Chapter II: Part 2

Adult weevils are attracted by the odor of fresh pine resin, and quickly invade logging areas. Eggs are laid in lateral roots of fresh pine stumps, where they hatch in approximately five to ten days. Larvae feed on the inner-bark tissues of roots. At maturity, larvae usually construct a chip cocoon in a chamber cut into the wood, and pupate in the cocoon. On emerging, adults feed on the tender bark of seedlings, or twigs of trees. The small irregular feeding patches in the bark are characteristic of weevil damage. Heavy feeding girdles the stem or twig, causing wilting and eventual death. Newly emerged adult females feed for approximately one month before laying eggs. Females may lay eggs sporadically through two growing seasons. The average female lays about 50 eggs in her lifetime. In the South there are two peaks in adult weevil population each year; the first occurs in the early spring (March-May) followed by a second somewhat lower peak in July and August.

This insect can be controlled by delaying planting in cut-over areas for at least nine months, or by treating seedlings with a suitable insecticide.

WHITE PINE WEEVIL, _Pissodes strobi_ (Peck)

The white pine weevil is generally regarded as the most serious insect pest of white pine. Although it usually does not cause mortality, trees suffering repeated attacks become stunted and deformed to the point of being commercially unusable. The weevil has become such a problem in some areas that it prohibits the growing of white pine. In addition to eastern white pine, the white pine weevils also attack Norway spruce and jack pine. Other pines and spruces are attacked to a lesser degree. The weevil is found throughout the range of eastern white pine.

During the latter half of April, the adults may be found on the terminal shoots of host trees where the female lays her eggs. Up to 200 eggs are deposited over a six-week period. The eggs are laid in feeding punctures in the bark, and hatch about two weeks later. Characteristically, the young larvae position themselves around the shoot and begin feeding as a group down the terminal through the inner bark. Small holes scattered over the bark are characteristic of white pine weevil attacks. After five or six weeks the larvae construct pupal chambers in the pith or wood of the terminal shoot and transform into adults. The young adults remain in the dead terminal until late October and November when they move to favorable overwintering sites on the ground, usually at the base of the host tree.

Control of the white pine weevil is difficult. It is possible, however, to reduce the damage by making conditions in a young stand unfavorable for egg laying. This is possible because the female weevil will only lay eggs within a rather narrow range of temperature and relative humidity. Various techniques involving the use of shade from “nurse trees” have been developed but require intensive management. Under certain circumstances, chemical control can be used.

PITCH-EATING WEEVIL, _Pachylobius picivorus_ (Germar)

In the Gulf Coast States the pitch-eating weevil is probably the most troublesome insect pest of pine seedlings. No accurate figures are available on the damage directly attributable to this pest, but mortality losses are estimated to average about 30 percent in susceptible areas. All of the southern hard pines and other conifers are probably suitable breeding and host material for the pitch-eating weevil. Its range overlaps that of the pales weevil, being reported from Labrador, Canada, south to Florida and west to Texas. It occurs in damage-causing numbers only in the Gulf Coast States.

Pitch-eating weevils breed in the roots of freshly cut stumps. The adults burrow down through the soil, sometimes a considerable distance from the stump, and lay their eggs in niches chewed in the root bark. On hatching, larvae mine the inner bark, packing their galleries with frass. Pupal cells are excavated in the sapwood, and a chip cocoon is constructed from the excelsior-like material removed during the cells’ construction. Development time varies from six to ten months depending on when the stumps are initially infested. Emerging adult pitch-eating weevils feed by night on the tender bark of seedlings. Small irregular patches of bark are removed, eventually girdling the seedling and causing its death. The pitch-eating weevil exhibits a population trend similar to that of the pales weevil, and is a threat mostly in early spring and in the fall.

The most effective control for pine reproduction weevils is to wait nine months before replanting or until the stumps in an area are no longer attractive to the weevil. Chemical control can be used when such a delay is considered impractical.

DEODAR WEEVIL, _Pissodes nemorensis_ (Germ.)

This snout beetle is very similar to the white pine weevil both in appearance and habits. It is found throughout the south- and mid-Atlantic states from southern New Jersey west to Missouri. Although deodar cedar is the preferred host, Atlas cedar, Lebanon cedar, and several species of southern pines are also attacked.

Adults emerge from April to May and feed briefly on the inner bark of leaders and lateral branches of host trees. Heavy feeding frequently girdles the stem and can kill small trees. The adults are dormant during the summer, but resume activity in the fall to lay their eggs. From one to four eggs are deposited in feeding punctures. The newly hatched larvae bore into the inner bark where they construct winding galleries which girdle the stem. Evidence of such infestations is often delayed until January when the branches begin to turn brown. Winter is spent in the larval stage. The larvae pupate in March or April and the cycle is complete.

Keeping shade trees in a vigorous condition by proper watering and fertilization helps reduce their susceptibility to weevil attack.

CONEWORMS, _Dioryctria_ spp.

Coneworms are perhaps the most destructive insect pests of pine cones in the South. They are particularly serious in superior-tree seed orchards where they frequently cause substantial economic loss. There are five important species of coneworms in the South, one or more of which attack all of the native and exotic pines.

Although the number of generations per year varies with the species, their general life history is similar. Female moths lay their eggs around wounds, cankers, galls, etc., but also deposit particularly on terminal growth. Eggs generally hatch in about a week. Larvae may stay at a single feeding site, or move to several different sites before completing their development. This latter behavior often results in a single larva destroying several cones or shoots. Pupation takes place in a chamber constructed by the larva at the feeding site. Depending on the species and time of year, the adult may emerge in two to three weeks or overwinter in the pupal stage. Coneworms cause several kinds of damage. They may mine through the inner bark, bore up the center of a shoot, or completely hollow out a cone. Their attacks are sometimes marked by fecal pellets and large pitch masses.

Several parasites attack coneworms but are seldom effective enough to prevent population build-ups. Chemical control is often necessary on seed orchards to ensure adequate protection of the cone crop.

PINE SEEDWORMS, _Laspeyresia_ spp.

Until recent years little has been known about pine seedworms. These insects are found throughout the South but seldom have population explosions. An exception to this is on slash pine in Florida where over 70 percent of one year’s cones were reported infested. Longleaf pine cones in Texas and Louisiana have also had over 60 percent cone infestation on occasion. Loblolly and shortleaf pine cones are seldom over 20 percent infested. Seedworms have been found infesting longleaf, loblolly, shortleaf, slash, and Virginia pine cones. _Laspeyresia anaranjada_ Miller attacks primarily slash pine, occasionally longleaf pine, and rarely loblolly pine. _L. ingens_ Heinrick attacks primarily longleaf and slash pine. _L. toreuta_ Grote attacks Virginia, shortleaf, and loblolly pine in the South.

The female moth lays eggs from April through May on second-year cones. There is one generation per year. Larvae feed within developing seeds until the cone matures. In late fall, larvae either bore into the cone axis or remain in a hollowed-out seed, and overwinter. Pupation occurs within the cone and moths emerge through the hollow seeds. External evidence of seedworm attack is not visible in immature cones. As cones mature, damaged seeds are retained in the cone. Heavily damaged cones do not open properly. In high-value seed orchards and seed production areas some protection from seedworm attack may be obtained through the use of pesticides applied in a carefully timed program.

BALSAM WOOLLY APHID, _Adelges piceae_ (Ratzeburg)

The balsam woolly aphid was introduced into northeastern North America from Europe around the turn of the century. Since then it has become a pest of major importance to true firs on the east and west coasts of the continent, and threatens some 60,000 acres of Fraser fir in the southern Appalachians. Usually the balsam woolly aphid has two generations per year in the southern Appalachians. Eggs of the first generation hatch in late June and July followed by the second generation in September and October. The immature stage of the aphid known as a “crawler” is the only motile stage in the aphid’s life cycle. Once the crawler begins feeding, it transforms into an adult and never again moves. Reproduction is parthenogenic with each female laying approximately 100 eggs during her lifetime.

In the feeding process the aphid injects a salivary substance into the host tree, which causes growth abnormalities. Initial symptoms of aphid attack may include “gouting” of buds or twig nodes and some twig and branch die-back. Heavy stem attacks reduce the tree’s ability to translocate food and water. Usually a heavily infested tree dies within two to seven years.

Chemical control is effective but extremely costly and thus limited to very high-value areas along scenic road-ways. Other control measures include removal and destruction of infested material.

DISEASES

NEEDLE CAST

Needle 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.

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.

BROWN SPOT NEEDLE BLIGHT

Brown 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.

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 RUST

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 RUST

Cedar 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.

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 BLIGHT

Cedar 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.

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 RUST

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.

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 RUST

White 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.

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 RUST

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 RUST

Eastern 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.

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 RUST

Southern 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.

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 CANKER

Pitch 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 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 DECAY

Wood 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.

RED HEART

The 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.

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.

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 ROT

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.

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.

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 CANKER

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.