Part 5

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.

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 ROT

_Polyporus 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.

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 ROT

_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 PINE

Littleleaf 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.

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 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.

WALNUT ANTHRACNOSE

Walnut 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 ANTRHACNOSE

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 ANTHRACNOSE

Dogwood 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.

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 RUST

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 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 CANKER

Nectria 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.

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 CANKER

Strumella 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 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 CANKER

Spiculosa canker, caused by _Poria spiculosa_, is found on bottomland oaks in the South. Occasionally this disease will also degrade hickories and honeylocust.

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 CANKER

Irpex 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.

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 CANKER

_Polyporus 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.

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 CANKER

_Botryosphaeria 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.