Bacterial wilt or Stewart’s disease of corn is caused by a bacterial parasite (Aplanobacter stewarti).  This organism grows abundantly in the vessels or water-conducting system of the corn plant and comes out as viscid yellow drops on the cut ends of badly infected stalks (fig. 2). The disease may attack the plants at any stage in their growth.  Young plants may wilt and die, or if they continue to grow may remain stunted. Tassels develop prematurely, and the leaves wilt one after the other (fig. 3). Long, light green to yellow streaks extend through the leaves. Infected plants that develop to normal height may be barren or produce only nubbins. Because of the dead and stunted plants, badly infected fields are very uneven.

FIGURE 2.—Cross section of stalk of corn badly infected with bacterial wilt and showing yellow ooze from cut ends of vessels. Magnified three times.

This disease was first described on sweet corn in 1897 by F. C. Stewart, who found it widespread and abundant in the market gardens of Long Island, N. Y., frequently causing losses of 20 to 40 percent and sometimes destroying whole fields. He found that the earliest-maturing varieties of sweet corn were the most susceptible and that late varieties were resistant. To control the disease he recommended that only late-maturing, resistant varieties be grown and that care be taken in selecting clean seed. His recommendations were not followed, for the most desirable varieties of sweet corn for table use are the early-maturing susceptible varieties.  Market and home gardeners continued to grow them, and so to produce much infected seed. In 1899 the disease was found in New Jersey, and in 1903 it was observed for the first time in Maryland and Virginia. It was gradually found southward through Pennsylvania, Maryland, and Virginia and in the Carolinas and Georgia and westward through the Corn Belt in Iowa, Missouri, Kansas, Texas, New Mexico, and California. The disease did not extend into the northern tier of States with the exception of southern New York, southern Michigan, Massachusetts, and possibly North Dakota and South Dakota.

Figure 3.—Golden Bantam hybrid: A, Normal plant; B, stunted plant infected with bacterial wilt, tassels premature.

Damage Heavy in Recent Years

   With the continued spread of the disease the annual losses also steadily increased. In most years losses were not great, but in the older disease areas, such as Maryland and Virginia, it finally became necessary to grow only the late-maturing, resistant varieties such as Stowell Evergreen and Country Gentleman. In a few exceptional years losses were heavy, and then again the disease became of minor importance. During the seasons of 1931-33 wilt was more widespread and destructive than ever before in its history. It spread northward into Wisconsin, central Michigan, and New York, into Ontario, Canada, and into Maine and New Hampshire.  Throughout the Corn Belt losses were heavy in susceptible varieties, and losses of 10 percent in late resistant varieties were common. In 1932 Indiana reported a loss of 50 percent in early plantings of susceptible varieties; Pennsylvania, 45 percent; Iowa, 5 percent; New York, 10 percent; Connecticut, 3 percent; and Massachusetts, 0.5 percent. In 1933 Michigan reported 93 to 100 percent infection in early varieties such as Spanish Gold, Golden Gem, and Extra Early Bantam; 64 to 91 percent infection in midseason varieties such as Sunshine and Golden Bantam; 10 to 29 percent in Stowell Evergreen; and 3 percent in Country Gentleman. These were percentages of infected plants and not actual losses.

This most recent epidemic of bacterial wilt occurred following a succession of mild winters. The winter of 1933-34 was much more severe throughout the Central and Northern States, and reports for the 1934 season indicate that the disease was again much less severe.  Introduction of the disease into new localities is at least partly brought about by infected seed. The wilt organism lives from one season to another inside the seed. It is not known how effective seed treatments are in controlling this seed-borne infection. The use of clean seed where the disease has not become established is important, but the use of clean seed of susceptible varieties grown where the disease does not occur is of doubtful value in wilt-infested areas. Experience has shown that such strains are often more susceptible than strains grown in wilt-infested areas.

The percentage of diseased plants even from badly infected seed is so low that it accounts for only a.small part of the early infections on young plants in the field. Recently it has been learned that the wilt organism lives over winter in one of the common flea beetles (Chaetocnema pulicaria). In the spring such beetles carry it to the young corn plants on which they feed. Possibly this accounts for a large part of the early infections. A great increase in number of diseased plants during midseason also is brought about by this same beetle.  Infections on the leaves may be seen starting from the feeding injuries on the outer halves of the leaves and progressing down through the leaf blade to the stalk. It was this type of leaf infection that occurred in dent corn in Illinois in 1932. The insects feed on resistant as well as susceptible varieties of corn, but on the resistant varieties the infections are much more restricted in area and develop more slowly, so that the injury is usually confined to the outer halves of the leaves.  On the other hand, in susceptible varieties the bacteria work back into the stalks more rapidly, and then out into the whole plant.

The wilt organism overwinters in old, infected cornstalks in the field, but it is not known how important this is in starting the disease in the spring. Crop rotation has not been shown to be effective in controlling the disease.

The control measures recommended by Stewart in 1897 still hold good. Use clean, disease-free seed in sections where the disease does not occur, and plant resistant varieties in sections where the disease has become established. The development of wilt-resistant, early-maturing, high-quality sweet corn is making it possible to practice the second and by far the most important method of control.

During the past several years plant breeders in the Central and Eastern States have been taking advantage of the marked differences in resistance and susceptibility of varieties of sweet corn. By methods of inbreeding ana crossing they have been developing early-maturing, wilt-resistant strains which are as desirable for table use as the original early varieties which were so susceptible to wilt. In 1933 seed of one of these early resistant strains known as Golden Cross Bantam, developed by the Department in cooperation with the Purdue University (Indiana) Agricultural Experiment Station, was sold for the first time by a number of seed companies.  This hybrid proved very popular. Reports from several States were encouraging.  Very little wilt occurred on Golden Cross Bantam when other early-maturing varieties suffered heavy losses. From Ohio it was reported that the only good fields of early sweet corn were Golden Cross Bantam. This variety is 4 to 8 days later than the earliest Golden Bantam, but still eaglier strains are being developed. A number of other early resistant strains of sweet corn, developed by the Connecticut Agricultural Experiment Station, are now being commercially produced. With the general planting of these resistant strains heavy losses from this disease can be avoided.