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Seweta Srivastava
CONTENTS
S.No.
Chapters
Page No
1.
Introduction
2 to 5
2.
Chestnut Blight
6 to 15
3.
Dutch Elm Disease
16 to 33
4.
Palm Lethal Yellowing
34 to 45
5.
Oak Wilt / Sudden Oak Death
46 to 62
6.
Butternut Canker
63 to 69
7.
Cypress Canker
70 to 76
8.
Xylella Outbreak
77 to 88
9.
References
89 to 99
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losses of 30 to 50 percent are common for major crops. In some years, losses are much greater, producing catastrophic results for those who depend on the crop for food. Major disease outbreaks among food crops have led to famines and mass migrations throughout history. The devastating outbreak of late blight of potato (Phytophthora infestans) that began in Europe in 1845 and brought about the Irish famine caused starvation, death, and mass migration of the Irish population. Of a population of eight million, approximately one million (about 12.5 percent) died of starvation and 1.5 million (almost 19 percent) emigrated, mostly to the United States, as refugees from the destructive blight. This fungus thus had a tremendous influence on the economic, political, and cultural development in Europe and the United States. During World War I, late blight damage to the potato crop in Germany may have helped end the war. Losses from plant diseases also can have a significant economic impact, causing a reduction in income for crop producers and distributors and higher prices for consumers. In 1993 the United States lost more than one million acres (405,000 hectares) of crops to disease. More than 800,000 acres of wheat succumbed to disease, exacting a monetary loss in the millions of dollars. Diseases²a normal part of nature Plant diseases are a normal part of nature and one of many ecological factors that help keep the hundreds of thousands of living plants and animals in balance with one another. Plant cells contain special signaling pathways that enhance their defenses against insects, animals, and pathogens. One such example involves a plant hormone called jasmonate (jasmonic acid). In the absence of harmful stimuli, jasmonate binds to special proteins, called JAZ proteins, to regulate plant growth, pollen production, and other processes. In the presence of harmful stimuli, however, jasmonate switches its signaling pathways, shifting instead to directing processes involved in boosting plant defense. Genes that produce jasmonate and JAZ proteins represent potential targets for genetic engineering to produce plant varieties with increased resistance to disease.
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Humans have carefully selected and cultivated plants for food, clothing, shelter, fiber, and beauty for thousands of years. Disease is just one of many hazards that must be considered when plants are taken out of their natural environment and grown in pure stands under what are often abnormal conditions. Many valuable crop and ornamental plants are very susceptible to disease and would have difficulty surviving in nature without human intervention. Cultivated plants are often more susceptible to disease than are their wild relatives. This is because large numbers of the same species or variety, having a uniform genetic background, are grown close together, sometimes over many thousands of square kilometers. A pathogen may spread rapidly under these conditions. Definitions of plant disease In general, a plant becomes diseased when it is continuously disturbed by some FDXVDO0003 DJHQW0003 WKDW0003 UHVXOWV0003 LQ0003 DQ0003 DEQRUPDO0003 SKVLRORJLFDO0003 SURFHVV0003 WKDW0003 GLVUXSWV0003 WKH0003 SODQW¶V0003 normal structure, growth, function, or other activities. This interference with one or more RI0003 D0003 SODQW¶V0003 HVVHQWLDO0003 Shysiological or biochemical systems elicits characteristic pathological conditions or symptoms. Plant diseases can be broadly classified according to the nature of their primary causal agent, either infectious or noninfectious. Infectious plant diseases are caused by a pathogenic organism such as a fungus, bacterium, mycoplasma, virus, viroid, nematode, or parasitic flowering plant. An infectious agent is capable of reproducing within or on its host and spreading from one susceptible host to another. Noninfectious plant diseases are caused by unfavorable growing conditions, including extremes of temperature, disadvantageous relationships between moisture and oxygen, toxic substances in the soil or atmosphere, and an excess or deficiency of an essential mineral. Because noninfectious causal agents are not organisms capable of reproducing within a host, they are not transmissible. In nature, plants may be affected by more than one disease-causing agent at a time. A plant that must contend with a nutrient deficiency or an imbalance between soil ϰ0003 0003
moisture and oxygen is often more susceptible to infection by a pathogen; a plant infected by one pathogen is often prone to invasion by secondary pathogens. The combinations of all disease-causing agents that affect a plant make up the disease complex. Knowledge of normal growth habits, varietal characteristics, and normal variability of plants within a species²as these relate to the conditions under which the plants are growing²is required for a disease to be recognized. The study of plant diseases is called plant pathology. Pathology is derived from the two Greek words pathos (suffering, disease) and logos (discourse, study). Plant pathology thus means a study of plant diseases. Invasive plant species are the second greatest threats to the natural ecosystems of the world today. Only direct habitat destruction poses a greater threat to the future of biological diversity. Invasive species disrupt the ecology of natural ecosystems by displacing native plant and animal species and reduce biological diversity by reducing the amount of light, water, nutrients and space available to native species.
The introduction of exotic plant species have resulted in the escape of plant pathogens which have greatly impacted our local flora, such as Dutch Elm Disease, Beech Bark Disease, Chestnut Blight and Dogwood Anthracnose.
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Usually prior to perithecia, pycnidia are produced in the same small stroma or in other stromata. They also can appear any time of year. The conidia ooze out in a tendril after rains. They are quite small, as small as 4 x 1 µm wide. In that little conidium is all the information and machinery necessary to wipe out one of the most important tree species in North America. Conidia may be carried by rain splash or catch a ride on an insect or bird. Identifying the Fungus: - The fungus forms yellowish or orange fruiting bodies (pycnidia) about the size of a pin head on the older portion of cankers. Spores may exude from the pycnidia as orange, curled horns during moist weather. Identifying the Injury: - Stem cankers are either swollen or sunken, and the sunken type may be grown over with bark. The bark covering swollen cankers is usually loose at the ends of the canker. Trees die back above the canker and may sprout below it. Frass and webs from secondary insects are common under loose bark.
Fig. 2.3: Cracking and fruiting bodies on chestnut Fig. 2.4: Basal cracking caused by chestnut blight fungus
Biology: - Host infection occurs when fresh wounds in the bark become infected with spores that are disseminated by wind, birds, rain, and insects. Cankers kill the cambium and girdle the stem. Multiple cankers on infected trees are common. ϴ0003 0003
Environment Within the range of environmental conditions found in the geographic range of chestnut, there do not appear to be important differential effects of the environment. Environmental conditions are conducive to disease throughout the range of chestnut. Disease Cycle Conidia and ascospores can infect wounds, even very small ones that don't go all the way to cambium. It is thought that insects of various kinds make most of the infection courts. The fungus grows in the inner bark and cambium, producing small brownish mycelial fans. Even after the branch or stem is girdled and killed, the fungus continues to colonize it, producing ever more inoculums. Symptoms Chestnut blight is a canker disease. Perhaps it is called blight because infected branches and stems die quickly, as in shoot blight. But it doesn't just infect shoots; it infects branches and stems of any size. The cankers are of the diffuse type. They grow rapidly and in most cases continue to develop until the stem is girdled and killed; then they continue to colonize the dead tree. Management We will never have chestnut like we did in 1900, at least not in the next few hundred years. But there are two areas of hope for some form of recovery. Breeding for resistance: Chinese chestnut is somewhat
resistant.
The
persistent perennial cankers
fungus
rather
than
causes diffuse
cankers. It can slow the fungus down. Reproduction is limited. But Chinese chestnut is not such a great tree.
So
traditional
breeding
followed
by
backcrossing is underway. Although it is slow and a ϵ0003 0003
It was later found that hypovirulent isolates have a piece of double-stranded RNA, which doesn't normally occur in fungi. It is now considered that the dsRNA is a virus in the family Hypoviridae, and essentially causes a disease in the fungus, making it less virulent. Hypovirulence has had limited success against chestnut blight. It shows promise in some locations in Europe and in Michigan in the United States. However, it has failed almost completely in eastern North America. Therapeutic treatment of individual cankers is successful in most cases, but the success of hypovirulence at the population level depends on the natural spread of viruses. It is not clear how well the hypovirulent strains can reproduce, disperse, and make contact with virulent strains in nature. Factors limiting spread of the virus are not well understood. One natural barrier to virus spread is hyphal fusion among individuals of the fungus. Hyphal fusion is necessary to transmit the virus. When hyphae can fuse and exchange material, they are said to be vegetatively compatible, and in the same vegetative compatibility group. In North America, we have more VC groups than they do in Europe, so getting the virus to spread around in nature is going to be difficult. But there is a lot of hope that it may yet succeed. Other Issues Most forest pathologists like tree diseases. Generally, I would like to see a diseased tree more than a healthy one. Although human society generally has a goal of reducing such diseases, if the truth be told, sometimes we root for the pathogen, just because it's such fun to see a disease really do a job. But chestnut blight is a different story. What it did to American forests is no joking matter. It's a tragedy. No one who loves forests can think about the decimation of such a fantastic and abundant tree species as anything else. An informal article by George Hepting gives some insight into the role of chestnut in American life as well as the chaos that ensued in scientific and political circles as society struggled to deal with the new disease. ϭϭ0003 0003
There is an emotional hook there that other diseases just don't have. Even today, many years after the American chestnut was essentially wiped out as a forest tree, there are many ordinary citizens deeply interested in doing something to bring it back. The reason there is little resistance in American Chestnut is that the pathogen was introduced. In 1904, the disease was observed in the New York Zoo killing chestnuts, but there is reason to suspect it was here as early as 1893. The pathogen was later found to be native to China and was apparently introduced on nursery stock. In Asia the fungus was a weak parasite. In America, it spread very quickly and never met a tree it couldn't kill. It spread up to 50 miles per year over the natural range of chestnut. By 1940, chestnut was destroyed as a commercial species. Today, incredibly, chestnut still survives in much of its former range, but only as sprouts from the old root systems. The roots and root collar are resistant. In many places, various oaks have replaced it. In the oak stands, you can hardly find chestnut. When the oaks are cut, fairly dense sprouts of chestnut pop up, trying to do their thing. But before they can get big enough to sexually reproduce, the damn disease cuts them down. They don't seem to stand much chance of adapting. Importance - The chestnut blight fungus has virtually eliminated the American chestnut, as a commercial species, from eastern hardwood forests. Although roots from trees cut or killed many years ago continue to produce sprouts that survive to the sapling stage before being killed, there is no indication that a cure for this disease will be found. The fungus is widespread and continues to survive as a nonlethal parasite on chinkapin, Spanish chestnut, and post oak. Control - No effective control has been developed for chestnut blight, even after decades of intensive research. Current research is targeted toward finding a blight resistant species and the further development of the hypovirulent strains of the fungus. These strains tend to inactivate the pathogen and promote healing, but only when applied directly to developing cankers.
ϭϮ0003 0003
Some Facts about Blight Resistance American chestnut seedlings are usually highly susceptible to the blight. In older trees (more than 1.5 inches in diameter at breast height), a resistant individual can slow down progress of the disease and may survive in spite of blight, but it is not immune. Many kinds of environmental stress may break down a tree's resistance to blight. Indeed, at higher elevations in areas exposed to severe climate, normally resistant, Oriental chestnuts have been killed by blight. When we search for possible sources of blight resistance, we look for American chestnuts greater than 10' DBH (Diameter at Breast Height) which have swollen blight cankers (as illustrated in the February 1990 National Geographic, page 132). Some Facts about Hypovirulence Hypovirulence is a virus disease of the blight fungus. Weakened by the virus, the blight's progress is slowed down, so that a chestnut tree which may have no resistance to blight can form the slow-growing swollen cankers normally produced only on resistant trees. Scientists have been trying to manipulate hypovirulence to develop an economical bio-control for blight. Among the obstacles to be overcome are 1) the blight spreads very rapidly in nature, while hypovirulence spreads very slowly; 2) there are many types of virulent strains in the forest which resist transfer of the virus responsible for hypovirulence; and 3) good, swollen, slow-growing cankers sometimes change into bad, sunken, rapid-growing cankers that kill trees. Integrated
management
for
American
chestnut
revival combines
hypovirulence (by inoculation) with blight-resistance (grafted) on sites identified as ideal American chestnut habitat, to produce blight control. In Virginia's Lesesne State Forest, 3 resistant American chestnuts were grafted in 1980. In 1982 and 1983 the first cankers were inoculated with hypovirulence. These trees are thriving; they have produced nuts for more than 10 years, and they make excellent annual growth. They are surrounded by nonresistant American chestnuts which are continuously killed back by the blight. Conservation Efforts There are approximately 2,500 chestnut trees growing on 60 acres near West Salem, Wisconsin, which is the world's largest remaining stand of American chestnut. ϭϯ0003 0003
These trees are the descendants of those planted by Martin Hicks, an early settler in the area. In the late 1800s, Hicks planted less than a dozen chestnuts. Planted outside the natural range of chestnut, these trees escaped the initial wave of infection by chestnut blight, but in 1987, scientists found blight also in this stand. Scientists are working to try to save the trees. There is a program to bring American chestnut back to the Eastern forest and funded by the American Chestnut Foundation, Wisconsin Department of Natural Resources, USDA Forest Service, University of West Virginia, Michigan State University, and Cornell University. Removing blighted trees to control the disease was first attempted when the blight was discovered, but this proved to be an ineffective solution. Scientists then set out to introduce a hypovirus into the chestnut blight fungus. The trees infected with virustreated fungus responded immediately and began to heal over their cankers. However, the virus was so efficient at attenuating fungal growth that it prevented spreading of the virus from an infected fungus growing on one tree to that growing on another tree. Only the virus-treated trees recovered. Scientific opinion regarding the future of the stand varies. Hybrid Chestnut Trees In the years since the chestnut blight, many scientists and botanists have worked to create a resistant hybrid chestnut tree that retains the main characteristics of the American chestnut tree. In the early 1950s, James Carpenter discovered a large living American chestnut in a grove of dead and dying trees in Salem, Ohio that showed no evidence of blight infection. Carpenter sent budwood to Dr. Robert T. Dunstan, a plant breeder in Greensboro, North Carolina. Dunstan grafted the scions onto chestnut rootstock and the trees grew well. He cross-pollinated one with a mixture of 3 Chinese chestnut selections: 'Kuling', 'Meiling', and 'Nanking'. The resulting fruit-producing hybrid was named the Dunstan Chestnut.[15] The trade off for resistance to the chestnut blight is that the Dunstan hybrid grew to a height of only twenty-five feet or 7.6 meters. Current efforts are under way by the Forest Health Initiative to use modern breeding techniques and genetic engineering to create resistant tree strains, with contributions from SUNY College of Environmental Science and Forestry, Penn State, UGA, and the US Forest Service. One of the most successful methods of breeding is to ϭϰ0003 0003
create a back cross of a resistant species (such as one from China or Japan) and American Chestnut. The two species are first bred to create a 50/50 hybrid. After three back crosses with American Chestnut, the remaining genome is approximate 1/16 that of the resistant tree, and 15/16 American. The strategy is to select blight-resistance genes during the back crossing, while preserving the more wild-type traits of American Chestnut as the dominant phenotype. Thus, the newly bred hybrid chestnut trees should reach the same heights as the original American chestnut. Research is also being conducted at the State University of New York College of Environmental Science and Forestry, by using the bacterial vector, Agrobacterium tumefaciens, to insert resistance genes from the Asian chestnuts into American chestnut. The inserted genes are present only in the resistant strain, and not in the Native American chestnut, and are tested for their potential to produce blight-resistant trees. Currently, SUNY ESF has over 100 individual events being tested, with more than 400 slated to be in the field or in the lab for various assay tests in the next several years. Ideal American Chestnut Revival Habitat Restoration projects (managing for American chestnut in aging clear cuts, or introducing improved blight resistance by grafting scions into available root systems or planting seedlings on former American chestnut lands) should concentrate on carefully selected sites which do not include the whole spectrum of choices mentioned above. Because the American chestnuts will be repeatedly challenged by blight, it is important to choose sites which avoid all other environmental stresses, as much as possible. These sites can be identified by the presence of large chestnut stumps or snags, chestnut sprouts, and other species that share similar site preferences, such as tulip poplar, northern red oak, and cucumber magnolia. Frequently, the best chestnut sites are located in shallow coves and slopes facing north to east. Dry sites should be avoided to limit stress by drought. Known frost pockets or cold air drainage routes should also be avoided, and lower elevation sites are generally preferable to sites over 2,000 or 3,000 feet, to minimize the stresses from extremes in temperature during winter. Full morning sun in coves or sloping, well-drained lands with acid soils (pH 5 to 6) is best. When in doubt, consult a professional forester.
ϭϱ0003 0003
Symptoms Dutch elm disease is a vascular wilt disease. The earliest external symptoms of infection are often yellowing and wilting (flagging) of leaves on individual branches (Fig. 3.2). These leaves often turn brown and curl up as the branches die, and eventually the leaves may drop off. This progressively spreads to the rest of the tree, with further dieback of branches. Eventually, the roots die, starved of nutrients from the leaves. Often, not all the roots die: the roots of some species, notably the English elm Ulmus procera, put up suckers which flourish for approximately 15 years, after which they too succumb (Spooner and Roberts, 2005). Although initially only a part of the tree crown may be affected, symptoms may progress rapidly throughout the crown. Highly susceptible trees often die in a single year, but others may linger for several years. Symptoms progress quickly and death may occur rapidly in trees infected in early spring, while trees infected later in the summer may survive longer.
Fig. 3.2
Fig. 3.3
If the bark of infected elm twigs or branches is peeled back, brown discoloration is seen in the outer layer of wood. This discoloration in the xylem actually occurs before the foliar symptoms described above are seen; foliar symptoms result when sap flow ceases in the infected wood. Xylem browning is often discontinuous. In cross section, it appears as a circle of brown dots or a ring (Fig. 3.3). Other wilt diseases of elm, such as Verticillium wilt, also cause sapwood discoloration, so positive diagnosis of Dutch elm disease depends on laboratory culturing and identification of the fungus.
ϭϳ0003 0003
The signs (fungal structures) of the Dutch elm disease pathogens are found within infected elm trees, and are described in the Pathogen Biology section. Pathogen The causative agents of DED are ascomycete microfungi. Three species are now recognized: x
Ophiostoma ulmi, which afflicted Europe from 1910, reaching North America on
imported timber in 1928. x Ophiostoma himal-ulmi, a species endemic to the western Himalaya0003;Brasier and Mehotra, 1995). x Ophiostoma novo-ulmi, an extremely virulent species which was first described in Europe and North America in the 1940s and has devastated elms in both areas since the late 1960s (Spooner and Roberts, 2005).0003
The origin of O. novo-ulmi remains unknown, but the species may have arisen as a hybrid between O. ulmi and O. himal-ulmi. The new species was widely believed to have originated in China, but a comprehensive survey there in 1986 found no trace of it, although elm bark beetles were very common (Brasier, 1996).
Fig. 3.4: Beetle feeding galleries on Wych Elm trunk
Fig. 3.5: An infected English elm at West Point, NY, July 2010
DED is spread in North America by three species of bark beetles (Family: Curculionidae, Subfamily: Scolytinae):
ϭϴ0003 0003
x
The native elm bark beetle, Hylurgopinus rufipes.
x
The European elm bark beetle, Scolytus multistriatus.
x
The banded elm bark beetle, Scolytus schevyrewi.
In Europe, while S. multistriatus again acts as vector for infection, it is much less effective than the large elm bark beetle, S. scolytus. H. rufipes can be a vector for the disease, but is inefficient compared to the other vectors. S. schevyrewi was found in 2003 in Colorado and Utah. Pathogen Biology The Ophiostoma species that cause Dutch elm disease grow and reproduce only within elms. At times they are parasites, feeding on living tissue of the elm tree; at other times they are saprophytes, getting nourishment from dead elm tissue. Ophiostoma ulmi caused the original Dutch elm disease epidemic in Europe and North America in the mid-1900s. Ophiostoma novo-ulmi, an even more aggressive pathogen of elms, largely replaced O. ulmi during the second half of the 20th century. These fungi spread within stems and roots of living elms both by passive transport of spores and by mycelial growth of colonies initiated by spores that germinate in the xylem. The mycelium of these fungi is creamy white (Fig. 3.6) and is composed of septate hyphae with haploid nuclei.
Fig. 3.6
Asexual reproduction Ophiostoma ulmi and O. novo-ulmi have two asexual forms that produce asexual spores called conidia. In the xylem vessels of living elm trees, small, white, oval conidia (Fig. 3.7) are formed in clusters on short mycelial branches. These conidia are carried in ϭϵ0003 0003
the xylem vessels where they reproduce by budding, germinate to produce mycelium, and thus spread the disease throughout the tree.
Fig. 3.7
Fig. 3.8
In dying or recently dead trees, conidia (Fig. 3.8) are produced by mycelium growing in the bark and in tunnels created by beetles just under the bark. These sticky conidia are produced at the tips of 1-2 mm tall synnemata. Each synnema consists of hyphae fused to form an erect, dark stalk with a round, nearly colorless head of sticky spores. Beetle vectors carry the sticky spores to new elm trees. Sexual reproduction Based on the structures produced by their sexual stage, the Dutch elm disease pathogens are placed in the ascomycete genus Ophiostoma. When two mating types come in contact, ascospores are produced in spherical, black, long-necked perithecia (Fig. 3.9). Perithecia form in the bark, either singly or in groups. Ascospores are produced in asci that degenerate inside of the perithecia. The free ascospores are discharged at the opening of the perithecial neck where they accumulate in sticky droplets that may be disseminated by beetle vectors.
Fig. 3.90003
ϮϬ0003 0003
Disease Cycle and Epidemiology
Fig. 2.10
Disease cycle The Dutch elm disease pathogens overwinter in the bark and outer wood of dying or recently dead elm trees and in elm logs as mycelia and synnemata with conidia. The fungi are spread from these sites by their vectors - elm bark beetles (Fig. 3.11). Two beetle species spread the pathogens in North America: the smaller European elm bark beetle (Scolytus multistriatus) and the native elm bark beetle (Hylurgopinus rufipes). The adult female beetle bores through the bark of dead or dying elm trees and elm logs and creates a tunnel in the wood as she feeds. She lays eggs in the tunnel behind her. The eggs hatch into larvae (Fig. 3.12) that begin to feed, creating tunnels at right angles to the maternal tunnel.
Ϯϭ0003 0003
Fig. 3.11
Fig. 3.12
The resulting pattern of tunnels is called a gallery (Fig. 3.13). The larvae pupate and emerge through the bark as adults (Fig. 3.14). If the fungi are present in the tree or log, the emerging adults carry thousands of sticky conidia on their bodies.
Fig. 3.13
Fig. 3.14
Newly-emerged S. multistriatus adults feed in the twig crotches of elm branches (Fig. 3.15); newly emerged H. rufipes DGXOWV¶ tunnel in the bark of elm branches and trunks. As the beetles feed, fungal spores are deposited. The beetle vectors only feed on healthy elms for a few days. Then they fly to dying or recently dead elm trees or to freshly cut elm wood to feed, create galleries, and lay eggs. The spores dislodged from elm bark beetles in feeding wounds and tunnels germinate and produce mycelium that grows into the xylem. The mycelium produces millions of small, white, oval conidia that spread through the xylem sap.
ϮϮ0003 0003
Fig. 3.15
Fig. 3.16
The fungi also produce enzymes and probably toxins that degrade plant cell walls and kill xylem parenchyma cells. In addition, the fungi induce hormonal imbalance that leads to the formation of tyloses (Fig. 3.16), overgrowths of parenchyma cells that push into and block the water-conducting xylem cells. The blockage of the xylem by tyloses and gums (thought to be products of plant cell wall breakdown) causes one of the diagnostic symptoms of Dutch elm disease, wilting of leaves. The killing of xylem parenchyma cells causes another diagnostic symptom, brown discoloration just under the bark. Epidemiology ,QIHFWLRQV0003 WKDW0003 WDNH0003 SODFH0003 LQ0003 WKH0003 VSULQJ0003 RU0003 HDUO0003 VXPPHU0003 LQYROYH0003 ³VSULQJZRRG´0003 which has very long xylem vessels. In these vessels the fungi can spread rapidly throughout the tree, which then may die quickly. Later in the season, the fungi are UHVWULFWHG0003WR0003WKH0003PXFK0003VKRUWHU0003YHVVHOV0003RI0003WKH0003³VXPPHUZRRG000f´0003DQG0003WKH0003IXQJL0003VSUHDG0003PXFK0003 Ϯϯ0003 0003
more slowly in the tree. Localized infections often result, and the tree is likely to survive longer.
Fig. 3.17
Healthy elm trees can become infected by the feeding of spore-contaminated elm bark beetles or through the development of grafts between their roots and the roots of infected trees (Fig. 3.17). Trees infected via beetle vectors often first develop symptoms in an upper section of the crown, whereas trees infected via root grafts often first develop symptoms lower in the crown. When the fungi are introduced through a root graft, they can be quickly distributed throughout the tree in the vascular system, and the entire tree may soon wilt and die. Root grafts form naturally between closely spaced elm trees with intertwined roots. Large elms growing within 7 meters (20 feet) of each other have almost 100% chance of becoming infected through root grafts. The likelihood of spread is lower when the elms are at least 13 meters (40 feet) apart. The severity and rate of spread of Dutch elm disease depend on the species of the pathogen, how rapidly the elm bark beetles reproduce the level of susceptibility of the elm hosts, and the environment. Temperatures around 20°C (68°F) favor the formation of conidia, whereas perithecia are induced at temperatures of 8-10°C (46-50°F). In the absence of effective disease management, Dutch elm disease increases exponentially until an affected elm population is greatly depleted. Seedlings and many saplings escape and live long enough to reproduce, so even the most susceptible elm species have never been threatened with extinction by Dutch elm disease. Wild elm Ϯϰ0003 0003
populations in the eastern and Midwestern U.S. have increased in recent decades, and this increase has led to renewed prominence of Dutch elm disease in landscapes. Dutch Elm Management Cultural Strategies Today, some communities maintain active programs to manage Dutch elm disease because they have found that it is cheaper to manage the disease than to remove the large dead trees that it leaves behind. Some communities focus on cultural practices for disease management, including the avoidance of monocultures of elm trees, the removal of all dying or recently dead branches, trees, and cut wood (sanitation), and the breakage of root grafts between adjacent elms. To be successful, diligent inspection of all elm trees in an area several times each growing season is required. Wood must be burned, chipped or buried so that it cannot provide a home for beetle vectors (Fig. 3.18).
Fig. 3.18
Organized community sanitation programs can delay the loss of elms. It has been estimated that the time when half of the elm trees in an area have been lost can be delayed by between 7 and 30 years. If privately owned trees are included in a program of inspection and mandatory removal, the longer end of this range is more likely. At best, this is a delaying tactic in the battle against Dutch elm disease.
Ϯϱ0003 0003
Chemical Strategies In the past, insecticides were sprayed on elm trees in attempts to kill the beetle vectors of Dutch elm disease (Fig. 3.19). This management strategy was expensive, not very effective, and came under attack from people concerned about the impact of insecticide use on wildlife and people.
Fig. 3.19
Fig. 3.20
Fig. 3.21
More recently, fungicides have been injected into trees infected by or at risk of infection by the Dutch elm disease pathogens (Fig. 3.20). These systemic chemicals are most effective if they are used to prevent new infections or to prevent the movement of the fungi into parts of a tree that are not yet colonized. Several different fungicides have been used, but all are relatively expensive, and none is completely effective. For these reasons, chemical management of Dutch elm disease is commonly used only to protect elm trees of high value, such as those along the Mall in Washington, D.C. (Fig. 3.21) or large trees in the yards of well-maintained properties. Biological Strategies Because of the ban on the use of chemicals on street and park trees in the Netherlands, the University of Amsterdam developed a biological vaccine by the late 1980s. Dutch Trig is nonchemical and nontoxic, consisting of a suspension in distilled water of spores of a strain of the fungus Verticillium albo-atrum that has lost much of its pathogenic capabilities, injected in the elm in spring. The strain is believed to have enough pathogenicity left to induce an immune response in the elm, protecting it against Ϯϲ0003 0003
DED during one growing season. This is called induced resistance. Trials in the US most notably Denver Colorado showed that Dutch Trig had no effect on saving Elms and that the treated trees were made sick by the treatment. Preventive treatment is usually only justified when a tree has unusual symbolic value or occupies a particularly important place in the landscape. Breeding for resistance The long-term solution to Dutch elm disease lies in the development of diseaseresistant cultivars of elms. Several Asian elm species have moderate to high resistance, and breeding programs in both Europe and the U.S. have introduced resistance from these species into native elm species. Other programs have focused on identifying and cloning individual American elm specimens that have moderate resistance to Dutch elm disease. The American elm breeders also would like to maintain the elegant vase shape of the American elm - the quality that made it a highly desirable shade tree. As a result of decades of efforts by elm breeders, several hybrid and clonal elms are now available that has very good resistance to Dutch elm disease. Resistant trees Research to select resistant cultivars and varieties began in the Netherlands in 1928, followed by the USA in 1937. Initial efforts in the Netherlands involved crossing varieties of U. minor and U. glabra, but later included the Himalayan or Kashmir elm U. wallichiana as a source of antifungal genes. Early efforts in the USA involved the hybridization of the Siberian elm U. pumila with American red elm U. rubra to produce resistant trees. Resulting cultivars lacked the traditional shape and landscape value of the American elm; few were planted. In 2005, the National Elm Trial (USA) began a 10-year evaluation of 19 cultivars in plantings across the United States. The trees in the trial are exclusively American developments; no European cultivars have been included. Recent research in Sweden has established that early-flushing clones are less susceptible to DED owing to an asynchrony between DED susceptibility and infection.[29] Hybrid cultivars Ϯϳ0003 0003
Many attempts to breed disease resistant cultivar hybrids have usually involved a genetic contribution from Asian elm species which have demonstrable resistance to this fungal disease. Much of the early work was undertaken in the Netherlands. The Dutch research programme began in 1928, and ended after 64 years in 1992, during which time well over 1000 cultivars were raised and evaluated. The programme had three major successes: 'Columella', 'Nanguen' LUTÈCE, and 'Wanoux' VADA,[30] all found to have an extremely high resistance to the disease when inoculated with unnaturally large doses of the fungus. Only 'Columella' was released during the lifetime of the Dutch programme, in 1987; patents for the LUTÈCE and VADA clones were purchased by the French Institut National de la Recherche Agronomique (INRA), which subjected the trees to 20 years of field trials in the Bois de Vincennes, Paris, before releasing them to commerce in 2002 and 2006, respectively. The Conservation Foundation, conservationfoundation.co.uk, is currently running two elm programmes - the Great British Elm Experiment and Ulmus londinium, an elm programme for London. These build on earlier elm projects in the past 30 years and both use saplings grown from mature parent elms found growing in the British countryside and cultivated through micro-propagation. The parent trees are monitored for Dutch elm disease. Saplings are offered free to schools and community groups, who are asked to monitor their tree's progress on the Foundation's online elm map. Elms are available at a small price to others who don't qualify for a free tree. In London, places with 'elm' in their name are offered a sapling. This is an experiment with the aim of finding over time why some elms have survived while others succumbed to Dutch elm disease. Asian species to feature in the American DED research programs were the Siberian elm U. pumila, Japanese elm U. davidiana var. japonica, and the Chinese elm U. parvifolia, giving rise to several dozen hybrid cultivars resistant not just to DED, but also to the extreme cold of Asian winters. Among the most widely planted of these, both in North America and in Europe are 'Sapporo Autumn Gold' and 'New Horizon'. Some hybrid cultivars, such as 'Regal', are the product of both Dutch and American research. Hybridization experiments using the slippery or red elm U. rubraresulted in the release of 'Coolshade' and 'Rosehill' in the 1940s and 50s. The species last featured in
Ϯϴ0003 0003
hybridization as the female parent of 'Repura' and 'Revera', both patented in 1993, although neither has yet appeared in commerce. In Italy, research is continuing at the Istituto per la Protezione delle Piante, Florence, to produce a range of disease-resistant trees adapted to the warmer Mediterranean climate, using a variety of Asiatic species crossed with the early Dutch hybrid 'Plantyn' as a safeguard against any future mutation of the disease (Santini et al. 2004). Two trees with very high levels of resistance, 'San Zanobi' and'Plinio' (Santini et al. 2002), were released in 2003. 'Arno' and 'Fiorente' were patented in 2006 and will enter commerce in 2012. All four have the Siberian elm U. pumila as a parent, the source of disease-resistance and drought-tolerance genes. Further releases are planned, notably of a clone derived from a crossing of Dutch elm Ulmus × hollandica with the Chinese species U. chenmoui. Species and species cultivars North America Ten resistant American elm U. americana cultivars are now in commerce in North America, but only two ('Princeton' and 'Valley Forge') are currently available in Europe. No cultivar is 'immune' to DED; even highly resistant cultivars can become infected, particularly if already stressed by drought or other environmental conditions where the disease prevalence is high. With the exception of 'Princeton', no trees have yet been grown to maturity. Trees cannot be said to be mature until they have reached an age of 60 years. Notable cultivars include: x
'Princeton', is a cultivar selected in 1922 by Princeton Nurseries for its landscape merit. By happy coincidence, this cultivar was found to be highly resistant in inoculation studies carried out by the USDA in the early 1990s. As trees planted in the 1920s still survive, the properties of the mature plant are well known.
x
'American Liberty', is, in fact, a set of six cultivars of moderate to high resistance produced through selection over several generations starting in the 1970s. Although 'American Liberty' is marketed as a single variety, nurseries selling the 'Liberty Elm' Ϯϵ0003
0003
actually distribute the six cultivars at random and thus, unfortunately, the resistance of any particular tree cannot be known. One of the cultivars, 'Independence', is covered by patent (U. S. Plant patent 6227). The oldest 'American Liberty' elm was planted in about 1980. x
'Valley Forge', released in 1995, has demonstrated the highest resistance of all the clones to Dutch elm disease in controlled USDA tests.
x
'Lewis and Clark' (Prairie Expedition TM ), released in 2004, was cloned from a tree found growing in North Dakota which had survived unscathed when all around had succumbed to disease. In 2007, the Elm Recovery Project from the University of Guelph in Ontario,
Canada reported that cuttings from healthy surviving old elms surveyed across Ontario had been grown to produce a bank of resistant trees, isolated for selective breeding of highly resistant cultivars. The University of Minnesota USA is testing various elms, including a huge nowpatented century-old survivor known as 'The St. Croix Elm', which is located in a Minneapolis-St. Paul, MN suburb (Afton) in the St. Croix River valley ² a designated National Scenic River way. The slippery or red elm U. rubra is marginally less susceptible to Dutch elm disease than the other American species, but this quality seems to have been largely ignored in American research. No cultivars were ever selected; although the tree was used in hybridization experiments (see above). Europe Among European species, there is the unique example of the European white elm U. laevis, which has little innate resistance to DED, but is eschewed by the vector bark beetles and only rarely becomes infected. Recent research has indicated it is the presence of certain organic compounds, such as triterpenes and sterols, which serves to make the tree bark unattractive to the beetle species that spread the disease (MartínBenito et al. 2005).
ϯϬ0003 0003
In 2001, English elm U. procera was genetically engineered to resist disease, in experiments at Abertay University, Dundee, Scotland, by transferring antifungal genes into the elm genome using minute DNA-coated ball bearings. However, owing to the hostility to GM developments, there are no plans to release the trees into the countryside. The spread of DED to Scotland has revealed a number of Wych elms U. glabra apparently surviving there unscathed, prompting the Royal Botanic Garden Edinburgh to clone the trees and inoculate them with the fungus to determine any innate resistance (2010) (Coleman, 2009). A similar programme in Europe, testing clones of surviving Field Elms for innate resistance, has been carried out since the 1990s by national research institutes, with findings centrally assessed and published. In the UK, clones from one of the elms that have so far survived in an area of high infectivity are now available commercially. Mr Paul King of King&Co The Tree Nursery took cuttings from an elm, thought to be nearly 200 years old, located in Essex (probably Ulmus minor subsp. minor, or a local hybrid), in 1990. Having potted the cuttings and found that the trees had indeed a high level of resistance to DED, Mr King then cultivated these cuttings via micro-propagation and now has over 2000 resistant trees for sale to the general public at around 10 foot tall. Historical Significance The first North American Dutch elm disease epidemic began when Ophiostoma ulmi was introduced in the 1920s by furniture makers who used imported European elm logs to make veneer for cabinets and tables. Some of the beetle vectors of the Dutch elm disease pathogens also were brought here from Europe, years before the fungi were introduced. When the more aggressive pathogen, O. novo-ulmi, was later introduced in North America, it killed many elms that had survived the original epidemic. Dutch elm disease epidemics that resulted from movement of Ophiostoma species between and across continents vividly illustrate the dangers inherent in our movement of plant material around the world. A Dutch scientist, Marie Beatrice Schwarz, is credited with first identifying the causal agent of what was to become known as Dutch elm disease. Another Dutch ϯϭ0003 0003
scientist, Christine Johanna Buisman, who had seen the disease in her homeland, first identified Dutch elm disease in Ohio in 1930. The disease spread up and down the U.S. East Coast and west across the continent, reaching the West Coast in 1973. Over 40 million American elm trees have been killed by this disease, and today it is still a very destructive disease of shade trees in the U.S. Many of the elm trees in North America and Europe were planted in rows along streets and walkways, or in hedgerows, or on dikes. The elm trees made effective windbreaks (Fig. 3.22), and the large, overarching branches created beautiful shady canopies (Fig. 3.23). These dense plantings of elm trees are examples of monocultures.
Fig. 3.22
Fig. 3.23
Monocultures are created when plants of the same species are grown in close proximity, with few other types of plants present. People have planted monocultures for hundreds of years and there are many reasons why monocultures are desirable. Monocultures provide uniformity, which is desirable both for aesthetic reasons and for production practices. Planting, management, and harvest are all simpler when one kind of plant is grown in an area. Dangers, however, are inherent in monocultures. Because all of the plants in a monoculture are very much alike, they are all subject to the same catastrophic problems. A disease, insect or weather condition that harms one plant is likely to harm them all. Monoculture is the main reason why Dutch elm disease has been so devastating in our towns and cities. The pathogens can move between closely spaced trees via insect vectors ϯϮ0003 0003
or root grafts, leaving devastation in their wake. The Dutch elm disease epidemics illustrate the value of diversity in plant populations.
ϯϯ0003 0003
Hosts Lethal Yellowing (LY) is a phytoplasma disease that attacks many species of palms, including some commercially important species such as the Coconut0003 and Date Palm. It is spread by the planthopper Haplaxius crudus (former name Myndus crudus) which is native to Florida, parts of the Caribbean and Central America. Infected plants will normally die in 3 to 6 months. The only effective cure is prevention, i.e. planting resistant varieties of coconut palm and preventing a park or 'golf course like' environments which attracts the planthopper. Some cultivars, such as the Jamaica Tall coconut cultivar nearly died out by lethal yellowing. Heavy turf grasses and similar green ground cover will attract the planthopper to lay its eggs and the nymphs develop at the roots of these grasses. The planthpoppers eggs and nymphs may pose a great threat to coconut growing countries' economies, into which grass seeds for golf courses and lawns are imported from the Americas. It is not clearly understood how the disease was spread to East Africa as the planthopper Haplaxius crudus is not native in East Africa.
Fig. 4.2: Coconut palms with various symptoms of LY.
Fig. 4.3: Coconut grove in Ghana badly affected by LY.
The only explanation is that it was imported with grass seed from Florida that were used to create golf courses and lawns in beach resorts. There is a direct connection between green lawns and the spread of lethal yellowing in Florida. Even so-called ϯϱ0003 0003
'resistant cultivars' such as the Malayan Dwarf or the Maypan hybrid between that dwarf and the Panama Tall were never claimed to have 100% immunity. The nymphs of the planthoppers develop on roots of grasses, hence the areas of grass in the vicinity of palm trees is connected with the spread of this phytoplasma disease. The problem arose as a direct result of using coconut and date palms for ornamental and landscaping purposes in lawns, golf courses and gardens together with these grasses. When these two important food palms were grown in traditional ways (without grasses) in plantations and along the shores, the palm grooves weren't noticeably affected by lethal yellowing. There is no evidence that disease can be spread when instruments used to cut an infected palm are then used to cut or trim a healthy one. Seed transmission has never been demonstrated, although the phytoplasma can be found in coconut seednuts, but phytosanitary quarantine procedures that prevent movement of coconut seed, seedlings and mature palms out of an LY epidemic area should be applied to grasses and other plants that may be carrying infected vectors.
Symptoms In general, an early symptom is the drying up of developing inflorescences. In coconut palms the spathes enclosing the flowers become discoloured and the tips blacken. The youngest leaves next to the buds show water- soaked streaks which spread until there is a terminal rot of the growing point. After the first symptoms there is a progressive leaf discoloration, beginning with the older leaves and spreading rapidly to the younger ones. The foliage turns light-yellow and eventually orange-yellow. This symptom coincides with the death of root tips. Death occurs in C. nucifera about 4 months after the initial symptoms appear. For the coconut palm, the progressive symptoms of LY are mainly the following (Dollet, et al. 1977): 1. premature drop of most of the fruit regardless of their development stage 2. blackening of newly opened inflorescences 3. ascending yellowing of the leaves (from the lower to the upper) 4. spear leaf death and collapse, with possibly a few green leaves remaining ϯϲ0003 0003
5. IDOO0003RI0003WKH0003ZKROH0003FURZQ000f0003OHDYLQJ0003D0003EDUH0003WUXQN0003RU0003µWHOHSKRQH0003SROH¶ Infected palms usually die within 3 to 7 months after the appearance of the first symptom (Mc Coy, 1983). No single symptom is diagnostic of lethal yellowing. Symptoms are variable among palm genera and, in the case of coconuts, among cultivars. It is the pattern of appearance and chronological progression of symptoms that accurately identifies the disease. Confirmation of lethal yellowing is based on a molecular diagnostic assay using the polymerase chain reaction (PCR). At least 36 palm species (Table 1) have been documented as susceptible to lethal yellowing, but coconut palm (Cocos nucifera) is most vulnerable to the disease, followed by Pritchardia species, Christmas palm (Adonidia merrillii), and date palm (Phoenix dactylifera). Table 1. Palm species susceptible to lethal yellowing disease. Adonidia merrillii
Dictyosperma album
Phoenix dactylifera
Aiphanes lindeniana
Dypsis cabadae
Phoenix reclinata
Allagoptera arenaria
Dypsis decaryi
Phoenix rupicola
Arenga engleri
Gaussia attenuata
Phoenix sylvestris
Borassus flabellifer
Howea belmoreana
Pritchardia affinis
Caryota mitis
Howea forsteriana
Pritchardia pacifica
Caryota rumphiana
Hyophorbe verschaffeltii
Pritchardia remota
Chelyocarpus chuco
Latania lontaroides
Pritchardia thurstonii
Cocos nucifera
Livistona chinensis
Ravenea hildebrantii
Corypha utan
Livistona rotundifolia
Syagrus schizophylla
Crysophila warsecewiczii
Nannorrhops ritchiana
Trachycarpus fortunei
Cyphophoenix nucele
Phoenix canariensis
Veitchia arecina
The first obvious symptom on mature palms (those able to produce fruit) is a premature drop of most or all fruits. For coconuts, the calyx end of the nut (fruit) will usually develop a brown to black, water-soaked appearance (Figure 1).
ϯϳ0003 0003
Nut or fruit-fall is accompanied or followed by flower necrosis. This symptom is most readily observed on newly mature flowers as they emerge from the spathe (Figure 2). Male flowers abscise, and no fruit is set.
Fig. 4.4
Fig. 4.5
The next symptom observed on mature palms (the first symptom for immature palms or non-fruit bearing palms) is foliar discoloration. This symptom varies markedly among coconut cultivars and other palm genera. For tall-WSH0003 FRFRQXW0003 FXOWLYDUV0003 H0011J0011000f0003 µ-DPDLFD0003 7DOO¶ 000f0003 WKH0003 IROLDJH0003 WXUQV0003 yellow, beginning with the lowermost (oldest) leaves and progressing until the entire crown is affected (Fig. 4.6). In some cases, this symptom is first seen as a VROLWDU000f0003 HOORZHG0003 OHDI0003 ³IODJ0003 OHDI´ 0003 LQ0003 WKH0003 PLGdle of the leaf canopy (Fig. 4.7). Typically, yellowed leaves remain turgid, but eventually turn brown, desiccate, and hang down to form a skirt around the trunk for several weeks before falling. As leaf yellowing advances, the spear (youngest) leaf collapses and hangs down in the crown. Death of the apical meristem (bud) usually occurs when one-half to two-thirds of the crown has yellowed. Eventually, the entire crown of the palm ϯϴ0003 0003
withers and topples, leaving a bare trunk standing (Fig. 4.8). Infected palms usually die within 3 to 5 months after the first appearance of symptoms.
Fig. 4.6
Fig. 4.7
Fig. 4.8
ϯϵ0003 0003
For dwarf-WSH0003FRFRQXW0003FXOWLYDUV0003000bH0011J0011000f0003µ0DODDQ0003*UHHQ0003'ZDUI¶ 000f0003OHDYHV0003JHQHUDOO0003 turn reddish to grayish-brown rather than yellow (Fig. 4.9). Leaflets on the green form of the Malayan Dwarf cultivar may be folded around the midvein (Fig. 4.10). Sometimes, affected leaves appear flaccid, giving an overall wilted appearance to the palm canopy.
Fig. 4.9
Fig. 4.10
Foliar yellowing also develops on Caryota mitis (clustering fishtail palm), C.
rumphiana,
album (hurricane
or
Chelyocarpus princess
chuco, Corypha
palm), Livistona
utan, Dictyosperma
chinensis (Chinese
fan
palm), Pritchardia spp., and Trachycarpus fortunei (windmill palm). In contrast, successively younger leaves turn varying shades of reddish-brown to dark brown or gray in other palm species, such as Adonidia merrillii (Christmas palm), Borassus
flabellifer(palmyra
palm), Dypsis
cabadae (cabada
palm), Phoenix spp. (date palm, Canary Island date palm, wild date palm), and Veitchia arecina (Montgomery palm). Differences may occur in the stage at which spear leaf collapse and necrosis appears on these species. For date palms and palmyra palm, death of the spear leaf often precedes foliar discoloration. For Adonidia andVeitchia spp., the spear leaf is usually not affected until after all other leaves have died. ϰϬ0003 0003
Pathogen Typical phytoplasma particles were found in sieve tubes of infected plants. They were ovoid, elongated and filamentous in shape and were bounded by a triple-layered structure comprising two electron-dense layers with a transparent layer between (Plavsic-Banjac et al., 1972). Pathogen Biology Lethal yellowing is caused by a phytoplasma, a cell wall-less bacterium that belongs to the class Mollicutes. The phytoplasma has been classified as a member of group 16S rDNA RFLP group 16SrIV, subgroup A (16SrIV-A). The proposed name IRU0003WKH0003SDWKRJHQ0003LV0003µCandidatus 3KWRSODVPD0003SDOPDH0011¶ The phytoplasma, which is not culturable, is found only in the phloem of host plants. When observed in phloem sieve elements by electron microscopy, the shape of phytoplasma cells varies from bead-like to filamentous (Fig. 4.11). Nonfilamentous forms average 295 nm in diameter and filamentous forms average 142 nm in diameter and at least 16 µm in length. Each phytoplasma cell is enclosed by a trilaminar unit membrane and contains cytoplasm with DNA strands and ribosomes.
Fig. 4.11
ϰϭ0003 0003
Molecular studies have determined that the lethal yellowing phytoplasma exists as a group of nearly identical strains in the western Caribbean region. Collectively, these strains are phylogenetically distinct from phytoplasmas that infect coconut in Africa or southeast Asia. The lethal yellowing phytoplasma is most closely related to, but distinct from, phytoplasmas associated with decline-type diseases of the monocot Carludovica palmata (Cyclanthaceae) in Yucatán, Mexico, Phoenix canariensis (Canary Island date palm) in the Corpus Christi area of southern Texas (United States), and phytoplasmas causing a newly recognized coconut leaf yellowing syndrome in southwestern Mexico. Insect Vector The pre-imaginal stages of M. crudus are subterranean, feeding on grass roots. They have been described by Wilson & Tsai (1982). The head and thorax of the adults are pale-brown; the forewings are hyaline with pale or light-brown veins. Males and females are 4.2-5.1 mm long. Characters of the male genitalia are essential for the specific identification (Kramer, 1979). In particular, the aedeagus is distinct. In left lateral view it has a long process originating in the distal half and directed ventrally and towards the head. 0003 Means of Movement and Dispersal Natural spread results from the movement of the vector M. crudus. Infected vegetative plant material, including ornamental species, could carry the pathogen in international trade. The vector is less likely to be carried by palms, which are infested only by the actively mobile adults. Since vector efficiency is said to be low, the probability of international movement of the phytoplasma in the vector may be correspondingly low. M. crudus itself could possibly be moved in international trade as nymphs in soil accompanying palms, but would not then be infected by the phytoplasma.
Disease Cycle and Epidemiology Experimental evidence implicates the planthopper Myndus crudus as a vector of the lethal yellowing phytoplasma (Fig. 4.12). The planthopper is an insect with piercing
ϰϮ0003 0003
and sucking mouthparts, and feeds on the contents of the plant host vascular system. The insect spreads the phytoplasma during feeding activity as it moves from palm to palm. The phytoplasma is not known to survive outside either its plant or insect hosts. The geographic range of lethal yellowing is limited in the United States to the subtropical southern third of Florida because the planthopper is not considered cold hardy.
Fig. 4.12
Inoculation of a susceptible plant initiates infection that is followed by a prolonged latent (incubation) phase estimated between 112 to 262 days. About 80 days prior to symptom appearance, the growth of infected palms is stimulated. This is followed by a period of gradual decline, and growth ceases about 1 month before the end of the incubation phase. Following an initial disease outbreak, further spread of lethal yellowing is characteUL]HG0003E0003D0003³MXPS-VSUHDG´0003SDWWHUQ000f0003LQGLFDWLQJ0003GLVVHPLQDWLRQ0003LQYROYLQJ0003DQ0003DLUERUQH0003 vector. Spread occurs among susceptible palms within a localized area, resulting in a random pattern around an active focus of disease that eventually claims most susceptible palms within the locality. Beyond this primary focus, further spread may occur in jumps of a few to 100 km or more, thus establishing new disease foci. Differences in the rates of spread of lethal yellowing at different geographical locations have also been noted. In Florida (United States), spread of the disease from the cities of Miami to Palm Beach, a distance of about 128 km, occurred within 3 years. In Jamaica, however, movement of ϰϯ0003 0003
the disease from the west to the east end of the island, a distance of approximately 238 km, took about 60 years.
Disease Management To discourage the spread of lethal yellowing in the tropics, commercial movement of living palms from locations affected by lethal yellowing to disease-free areas is generally not permitted. However, quarantine requirements vary according to the specific geographical areas involved. Technical guidelines for the safe movement of coconut germplasm have been developed under the auspices of the FAO International Board for Plant Genetic Resources. Chemical control of lethal yellowing is accomplished with the antibiotic oxytetracycline HCl (Terramycin), which is administered to palms as a liquid injection into the trunk. As a therapeutic measure, systemic treatment on a 4-month treatment schedule should begin as early as possible after the onset of symptoms. Palms with >25% discolored leaves should be removed, since they are unlikely to respond to Terramycin treatment. The antibiotic can also be used preventively to protect palms when lethal yellowing is known to occur in the area. The dosage recommended depends on the size of the treated palm. The approximate cost of Terramycin ranges from $1.50 to $4.00 per palm per treatment, depending on the number of palms treated. Control of planthopper populations with insecticides is currently insufficient to justify repeated applications in landscapes or palm plantations. Use of host resistance represents the most practical long-term tool for managing lethal yellowing. Many palm species are not susceptible to lethal yellowing and provide important alternative choices for ornamental landscape plantings. To date, lethal yellowing has not been reported on most palm species native to Florida and the Caribbean Basin. These include Sabal palmetto (cabbage palm),Roystonea regia (royal palm), Acoelorrhaphe wrightii (Paurotis or Everglades palm), and Thrinaxspecies (thatch palms). On the other hand, Cocos nucifera (coconut), Pritchardia spp., Adonidia merrillii (Christmas palm), and Phoenix dactylifera (date palm) have sustained consistent ϰϰ0003 0003
losses and are not recommended for widespread landscape use in areas where lethal yellowing occurs. &RFRQXW0003 FXOWLYDUV000f0003 VXFK0003 DV0003 WKH0003 µ0DODDQ0003 'ZDUI¶0003 RU0003 KEULG0003 µ0D3DQ¶0003 µ0DODDQ0003 'ZDUI¶0003 [0003 µ3DQDPD0003 7DOO¶ 000f0003 KDYH0003 H[KLELWHG0003 DFFHSWDEOH0003 OHYHOV0003 RI0003 UHsistance in most areas. +RZHYHU000f0003UHFHQW0003UHSRUWV0003RI0003OHWKDO0003HOORZLQJ0003ORVVHV0003LQ0003µ0DODDQ0003'ZDUI¶0003DQG0003µ0D3DQ¶0003RI0003 70% and 83%, respectively, at localized sites in southeastern Florida and 95 to 99% in Jamaica cast doubt on the long-term resistance of these cultivars. Significance While coconut palm is highly valued as a woody ornamental plant in the United States, it is an important subsistence crop in the coastal tropics. Almost all parts of the coconut palm are used, providing food, drink, fuel, shelter, and cash income for producers. The term lethal yellowing (often shortened to LY) was first used in the mid1950s to describe a fatal disease of unknown etiology that had affected coconuts in western Jamaica since the 1800s. During the last four decades, outbreaks of lethal yellowing disease have killed most of the once prevalent tall-type coconut cultivars in both Jamaica and Florida (United States). The disease has also been reported from the Bahamas, Belize, the Cayman Islands, Cuba, Dominican Republic, Guatemala, Haiti, Honduras, Leeward Islands (Nevis), and southern Mexico (Yucatan peninsula). Recurrent coconut diseases that resemble lethal yellowing have been recorded elsewhere in the tropics under a variety of names depending on location. Collectively refeUUHG0003 WR0003 DV0003 ³OHWKDO0003 HOORZLQJ-WSH0003 GLVHDVHV000f´0003 WKH0003 LQFOXGH0003 $ZND0003 ZLOW0003 1LJHULD 000f0003 &DSH0003 St. Paul wilt (Ghana), Kaïncopé (Togo), and Kribi (Cameroon) in West Africa; lethal disease (Kenya, Tanzania and Mozambique) in East Africa; and Kalimantan wilt (Central Kalimantan), Natuna wilt (Natuna Islands), and Malaysian wilt (Peninsula Malaysia) in South East Asia.
ϰϱ0003 0003
huckleberry (Vaccinium ovatum), bay laurel (Umbellularia californica), madrone (Arbutus menziesii), bigleaf maple (Acer macrophyllum), manzanita (Arctostaphylos manzanita), and California buckeye (Aesculus californica). On these hosts the fungus causes leaf spot and twig dieback. As of January 2002, the disease was known to occur only in California and southwestern Oregon; however, transporting infected hosts may spread the disease. The pathogen has the potential to infect oaks and other trees and shrubs elsewhere in the United States. Limited tests show that many oaks are susceptible to the fungus, including northern red oak and pin oak, which are highly susceptible. Symptoms
Fig. 5.2: Leaf death caused by P. ramorum
In tanoaks, the disease may be recognized by wilting new shoots, older leaves becoming pale green, and after a period of two to three weeks, foliage turns brown while clinging to the branches. Dark brown sap may stain the lower trunk's bark. Bark may split and exude gum, with visible discoloration. Necrotic bark tissues surrounded by black zone lines are usually present under affected bark. After the tree dies back, suckers will try to sprout the next year, but their tips soon bend and die. Ambrosia beetles (Monarthrum scutellare) will most likely infest a dying tree during midsummer, producing
piles
of
fine
white
dust
near
tiny
holes.
Later, bark
beetles
(Pseudopityophthorus pubipennis) produce fine red boring dust. Small black domes, the fruiting bodies of the Hypoxylon fungus, may also be present on the bark. Leaf death may
ϰϳ0003 0003
occur more than a year after the initial infection and months after the tree has been girdled by beetles. In Coast Live Oaks and Californian Black Oaks, the first symptom is a burgundy-red to tar-black thick sap bleeding from the bark surface. These are often referred to as bleeding cankers.
Fig. 5.3
Fig. 5.4 Pathogen Sudden
oak
death is
the
common
name
of
a
disease
caused
by
the oomycete plant pathogen Phytophthora ramorum. P. ramorum was first reported in 1995, and the origins of the pathogen are still unclear but most evidence suggests it was repeatedly introduced as an exotic species (Grünwald, et al. 2012). Very few control mechanisms exist for the disease, and they rely upon early detection and proper disposal of infected plant material. ϰϴ0003 0003
The Two Mating Types
Fig. 4.5: Mating Structures
P. ramorum is heterothallic and has two mating types A1 and A2 required for sexual reproduction (Boutet, et al. 2010). Interestingly, the European population is predominantly A1 while both mating types A1 and A2 are found in North America (Grünwald, et al. 2008). Genetics of the two isolates indicate that they are reproductively isolated (Ivors, et al. 2004). On average the A1 mating type is more virulent than the A2 mating type but there is more variation in the pathogenicity of A2 isolates (Brasier, et al. 2002). It is currently not clear whether this pathogen can reproduce sexually in nature and genetic work has suggested that the lineages of the two mating types might be isolated reproductively or geographically given the evolutionary divergence observed (Grünwald and Goss, 2011). Transmisson P. ramorum produces both resting spores (chlamydospores) and zoospores, which have flagella enabling swimming. P. ramorum is spread by air; one of the major mechanisms of dispersal is rainwater splashing spores onto other susceptible plants, and into watercourses to be carried for greater distances. Chlamydospores can withstand harsh conditions and are able to overwinter (Davidson, et al. 2001). The pathogen will take advantage of wounding, but it is not necessary for infection to occur (Anon, 2005).
ϰϵ0003 0003
As mentioned above, P. ramorum does not kill every plant that can be used as a host, and it is these plants that are most important in the epidemiology of the disease as they act as sources of inoculum (Garbelotto, et al. 2003). In the USA bay laurel seems to be the main source of inoculum in forests. Green waste, such as leaf litter and tree stumps are also capable of supporting P. ramorum as a saprotroph and acting as a source of inoculum. Because P. ramorum is able to infect many ornamental plants, it can be transmitted by ornamental plant movement.
Oak Wilt
Oak wilt is an aggressive fungus disease caused by Ceratocystis fagacearum. It is one of the most serious diseases in the Eastern United States, killing thousands of oak trees in forests, woodlots, and home landscapes. Susceptible hosts include most oaks in the red oak group and Texas live oak. Symptoms include wilting and discoloration of the foliage, premature leaf drop, and rapid death of the tree within days or weeks of the first symptoms. Trees become infected with oak wilt in two ways: through connections between root systems of adjacent trees, and through insects that carry the fungus to other trees that have been wounded.
Similarities: Oak wilt can also kill trees very quickly, especially if infection begins through root grafts. Differences: The oak wilt pathogen does not cause cankers on the stems, and no bleeding is associated with this disease. Dark staining may be evident
ϱϬ0003 0003
under the bark of trees with oak wilt, but there are no conspicuous zone lines. Oak wilt typically causes red oak leaves to turn brown around the edges while the veins remain green. Leaves are rapidly shed as the tree dies. Conversely, in live oak with the sudden oak death pathogen, the veins first turn yellow and eventually turn brown. Leaves are often retained on the tree after it dies. Oak Decline
Oak decline is a slowacting disease complex that
can
kill
physiologically
mature
trees in the upper canopy. Decline
results
from
interactions of multiple stresses,
such
as
prolonged drought and spring defoliation by late frost
or
insects,
opportunistic root disease fungi such as Armillaria mellea, and inner-barkboring insects such as the two lined chestnut borer and
red
oak
borer.
Progressive dieback of the crown is the main symptom of oak decline and is an expression of an impaired root system. This disease can kill susceptible oaks within 3-5 years of the onset of crown symptoms. Oak decline occurs throughout the range of eastern hardwood forests, but is particularly common in the Southern Appalachian Mountains in North Carolina, Tennessee, and Virginia, as well as the Ozark Mountains in Arkansas and Missouri. ϱϭ0003 0003
Similarities: Oak decline can cause death of many oaks on a landscape scale. Moist, dark stains may be present on the trunk of trees affected by oak decline. Differences: Oak decline shows evidence that dieback has occurred over several years from the top down and outside inward. Newly killed branches with twigs attached are usually found in the same crown as those in a more advanced state of deterioration killed years before. Dieback associated with sudden oak death occurs over a growing season or two. The inner bark beneath the dark stain associated with stem-boring-insect attacks has a discrete margin with no zone lines or evidence of canker development beyond the attack site. Red Oak Borer
Red
oak
borer
(Enaphalodes
rufulus (Haldeman)) attacks oaks of both red and white groups throughout the eastern United States, but prefers members of the red oak group; however, it does not kill trees. Outbreaks are associated with stressed trees that eventually die from oak decline. The complete life cycle takes 2 years. Adults are 1-1.5 inches long with antennae one to two times as long as the body. Larvae are the damaging life stage. Adult females lay eggs in mid-summer in refuges in the crevices of the bark. Newly hatched larvae bore into the phloem, where they mine an irregular burrow 0.5-1 inch in diameter before fall. In spring and summer of the second year, dark, moist stains and fine, granular frass ϱϮ0003 0003
may be seen on the trunk. Exposure of the inner bark reveals the frass-packed burrow and the larva, if it has not bored more deeply into the wood to complete development. Mature larvae are stout, round-headed grubs about 2 inches long before they pupate deep in the wood.
Similarities: Moist, dark stains and fine frass may be present at sites of red oak borer attack. Differences: With red oak borer the inner bark beneath the dark stain contains a frass-packed burrow and has a discrete margin with no zone lines or evidence of canker development beyond it. Disease Management Early detection Early detection of P. ramorum is essential for its control. On an individualtree basis, preventative treatments, which are more effective than therapeutic treatments (Garbelotto, et al. 2007), GHSHQG0003 RQ0003 NQRZOHGJH0003 RI0003 WKH0003 SDWKRJHQ¶V0003 movement through the landscape to know when it is nearing prized trees. On the landscape level, 300110003UDPRUXP¶V fast and often undetectable movement means that any treatment hoping to slow its spread must happen very early in the development of an infestation. Since 300110003 UDPRUXP¶V discovery, researchers have been working on the development of early detection methods on scales ranging from diagnosis in individual infected plants to landscape-level detection efforts involving large numbers of people. Detecting
the
presence
of Phytophthora species
requires
laboratory
confirmation. The traditional method of culturing is on a growth medium that is selective against fungi (and, in some cases, against other oomycetes such as Pythium species). Host material is removed from the leading edge of a plant tissue canker caused by the pathogen; resulting growth is examined under a microscope to confirm the unique morphology of P. ramorum. Successful isolation of the pathogen often depends on the type of host tissue and the time of year that detection is attempted (Kliejunas, 2007a).
ϱϯ0003 0003
Because of these difficulties, researchers have developed some other approaches for identifying P. ramorum. The ELISA (enzyme-linked immunosorbent assay) test can be the first step in non-culture methods of identifying P. ramorum, but it can only be a first step, because it detects the presence of proteins that are produced by
all Phytophthora species.
In
other
words,
it
can
identify
to
the Phytophthora genus level, but not to the species level. ELISA tests can process large numbers of samples at once, so researchers often use it to screen out samples that are likely positive from those that are not when the total number of samples is very large (Kliejunas, 2007a). Some manufacturers produce small-VFDOH0003(/,6$0003³ILHOG0003 NLWV´0003 WKDW0003 WKH0003 KRPHRZQHU0003 FDQ0003 XVH0003 WR0003 GHWHUPLne if plant tissue is infected by Phytophthora. Researchers have also developed numerous molecular techniques for P. ramorum identification. These include amplifying DNA sequences in the internal transcribed spacer region
of the P. ramorum genome (ITS Polymerase Chain
Reaction, or ITS PCR); real-time PCR, in which DNA abundance is measured in real time during the PCR reaction, using dyes or probes such as SBYR-Green or TaqMan; multiplex PCR, which amplifies more than one region of DNA at the same time; and Single Strand Conformation Polymorphism (SSCP), which uses the ITS DNA sequence amplified by the PCR reaction to differentiate Phytophthora species according to their differential movement through a gel (Kliejunas, 2007a). Additionally, researchers have begun using features of the DNA sequence of P. ramorum to pinpoint the minuscule differences of separate P. ramorum isolates from each other. Two techniques for doing this are amplified fragment length polymorphism, which through comparing differences between various fragments in the sequence has enabled researchers to differentiate correctly between EU and U.S. isolates, and the examination of microsatellites, which are areas on the sequence featuring repeating base pairs. When P. ramorum propagules arrive in a new geographic location and establish colonies, these microsatellites begin to display mutation in a relatively short time, and they mutate in a stepwise fashion. Based on this, researchers in California have been able to construct trees, based on microsatellite analyses of isolates collected from around the state, that trace the ϱϰ0003 0003
movement of P. ramorum from two likely initial points of establishment in Marin andSanta Cruz counties and out to subsequent points (Mascheretti, et al. 2008). Early detection of P. ramorum on a landscape scale begins with the observation
of
symptoms
on
individual
plants
(and/or
detecting P.
ramorum propagules in watercourses). Systematic ground-based monitoring has been difficult within the range of P. ramorum because most infected trees stand on a complex mosaic of lands with various ownerships. In some areas, targeted groundbased surveys have been conducted in areas of heavy recreation or visitor use such as parks, trailheads, and boat ramps. In California, when conducting ground-based detection, looking for symptoms on bay laurel is the most effective strategy, since P. ramorum infection of true oaks and tanoaks is almost always highly associated with bay laurel, the main epidemiological springboard for the pathogen (Davidson, et al. 2001; Davidson and Shaw, 2003; Maloney, et al. 2005). Moreover, on many sites in California (though not all), P. ramorum can typically be detected from infected bay laurel tissues via culturing techniques year-round; this is not the case for most other hosts, nor is it the case in Oregon, where tanoak is the most reliable host. As part of a nationwide USDA program, a ground-based detection survey was implemented from 2003 to 2006 in thirty-nine U.S. states to determine whether the pathogen was established outside the West Coast areas already known to be infested. Sampling areas were stratified by environmental variables likely to be conducive to pathogen growth and by proximity to possible points of inoculum introduction such as nurseries. Samples were collected along transects established in potentially susceptible forests or outside the perimeters of nurseries. The only positive samples were collected in California, confirming that P. ramorum was not yet established in the environment outside the West Coast (Oak, et al. 2008). Aerial surveying has proven useful for detection of P. ramorum infestations DFURVV0003 ODUJH0003 ODQGVFDSHV000f0003 DOWKRXJK0003 LW0003 LV0003 QRW0003 DV0003 ³HDUO´0003 D0003 WHFKQLTXH0003 DV0003 VRPH0003 RWKHUV0003 because it depends on spotting dead tanoak crowns from fixed-wing aircraft. Sophisticated GPS and sketch-mapping technology enables spotters to mark the ϱϱ0003 0003
locations of dead trees so that ground crews can return to the area to sample from nearby vegetation (Mai, et al. 2006). Detection of P. ramorum in watercourses has emerged as the earliest of early detection methods. This technique employs pear or rhododendron baits suspended in the watercourse using ropes, buckets, mesh bags, or other similar devices. If plants in the watershed are infected with P. ramorum, zoospores of the pathogen (as well as other Phytophthora spp.) are likely present in adjacent waterways. Under conducive weather conditions, the zoospores are attracted to the baits and infect them, causing lesions that can be isolated to culture the pathogen or analyzed via PCR assay (Murphy, et al. 2006; Murphy, et al. 2008). This method has detected P. ramorum at scales ranging from small, intermittent seasonal drainages to the Garcia, Chetco, and South Fork Eel Rivers in California and Oregon (144, 352 and 689 m2 drainage areas, respectively). It can detect the existence of infected plants in watersheds before any mortality from the infections becomes evident. Of course, it cannot detect the exact locations of those infected plants: at the first sign of P. ramorum propagules in the stream, crews must scour the watershed using all available means to find symptomatic vegetation. A less technical means of detecting P. ramorum at the landscape level involves engaging local landowners across the landscape in the search. Many local county Agriculture Departments and University of California Cooperative Extension offices in California have been able to keep track of the distribution of the pathogen in their regions through reports and samples brought to them by the public. In 2008, the Garbelotto Laboratory at UC Berkeley, along with local collaborators, hosted a VHULHV0003RI0003HGXFDWLRQDO0003HYHQWV000f0003FDOOHG0003³62'0003%OLW]HV000f´0003GHVLJQHG0003WR0003JLve local landowners basic information about P. ramorum and how to identify its symptoms; each participant was provided with a sampling kit, sampled a certain number of trees on his or her property, and returned the samples to the lab for analysis. It is hoped that WKLV0003 NLQG0003 RI0003 ³FLWL]HQ0003 VFLHQFH´0003 FDQ0003 KHOS0003 JHQHUDWH0003 DQ0003 LPSURYHG0003 PDS0003 RI P. ramorum distribution in the areas where the workshops are held.
ϱϲ0003 0003
General sanitation in infested areas One of the most important aspects of P. ramorum control involves interrupting the human-mediated movement of the pathogen by ensuring that infested materials do not move from location to location. While enforceable quarantines perform part of this function, basic cleanliness when working or recreating in infested areas is also important. In most cases, cleanliness practices involve ridding potentially infested surfaces²such as shoes, vehicles, and pets²of foliage and mud before leaving the infested area. The demands of implementing these practices become more complex when large numbers of people are working in infested areas, as in construction, timber harvesting, or wildfire suppression. The California Department of Forestry and Fire Protection and USDA Forest Service have implemented guidelines and mitigation requirements for the latter two situations; basic information about cleanliness in P. ramorum-infested areas can be found at the California Oak Mortality Task Force web site (www.suddenoakdeath.org 0003XQGHU0003WKH0003³7UHDWPHQW0003DQG0003 0DQDJHPHQW´0003VHFWLRQ0003000bVXEVHFWLRQ0003³6DQLWDWLRQ0003DQG00035HGXFLQJ00036SUHDG´ 0011 Wildland management The course that P. ramorum management should take depends on a number of factors, including the scale of the landscape upon which one hopes to manage it. Management of P. ramorum has been undertaken at the landscape/ regional level in Oregon in the form of a campaign to completely eradicate the pathogen from the forests in which it has been found (mostly private, but also USDA Forest Service and USDI Bureau of Land Management ownership) (Goheen, et al. 2002; Goheen, et al. 2004; Kanaskie, et al. 2006). The eradication campaign involves vigorous early detection by airplane and watercourse monitoring, a U.S. Department of Agriculture Animal and Plant Health Inspection Service (USDA APHIS) and Oregon Department of Agriculture-led quarantine to prevent movement of host materials out of the area where infected trees are found, and immediate removal of P. ramorum host vegetation, symptomatic or not, within a 300-foot (91 m) buffer around each infected tree.
ϱϳ0003 0003
The Oregon eradication effort, which began near the town of Brookings in southwest Oregon in 2001, has adapted its management efforts over the years in response to new information about P. ramorum. For example, after inoculation trials of various tree species more clearly delineated which hosts are susceptible, the Oregon cooperators began leaving non-host species such as Douglas-fir and red alder on site. In another example, after finding that a small percentage of tanoak stumps that were resprouting on the host removal sites were infected with the pathogen² whether these infections were systemic or reached the sprouts from the surrounding environment is unknown²the cooperators began pretreating trees with very small, targeted amounts of herbicide to kill the root systems of infected tanoaks before cutting them down. The effort has been successful in that while it has not yet completely eradicated the pathogen from Oregon forests, the epidemic in Oregon has not taken the explosive course that it has in California forests. California, on the other hand, faces significant obstacles that preclude it from mounting the same kind of eradication effort. For one thing, the organism was too well established in forests in the Santa Cruz and San Francisco Bay areas by the time the cause of sudden oak death was discovered to enable any eradication effort to succeed. Even in still relatively uninfested areas of the north coast and southern Big Sur, regionally coordinated efforts to manage the pathogen face huge challenges of leadership, coordination, and funding. Nevertheless, land managers are still working to coordinate efforts between states, counties, and agencies to provide P. ramorum management in a more comprehensive manner. Several options exist for landowners who want to treat to limit the impacts of sudden oak death on their properties. None of these options is foolproof, guaranteed to eradicate P. ramorum, or guaranteed to prevent a tree from becoming infected. Some are still in the initial stage of testing. Nevertheless, when used thoughtfully and thoroughly, some of the treatments do improve the likelihood of either slowing the spread of the pathogen or of limiting its impacts on trees or stands of trees. Assuming that the landowner has correctly identified the host tree(s) and symptom(s), has submitted a sample to a local authority to send to an approved laboratory for testing, and has received confirmation that the tree(s) are indeed infected with P. ramorum² ϱϴ0003 0003
or, alternatively, assuming that the landowner knows that P. ramorum-infected trees are nearby and wants to protect the resources on his or her property²he or she can attempt control by cultural (individual-tree), chemical, or silvicultural (stand-level) means. The best evidence that cultural techniques might help protect trees against P. ramorum comes from research that has established a correlation between disease risk LQ0003FRDVW0003OLYH0003RDN0003WUHHV0003DQG0003WKH0003WUHHV¶0003SUR[LPLW0003WR0003ED0003ODXUHO (Swiecki and Bernhardt, 2007). In particular, this research found that bay laurel trees growing within 5m of the trunk of an oak tree were the best predictors of disease risk. This implies that strategic removal of bay laurel trees near coast live oaks might decrease the risk of oak infection. Wholesale removal of bay laurel trees would not be warranted, since the bay laurels close to the oak trees appear to provide the greatest risk factor. Whether the same pattern is true for other oaks or tanoaks has yet to be established. Research on this subject has been started for tanoak, but any eventual cultural recommendations will be more complicated, because tanoak twigs also serve as sources of P. ramorum inoculum. A promising treatment for preventing infection of individual oak and tanoak trees²not
for
curing
an
already
established
infection²is
a phosphonate fungicide marketed under the trade name Agri-fos. Phosphonate is a neutralized form of phosphorous acid that works not by direct antagonism of Phytophthora, but by stimulating several of kinds of immune responses on the part of the tree.[28] It is mostly environmentally benign if not applied to non-target plants and can be applied either as an injection into the tree stem or as a spray to the bole. When applying Agri-fos as a spray, it must be combined with an organosilicate surfactant, Pentra-bark, to enable the product to adhere to the bole long enough to be absorbed by the tree. Agri-fos has been very effective in preventing tree infections, but it must be applied when visible symptoms of P. ramorum on other trees in the immediate neighborhood are still relatively distant; otherwise, it is likely that the tree one wishes to treat is already infected but that visible symptoms have not yet developed (this is especially true for tanoak).
ϱϵ0003 0003
Trials of silvicultural methods for treating P. ramorum began in Humboldt County in northwest coastal California in 2006. The trials have taken place on a variety of infested properties both private and public and have generally focused on varying levels and kinds of host removal. The largest (50 acres (200,000 m2)) and most replicated trials have involved removal of tanoak and bay laurel by chainsaw throughout the infested stand, both with and without subsequent under burning designed to eliminate small seedlings and infested leaf litter (Valachovic, et al. 2008). 2WKHU0003WUHDWPHQWV0003LQFOXGHG0003KRVW0003UHPRYDO0003LQ0003D0003PRGLILHG0003³VKDGHG0003 fuel break´0003 design in which all bay laurel is removed, but not all tanoaks; bay and tanoak removal using herbicides; and removal of bay laurel alone. The results of these treatments are still being monitored, but repeated sampling has so far detected only very small amounts of P. ramorum in the soil or on vegetation in the treated sites. Nursery management Research and development in managing P. ramorum in nursery settings extends from P. ramorum in the individual plant, to P. ramorum in the nursery HQYLURQPHQW000f0003 WR0003 WKH0003 SDWKRJHQ¶V0003 PRYHPHQW0003 DFURVV0003 VWDWH0003 DQG0003 QDWLRQal borders in infected plants. An array of studies have tested the curative and protective effects of various chemical compounds against P. ramorum in plants valued as ornamentals or Christmas trees. Many studies have focused on the four main ornamental hosts of P. ramorum (Rhododendron, Camellia, Viburnum, compounds
have
been
found;
some
and Pieris). of
the
most
Several effective
effective include
mefenoxam, metalaxyl, dimethomorph, and fenamidone. Many of these studies have converged upon the following conclusions: chemical compounds are, in general, more effective as preventatives than in curatives; when used preventatively, chemical compounds must be reapplied at various intervals; and chemical compounds can mask the symptoms of P. ramorum infection in the host plant, potentially interfering with inspections for quarantine efforts. In general, these compounds suppress but do not eradicate the pathogen, and some researchers are concerned that with repeated use
ϲϬ0003 0003
the pathogen may become resistant to them. These studies and conclusions are summarized by Kliejunas (Kliejunas, 2007b). Another area of research and evolving practice deals with eliminating P. ramorum from nursery environments in which it is established to prevent humanmediated pathogen movement within the ornamental plant trade. One way of approaching this is through a robust quarantine and inspection program, which the various federal and state regulatory agencies have implemented. Under the federal P. ramorum quarantine program implemented by USDA APHIS, nurseries in California, Oregon, and Washington are regulated and must participate in an annual inspection regime; nurseries in the fourteen infested counties in coastal California, plus the limited infested area in Curry County, Oregon, must participate in a more stringent inspection schedule when shipping out of this area (USDA APHIS, 2007). Much of the research into disinfesting nurseries has focused on the voluntary Best Management Practices (BMPs) that nurseries can implement to prevent 300110003 UDPRUXP¶V introduction into the nursery and movement from plant to plant. In 2008, a group of nursery industry organizations issued a list of BMPs that includes subsections on Pest Prevention/Management, Training, Internal/External Monitoring/Audits, Records/Traceability, and Documentation. The document LQFOXGHV0003 VXFK0003 VSHFLILF0003 UHFRPPHQGDWLRQV0003 DV0003 ³$YRLG0003 overhead irrigation of high-risk SODQWV´001e0003 ³$IWHU0003 HYHU crop rotation, disinfect propagation mist beds, sorting area, cutting benches, machines and tools to minimize the spread or introduction of SDWKRJHQV´001e0003DQG0003³1XUVHU0003SHUVRQQHO0003VKRXOG0003DWWHQG0003RQH0003RU0003PRUH0003P. ramorum trainings conducted by qualified personnel or document self-WUDLQLQJ´ (Suslow, 2008; HRI P. ramorum Industry Working Group, 2008). Research on control of P. ramorum in nurseries has also focused on disinfesting irrigation water containing P. ramorum inoculum. Irrigation water can become infested from bay trees in the forest (if the irrigation source is a stream), from bay trees overhanging irrigation ponds, from runoff from infested forests (Tjosvold, et al. 2006), or from recirculated irrigation water (Werres, et al. 2007). Experiments in Germany with three types of filters²slow sand filters, lava filters, and constructed ϲϭ0003 0003
wetlands²showed that the first two removed P. ramorum from the irrigation water completely, while 37% of the post-treatment water samples from the constructed wetland still contained P. ramorum (Ufer, et al. 2008). Since P. ramorum can persist for an undetermined period of time within the soil profile, management programs in nurseries should also deal with delineating the SDWKRJHQ¶V0003 GLVWULEXWLRQ0003 LQ0003 QXUVHU0003 VRLO0003 DQG0003 HOLPLQDWLQJ0003 LW0003 IURP0003 LQIHVWHG0003 DUHDV00110003 $0003 variety of chemical options have been tested for soil disinfestation, including such chemicals as chloropicrin, metham sodium, iodomethane and dazomet. Lab tests indicated that all of these chemicals were effective when applied to infested soil in glass jars. Additionally, tests on volunteer nurseries with infested soil demonstrated that dazomet (trade name Basamid) fumigation followed by a 14-day tarping period successfully removed P. ramorum from the soil profile (Yakabe and MacDonald, 2008). Other soil disinfestation practices under investigation, or in which interest has been expressed, include steam sterilization, solarization, and paving of infested areas. Government Agency Involvement In England in 2009, the Forestry Commission, DEFRA, the Food and Environment Research Agency, Cornwall County Council, and Natural England are working together to record the locations and deal with this disease. Natural England is offering
grant
funding
through
Stewardship and Environmentally
its Environmental Sensitive
Stewardship, Countryside
Area schemes
to
clear
rhododendron.[52] In 2011, the Forestry Commission started felling 10,000 acres (40 km2) of larch forest in the SW of England, as an attempt to halt the spread of the disease.[53] In Northern Ireland at the end of 2011, the Department of Agriculture and 5XUDO0003 'HYHORSPHQW¶V0003 )RUHVW0003 6HUYLFH0003 EHJDQ0003 IHOOLQJ0003 001400170003 KHFWDUHV0003 RI0003 DIIHFWHG0003 /DUFK0003 woodland at Moneyscalp, on the edge of Tollymore Forest Park in County Down.
ϲϮ0003 0003
Host Butternut (Juglans cinerea) is an endangered species, threatened by a fungal disease called Butternut Canker (Sirococcus clavigignenti-juglandacearum).0003Trees of all ages, all sizes and on all sites are at risk. The USA has lost significant numbers of butternut to the canker. In Canada, butternut was officially listed as endangered under the Species at Risk Act (SARA) in 2005. In Ontario Butternut is listed as an endangered species under the Endangered Species Act (ESA 2007). Open grown butternut trees have a short trunk with a broad, spreading crown. In the forest they have taller, less branchy trunks with smaller crowns. The small branches tend to bend downward and turn up at the ends. Butternut (also known as white walnut) and black walnut can be confused. Also, people have been growing exotic walnuts and creating hybrids in North $PHULFD0003VLQFH0003WKH00030014001b00130013¶V0003± they are not uncommon in urban and long settled areas. Table: - Help to identify the species Butternut Juglans cinerea Larger range than black walnut, North into Central and Eastern Ontario Thick, buff colored 4XLWH0003IX]] &KDPEHUHG0003 SLWK0003 LV0003QDUURZ0003 DQG0003GDUN0003 brown(2 yr twig) +DLU0003IULQJH0003DERYH0003HDFK0003OHDI0003VFDU 8SSHU0003PDUJLQ0003RI0003OHDI0003VFDU0003VWUDLJKW
Black Walnut Juglans nigra Native to Southwestern Ontario
Butternut hybrids & exotic walnuts
If your tree has a few of these characteristics, you might have a hybrid or exotic walnut tree: $0003SODQWHG0003WUHH /LWWOH0003VLJQ0003RI0003FDQNHU 3LWK0003 LV0003 ZLGHU0003 DQG0003 OLJKWHU0003 brown (top 2 yr twig; bottom twig is butternut) /HDYHV0003 VWD0003 JUHHQ0003 DQG0003 RQ0003 tree in the fall weeks later than other native species 0DOH0003 FDWNLQV0003 ORQJHU0003 WKDQ0003 15cm *RRG0003 VHHG0003 FURSV0003 DOPRVW0003 every year +HDUW0003VKDSHG0003QXW0003VKHOO
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Seweta Srivastava
CONTENTS
S.No.
Chapters
Page No
1.
Introduction
2 to 5
2.
Chestnut Blight
6 to 15
3.
Dutch Elm Disease
16 to 33
4.
Palm Lethal Yellowing
34 to 45
5.
Oak Wilt / Sudden Oak Death
46 to 62
6.
Butternut Canker
63 to 69
7.
Cypress Canker
70 to 76
8.
Xylella Outbreak
77 to 88
9.
References
89 to 99
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losses of 30 to 50 percent are common for major crops. In some years, losses are much greater, producing catastrophic results for those who depend on the crop for food. Major disease outbreaks among food crops have led to famines and mass migrations throughout history. The devastating outbreak of late blight of potato (Phytophthora infestans) that began in Europe in 1845 and brought about the Irish famine caused starvation, death, and mass migration of the Irish population. Of a population of eight million, approximately one million (about 12.5 percent) died of starvation and 1.5 million (almost 19 percent) emigrated, mostly to the United States, as refugees from the destructive blight. This fungus thus had a tremendous influence on the economic, political, and cultural development in Europe and the United States. During World War I, late blight damage to the potato crop in Germany may have helped end the war. Losses from plant diseases also can have a significant economic impact, causing a reduction in income for crop producers and distributors and higher prices for consumers. In 1993 the United States lost more than one million acres (405,000 hectares) of crops to disease. More than 800,000 acres of wheat succumbed to disease, exacting a monetary loss in the millions of dollars. Diseases²a normal part of nature Plant diseases are a normal part of nature and one of many ecological factors that help keep the hundreds of thousands of living plants and animals in balance with one another. Plant cells contain special signaling pathways that enhance their defenses against insects, animals, and pathogens. One such example involves a plant hormone called jasmonate (jasmonic acid). In the absence of harmful stimuli, jasmonate binds to special proteins, called JAZ proteins, to regulate plant growth, pollen production, and other processes. In the presence of harmful stimuli, however, jasmonate switches its signaling pathways, shifting instead to directing processes involved in boosting plant defense. Genes that produce jasmonate and JAZ proteins represent potential targets for genetic engineering to produce plant varieties with increased resistance to disease.
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Humans have carefully selected and cultivated plants for food, clothing, shelter, fiber, and beauty for thousands of years. Disease is just one of many hazards that must be considered when plants are taken out of their natural environment and grown in pure stands under what are often abnormal conditions. Many valuable crop and ornamental plants are very susceptible to disease and would have difficulty surviving in nature without human intervention. Cultivated plants are often more susceptible to disease than are their wild relatives. This is because large numbers of the same species or variety, having a uniform genetic background, are grown close together, sometimes over many thousands of square kilometers. A pathogen may spread rapidly under these conditions. Definitions of plant disease In general, a plant becomes diseased when it is continuously disturbed by some FDXVDO0003 DJHQW0003 WKDW0003 UHVXOWV0003 LQ0003 DQ0003 DEQRUPDO0003 SKVLRORJLFDO0003 SURFHVV0003 WKDW0003 GLVUXSWV0003 WKH0003 SODQW¶V0003 normal structure, growth, function, or other activities. This interference with one or more RI0003 D0003 SODQW¶V0003 HVVHQWLDO0003 Shysiological or biochemical systems elicits characteristic pathological conditions or symptoms. Plant diseases can be broadly classified according to the nature of their primary causal agent, either infectious or noninfectious. Infectious plant diseases are caused by a pathogenic organism such as a fungus, bacterium, mycoplasma, virus, viroid, nematode, or parasitic flowering plant. An infectious agent is capable of reproducing within or on its host and spreading from one susceptible host to another. Noninfectious plant diseases are caused by unfavorable growing conditions, including extremes of temperature, disadvantageous relationships between moisture and oxygen, toxic substances in the soil or atmosphere, and an excess or deficiency of an essential mineral. Because noninfectious causal agents are not organisms capable of reproducing within a host, they are not transmissible. In nature, plants may be affected by more than one disease-causing agent at a time. A plant that must contend with a nutrient deficiency or an imbalance between soil ϰ0003 0003
moisture and oxygen is often more susceptible to infection by a pathogen; a plant infected by one pathogen is often prone to invasion by secondary pathogens. The combinations of all disease-causing agents that affect a plant make up the disease complex. Knowledge of normal growth habits, varietal characteristics, and normal variability of plants within a species²as these relate to the conditions under which the plants are growing²is required for a disease to be recognized. The study of plant diseases is called plant pathology. Pathology is derived from the two Greek words pathos (suffering, disease) and logos (discourse, study). Plant pathology thus means a study of plant diseases. Invasive plant species are the second greatest threats to the natural ecosystems of the world today. Only direct habitat destruction poses a greater threat to the future of biological diversity. Invasive species disrupt the ecology of natural ecosystems by displacing native plant and animal species and reduce biological diversity by reducing the amount of light, water, nutrients and space available to native species.
The introduction of exotic plant species have resulted in the escape of plant pathogens which have greatly impacted our local flora, such as Dutch Elm Disease, Beech Bark Disease, Chestnut Blight and Dogwood Anthracnose.
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Usually prior to perithecia, pycnidia are produced in the same small stroma or in other stromata. They also can appear any time of year. The conidia ooze out in a tendril after rains. They are quite small, as small as 4 x 1 µm wide. In that little conidium is all the information and machinery necessary to wipe out one of the most important tree species in North America. Conidia may be carried by rain splash or catch a ride on an insect or bird. Identifying the Fungus: - The fungus forms yellowish or orange fruiting bodies (pycnidia) about the size of a pin head on the older portion of cankers. Spores may exude from the pycnidia as orange, curled horns during moist weather. Identifying the Injury: - Stem cankers are either swollen or sunken, and the sunken type may be grown over with bark. The bark covering swollen cankers is usually loose at the ends of the canker. Trees die back above the canker and may sprout below it. Frass and webs from secondary insects are common under loose bark.
Fig. 2.3: Cracking and fruiting bodies on chestnut Fig. 2.4: Basal cracking caused by chestnut blight fungus
Biology: - Host infection occurs when fresh wounds in the bark become infected with spores that are disseminated by wind, birds, rain, and insects. Cankers kill the cambium and girdle the stem. Multiple cankers on infected trees are common. ϴ0003 0003
Environment Within the range of environmental conditions found in the geographic range of chestnut, there do not appear to be important differential effects of the environment. Environmental conditions are conducive to disease throughout the range of chestnut. Disease Cycle Conidia and ascospores can infect wounds, even very small ones that don't go all the way to cambium. It is thought that insects of various kinds make most of the infection courts. The fungus grows in the inner bark and cambium, producing small brownish mycelial fans. Even after the branch or stem is girdled and killed, the fungus continues to colonize it, producing ever more inoculums. Symptoms Chestnut blight is a canker disease. Perhaps it is called blight because infected branches and stems die quickly, as in shoot blight. But it doesn't just infect shoots; it infects branches and stems of any size. The cankers are of the diffuse type. They grow rapidly and in most cases continue to develop until the stem is girdled and killed; then they continue to colonize the dead tree. Management We will never have chestnut like we did in 1900, at least not in the next few hundred years. But there are two areas of hope for some form of recovery. Breeding for resistance: Chinese chestnut is somewhat
resistant.
The
persistent perennial cankers
fungus
rather
than
causes diffuse
cankers. It can slow the fungus down. Reproduction is limited. But Chinese chestnut is not such a great tree.
So
traditional
breeding
followed
by
backcrossing is underway. Although it is slow and a ϵ0003 0003
It was later found that hypovirulent isolates have a piece of double-stranded RNA, which doesn't normally occur in fungi. It is now considered that the dsRNA is a virus in the family Hypoviridae, and essentially causes a disease in the fungus, making it less virulent. Hypovirulence has had limited success against chestnut blight. It shows promise in some locations in Europe and in Michigan in the United States. However, it has failed almost completely in eastern North America. Therapeutic treatment of individual cankers is successful in most cases, but the success of hypovirulence at the population level depends on the natural spread of viruses. It is not clear how well the hypovirulent strains can reproduce, disperse, and make contact with virulent strains in nature. Factors limiting spread of the virus are not well understood. One natural barrier to virus spread is hyphal fusion among individuals of the fungus. Hyphal fusion is necessary to transmit the virus. When hyphae can fuse and exchange material, they are said to be vegetatively compatible, and in the same vegetative compatibility group. In North America, we have more VC groups than they do in Europe, so getting the virus to spread around in nature is going to be difficult. But there is a lot of hope that it may yet succeed. Other Issues Most forest pathologists like tree diseases. Generally, I would like to see a diseased tree more than a healthy one. Although human society generally has a goal of reducing such diseases, if the truth be told, sometimes we root for the pathogen, just because it's such fun to see a disease really do a job. But chestnut blight is a different story. What it did to American forests is no joking matter. It's a tragedy. No one who loves forests can think about the decimation of such a fantastic and abundant tree species as anything else. An informal article by George Hepting gives some insight into the role of chestnut in American life as well as the chaos that ensued in scientific and political circles as society struggled to deal with the new disease. ϭϭ0003 0003
There is an emotional hook there that other diseases just don't have. Even today, many years after the American chestnut was essentially wiped out as a forest tree, there are many ordinary citizens deeply interested in doing something to bring it back. The reason there is little resistance in American Chestnut is that the pathogen was introduced. In 1904, the disease was observed in the New York Zoo killing chestnuts, but there is reason to suspect it was here as early as 1893. The pathogen was later found to be native to China and was apparently introduced on nursery stock. In Asia the fungus was a weak parasite. In America, it spread very quickly and never met a tree it couldn't kill. It spread up to 50 miles per year over the natural range of chestnut. By 1940, chestnut was destroyed as a commercial species. Today, incredibly, chestnut still survives in much of its former range, but only as sprouts from the old root systems. The roots and root collar are resistant. In many places, various oaks have replaced it. In the oak stands, you can hardly find chestnut. When the oaks are cut, fairly dense sprouts of chestnut pop up, trying to do their thing. But before they can get big enough to sexually reproduce, the damn disease cuts them down. They don't seem to stand much chance of adapting. Importance - The chestnut blight fungus has virtually eliminated the American chestnut, as a commercial species, from eastern hardwood forests. Although roots from trees cut or killed many years ago continue to produce sprouts that survive to the sapling stage before being killed, there is no indication that a cure for this disease will be found. The fungus is widespread and continues to survive as a nonlethal parasite on chinkapin, Spanish chestnut, and post oak. Control - No effective control has been developed for chestnut blight, even after decades of intensive research. Current research is targeted toward finding a blight resistant species and the further development of the hypovirulent strains of the fungus. These strains tend to inactivate the pathogen and promote healing, but only when applied directly to developing cankers.
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Some Facts about Blight Resistance American chestnut seedlings are usually highly susceptible to the blight. In older trees (more than 1.5 inches in diameter at breast height), a resistant individual can slow down progress of the disease and may survive in spite of blight, but it is not immune. Many kinds of environmental stress may break down a tree's resistance to blight. Indeed, at higher elevations in areas exposed to severe climate, normally resistant, Oriental chestnuts have been killed by blight. When we search for possible sources of blight resistance, we look for American chestnuts greater than 10' DBH (Diameter at Breast Height) which have swollen blight cankers (as illustrated in the February 1990 National Geographic, page 132). Some Facts about Hypovirulence Hypovirulence is a virus disease of the blight fungus. Weakened by the virus, the blight's progress is slowed down, so that a chestnut tree which may have no resistance to blight can form the slow-growing swollen cankers normally produced only on resistant trees. Scientists have been trying to manipulate hypovirulence to develop an economical bio-control for blight. Among the obstacles to be overcome are 1) the blight spreads very rapidly in nature, while hypovirulence spreads very slowly; 2) there are many types of virulent strains in the forest which resist transfer of the virus responsible for hypovirulence; and 3) good, swollen, slow-growing cankers sometimes change into bad, sunken, rapid-growing cankers that kill trees. Integrated
management
for
American
chestnut
revival combines
hypovirulence (by inoculation) with blight-resistance (grafted) on sites identified as ideal American chestnut habitat, to produce blight control. In Virginia's Lesesne State Forest, 3 resistant American chestnuts were grafted in 1980. In 1982 and 1983 the first cankers were inoculated with hypovirulence. These trees are thriving; they have produced nuts for more than 10 years, and they make excellent annual growth. They are surrounded by nonresistant American chestnuts which are continuously killed back by the blight. Conservation Efforts There are approximately 2,500 chestnut trees growing on 60 acres near West Salem, Wisconsin, which is the world's largest remaining stand of American chestnut. ϭϯ0003 0003
These trees are the descendants of those planted by Martin Hicks, an early settler in the area. In the late 1800s, Hicks planted less than a dozen chestnuts. Planted outside the natural range of chestnut, these trees escaped the initial wave of infection by chestnut blight, but in 1987, scientists found blight also in this stand. Scientists are working to try to save the trees. There is a program to bring American chestnut back to the Eastern forest and funded by the American Chestnut Foundation, Wisconsin Department of Natural Resources, USDA Forest Service, University of West Virginia, Michigan State University, and Cornell University. Removing blighted trees to control the disease was first attempted when the blight was discovered, but this proved to be an ineffective solution. Scientists then set out to introduce a hypovirus into the chestnut blight fungus. The trees infected with virustreated fungus responded immediately and began to heal over their cankers. However, the virus was so efficient at attenuating fungal growth that it prevented spreading of the virus from an infected fungus growing on one tree to that growing on another tree. Only the virus-treated trees recovered. Scientific opinion regarding the future of the stand varies. Hybrid Chestnut Trees In the years since the chestnut blight, many scientists and botanists have worked to create a resistant hybrid chestnut tree that retains the main characteristics of the American chestnut tree. In the early 1950s, James Carpenter discovered a large living American chestnut in a grove of dead and dying trees in Salem, Ohio that showed no evidence of blight infection. Carpenter sent budwood to Dr. Robert T. Dunstan, a plant breeder in Greensboro, North Carolina. Dunstan grafted the scions onto chestnut rootstock and the trees grew well. He cross-pollinated one with a mixture of 3 Chinese chestnut selections: 'Kuling', 'Meiling', and 'Nanking'. The resulting fruit-producing hybrid was named the Dunstan Chestnut.[15] The trade off for resistance to the chestnut blight is that the Dunstan hybrid grew to a height of only twenty-five feet or 7.6 meters. Current efforts are under way by the Forest Health Initiative to use modern breeding techniques and genetic engineering to create resistant tree strains, with contributions from SUNY College of Environmental Science and Forestry, Penn State, UGA, and the US Forest Service. One of the most successful methods of breeding is to ϭϰ0003 0003
create a back cross of a resistant species (such as one from China or Japan) and American Chestnut. The two species are first bred to create a 50/50 hybrid. After three back crosses with American Chestnut, the remaining genome is approximate 1/16 that of the resistant tree, and 15/16 American. The strategy is to select blight-resistance genes during the back crossing, while preserving the more wild-type traits of American Chestnut as the dominant phenotype. Thus, the newly bred hybrid chestnut trees should reach the same heights as the original American chestnut. Research is also being conducted at the State University of New York College of Environmental Science and Forestry, by using the bacterial vector, Agrobacterium tumefaciens, to insert resistance genes from the Asian chestnuts into American chestnut. The inserted genes are present only in the resistant strain, and not in the Native American chestnut, and are tested for their potential to produce blight-resistant trees. Currently, SUNY ESF has over 100 individual events being tested, with more than 400 slated to be in the field or in the lab for various assay tests in the next several years. Ideal American Chestnut Revival Habitat Restoration projects (managing for American chestnut in aging clear cuts, or introducing improved blight resistance by grafting scions into available root systems or planting seedlings on former American chestnut lands) should concentrate on carefully selected sites which do not include the whole spectrum of choices mentioned above. Because the American chestnuts will be repeatedly challenged by blight, it is important to choose sites which avoid all other environmental stresses, as much as possible. These sites can be identified by the presence of large chestnut stumps or snags, chestnut sprouts, and other species that share similar site preferences, such as tulip poplar, northern red oak, and cucumber magnolia. Frequently, the best chestnut sites are located in shallow coves and slopes facing north to east. Dry sites should be avoided to limit stress by drought. Known frost pockets or cold air drainage routes should also be avoided, and lower elevation sites are generally preferable to sites over 2,000 or 3,000 feet, to minimize the stresses from extremes in temperature during winter. Full morning sun in coves or sloping, well-drained lands with acid soils (pH 5 to 6) is best. When in doubt, consult a professional forester.
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Symptoms Dutch elm disease is a vascular wilt disease. The earliest external symptoms of infection are often yellowing and wilting (flagging) of leaves on individual branches (Fig. 3.2). These leaves often turn brown and curl up as the branches die, and eventually the leaves may drop off. This progressively spreads to the rest of the tree, with further dieback of branches. Eventually, the roots die, starved of nutrients from the leaves. Often, not all the roots die: the roots of some species, notably the English elm Ulmus procera, put up suckers which flourish for approximately 15 years, after which they too succumb (Spooner and Roberts, 2005). Although initially only a part of the tree crown may be affected, symptoms may progress rapidly throughout the crown. Highly susceptible trees often die in a single year, but others may linger for several years. Symptoms progress quickly and death may occur rapidly in trees infected in early spring, while trees infected later in the summer may survive longer.
Fig. 3.2
Fig. 3.3
If the bark of infected elm twigs or branches is peeled back, brown discoloration is seen in the outer layer of wood. This discoloration in the xylem actually occurs before the foliar symptoms described above are seen; foliar symptoms result when sap flow ceases in the infected wood. Xylem browning is often discontinuous. In cross section, it appears as a circle of brown dots or a ring (Fig. 3.3). Other wilt diseases of elm, such as Verticillium wilt, also cause sapwood discoloration, so positive diagnosis of Dutch elm disease depends on laboratory culturing and identification of the fungus.
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The signs (fungal structures) of the Dutch elm disease pathogens are found within infected elm trees, and are described in the Pathogen Biology section. Pathogen The causative agents of DED are ascomycete microfungi. Three species are now recognized: x
Ophiostoma ulmi, which afflicted Europe from 1910, reaching North America on
imported timber in 1928. x Ophiostoma himal-ulmi, a species endemic to the western Himalaya0003;Brasier and Mehotra, 1995). x Ophiostoma novo-ulmi, an extremely virulent species which was first described in Europe and North America in the 1940s and has devastated elms in both areas since the late 1960s (Spooner and Roberts, 2005).0003
The origin of O. novo-ulmi remains unknown, but the species may have arisen as a hybrid between O. ulmi and O. himal-ulmi. The new species was widely believed to have originated in China, but a comprehensive survey there in 1986 found no trace of it, although elm bark beetles were very common (Brasier, 1996).
Fig. 3.4: Beetle feeding galleries on Wych Elm trunk
Fig. 3.5: An infected English elm at West Point, NY, July 2010
DED is spread in North America by three species of bark beetles (Family: Curculionidae, Subfamily: Scolytinae):
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x
The native elm bark beetle, Hylurgopinus rufipes.
x
The European elm bark beetle, Scolytus multistriatus.
x
The banded elm bark beetle, Scolytus schevyrewi.
In Europe, while S. multistriatus again acts as vector for infection, it is much less effective than the large elm bark beetle, S. scolytus. H. rufipes can be a vector for the disease, but is inefficient compared to the other vectors. S. schevyrewi was found in 2003 in Colorado and Utah. Pathogen Biology The Ophiostoma species that cause Dutch elm disease grow and reproduce only within elms. At times they are parasites, feeding on living tissue of the elm tree; at other times they are saprophytes, getting nourishment from dead elm tissue. Ophiostoma ulmi caused the original Dutch elm disease epidemic in Europe and North America in the mid-1900s. Ophiostoma novo-ulmi, an even more aggressive pathogen of elms, largely replaced O. ulmi during the second half of the 20th century. These fungi spread within stems and roots of living elms both by passive transport of spores and by mycelial growth of colonies initiated by spores that germinate in the xylem. The mycelium of these fungi is creamy white (Fig. 3.6) and is composed of septate hyphae with haploid nuclei.
Fig. 3.6
Asexual reproduction Ophiostoma ulmi and O. novo-ulmi have two asexual forms that produce asexual spores called conidia. In the xylem vessels of living elm trees, small, white, oval conidia (Fig. 3.7) are formed in clusters on short mycelial branches. These conidia are carried in ϭϵ0003 0003
the xylem vessels where they reproduce by budding, germinate to produce mycelium, and thus spread the disease throughout the tree.
Fig. 3.7
Fig. 3.8
In dying or recently dead trees, conidia (Fig. 3.8) are produced by mycelium growing in the bark and in tunnels created by beetles just under the bark. These sticky conidia are produced at the tips of 1-2 mm tall synnemata. Each synnema consists of hyphae fused to form an erect, dark stalk with a round, nearly colorless head of sticky spores. Beetle vectors carry the sticky spores to new elm trees. Sexual reproduction Based on the structures produced by their sexual stage, the Dutch elm disease pathogens are placed in the ascomycete genus Ophiostoma. When two mating types come in contact, ascospores are produced in spherical, black, long-necked perithecia (Fig. 3.9). Perithecia form in the bark, either singly or in groups. Ascospores are produced in asci that degenerate inside of the perithecia. The free ascospores are discharged at the opening of the perithecial neck where they accumulate in sticky droplets that may be disseminated by beetle vectors.
Fig. 3.90003
ϮϬ0003 0003
Disease Cycle and Epidemiology
Fig. 2.10
Disease cycle The Dutch elm disease pathogens overwinter in the bark and outer wood of dying or recently dead elm trees and in elm logs as mycelia and synnemata with conidia. The fungi are spread from these sites by their vectors - elm bark beetles (Fig. 3.11). Two beetle species spread the pathogens in North America: the smaller European elm bark beetle (Scolytus multistriatus) and the native elm bark beetle (Hylurgopinus rufipes). The adult female beetle bores through the bark of dead or dying elm trees and elm logs and creates a tunnel in the wood as she feeds. She lays eggs in the tunnel behind her. The eggs hatch into larvae (Fig. 3.12) that begin to feed, creating tunnels at right angles to the maternal tunnel.
Ϯϭ0003 0003
Fig. 3.11
Fig. 3.12
The resulting pattern of tunnels is called a gallery (Fig. 3.13). The larvae pupate and emerge through the bark as adults (Fig. 3.14). If the fungi are present in the tree or log, the emerging adults carry thousands of sticky conidia on their bodies.
Fig. 3.13
Fig. 3.14
Newly-emerged S. multistriatus adults feed in the twig crotches of elm branches (Fig. 3.15); newly emerged H. rufipes DGXOWV¶ tunnel in the bark of elm branches and trunks. As the beetles feed, fungal spores are deposited. The beetle vectors only feed on healthy elms for a few days. Then they fly to dying or recently dead elm trees or to freshly cut elm wood to feed, create galleries, and lay eggs. The spores dislodged from elm bark beetles in feeding wounds and tunnels germinate and produce mycelium that grows into the xylem. The mycelium produces millions of small, white, oval conidia that spread through the xylem sap.
ϮϮ0003 0003
Fig. 3.15
Fig. 3.16
The fungi also produce enzymes and probably toxins that degrade plant cell walls and kill xylem parenchyma cells. In addition, the fungi induce hormonal imbalance that leads to the formation of tyloses (Fig. 3.16), overgrowths of parenchyma cells that push into and block the water-conducting xylem cells. The blockage of the xylem by tyloses and gums (thought to be products of plant cell wall breakdown) causes one of the diagnostic symptoms of Dutch elm disease, wilting of leaves. The killing of xylem parenchyma cells causes another diagnostic symptom, brown discoloration just under the bark. Epidemiology ,QIHFWLRQV0003 WKDW0003 WDNH0003 SODFH0003 LQ0003 WKH0003 VSULQJ0003 RU0003 HDUO0003 VXPPHU0003 LQYROYH0003 ³VSULQJZRRG´0003 which has very long xylem vessels. In these vessels the fungi can spread rapidly throughout the tree, which then may die quickly. Later in the season, the fungi are UHVWULFWHG0003WR0003WKH0003PXFK0003VKRUWHU0003YHVVHOV0003RI0003WKH0003³VXPPHUZRRG000f´0003DQG0003WKH0003IXQJL0003VSUHDG0003PXFK0003 Ϯϯ0003 0003
more slowly in the tree. Localized infections often result, and the tree is likely to survive longer.
Fig. 3.17
Healthy elm trees can become infected by the feeding of spore-contaminated elm bark beetles or through the development of grafts between their roots and the roots of infected trees (Fig. 3.17). Trees infected via beetle vectors often first develop symptoms in an upper section of the crown, whereas trees infected via root grafts often first develop symptoms lower in the crown. When the fungi are introduced through a root graft, they can be quickly distributed throughout the tree in the vascular system, and the entire tree may soon wilt and die. Root grafts form naturally between closely spaced elm trees with intertwined roots. Large elms growing within 7 meters (20 feet) of each other have almost 100% chance of becoming infected through root grafts. The likelihood of spread is lower when the elms are at least 13 meters (40 feet) apart. The severity and rate of spread of Dutch elm disease depend on the species of the pathogen, how rapidly the elm bark beetles reproduce the level of susceptibility of the elm hosts, and the environment. Temperatures around 20°C (68°F) favor the formation of conidia, whereas perithecia are induced at temperatures of 8-10°C (46-50°F). In the absence of effective disease management, Dutch elm disease increases exponentially until an affected elm population is greatly depleted. Seedlings and many saplings escape and live long enough to reproduce, so even the most susceptible elm species have never been threatened with extinction by Dutch elm disease. Wild elm Ϯϰ0003 0003
populations in the eastern and Midwestern U.S. have increased in recent decades, and this increase has led to renewed prominence of Dutch elm disease in landscapes. Dutch Elm Management Cultural Strategies Today, some communities maintain active programs to manage Dutch elm disease because they have found that it is cheaper to manage the disease than to remove the large dead trees that it leaves behind. Some communities focus on cultural practices for disease management, including the avoidance of monocultures of elm trees, the removal of all dying or recently dead branches, trees, and cut wood (sanitation), and the breakage of root grafts between adjacent elms. To be successful, diligent inspection of all elm trees in an area several times each growing season is required. Wood must be burned, chipped or buried so that it cannot provide a home for beetle vectors (Fig. 3.18).
Fig. 3.18
Organized community sanitation programs can delay the loss of elms. It has been estimated that the time when half of the elm trees in an area have been lost can be delayed by between 7 and 30 years. If privately owned trees are included in a program of inspection and mandatory removal, the longer end of this range is more likely. At best, this is a delaying tactic in the battle against Dutch elm disease.
Ϯϱ0003 0003
Chemical Strategies In the past, insecticides were sprayed on elm trees in attempts to kill the beetle vectors of Dutch elm disease (Fig. 3.19). This management strategy was expensive, not very effective, and came under attack from people concerned about the impact of insecticide use on wildlife and people.
Fig. 3.19
Fig. 3.20
Fig. 3.21
More recently, fungicides have been injected into trees infected by or at risk of infection by the Dutch elm disease pathogens (Fig. 3.20). These systemic chemicals are most effective if they are used to prevent new infections or to prevent the movement of the fungi into parts of a tree that are not yet colonized. Several different fungicides have been used, but all are relatively expensive, and none is completely effective. For these reasons, chemical management of Dutch elm disease is commonly used only to protect elm trees of high value, such as those along the Mall in Washington, D.C. (Fig. 3.21) or large trees in the yards of well-maintained properties. Biological Strategies Because of the ban on the use of chemicals on street and park trees in the Netherlands, the University of Amsterdam developed a biological vaccine by the late 1980s. Dutch Trig is nonchemical and nontoxic, consisting of a suspension in distilled water of spores of a strain of the fungus Verticillium albo-atrum that has lost much of its pathogenic capabilities, injected in the elm in spring. The strain is believed to have enough pathogenicity left to induce an immune response in the elm, protecting it against Ϯϲ0003 0003
DED during one growing season. This is called induced resistance. Trials in the US most notably Denver Colorado showed that Dutch Trig had no effect on saving Elms and that the treated trees were made sick by the treatment. Preventive treatment is usually only justified when a tree has unusual symbolic value or occupies a particularly important place in the landscape. Breeding for resistance The long-term solution to Dutch elm disease lies in the development of diseaseresistant cultivars of elms. Several Asian elm species have moderate to high resistance, and breeding programs in both Europe and the U.S. have introduced resistance from these species into native elm species. Other programs have focused on identifying and cloning individual American elm specimens that have moderate resistance to Dutch elm disease. The American elm breeders also would like to maintain the elegant vase shape of the American elm - the quality that made it a highly desirable shade tree. As a result of decades of efforts by elm breeders, several hybrid and clonal elms are now available that has very good resistance to Dutch elm disease. Resistant trees Research to select resistant cultivars and varieties began in the Netherlands in 1928, followed by the USA in 1937. Initial efforts in the Netherlands involved crossing varieties of U. minor and U. glabra, but later included the Himalayan or Kashmir elm U. wallichiana as a source of antifungal genes. Early efforts in the USA involved the hybridization of the Siberian elm U. pumila with American red elm U. rubra to produce resistant trees. Resulting cultivars lacked the traditional shape and landscape value of the American elm; few were planted. In 2005, the National Elm Trial (USA) began a 10-year evaluation of 19 cultivars in plantings across the United States. The trees in the trial are exclusively American developments; no European cultivars have been included. Recent research in Sweden has established that early-flushing clones are less susceptible to DED owing to an asynchrony between DED susceptibility and infection.[29] Hybrid cultivars Ϯϳ0003 0003
Many attempts to breed disease resistant cultivar hybrids have usually involved a genetic contribution from Asian elm species which have demonstrable resistance to this fungal disease. Much of the early work was undertaken in the Netherlands. The Dutch research programme began in 1928, and ended after 64 years in 1992, during which time well over 1000 cultivars were raised and evaluated. The programme had three major successes: 'Columella', 'Nanguen' LUTÈCE, and 'Wanoux' VADA,[30] all found to have an extremely high resistance to the disease when inoculated with unnaturally large doses of the fungus. Only 'Columella' was released during the lifetime of the Dutch programme, in 1987; patents for the LUTÈCE and VADA clones were purchased by the French Institut National de la Recherche Agronomique (INRA), which subjected the trees to 20 years of field trials in the Bois de Vincennes, Paris, before releasing them to commerce in 2002 and 2006, respectively. The Conservation Foundation, conservationfoundation.co.uk, is currently running two elm programmes - the Great British Elm Experiment and Ulmus londinium, an elm programme for London. These build on earlier elm projects in the past 30 years and both use saplings grown from mature parent elms found growing in the British countryside and cultivated through micro-propagation. The parent trees are monitored for Dutch elm disease. Saplings are offered free to schools and community groups, who are asked to monitor their tree's progress on the Foundation's online elm map. Elms are available at a small price to others who don't qualify for a free tree. In London, places with 'elm' in their name are offered a sapling. This is an experiment with the aim of finding over time why some elms have survived while others succumbed to Dutch elm disease. Asian species to feature in the American DED research programs were the Siberian elm U. pumila, Japanese elm U. davidiana var. japonica, and the Chinese elm U. parvifolia, giving rise to several dozen hybrid cultivars resistant not just to DED, but also to the extreme cold of Asian winters. Among the most widely planted of these, both in North America and in Europe are 'Sapporo Autumn Gold' and 'New Horizon'. Some hybrid cultivars, such as 'Regal', are the product of both Dutch and American research. Hybridization experiments using the slippery or red elm U. rubraresulted in the release of 'Coolshade' and 'Rosehill' in the 1940s and 50s. The species last featured in
Ϯϴ0003 0003
hybridization as the female parent of 'Repura' and 'Revera', both patented in 1993, although neither has yet appeared in commerce. In Italy, research is continuing at the Istituto per la Protezione delle Piante, Florence, to produce a range of disease-resistant trees adapted to the warmer Mediterranean climate, using a variety of Asiatic species crossed with the early Dutch hybrid 'Plantyn' as a safeguard against any future mutation of the disease (Santini et al. 2004). Two trees with very high levels of resistance, 'San Zanobi' and'Plinio' (Santini et al. 2002), were released in 2003. 'Arno' and 'Fiorente' were patented in 2006 and will enter commerce in 2012. All four have the Siberian elm U. pumila as a parent, the source of disease-resistance and drought-tolerance genes. Further releases are planned, notably of a clone derived from a crossing of Dutch elm Ulmus × hollandica with the Chinese species U. chenmoui. Species and species cultivars North America Ten resistant American elm U. americana cultivars are now in commerce in North America, but only two ('Princeton' and 'Valley Forge') are currently available in Europe. No cultivar is 'immune' to DED; even highly resistant cultivars can become infected, particularly if already stressed by drought or other environmental conditions where the disease prevalence is high. With the exception of 'Princeton', no trees have yet been grown to maturity. Trees cannot be said to be mature until they have reached an age of 60 years. Notable cultivars include: x
'Princeton', is a cultivar selected in 1922 by Princeton Nurseries for its landscape merit. By happy coincidence, this cultivar was found to be highly resistant in inoculation studies carried out by the USDA in the early 1990s. As trees planted in the 1920s still survive, the properties of the mature plant are well known.
x
'American Liberty', is, in fact, a set of six cultivars of moderate to high resistance produced through selection over several generations starting in the 1970s. Although 'American Liberty' is marketed as a single variety, nurseries selling the 'Liberty Elm' Ϯϵ0003
0003
actually distribute the six cultivars at random and thus, unfortunately, the resistance of any particular tree cannot be known. One of the cultivars, 'Independence', is covered by patent (U. S. Plant patent 6227). The oldest 'American Liberty' elm was planted in about 1980. x
'Valley Forge', released in 1995, has demonstrated the highest resistance of all the clones to Dutch elm disease in controlled USDA tests.
x
'Lewis and Clark' (Prairie Expedition TM ), released in 2004, was cloned from a tree found growing in North Dakota which had survived unscathed when all around had succumbed to disease. In 2007, the Elm Recovery Project from the University of Guelph in Ontario,
Canada reported that cuttings from healthy surviving old elms surveyed across Ontario had been grown to produce a bank of resistant trees, isolated for selective breeding of highly resistant cultivars. The University of Minnesota USA is testing various elms, including a huge nowpatented century-old survivor known as 'The St. Croix Elm', which is located in a Minneapolis-St. Paul, MN suburb (Afton) in the St. Croix River valley ² a designated National Scenic River way. The slippery or red elm U. rubra is marginally less susceptible to Dutch elm disease than the other American species, but this quality seems to have been largely ignored in American research. No cultivars were ever selected; although the tree was used in hybridization experiments (see above). Europe Among European species, there is the unique example of the European white elm U. laevis, which has little innate resistance to DED, but is eschewed by the vector bark beetles and only rarely becomes infected. Recent research has indicated it is the presence of certain organic compounds, such as triterpenes and sterols, which serves to make the tree bark unattractive to the beetle species that spread the disease (MartínBenito et al. 2005).
ϯϬ0003 0003
In 2001, English elm U. procera was genetically engineered to resist disease, in experiments at Abertay University, Dundee, Scotland, by transferring antifungal genes into the elm genome using minute DNA-coated ball bearings. However, owing to the hostility to GM developments, there are no plans to release the trees into the countryside. The spread of DED to Scotland has revealed a number of Wych elms U. glabra apparently surviving there unscathed, prompting the Royal Botanic Garden Edinburgh to clone the trees and inoculate them with the fungus to determine any innate resistance (2010) (Coleman, 2009). A similar programme in Europe, testing clones of surviving Field Elms for innate resistance, has been carried out since the 1990s by national research institutes, with findings centrally assessed and published. In the UK, clones from one of the elms that have so far survived in an area of high infectivity are now available commercially. Mr Paul King of King&Co The Tree Nursery took cuttings from an elm, thought to be nearly 200 years old, located in Essex (probably Ulmus minor subsp. minor, or a local hybrid), in 1990. Having potted the cuttings and found that the trees had indeed a high level of resistance to DED, Mr King then cultivated these cuttings via micro-propagation and now has over 2000 resistant trees for sale to the general public at around 10 foot tall. Historical Significance The first North American Dutch elm disease epidemic began when Ophiostoma ulmi was introduced in the 1920s by furniture makers who used imported European elm logs to make veneer for cabinets and tables. Some of the beetle vectors of the Dutch elm disease pathogens also were brought here from Europe, years before the fungi were introduced. When the more aggressive pathogen, O. novo-ulmi, was later introduced in North America, it killed many elms that had survived the original epidemic. Dutch elm disease epidemics that resulted from movement of Ophiostoma species between and across continents vividly illustrate the dangers inherent in our movement of plant material around the world. A Dutch scientist, Marie Beatrice Schwarz, is credited with first identifying the causal agent of what was to become known as Dutch elm disease. Another Dutch ϯϭ0003 0003
scientist, Christine Johanna Buisman, who had seen the disease in her homeland, first identified Dutch elm disease in Ohio in 1930. The disease spread up and down the U.S. East Coast and west across the continent, reaching the West Coast in 1973. Over 40 million American elm trees have been killed by this disease, and today it is still a very destructive disease of shade trees in the U.S. Many of the elm trees in North America and Europe were planted in rows along streets and walkways, or in hedgerows, or on dikes. The elm trees made effective windbreaks (Fig. 3.22), and the large, overarching branches created beautiful shady canopies (Fig. 3.23). These dense plantings of elm trees are examples of monocultures.
Fig. 3.22
Fig. 3.23
Monocultures are created when plants of the same species are grown in close proximity, with few other types of plants present. People have planted monocultures for hundreds of years and there are many reasons why monocultures are desirable. Monocultures provide uniformity, which is desirable both for aesthetic reasons and for production practices. Planting, management, and harvest are all simpler when one kind of plant is grown in an area. Dangers, however, are inherent in monocultures. Because all of the plants in a monoculture are very much alike, they are all subject to the same catastrophic problems. A disease, insect or weather condition that harms one plant is likely to harm them all. Monoculture is the main reason why Dutch elm disease has been so devastating in our towns and cities. The pathogens can move between closely spaced trees via insect vectors ϯϮ0003 0003
or root grafts, leaving devastation in their wake. The Dutch elm disease epidemics illustrate the value of diversity in plant populations.
ϯϯ0003 0003
Hosts Lethal Yellowing (LY) is a phytoplasma disease that attacks many species of palms, including some commercially important species such as the Coconut0003 and Date Palm. It is spread by the planthopper Haplaxius crudus (former name Myndus crudus) which is native to Florida, parts of the Caribbean and Central America. Infected plants will normally die in 3 to 6 months. The only effective cure is prevention, i.e. planting resistant varieties of coconut palm and preventing a park or 'golf course like' environments which attracts the planthopper. Some cultivars, such as the Jamaica Tall coconut cultivar nearly died out by lethal yellowing. Heavy turf grasses and similar green ground cover will attract the planthopper to lay its eggs and the nymphs develop at the roots of these grasses. The planthpoppers eggs and nymphs may pose a great threat to coconut growing countries' economies, into which grass seeds for golf courses and lawns are imported from the Americas. It is not clearly understood how the disease was spread to East Africa as the planthopper Haplaxius crudus is not native in East Africa.
Fig. 4.2: Coconut palms with various symptoms of LY.
Fig. 4.3: Coconut grove in Ghana badly affected by LY.
The only explanation is that it was imported with grass seed from Florida that were used to create golf courses and lawns in beach resorts. There is a direct connection between green lawns and the spread of lethal yellowing in Florida. Even so-called ϯϱ0003 0003
'resistant cultivars' such as the Malayan Dwarf or the Maypan hybrid between that dwarf and the Panama Tall were never claimed to have 100% immunity. The nymphs of the planthoppers develop on roots of grasses, hence the areas of grass in the vicinity of palm trees is connected with the spread of this phytoplasma disease. The problem arose as a direct result of using coconut and date palms for ornamental and landscaping purposes in lawns, golf courses and gardens together with these grasses. When these two important food palms were grown in traditional ways (without grasses) in plantations and along the shores, the palm grooves weren't noticeably affected by lethal yellowing. There is no evidence that disease can be spread when instruments used to cut an infected palm are then used to cut or trim a healthy one. Seed transmission has never been demonstrated, although the phytoplasma can be found in coconut seednuts, but phytosanitary quarantine procedures that prevent movement of coconut seed, seedlings and mature palms out of an LY epidemic area should be applied to grasses and other plants that may be carrying infected vectors.
Symptoms In general, an early symptom is the drying up of developing inflorescences. In coconut palms the spathes enclosing the flowers become discoloured and the tips blacken. The youngest leaves next to the buds show water- soaked streaks which spread until there is a terminal rot of the growing point. After the first symptoms there is a progressive leaf discoloration, beginning with the older leaves and spreading rapidly to the younger ones. The foliage turns light-yellow and eventually orange-yellow. This symptom coincides with the death of root tips. Death occurs in C. nucifera about 4 months after the initial symptoms appear. For the coconut palm, the progressive symptoms of LY are mainly the following (Dollet, et al. 1977): 1. premature drop of most of the fruit regardless of their development stage 2. blackening of newly opened inflorescences 3. ascending yellowing of the leaves (from the lower to the upper) 4. spear leaf death and collapse, with possibly a few green leaves remaining ϯϲ0003 0003
5. IDOO0003RI0003WKH0003ZKROH0003FURZQ000f0003OHDYLQJ0003D0003EDUH0003WUXQN0003RU0003µWHOHSKRQH0003SROH¶ Infected palms usually die within 3 to 7 months after the appearance of the first symptom (Mc Coy, 1983). No single symptom is diagnostic of lethal yellowing. Symptoms are variable among palm genera and, in the case of coconuts, among cultivars. It is the pattern of appearance and chronological progression of symptoms that accurately identifies the disease. Confirmation of lethal yellowing is based on a molecular diagnostic assay using the polymerase chain reaction (PCR). At least 36 palm species (Table 1) have been documented as susceptible to lethal yellowing, but coconut palm (Cocos nucifera) is most vulnerable to the disease, followed by Pritchardia species, Christmas palm (Adonidia merrillii), and date palm (Phoenix dactylifera). Table 1. Palm species susceptible to lethal yellowing disease. Adonidia merrillii
Dictyosperma album
Phoenix dactylifera
Aiphanes lindeniana
Dypsis cabadae
Phoenix reclinata
Allagoptera arenaria
Dypsis decaryi
Phoenix rupicola
Arenga engleri
Gaussia attenuata
Phoenix sylvestris
Borassus flabellifer
Howea belmoreana
Pritchardia affinis
Caryota mitis
Howea forsteriana
Pritchardia pacifica
Caryota rumphiana
Hyophorbe verschaffeltii
Pritchardia remota
Chelyocarpus chuco
Latania lontaroides
Pritchardia thurstonii
Cocos nucifera
Livistona chinensis
Ravenea hildebrantii
Corypha utan
Livistona rotundifolia
Syagrus schizophylla
Crysophila warsecewiczii
Nannorrhops ritchiana
Trachycarpus fortunei
Cyphophoenix nucele
Phoenix canariensis
Veitchia arecina
The first obvious symptom on mature palms (those able to produce fruit) is a premature drop of most or all fruits. For coconuts, the calyx end of the nut (fruit) will usually develop a brown to black, water-soaked appearance (Figure 1).
ϯϳ0003 0003
Nut or fruit-fall is accompanied or followed by flower necrosis. This symptom is most readily observed on newly mature flowers as they emerge from the spathe (Figure 2). Male flowers abscise, and no fruit is set.
Fig. 4.4
Fig. 4.5
The next symptom observed on mature palms (the first symptom for immature palms or non-fruit bearing palms) is foliar discoloration. This symptom varies markedly among coconut cultivars and other palm genera. For tall-WSH0003 FRFRQXW0003 FXOWLYDUV0003 H0011J0011000f0003 µ-DPDLFD0003 7DOO¶ 000f0003 WKH0003 IROLDJH0003 WXUQV0003 yellow, beginning with the lowermost (oldest) leaves and progressing until the entire crown is affected (Fig. 4.6). In some cases, this symptom is first seen as a VROLWDU000f0003 HOORZHG0003 OHDI0003 ³IODJ0003 OHDI´ 0003 LQ0003 WKH0003 PLGdle of the leaf canopy (Fig. 4.7). Typically, yellowed leaves remain turgid, but eventually turn brown, desiccate, and hang down to form a skirt around the trunk for several weeks before falling. As leaf yellowing advances, the spear (youngest) leaf collapses and hangs down in the crown. Death of the apical meristem (bud) usually occurs when one-half to two-thirds of the crown has yellowed. Eventually, the entire crown of the palm ϯϴ0003 0003
withers and topples, leaving a bare trunk standing (Fig. 4.8). Infected palms usually die within 3 to 5 months after the first appearance of symptoms.
Fig. 4.6
Fig. 4.7
Fig. 4.8
ϯϵ0003 0003
For dwarf-WSH0003FRFRQXW0003FXOWLYDUV0003000bH0011J0011000f0003µ0DODDQ0003*UHHQ0003'ZDUI¶ 000f0003OHDYHV0003JHQHUDOO0003 turn reddish to grayish-brown rather than yellow (Fig. 4.9). Leaflets on the green form of the Malayan Dwarf cultivar may be folded around the midvein (Fig. 4.10). Sometimes, affected leaves appear flaccid, giving an overall wilted appearance to the palm canopy.
Fig. 4.9
Fig. 4.10
Foliar yellowing also develops on Caryota mitis (clustering fishtail palm), C.
rumphiana,
album (hurricane
or
Chelyocarpus princess
chuco, Corypha
palm), Livistona
utan, Dictyosperma
chinensis (Chinese
fan
palm), Pritchardia spp., and Trachycarpus fortunei (windmill palm). In contrast, successively younger leaves turn varying shades of reddish-brown to dark brown or gray in other palm species, such as Adonidia merrillii (Christmas palm), Borassus
flabellifer(palmyra
palm), Dypsis
cabadae (cabada
palm), Phoenix spp. (date palm, Canary Island date palm, wild date palm), and Veitchia arecina (Montgomery palm). Differences may occur in the stage at which spear leaf collapse and necrosis appears on these species. For date palms and palmyra palm, death of the spear leaf often precedes foliar discoloration. For Adonidia andVeitchia spp., the spear leaf is usually not affected until after all other leaves have died. ϰϬ0003 0003
Pathogen Typical phytoplasma particles were found in sieve tubes of infected plants. They were ovoid, elongated and filamentous in shape and were bounded by a triple-layered structure comprising two electron-dense layers with a transparent layer between (Plavsic-Banjac et al., 1972). Pathogen Biology Lethal yellowing is caused by a phytoplasma, a cell wall-less bacterium that belongs to the class Mollicutes. The phytoplasma has been classified as a member of group 16S rDNA RFLP group 16SrIV, subgroup A (16SrIV-A). The proposed name IRU0003WKH0003SDWKRJHQ0003LV0003µCandidatus 3KWRSODVPD0003SDOPDH0011¶ The phytoplasma, which is not culturable, is found only in the phloem of host plants. When observed in phloem sieve elements by electron microscopy, the shape of phytoplasma cells varies from bead-like to filamentous (Fig. 4.11). Nonfilamentous forms average 295 nm in diameter and filamentous forms average 142 nm in diameter and at least 16 µm in length. Each phytoplasma cell is enclosed by a trilaminar unit membrane and contains cytoplasm with DNA strands and ribosomes.
Fig. 4.11
ϰϭ0003 0003
Molecular studies have determined that the lethal yellowing phytoplasma exists as a group of nearly identical strains in the western Caribbean region. Collectively, these strains are phylogenetically distinct from phytoplasmas that infect coconut in Africa or southeast Asia. The lethal yellowing phytoplasma is most closely related to, but distinct from, phytoplasmas associated with decline-type diseases of the monocot Carludovica palmata (Cyclanthaceae) in Yucatán, Mexico, Phoenix canariensis (Canary Island date palm) in the Corpus Christi area of southern Texas (United States), and phytoplasmas causing a newly recognized coconut leaf yellowing syndrome in southwestern Mexico. Insect Vector The pre-imaginal stages of M. crudus are subterranean, feeding on grass roots. They have been described by Wilson & Tsai (1982). The head and thorax of the adults are pale-brown; the forewings are hyaline with pale or light-brown veins. Males and females are 4.2-5.1 mm long. Characters of the male genitalia are essential for the specific identification (Kramer, 1979). In particular, the aedeagus is distinct. In left lateral view it has a long process originating in the distal half and directed ventrally and towards the head. 0003 Means of Movement and Dispersal Natural spread results from the movement of the vector M. crudus. Infected vegetative plant material, including ornamental species, could carry the pathogen in international trade. The vector is less likely to be carried by palms, which are infested only by the actively mobile adults. Since vector efficiency is said to be low, the probability of international movement of the phytoplasma in the vector may be correspondingly low. M. crudus itself could possibly be moved in international trade as nymphs in soil accompanying palms, but would not then be infected by the phytoplasma.
Disease Cycle and Epidemiology Experimental evidence implicates the planthopper Myndus crudus as a vector of the lethal yellowing phytoplasma (Fig. 4.12). The planthopper is an insect with piercing
ϰϮ0003 0003
and sucking mouthparts, and feeds on the contents of the plant host vascular system. The insect spreads the phytoplasma during feeding activity as it moves from palm to palm. The phytoplasma is not known to survive outside either its plant or insect hosts. The geographic range of lethal yellowing is limited in the United States to the subtropical southern third of Florida because the planthopper is not considered cold hardy.
Fig. 4.12
Inoculation of a susceptible plant initiates infection that is followed by a prolonged latent (incubation) phase estimated between 112 to 262 days. About 80 days prior to symptom appearance, the growth of infected palms is stimulated. This is followed by a period of gradual decline, and growth ceases about 1 month before the end of the incubation phase. Following an initial disease outbreak, further spread of lethal yellowing is characteUL]HG0003E0003D0003³MXPS-VSUHDG´0003SDWWHUQ000f0003LQGLFDWLQJ0003GLVVHPLQDWLRQ0003LQYROYLQJ0003DQ0003DLUERUQH0003 vector. Spread occurs among susceptible palms within a localized area, resulting in a random pattern around an active focus of disease that eventually claims most susceptible palms within the locality. Beyond this primary focus, further spread may occur in jumps of a few to 100 km or more, thus establishing new disease foci. Differences in the rates of spread of lethal yellowing at different geographical locations have also been noted. In Florida (United States), spread of the disease from the cities of Miami to Palm Beach, a distance of about 128 km, occurred within 3 years. In Jamaica, however, movement of ϰϯ0003 0003
the disease from the west to the east end of the island, a distance of approximately 238 km, took about 60 years.
Disease Management To discourage the spread of lethal yellowing in the tropics, commercial movement of living palms from locations affected by lethal yellowing to disease-free areas is generally not permitted. However, quarantine requirements vary according to the specific geographical areas involved. Technical guidelines for the safe movement of coconut germplasm have been developed under the auspices of the FAO International Board for Plant Genetic Resources. Chemical control of lethal yellowing is accomplished with the antibiotic oxytetracycline HCl (Terramycin), which is administered to palms as a liquid injection into the trunk. As a therapeutic measure, systemic treatment on a 4-month treatment schedule should begin as early as possible after the onset of symptoms. Palms with >25% discolored leaves should be removed, since they are unlikely to respond to Terramycin treatment. The antibiotic can also be used preventively to protect palms when lethal yellowing is known to occur in the area. The dosage recommended depends on the size of the treated palm. The approximate cost of Terramycin ranges from $1.50 to $4.00 per palm per treatment, depending on the number of palms treated. Control of planthopper populations with insecticides is currently insufficient to justify repeated applications in landscapes or palm plantations. Use of host resistance represents the most practical long-term tool for managing lethal yellowing. Many palm species are not susceptible to lethal yellowing and provide important alternative choices for ornamental landscape plantings. To date, lethal yellowing has not been reported on most palm species native to Florida and the Caribbean Basin. These include Sabal palmetto (cabbage palm),Roystonea regia (royal palm), Acoelorrhaphe wrightii (Paurotis or Everglades palm), and Thrinaxspecies (thatch palms). On the other hand, Cocos nucifera (coconut), Pritchardia spp., Adonidia merrillii (Christmas palm), and Phoenix dactylifera (date palm) have sustained consistent ϰϰ0003 0003
losses and are not recommended for widespread landscape use in areas where lethal yellowing occurs. &RFRQXW0003 FXOWLYDUV000f0003 VXFK0003 DV0003 WKH0003 µ0DODDQ0003 'ZDUI¶0003 RU0003 KEULG0003 µ0D3DQ¶0003 µ0DODDQ0003 'ZDUI¶0003 [0003 µ3DQDPD0003 7DOO¶ 000f0003 KDYH0003 H[KLELWHG0003 DFFHSWDEOH0003 OHYHOV0003 RI0003 UHsistance in most areas. +RZHYHU000f0003UHFHQW0003UHSRUWV0003RI0003OHWKDO0003HOORZLQJ0003ORVVHV0003LQ0003µ0DODDQ0003'ZDUI¶0003DQG0003µ0D3DQ¶0003RI0003 70% and 83%, respectively, at localized sites in southeastern Florida and 95 to 99% in Jamaica cast doubt on the long-term resistance of these cultivars. Significance While coconut palm is highly valued as a woody ornamental plant in the United States, it is an important subsistence crop in the coastal tropics. Almost all parts of the coconut palm are used, providing food, drink, fuel, shelter, and cash income for producers. The term lethal yellowing (often shortened to LY) was first used in the mid1950s to describe a fatal disease of unknown etiology that had affected coconuts in western Jamaica since the 1800s. During the last four decades, outbreaks of lethal yellowing disease have killed most of the once prevalent tall-type coconut cultivars in both Jamaica and Florida (United States). The disease has also been reported from the Bahamas, Belize, the Cayman Islands, Cuba, Dominican Republic, Guatemala, Haiti, Honduras, Leeward Islands (Nevis), and southern Mexico (Yucatan peninsula). Recurrent coconut diseases that resemble lethal yellowing have been recorded elsewhere in the tropics under a variety of names depending on location. Collectively refeUUHG0003 WR0003 DV0003 ³OHWKDO0003 HOORZLQJ-WSH0003 GLVHDVHV000f´0003 WKH0003 LQFOXGH0003 $ZND0003 ZLOW0003 1LJHULD 000f0003 &DSH0003 St. Paul wilt (Ghana), Kaïncopé (Togo), and Kribi (Cameroon) in West Africa; lethal disease (Kenya, Tanzania and Mozambique) in East Africa; and Kalimantan wilt (Central Kalimantan), Natuna wilt (Natuna Islands), and Malaysian wilt (Peninsula Malaysia) in South East Asia.
ϰϱ0003 0003
huckleberry (Vaccinium ovatum), bay laurel (Umbellularia californica), madrone (Arbutus menziesii), bigleaf maple (Acer macrophyllum), manzanita (Arctostaphylos manzanita), and California buckeye (Aesculus californica). On these hosts the fungus causes leaf spot and twig dieback. As of January 2002, the disease was known to occur only in California and southwestern Oregon; however, transporting infected hosts may spread the disease. The pathogen has the potential to infect oaks and other trees and shrubs elsewhere in the United States. Limited tests show that many oaks are susceptible to the fungus, including northern red oak and pin oak, which are highly susceptible. Symptoms
Fig. 5.2: Leaf death caused by P. ramorum
In tanoaks, the disease may be recognized by wilting new shoots, older leaves becoming pale green, and after a period of two to three weeks, foliage turns brown while clinging to the branches. Dark brown sap may stain the lower trunk's bark. Bark may split and exude gum, with visible discoloration. Necrotic bark tissues surrounded by black zone lines are usually present under affected bark. After the tree dies back, suckers will try to sprout the next year, but their tips soon bend and die. Ambrosia beetles (Monarthrum scutellare) will most likely infest a dying tree during midsummer, producing
piles
of
fine
white
dust
near
tiny
holes.
Later, bark
beetles
(Pseudopityophthorus pubipennis) produce fine red boring dust. Small black domes, the fruiting bodies of the Hypoxylon fungus, may also be present on the bark. Leaf death may
ϰϳ0003 0003
occur more than a year after the initial infection and months after the tree has been girdled by beetles. In Coast Live Oaks and Californian Black Oaks, the first symptom is a burgundy-red to tar-black thick sap bleeding from the bark surface. These are often referred to as bleeding cankers.
Fig. 5.3
Fig. 5.4 Pathogen Sudden
oak
death is
the
common
name
of
a
disease
caused
by
the oomycete plant pathogen Phytophthora ramorum. P. ramorum was first reported in 1995, and the origins of the pathogen are still unclear but most evidence suggests it was repeatedly introduced as an exotic species (Grünwald, et al. 2012). Very few control mechanisms exist for the disease, and they rely upon early detection and proper disposal of infected plant material. ϰϴ0003 0003
The Two Mating Types
Fig. 4.5: Mating Structures
P. ramorum is heterothallic and has two mating types A1 and A2 required for sexual reproduction (Boutet, et al. 2010). Interestingly, the European population is predominantly A1 while both mating types A1 and A2 are found in North America (Grünwald, et al. 2008). Genetics of the two isolates indicate that they are reproductively isolated (Ivors, et al. 2004). On average the A1 mating type is more virulent than the A2 mating type but there is more variation in the pathogenicity of A2 isolates (Brasier, et al. 2002). It is currently not clear whether this pathogen can reproduce sexually in nature and genetic work has suggested that the lineages of the two mating types might be isolated reproductively or geographically given the evolutionary divergence observed (Grünwald and Goss, 2011). Transmisson P. ramorum produces both resting spores (chlamydospores) and zoospores, which have flagella enabling swimming. P. ramorum is spread by air; one of the major mechanisms of dispersal is rainwater splashing spores onto other susceptible plants, and into watercourses to be carried for greater distances. Chlamydospores can withstand harsh conditions and are able to overwinter (Davidson, et al. 2001). The pathogen will take advantage of wounding, but it is not necessary for infection to occur (Anon, 2005).
ϰϵ0003 0003
As mentioned above, P. ramorum does not kill every plant that can be used as a host, and it is these plants that are most important in the epidemiology of the disease as they act as sources of inoculum (Garbelotto, et al. 2003). In the USA bay laurel seems to be the main source of inoculum in forests. Green waste, such as leaf litter and tree stumps are also capable of supporting P. ramorum as a saprotroph and acting as a source of inoculum. Because P. ramorum is able to infect many ornamental plants, it can be transmitted by ornamental plant movement.
Oak Wilt
Oak wilt is an aggressive fungus disease caused by Ceratocystis fagacearum. It is one of the most serious diseases in the Eastern United States, killing thousands of oak trees in forests, woodlots, and home landscapes. Susceptible hosts include most oaks in the red oak group and Texas live oak. Symptoms include wilting and discoloration of the foliage, premature leaf drop, and rapid death of the tree within days or weeks of the first symptoms. Trees become infected with oak wilt in two ways: through connections between root systems of adjacent trees, and through insects that carry the fungus to other trees that have been wounded.
Similarities: Oak wilt can also kill trees very quickly, especially if infection begins through root grafts. Differences: The oak wilt pathogen does not cause cankers on the stems, and no bleeding is associated with this disease. Dark staining may be evident
ϱϬ0003 0003
under the bark of trees with oak wilt, but there are no conspicuous zone lines. Oak wilt typically causes red oak leaves to turn brown around the edges while the veins remain green. Leaves are rapidly shed as the tree dies. Conversely, in live oak with the sudden oak death pathogen, the veins first turn yellow and eventually turn brown. Leaves are often retained on the tree after it dies. Oak Decline
Oak decline is a slowacting disease complex that
can
kill
physiologically
mature
trees in the upper canopy. Decline
results
from
interactions of multiple stresses,
such
as
prolonged drought and spring defoliation by late frost
or
insects,
opportunistic root disease fungi such as Armillaria mellea, and inner-barkboring insects such as the two lined chestnut borer and
red
oak
borer.
Progressive dieback of the crown is the main symptom of oak decline and is an expression of an impaired root system. This disease can kill susceptible oaks within 3-5 years of the onset of crown symptoms. Oak decline occurs throughout the range of eastern hardwood forests, but is particularly common in the Southern Appalachian Mountains in North Carolina, Tennessee, and Virginia, as well as the Ozark Mountains in Arkansas and Missouri. ϱϭ0003 0003
Similarities: Oak decline can cause death of many oaks on a landscape scale. Moist, dark stains may be present on the trunk of trees affected by oak decline. Differences: Oak decline shows evidence that dieback has occurred over several years from the top down and outside inward. Newly killed branches with twigs attached are usually found in the same crown as those in a more advanced state of deterioration killed years before. Dieback associated with sudden oak death occurs over a growing season or two. The inner bark beneath the dark stain associated with stem-boring-insect attacks has a discrete margin with no zone lines or evidence of canker development beyond the attack site. Red Oak Borer
Red
oak
borer
(Enaphalodes
rufulus (Haldeman)) attacks oaks of both red and white groups throughout the eastern United States, but prefers members of the red oak group; however, it does not kill trees. Outbreaks are associated with stressed trees that eventually die from oak decline. The complete life cycle takes 2 years. Adults are 1-1.5 inches long with antennae one to two times as long as the body. Larvae are the damaging life stage. Adult females lay eggs in mid-summer in refuges in the crevices of the bark. Newly hatched larvae bore into the phloem, where they mine an irregular burrow 0.5-1 inch in diameter before fall. In spring and summer of the second year, dark, moist stains and fine, granular frass ϱϮ0003 0003
may be seen on the trunk. Exposure of the inner bark reveals the frass-packed burrow and the larva, if it has not bored more deeply into the wood to complete development. Mature larvae are stout, round-headed grubs about 2 inches long before they pupate deep in the wood.
Similarities: Moist, dark stains and fine frass may be present at sites of red oak borer attack. Differences: With red oak borer the inner bark beneath the dark stain contains a frass-packed burrow and has a discrete margin with no zone lines or evidence of canker development beyond it. Disease Management Early detection Early detection of P. ramorum is essential for its control. On an individualtree basis, preventative treatments, which are more effective than therapeutic treatments (Garbelotto, et al. 2007), GHSHQG0003 RQ0003 NQRZOHGJH0003 RI0003 WKH0003 SDWKRJHQ¶V0003 movement through the landscape to know when it is nearing prized trees. On the landscape level, 300110003UDPRUXP¶V fast and often undetectable movement means that any treatment hoping to slow its spread must happen very early in the development of an infestation. Since 300110003 UDPRUXP¶V discovery, researchers have been working on the development of early detection methods on scales ranging from diagnosis in individual infected plants to landscape-level detection efforts involving large numbers of people. Detecting
the
presence
of Phytophthora species
requires
laboratory
confirmation. The traditional method of culturing is on a growth medium that is selective against fungi (and, in some cases, against other oomycetes such as Pythium species). Host material is removed from the leading edge of a plant tissue canker caused by the pathogen; resulting growth is examined under a microscope to confirm the unique morphology of P. ramorum. Successful isolation of the pathogen often depends on the type of host tissue and the time of year that detection is attempted (Kliejunas, 2007a).
ϱϯ0003 0003
Because of these difficulties, researchers have developed some other approaches for identifying P. ramorum. The ELISA (enzyme-linked immunosorbent assay) test can be the first step in non-culture methods of identifying P. ramorum, but it can only be a first step, because it detects the presence of proteins that are produced by
all Phytophthora species.
In
other
words,
it
can
identify
to
the Phytophthora genus level, but not to the species level. ELISA tests can process large numbers of samples at once, so researchers often use it to screen out samples that are likely positive from those that are not when the total number of samples is very large (Kliejunas, 2007a). Some manufacturers produce small-VFDOH0003(/,6$0003³ILHOG0003 NLWV´0003 WKDW0003 WKH0003 KRPHRZQHU0003 FDQ0003 XVH0003 WR0003 GHWHUPLne if plant tissue is infected by Phytophthora. Researchers have also developed numerous molecular techniques for P. ramorum identification. These include amplifying DNA sequences in the internal transcribed spacer region
of the P. ramorum genome (ITS Polymerase Chain
Reaction, or ITS PCR); real-time PCR, in which DNA abundance is measured in real time during the PCR reaction, using dyes or probes such as SBYR-Green or TaqMan; multiplex PCR, which amplifies more than one region of DNA at the same time; and Single Strand Conformation Polymorphism (SSCP), which uses the ITS DNA sequence amplified by the PCR reaction to differentiate Phytophthora species according to their differential movement through a gel (Kliejunas, 2007a). Additionally, researchers have begun using features of the DNA sequence of P. ramorum to pinpoint the minuscule differences of separate P. ramorum isolates from each other. Two techniques for doing this are amplified fragment length polymorphism, which through comparing differences between various fragments in the sequence has enabled researchers to differentiate correctly between EU and U.S. isolates, and the examination of microsatellites, which are areas on the sequence featuring repeating base pairs. When P. ramorum propagules arrive in a new geographic location and establish colonies, these microsatellites begin to display mutation in a relatively short time, and they mutate in a stepwise fashion. Based on this, researchers in California have been able to construct trees, based on microsatellite analyses of isolates collected from around the state, that trace the ϱϰ0003 0003
movement of P. ramorum from two likely initial points of establishment in Marin andSanta Cruz counties and out to subsequent points (Mascheretti, et al. 2008). Early detection of P. ramorum on a landscape scale begins with the observation
of
symptoms
on
individual
plants
(and/or
detecting P.
ramorum propagules in watercourses). Systematic ground-based monitoring has been difficult within the range of P. ramorum because most infected trees stand on a complex mosaic of lands with various ownerships. In some areas, targeted groundbased surveys have been conducted in areas of heavy recreation or visitor use such as parks, trailheads, and boat ramps. In California, when conducting ground-based detection, looking for symptoms on bay laurel is the most effective strategy, since P. ramorum infection of true oaks and tanoaks is almost always highly associated with bay laurel, the main epidemiological springboard for the pathogen (Davidson, et al. 2001; Davidson and Shaw, 2003; Maloney, et al. 2005). Moreover, on many sites in California (though not all), P. ramorum can typically be detected from infected bay laurel tissues via culturing techniques year-round; this is not the case for most other hosts, nor is it the case in Oregon, where tanoak is the most reliable host. As part of a nationwide USDA program, a ground-based detection survey was implemented from 2003 to 2006 in thirty-nine U.S. states to determine whether the pathogen was established outside the West Coast areas already known to be infested. Sampling areas were stratified by environmental variables likely to be conducive to pathogen growth and by proximity to possible points of inoculum introduction such as nurseries. Samples were collected along transects established in potentially susceptible forests or outside the perimeters of nurseries. The only positive samples were collected in California, confirming that P. ramorum was not yet established in the environment outside the West Coast (Oak, et al. 2008). Aerial surveying has proven useful for detection of P. ramorum infestations DFURVV0003 ODUJH0003 ODQGVFDSHV000f0003 DOWKRXJK0003 LW0003 LV0003 QRW0003 DV0003 ³HDUO´0003 D0003 WHFKQLTXH0003 DV0003 VRPH0003 RWKHUV0003 because it depends on spotting dead tanoak crowns from fixed-wing aircraft. Sophisticated GPS and sketch-mapping technology enables spotters to mark the ϱϱ0003 0003
locations of dead trees so that ground crews can return to the area to sample from nearby vegetation (Mai, et al. 2006). Detection of P. ramorum in watercourses has emerged as the earliest of early detection methods. This technique employs pear or rhododendron baits suspended in the watercourse using ropes, buckets, mesh bags, or other similar devices. If plants in the watershed are infected with P. ramorum, zoospores of the pathogen (as well as other Phytophthora spp.) are likely present in adjacent waterways. Under conducive weather conditions, the zoospores are attracted to the baits and infect them, causing lesions that can be isolated to culture the pathogen or analyzed via PCR assay (Murphy, et al. 2006; Murphy, et al. 2008). This method has detected P. ramorum at scales ranging from small, intermittent seasonal drainages to the Garcia, Chetco, and South Fork Eel Rivers in California and Oregon (144, 352 and 689 m2 drainage areas, respectively). It can detect the existence of infected plants in watersheds before any mortality from the infections becomes evident. Of course, it cannot detect the exact locations of those infected plants: at the first sign of P. ramorum propagules in the stream, crews must scour the watershed using all available means to find symptomatic vegetation. A less technical means of detecting P. ramorum at the landscape level involves engaging local landowners across the landscape in the search. Many local county Agriculture Departments and University of California Cooperative Extension offices in California have been able to keep track of the distribution of the pathogen in their regions through reports and samples brought to them by the public. In 2008, the Garbelotto Laboratory at UC Berkeley, along with local collaborators, hosted a VHULHV0003RI0003HGXFDWLRQDO0003HYHQWV000f0003FDOOHG0003³62'0003%OLW]HV000f´0003GHVLJQHG0003WR0003JLve local landowners basic information about P. ramorum and how to identify its symptoms; each participant was provided with a sampling kit, sampled a certain number of trees on his or her property, and returned the samples to the lab for analysis. It is hoped that WKLV0003 NLQG0003 RI0003 ³FLWL]HQ0003 VFLHQFH´0003 FDQ0003 KHOS0003 JHQHUDWH0003 DQ0003 LPSURYHG0003 PDS0003 RI P. ramorum distribution in the areas where the workshops are held.
ϱϲ0003 0003
General sanitation in infested areas One of the most important aspects of P. ramorum control involves interrupting the human-mediated movement of the pathogen by ensuring that infested materials do not move from location to location. While enforceable quarantines perform part of this function, basic cleanliness when working or recreating in infested areas is also important. In most cases, cleanliness practices involve ridding potentially infested surfaces²such as shoes, vehicles, and pets²of foliage and mud before leaving the infested area. The demands of implementing these practices become more complex when large numbers of people are working in infested areas, as in construction, timber harvesting, or wildfire suppression. The California Department of Forestry and Fire Protection and USDA Forest Service have implemented guidelines and mitigation requirements for the latter two situations; basic information about cleanliness in P. ramorum-infested areas can be found at the California Oak Mortality Task Force web site (www.suddenoakdeath.org 0003XQGHU0003WKH0003³7UHDWPHQW0003DQG0003 0DQDJHPHQW´0003VHFWLRQ0003000bVXEVHFWLRQ0003³6DQLWDWLRQ0003DQG00035HGXFLQJ00036SUHDG´ 0011 Wildland management The course that P. ramorum management should take depends on a number of factors, including the scale of the landscape upon which one hopes to manage it. Management of P. ramorum has been undertaken at the landscape/ regional level in Oregon in the form of a campaign to completely eradicate the pathogen from the forests in which it has been found (mostly private, but also USDA Forest Service and USDI Bureau of Land Management ownership) (Goheen, et al. 2002; Goheen, et al. 2004; Kanaskie, et al. 2006). The eradication campaign involves vigorous early detection by airplane and watercourse monitoring, a U.S. Department of Agriculture Animal and Plant Health Inspection Service (USDA APHIS) and Oregon Department of Agriculture-led quarantine to prevent movement of host materials out of the area where infected trees are found, and immediate removal of P. ramorum host vegetation, symptomatic or not, within a 300-foot (91 m) buffer around each infected tree.
ϱϳ0003 0003
The Oregon eradication effort, which began near the town of Brookings in southwest Oregon in 2001, has adapted its management efforts over the years in response to new information about P. ramorum. For example, after inoculation trials of various tree species more clearly delineated which hosts are susceptible, the Oregon cooperators began leaving non-host species such as Douglas-fir and red alder on site. In another example, after finding that a small percentage of tanoak stumps that were resprouting on the host removal sites were infected with the pathogen² whether these infections were systemic or reached the sprouts from the surrounding environment is unknown²the cooperators began pretreating trees with very small, targeted amounts of herbicide to kill the root systems of infected tanoaks before cutting them down. The effort has been successful in that while it has not yet completely eradicated the pathogen from Oregon forests, the epidemic in Oregon has not taken the explosive course that it has in California forests. California, on the other hand, faces significant obstacles that preclude it from mounting the same kind of eradication effort. For one thing, the organism was too well established in forests in the Santa Cruz and San Francisco Bay areas by the time the cause of sudden oak death was discovered to enable any eradication effort to succeed. Even in still relatively uninfested areas of the north coast and southern Big Sur, regionally coordinated efforts to manage the pathogen face huge challenges of leadership, coordination, and funding. Nevertheless, land managers are still working to coordinate efforts between states, counties, and agencies to provide P. ramorum management in a more comprehensive manner. Several options exist for landowners who want to treat to limit the impacts of sudden oak death on their properties. None of these options is foolproof, guaranteed to eradicate P. ramorum, or guaranteed to prevent a tree from becoming infected. Some are still in the initial stage of testing. Nevertheless, when used thoughtfully and thoroughly, some of the treatments do improve the likelihood of either slowing the spread of the pathogen or of limiting its impacts on trees or stands of trees. Assuming that the landowner has correctly identified the host tree(s) and symptom(s), has submitted a sample to a local authority to send to an approved laboratory for testing, and has received confirmation that the tree(s) are indeed infected with P. ramorum² ϱϴ0003 0003
or, alternatively, assuming that the landowner knows that P. ramorum-infected trees are nearby and wants to protect the resources on his or her property²he or she can attempt control by cultural (individual-tree), chemical, or silvicultural (stand-level) means. The best evidence that cultural techniques might help protect trees against P. ramorum comes from research that has established a correlation between disease risk LQ0003FRDVW0003OLYH0003RDN0003WUHHV0003DQG0003WKH0003WUHHV¶0003SUR[LPLW0003WR0003ED0003ODXUHO (Swiecki and Bernhardt, 2007). In particular, this research found that bay laurel trees growing within 5m of the trunk of an oak tree were the best predictors of disease risk. This implies that strategic removal of bay laurel trees near coast live oaks might decrease the risk of oak infection. Wholesale removal of bay laurel trees would not be warranted, since the bay laurels close to the oak trees appear to provide the greatest risk factor. Whether the same pattern is true for other oaks or tanoaks has yet to be established. Research on this subject has been started for tanoak, but any eventual cultural recommendations will be more complicated, because tanoak twigs also serve as sources of P. ramorum inoculum. A promising treatment for preventing infection of individual oak and tanoak trees²not
for
curing
an
already
established
infection²is
a phosphonate fungicide marketed under the trade name Agri-fos. Phosphonate is a neutralized form of phosphorous acid that works not by direct antagonism of Phytophthora, but by stimulating several of kinds of immune responses on the part of the tree.[28] It is mostly environmentally benign if not applied to non-target plants and can be applied either as an injection into the tree stem or as a spray to the bole. When applying Agri-fos as a spray, it must be combined with an organosilicate surfactant, Pentra-bark, to enable the product to adhere to the bole long enough to be absorbed by the tree. Agri-fos has been very effective in preventing tree infections, but it must be applied when visible symptoms of P. ramorum on other trees in the immediate neighborhood are still relatively distant; otherwise, it is likely that the tree one wishes to treat is already infected but that visible symptoms have not yet developed (this is especially true for tanoak).
ϱϵ0003 0003
Trials of silvicultural methods for treating P. ramorum began in Humboldt County in northwest coastal California in 2006. The trials have taken place on a variety of infested properties both private and public and have generally focused on varying levels and kinds of host removal. The largest (50 acres (200,000 m2)) and most replicated trials have involved removal of tanoak and bay laurel by chainsaw throughout the infested stand, both with and without subsequent under burning designed to eliminate small seedlings and infested leaf litter (Valachovic, et al. 2008). 2WKHU0003WUHDWPHQWV0003LQFOXGHG0003KRVW0003UHPRYDO0003LQ0003D0003PRGLILHG0003³VKDGHG0003 fuel break´0003 design in which all bay laurel is removed, but not all tanoaks; bay and tanoak removal using herbicides; and removal of bay laurel alone. The results of these treatments are still being monitored, but repeated sampling has so far detected only very small amounts of P. ramorum in the soil or on vegetation in the treated sites. Nursery management Research and development in managing P. ramorum in nursery settings extends from P. ramorum in the individual plant, to P. ramorum in the nursery HQYLURQPHQW000f0003 WR0003 WKH0003 SDWKRJHQ¶V0003 PRYHPHQW0003 DFURVV0003 VWDWH0003 DQG0003 QDWLRQal borders in infected plants. An array of studies have tested the curative and protective effects of various chemical compounds against P. ramorum in plants valued as ornamentals or Christmas trees. Many studies have focused on the four main ornamental hosts of P. ramorum (Rhododendron, Camellia, Viburnum, compounds
have
been
found;
some
and Pieris). of
the
most
Several effective
effective include
mefenoxam, metalaxyl, dimethomorph, and fenamidone. Many of these studies have converged upon the following conclusions: chemical compounds are, in general, more effective as preventatives than in curatives; when used preventatively, chemical compounds must be reapplied at various intervals; and chemical compounds can mask the symptoms of P. ramorum infection in the host plant, potentially interfering with inspections for quarantine efforts. In general, these compounds suppress but do not eradicate the pathogen, and some researchers are concerned that with repeated use
ϲϬ0003 0003
the pathogen may become resistant to them. These studies and conclusions are summarized by Kliejunas (Kliejunas, 2007b). Another area of research and evolving practice deals with eliminating P. ramorum from nursery environments in which it is established to prevent humanmediated pathogen movement within the ornamental plant trade. One way of approaching this is through a robust quarantine and inspection program, which the various federal and state regulatory agencies have implemented. Under the federal P. ramorum quarantine program implemented by USDA APHIS, nurseries in California, Oregon, and Washington are regulated and must participate in an annual inspection regime; nurseries in the fourteen infested counties in coastal California, plus the limited infested area in Curry County, Oregon, must participate in a more stringent inspection schedule when shipping out of this area (USDA APHIS, 2007). Much of the research into disinfesting nurseries has focused on the voluntary Best Management Practices (BMPs) that nurseries can implement to prevent 300110003 UDPRUXP¶V introduction into the nursery and movement from plant to plant. In 2008, a group of nursery industry organizations issued a list of BMPs that includes subsections on Pest Prevention/Management, Training, Internal/External Monitoring/Audits, Records/Traceability, and Documentation. The document LQFOXGHV0003 VXFK0003 VSHFLILF0003 UHFRPPHQGDWLRQV0003 DV0003 ³$YRLG0003 overhead irrigation of high-risk SODQWV´001e0003 ³$IWHU0003 HYHU crop rotation, disinfect propagation mist beds, sorting area, cutting benches, machines and tools to minimize the spread or introduction of SDWKRJHQV´001e0003DQG0003³1XUVHU0003SHUVRQQHO0003VKRXOG0003DWWHQG0003RQH0003RU0003PRUH0003P. ramorum trainings conducted by qualified personnel or document self-WUDLQLQJ´ (Suslow, 2008; HRI P. ramorum Industry Working Group, 2008). Research on control of P. ramorum in nurseries has also focused on disinfesting irrigation water containing P. ramorum inoculum. Irrigation water can become infested from bay trees in the forest (if the irrigation source is a stream), from bay trees overhanging irrigation ponds, from runoff from infested forests (Tjosvold, et al. 2006), or from recirculated irrigation water (Werres, et al. 2007). Experiments in Germany with three types of filters²slow sand filters, lava filters, and constructed ϲϭ0003 0003
wetlands²showed that the first two removed P. ramorum from the irrigation water completely, while 37% of the post-treatment water samples from the constructed wetland still contained P. ramorum (Ufer, et al. 2008). Since P. ramorum can persist for an undetermined period of time within the soil profile, management programs in nurseries should also deal with delineating the SDWKRJHQ¶V0003 GLVWULEXWLRQ0003 LQ0003 QXUVHU0003 VRLO0003 DQG0003 HOLPLQDWLQJ0003 LW0003 IURP0003 LQIHVWHG0003 DUHDV00110003 $0003 variety of chemical options have been tested for soil disinfestation, including such chemicals as chloropicrin, metham sodium, iodomethane and dazomet. Lab tests indicated that all of these chemicals were effective when applied to infested soil in glass jars. Additionally, tests on volunteer nurseries with infested soil demonstrated that dazomet (trade name Basamid) fumigation followed by a 14-day tarping period successfully removed P. ramorum from the soil profile (Yakabe and MacDonald, 2008). Other soil disinfestation practices under investigation, or in which interest has been expressed, include steam sterilization, solarization, and paving of infested areas. Government Agency Involvement In England in 2009, the Forestry Commission, DEFRA, the Food and Environment Research Agency, Cornwall County Council, and Natural England are working together to record the locations and deal with this disease. Natural England is offering
grant
funding
through
Stewardship and Environmentally
its Environmental Sensitive
Stewardship, Countryside
Area schemes
to
clear
rhododendron.[52] In 2011, the Forestry Commission started felling 10,000 acres (40 km2) of larch forest in the SW of England, as an attempt to halt the spread of the disease.[53] In Northern Ireland at the end of 2011, the Department of Agriculture and 5XUDO0003 'HYHORSPHQW¶V0003 )RUHVW0003 6HUYLFH0003 EHJDQ0003 IHOOLQJ0003 001400170003 KHFWDUHV0003 RI0003 DIIHFWHG0003 /DUFK0003 woodland at Moneyscalp, on the edge of Tollymore Forest Park in County Down.
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Host Butternut (Juglans cinerea) is an endangered species, threatened by a fungal disease called Butternut Canker (Sirococcus clavigignenti-juglandacearum).0003Trees of all ages, all sizes and on all sites are at risk. The USA has lost significant numbers of butternut to the canker. In Canada, butternut was officially listed as endangered under the Species at Risk Act (SARA) in 2005. In Ontario Butternut is listed as an endangered species under the Endangered Species Act (ESA 2007). Open grown butternut trees have a short trunk with a broad, spreading crown. In the forest they have taller, less branchy trunks with smaller crowns. The small branches tend to bend downward and turn up at the ends. Butternut (also known as white walnut) and black walnut can be confused. Also, people have been growing exotic walnuts and creating hybrids in North $PHULFD0003VLQFH0003WKH00030014001b00130013¶V0003± they are not uncommon in urban and long settled areas. Table: - Help to identify the species Butternut Juglans cinerea Larger range than black walnut, North into Central and Eastern Ontario Thick, buff colored 4XLWH0003IX]] &KDPEHUHG0003 SLWK0003 LV0003QDUURZ0003 DQG0003GDUN0003 brown(2 yr twig) +DLU0003IULQJH0003DERYH0003HDFK0003OHDI0003VFDU 8SSHU0003PDUJLQ0003RI0003OHDI0003VFDU0003VWUDLJKW
Black Walnut Juglans nigra Native to Southwestern Ontario
Butternut hybrids & exotic walnuts
If your tree has a few of these characteristics, you might have a hybrid or exotic walnut tree: $0003SODQWHG0003WUHH /LWWOH0003VLJQ0003RI0003FDQNHU 3LWK0003 LV0003 ZLGHU0003 DQG0003 OLJKWHU0003 brown (top 2 yr twig; bottom twig is butternut) /HDYHV0003 VWD0003 JUHHQ0003 DQG0003 RQ0003 tree in the fall weeks later than other native species 0DOH0003 FDWNLQV0003 ORQJHU0003 WKDQ0003 15cm *RRG0003 VHHG0003 FURSV0003 DOPRVW0003 every year +HDUW0003VKDSHG0003QXW0003VKHOO
Leaves
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Bark
Young ± Ash grey, smooth
Thick, orange-brown 6OLJKWO0003IX]] &KDPEHUHG0003 SLWK0003 LV0003 RUDQJHyellow 1R0003KDLU0003IULQJH0003DERYH0003OHDI0003VFDU 8SSHU0003 PDUJLQ0003 RI0003 OHDI0003 VFDU0003 LV0003 notched Slightly fuzzy 7HUPLQDO0003 EXG0003 LV0003 URXQGHG0003 DQG0003 blunt &RPSRXQG0003ZLWK000300140018-23 leaflets 001600130003FP0003ORQJ 7HUPLQDO0003OHDIOHW0003VPDOOHU or missing /HDIOHts are stalked 6OLJKWO0003KDLU0003XQGHUVLGH