The Cultivated Highbush Blueberry

Austin C. Goheen.

Our cultivated highbush blueberries are mostly hybrids and selected wild plants of Vaccinium australe and V. corymbosum, the native blueberries of eastern North America. A few are hybrids between the species V. australe and V. lamarckii, the lowbush blueberry that forms the bulk of the wild blueberry crop that is harvested in Maine.

When the commercial cultivation of blueberries was first started, the fields were small and isolated, and the plants remained relatively free from disease blueberries, in fact, were hailed as one crop without serious disease problems. But that happy condition no longer prevails. Modern plantings, in large fields of genetically similar bushes, are subject to considerable damage from several disease-producing agencies. The most serious diseases are stunt, mummy berry, botrytis blight, powdery mildew, and stem canker.

STUNT, a virus disease of the yellows type, is prevalent in New Jersey and North Carolina. Entire fields may become so badly diseased that little or no crop is produced. The disease also occurs in Massachusetts, New York, Michigan, Maryland, and eastern Canada. It occurs in wild highbush blueberries in New Jersey.

In nature it is transmitted by the leafhopper, Scaphytopius magdalensis. It can also be spread in diseased cuttings and nursery stock. In experiments it has been transmitted in diseased buds and grafting wood. We know from tests that dodder, a parasitic seed plant, can transmit the disease from blueberry plants to other blueberry plants and to Vinci rosea, but such transmission has not been observed under natural conditions. Inoculating healthy plants with the juices of diseased plants has not transmitted the disease. Stunt is not spread in the field by pruning knives or other mechanical methods.

Its symptoms are variable, differing with variety, time of year, stage of growth, and age of infection. Stunt dwarfs the bush, reduces the size of the leaves, and causes an abnormal coloring of the leaves. The fruit on bushes that have been infected for a number of years are inferior in size and quality. Diseased bushes eventually fail to set fruit.

The most marked symptom is found in the terminal leaves of young shoots, which in spring and early summer develop pale-green or yellowish margins. Often they are cupped. By holding the leaves perpendicular, one can see a pattern like a Christmas tree: The midrib and lateral veins remain dark green and the pale colors extend inward in the areas between the lateral veins. In late summer the inter-veinal areas redden brilliantly before healthy plants show any normal red fall coloring. Then the Christmas tree pattern is very striking. Leaf symptoms; vary with variety. Rubel shows the spring symptoms throughout the season. Infected Rancocas bushes exhibit only late-summer symptoms. Bushes infected for some time frequently do not show the leaf symptoms.

Stunt was first observed in New Jersey in 1926. In 1942 R. B. Wilcox, of the Department of Agriculture, described the trouble as of virus origin. In 1945 C. A. Doehlert, of the New Jersey Agricultural Experiment Station, found that the disease could be transmitted by mixed colonies of leafhoppers. Subsequently P. E. Marucci and W. E. Tomlinson, Jr., of the same station, proved that the vector was either S. magdalensis or S. verecundus, two similar insects that are widely distributed on ericaceous plants in swamps of eastern North America. M. T. Hutchinson, also of the New Jersey station, found that S. verecundus does not occur in appreciable numbers in the cultivated blueberry fields although it is common in nearby cranberry bogs. S. magdalensis therefore seems to be the principal vector for stunt virus.

No variety is immune to stunt. Rancocas appears to be tolerant to the virus. Plantings of Rancocas in badly infected fields have continued to produce crops of berries long after the disease has destroyed other varieties.

Three control practices are each partly successful. Prompt removal of plants that show stunt symptoms reduces the reservoir of diseased plants that the leafhopper may feed on. In districts where the disease occurs sporadically this practice is effective.

In areas where the disease is bad and the leafhopper is abundant, roguing alone is not successful. Here the second practice, control of the leafhopper, is necessary. Four applications of DDT or methoxychlor (3 pounds in 100 gallons of water) have greatly reduced the numbers of leafhoppers in tests in New Jersey but have never completely destroyed them. Roguing and insect control together are the best control procedures for use in New Jersey and North Carolina.

Use of disease-free plants in setting new fields is the third practice. Rigid specifications have been set up for the certification of healthy plants in New Jersey. But even with certified plants, new fields in New Jersey and North Carolina should be rogued and the leafhoppers controlled.

The ultimate control of stunt in areas where the vector is abundant seems to rest on the development of immune varieties or elimination of sources of the disease. No truly immune varieties were available in 1953. A number of wild species and varieties of blueberries have been put under test in New Jersey in the hope that among them an immune plant might be found to form the basis of a breeding program whose objective would be the development of resistance to stunt.

MUMMY BERRY, a fungus disease, is widespread in commercial blueberry fields in eastern North America. In the northern zones it sometimes destroys the crop of some varieties. In the Pacific Northwest and in North Carolina it is rare on the cultivated blueberry but more or less abundant on other blueberry species.

The causal fungus, Monilinia urnula, has a complicated life cycle. From harvest in early summer until the blueberry buds open the following spring, the fungus is found on the ground under the bushes in the form of mummies. The mummies are compact masses of fungus tissues that formed in infected berries the previous season. In early spring, when the blueberry buds start to open, the fungus renews its development, and mummy cups; the apothecia are produced from the old mummies. Along the inner surface of the mummy cup sexual spores, or ascospores, of the fungus are produced in profusion. The ascospores, released during periods of rainy, cool weather, are carried by wind to the young flower and leaf buds. Ascospores landing on the moist surfaces of the young buds grow into the young leaf and flower bud tissues. After about a week the infections become apparent as necrotic areas on the petioles and along the midveins of the leaves in spur infections or at the base of the flowers in cluster infections. The infected spurs and clusters soon die, and conidia of the fungus are formed along the central axes of the spurs or clusters. The conidia are carried by wind or by insects to the stigmas of open flowers. The young berries become infected and develop into new mummies, which carry the fungus through the summer and the following winter.

Weather conditions are important. In early spring the mummies must have moisture before apothecia and ascospores are produced. Primary infection of the spurs and clusters depends on wet weather at the time the buds are beginning to open. Secondary infection of the flowers depends on weather conditions that affect dispersal of the conidia. Differences in spring weather may explain the differences in the amount of damage done by mummy berry in different years. A cool, wet spring favors the outbreak of an epiphytotic.

Mummy berry was first identified in 1832 in Russia on the wild European lingberry, Vaccinium vitis-idaea. It was first discovered in North America on various wild blueberries in Michigan in 1898 by B. O. Longyear, of the Michigan Agricultural Experiment Station. He described the life cycle of the fungus essentially as we know it today.

Varieties differ considerably in susceptibility. June and Rancocas are blighted more severely by primary infections than are Weymouth, Cabot, and Stanley. There are also differences in the amount of secondary infection with different varieties.

It can be controlled at the time of primary infection in the spring. The young blueberry buds can be protected from infection through the use of ziram fungicide applied as a heavy spray over all the surfaces of the bushes, or the spores of the fungus can be destroyed before they blow to the bushes through the mechanical or chemical destruction of the mummy cups. Protection with ziram is more effective than destruction of the cups because the wind can blow spores to the bushes from distant sources. In order to obtain control, treatments must be applied just before the release of the spores from the cups. In New Jersey this usually occurs during the first or second week in April.

BOTRYTIS BLIGHT is widespread in areas where blueberries are grown, but it often is overlooked because it is confused with mummy berry. It destroys the fruit when whole flower clusters are blighted at blossom time, when individual green berries become infected and rot, or when berries become infected at harvesttime and rot during marketing or in cold storage.

The fungus can develop on stored berries at temperatures only slightly above freezing.

The disease attacks a variety of species. It is most severe in places where the weather is cool and wet when the blueberries are maturing and the bushes are producing new growth. The disease organism has been isolated from dead blueberry tips gathered in Washington, Michigan, Maryland, New Jersey, New York, Massachusetts, and Maine.

The cause is the common gray mold fungus, Botrytis cinerea. Besides producing blueberry fruit rots and tip blights, it occasionally produces leaf spots. It is abundant on such debris as fallen corollas, insect-damaged berries, and mummy lesions on or under the bush. Its production of spores reaches a peak during the period just after blossoming. After the weather becomes warm and dry in the summer, sporulation occurs only for short periods following rains. The fungus has been isolated from dead blueberry tips at all times during the year. In the spring the first sporulation of the fungus is observed on the dead tips.

The blight was one of the first diseases reported on commercial blueberries but no investigations of methods to control the disease were undertaken until 1949. No control method has been found for the disease.