Many diseases occur in southern Appalachian forests. Most forest diseases are native and a natural part of the ecosystem. Diseases can help to keep the forest healthy by removing weak or injured trees. They also can improve wildlife habitat by creating holes in trees and snags. However, some exotic diseases have been devastating to the ecosystem. These diseases are not native to the ecosystem and thus can spread unchecked, killing many trees and threatening the health of Appalachian forests. The biology, symptoms, spread, and management of these important diseases are outlined here.

Chestnut blight	This disease decimated the once abundant native American chestnut (Castanea dentata) populations in the first part of the 1900s.
Dogwood anthracnose	This disease is currently killing the majority of dogwoods (Cornus spp.) that occur at high elevations in the southern Appalachians.
Dutch elm disease	Introduced in the 1930s, this disease has affected mostly urban populations of American elm (Ulmus americana), but American elm is slowly declining in forest stands as well.
Beech bark disease	This disease has been in North America since the 1890s but didnt reach the southern Appalachians until the 1980s. The disease is caused by a combination of a beech scale insect and a fungus.
Oak decline	This is a slow-acting disease complex with interactions between biotic and abiotic factors that combine to stress oaks (Quercus spp.). It has existed in eastern oak forests since the mid 1800s. Oak decline leads to gradual crown dieback and eventual mortality.
Butternut canker	Butternut (Juglans cinerea) populations have continued to decline since this disease was discovered in 1967. An estimated 77% of the trees of this rare species have already been killed by butternut canker.
Sudden oak death	This disease has recently been introduced into ornamental nurseries in the eastern United States on non-oak hosts. Oaks (Quercus spp.) are most at risk but the host list continues to grow. The potential impact of this disease on the southern Appalachians is unknown but it could severely alter the biodiversity by decimating the oak population, one of the most abundant group of trees in the eastern United States.

Chestnut blight altered the hardwood forests of the eastern United States perhaps more than any other forest disease.  Its history in the US starts around 1900 when it was acidentally introduced.  The biology of the fungus is such that it spreads and kills trees rapidly, although the trees can persist from root sprouts.  Chestnuts, once dominant in the eastern United States and very dominant in the southern Appalachians, are all but removed from the ecosystem.  Several different restoration techniques are being researched and developed but the potential success of these techniques remains in question.  Several other exotic pests also affect the American chestnut.  Some chestnuts have shown varying degrees of blight resistance but environmental factors, such as air pollution, can diminish any resistance.

• History
• Biology
• Restoration
• Other Exotic Pests of Chestnut
• Blight Resistance

Americn Chestnut Range

Chestnut blight, caused by the fungus (Cryphonectria parasitica (Murrill) M.E. Barr) has probably had the most pervasive influence on forest structure and composition in the southern Appalachians of any disease or insect. Prior to the introduction of this disease, the American chestnut (Castanea dentata (Marsh.) Borkh.) was the tallest and most dominant hardwood species in the eastern United States. It grew in vast stands from Maine to Florida, with the largest trees occurring in the southern Appalachians (Schlarbaum and others 1997). After the introduction of the fungus, which probably arrived on nursery stock from Asia around 1900, native chestnut trees, which had no resistance, quickly succumbed. By 1929, nearly all counties in the southern Appalachians were infested; by about 1940, most of the standing chestnut trees were dead (SAMAB 1996). The chestnut blight fungus kills the above-ground portion of trees but does not affect root systems. Therefore, American chestnut persists throughout its former range as root sprouts growing in the understory.

Chesnut blight canker

The fungus enters a host through cracks or wounds in the bark and multiplies rapidly. It produces sunken cankers which expand and girdle the stem, killing everything above the canker, usually in one growing season. Fungal spores are formed 3-6 weeks after intial infestion (Tainter and Baker 1996). Spores can be produced for years after death of the tree. Fungus spores can be transported by wind or on the feet of migrating birds and insects. The disease, therefore, can spread rapidly -about 24 miles per year (Schlarbaum and others 1997).

Sprouts, resulting from the live, unaffected root systems, generally live for 5 to 10 years before being top-killed by the blight. Often chestnut sprouts reach heights of 25 feet or more, but they rarely flower and bear fruit before dieback. Some chestnuts display varying amounts of blight resistance and may survive long enough to permit nut production before succumbing to the disease. Despite the persistence of spouts, there is a gradual loss of this genetic resource. Areas with extensive chestnut rootstocks should be identified and silvicultural practices that favor its shade-intolerant regeneration should be employed to protect or enhance sprout survival.

There have been two primary research approaches to restore chestnuts to American forests: use of hypovirulent strains and breeding.

Hypovirulence research

Hypovirulence is a condition resulting from a virus disease that weakens the chestnut blight fungus. Hypovirulence allows a chestnut tree with no resistance to blight to form slow-growing swollen cankers normally produced only on resistant trees. Scientists have been trying to manipulate hypovirulence to develop an economical biocontrol for blight. However, several obstacles to this approach exist including: (1) the blight spreads very rapidly in nature, while hypovirulence spreads very slowly; and (2) there are many types of virulent strains in the forest which resist transfer of the virus responsible for hypovirulence. Despite these limitations, hypovirulent strains have been used to effect recovery from chestnut blight in certain situations (Scibilia and Shain 1989, Anagnostakis 1990, MacDonald and Fulbright 1991, Brewer 1995). For example, some positive results have been achieved by using molecular biology to transfer the debilitating genes of the virus into the fungus (Choi and Nuss 1992, Schlarbaum and others 1997).

Breeding research

Two strategies have been pursued to breed a blight-resistant American chestnut: (1) breeding within the American chestnut gene pool and (2) hybridization with Asian chestnut species.

Breeding within American chestnut populations was begun with the occasional surviving trees that were thought to possess some resistance. Enzymatic studies of inner bark tissue revealed small resistance differences among trees (Samman and Barnett 1973, McCarroll and Thor 1985). Cross pollinations were made among putatively resistant trees, but resistance could not be increased to an acceptable level and the approach was abandoned (Thor 1978, Schlarbaum and others 1997).

Chinese chestnut

Resistance in Asian chestnut species, particularly C. mollissima (Chinese chestnut) and Japanese chestnut (C. crenata) was evident to scientists in the early 1900s. Early breeding programs were initiated by state and federal agencies in the 1930s. However, the initial hybrids generated by these programs were not as blight resistant as the oriental chestnut parent. To increase resistance, these first hybrids were crossed back to a resistant oriental parent. Unfortunately, this strategy produced trees that were short and branching, and not competitive in eastern forests (Schlarbaum and others 1997). A number of breeding programs were more successful with the backcross method, which aimed to transfer blight resistance from Chinese chestnut to American chestnut, while retaining the desirable growth, form, and adaptability of the American chestnut (Burnham and others 1986, Burnham 1990). These trials produced two partially blight-resistant first backcrosses (BC1), the "Graves" tree and the "Clapper" tree, which were first generation hybrids (Schlarbaum and others 1997).

Although these early breeding programs did not produce a blight-resistant American chestnut, they left a valuable legacy of knowledge and germplasm. There is now evidence that only a few genes control blight resistance in Chinese chestnut, specifically, two or three incompletely dominant genes. A genetic map of chestnut with regions associated with blight resistance was identified, and could be used to screen newly germinated nuts for blight resistance. This screening process may enable several generations of backcrossing to be bypassed. The American Chestnut Foundation estimates that by 2012, nuts will be produced from the most blight-resistant breeding lines that can be used in reforestation (Schlarbaum and others 1997).

Some promising results have also been seen with an integrated management approach for American chestnut revival. This approach combines hypovirulence (by inoculation) with blight-resistance (grafted). In Virginias Lesesne State Forest, trees grafted with blight resistant strains and inoculated with hypovirulence have been thriving for 20 years, but they are surrounded by nonresistant chestnuts, which are continuously killed back by the blight. While these methods may lead to the restoration of chestnuts throughout the eastern United States, the results are still unknown and the American chestnut may not ever be restored as a viable, reproducing canopy tree.

Chestnut gall wasp

Chestnut blight was preceded by another exotic fungal disease, Phytophthora cinnamomi, which infected southern American chestnuts and related Allegheny chinkapins as early as 1824 (Crandall and others 1945). This root rot disease constricted the natural range of chestnut to upland areas. On these upland sites, chestnuts are challenged by yet another exotic pest, the chestnut gall wasp (Dryocosmus kuriphilus). Chestnut gall wasp larvae feed upon bud and flower tissues forming a characteristic gall and producing a toxin that can kill the infested branch. Infestations by this insect, which can cause mortality, were first reported in 1974 (Payne and others 1975) and now have spread north into Tennessee and North Carolina (Schlarbaum and others 1997).

Some Facts about Blight Resistance

American Chestnut Leaf

American chestnut seedlings are usually highly susceptible to the blight. In older trees (more than 1.5 inches in diameter at breast height), a resistant individual can slow down progress of the disease and may survive in spite of blight, but it is not immune. Many kinds of environmental stresses may break down a trees resistance to blight. Indeed at high elevations in areas exposed to severe climate, normally resistant Oriental chestnuts have been killed by blight.

Even where all the American chestnuts have been killed, the blight fungus is still present. Planting so-called "blight-free" chestnut has been widely publicized, but this practice is ineffective. "Blight-free" merely means a tree is uninfected, grown in an area where no blight is present, outside the natural range, or inside a greenhouse. This is no guarantee that the tree will not contract blight in the future. Furthermore, this practice raises false hopes among the public and may discourage research funding (SAMAB 1996).

For more information on this disease, see Revitalization of the Majestic Chestnut: Chestnut Blight Disease at the American Pathological Societys website.

Dogwood anthracnose is a relatively new disease to the southern Appalachians. In the past decade, it has killed millions of flowering dogwoods (Cornus florida L.) particularly at high elevations in the Blue Ridge Province. Dogwood is an important understory and midstory component in the southern Appalachians. Aside from the aesthetic impact to both forest and shade trees, dogwood anthracnose can have significant impacts on wildlife and ecosystem processes.

The history of the disease in the United States has been very short (since 1976) yet its spread in the South has been rapid. Symptoms caused by the disease appear on foliage, twigs, fruits, seeds, and stems. The pathogens biology is well understood and spread of infection has been related to several environmental factors. Consequently, several management options exist to control dogwood anthracnose. Still, the diseases impacts and highly effective management alternatives remain important research questions.

Dogwood anthracnose is a relatively new disease to North America. It was first observed in 1976 affecting a population of Cornus nuttallii in Washington state (BROKEN-LINK Byther and Davidson 1979). Two years later, Pirone (1980) noticed a widespread and rapid deterioration of flowering dogwoods in New York and Connecticut. In 1983, fungus associated with anthracnose on C. nuttallii was identified as a species of Discula, and flowering dogwood (Cornus florida) and Japanese dogwood (Cornus kousa) were noted as minor hosts (Salogga and Ammirati 1983). Finding the disease distinct from other Discula spp. that cause anthracnose of ash, oak, and sycamore, Redlin (1991) described and named the pathogen Discula destructiva Redlin in 1991 (Daughtrey and Hibben 1994, Daughtrey and others 1996).

Although the origin of dogwood anthracnose is unknown, results of DNA analysis combined with its rapid spread have led many to conclude it was introduced (Daughtrey and others 1996). Researchers also speculate that climatic changes and droughts may have predisposed trees to infection, thus causing coincidental outbreaks in the Northeast and the Pacific Northwest (BROKEN-LINK Anderson and others 1994).

In the eastern US, the disease has spread rapidly down the Appalachians, primarily on Cornus florida, the eastern flowering dogwood. By 1995, the disease had been confirmed in northern Georgia (1987), western North Carolina (1988), and as far south as northern Alabama. Dogwood anthracnose has been reported on over 12 million acres in 180 counties (BROKEN-LINK Anderson and others 1994, SAMAB 1996).

1999 Incidence of dogwood
anthracnose in the South

Disease severity within infected areas also has increased rapidly. Anthracnose was monitored on permanent plots in the Great Smoky Mountains National Park (GSMNP) from 1988-1991 (Windham and others 1993). During that period, the number of plots with severe epidemics (more than 25 percent of foliage blighted) increased by 638 percent. As of 1999, anthracnose had killed 49.7 percent of the native dogwood trees in 24 western counties of North Carolina (Forest Health and Protection 2001). In the GSMNP, it is estimated that more than 90 percent of the dogwoods have died in heavily shaded coves and alluvial forests. Disease severity in the South seems to be more intense at higher elevations. In general, damage is most severe at elevations above 3,000 feet, where forest and ornamental dogwoods will be largely eliminated. At elevations between 2,000 to 3,000 feet, dogwoods in shade are affected. At elevations below 2,000 feet, only dogwoods in cool, wet areas are dying (BROKEN-LINK Anderson and others 1994).

The decline of dogwood populations resulting from dogwood anthracnose has several serious impacts in the southern Appalachians. Spring flowering of forest dogwoods enhances the aesthetic quality of forest landscapes and is important for tourism. Beyond this aesthetic loss, absence of native dogwoods and their fruits is detrimental to wildlife. Dogwood fruits, rich in fat and protein, are a preferred food for turkeys, bobwhite quail, squirrels, rabbits, and deer, as well as for numerous nongame species of birds. Dogwood leaves also have a high calcium content and decompose rapidly. Their loss hastens soil acidification, reduce nutrient availability, and influences numerous ecological relationships (Daughtrey and Hibben 1994).

Dogwood anthracnose affects leaves, bracts, current-year shoots, localized areas of bark and cambium of trunk or branches, fruits, and seeds of Cornus florida (Britton and others 1993, Daughtrey and Hibben 1983). C. kousa also is considered a host, but leaf infection is generally minimal (BROKEN-LINK Daughtrey and others 1996).

Dogwood anthracnose leaf symptoms

Leaf symptoms on C. florida generally occur within 4 weeks after flowering (Britton 1993, Hibben and Daughtrey 1988). Symptoms and include: (1) necrotic lesions surrounded by a reddish or brown-purple zone (some with chlorotic halo), (2) shot holes, (3) necrotic blotches at the leaf tip or along the blade periphery, or (4) blight of the entire blade (Hibben and Daughtrey 1988). Leaf spots vary according to light exposure. Purple-rimmed lesions (BROKEN-LINK Parham and Windham 1992) or shot holes predominate on leaves exposed to sunlight, while necrotic blotches predominate on shaded leaves (BROKEN-LINK Parham and Windham 1992). Blighting commonly occurs throughout the canopy of understory C. florida, or within the interior canopy or on epicormic branches of exposed trees. Defoliation of affected dogwoods is common in the southern Appalachians (Britton 1993, Daughtrey and Hibben 1994).

Dogwood Anthracnose twig dieback

Twig dieback is caused by infection, which may occur directly through bark or indirectly through spread from the petioles of affected leaves (BROKEN-LINK Daughtrey and others 1996). Epicormic shoots often form along the entire length of the main stem and on major branches of infected C. florida (Hibben and Daughtrey 1988). Infection of epicormic branches via petioles of blighted leaves is very common. Infections then spread from infected shoots into the main stem, forming annual cankers that can kill the entire tree (Hibben and Daughtrey 1988, BROKEN-LINK Daughtrey and others 1996, Daughtrey and Hibben 1994).

The disease kills dogwoods of all sizes but it is most severe on young seedlings. Regeneration can be eliminated in some areas. Large C. florida often die 2 to 3 years after the first symptoms are found in the leaves (BROKEN-LINK Anderson and others 1994). Overall, vigorous trees tend to be less damaged than weak trees. Trees that survive one or more seasons of severe anthracnose usually have swollen areas on trunks and branches where cankers were enveloped by new tissue (Daughtrey and Hibben 1994).

Environmental factors influence dogwoods susceptibility to disease. Understory forest dogwoods are more prone to infection than trees growing in full sunlight. For this reason, ornamentals grown in open, sunny sites are often disfigured without being killed. In the southern Appalachians, mortality is most likely at elevations above 3,000 feet. Below 3,000 feet, damage is most severe on moist, cool sites such as northeast-facing slopes (Chellemi and others 1992, Hoffard and others 1995).

Infection of dogwoods is most likely to occur during cool, wet weather in spring and fall, but can occur at any time during the growing season. Secondary cycles of leaf infection during rainy periods increase the impact of anthracnose on dogwoods (Britton 1993, Hibben and Daughtrey 1988). Drought and winter injury appear to increase susceptibility (Daughtrey and Hibben 1994).

Diseases with similar symptoms

The symptoms of dogwood anthracnose (D. destructiva) are often similar to symptoms of less serious diseases. BROKEN-LINK Anderson and others (1994) point out the following:

• Spot anthracnose, caused by Elsin orni, infects leaves in the spring, causing numerous round lesions (1 to 2 mm diameter) that can coalesce into large spots.
• Leaf spots, caused by Septoria cornicola, appear in late summer or fall. Spots, about 1/4 inch in diameter with square margins, may merge to form large blotches.
• Bracts infected by Botrytis cinerea have irregular brown patches, and can be easily confused with bracts infected by D. destructiva.
• The dogwood twig borer (Oberea tripunctata) kills shoots in clumped areas of the crown. The emerging borer causes a hole in the affected shoot.
• Mechanical injuries and drought can also cause symptoms in foliage and branches that mimic dogwood anthracnose.

Due to the difficulty of distinguishing similar diseases and pests, researchers recommend that the presence of D. destructiva should be confirmed by directly examining fungal sporulation in tissue lesions (BROKEN-LINK Anderson and others 1994).

D. destructiva, the pathogen causing dogwood anthracnose on leaves, asexual fruiting bodies (conidiomata) form most often on the undersurface, beneath a trichome (Redlin 1992). Twigs with conidiomata remain on trees over winter and provide primary inoculum for new infection cycles in the spring. Under wet conditions, conidia ooze from these fruiting bodies in a slimy white to beige or pinkish cirrhus. Most short-distance dispersal of conidia probably occurs via splashing rain, although dispersal by convergent lady beetles (Hippodamia convergens) (Colby and others 1995) and birds is possible (Britton and others 1993). Conidial germ tubes penetrate leaves directly (Graham and others 1991). Necrosis precedes hyphal proliferation in palisade and spongy parenchyma cells (Walkinshaw and Anderson 1991), indicating toxin activity. Four phytotoxic phenols have been identified in culture filtrates of the pathogen (BROKEN-LINK Venkatasubbaiah and Chilton 1991, Daughtrey and Hibben 1994, BROKEN-LINK Daughtrey and others 1996).

Light exposure, water relations, acid rain, and topographic factors have all been correlated with incidence and severity of dogwood anthracnose. Research on the effects of these factors is summarized below.

There is an inverse correlation between leaf exposure to sunlight and disease severity. Infection is greater in shaded understory dogwoods (BROKEN-LINK Gould and Peterson 1994, Hibben and Daughtrey 1988), in the interior and on north side of canopies (Chellemi and Britton 1992, BROKEN-LINK Parham and Windham 1992), and in trees with north to east aspects (Chellemi and others 1992, BROKEN-LINK Windham and others 1992). Light is important for both the vigor of the host and for production of anthocyanin, a light-activated disease-limiting compound. Also, reduced light is often correlated with reduced evaporative potential, which promotes conidial germination, infection, and lesion development. For example, Chellimi and Britton (1992) measured photosynthetically active radiation (PAR) values within three types of dogwood canopies, and found evaporative potential was more correlated with differences in disease severity than PAR. The heating effects of sunlight may also affect lesion type and sporulation (BROKEN-LINK Parham and Windham 1992, Daughtrey and Hibben 1994).

The amount of rainfall also affects the intensity of anthracnose infection. Periods of drought have preceded severe dogwood anthracnose epidemics (BROKEN-LINK Gould and Peterson 1994, Hartman and others 1992). BROKEN-LINK Erbaugh and others (1994) hypothesized that drought mayincrease tree vulnerability to the disease. However, moisture also plays a key role in facilitating epidemics by fostering infection. In the Northeast, leaf symptoms begin to appear following the first extended rainy period after leaf expansion (Hibben and Daughtrey 1988, Smith 1992). A 3-year study in North Carolina (Britton 1993) confirmed that disease severity was correlated with rainfall, particularly in the summer when temperatures averaged 64-70°F. Although rainfall clearly is conducive to infection, it also promotes host vigor and lessens disease impact (BROKEN-LINK Gould and Peterson 1994, Williams and others 1987, Daughtrey and Hibben 1994).

Acidic rainfall may also predispose dogwoods to infection. Anderson and others (1993) reported that disease incidence and severity increased with decreasing pH (2.5 to 5.5) caused by destruction of leaf cuticles by acid treatments (Anderson 1991, Brown and others 1994, Thornham and others 1992), or by changes in soil nutrient status. The mechanism is complicated by the neutralizing effect dogwood leaves can have on acid droplets by releasing calcium and magnesium ions (Wiley and Hackney 1991, Daughtrey and Hibben 1994).

Topography of dogwood habitat may also affect disease incidence. At several sites in the southern Appalachians, dogwoods growing on north-facing slopes had higher frequencies of disease incidence than did trees growing on east-, south-, or west-facing slopes (BROKEN-LINK Windham and others 1992, Windham and others 1993). Aspect also influenced disease development; lesions developed more rapidly on the north side of trees than east, west, or south sides of the same trees (Chellemi and others 1992). Evaporative demand (an index of drying potential) was found to be lowest at sites with north-facing slopes. Early-morning fogs may be a disease-promoting factor. Disease-prediction models based on these geographic factors have been generally accurate when tested against field survey data (Chellemi and others 1992, Langdon and others 1992). Notably, Wilds (1997) found that although the degree of infection is influenced by elevation, slope curvature, slope position, and potential soil moisture, stem density alone explains 25 percent of the variation in disease severity.

Proximity of trees to streams is also associated with greater dogwood anthracnose severity (Anderson 1991, Chellemi and others 1992, Knighten and Anderson 1992). For example, dogwoods located within 60 feet of streams declined more rapidly from anthracnose than did trees located further from streams (Knighten and Anderson 1993). These relationships mean that the highest mortality rates are restricted to dense stands in damp, sheltered sites at low slope positions. As a result, Wilds (1997) suggests surviving populations of flowering dogwood may represent a biased genetic subset of the original population.

More options exist for managing ornamental dogwoods in landscaped areas than natural populations in forested sites. Cultural conditions that favor growth of dogwood, such as optimum fertilization, trickle irrigation (Daughtrey and others 1988, Mielke and Daughtrey 1989), mulching, and at least 30 percent full sun, have been recommended for ornamental dogwoods (Bailey and Brown 1991, BROKEN-LINK Gould and Peterson 1994). Under severe disease pressure, these cultural treatments should be combined with fungicide application to provide adequate control. The protectant fungicides chlorothalonil, mancozeb, or mancozeb plus thiophanate-methyl and the systemic fungicides: propiconazole, tebuconazole, andtriforine are registered for control of dogwood anthracnose (Anderson and others 1993, Windam and Windam 1991). Pruning to reduce inoculum, although originally recommended, has proven ineffective or only slightly effective (Anderson and others 1993, Windam and Windam 1991). These management guidelines for ornamental dogwoods are summarized in a 10-point control program (Bailey and Brown 1991) and further refined into a decision tree (BROKEN-LINK Anderson and others 1994, Daughtrey and Hibben 1994, BROKEN-LINK Daughtrey and others 1996).

In forested environments, managing individual trees for dogwood anthracnose is prohibitively expensive. Sometimes, however, it is practical to manage the disease with stand-level treatment. Clearcutting forest sites where dogwood regeneration is desired may lead to development of a C. florida population that is less susceptible to anthracnose (Britton and others 1994). Britton and others (1994) found anthracnose was less severe in stands of C. florida where timber had been clearcut 30 years previously than in stands where timber had been partially harvested. However, the effects of harvesting stands after anthracnose is present are not yet known. Identifying ideal sites for dogwood will be as important as identifying site factors most likely to favor anthracnose (Langdon and others 1991, Windham and others 1993). Disease severity often is low on undisturbed sites that support the largest C. florida populations, possibly because these are the most favorable sites for the species (Chellemi and others 1992, Daughtrey and Hibben 1994, BROKEN-LINK Daughtrey and others 1996).

Resistant host material may be the greatest hope for long-term management of anthracnose. Research continues to find potentially resistant trees in woodlands where dogwood anthracnose was present. Potentially resistant survivors have been identified from populations of flowering dogwoods devastated by anthracnose in southeastern New York (Hibben and McArdle 1992) and in Catoctin Mountain Park (Graham and Windham 1993). These selections can be included in breeding programs after their disease resistance is confirmed (Daughtrey and Hibben 1994, BROKEN-LINK Daughtrey and others 1996).

Resistant genes in other dogwood species make them useful as current planting alternatives for high-hazard areas, as well as candidates for resistance gene donors. Cornus kousa is a known host of D. destructiva but seldom shows severe symptoms. The first-generation hybrids of C. florida x C. kousa, introduced as the Stellar series by Rutgers University, possess increased genetic resistance to anthracnose (Britton 1993). Other resistant species native to North America include C. racemosa and C. canadensis, C. amomum, C. alternifolia, and C. mas (Brown and others 1992, Daughtrey and Hibben 1994, BROKEN-LINK Daughtrey and others 1996).

There are still many gaps in our knowledge of this relatively new disease. Daughtrey and others (1996) highlighted the following research questions regarding dogwood anthracnose.

1. Where did anthracnose originate? Several lines of evidence, such as lack of disease symptoms prior to 1970, appearance of the disease near ports of entry (Seattle and New York), its rapid spread, and its lethal nature, suggest that dogwood anthracnose was introduced. However, the origin of the fungus remains unknown (Daughtrey and others 1996).
2. What are its long-term effects on dogwood populations? Relatively little is known about long-term effects of anthracnose on native dogwood populations. In woodland areas where mortality of dogwoods was severe over a decade ago, there is little regeneration by seedlings even though seed-bearing trees have survived (Daughtrey and Hibben 1994). Will such sites gradually become repopulated with C. florida, and how long will D. destructiva remain at a high enough level to initiate new infections (Daughtrey and others 1996)?
3. What are the effects of this disease on wildlife and nutrient cycling? The decline of dogwood populations will likely effect wildlife populations and nutrient cycling in forest soil, but these impacts have not been measured. Dozens of bird species, bears, and deer use dogwood as a source of mast or browse (Nash 1999). How will the decline of dogwood affect these wildlife populations? Dogwood leaves are high in calcium. Decomposition of dogwood leaves not only makes this critical element available for other plants, but buffers soil acidity (Nash 1999). How will removal of this source of calcium affect nutrient cycling?
4. Can we induce genetic improvements in dogwoods susceptible to anthracnose? Conventional breeding methods to produce interspecific hybrids have been successful but results take a long time (Orton 1993). Selecting disease resistance in native populations of C. florida have also been attempted but results are inconclusive (Daughtrey and Hibben 1994, Santamour and others 1989). Will it be possible to use new genetic engineering techniques for direct transfer of disease-resistance genes? This approach could produce quicker results without compromising ornamental qualities of dogwoods (Daughtrey and others 1996).
5. Will hypovirulent strains of the anthracnose pathogen slow the disease? Hypovirulent (weakened) strains of the chestnut blight pathogen cause a less severe reaction in their woody hosts than do the normal virulent strains. Research into possible hypovirulence in D. destructiva may uncover a biocontrol for this disease (Daughtrey and others 1996).

Dutch elm disease devastated urban elms throughout both Europe and America.  With the origin of the disease unclear, Dutch elm disease history begins in the Netherlands in 1919.  It was accidentally introduced into the United States in the 1930s.  The disease can be spread both by root grafting and by two species of bark beetle.  This aspect of the diseases biology has allowed it to rapidly spread throughout the United States, including the southern Appalachians.  Urban elms are generally more affected, often occuring in monocultures and stressful environments.  Elms occuring in forests decline at a slower pace.  Several management options exist but rely on quick identification and rapid response to new infestations.

• History
• Biology
• Management

Tree Mortality due to Dutch Elm Disease

Dutch elm disease, caused by two fungal strains, a non-aggressive strain (Ophiostoma ulmi (Buisman) Nannf., formerly called Ceratocystis ulmi)) and an aggressive strain (O. nova-ulmi), was introduced to the United States through shipments of unpeeled veneer logs from Europe in the 1930s. By 1977, the disease had spread through most of the country, killing an estimated 46 million elms. (Schlarbaum and others 1997). Dutch elm disease was first discovered in the Netherlands in 1919. The origin of the disease is not known but it is believed to have originated in Europe or Asia (Tainter and Baker 1996).

Dutch elm disease has mostly affected urban populations of American elm (Ulmus americana L.), a widely planted shade tree. In Europe, 60-70% of the Ornamental American elms were killed due to Dutch elm disease. American elms were planted along roads and as shade trees in many cities and towns in America and Europe because of their ability to grow in adverse conditions (Tainter and Baker 1996). Towns in the midwestern United States suffered greater losses than the towns in the eastern United States because of harsher conditions and extensive use of elms for urban plantings, often the dominant/only tree planted.

In forest stands where elms are relatively isolated from one another and spread of the disease is sporadic, American elm is declining more slowly (SAMAB 1996). This is true in the southern Appalachians where elms are present in the forested ecosystems but often not a dominant feature of the forest. Other native elm species, such as red elm (Ulmus rubra), can be infected with Dutch elm disease, but appear to have greater resistance (Schlarbaum and others 1997).

Dutch Elm Disease Vector Galleries

The fungi responsible for causing Dutch elm disease are usually spread by two species of elm bark beetles, the smaller European elm beetle (Scolytus multistriatus (Marsham)) and the native elm bark beetle ((Eichhoff)) (Tainter and Baker 1996). Fungal spores are prodcued in beetle galleries and emerging adults will carry the spores to new trees, spreading the disease. Dutch elm disease can also be spread by root grafts between trees in urban settings (Hanisch and others 1983 in SAMAB 1996).

Symptoms of Dutch Elm Disease

Once established in a tree, the fungus grows and can spread throughout the tree via the cells of the outer sapwood (Tainter and Baker 1996). The tree reacts to the fungus by producing gums and tyloses (outgrowths from living cells adjacent to vessels). These, along with fungal structures, block the vascular system of the tree, reducing the trees ability to transport water. The vascular system blockages leads to severe water stress and wilting of tree foliage, often the first outward sign of infection. The tyloses, which develop in large vessels combined with large accumulations of tannins, form a discoloration in the vessels which can be seen in cross sections of stems. Blockage in small stems will cause more severe wilting than in large stems (Tainter and Baker 1996). External symptoms often take weeks on months to appear. The fungus can rapidly spread throughout the tree. One estimate states that the fungus can move through young stems at a rate of up to 2.5 cm/day (Tainter and Baker 1996). Defoliation and death of the tree, due to severe vessel blockage, can occur in the following year.

Dutch elm Disease discolored stem vessels

Elms are most susceptible in spring, but this varies geographically. Susceptibility seems to be timed with the trees production of large xylem vessels (Tainter and Baker 1996). Weather also affects the incidence of Dutch elm disease, both by affecting beetle vectors and tree susceptibility. Cool weather slows beetle development, slowing the spread of the fungal spores. Hot and dry weather speeds beetle development and stresses the elm trees, both of which increase the incidence of Dutch elm disease. (Tainter and Baker 1996).

Dutch Elm Disease Symptoms

Disease Management and Breeding Programs

The first step to successful control/containment program for Dutch elm disease is rapid detection.  Detecting the disease early allows for measures to be taken before the spore-carrying beetles can emerge and spread the disease to other elms.  Frequent inspections focused on the early wilting symptoms can help catch the disease at an early stage.  Once an infected tree is found, it should be promptly removed.

The most important step to sucessfully controlling/containing Dutch elm disease is correct and rapid sanitation of an infected tree (Tainter and Baker 1996).  Sanitation involves reducing the ability of the disease to spread by disrupting root grafts and reducing brood habitat for beetle vectors.  Remove any dead, dying, or damaged elm material that could harbor beetle broods.  Remove the material before the spring beetle emergence if possible.  Debark elm firewood to prevent any larvae present from finishing development.  Several chemical treatments are also available for treating elms to prevent beetle colonization of uninfested trees or to prevent beetle emergence in infected trees (Tainter and Baker 1996).

Transfer of the disease via root grafting is a major step to preventing transfer of Dutch elm disease in urban settings.  Both chemical and mechanical methods exist for severing common root systems.  Pruning infected limbs may remove any beetle-inoculated fungus before it reaches the main stem and requires the removal of the entire tree (Tainter and Baker 1996).  For highly valued trees, some fungicides are available but are very expensive. 

Resistance has been bred into cultivars using American elm strains that are tolerant of Dutch elm disease. Two new cultivars, "Valley Forge" and "New Harmony," were released by the US National Arboretum in 1996 (US National Arboretum 1996). Attempts to breed resistance into American elm using other Ulmus species generally fail due to a reproductive barrier between American elm and other elm species (Santamour 1969, Schlarbaum and others 1997).

Although trees with good tolerance to Dutch elm disease have been found, very little is known about the mechanisms of tolerance. A current joint project by the USDA Forest Service and the US National Arboretum is studying the genetics of host resistance to improve tree selection in breeding programs and to illucidate quantitative inheritance of disease tolerance (Schlarbaum and others 1997).

For more information on Dutch elm disease, see "How to identify and manage Dutch elm disease", on the Northeastern Area State and Private Forestrys website.

Beech bark disease has devastated American beech trees in the northeast United States and adjacent Canada.  Its known history starts in Europe in the mid 1800s. This disease was first found in North America in 1914 in Nova Scotia.  In the early 1990s, beech bark disease was found in the southern Appalachians.  A unique characteristic of the biology of beech bark disease is that it is a complex resulting from combined attacks from a scale insect and a fungus.  The scale insect wounds the bark allowing the fungus to enter into the tree.  Once the fungus is in the tree, it spreads rapidly creating wounds and cankers along the bark that weaken and may girdle the tree.  Management of ornamental beech trees can involve insecticidal sprays to remove scale insects but this is not a cost-effective option for forest situations.  In a forest situation, removal of dead and dying material as well as favoring any trees which seem to have blight resistance may aid in keeping beech in the overstory.

• History
• Biology
• Management

Beech Bark Disease Map

Beech bark disease is a disease complex resulting from combined attacks of a scale insect and a fungus. It has caused considerable amounts of beech mortality in the northeastern United States and adjacent Canada. It was killing European beech (Fagus sylvatica) before 1849 but it was not until 1914 that the disease complex was discovered and Nectria fungus identified. In 1890, the scale insect was introduced accidentally in North America in Halifax, Nova Scotia. The disease was first reported in North America in the 1920s on American beech in Nova Scotia. After establishing in Nova Scotia, the disease started to spread its range at a rate of 10-15 km/yr (Tainter and Baker 1996). Beech bark disease was first found in the United States in Massachusetts in 1929. During the 1930s, the disease spread throughout New England and by the 1980s, the disease was in Monongahela National Forest in West Virginia (Houston and OBrien 1983). In 1993, the first case of beech bark disease in the southern Appalachians was found in the Great Smoky Mountains National Park in both North Carolina and Tennessee (Johnson 1995, SAMAB 1996). Heavy mortality of some beech coves in the Great Smoky Mountains National Park is being found despite an aggressive control program.

Initially great concern arose over beech bark disease in the United States, but interest faded quickly because beech was not commercially valuable at that point due to problems with wood drying techniques. During the 1950s, innovations in the drying process of beech allowed for commercial use, but by then much of the northeastern beeches were killed or not fit for commercial use (Tainter and Baker 1996).

Symptoms of beech
bark disease

Beech bark disease is caused by a complex of two agents: the beech scale insect, Cryptococcus fagisuga, and a fungus, Nectria coccinea faginata. Beech bark disease affects both the American beech (Fagus grandifolia) and the European beech (Fagus sylvatica). By themselves, the scale insects do not fatally injure beech. However, scale insects form a symbiotic and fatal combination with Nectria; by penetrating the bark, the scale insect allows the fungus to invade (Houston 1975, SAMAB 1996).

Beech scale insects reproduce pathernogenically (entire population is female). The adult females die after laying eggs on the bark in midsummer. The eggs hatch from late summer to early winter. The first instar stage of the larvae is the only life cycle that has legs, making it the principal stage for spread. Once hatched, larvae can either remain on the current position on the tree, migrate to cracks or other protected areas, or get carried from the tree by wind, rain, birds, or ladybugs (Tainter and Baker 1996). If the larvae lands in an unfavorable host or on the ground, it will die. If it lands on a favorable host (beech), it will establish itself in the feeding position where it will remain for the rest of its life (Tainter and Baker 1996).

Infestations can contain countless individuals. Each individual will produce a waxy secretion, which over time and scale generations, will develop to produce a waxy mass that covers and protects the scale insects. The Nectria fungus can infect bark that has been damaged and stressed by the scale infestations. Once the fungus has infected a wound site, fungal mycelium develops stromata which rupture the bark (Tainter and Baker 1996). The fungus then goes through several stages, including a stage where dense white clusters of material is formed that resemble the waxy secretions of the scale insect. Another stage is characterized by tiny red globe-shaped material. Both of the previous stages can be wind dispersed (Tainter and Baker 1996). Beech coves in the southern Appalachian mountains are very susceptible due to the high dominance of beech within that ecosystem.

Beech Bark Disease Mortality

The infections spread throughout the tree as well as throughout the forest. Lesions caused by the funus weaken the tree, forming larger cankers. These lesions may girdle the tree, killing the cabium layer. Spread of beech bark disease is limited by the dispersal ability of the beech scale insect.

The pattern of spread of beech bark disease and subsequent impact on trees can be characterized by a three-stage development (Tainter and Baker 1996):

1. Advancing front
   • Large, old trees
   • Building scale population
   • Fungus is scarce
2. Killing front
   • Large populations of scale
   • Severe outbreaks of fungal infection
   • Massive mortality of beech trees
   • This is the most spectacular and noticable stage of infestation
3. Aftermath zone
   • Evidence of prior mortality
   • Few old trees remain
   • Beech population consist primarily of small trees and sprouts

Diagnosing Beech Bark Disease

Several characteristics make diagnosing beech bark disease relatively easy. The first symptom is the wooly, waxy secretions produced by the scale insect. Symptoms and signs of a fungal infection include:

• Reddish-brown fluid oozing from wounds
• Sunken, necrotic areas of bark
• Small, white "pin cushions" on bark (midsummer-fall)
• Small, bright-red, lemon-shaped clusters of perithecia (Fall)

An infected tree may display foliar symptoms such as chlorotic leafs and sparse or small foliage.

Twicestabbed lady beetle

The lady bird beetle, Chilocorus stigma, feeds on the scale insect. It was once thought to be a promising biological control agent, but doesnt seem to have an impact on scale populations. However, it may serve as a dispersal agent for scale larvae and actually aid in dispersing the disease (Tainter and Baker 1996).

Inspecting nursery stock and limited transport of infested material will help to slow the spread of of the scale insect. This is especially important in long distance dispersal events. Ornamental or landscape trees can be treated with insecticides to remove the scale insect and protect the tree from infestation. Economically and practically, this is not an option in a forested stand. Since some beech trees seem to have a genetically-related resistance to beech bark disease, silvicultural options promoting resistant trees should be taken if beech is desired as an overstory component. This involves determining which, if any, trees seem to be resistant in a forest. Any dead or diseased material should be promptly removed and discouraged from resprouting (the sprouts are genetically the same as the parent tree and thus susceptible to the disease).

Causal agents

Oak decline is the name given to a slow-acting disease complex stemming from interactions between biotic and abiotic stressors of oaks (Quercus spp.). Abiotic factors that contribute to oak decline include low site productivity, drought, and spring frost. Biotic factors include tree maturity, root diseases such as Armillaria root disease (Armillaria spp.), canker causing fungi such as Hypoxylon canker (Hypoxylon spp.), defoliating insects such as gypsy moth (Lymantria dispar), and boring insects such as the two-lined chestnut borer (Agrilus bilineatus) (Wargo and others 1983).

Two-lined chesnut borer

Armillaria root disease

Hypoxylon canker

Gypsy moth caterpillar

Hosts

Black oak

Oak species differ in susceptibility to oak decline. Species in the red oak group are more susceptible than white oaks. Within the red oak group, black oak (Q. velutina) and scarlet oak (Q. coccinea) had been impacted most severly along with northern red oak (Q. rubra) and pin oak (Q. paulstris) (Wargo and others 1983). White oak (Q. alba) and chestnut oak (Q. prinus) have been most affected in the white oak group. Other species reported to have had some effects from decline include ash (Fraxinus spp.), hickory (Carya spp.), birch (Betula spp.), beech (Fagus grandifolia), and maple (Acer spp.) (Wargo and others 1983).

History

Symptoms of oak decline have been described in the eastern United States since the late 1800s (Oak 1994). Oak decline has become more prevalent since the 1950s, likely because of the shift in dominance to oaks during the early 1900s and severe droughts during the 1950s (SAMAB 1996). Another increase in incidence and severity occurred in the early 1980s. Oak decline has been reported throughout the entire range of the oak dominated eastern hardwood forest. Within the southern Appalachians, oak decline has been more prevalent on public lands than in private lands. North Carolina and Virginia has had the highest incidences of oak decline within the southern Appalachians (SAMAB 1996).

Symptoms

Oak decline leads to a reduction on radial growth and dieback of the canopy, leading to tree mortality. Older, mature trees are most likely to be affected by oak decline. The most easily recognized symptom of oak decline is progressive dieback of tree crowns starting from the outside of the crown and working inward. As the disease progresses, larger branches are killed. Branches having various states of decay, indicating death over time instead of in one event, help diagnose this disease (Oak 1994). Other symptoms may include:

• Chlorotic, dwarfed, or sparse foliage
• Epicormic growth (sprouting from the main stem and large branches)
• Premature autumn coloration
• Foliage death

Areas with new infestations of gypsy moth will show some of the most severe impacts due to oak decline. The defoliation caused by gypsy moth caterpillar feeding greatly increases tree susceptibility to oak decline.

Impacts

Oak will not be eliminated from the southern Appalachians due to oak decline but they will decrease in numbers and overstory dominance. Oak decline is a natural part of the ecosystem and positive and negative impacts will result from oak decline occurrences (SAMAB 1996).

Cavity nest

Positive benefits include:

• Higher overstory richness and eveness
• Increase in cavity nesting and den sites
• Creation of small openings
• Stimulation of understory species
• Increase in coarse woody debris

Negative impacts include:

• Reduction in oak regeneration
• Lower harvest volumes
• Increased fire hazard
• Smaller mast crops (decrease in wildlife food)

Butternut canker is a fungal disease that has caused massive amounts of butternut mortality.  The origin of the disease is unclear but known history begins in 1967 in Wisconsin.  The disease quickly spread into the southern Appalachians where most (up to 90% is some areas) of the butternuts were killed (biology).  This disease is spread by air, rain splashes, and insects.  Once infected, a tree produces oozing cankers that can girdle and kill the tree.  Butternut was never an abundant tree in the forest, so the disease went unnoticed in areas for a long time.  Management options are few but promotion of seemingly genetically resistant trees provides hope of maintaining butternuts as part of the ecosystem.

• History
• Biology
• Management and Research

Butternut distribution and butternut
canker distribution by county.

Butternut canker, a disease caused by the nonnative fungus, Sirococcus clavigignenti-juglandacerum (USDA Forest Service 1994), produces multiple cankers on the main stem and branches of butternut (Juglans cinera). First identified in 1967 in Wisconsin (Anderson 1988), it appears that butternut canker has spread throughout the range of butternut in the South, except for some isolated pockets. An estimated 77% of butternut trees have died in the South from this disease in the last 30 years. In the southern Appalachians, the disease has killed 90% of butternut trees. From 1966 to 1986, butternuts in parts of the southern Appalachians (North Carolina and Virginia) fell from 7.5 million trees to 2.5 million (Tainter and Baker 1996).

Unfortunately, the fungus went largely unnoticed because butternut trees are generally scattered and death from the disease is slow. Since nuts from infected trees generally are not viable, declining trees do not reproduce (Hoffard and others 1995). Butternut is a unique tree that adds to the biodiversity of the southern Appalachian forests. It also has importance as a food source. Butternut canker seriously threatens the existence of this tree, prompting the initiation of many research programs aimed at getting a clearer picture of the situation.

Butternut Branch Canker

Butternut Cankers

Spores of the causal fungus are disseminated from fruiting bodies by rain splash and insects. Produced throughout the growing season, the spores can survive and be dispersed long distances during cool weather. The fungus enters the host via leaf scars, buds, and bark wounds (Tainter and Baker 1996). Branch cankers caused by the fungus usually occur first in the lower crown, and stem cankers develop later from spores washing down from cankers above. Cankers are elongated sunken areas, often with an inky black center and whitish margins. Brown-to-black elliptical areas of killed cambium can be seen under peeled bark. Older branch and stem cankers are perennial, often covered by shredded bark and bordered by successive callus layers (Hoffard and others 1995). The cankers eventually girdle the tree, moisture stressing the tree. The canopy becomes thin or dies back and the tree eventually dies. Nuts produced from infected trees are usually not viable, limiting reproduction of this rare tree.

High mositure levels favor the spread and impact of this disease. The high humidity favors high spore germination and spore production may continue for up to 20 months on dead host tissue (Tainter and Baker 1996).

Butternut Canker

Genetic resistance to this fungus appears to exist among natural populations of butternut. Currently, harvest of all butternut is restricted on federal land (Ostry and others 1996, USDA Forest Service 1994, SAMAB 1996). Two research and development efforts have been formed to address the decline of butternut. The USDA Forest Service North Central Experiment Station initiated a cooperative effort with northern states and northern national forests to locate surviving butternuts and graft putative resistant trees into clone banks to preserve the germplasm (Nicholls and others 1978, Ostry and others 1996). Research is being conducted to develop laboratory and field protocols for screening trees for resistance and host range (Pijut 1993) and the role of insects in dissemination of the fungus (Schlarbaum and others 1997). A coalition has also been formed by the University of Tennessee, USDA Forest Service Southern Region and Southern Research Station, Great Smoky Mountains National Park, Tennessee Division of Forestry, and USGS Biological Research Division. This coalition is working to locate surviving trees or populations, characterize sites, identify trees with putative resistance, develop methods for disease resistance screening, study fungal physiology, and preserve germplasm (Schlarbaum and others 1997).

Management

No management techniques, other than attempted containment, is known for this disease. Promotion of trees which appear to have some genetic resistance appears to be the best chance of maintaining butternuts as a viable part of the ecosystem. In the late 1980s the need for identification and conservation of butternut for tree selection and breeding was recognized. The following guidelines have been prepared (taken from Ostry and others 1996):

• Retain trees with more than 70 percent live crown and with less than 20 percent of the combined circumference of stem and root flares affected by cankers.
• Harvest dead or declining trees to salvage quality and value of the wood, or maintain trees in the forest for their wildlife value.
• Retain trees free of cankers with at least 50 percent live crown and growing among diseased trees. These trees may be resistant and have potential for propagation by grafting or future breeding.

For more information on Butternut Canker - Click Here.