Transcript Chestnut Blight Endothia parasitica

Threats to biological diversity
3: Exotic Species
Vanessa Couldridge &
Sam Hopkins
Biodiversity & Conservation Biology
Department
Matteo Garbelotto
University of California
Available at http://planet.uwc.ac.za/nisl
Introduction
 The Invasion Biology course discusses exotic
species in detail.
 Rather than repeat everything, the following
examples of invasive species have been selected
for discussion:

Rinderpest

The black rat (Rattus rattus)

The toad/platanna – Xenopus laevis

Chestnut blight
 Viral disease that affects
primarily cattle (also
known as cattle plague)
http://www.virology.net
Rinderpest
 All cloven-hoofed wild and
domestic are animals susceptible to the disease
 Belongs to the genus Morbillivirus
 Affects gastrointestinal and respiratory systems
 Highly contagious and usually fatal; it can wipe
out entire populations
 Death occurs 6-12 days after the first symptoms
Rinderpest: Introduction to Africa
 Introduced to Africa from Asia in 1887
 Disease was present in Indian cattle imported to
the east coast of Africa to feed the Italian army,
which was invading Ethiopia at the time
 Quickly spread to local cattle and wildlife
populations
 From there the disease swept across eastern and
southern Africa, with devastating consequences
 Within 10 years it had reached South Africa
Rinderpest: Spread in Africa
 This map shows
the spread of the
disease across
the African
continent
 The fauna and
flora of Africa
south of the
Sahara changed
completely as a
result
Rinderpest: Plague of 1890s
 Millions of animals died, both wild and domestic
http://www.Aleffgroup.com
 Reports indicate more than 90% of cattle and
wildebeest were wiped out
Rinderpest: Devastation Caused
 Wildlife killed by rinderpest included wildebeest,
buffalo, giraffe, warthog, eland, kudu, and other
buck species
 Predators also suffered as their prey species
disappeared; lions reportedly became maneaters
 Pastoralists depending on cattle for their
livelihood faced severe hardship and death
 Ox-wagon transport was brought to a standstill
 Loss of grazers transformed the landscape
Rinderpest: Control
 The disease was eventually brought under
control through early attempts at vaccination and
natural immunity among surviving animals
 In the early 1960s a more reliable vaccine was
developed and between 1962 and 1976 there was
a large-scale attempt to eradicate rinderpest
entirely from Africa through mass vaccination
 This was largely successful – 15 out of 17
countries were freed of the disease
 Outbreaks still occur from time to time, but none
as severe as the original plague of the 1890s
Rinderpest: Recovery
 Vaccination of cattle in the 1960s eliminated
rinderpest from wildlife populations, as cattle
could no longer act as a reservoir for the disease
http://geoimages.berkeley.edu
 Wildebeest numbers in the Serengeti increased
by about six-fold over a period of 15 years;
Buffalo numbers also increased dramatically
Rinderpest: Landscape Change
1980
http://www.circa.gbif.net/Public/irc/gbif/pr/library?!=/
science_symposia/2006/mduma_ppt/_EN_1.0_&a=d
 This had an impact on the environment by
changing grassland into woodland – an increase
in grazers eliminated the fuel for fires that
control tree growth. Fires are now less frequent
and do not burn as hot
2003
Rinderpest and Canine Distemper
 Ironically, it has been suggested that eradication
of rinderpest has led to an increase in canine
distemper among lions
http://www.eecs.umich.edu
 Lions feeding on wildebeest infected with
rinderpest may have gained immunity to canine
distemper, since the two
viruses are very similar
to each other
(both Morbilliviruses)
The Rat1
 The Black Rat (Rattus rattus) was originally from
Asia
 It made its way to the near East in Roman time
 It was in Europe in the 8th century
 From Europe it had a boat ticket to the rest of the
world
 Rats are nocturnal
 Rats are omnivorous
 They are good breeders
The Rat and the plague2
 The rat and a number of
other rodents are largely
responsible for out
breaks of plague
through history
 Humans as carriers of
rats also participated in
the spread of the
disease
 Often the rats would
then infect native
rodents with the disease
History of the Plague
 An early example is the plague of Justintian 3
 544, The first great plague 4
 1348, Black Death 5
 1665, Great Plague 6
 1899, Plague in South Africa 7
 Recent plague – 2005/ 2006 DRC 8,9
Other effects of rat invasion –
Lundy Puffins 10, 11
 Lundy island is off the coast of
North Devon, UK
 Rats reached the island 200
years ago
 Rat numbers reached 40,000
 Extermination started in 2003
 Puffin and Manx Shearwater
numbers had declined
 Now rats gone, hopefully bird
numbers will increase
Other effects of rat invasion –
Pacific Islands 12,13
 Reached Pacific Islands in the 17th century
 Now established on 28 groups of islands
 Eat native snails, beetles, spiders, moths, stick insects, and
fruit, eggs and young of birds
 Largest threat to the Rarotonga flycatcher
 Other Island birds affected
 Sooty terns, Seychelles
 Bonin Petrels, Hawaii
 Galapagos dark-rumped petrels Galapagos islands
 White tailed tropic birds Bermuda
The Toad –
Xenopus laevis 14
 Xenopus laevis is the
common platanna in
Southern Africa
 It is mainly aquatic
 Females reach 130 mm
 Eats insects, small fish,
young and larvae of its
own species or other
species of frogs
 Adults can breed more
than once per season
The Toad –
Xenopus laevis 14
 Xenopus laevis is found about the world owing to
 Lab animals
 Pet trade
 Pregnancy tests
 These animals escape and can form viable populations
 Now found in USA, Chile, Mexico, France, Indonesia and the UK
 These frogs are a great invader owing to
 Good in disturbed environments
 Has a varied diet
 High reproductive rate
 High salt tolerance
 Disease resistant
 Can move overland or through rivers and streams
The Toad –
Xenopus laevis 14
 Xenopus laevis are a
problem because they
 Predate upon and
compete with native
species
 Are toxic to predators
 Make water turbid
The Toad –
Xenopus laevis
 Seen in Southern California
 X. laevis has been present
since the 1960s
 Preys on the Tide Water Goby
 Preys on the Endangered
Red-legged frog
 Also managed to establish parasites that need alternate
hosts 15
 In South Wales, Xenopus were found to have a very varied
diet ranging from zooplankton to bank voles to Xenopus
eggs 16
The Toad –
Xenopus laevis 17
 In South Africa X. laevis is an invasive
 Animals are moved out of their natural range by
fisherman
 Animals make use of the habitat disturbed by
humans
 Have hybridized with Xenopus gilli
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.
Map of 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 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”
Cumulative Impacts
Chestnut in Southern range was first
affected by Phytophtera cinnamomum
Now affecting hybrids
Cumulative 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
infected between 1-12 yrs of
age.
Blight Control and Restoration
Approaches:
Hypovirulent
Asian
strains
blight resistance
Natural
Forest
resistance
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
Graph of Numbers of
Living Stems of
Intensively treated
American Chestnuts
Intensively treated - cankers sampled, paired with
hypovirulent strains, and reintroduced into the canker.
Graph of Numbers of
Living Stems of
American Chestnuts
with Limited
Treatment
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.
Graph of Numbers of
Living Stems of
American Chestnuts
with the Control
Treatment
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
Concluding Remarks
 The selected examples demostrate the damage that
invasive species can do to both the natural environment
and human interests.
 For more information on invasive species see the Invasion
Biology course.
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