Chestnut Blight Cryphonectria parasitica

The American Chestnut (Castanea dentata)

American Chestnut: Range Maine to Georgia and west to Ohio and Tennessee. (Braun, 1950) Commonly made up 25% or more of mixed stands Formed pure stands on many dry Appalachian ridgetops and near densely populated areas. Historical Range of Castanea dentata (Saucier, 1973)

American Chestnut: Habitat Common on midslopes and other moderately dry soils Shared moist meso-phytic soils with many other species Tap root 4 to 5 ft down

“Redwoods of the East” Mature chestnuts could be 600 years old and average up to five feet in diameter and 100 feet tall Many specimens of 8 to 10 feet in diameter were recorded

American Chestnut: Ecological Importance Wildlife depended on the abundant crop of chestnuts Many species of insects fed on the leaves, flowers, and nuts

American Chestnut: Economic Importance Throughout much of the range chestnut had the most timber volume of any species – Half the standing timber volume of CT Was the major source of tannin for leather production (6-11 % tannin content) Chestnuts

“From cradle to casket…” Fast growing –reached half ultimate height by 20 th year Resistant to decay Straight and tall – often branch free for 50 feet Only white pine & tulip poplar could grow taller

“From cradle to casket…” Posts & railroad ties Telephone poles (65 feet) Construction Fuel Fine furniture & musical instruments

American Chestnut: Economic Importance Scientific forest management in the US was just getting started when the country lost its most important hard wood species (Smith, 2000) Foresters had begun to develop comprehensive plans for intensive management

Near densely populated areas Chestnut often formed nearly complete stands –due to rapid growth from stump sprouts –repeated coppicing for fuelwood

Experts estimate that American Chestnut represented half the commercial value of all Eastern North American hardwoods Pure stand of Chestnut in CT 90 years after clear-cutting, 1905.

“… the most valuable and usable tree that ever grew in the Eastern United States.”

Introduction of Cryphonectria parasitica In 1904, Herman Merkel, a forester at the New York Zoological Garden, found odd cankers on American chestnut trees in the park

Introduction of Cryphonectria parasitica "rapid & sudden death of many branches stems & trees"

Introduction of Cryphonectria parasitica American Chestnut produces a sweet but small nut Chinese chestnut produces a large but generally tasteless nut

Introduction of Cryphonectria parasitica Thomas Jefferson –imported European or Spanish chestnut (Castanea sativa) – grafted it onto native root stocks at Monticello. In 1876, a nurseryman in Flushing, NY, imported the Japanese chestnut (C. crenata). –More were brought over in 1882 and Chinese chestnut (C. Molissima) was brought here from Ichang in –to hybridize for ornamentals and nut production

Cryphonectria parasitica Ascomycete Produces both conidia & ascospores Pycnidia stromata break through the lenticels and produce conidia and perithecia producing ascospores are formed

Cryphonectria parasitica: Life Cycle

Dispersal Animals and insects Ascospores are shot into the air after rain storms in the fall Rain (conidia)

Infects trunk and branches –Only above ground parts of trees active growth & sporulation

How does it kill the tree? Enters through fissures or wounds in the bark Grows in and under the bark, girdling the cambium. Kill the tree above the point of infection.

Causes swollen or sunken orange-colored cankers on the limbs and trunks of the chestnut trees.

How does it kill the tree? The leaves above the point of infection die, followed by the limbs. Within two to ten years the entire tree is dead. Not uncommon to find many cankers on one tree

How does it kill the tree? The fungus has girdled the tree and is producing yellow conidia asexual spores

Host Range Like most cankers - fairly specific host range Serious pathogen: American & European (infects Japanese and Chinese much less) Moderate pathogen: Chinquapin & Live Oak Can also be found infecting/living on numerous oak species in the US

Rate of Spread Aggressive attempts to halt the spread of the blight were made by PA and NY –removed chestnut over a large area to halt southward spread In , the U.S. Congress appropriated special funds to enable foresters to study and control the blight

Rate of Spread Horticulturalists, found a blight-free area in Pennsylvania and quickly imported trees to form an experiment station –transported the blight and created a new epicenter –Accelerated spread in PA Cuts in funding for Chestnut blight research: –With the onset of World War I in 1914 –The evident futility of control efforts

By 1926, fungus reported throughout native range By 1940, virtually all (an estimated 4 billion) were dead or infected with the blight Chestnut was the dominant wood processed at PA sawmills in the early 1920s, – salvage logging to make use of the dead and dying trees

“…a tragic loss, one of the worst natural calamities ever experienced by this nation”

Cummulative Impacts Chestnut in Southern range was first affected by Phytophtera cinnamomum Now affecting hybrids

Cummulative Impacts In 1974, the Oriental Chestnut Gall Wasp (Dryocosmus kuriphilus) was brought to the US –Female lays eggs in chestnut vegetative buds –Galls suppress shoot elongation and reduce fruiting –Heavy infestations can kill the trees (afflicts both American and Chinese chestnuts at the southern end of their ranges) Threatening complete extinction (Anagnostakis, 1994)

Varying Outcomes: Europe The fungus was later introduced into Europe (for tree breeding) from America Moved through Europe killing European Chestnut However, it was observed that many trees, while infected and full of cankers, did not die

Instead of sunken diffuse cankers, surviving European chestnuts had swollen cankers with evidence of "healing" along the margins.

Many forest pathologists began working on this healing canker Speculation that: – European Chestnut was less susceptible – That the fungus had mutated – That it was a different fungus altogether

Noticed that a different colored fungus was recovered from "healing cankers" Instead of the typical orange colored Cryphonectria parasitica fungus, a white-colored fungus was found. –White fungus was slower growing and produced fewer spores When you "sprayed" the white fungus on a "killing canker" the "killing canker" became a "healing canker" (Europe)

Determined that the white hypovirulent strains had become infected with a simple dsRNA virus This virus was making the fungus "sick“ A slower fungus allowed the tree to respond to a point where the tree could survive infection

Varying Outcomes: Europe Grente reported in 1965 that ‘hypovirulent’ strains from Italy did not kill chestnut trees Began a program of active intervention when blight was found in France –blight strains with dsRNA passed hypovirulence to lethal strains Treatment of new cankers as they formed resulted in a successful ‘biological therapy’ of the disease. – treat every canker for several years

For a number of reasons biological control of chestnut blight does not work as well in the US –Different mating types of the fungus –Lack of chestnut to support conversion of the fungus by the virus –The many different types of virus in the United States

Varying Outcomes: Michigan Hypovirulent strains were found in the United States –Most notably in Michigan Successful because: –Few mating types –High number of Chestnut –Isolated from the native range Less diversity of pathogen in MI so that hypovirulence can transfer more readily

The transmission of hypovirulence from strain to strain of the fungus is restricted by a genetic system of vegetative incompatibility Six loci, each with two alleles in a system of heterogenic incompatibility which keep the strains of the fungus from fusing and passing hypovirulence (Huber and Milgroom) Virus transfer is restricted when there are different alleles at the vegetative incompatibility loci

Current Status Reduced to a short lived sprouting understory tree Fungus can not survive below the ground. –roots continue to live and they send up stump sprouts.

Current Status Stump sprouts grow until infected – the stump re-sprouts again Little chance for resistance to evolve –sprouts typically killed before they become sexually mature –sexual reproduction rare

Last remaining stand of American Chestnut Trees were blight free due to isolation until a canker was found in 1986 Now over 1600 cankers are present on 530 trees. Virus was introduced in 1992 – not successful Largest living (>3 ft dbh) about 20 miles east of La Crosse, WI. 10 chestnuts planted in 1885 Seeds propagated around 50 acres and more than 3000 trees

Where are we now? Upper slopes – scarlet oak, hickory, black gum Mid slopes – red and white oak, red maple, & hickory Coves – Poplar, hard maple, beech Understory - American chestnut sprouts still persist, however they become infected between 1-12 yrs of age.

Blight Control and Restoration Approaches: –Hypovirulent strains –Asian blight resistance –Natural resistance –Forest management practices

Hypovirulent Strains Italian and French scientists observed non-lethal cankers growing on trees in Italy (1960’s) –Found that strains of the fungus associated with the blight produced colonies of abnormal shape and pigment –Demonstrated that these strains contained some “contagious factor” responsible for the inability to produce lethal infections (i.e., Hypoviruses) In North America, hypovirus-infected strains have been found in stands in Michigan.

Hypovirulent Strains In the last two decades, scientists have attempted to debilitate the fungus by infecting it with a virus, a process called hypovirulence. Hypovirulence gives chestnut trees a much less potent form of the disease and gives chestnuts a fighting chance for survival (i.e., fungus is restricted to the outer bark). Once introduced into a few trees, hopes are that hypovirulence will spread throughout the forest, offering hope to surrounding trees as well.

Varied success –increase in stem size and stem number (Anagnostakis 2001) –strains do not persist (Peever et al. 1997) Virulent strains Hypovirulent strains

Intensively treated - cankers sampled, paired with hypovirulent strains, and reintroduced into the canker.

Limited treatment - cankers were sprayed with a mixture of conidia from Hypovirus-infected strains that had been used for treatment of the intensively treated plot.

Control Treatment

Factors contributing to failure high blight susceptibility abundance of virulent inoculum restricted movement of the hypovirulence viruses among the many strains –Europe and Michigan strains

Factors contributing to failure The transmission of hypovirulence from strain to strain of the fungus is restricted by a genetic system of vegetative incompatibility. Genetic studies found that there are six loci, each with two alleles in a system of heterogenic incompatibility which keep the strains of the fungus from fusing and passing hypovirulence (Milgroom and Cortesi).

More factors contributing to failure environmental stress superficial canker instability (i.e., hypovirulent cankers produced change back into a killing canker after one or more winters)

Asian blight resistance Early breeding efforts unsuccessful: –Poor form –< 50% AC parentage –Poor survival 1981 backcross breeding method proposed (Burnham) –Better form –Field blight resistance

Resistant Asian X Susceptible American Partially resistant X American again 1 out of the 4 will have 1 copy of both resistant genes Process repeated until a final cross of 2 trees with partial resistance yields 1 having 2 copies of both resistant genes making it fully resistant

American chestnut resistance Breeding programs –Scions were grafted into chestnut rootstocks to establish seed orchards Seeds and seedlings have been distributed that have low levels of blight resistance by artificial inoculation with a standard virulent strain

Site Factors High vs. low elevation –High elevation sites contain the highest density of chestnut sprouts –Studies found the superficiality rating of cankers to decrease greatly (disease developed at the vascular cambium) after several winters at high elevation sites –May be a result of physiological stress from low temperatures in mid- to late winter which may decrease host defense mechanisms in chestnut towards weak pathogens, such as hypovirulent strains

Site Factors Xeric vs. mesic sites –Blight control greatest on mesic sites Competition- high levels of hardwood competition, especially on mesic sites Browse damage

Restoration Combination of the four approaches can bring the chestnut back –Individual or group selection openings- an integrated management system using grafted trees, inoculating them with hypovirulent strains, and controlling hardwood competition –Timber production- backcross approaches