  NEEDLE CASTNeedle cast is a very common disease of conifers throughout eastern and southern United States. Eastern white, loblolly, longleaf, pitch, pond, shortleaf, table mountain, and Virginia pines are all susceptible. Hypoderma lethale is probably the most common cause of needle cast on the above hosts, with the exception of longleaf pine. Lophodermium pinastri is also associated with needle cast. Hypoderma needle cast on loblolly pine. Current pine needles are infected in the early summer, and by winter or early spring begin to turn brown at the tips. At this time the tree usually has a scorched appearance. Later, the browning progresses down the needle and the fungal fruiting bodies are produced. These are small, black, elongated structures known as hysterothecia, which open along a slit during moist weather to release their spores. The infected needles are often “cast,” leaving only the new growth, and causing the tree to have a tufted appearance. Controls are seldom needed for this disease in forest stands. Infected trees usually recover and put out new foliage the year following heavy attacks. Nurseries or plantations should not be established in areas where needle cast is prevalent. Lophodermium needle cast on 2-0 nursery stock and 5 year old scotch pine, Spanish variety. (cont.) BROWN SPOT NEEDLE BLIGHTBrown spot or brown spot needle blight is caused by the fungus Scirrhia acicola. Brown spot occurs in all the coastal states from Virginia to Texas, and inland to Arkansas and Tennessee. All southern pines are attacked by the fungus, but only longleaf pine seedlings are seriously damaged. Brown spot needle blight on longleaf pine reproduction. Initial infection of pine needles results in the development of small, circular spots of grey green color, which later turn brown. As the fungus continues to grow, a necrotic area encircles the needle, appearing as a brown band. The infected area will then increase in size, eventually resulting in the death of the needle. Fruiting bodies, called acervuli, develop in the dead areas of the needle. Spores are extruded from the acervuli in a water soluble gelatinuous matrix throughout the entire year. The spores are washed apart and splashed short distances by rain drops. These spores spread the disease from seedling to seedling. During the winter and early spring, the sexual stage of the fungus is produced on dead needles. Ascospores, produced in a fruiting body called a perithecium, are light and wind-disseminated. These spores are responsible for disease spread. During the grass stage, seedlings often become heavily infected by the brown spot fungus, resulting in partial to complete defoliation. Seedlings which are nearly defoliated every year remain in the grass stage and eventually die. Three successive years of complete defoliation will result in death. The disease is very damaging during wet years, especially in areas where the fungus has become well established in the absence of controls. The disease can be reduced by control burning during the winter months. On seedlings, fire burns the diseased needles and reduces the amount of available inoculum for reinfection, leaving the large terminal bud unharmed. Often a single prescribed burn reduces the disease intensity to such low levels that vigorous seedling height growth begins the following year. Fungicide sprays will also reduce brown spot on high valued trees. PINE NEEDLE RUSTFruiting bodies of pine needle rust on loblolly pine. Nearly all the native pines in southern United States are attacked by various needle rust fungi of the genus Coleosporium. This disease is very common, but causes little harm to the trees. Many species of this rust also attack broadleaved weeds in addition to the pines, needing both host types to complete their life cycle. Needle rusts are most prevalent on young trees in the seedling to sapling stage. In the spring or early summer small, delicate white fungus “cups” filled with yellow to orange spores are produced on the needles. From a distance entire seedlings may appear to have a whitish or yellowish cast. Individual needles which are heavily infected may die, turn brown, and drop from the tree. However, the entire tree is rarely defoliated. Small red “rust pustules” form on the undersurface of the weed leaves. These are replaced by dark structures later in the summer. The needle rusts are not important enough to warrant control in natural forests or plantations. If the weed (alternate) host is known, it can be eradicated around nurseries of susceptible pine species. However, it would be better to establish nurseries in rust free areas. CEDAR APPLE RUSTCedar apple rust, caused by Gymnosporangium juniperi-virginianae, is important commercially in the apple-growing regions of the Virginias, Carolinas, and the Mississippi Valley. The alternate hosts of this rust are eastern red cedar and several species of junipers. Fruiting galls containing spores on cedar tree. Fruiting on apple leaf the alternate host. Cedar “apples” or galls are the characteristic signs of the fungus on cedars. Cedar needles are infected in the summer by wind-borne spores from apple leaves. By the next spring or early summer galls begin to appear as small greenish brown swellings on the upper needle surfaces. By fall, the infected needle turns into a chocolate brown gall covered with small circular depressions. The following spring, orange jelly-like tendrils protrude from the galls producing an attractive ornament for the cedar tree. Spores produced from these orange spore masses are then capable of reinfecting apple leaves, thus completing the fungus life cycle. No practical control of the rust on cedars is available because of the low value of cedar. However, considerable effort is expended to protect apple trees. Where apple is to be protected, cedars should be eliminated in the vicinity or, rust galls should be picked or cut off cedars before the galls mature. CEDAR BLIGHTCedar blight, caused by Phomopsis juniperovora, is most severe on eastern red and Rocky Mountain cedars. Other hosts include arborvitae, cypress, and Atlantic white cedar. The disease ranges from the mid-West to the Atlantic coast and south to Alabama where it is most common in nurseries. Needle symptoms on 1-0 eastern red cedar nursery stock and 5 year old Arizona cypress. (cont.) Symptoms on red cedar resemble that of drought. The tips of branches are killed back and sometimes entire trees will turn brown. The fungus forms black fruiting bodies on needles and stem lesions. Fungus spores are distributed by rainwater; nursery overhead sprinkling systems also facilitate blight spread. Control of cedar blight is initiated by removing and burning infected nursery stock early in the season before infection becomes heavy. Seedbeds should be well drained. Avoid introducing cedar stock to an infected nursery. The location of cedars in the nursery should be changed frequently and, where possible, cedar beds should be kept well away from older cedar or cedar hedges. Seedlings growing in low-density seed beds are more vulnerable to the blight; thus beds should be fully stocked. Cedar mulch should never be used on cedar beds. Avoid wounding nursery transplants. No economically feasible control is available for forest stands. FUSIFORM RUSTGalls on 1-0 pine nursery stock. Damage caused by fusiform rust infection. Fusiform rust, caused by Cronartium fusiforme, is one of the most important diseases on southern pines. This rust is found from Maryland to Florida and west to Texas and southern Arkansas. The rust’s most important impact is in nurseries, seed orchards, and young plantations. Loblolly and slash pines are very susceptible to this rust. Pitch and pond pines are moderately susceptible, longleaf pine is fairly resistant, and shortleaf pine is highly resistant. The most easily recognized symptom is the spindle-shaped canker on the pine branches or main stem. In early spring these swellings appear yellow to orange as the fungus produces powdery spores. As host tissue is killed, older stem cankers may become flat or sunken. Cankers often girdle trees and wind breakage at the canker is common. Fungus spores from the pine infect oak leaves. Brown hair-like structures, produced on the underside of the leaves in late spring, are the most conspicuous signs. These projections produce spores which in turn reinfect the pine trees, completing a “typical” rust cycle. Fruiting fusiform-shaped canker on main stem of southern pine. Silvicultural practices may lessen the incidence of infection in plantations. Avoid planting highly susceptible species such as slash and loblolly pines in areas of known high rust incidence. In these areas more resistant species such as longleaf or shortleaf pine should be planted. Pruning infected branches will prevent stem infection in young plantations. Rust-resistant pines should be readily available from the nurseries in the near future. Culling out seedlings with obvious galls before outplanting will reduce the disease incidence in new plantations. WHITE PINE BLISTER RUSTWhite pine blister rust, caused by Cronartium ribicola, was introduced to North America on nursery stock about 1900. It is the most important disease on white pine in the United States. In the South, the disease is found on eastern white pine in the Appalachian mountains. Fruiting cankers showing yellow-colored spores of blister rust on eastern white pine. (cont.) The disease is caused by a fungus that attacks both white pine and wild and cultivated currant and gooseberry bushes, called Ribes. Both hosts must be present if the fungus is to complete its life cycle. Attack by the disease is followed by the development of cankers on the main stem or branches. Infected pines die when a canker completely girdles the main stem or when many of the branches are killed by girdling. The most conspicuous symptoms of the disease are the dying branches or crowns (“flags”) above the girdling cankers, and the cankers themselves. Initially, a narrow band of yellow-orange bark marks the edges of the canker. Inside this band are small irregular dark brown scars. As the canker grows, the margin and bank of dark scars expand and the portion formerly occupied by the dark scars is now the area where the spores that infect Ribes are produced. During the months of April through June white sacs or blisters containing orange-yellow spores (called aeciospores) push through the diseased bark. The blisters soon rupture and the orange-yellow spores are wind-dispersed for great distances. Generally, there is some tissue swelling associated with the canker, which results in a spindle-shaped swelling around the infected portion of the stem. Loss of white pines from blister rust can be prevented by destroying the wild and cultivated Ribes bushes. Bushes may be removed by uprooting by hand, grubbing with a hand tool, or with herbicides. Pruning infected branches on young trees will prevent stem infections and probably tree mortality. COMANDRA BLISTER RUSTFruit gall showing orange colored spores on loblolly pine. Alternate host—false toadflax. Comandra blister rust, caused by the fungus Cronartium comandrae, is a canker disease of hard pines. The disease presently occurs in widely scattered areas throughout the western, central, and southern United States. In the South, the primary hosts are loblolly, shortleaf, pond, and Virginia pine. Herbaceous plants of the genus Comandra, commonly known as false toadflax or comandra, are also attacked. The fungus infects pines through the needles and grows from the needle into the branch or main stem where it forms a gall or canker. Dark orange-colored spores which are produced on the surface of the gall in the spring are wind-blown and infect the leaves or stems of the comandra plants. Two to three weeks after infection, urediospores are produced on the underside of the comandra leaf. These are wind-blown and can only infect other comandra plants. Eventually hair-like structures known as telia are produced on the comandra leaves and stems. The telia produce spores which are wind-blown and infect the pine host through the needle. The necessary combination of a susceptible pine host, the alternate host, and the pathogen is presently known to occur only in northern Arkansas, eastern Tennessee, and northern Alabama. No effective method of controlling the disease in forest stands is presently known. Silvicultural or forest management practices which reduce the abundance of the alternate host offer promise of long term control. Maintenance of dense stands and heavy ground cover as a means of shading out the intermediate host plants, may be helpful in reducing rust damage in many areas. EASTERN GALL RUSTEastern gall rust, caused by the fungus Cronartium cerebrum, attacks many species of eastern hard pines. The disease ranges eastward from the Great Plains and is most severe in the South on Virginia and shortleaf pines. Like most rusts this fungus requires an alternate host in addition to its pine host. In this case oaks, especially the red oak group (black, red, scarlet and pin) are the alternate hosts. Damage to the oaks is generally not of economic importance as only the leaves are affected. Fruiting gall showing red-orange spores on Virginia pine. On pines the fungus causes the formation of globose to sub-globose galls. Canker formation occurs occasionally but mortality generally results from wind breakage at the gall rather than by canker formation as literally hundreds of galls may appear on a single tree. They are not lethal to the tree, but may ruin tree form and on a large stem they can lead to an open decayed wound, as decay fungi are often secondary invaders of rust infections. The shape of galls and the arrangement of the spore sacs filled with red-orange spores present a cerebroid (brain-like) appearance. During the spring the bright orange galls are very striking. This disease is sometimes a problem in nurseries where seedlings are attacked and killed. This is where control efforts are concentrated. Fungicide protectants are applied to the seedling foliage to prevent infection from spores produced on oaks. Contact your local forestry extension agent or the nearest Division of Forest Pest Management for the latest recommendations. Under forest conditions, control is not economically feasible. Trees of poor form should be removed during thinning operations. SOUTHERN CONE RUSTSouthern cone rust is caused by the fungus Cronartium strobilinum. It has been reported to completely destroy slash and longleaf pine cone crops in Georgia and along the Gulf Coast from Florida to Texas. Cone rust symptoms on slash pine. (cont.) Like most other rusts, the fungus requires oaks and pines to complete its life cycle. Although infection of oak leaves occurs annually, no significant economic damage is done to the oaks. Fungus spores produced on oak leaves infect the mature female pine flowers about the time of pollination (January-February). The fungus grows through the developing conelet causing it to swell abnormally. By early April or late May the infected cones are three to four times larger than the normal first-year cones and even exceed the maturing second-year cones in size. The swollen cone scales are reddish in color. Cavities in the cone filled with orange-yellow spores burst and the cones become orange-yellow. The swollen orange-yellow cones in the tree crowns can be easily distinguished from normal cones by an observer on the ground. By late summer most of the diseased cones have died and fallen. Control at present is confined to seed orchards. Hydraulic spraying of the flowers with fungicides gives a significant reduction in infections. Consult your local forester, county extension agent or the nearest Forest Pest Management Office for current control recommendations. PITCH CANKERPitch canker, caused by the fungus Fusarium lateritium forma pini, is rapidly becoming widespread throughout the South. The disease apparently is most serious on Virginia, slash and south Florida slash pine. The fungus also attacks shortleaf, pitch, and table-mountain pine. Pitch canker infection in terminal branch and main stem of pine. (cont.) Pitch canker may cause tree mortality. On Virginia pines the fungus reportedly enters through small insect wounds in the twigs or mechanical wounds in the bole. Shoots may be girdled and killed within a few weeks, but it takes a period of years for the fungus to girdle the bole of larger trees. On slash pine the disease apparently attacks plantations in wave years. During years of heavy attack the fungus can cause rapid crown deterioration in addition to causing bole canker infections. Cankers on leaders in the crown can result in death of two-thirds or more of the crown by mid-summer in a tree that appeared healthy in the spring. In the majority of tree infections only the leader and one or two laterals will be infected. The tree recovers in a few years with a crook in the bole as the only evidence of attack. Pitch cankers usually retain the bark and old cankers on the hole may be sunken. The most diagnostic characteristic of the disease, and the one that definitely separates it from similar disease, is the heavy pitch soak of the wood beneath the canker. Pitch cankers are often so soaked with pitch that heavy flow of pitch is observed flowing down the bole. At the present time, no known method of control exists. Observations in slash pine plantations indicate that some trees are resistant while others range in their degree of susceptibility. WOOD DECAYWood decay of southern forest trees is responsible for nearly 80 percent of all loss attributed to disease. This decay is caused by fungi which mainly attack heartwood in the central portion of stems, branches, and roots. Wood-rotting fungi gain entrance into the tree through broken branches, wounds, and damaged or exposed roots. Spores, which land at these damaged areas, germinate and produce a microscopic mycelium which attacks and spreads throughout the heartwood. The decay is caused by the action of the mycelium, which penetrate the cell walls and dissolve or alter the wood in various ways. Fungus development within the tree may continue for many years without any apparent effect on the growth of the host. Eventually the mycelium will aggregate and break through the bark to form the reproductive stage, either before or after the death of the host. The fruiting body (sporophore, conk) produces vast amounts of spores which are capable of spreading the fungus to other trees. Heartrots may be separated into broad classes on the basis of the host portion attacked, such as root rots, root and butt rots, stem rots, and top rots. Decay fungi may be further separated into two broad classes based on their effect on wood. The first class causes white rots, decomposing all components of the wood and reducing it to a spongy mass with white pockets or streaks separated by firm wood. The second class, causing brown rots, utilize the cellulose, leaving the lignin more or less unaffected. This usually results in a rot which appears as some shade of brown. The separation of wood decay fungi on the basis of their host range, the portion of the host attacked, and the type of rot produced are useful aids to a pathologist in determining a tentative identification of the fungus responsible for a particular type of rot. However, there are numerous fungi which cause decay, many of which are exceptions to the various methods of classification. This forces the pathologist to use microscopic examination and various artificial keys to arrive at the proper identification of a given rot-producing fungus. Sectioned stump showing rot and decay in heartwood. RED HEARTThe fungus, Fomes pini, is the cause of a heartrot of widespread distribution. Common names for the rot produced by this fungus are: red heart, red ring rot, or white peck. The disease is commonly associated with mature and over-mature conifers, especially Douglas fir, larch, spruce, and pine. In the southern United States, the fungus attacks all species of mature pine. Fruiting body of redheart on southern pine. Generally, infection of all hosts occurs through dead branch stubs. Early stages of decay caused by F. pini are characterized by a discoloration of the heartwood, often appearing light red to reddish brown. The advanced stages of heartrot appear as elongated white pockets or flecks, formed parallel to the grain and separated by apparently firm wood. Often the pockets become resin filled. On southern pine hosts, the conks are often bracket-like or hoof-shaped. The upper surface appears dull grey to dark brown, with concentric furrows parallel to the margin of the fruiting body. The lower side is a light brown to brownish gold, rimmed by a velvety golden brown margin. Swollen knots result from the living wood tissue trying to overgrow the knot where a conk is forming. Cross section of infected tree showing rotted and decayed heart wood. In southern forest stands, heartrot damage may be reduced by harvesting mature pines prior to the age of extreme susceptibility to fungus attack. Some degree of shade tree protection can be obtained by pruning dead and dying branches flush with the main stem. This will allow the knot to be quickly overgrown by sap wood, preventing the heartrot fungus from entering through the branch stub. ANNOSUS ROOT AND BUTT ROTFomes annosus fruiting bodies on stump. Annosus root and butt rot is caused by the fungus Fomes annosus. This pathogen is common throughout coniferous stands of the North Temperate Zone. Hardwoods may be attacked, but damage is usually of minor consequence. In the South, the disease is most serious in pine plantations on sandy soils with low organic matter. All species of southern pine are susceptible. Slash and loblolly plantations are often severely affected. The disease gains entry into plantations by spore infection of freshly cut stumps during thinnings. The fungus then spreads from the infected stumps to residual trees by growth along the roots to points of root contact. Residual trees usually begin to die within a few years after thinning. The sporophores or fruiting bodies are generally found at ground line or in the root crotch. Pines in initial stages of the disease usually exhibit sparsely foliated crowns; however, white pine with full crown may have extensive butt and root decay. Occasionally trees may die rapidly with a sudden red discoloration of a nearly full crown. Diseased trees are often found in groups or circular pockets in the stand. The indication of F. annosus decay may include the pink to violet stain of incipient decay, the narrow elongated white pockets and scattered black flecks in the wood of the early decay stages, and the yellow stringy rot of the late stages of decay. Infection center in pulpwood size pine stand. Control includes avoidance of planting on soils of low organic matter and elimination of thinning. Stump infection following thinning or harvest may be prevented using various methods. BROWN CUBICAL BUTT ROTPolyporus schweinitzii is a common cause of root and butt rot of conifers throughout North America. The primary hosts of the fungus are Douglas fir, spruce, and pine. All southern pines are susceptible to attack by P. schweinitzii. Common names of the rot are: red-brown butt rot and brown cubical butt rot. Fruiting body of brown cubical root and butt rot of pine. The fungus enters living hosts through damaged roots, fire scars, and other wounds near the tree base. The initial stage of decay appears as a light yellow stain. In the advanced stage, the heartwood becomes brittle and breaks into large yellow-brown to reddish-brown cubes. The fungus develops primarily in the roots and butt and seldom extends more than 15 or 20 feet up into the stem. Diseased trees are subject to wind-throw and wind breakage. Although the volume of wood destroyed by the rot is small, the total volume lost through wind-throw is quite large. Mature, suppressed, and weakened off-site trees are commonly attacked by the fungus. It is assumed that the fungus may also spread from infected to healthy trees through root contacts and grafts. The only outward signs of decay are the annual sporophores, which develop in late summer and fall during moist weather. Conks formed at the base of infected trees are bracket shaped, while those arising from decayed roots appear circular, sunken in the center, and supported by a short stalk. When fresh, the upper surface is velvety, concentrically zoned, and reddish-brown in color with a light yellow margin. The underside is dark olive or green with large irregular pores. In forest stands, no method of controlling the disease is known. Losses may be prevented to some extent by reducing the amount of root damage and wounding from heavy logging equipment. The prevention of basal fire scars in conifer stands will also reduce the incidence of this disease. Trees which show signs of advanced root and butt rot should be removed from around recreation areas, parking lots, power lines, and buildings to avoid damage from wind-throw and wind breakage. RED ROOT AND BUTT ROTFruiting body of red root and butt rot of pine. Polyporus tomentosus causes red root and butt rot of living conifers throughout North America. Common hosts of the fungus are: spruce, larch, pine, fir, Douglas fir, hemlock, and cedar. Throughout the southern United States, P. tomentosus has been reported in two general areas; causing extensive degrade of mature shortleaf pine in northern Arkansas and root and butt rot of slash pine in South Carolina, Georgia, and Florida. The fungus is believed to enter living hosts through basal wounds and damaged roots. Under ideal conditions, the fungus may spread from infected to healthy trees by way of root contacts or grafts. Growth of the fungus is very slow, often causing host mortality 20 to 30 years after initial infection. Wood decayed initially appears firm, but dark reddish-brown in color. In advanced stages, the wood is flecked with elliptical white pockets separated by brown-colored wood. Infected conifers generally express typical root rot symptoms. Trees show evidence of reduced radial and internodal growth, accompanied by death of the crown from the base upward. The foliage appears off-color and reduced in length. Under moist conditions, sporophores are produced either at the base of infected trees or on the forest floor. Bracket-shaped sporophores are produced at the base of infected trees while stipitate conks are produced on the ground directly over infected or dead roots. Fresh sporophores appear yellow-brown in color from above with a lighter colored pore surface below. No effective method of controlling the disease in forest stands is presently known. However, damage and losses may be reduced by management practices which reduce or eliminate the chance introduction of the disease into healthy stands. In areas where red root and butt rot is common, attempts should be made to conduct logging and thinning operations during the dry season to avoid mechanical damage to the root systems of the residual trees. LITTLELEAF OF PINELittleleaf of pine, caused by Phytophthora cinnamomi, is the most serious disease of shortleaf pine in the Piedmont region of the South. Loblolly is also affected, usually where associated with infected shortleaf pine. The disease is most evident in older age classes, rarely attacking stands under 20 years old. Needle symptoms and damage of littleleaf on shortleaf pine. (cont.) The disease is caused by a malfunctioning of the root system due to a combination of biological and physical factors. A fungus, Phytophthora cinnamomi attacks and kills the root tips. When conditions of moisture, fertility, and drainage are adverse, they reduce tree vigor and prevent the tree from rapidly replacing the destroyed root tips. Trees on good sites are reportedly also attacked by the fungus, but their vigor is such that they quickly overcome the disease by producing new root tips. The disease usually progresses rather slowly. Some trees may persist fifteen or more years after the appearance of initial symptoms. In general, trees live only five or six years after attack, but they may die in as little as one year. Symptoms are those typical of trees in stress due to a malfunction of the root system. In the early stage of the disease the foliage may turn yellow-green and the current year’s needles are shorter than normal. Later stages of the disease are sparsely foliated crowns with short needles (reduced from three to five to only one-half to three inches in length) and dead branches. Abundant foliage sprouting on the hole of infected shortleaf is common. Losses are minimized by salvage cuttings and by favoring loblolly and hardwoods in regeneration plans. SYCAMORE ANTHRACNOSEDefoliation of sycamore tree caused by sycamore anthracnose. Sycamore anthracnose, caused by Gnomonia veneta, is common on American sycamore throughout its range in the eastern United States. Anthracnose is a disease characterized by distinctive limited lesions on stem, leaf, or fruit, often accompanied by dieback or blight and usually caused by fungi that produce slimy spores that ooze from small cup-shaped fruiting bodies that are visible with a hand lens. This disease has four distinct symptom stages identified as twig blight, bud blight, shoot blight, and leaf blight. Twig blight appears before leaf emergence and kills the tips of small one-year-old twigs. Infection comes initially from leaf litter and twig cankers. The second stage, bud blight, develops during bud expansion in April and early May. Shoot blight, the most frequently observed symptom, causes the sudden dying of expanding shoots and also young leaves. Leaf blight, the final stage, involves the actual infection of expanding or mature leaves. Diseased portions of the leaf involve irregular brown areas adjacent to the midrib and veins which are dotted with diseased spots. Incidence of anthracnose is directly related to the amount of spring rainfall. Shoot blight is severe if the weather for two weeks after leaf emergence is cool and moist. The disease may defoliate trees, which usually put out a new crop of leaves by late spring or summer. Control of sycamore anthracnose under forest conditions is not economically feasible. Where the disease is prevalent, other species should be favored during thinnings. In shade and ornamental trees, pruning of infected twigs, burning of leaves, and fertilization will reduce the disease impact. Leaf and twig symptoms. WALNUT ANTHRACNOSEWalnut anthracnose is a fungus disease caused by Gnomonia leptostyla. This worldwide disease attacks most species of walnut in the United States. Black walnut is most severely affected, but with favorable weather for the fungus, even less susceptible individuals may be defoliated. Butternut, Persian walnut, and two species from California (Hinds walnut and California walnut) are all susceptible. Anthracnose has also been reported on species of walnut from most of the European countries, Argentina, Canada, and South Africa. Wet weather greatly favors this leaf disease which may defoliate black walnuts by late July or early August. Defoliation slows growth, weakens trees, and sometimes causes mortality. Infected leaves reveal circular spots of dark brown or black. These spots often grow together, leaving large dead areas. These spots or blotches are bordered with yellow to golden tissue. While severely affected leaves fall, some “anthracnose” leaves remain on the tree. This disease also affects the growth and quality of the nuts. Nutmeats from infected trees are dark, unattractive, and shrivelled. Sunken, killed areas appear on the husks as dark circular spots smaller than those on the leaves. Infected nuts, like the leaves, may also fall from the tree. Lesions may appear on the current year’s shoots and later form dead sunken areas that are oval to irregularly circular with reddish brown margins. As with the other anthracnose diseases, no practical control is available for forest trees. Control of walnut anthracnose on ornamentals and nut trees is partially achieved by raking and burning of old leaves. OAK ANTRHACNOSELeaf symptoms of oak anthracnose. Oak anthracnose is caused by the fungus Gnomonia veneta. Trees of the white oak group, particularly white oak, are susceptible to this disease. Oaks throughout the entire eastern United States are affected by the disease, although it is less common in the Northeast. Infection occurs in the early spring or mid-summer. Symptoms on leaves develop as irregular brown diseased areas (blotches) along the midrib and the major side veins. These blotches may grow together by late spring or early summer if infection occurs early. Blotches are usually confined to the areas bordered by the larger veins. Leaves on the lower branches are frequently killed and occasionally trees will be defoliated. However, a second crop of leaves soon develops and mortality is rare. Fruiting bodies of Gloeosporium, the imperfect fungus fruiting stage of anthracnose, are located on the midrib and veins of infected leaves. When the disease spreads to the twigs, cankers and crown dieback may occur. The anthracnose fungus overwinters on diseased twigs and in the leaf litter. Oak anthracnose has the same causal agent as sycamore anthracnose, and the weather conditions favoring the sycamore disease also increases the anthracnose on oak. Control is similar to sycamore anthracnose and involves an integrated program of pruning disease tissue, fertilization, and burning of leaf litter. No practical control is available for forest trees. DOGWOOD ANTHRACNOSEDogwood anthracnose, caused by the fungus Elsinoe corni, occurs in states bordering the Atlantic Ocean and has also been reported in Louisiana. Its primary host is flowering dogwood, Cornus florida L. Leaf and flower symptoms of dogwood anthracnose. (cont.) Anthracnose occurs in the spring and affects not only the leaves, but also the buds and “flowers”. The buds may fail to open or they may produce stunted flowers. These have many circular to elongated spots with light tan centers. Margins of these spots are purple to brown. Often the flowers abort before development. Foliage spots (1-2 mm. in diameter) are raised at the margins. They are purple at the edges and yellow-gray in the center. Later centers of spots may fall out causing a “shothole” effect. Dozens of spots may be present on a single leaf and may be scattered or concentrated at tip, margin, or midrib. Twisting and malformation of the leaves are common. In addition to floral and foliage spots, infected areas may also occur on petioles, stems, and fruit clusters. All three areas have spots similar to those on the foliage. Other diseases which may be confused with anthracnose include Septoria and Ascochyta leaf spots. Septoria usually begins around July and unlike anthracnose has more angular lesions that are between the veins. Ascochyta spots may be larger (6 mm. in diameter) than anthracnose, and tissue discoloration may extend outside of their borders. Occasionally the leaves may totally blacken. This disease may occur as early as June. Wet, humid weather at certain stages of plant development is required for infection. Homeowners may obtain effective control by removing and burning infected plant parts. Various fungicide sprays are recommended by authors of ornamental handbooks. COTTONWOOD RUSTRust infected cottonwood leaf. Cottonwood rust, caused by Melampsora medusae, is probably the most important leaf disease of cottonwoods wherever they are grown. In the Lower Mississippi Valley, all sizes of eastern cottonwood trees may be infected with this rust. However, the disease is probably of most importance in cottonwood nurseries. In mid-summer, yellow to orange pustules containing spores of the fungus form on the under surface of the cottonwood leaves. In late summer and early fall, dark brown fungal growths replace the orange structures. Cottonwood may be prematurely defoliated or even killed by successive attacks. The rust may weaken trees and subject them to attack by other disease-causing organisms. Also, there is often a reduction in growth in these normally fast growing species. This is very important since there is presently a wide interest in the use of hybrid poplars for pulp and timber production. There is generally no accepted control for cottonwood rust. Rust-resistant varieties of hybrid and exotic cottonwoods are being developed and may provide the best control of this disease. BLACK KNOTBlack swellings of cherry black knot. Black knot, caused by Dibotryon morbosum, is prevalent throughout the Southeast (with the exception of southern Florida) wherever black cherry grows, and in orchards on plums and domestic cherries. The most prominent symptoms are the elongated black swellings which appear in summer on small twigs and branches. Heavily infected trees appear quite grotesque, with large swellings which may be several times the diameter of the twigs. Cankers occurring on black cherry trunks usually ruin the commercial tree value. Initial infection occurs on lateral branches and twigs in the spring, but the swellings do not become noticeable until the following spring. The most practical control for black knot is removal of infected black cherry from the stand. Twigs and branches with knots should be burned. NECTRIA CANKERNectria canker of hardwoods, caused by Nectria galligena and N. magnoliae, is frequently found on yellow birch and black walnut. Common hosts also include bigtooth aspen, sassafras, northern red oak, red maple, beech, Carolina poplar, paper birch, and sweet birch. A closely related canker disease is also found on yellow-poplar and magnolias. The range of this disease includes the Lake States, the Northeast, and the southern Appalachians. Target-shaped canker of Nectria on sassafras and yellow-poplar. (cont.) Older Nectria cankers are easily recognized in forest stands because of their typical “target” shape. “Target” cankers have rings, each of which represent a year’s growth. Younger cankers tend to be grown over by bark and callus tissue attempting to heal the wound. Such cankers are difficult to recognize, but close examination of the affected area may reveal tiny red bodies, which are the fruiting bodies of the Nectria fungi. Mortality rarely occurs from this disease, but stems may break at canker locations during high winds. Control of Nectria canker is the same as for Strumella canker—the removal of infected trees during thinning operations. STRUMELLA CANKERStrumella canker of hardwoods, caused by Strumella coryneoidia, most frequently attacks trees of the red oak group. Other hosts include species in the white oak group. Beech, basswood, blackgum, shagbark hickory and red maple are also occasionally affected. This disease is found in the East, from the southern Appalachians to northern New England. Strumella canker on black oak. Strumella cankers are of two types: diffuse, and the more common “target-shaped.” The first develops on smooth-barked saplings and rapidly girdles and kills the tree. Killing results because callus tissue, which tends to heal over cankers, does not have time to develop. Target-shaped cankers are more common. “Targets” are formed by the alternation of killing of bark by the fungus around the canker’s perimeter and the formation, in turn, of a callus ridge by the host tree. The fungus is active usually in the dormant season, while callusing occurs in the spring. As with most canker-causing fungi, Strumella usually enters the tree through a branch stub. Cankers are quite large and may reach several feet in circumference or length. The presence of the causal fungus is revealed by dark brown, cushion-like structures about one to three millimeters in diameter on the dead bark and surrounding tissue. No feasible control method is available under forest conditions. However, the disease impact can be greatly reduced by removing cankered trees during thinning operations. SPICULOSA CANKERSpiculosa canker, caused by Poria spiculosa, is found on bottomland oaks in the South. Occasionally this disease will also degrade hickories and honeylocust. Fruiting body of Poria rot and canker on oak. Cross section of tree showing rot and decay. Spiculosa canker is considered to be a canker-rot disease, a type of decay in which the causal organism incites not only heart-rot but also large irregular cankers. Infected trees have cankers that appear as rough circular swellings on the bole. The canker centers are depressed and old branch stubs are discernible. Fungus fruiting bodies, or conks, usually are not present on living trees but develop on snags or decayed logs. The conks grow flat under the bark and push it off to expose the brown fungus fruiting surface. Control for Spiculosa canker is similar to other canker rots: salvage to remove undesirable cankered trees that may be later replaced by better quality trees. IRPEX CANKERIrpex canker, caused by Irpex mollis, is prevalent in bottomlands and on upland areas of the Southeast. In the bottoms, Nuttall, water, and willow oaks are affected. White, chestnut, southern red, and black oaks are the hosts of this disease on upland sites. Fruiting body of Irpex rot. Cross section of tree showing rot and decay. Irpex canker is also considered to be a canker-rot disease. Symptoms on infected trees frequently involve irregular cankers up to two feet in length. Cankers are usually found on trees eight to ten inches in diameter or larger, at a height of twenty feet above the ground. Branch stubs, signifying probable infection points, are usually present in the centers of cankers. The portion of the trunk affected is usually swollen but sometimes may be sunken. At the base of the sunken portion of the canker are small, creamy-white, toothed fruiting bodies or conks with a leathery texture. Conks also appear on hardwood logs. The wood behind cankers is characterized by a tough, spongy, white rot which extends as much as eight feet above and below the canker. The decay pattern may also extend downward into the roots. In cross-section, the rotted areas appear as finger-like projections radiating out toward the sapwood. Gradually the rot column tapers to a thin central core beyond which white flecks appear, and this early rot stage is concentrated along the rays of the oaks. Control for Irpex canker is the same as for other canker-rots—salvage of undesirable cankered trees. HISPIDUS CANKERPolyporus hispidus is the cause of trunk cankers and localized decay of hardwoods throughout eastern, central, and southern United States. The fungus is also known to attack hardwoods in Oregon and California. Reported hosts are: hickory, ash, mulberry, willow, walnut, and oak. In the south, P. hispidus is common on oaks, including willow, water, black, white, Nuttall, and cherrybark. Fruiting body and canker of Hispidus on oak. The fungus usually enters the tree through dead branch stubs, from which it grows into the heartwood. After becoming established, the fungus begins penetrating the sapwood and attacks the living cambium. Callus folds are formed by the host around the dead cambial area, forming an elongated swollen canker, commonly referred to as a “hispidus canker”. The cankered area of the stem is bark-covered and sunken, usually containing a remnant of a branch stub or branch scar. During late summer, fall or early winter, the fungus produces conks (sporophores) on the surface of the cankers. The annual bracket-shaped conks are large, spongy, and yellowish-brown to rusty-brown on the upper surface. When fresh, the under surface is a light tan color. After a few months, the mature conks dry to a rigid black mass and fall from the canker. Old conks are commonly found at the base of cankered trees during the spring and early summer. Decay produced by the fungus appears spongy, light yellow, and is commonly separated from the sound wood by a black zone line. The rot is of the delignifying white rot type. On southern oaks, the rate of canker elongation has been estimated at one-half foot per year, with the internal rot usually extending about one foot above and below the cankered area. No effective control in forest stands is known. Removal of diseased trees provides additional growing space for crop trees. Some degree of shade tree protection can be obtained by pruning of dead branches flush with the main stem of the tree. BOTRYOSPHAERIA CANKERBotryosphaeria ribis causes cankering and mortality of more than 50 woody plants. The fungus is widely distributed throughout the eastern one-half of the United States. The pathogen infects the following economically important hosts: sweetgum, redbud, willow, poplar, tupelo, pecan, and hickory. Botryosphaeria canker on sweetgum. The fungus gains entry into susceptible hosts primarily through wounds or dead and dying twigs. Small oval cankers on stems or branches are the first symptoms of infection. As the fungus continues to attack and kill the cambium, the sunken cankers enlarge, eventually girdling and killing the branch or stem above the cankered area. In the spring and early summer, cankers on living portions of the host often produce an exudate. Infected sweetgums generally produce the exudate in great quantities, to which the common name of bleeding necrosis has been applied. Reproductive structures called stroma are produced by the fungus on dead cankered stems and branches during moist periods of the spring and summer. No practical method of control is known. Diseased trees seldom recover. Infection of high value shade and ornamental trees may be prevented to some degree by avoiding mechanical damage. Dead limbs and branches should be pruned and wounds covered with a suitable tree paint. Infected trees should be removed and burned. SEPTORIA CANKERSeptoria canker on young cottonwood saplings. Septoria canker is caused by the fungus Septoria musiva. Although this is a disease of poplars, native poplar species are not severely attacked. However, this is an important problem wherever hybrid or introduced poplars are grown. With the ever-increasing emphasis on poplar planting, this will probably become a much more important problem in the near future. Young stem cankers usually develop around openings such as wounds, lenticels, or leaf scars, appearing first as sunken, dark areas of the bark. The infected area later becomes more depressed and darker as tissue dies, and often a black margin will be formed around the canker. Small, pink, hair-like spore tendrils are produced by the fungus around the canker margin, especially during moist weather. These tendrils contain spores which can cause further infection, and arise from small dark fungal fruiting structures called pycnidia. This cankered area is often invaded by insects and other fungi and is also a weakened area at which wind breakage may occur. The fungus also causes a gray to black leaf spot, which usually has a light colored center. These spots may coalesce on a severely infected leaf and involve the entire leaf surface. This leaf spot in itself causes slight damage, but acts as a source of fungus spores which can cause stem cankers, and thus is important in the overall consideration of the disease. Defoliation in cottonwood caused by Septoria leafspot. A control for this disease is to use native poplars or resistant hybrids wherever possible. Wider spacing in plantations may also reduce the humidity, decreasing the amount of infection. CYTOSPORA CANKERCytospora canker is caused by Cytospora chrysosperma. This fungus attacks more than 70 species of hardwood trees and shrubs as well as some conifers. Poplars and willows are among the most common hosts, and are attacked throughout their range. Trees used for shade or windbreak, and also cuttings in propagation beds are particularly susceptible to this canker. This disease is most severe on trees growing under stress, such as those growing on an unfavorable site, or injured by drought, frost, fire, or severe pruning. The fungus is a normal inhabitant of the bark and becomes parasitic only when the tree is weakened. Cytospora canker on cottonwood. A canker begins as a gradual, circular killing of the bark of a limb or stem. This infected tissue soon appears as a brownish, sunken patch, around which the host often produces raised callus tissue. Small black fungal structures (pycnidia) appear as small pimples on the dead bark. During moist weather, thin threads of spores exude out from the pycnidia. The inner diseased bark becomes dark and odorous. The cambium is killed and the sapwood becomes watery and reddish brown as it becomes infected. Water spouts may form below the canker before the tree dies. Since this disease is most severe on weakened trees, shade trees should be watered and fertilized to maintain healthy, vigorous growth. Wounding and severe pruning should be avoided. Cuttings should be selected from healthy planting material grown in disease free areas. If cuttings are to be stored for any length of time, they should be kept at a temperature below 35°. This low temperature will keep new infections from occurring, even if spores are present. CHESTNUT BLIGHTStem canker caused by chestnut blight organism. Chestnut blight is caused by the fungus Endothia parasitica. It can be found on American chestnut throughout its range where it has virtually eliminated this valuable species from eastern hardwood forests. The chestnut blight fungus is also parasitic on other hosts including common chinkapin, Spanish chestnut, and post oak. Japanese and Chinese chestnuts are resistant. Stem cankers are either swollen or sunken and the sunken type may be grown over with bark. The fungus forms fruiting bodies some distance back from the advancing cankers, and the spores may exude from bark crevices as orange curl-like masses during moist weather. Young cankers are yellow-brown in sharp contrast to the normal olive-green color of the bark. The chestnut is a vigorous sprouting species but the fungus survives in previously killed stumps and later kills the new sprout growth. No effective control has been developed for chestnut blight, even after several decades of intensive research. The most promising control involves the development of a blight-resistant species. Research is presently underway on this matter but results are inconclusive. Fruiting bodies on surface of canker. OAK WILTThis serious vascular wilt of oaks is caused by the fungus Ceratocystis fagacearum. At least fifty species and varieties of oak are susceptible. The disease has been most damaging in the Lake States but is also found in the eastern United States. Oak wilt symptoms on red oak trees and leaves. (cont.) Oak wilt symptoms are most noticeable during late spring or early summer. Red oaks may be killed in as little as three weeks, the lower branches being affected last. In white oaks, symptoms are usually confined to a few branches each year and trees may live several years before death. Leaf symptoms are similar for both red and white oaks. Leaves turn yellow or brown and become dry progressively from the edge or tip to the midrib and base. Mature leaves may fall at any symptom stage from green to brown. Premature leaf shedding is the most outstanding symptom. A definite characteristic of the disease is the raising and cracking of the bark due to pressure of mats of the fungus growing between the bark and wood. Oak wilt is spread over long distances by insects that pick up spores while crawling on the mats of infected trees. The disease may also spread from tree to tree via root graft. Short-distance spread is controlled by severing all roots of living trees around infected trees by use of a ditchdigger. Another control is to fell all trees in a 50-foot radius of infected trees; felling and burning of all parts of infected trees is sometimes done to prevent overland spread. DUTCH ELM DISEASEDying tree infected with Dutch elm disease. Dutch elm disease, caused by Ceratocystis ulmi, is the most devastating disease of elm trees in the United States. This disease has been recorded in most states east of the Mississippi and as far as Idaho in the Northwest and Texas in the Southwest. All of the native elm species are susceptible, while many of the ornamental Asiatic species are highly resistant. Trees suffering from Dutch elm disease may show a variety of symptoms. Leaves become yellow, wilt, and turn brown. Premature defoliation and death of branches usually occurs, causing the crown to appear thin and sparse. Internally, a brown discoloration appears in the outer sapwood. C. ulmi is transmitted from diseased to healthy elms by elm bark beetles, mainly the small European elm bark beetle and the native elm bark beetle. These beetles make characteristic galleries under the bark of dead and dying elms. Adult beetles pick up the sticky fungus spores from under the bark and then feed on the young tender elm twigs of healthy trees, inadvertently inoculating the healthy tree with the fungus. The fungus may also spread from diseased elms to adjacent healthy elms through root grafts. Discoloration and streaking symptoms in the sapwood. Controls to combat this disease generally involve sanitary measures aimed at the beetles. Dead and dying elms should be burned. This eliminates the elm wood which normally serves as a breeding place for elm bark beetles and thus reduces the beetle population. In areas where most native elms are infected, other tree species or resistant elm species, such as the Chinese or Siberian elm, should be planted rather them native elms. ELM PHLOEM NECROSISElm phloem necrosis is a disease of elm, caused by a virus or virus-like organism. The disease has occurred in the United States for many years, probably as early as 1882. The pathogen is transmitted from infected to healthy trees by the adult white-banded elm leafhopper, Scaphoideus luteolus, which feeds on the leaf veins. It is now present throughout most of the central, eastern, and southern portions of the United States. The disease is known to occur on American and winged elm, but all native elms are probably susceptible to attack by the pathogen. Foliage symptoms of elm phloem necrosis. The earliest symptoms of the disease appear in the top of the crown, at the outer tips of the branches. Here the elm leaves suddenly wilt, turn yellow, the margins curl upward and the leaves die. Leaf-fall causes the crown to appear sparse. In large trees, the foliage symptoms may initially appear on one branch or only a portion of the crown. However, the symptoms during the advanced stage of the disease are exhibited throughout the crown. The most reliable symptom appears as a yellow to butterscotch discoloration on the inner bark surface or phloem. This symptom initially appears under the bark of large roots, later spreading to the base of the main stem and finally to the larger branches. Phloem and cambial discoloration is often found in advance of the foliage symptoms. The moderately discolored phlomen has a slight odor of wintergreen. Thus far, all trees known to be infected with the pathogen have died. Acutely infected trees, while initially appearing healthy, may wilt and die in three to four weeks. Stem sample showing discoloration of sapwood. No effective controls are known. The “Christine Buisman” elm, which is highly resistant to Dutch elm disease, has demonstrated resistance to elm phloem necrosis. MIMOSA WILTMimosa branches showing wilt symptoms. A vascular wilt of the mimosa (silktree) is caused by the fungus Fusarium oxysporum forma perniciosum. The fungus is known only to attack the mimosa, a tree imported from eastern Asia and grown throughout the southeast as an ornamental. Since the discovery of the disease in North Carolina in 1935, the fungus has spread north to Maryland, south to Florida, and west to Texas. The fungus causing mimosa wilt is soil-borne and gains entrance into the tree by attacking the roots. Once entrance is gained by the fungus, the pathogen enters the outer water-conductive system in the sapwood. As the fungus grows throughout the system, it hinders or completely inhibits the water movement from the roots to the aerial portion of the tree. The first outward symptom of disease is the wilting of leaflets, usually in the upper portion of the crown. The wilted leaflets turn yellow, then brown, and die. Often a branch or two will succumb at a time until the entire crown is dead. A second symptom of the disease is found in the outer sapwood of the tree. A brown discoloration, appearing as spots or a ring, is observed by cutting into the outer sapwood of the infected stem or branch. Control of the fungus is very difficult, since it is soil-borne and enters through the roots. However, resistant varieties of mimosa trees, developed by the U.S. Department of Agriculture, are now available at most commercial nurseries. Branch sample showing brown discoloration of sapwood. VERTICILLIUM WILTVerticillium wilt, caused by common soil-inhabiting fungi belonging to the genus Verticillium, is found on a number of hardwood hosts. In southern and eastern United States elms and maples are attacked throughout their natural ranges. Wilting foliage and defoliation of elms caused by Verticillium wilt. Infected trees may die within a few weeks after the first symptoms are observed, or they may survive for years. The first symptoms of the disease involve a wilting of the foliage, with the leaves turning yellow and finally brown. The early symptoms are often restricted to a single limb or portion of the crown. Vascular discoloration, which is brown in elms and green in maples, is present in the outer sapwood. In elms, this discoloration is similar to that produced in trees having Dutch elm disease. This disease is not of serious consequence in forest stands. However, it is often extremely important in high value shade trees. Dead or dying limbs on lawn trees may be pruned out. This may not always save the tree, but may help keep it alive for years. Trees should be well watered and fertilized as necessary. If a lawn tree dies from Verticillium wilt, it should be replaced by a resistant species. ARMILLARIA ROOT AND BUTT ROTMushroom or fruiting bodies of the “honey mushroom” rot. Armillaria root and butt rot is caused by the fungus Armillaria mellea. This disease is common in orchards, vineyards, gardens, parks, and forests throughout the world. Both coniferous and hardwood forest trees are attacked. The fungus is especially troublesome in plantations, particularly in stands recently thinned. The fungus is spread by spores produced by honey-colored mushrooms, rhizomorphs, and root contacts between diseased trees or stumps and healthy trees. Rhizomorphs are visible strands of compacted mycelium (fungus material) that appear as black or reddish-brown “shoestrings.” They may be flattened when found between bark and wood or cylindrical when found in decayed wood or soil. Rhizomorphs increase in length at their tips and in this manner the fungus may move through the soil from infected trees to uninfected trees. The honey-colored mushrooms are produced annually and are fairly short lived; they are subject to desiccation, and are favored by small mammals. The size of the top varies from two to five inches in diameter. The top is usually flecked with dark brown scales. White to light yellow gills are borne underneath. Crown symptoms of the trees affected are similar to those caused by any malfunctioning of the roots. A reduction in size and production of leaves or needles, a general thinning of the crown, branch dying, and yellowing of foliage may precede death or trees may die rapidly with a rapid red discoloration of the foliage. Trees often die in groups, but single-tree kill is also common. Cankers bleeding resin, gum or other exudate at the tree base are common symptoms. Control is not attempted for this disease under forest conditions. Losses may be reduced by following proper planting procedures, and by salvage cutting. Shoestrings of armillaria. CYLINDROCLADIUM ROOT ROTThis nursery disease is caused by two fungi species. Cylindrocladium scoparium and C. floridanum: Cylindrocladium root rot has been found on two hardwoods (yellow-poplar and black walnut) and two conifers (white pine and Fraser fir) in forest tree nurseries in six southern states. These include Virginia, West Virginia, North Carolina, Tennessee, Alabama, and Mississippi. Leaf symptoms on 1-0 black walnut nursery stock. Root rot symptoms on hardwoods and conifers are quite different. The most characteristic root symptoms on yellow-poplar and black walnut are the blackened and longitudinally-cracked infected roots that are in sharp contrast with healthy white roots of these two species. Infected seedling leaves become yellow and later turn reddish-brown. Root rot symptoms on conifers involve either rotting of the seed or seedling (pre-emergence damping off) before emergence from the soil or seedling root rot following emergence. These symptoms also involve a shrivelling and reddening of foliage, needle blight, and stem cankers. The most characteristic symptoms are the “patchy” irregularly scattered pattern of infection in conifer seedling beds and the loosening of the root epidermis on infected roots—making it very easy to pull off. Root symptoms on 1-0 yellow-poplar nursery stock. The most practical and effective control for root rot diseases of this type involves strict quarantine to either keep the disease out of the nursery or keep it confined to known infected areas by avoiding the transportation of root material, organic matter, and soil from infected to non-infected seed beds. Soil fumigation may control this disease if applied under favorable conditions. LUCIDUS ROOT AND BUTT ROTFruiting body of Lucidus root and butt rot on mimosa. Polyporus lucidus is the cause of root and basal stem decay of hardwood trees throughout the eastern, central, and southern portions of the United States. The fungus is known to attack and kill maple, hackberry, orange, lemon, ash, sweetgum, oak, locust, elm, tupelo, willow, and mimosa. Mimosa trees are very susceptible to attack by P. lucidus throughout the South. The disease is characterized by a rapid decline and death of the host. Examination of infected roots will reveal a soft spongy white rot with black spots scattered throughout. Fruiting bodies are formed at the base of infected trees or on the surface of exposed roots. The mature fruiting bodies are a reddish brown above and white below, with the tops and stems appearing glazed or varnished. The fungus is believed to gain entrance into the host through bark and root injuries and can spread from infected to healthy trees through root contacts and grafts. No control is known for this disease. Avoidance of lawnmower and other mechanical injuries to the base of roots of susceptible shade trees will reduce the chance of infection by the fungus. The spread of the disease from infected to healthy trees can be reduced by planting at a wide enough spacing to avoid root contacts and grafts. If you find damage on your trees from insects or diseases you may consult with any of the following offices or your state forester.
Forest Environment: WEATHER FIRE PEOPLE SOIL ABUSE PESTS FOREST PEST MANAGEMENT GROUP Southeastern Area S. and P. F.—7 1972 |
|
