Wilt Diseases

i R. Kenneth Horst: Westcott’s Plant Disease i Handbook — 2008/3/14 — 18:36 — page 681 — LE-TEX i i WILT DISEASES To wilt means to lose freshness or to become flaccid. Wilting in plants may be temporary, due to too rapid transpiration; or it may be permanent, due to continued loss of water beyond the recovery point. Disease organisms, by reducing or inhibiting water conduction, may cause permanent wilting. Because wilt diseases are systemic, and tied up with the entire vascular sys- tem of a plant, they are usually more important, and harder to control, than localized spots or cankers. In many cases the fungus enters the plant from the soil through wounds or root hairs and cannot be controlled by protec- tive spraying. Often, although the fungus is present only near the base of a plant, the first symptom is a flagging or wilting or yellowing of a branch near the top. Many species of Fusarium are responsible for important wilts and “yellows.” Verticillium is a common cause of wilt in maples, other trees, and shrubs, but most important among the wilt pathogens are two species of Ceratocystis, one causing oak wilt, the other Dutch elm disease. Acremonium (Cephalosporium) Leaf Spots. Acremonium diospyri (formerly Cephalosporium diospyri). Persimmon Wilt, a lethal disease of common persimmon. Wilt appears in scattered local- ities from North Carolina to Florida and west to Oklahoma and Texas, but most infection is in north central Florida and central Tennessee. Spread is rapid and death quick. First notice of the disease was in Tennessee in 1933. By 1938 only 5% of the persimmons in the infected stand were alive. Top- most branches wilt suddenly, then the rest of the tree, with defoliation and death. The fungus fruits in salmon-colored spore masses in cracks in dead bark of dying trees or under bark of dead rings. Fine, blackish streaks are present in five or six outer rings of trunk, branches, and roots. No control is known. i i i i i R. Kenneth Horst: Westcott’s Plant Disease i Handbook — 2008/3/14 — 18:36 — page 682 — LE-TEX i i 682 Plant Diseases and Their Pathogens Cephalosporium diospyri (see Acremonium diospyri). Persimmon Wilt, a lethal disease of common persimmon. Cephalosporium sp. Sunflower wilt. Ophiostoma (Ceratocystis) Ascomycetes, Ophiostomatales Perithecia enlarged at base, with thin walls, and long slender neck, ascus wall evanes- cent, ascospores hyaline. Conidial stage may be Chalara with endogeneous spores or Graphium with external conidia or conidiophores united into a dark stalk (synnema). Ceratocystis fagacearum (Chalara quercina, Endoconidiophora fagacearum). Oak Wilt, our most serious disease of oaks, now known in 20 states from Texas and Oklahoma east to Pennsylvania and South Carolina. It has also been reported in Florida. Although apparently present in the Upper Mississippi Valley for many years, the disease did not cause concern, and the fungus was not described until 1943, since when it has become a major threat to our forest economy and to trees in residential areas. All native oak species are susceptible, also chinquapin, chestnut, lithocarpus (and apples in experimental inoculation); but red oaks succumb most rapidly. Scouting for the disease has been done largely by airplane, the discolored foliage being visible up to a half mile. First symptoms are a slight crinkling and paling of leaves, followed by pro- gressive wilting, bronzing, and browning of leaf blades from margins toward midribs and defoliation progressively downward and inward throughout the tree. Red oaks almost never recover and may be killed within 4 to 8 weeks after symptoms appear. White and burr oaks may persist for some years, with affected branches dying in a staghead effect. The first internal symptoms are the formation of gums and tyloses in the xylem. After wilting, mycelial mats are formed between the bark and wood, and the bark cracks from the pressure exerted. Perithecia are formed in these mats, which have a sour odor and attract insects. Nitulid beetles, fruit flies, brentids, springtails, bark beetles, and possibly other insects get conidia and ascospores on or in their bodies as they feed, and can inoculate other trees through wounds. We know that ascospores remain viable several months on insects and can be distributed through fecal pellets, but we do not yet know how great a role they play in the spread of oak wilt. Birds have been suspected as carriers but are not yet indicted. Local spread is largely by root grafts, i i i i i R. Kenneth Horst: Westcott’s Plant Disease i Handbook — 2008/3/14 — 18:36 — page 683 — LE-TEX i i WILT DISEASES 683 one tree infecting others within 50 feet and with grafts possible between red and white oaks, not limited to the same species. Control. In residential areas infected trees should be removed. In forests, felling may wound other trees and spread the disease more than letting the dead tree remain but treated so that it is not infective. Different states handle the problem in different ways. In Pennsylvania, each infected tree is cut, with all other oaks within 50 feet, and ammate crystals are placed on each stump. In North Carolina stumps and felled trees are thoroughly sprayed. In West Virginia the trees are left standing, but a deep girdle into the heartwood dries out the tree so that mycelial mats and spores do not form. Ceratocystis (Ceratostomella) ulmi (Graphium ulmi) (see Ophiostoma ulmi and O. novo-ulmi). Dutch Elm Disease, on American, Sibirian, Slip- pery and European elms in 31 states, Maine to North Carolina and west to Oklahoma, and on cedar. Ophiostoma ulmi and O. novo-ulmi (formerly Ceratocystis (Ceratostomel- la) ulmi (Graphium ulmi)). Dutch Elm Disease, on American, Sibirian, Slippery and European elms in 31 states, Maine to North Carolina and west to Oklahoma, and on cedar. This fatal disease is not really of Dutch origin but is so named because it was first investigated in Holland. It was noticed in Europe about 1918, first in France, then in Belgium and Holland. It spread throughout central and southern Europe, then into England and Wales. In many places it virtually exterminated the elms, including those on the famous avenues at Versailles. It is suspected that the fungus came to Europe from Asia during World War I. Dutch elm disease was discovered in Ohio in 1930 and in New Jersey in 1933. It has spread north through New England and has become very serious in the Midwest. In 1948, the disease was found in Denver, Colorado, and in 1976 in California. It is now fairly widespread in reports of its occurrence in the United States. The spread of the fungus is linked with the presence of the large and small European bark beetles, Scolytus scolytus and S. multistriatus. Only the latter is established in this country, having arrived in Boston about 1919. Patient detective work established the fact that the fungus came here in elm burl logs imported for furniture veneer. After one such infected elm burl was found in Baltimore in 1934, months of scouting went on in the vicinity of ports of entry, railroad distributing yards, and veneer plants. Such backtracking showed the infected material had come in at four ports of entry and had been carried by 16 railroads over 13,000 miles in 21 states. From this source the disease got its start in at least 13 areas in 7 states. i i i i i R. Kenneth Horst: Westcott’s Plant Disease i Handbook — 2008/3/14 — 18:36 — page 684 — LE-TEX i i 684 Plant Diseases and Their Pathogens Elm nursery stock is, of course, quarantined, and elm burls are embargoed; but who who would have believed that dishes could have anything to do with killing our elms? Dishes have to be crated, however, and several times since 1933 English dishes crated with elm wood carrying bark beetles and Ceratocystis have been intercepted. All American and European elms are susceptible. Asiatic elms, Ulmus parvifolia and U. pumila, are resistant. A seedling elm, named Christine Buisman for its Netherlands’ discoverer, is highly resistant, though not immune, and is now available. Other promising seedlings have been tested by the U.S. Department of Agriculture. Symptoms are apparent from the latter part of May until late fall. The acute form of the disease is characterized by sudden and severe wilting. First the young leaves, then all leaves wilt and wither, sometimes so rapidly that they dry, curl, and fall while still green, before they can turn the usual brown of dead leaves. Sometimes terminal twigs are curled into a shepherd’s crook. Chronic disease symptoms are gradual, often taking all summer for com- plete defoliation. In many cases individual branches or “flags” appear, the yellowed leaves conspicuous against the rest of the tree; but sometimes all leaves gradually turn yellow. In another type of chronic disease, trees leaf out late in spring, with sparse chlorotic foliage and a staghead appearance. When an affected twig is cut across, the vessels or water-conducting tubes show dark brown or black, being clogged with bladderlike tyloses and brown gummy substances (see Fig. 3.62). The production of these substances is thought to be stimulated by a toxin secreted by the fungus and carried in the sapstream. Symptoms are not dependent on the physical presence of fungal hyphae in all parts of the tree. The fungus lives in the sapwood, fruiting in cracks between wood and loosened bark and in bark beetle galleries under the bark. This fruiting is of the anamorph state, spores being produced in structures called coremia.

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