on lighter soils, where early rains can easily leach out some of the available potash supplied before planting, is to apply some potash along with nitrogen as a side dressing after the plants are established.

Potash hunger should not be confused with the true rust of cotton, which is caused by attack of the parasitic fungus Puccinia stakmanii, and occurs in limited areas of the Western States. Fusarium wilt and root knot nematodes also are often prevalent in the soils where potash hunger is common. It is not always easy to determine the exact degree of damage associated with each cause in this complex.

THE CRAZY Top disorder of cotton was first recognized by C. J. King and H. F. Loomis in a field of Pima cotton near Scottsdale, Ariz., in 1919. Three years later it was observed in a field of upland cotton near Casa Grande, Ariz. By 1924 the disorder had become common in Arizona and by 1936 it was still considered one of the most important problems of cotton production in certain districts of the State. Mild stages of the disease were also known to have appeared in the San Joaquin and Imperial Valleys of California between 1926 and 1933.

O. F. Cook was first to present an accurate description of the disorder. He named the disease acromania, but the term crazy top, which is descriptive of the abnormal branching and fruiting in the upper part of affected plants, has remained the one in common use. The first symptom is an abrupt change in the type of new growth made in the top of the cotton plants. Fruiting branches frequently are replaced by vegetative branches, which have regrown in an upright position and are developing an abnormal or crazy appearance in the tops of the plants. Typical features of the abnormality include reductions and distortions of leaves, internodes, bracts, and floral parts. The leaves are small, rounded, cupped, and thickened. Flowers are small and distorted. Sterility is common and may be expressed either as complete suppression of floral buds or as profuse shedding of flowers. The few bolls that develop are usually small and malformed and contain a reduced number of seed.

The disease occurs only on calcareous soils and has been found almost entirely related to irrigation practice. It is associated with the checking of growth from water shortages and the resumption of growth when abundant moisture is restored. The disease is controlled easily by applying irrigation water frequently enough to prohibit a checking of plant growth during the summer months. Water shortage may not be the only factor involved in bringing about the abnormalities maintaining organic matter at higher levels by rotation with alfalfa is beneficial.

CRINKLE LEAF is the name given by D. C. Neal in 1937 to a peculiar disorder of cotton plants occurring in Lintonia and Oliver silt loam soils of Louisiana and Arkansas. The typical symptoms are a puckering, mottling, partial chlorosis, and distortion of the leaves. The branches are often fasciated and the floral buds, flowers, and bolls are distorted. The fiber from affected bolls is often so weak as to be considered worthless.

Dr. Neal and H. C. Lovett demonstrated by experiments they conducted in Louisiana in 1937 and 1938 that the disease was associated with high soil acidity, calcium deficiency, and manganese toxicity. The typical symptoms were readily produced by adding increasing amounts of manganese sulfate to pot cultures of cotton. But it was easy to control the disease in the field by adding limestone. At the higher pH produced by treating the soil with limestone, or with other material containing basic carbonates, the manganese apparently is precipitated, and so the plants remain healthy.

THRIPS INJURY is not strictly a nonparasitic disease of cotton, but I include a brief description because its symptoms are not unlike those of certain stages of crinkle leaf and crazy top.

Infestation by thrips frequently causes serious injury to cotton plants. Reduced stands or reduced yields result from stunting and delayed fruiting of the plants. Damage is severe only in the early-season development of the plants and is usually restricted to mutilation of seedling leaves as they unfold from the bud. Often, however, the terminal bud is destroyed, so that the plant gets a stunted appearance. Until it outgrows the disorder around mid-season, the branching is bunched or fasciated. The leaves may appear torn, perforated, cupped, and distorted. Usually there will be little if any change from normal green color.

A serious aspect of the disease is that the injury and decreased vigor tend to make plants more susceptible to the sore shin disease of cotton seedlings caused by Rhizoctoma solani a fact demonstrated in experiments conducted by Neal and L. D. Newsome in Louisiana in 1950.

Considerable variation in susceptibility among commercial varieties of cotton was observed by W. W. Ballard in Georgia. He pointed out that dense pubescence of juvenile terminal leaves appeared to be associated with resistance to thrips in some cases. He noted also that the degree of injury was usually correlated with the amount of aborted terminal buds, although a few varieties exhibited a degree of injury independent of the proportion of terminal buds aborted.

2,4-D (2,4-dichlorophenoxyacetic acid), a hormone-type herbicide commonly used to kill broadleaf pests in lawns, is extremely toxic to cotton plants. The minute quantities that light on cotton plants when the drift from adjacent applications is not controlled can cause severe injury. The danger has been thoroughly recognized since this weed killer was first introduced commercially in 1946 but, despite adequate and repeated warnings, cotton may be found injured occasionally from drift, from accidental contamination of other chemicals used on cotton, or from improperly cleaned machinery and containers that have been used with 2,4-D.

The symptoms on cotton are characteristic and specific formative effects, except where the dosage is sufficiently high to kill the plants or plant parts outright. The effects are first noted near the growing points and the characteristic symptoms are usually the result of an abnormal stimulation of growth of the affected parts. Leaves are greatly modified. They become narrow, closely and conspicuously veined, and deeply lobed. Affected flowers are modified in a manner similar to the leaf elongated and narrow. Bracts are modified. They become deeply lobed and elongated and they fail to separate; they grow as a sheath around the developing boll.

When enough material is absorbed to kill or inhibit the terminal bud, the plant may become branched and fasciated, with slender and malformed leaves, branches, buds, and flowers. Affected bolls and squares may turn yellow and then drop, although some malformed and partially fertile mature bolls have been observed. Often, however, the squares or bolls die without shedding. Excessive shedding of leaves as a result of 2,4-D injury has not been reported. If the tops of plants are damaged, they may send out strong laterals, which produce apparently normal branches. The fully grown leaves, branches, or bolls seldom show much injury from the low dosages.

The formative effects in cotton continue to develop for some weeks following application of 2,4-D but the persistence of the stimulus depends on the stage of plant development and the concentration applied. If young bolls are present, the seed may be, injured. The likelihood of damage is greater for seed developing from plants treated at the time of flowering and, normally, no effects on the seed will be noted if parent plants are treated before the young square stage of growth.

Some instances have been reported where applications of organic insecticides have been associated with injury to cotton plants similar to that produced by 2,4-D. Many are undoubtedly cases of contamination, but with the use of certain of the organic phosphates it may be the insecticide itself causing the injury. Wayne J. McIlrath has shown a striking similarity of symptoms produced by treating comparable plants with 2,4-D and with commercial HETP (hexaethyl tetra-phosphate), and to some extent with TEPP (tetraethyl pyrophosphate).

W. HARDY THARP is a project leader for plant physiology in the Department of Agriculture. He was graduated from Montana State College. He received his advanced training at the University of Wisconsin and Cornell University. He joined the Department in 1934.