The pathogenic fungus Cryphonectria parasitica (formerly Endothia parasitica) is a member of the Ascomycota (sac fungi). This necrotrophic fungus is native to East Asia and South East Asia and was introduced into Europe and North America in the early 1900s. Strains of the fungus spread more or less rapidly and caused significant tree loss in both regions. Strains of the fungus can be more or less virulent.
Overview Cryphonectria parasitica is a parasitic fungus of chestnut trees. This disease came to be known as chestnut blight. Naturally found in Southeast Asia, accidental introductions led to invasive populations of C. parasitica in North America and Europe. In the first half of the 20th century, the fungal disease had a devastating economic and social impact on communities in the eastern United States. It killed an estimated four billion trees; or, by another count, 3.5 billion trees through 2013. Less severe impacts have occurred in Europe due to widespread CHV1-induced hypovirulence. CHV1 is one of at least two viral pathogens that weaken the fungus through hypovirulence and helps trees survive a blight infection.
The American chestnut (Castanea dentata) and American chinquapin (Castanea pumila) are highly susceptible to chestnut blight. The European chestnut (Castanea sativa) is also susceptible, but due to widespread CHV1 hypovirulence, blight-induced tree death is less common. The fungus can infect other tree species such as oaks, red maples, staghorn sumacs, and shagbark hickories. Once infected, these trees' bark also exhibit orange cankers but may not die. The pathogen can persist in these trees, producing spores that may infect other trees.
Fungal strains spread by wind-borne ascospores and, over a shorter distance, conidia distributed by rain-splash action. Infection can be local in range, so some isolated American chestnuts survive where there is no other infected tree within . Soil organisms at the root collar and root system of the chestnut tree are antagonistic to the fungus. Chestnut tree roots are resistant to blight infections. Consequently, a large number of small American chestnut trees still exist as shoots growing from existing root bases. However, these regrown shoots seldom reach the reproductive stage before above ground growth is again girdled by the fungus. Fungal strains originally infected the Chinese chestnut (Ca. mollissima) and the Japanese chestnut (Ca. crenata). These two species have co-evolved with the pathogen, making them most variably resistant to its ill effects.
History
Infections in North America
In 1904, the chestnut blight was accidentally introduced to North America by Robert Fortune. Cryphonectria parasitica was introduced into the United States from East Asia via import of Japanese chestnut trees. Commercial breeding purposes motivated these imports. Infection of American chestnut trees with C. parasitica simultaneously appeared in numerous places on the East Coast, most likely from Japanese chestnuts, which had become popular imports.
Herman W. Merkel, a forester at the New York Zoological Garden (Bronx Zoo) first found infected chestnut trees on the grounds of the zoo. In 1905, American mycologist William Murrill isolated and described the fungus responsible (which he named Diaporthe parasitica), and demonstrated by inoculation into healthy plants that the fungus caused the disease. By 1940, most mature American chestnut trees had been girdled by the disease. It took about 40 years to devastate the nearly four-billion-strong American chestnut population in North America. Today, uninfected wild American chestnut trees are extraordinarily rare, with researchers encouraging members of the public to report sightings. The world's largest remaining stand of genetically pure, mature American chestnut trees is near West Salem, Wisconsin, where scientists have been trying for decades to save the trees while studying the efficacy of hypoviruses that target the blight fungus. Other sightings of mature American chestnut trees have been reported within and outside of its original range, including in Alabama, Kentucky, Maine, Michigan, Ohio, Tennessee, and Vermont.
Japanese and Chinese chestnut trees may resist an infection from C. parasitica. Because of the disease, American chestnut wood almost disappeared from the market for decades, although it can still be obtained as reclaimed lumber.
It is estimated that in some places, such as the Appalachian Mountains, one in every four hardwoods was an American chestnut. Mature trees often grew straight and branch-free for and could grow up to tall with a trunk diameter of at a few feet above ground level. The reddish-brown wood was lightweight, soft, easy to split, very resistant to decay, and did not warp or shrink. For three centuries many barns and homes near the Appalachian Mountains were made from American chestnut. Its straight-grained wood was ideal for building furniture and caskets. The bark and wood were rich in tannic acid, which provided tannins for use in the tanning of leather.Davis Conference 2004, ecosystems.psu.edu
Chestnuts were an important cash crop and food source. Many native animals fed on chestnuts, and chestnuts were used for livestock feed, which kept the cost of raising livestock low.American-Chestnut: Appalachian Apocalypse, Cornett Media, 2010.
Since the 1930s, there have been various efforts to repopulate chestnut trees in the United States.American Chestnut Foundation. Surviving American chestnut trees are being bred for resistance to the blight, notably by The American Chestnut Foundation, which aims to reintroduce a blight-resistant American chestnut to its original forest range within the early decades of the 21st century. Japanese chestnut and Chinese chestnut, as well as Seguin's chestnut and Henry's chestnut, have been used in these breeding programs in the US to create disease-resistant hybrids with the American chestnut.New RHS Dictionary of Gardening. By A. Huxley ed. 1992. Macmillan . Chinese chestnut trees have been found to have the highest resistance to chestnut blight; however, individuals within the Chinese chestnut species may vary in blight resistance. Some individuals are still quite susceptible while others are essentially immune.Dr. Greg Miller, Empire Chestnut Company, FAQ http://www.empirechestnut.com/faqpests.htm Retrieved January 13, 2016
Hypovirulence is not widespread in the US and attempts to commercially introduce CHV1 virus have not been widely successful . Though CHV1 persists in applied trees, it does not spread naturally as it does in Europe , preventing it from being an effective form of biocontrol.
Infections in Europe
In 1938, chestnut blight was first identified around Genoa. Infection quickly spread and was identified in France in 1946, Switzerland in 1951, and Greece in 1963. It has most recently been found in the UK. Due to genetic differences between the fungal populations (strains), it is likely that a second introduction of chestnut blight occurred in Georgia and Azerbaijan in 1938. The fungal infections initially caused widespread tree death in Europe. However, in the early 1950s trees were identified in Italy that survived fungal infection. On these trees, the fungus caused more superficial cankers, that appeared to be healing. The milder infection outcome was due to the presence of CHV1, an RNA virus that infects C. parasitica. CHV1 spread naturally throughout Europe but is also spread artificially as a biocontrol measure (particularly in France). CHV1 is currently not present in the UK, Northern France, or Eastern Georgia but an introduction for biocontrol is being considered.
Symptoms
The fungus enters through wounds on susceptible trees and grows in and beneath the bark, eventually killing the vascular cambium all the way around the twig, branch, or trunk.Anagnostakis SL (2000) Revitalization of the Majestic Chestnut: Chestnut Blight Disease. The first symptom of C. parasitica infection is a small orange-brown area on the tree bark. A sunken canker then forms as the mycelial fan spreads under the bark. As the hyphae spread, they produce several toxic compounds, the most notable of which is oxalic acid. This acid lowers the pH of the infected tissue from around the normal 5.5 to approximately 2.8, which is toxic to cambium cells. The canker eventually girdles the tree, killing everything above it. Distinctive yellow tendrils (cirrus) of conidia can be seen extruding in wet weather.Crop Protection Compendium 2005 Edition. Cryphonectria parasitica (blight of chestnut). CAB International, Wallingford, UK.
Life cycle and reproduction The primary plant tissues targeted by C. parasitica are the inner bark, an area containing the conductive tissue, and the vascular cambium, a layer of actively dividing cells that give rise to secondary vascular tissues. In these tissues, the pathogen forms diffuse cankers in which the mycelium overwinters. In the following spring, two types of fruiting bodies will form: pycnidia, usually first, and perithecia. Following rainfall, the pycnidia ooze orange tendrils of conidia, the asexual spores, while perithecia forcibly eject ascospores, the sexual spores. Upon becoming airborne, ascospores are carried by eddies of wind to new hosts or infect other parts of the same tree. When insects, birds, or other wildlife come into contact with the cankers, they can mechanically disperse the conidia to a new host. Additionally, the asexual spores can be dispersed by rain splash. Once on the new host, or new area of the tree, the spores can germinate and infect the inner bark through insect wounds and fissures in the outer bark.
If cankers continue to form and expand, the fungus can girdle the stem, severing the flow of nutrients and water to the vital vegetative tissues. The absence of nutrient dispersal will result in above ground tree death. However, the root system may survive. As a result, American chestnuts exist mainly as shrubs sprouting from the old, surviving roots. These sprouts usually die of infection by C. parasitica before reaching sexual maturity.
Management: hypovirulence, sanitation, and chemical control In Europe, during the late 1960s, it was found that a strain of C. parasitica was less virulent, only able to produce shallow cankers that the tree's callus tissue could eventually limit and isolate. The trait of hypovirulence could be transferred from an avirulent strain to a lethal strain through anastomosis—the fusion of hyphae. It was later discovered that this attenuated virulence was due to infection by a dsRNA mycovirus, Cryphonectria hypovirus 1 (CHV1) of genus Hypovirus.
Considering the nature of hypovirulent strains, there has been a strong interest to use them to manage lethal C. parasitica strains. In Europe, natural dissemination of hypovirulence in pathogen populations resulted in the restoration of economically valuable chestnuts. Unfortunately, this was not the case in the United States. Compared to Europe, the US has a greater diversity of C. parasitica strains. Thus, the spread of the mycovirus in American C. parasitica populations is inhibited by vegetative incompatibility, an allorecognition system that inhibits the fusion of hyphae between individuals that are genetically distinct at specific loci. In 2016, however, "super mycovirus donor strains" of C. parasitica were engineered to overcome this incompatibility system. This could potentially be employed as a method of biological control.
As mentioned above some soil microorganisms suppress C. parasitica. This can be used to treat the cankers, by using a soil compress, a quantity of soil held against the trunk itself with plastic wrap and some adhesive tape around that.