Petal Blight of Azalea

D. L. Gill.

Azalea petal blight, or flower spot, is a striking disease. One day all the flowers on a plant or in a garden may appear normal to the casual observer. The next day they may be blighted as though hot water had been poured over them.

The disease was first noticed near Charleston, S. C., in 1931. In 1932, men who conducted a survey for the Department of Agriculture found the disease in all the gardens they visited within 20 miles of Charleston on both sides of the Ashley and Cooper Rivers. The disease spread rapidly. In 1935 it was discovered in Wilmington, N. C., and in 1936 in Savannah, Ga., Mobile, Ala., and New Orleans.

Freeman Weiss, then of the Department of Agriculture, found the disease in 1937 along the Coastal Plain from Wilmington, N. C., to Lafayette, La., where his survey stopped. It was not present in some of the isolated azalea plantings into which no new plants had been brought shortly before. The disease was reported in 1940 in Texas, where apparently it had been present for several years. California reported its presence in 1941, Maryland in 1946, and Virginia in 1947.

Moved by the severity of the disease and the great value of the azalea flowers throughout the South, Dr. Weiss began investigations in 1933 at Charleston. He believed at first that the sudden appearance and rapid spread of the disease meant it was spread otherwise than by wind or rain. As insects were considered possible vectors, Floyd F. Smith, an entomologist in the Department, joined Weiss in the investigation in 1935. They continued to work together on the project through 1938.

Azalea petal blight appears first as small white spots on the colored flowers, or as brown spots on white-flowered varieties. The spots enlarge rapidly under favorable conditions until the whole petal or flower softens and collapses. Affected petals fall apart if rubbed gently between the fingers. Flowers injured by insects or weather or otherwise will not do so. The diseased flowers cling to the plant and present an unsightly appearance. Normally healthy flowers of Indian azaleas fall to the ground while still displaying their original color and shape and thus prolong their attractiveness.

Weiss and Smith found the fungus most commonly associated with the diseased flowers to be the cause of it. That point had been hard to prove because the fungus grows slowly and fails to produce spores in artificial culture. Because the fungus was previously unknown, Dr. Weiss named it Ovulinia azaleae.

Hard, black objects the sclerotia, are produced on the old, diseased flowers while they still cling to the plant or after they fall to the ground. The sclerotia are one-eighth to one-fourth inch long. In that stage the fungus can live through the period when flowers are not present. Their presence confirms diagnosis of the disease.

Sclerotic spread Ovulinia into new areas when some of the surrounding soil is moved with the plants in transplanting. In spring, about the time azaleas bloom, the sclerotia on or just below the soil surface produce on the ends of short stalks small, brown, cup-shaped bodies, known as apothecia. The apothecia are one-sixteenth to one-eighth inch across. Apothecia continue to be produced for 4 or 5 weeks. They flatten as they mature, and spores (ascospores) of the Ovulinia are forcibly y discharged from their flat upper surface. A spore may reach a flower by the force of its discharge, or it may be caught in wind currents and carried to a nearby plant. If such a spore reaches a flower when conditions are favorable it germinates, sends a germ tube into the flower, and initiates a new infection. A few days later, as the flower blight progresses, secondary spores (conidia) are produced.

Up to several hundred thousand conidia are produced on a single flower. They spread the disease quickly. Infection thus is produced on successively opening flowers. Spores can produce infection at 40 to 80 F.; infection normally occurs between 50 and 72 and is at a peak at 65 .

High humidity, rain, fog, and dew favor the development of the petal blight disease conditions frequently present in the South during the azalea season.

Azalea petal blight attacks all varieties of azaleas (Rhododendron species).

Early-blooming varieties like Elegans may largely escape infection because there is not enough inoculum when they flower. The Macrantha azaleas usually bloom so late that conidial inoculum, is again very low.

Weiss and Smith found the disease on several unidentified hybrid rhododendrons growing inter-planted with azaleas. Two true rhododendrons (R. catawbiense and R. carolinianum) became infected following inoculation.

Ovulinia attacks mountain-laurel (Kalmia latifolia) when it grows near azaleas.

Flowers of highbush blueberry (Vacanium corymbosum and its varieties fuscatum and tenellum) and of huckleberry (Gaylussacia baccata) were experimentally infected. The disease has been of little importance on them. All plants known to be susceptible belong to the family Ericaceae. Research workers could not infect plant parts other than flowers.

Because many insects visit azalea flowers, Weiss and Smith undertook an investigation to determine their relationship to the spread of petal blight. They soon learned that insect injuries were not necessary for the fungus to enter the flower. Early in the study, they thought it probable that spores carried by insects were responsible for the initial infection in the spring. It seemed unlikely that honey bees harbored the fungus in their colony or initiated early infection.

Because primary infection occurred near the ground, soil-inhabiting insects and animals and insects emerging from the soil were investigated, but these workers rarely found that they harbored Ovulinia. They could not indict them as carriers of primary inoculum.

Insects, they learned, can carry Ovulinia conidia from flower to flower but are not effective carriers until infection becomes general and large numbers of conidia are present. Some of the spore-bearing insects were observed to travel 5 miles in 8 days. Inoculation tests showed that they sometimes released spores gradually for several days. Insects therefore may be responsible for the introduction of the disease into nearby uninfected azalea gardens. Consequently any eradication program must be on an area basis if it is to succeed.

Some combined insecticidal-fungicidal dusts had no repelling effect on bees lighting on the flowers. The combination, or fungicidal dusts alone, did reduce the number of spores produced on the flowers and so reduced the number carried by the insects. Dusts made of stomach poisons had no effect on the insects carrying the fungus. Dusts that contained a contact insecticide, derris, pyrethrum, or nicotine sulfate killed adults of most species in 1 to 4 days. The insects were not attracted to poisoned sugar spray applied to the flowers.

The entomological investigations were closed with the conclusion that disease control, rather than insect control, appeared the logical method of attacking the problem. The studies showed that insects were involved in the secondary spread of the disease, but that their role was less important than it had been thought to be.

Weiss and Smith pointed out that since the Ovulinia persists in the sclerotial stage from one flowering season to another, the chief control efforts should be prevention of sclerotial formation, removal and destruction of sclerotia that may form and reach the ground, and prevention of apothecial development by sclerotia that escape.

In accord with those recommendations, large numbers of diseased flowers were picked from the plants and destroyed. The suggestion was made that in isolated plantings the entire bloom for i year be destroyed as a means of eliminating the disease but that was of no value, because some sclerotia were found to live at least 2 years. Because picking off all infected flowers proved to be an almost impossible task, the mulch around the plants was removed and destroyed after the old flowers had fallen. Many sclerotia were destroyed. A heavier mulch replacing the old then tended to prevent apothecia from pushing through to a point from which they could eject spores onto the flowers.

Those practices effected little or no control at least a few apothecia were always produced to initiate infection, and (except in isolated plantings) secondary infections could be initiated by conidia from outside the treated area. Besides, old sclerotia sometimes remained hanging on plants a year after they were produced, and some sclerotia produced apothecia in the second flowering season.

Drenches applied to the soil about the plants were also tested. The shallow root system of azaleas makes injury from such applications a hazard. Surface applications of sulfur and copper, commonly used as dormant sprays, were ineffective. Acetic acid (1 1,000 to 1-600) did not injure azaleas even with repeated applications and was toxic to the Ovulinia.

Fungicidal sprays were applied to the plants before the flowers opened Because Ovulinia azaleae infects only flowers after they show color, the sprays were valueless.

Spraying the open flowers with fungicides was also tried. Effective control by this method was considered unlikely by Weiss and Smith because the waxy surface of the blossoms prevented wetting, therein the difficulty in obtaining coverage in the dense masses of blooms, and frequent spraying was necessary because of continuous opening of the flowers over several weeks. Lime-sulfur and copper sprays gave no control but produced no injury in azaleas except flower discoloration. Acetic acid (80 percent diluted to 1 part to 600 parts water) offered some promise when sprayed on open flowers and on the ground, but; because of its solubility in water rains, dews, and fogs removed it and left the flowers exposed to infection.

A copper-clay or copper-lime dust containing 6.5 percent copper was effective in laboratory tests. Dusting azaleas in the open failed to control the disease if secondary infection was severe. The dusts left an objectionable residue on the flowers. Weiss and Smith concluded that overwintering sources of Ovulinia must be largely eliminated if spraying or dusting was to be effective.

Philip Brierley, of the Department of Agriculture, followed Weiss and Smith at Charleston, working through the 1941 season. His approach was to attempt suppression of apothecial formation by application of chemicals to the soil just before the apothecia developed.