Transcript Chestnut Blight Endothia parasitica

BCB 341: Principles of
Conservation Biology
THREATS TO BIOLOGICAL DIVERSITY
3: EXOTIC SPECIES
Lecturer: James Reeler
Material by: Sam Hopkins & Vanessa
Couldridge
INTRODUCTION
 Invasion by alien species can have a significant impact
on biodiversity
 Usually there are few predatory species/diseases for
successful invaders (competitive advantage)
 Exacerbated by habitat destruction/disturbance
 Possibly exacerbated by climate shifts – expansion into
new suitable ranges
 Primary contemporary cause – humans
 Deliberate (plants/animals with economic/aesthetic
uses)
 Accidental – “piggybacking” on other species
INVASION – WHO?
 Not all species that are transported to new areas
become invasive.
 There are several characteristics of good
invaders:
 High reproductive rate (quickly build up a large
population under favourable conditions)
 Generalist species (variable diet, no strong
habitat requirements)
 Good dispersers (can rapidly spread to new
areas & find suitable habitats)
INVASION – WHERE?
 Certain areas are more vulnerable to invasion
 Disturbed areas/early succession
 Tend to have unexploited resources/empty
niches
 Little competition
 Remote islands with low diversity
 Simple food webs/empty niche space
 Remote islands/fragments with no predators
 Often naive prey (included plants poorly
adapted to herbivory
INVASION – HOW?
 Generally follows three stages:
 1. Usually start with a few individuals
 High initial likelihood of population extinction
 Initial establishment phase – growing
population, little size expansion
 2. Spreads from initial site and increases range
(expansion phase)
 3. Fills all available habitat and enters saturation
phase.
CASE STUDIES
 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 Justinian 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 habitats 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
 It was 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 CLEARCUTTING, 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 across 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 whitecolored 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
BLIGHT CONTROL AND RESTORATION
Approaches:
Hypovirulent
Asian
strains
blight resistance
Natural
Forest
resistance
management practices
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.
REFERENCES FOR THE RAT AND THE TOAD
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2.
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3.
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Maddicott, J. R.(1997) Plague in Seventh -Century England. The past and present society
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G. McCormack. (2005). The Status of Cook Island Birds 1996, Cook Island Biodiversity and natural heritage
http://cookislands.bishopmuseum.org/showarcticle.asp?id=7
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Measy, J. (2004). Global Invasive species database Xenopus laevis. [accessed 30th July 2006] Found at
http://www.issg.org/database/species/ecology.asp?si=ISO&fr=1&sts=sss
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Lafferty, K. and Page, C. (1997) Predation on the endangered Tide Water Goby, Eucyclobius newberryi, by the introduced African
clawed frog I, Xenopus laevis, with notes on the frogs parasites. Copeia 1997: 589-592.
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et al.