Eugene S. Schultz.
The Irish potato is susceptible to many diseases. The fungi that might attack it range from the slime molds to the smuts and rusts. It is subject to several viruses of the yellows and mosaic groups. Such nonparasitic diseases as black heart, sunscald, freezing injury, and a malnutrition caused by deficiency in magnesium, potash, and boron may cause damage. Several nematode diseases have been found on it.
Unless effective methods of control are practiced, serious diseases, such as late blight, ring rot, and leaf roll, can cause the total loss of a crop.
LATE BLIGHT of potato is a downy mildew caused by a fungus, Phytophthora infestans. The mildew, or flour-like spots, usually on the lower surface of the leaf, distinguishes the disease from other leaf spots on the potato plant. Humid conditions favor it. Despite its name, the first infection often occurs soon after the plants emerge when favorable moisture and temperature prevail. At 70 to 75 F. the fungus grows so fast inside the leaves that within a week after infection it causes dead spots one-half to 1 inch in diameter. The entire plant may be killed within 2 weeks. The brown discoloration of the foliage brings to mind the terms "blight" and "rust."
Late blight destroyed potato crops so often during the nineteenth century that it outranked other potato diseases and was called "the potato disease." In 1845 it was responsible for the potato famine in Ireland.
The late blight fungus produces a mycelium, or moldlike growth, which invades and kills the plant tissue. From the mycelium grow treelike sporangiophores, which bear sporangia, the agents involved in spreading infection. At about 70 and 90 percent relative humidity, sporangia develop in 5 to 7 days after infection. In water at 72 to 77 , sporangia form germ tubes. At lower temperatures, 58 to 63 , they develop swarmspores, or zoospores. The two methods of germination enable the fungus to adapt itself to a rather wide range of temperature. The higher temperature favors mycelial development, rapid invasion, and killing of the plant. The lower temperature favors formation of zoospores and rapid increase in inoculum to spread infection.
The fungus infects the potato tuber as well as the tops. Spores from infected tops are carried by rain to the tubers in the soil. Tubers also are readily infected if they are harvested before the blighted tops are killed. Infected tubers quickly show a brown discoloration, which changes to a purplish color. The fungus usually invades the tuber to about one-fourth to one-half inch below the skin. At about 36 to 40 , the affected tubers persist in a dry rot condition. Higher temperatures favor secondary infection with bacteria, and the blighted tubers develop soft rot.
The organism is carried into the following season in infected tubers. When such tubers are planted, the fungus invades the shoots on which form the spores that infect the foliage. Another source of infection is the blighted tubers in the potato refuse or dump pile. Late blight appears on potato tops on waste piles a few weeks before the plants in the fields emerge, so that the potato tops in the fields become infected as soon as the plants emerge and before spraying begins.
The spread of late blight is favored by humid conditions such as may prevail in the New England States, other regions along the Atlantic coast, the North Central States. With favorable moisture, it also appears in the Middle Western, Southern, and Pacific Coast States. It occurs in long periods of rain, fog, and dew, which favor fruiting, infection, and dissemination of the fungus.
Control measures are sanitation, protection, and the use of resistant varieties.
Sanitation involves careful inspection and removal of blighted tubers from seed potatoes and elimination of piles of waste potatoes. Waste potatoes that have to be dumped should be given a dormancy or sprout-inhibiting treatment 0.25 percent isopropyl ester of trichlorophenoxy acetic acid before dumping to prevent sprouting.
For many years a combination of copper sulfate and lime bordeaux mixture has been used to control late blight. Weekly spraying with it during the growing season effectively, although not absolutely, controls late blight even during epidemics. Copper-lime dusts control late blight if applied at rates of 25 to 30 pounds the acre at weekly intervals.
Some of the more recently developed products like Dithane and Parzate are less toxic to foliage and therefore favor higher yields than when bordeaux mixture is used. Because these products are not generally so effective for control of late blight as bordeaux mixture, some growers change to bordeaux mixture during the latter part of the season when conditions favor an epidemic of late blight.
Because lime in bordeaux mixture increases transpiration to a harmful degree and because one-half the amount of lime used formerly in bordeaux mixture is satisfactory, many growers use a recommended formula such as 10-5-100-10 pounds of copper sulfate and 5 pounds of lime in 100 gallons of water.
Search for resistant varieties began about the middle of the nineteenth century. Varying degrees of resist- ante appeared in different varieties, but no cultivated varieties manifested immunity from late blight. Sebago, 'Menominee, and Calrose, though not immune, are somewhat blight-resistant. The tubers in some varieties, such as Sebago, are more blight-resistant than the foliage.
Among certain wild species, such as Solanum demissum, some lines or strains are immune. Some lines of that species also are blight-susceptible. Empire, Ashworth, Chenango, Essex, Placid, Virgil, and Kennebec are varieties in which S. demissum was one of the parents and are immune to some races of late blight.
The development of blight-resistant varieties is a complicated procedure actually, the plant breeder has to develop resistance to several biological races that vary in ability to cause disease. A blight-immune variety may be immune to one race but susceptible to other races. Within the past decade, however, efforts to develop blight-immune varieties show that varieties can harbor immunity to more than one race of the fungus of late blight.
COMMON SCAB, caused by Streptomyces scabies, is recognized by slightly raised spots or lesions of rough, corky tissue on the tuber. The lesions may be so numerous as to involve the entire surface. They may involve distinct russeting or deep scab. Scab lesions spoil the looks of the tuber and cause waste in peeling and reduction in grade.
The fungus lives in the soil and on infected tubers. It occurs in nearly every potato-growing region. Soil acidity, moisture, temperature, and aeration influence the development of scab. A soil reaction below pH 5.2 is unfavorable for most of the common scab races, although some strains are said to cause infection below pH 5. In general, the fungus is favored at pH 5.2 to 7. Common scab develops at a wide range of temperatures, 50 to 85 , but it thrives best at about 70 . Relatively high soil moisture tends to check the disease in some localities, but in other districts high moisture may favor scab. Lack of aeration inhibits development of the organism.
The several races of the fungus vary in type and color of mycelium, color in the medium, and pathogenicity. Apparently the races result by mutation and some races mutate more than others.
Treatment of seed tubers with disinfectants kills the scab fungus on the tuber, but it fails to control the disease if the treated tubers are planted in scab-infested soil. The use of 300 to 500 pounds of sulfur an acre reduces the severity of scab in some soils. The use of ammonium sulfate in fertilizer that increases soil acidity may inhibit the disease somewhat. None of the treatments has been entirely adequate for scab control, however.
The most promising method involves the development of scab-resistant varieties. Studies in Europe have disclosed that Jubel, Hindenburg, Ostragis, and Arnica are scab-resistant. In this country, scab resistance was noted in Russet Rural and Russet Burbank. Although the scab-resistant European varieties are not adapted to growing conditions in America, they do serve as resistant parents. From them the resistant Cayuga, Menominee, Ontario, and Seneca were derived. Investigations on scab resistance by the Department of Agriculture and State experiment stations are designed to develop varieties that are superior to them in scab resistance, quality, adaptability, and yield.
VERTICILLIUM WILT, caused by Verticillium albo-atrum, induces wilting of the tops and vascular discoloration of the stems, tubers, and roots symptoms similar to those associated with other wilt-inciting fungi. Since V. albo-atrum is favored by lower temperatures than are wilt-inciting Fusaria, it often occurs in the cool seed-potato areas.
Verticillium wilt is recognized by flaccid, drooping leaves. Often only one stalk in the hill or a part of a stalk may be wilted. Later all the plants in the hill are involved and finally are killed.
Cross sections near the stem or stolon end of the tubers expose dark-colored vascular elements, the sap-conducting elements. The verticillium wilt fungus does not cause a disintegration or rot of the invaded tissues. Sometimes other organisms may enter the wilt-invaded parts, however.
Verticillium wilt on potato was reported in Europe and America early in the twentieth century. It occurs in the seed-potato areas in the New England, North Central, and Northwestern States.
The wilt fungus is harbored in the tubers and persists in the soil. If conditions are favorable, wilt-free soil can be infested by wilt-infected seed potatoes. Attempts at getting wilt-free seed tubers by cutting off the discolored stem end of infected tubers have met with failure because fungus hyphae may penetrate beyond the discolored section of the tuber.
Roguing wilted tops has reduced the amount of wilt of seed potatoes if the tops in the three hills on each side of the wilted hill also were removed. In some regions the wilt fungus persisted in the soil after a 2-year rotation, but infestation was practically eliminated after a 3- to 4-year rotation.
Some varieties Menominee, Saranac, and Sequoia are more resistant than others.
BLACKLEG, caused by Erwinia atroseptica, is recognized by an inky-black lesion on the base of the stem, which is a primary distinguishing character from similar soft rot caused by bacteria.
The blackleg bacteria invade tops and tubers. Infection may enter the stalks from the infected seed piece. Diseased tops manifest slight to severe dwarfing and somewhat rigid and rolled leaves that in the later stages yellow, wilt, and die.
In very wet weather, the inky-black lesions at the base of the stalk may spread to most of the plant. The bacteria enter the new tubers through the stolons of a blackleg stalk and invade the vascular elements, as well as other tissues of the tuber. Affected tubers show soft rot, involving the entire tuber. Under less favorable conditions the decay is arrested so that only the tissues in the center of the tubers are disintegrated.