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Nonnative Diseases of Hardwoods

Dogwood anthracnose

The eastern flowering dogwood is a small tree that is valued as an ornamental and for its beauty in both forest and urban landscapes. It is also an important source of soft mast for over 100 different species of wildlife that feed on its berries (Kasper 2000). It is typically an understory tree found growing mixed with other hardwoods such as oak and hickory. The southern range of this disease is presented as figure 17.11.

Dogwood anthracnose is caused by an introduced fungus, Discula destructiva. It was first reported in the United States on flowering dogwood in 1978 and on western flowering dogwood in 1979.

For the past two decades, flowering dogwoods have been declining at an alarming rate. In some areas, they have been all but eliminated from the forest ecosystem above 3,000 feet in elevation.

Dogwood anthracnose affects all ages and sizes of dogwoods. The impact is most severe on fully shaded, understory trees, which are normally killed in 2 to 5 years. The most characteristic symptom of dogwood anthracnose is the yearly twig and branch death beginning in the lower part of the canopy (Britton and others 1993, Daughtrey and others 1988).

In the South, the most severe hazard for infection and mortality is at elevations above 3,000 feet and on shaded north-facing slopes. At lower elevations, the hazard is most severe in shaded, moist, and cool areas. Trees growing in full sunlight or on southern or western facing slopes at elevations below 3,000 feet sustain little damage from the disease.

Ornamentals are often disfigured without being killed, particularly if they are growing on open, sunny sites. In the last 10 years, the popularity of this tree as a landscape ornamental has declined because of the sudden destructive outbreak of dogwood anthracnose (Daughtrey and others 1996).

There is no known control of the disease for dogwoods growing in the forest, but vigorously growing trees tend to suffer less damage than weakened or stressed trees. Stress factors such as drought and winter injury appear to increase susceptibility (Anderson and others 1994). High-value trees can generally be protected by mulching, watering during droughts, and applying a fungicide.

While there is no practical control strategy for this disease in forest settings, hotter, drier climate in the southern and western portions of dogwood’s range may limit its spread. Neither ownership nor intensity of management has had any significant effect on this disease.

A few disease-free trees have been found in the native population of dogwoods in areas of high dogwood mortality. An anthracnose-resistant flowering dogwood was introduced into the marketplace in the fall of 2000 (Windham and others 1998). Planting resistant trees in high-value areas is practical and wildlife may ultimately spread anthracnose-resistant seeds throughout the forest. However, the native population of dogwood is expected to continue to decline.

Beech bark disease

Beech bark disease is caused by a complex of two or more agents working in concert. The beech scale attacks the bark of American beech, creating infection courts subsequently colonized by the fungus Nectria coccinea var. faginata. This fungus causes cankers that coalesce and girdle host trees.

While the beech scale is now a common pest of the American beech, it is nonnative, having been introduced through Nova Scotia (Canada) in the late 1800s. There is speculation that the fungus was also introduced. Discussion on that point is somewhat pointless since a native fungus, Nectria galligena is also capable of inciting cankers and killing hosts after entering through scale-damaged bark. The scale must be considered the pivotal introduction that allowed the invasive spread of this disease complex (Houston and O’Brien 1983, Southern Appalachian Man and the Biosphere 1996). This disease complex was first identified in southern forests in the early 1990s.

The disease range continues to spread along a broad front. In the early phase of the disease cycle, more than 50 percent of the American beech trees 10 inches or larger in diameter at breast height are killed. Openings created by death or removal of the beech result in dense stands of root-sprouts, which in turn yield stands abnormally rich in beech and deficient in its normal associates.

In the second phase of the disease cycle, revegetated beech stands are attacked less severely, resulting in diseased survivors rather than in extensive mortality. Trees infected in this phase are rarely girdled, but they are generally severely deformed.

Since this disease complex affects only American beech, there is a direct relationship between the amount of beech in a stand and the intensity of the disease. Houston (1997) reports that ”stand age and density, tree size, and species composition affect disease severity, especially in forests affected for the first time.” The disease is expected to spread throughout the range of the host (fig. 17.12).

Silvicultural, chemical, and genetic strategies are available to manage this disease. Owners who depend on extensive (low intensity) management are expected to suffer significantly more quality (and value) loss than those who manage more intensively. Favoring genetic resistance is more effective in intensively managed forest stands.

Progeny from breeding programs designed to increase resistance have not been tested in field outplantings. They appear to hold promise, however, because some disease-free trees are known in most areas devastated by the disease. There is also some hope for biological control since a fungus and an insect are reported to attack the scale. High-value trees are sometimes protected with insecticides, but this method is impractical and uneconomical in the forest.

Damage to the South’s beech resource has only just begun. Explosive buildups of scale population have not yet occurred in many places where the scales are known to be present. We anticipate significant additional mortality and deformation from this disease before prevention strategies are developed for use in forests.

Butternut canker

Butternut is a small to medium sized tree. Butternut typically is mixed with other hardwoods, such as black walnut, in the upland northern hardwood forest types (mapped as maple-beech-birch, oak-hickory, and oak-pine). Primarily found in riparian areas, this species was a significant producer of mast for wildlife. It hybridizes with other Juglans spp., such as heartnut, Japanese walnut, English walnut, little walnut, and Manchurian walnut. Although butternut is seldom found growing in great numbers, there is a strong desire to maintain a viable butternut population to preserve biodiversity (Clark 1965).

Butternut is being killed throughout its range in North America by a fungus, Sirococcus clavigignenti-juglandacearam. The fungus causes multiple cankers on the main stem and branches. Butternut canker has been found in 55 counties in the Southern United States (fig. 17.13). Butternut numbers have been dramatically reduced and it is now a candidate for listing under the Endangered Species Act.

Detailed examination of cankers indicates that butternut canker has been present in the United States since the early 1960s. Its origin is unknown but its rapid spread throughout the butternut range, its highly aggressive nature on infected trees, the scarcity of resistant trees, the lack of genetic diversity in the fungus, and the age of the oldest cankers (40 years) support the theory that it is a recent introduction.

Inventory data from FIA show a dramatic decrease in the number of live butternut trees in the United States. Surveys reveal that 77 percent of the butternut trees have been killed in North Carolina and Virginia.

Butternut canker kills trees of all ages. Trees in all settings and ownerships appear to be equally affected, except in urban settings that have been fertilized. (Fleguel 1996, Nicholls 1979).

Since butternut makes up less than 0.5 percent of the trees in the South, the overall impact of its loss to the forested ecosystem is considered by some to be minor. However, as butternut trees die, they are replaced by other species with a subsequent loss of biodiversity. The long-term outlook for butternut is not good; there is no known control for butternut canker. It appears the species will continue to decline and die, making up less and less of the forest population over time. At this time, the only hope for restoration is genetic selection and breeding.

The primary potential for control of the butternut canker is genetic. Disease-free trees are rare but have been found (Orchard and others 1981; Ostry and others 1994, 1996).

Chestnut blight

No event in the history of American forests is better known or sadder than the introduction of the chestnut blight fungus, Cryphonectria parasitica, from Asia, probably in the middle to late 1890s. The effects of this introduction will be felt for all time. The American chestnut tree was lost not only as a valuable timber species but also as the most important producer of hard mast for wildlife. The fungus continues to survive on infected sprouts from old chestnut rootstocks, various oaks, and some other hardwoods (Boyce 1961). Thus, there is virtually no hope the disease will be eradicated or that the American chestnut will naturally recover its preeminent position in eastern forest ecosystems.

Species associated with chestnut, including oaks, filled voids in forest stands left by the death of chestnut (Hepting 1974, Oak 1994). Unfortunately within about 60 years in the Southern Appalachians, the oaks that replaced the chestnut began to decline and die back (see Oak Decline) due in part to stressed growth on sites better adapted to chestnut.

No forest management practice of any intensity could overcome the ravages of chestnut blight nor did ownership affect disease progression. No control was found to stop the rapid devastation caused by this blight. Current attempts to cross American chestnuts with oriental varieties and then backcross to the American parent appear to offer a viable method of maintaining resistant chestnut in the forest (Schlarbaum 1988). Chromosome and gene manipulations now employed with other plants and animals may provide new avenues for resurrecting the American chestnut. Research into hypovirulence, the discovery of reduced pathogenicity because of a disease of C. parasitica itself, showed early promise as well (Anagnostakis 1978). Genetic engineering of the virus that causes a hypovirulent reaction has the potential to increase the efficiency of spread of hypovirulence in the fungal population and is currently being field-tested. Neither method has yet provided the needed answers but research is ongoing.