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
Historical Range of Castanea dentata
(Saucier, 1973)
• Formed pure stands on
many dry Appalachian
ridgetops and near densely
populated areas.
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 20th 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
Pure stand of Chestnut in CT 90 years after clear-cutting, 1905.
Experts estimate that American Chestnut represented
half the commercial value of all Eastern North
American hardwoods
“… 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 1886.
• Chinese chestnut (C. Molissima) was brought here
from Ichang in 1900.
– 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)
active growth & sporulation
• Infects trunk and branches
– Only above ground parts of trees
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 1911-1913, 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
• 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
• 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
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
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