Transcript Lecture #4 PPT

2013 2nd Quizzes
• What are the differences between a native and an
emergent disease
• What role do native forest diseases play
• What is the Janzen-Connell hypothesis
• What is the relationship between disease and density and
what are the notable exceptions
• What are the counterweights to numerical effects of
disease, why do they count
• What are soil feed-backs and why are they important
More Ecology of Forest
Diseases (Gilbert 2002)
• Density Dependence
• Counterweights to numerical effects
• Disease and competition
• Dispersal and Local Adaptation
Density Dependence
• Most studies have shown a positive
relationship between density and
disease incidence
– Shorter distance to be covered
– Potentially limiting resources
– However there are examples that show a
different pattern, in particular for diseases
that are vectored, and for diseases that
require an alternate host
Counterweights to numerical
effects
• Disease = damage, but communities will compensate
– Disease reduced number and size of survivors,
but at maturity disease-infested plots had the
largest trees
– Survivors produce more seed
• Cross generational effects
– Diseased mothers will produce inferior seed
– Diseased mothers will generate progeny that is more
resistant to that disease
Disease and Competition
• More competition = more stress=more disease
• Disease reduces competitivity, by reducing growth
and ability to use light. Effect is larger than damage
• Apparent Competition: a generalist pathogen reduces
growth of two hosts, but allows for the second host to
coexist
• Soil feedbacks: Negative feedbacks: build-up of soil
pathogens with growth of same species (reason
behind need for crop rotation. The more limited the
dispersal of the pathogen, the stronger the effect
(that’s why effect is measurable for soil pathogens).
The more important sexual reproduction is in hosts ,
the slower the effect
Dispersal
• Dispersal of pathogen, pollen, and seed
– Pathogen: effective dispersal depends on
traits of spores (size, moisture, UV
susceptibility) and threshold number
needed for infection
– Dilution is not linear, but rather exponential
– Longer movement sometimes through
stepping stones
– Usually infection shows patterns of
aggregation (clustering) that is an easy
way to show infectious disease
Infectious diseases spread not randomly but around initial
infections
Site
Mantel test among all individuals.
[Moran’s I vs ln (geographic
distance)]
ID
ALL
Correlation
coeff. (r)
P-value
(1000,000
perm)
-0.2153
<0.000001
0.5
0.4
Moran's I
0.3
0.2
0.1
0
-0.1
-0.2
10
100
1000
Mean Geographic Distance (m)
10000
100000
Local Adaptation
• Process strongly dependent on generational rates, that is why
microbes increase virulence more rapidly than hosts, however a
generational turn over of the host may increase host resistance
• Importance of metapopulations: locally co-evolving hosts and
pathogens are more likely to undergo selective processes. If
long distance effective dispersal occurs, resistance will be
slower to show up in hosts, and virulence will increase more
slowly in pathogens
• Red queen hypothesis: relationship between hosts and
pathogens is always dynamic: pathogen increases virulence,
plants will be selected for increased resistance. Often virulence
and resistance are determined by individual genes, but these
genes cannot be accumulated indefinitely due to their cost
Forest Disease Concepts
(Tainter and Baker, chapter 5)
• Inoculum and its sources: inoculum
defined as the organism itself or
specialized cells of an organism that are
capable of infecting a host
• Viruses, bacteria, mycoplasmas the
organisms themselves, nematodes also
their eggs
• Fungi: mycelia, rhizomorphs or strands,
chlamydospores, spores, sclerotia
• Release: active or passive (weather
controlled)
• Dispersal: in general limited, vast majority of
spores stay within 100 m, however, longer
distances are reported: 500 m up to 500 Kms,
Some fungi are vectored by insects, others by
water. Insects can carry spores on surface or
mycelia in specialized organs called
mycangia
• Dormancy and survival: fungal spores usually
survive from a few days to about a year.
Oomycete mycelia: 2 months, Basidiomycete
mycelia 63 years, zoospores three weeks
• Disease Expression=Inoculum potential x
disease potential, where ip=effective
inoculum density and dp=host susceptibility
Infection rate
S
e
q
u
e
n
t
DISEASE TRIANGLE
Pathogen
Host
Environment
DISEASE TRIANGLE
HIGH DISEASE
Pathogen
Host
Environment
Pathogen
Does it need a wound to infect a host?
Can it survive in the environment without a host?
soil, water
on alternate host
How does it move around?
airborne/waterborne
animal vectors
humans
Virulence + reproductive potential=transmission
Host
Must be physically present with pathogen
Must be physically compatible with pathogen
Must provide window of opportunity for infection
Tolerance
losses where infected
but ability to redirect resources
What type of resistance?
simple= one gene
complex=several genes
100
90
80
70
60
50
40
30
20
10
0
Simple
Complex
Environment
Climatic
Climate patterns match pathogen biology
(high RH, rainfall when needed, temp range for
growth: thermophilic vs. psychrophilic organisms,
Max-min temperatures)
Host phenology: synchrony between pathogen and
host
Average lesion (mm_)
80
60
40
Wetness > 12 h
20
0
0
6
12
18
24
30
36
42
48
54
Time (h)
2
Lesion area (mm )
50
40
30
Temp >19 C
20
10
0
15
17
19
21
23
25
Temperature (¡C)
27
29
Bay Laurel / Tanoak SOD Spore Survey
35
Temp (C)
30
Rain (mm)
25
20
15
10
5
0
Date
Synchrony pathogen-host
High sporulation by pathogen
Susceptibility of oaks
(lesion size)
Host
Disease
Pathogen
• Monocultures
• Off site
• Exotic
• Artificial cross
•Enemy Release
Hypothesis
Environment
Hevea brasiliensis:
severely affected by
foliar pathogen in
South America, but
does extremely well
In Asia where the
pathogen has not
been introduced
Swiss needle cast
on Douglas-fir: excessive
homogeneity in
plantations
Caused by
Phaeocryptopus
gaeumannii
Pathogen
Disease
Host
Environment
Pathogen
•Exotic pathogens
•Pesticide resistance
Disease
Host
Environment
American chestnutCastanea dentata
Chestnut blight caused by
Cryphonectria parasitica
Stump sprouts
Migration of Cryphonectria parasitica
1910
1920
1930
1940
Modified from
Anagnostakis 1987
Introduced Forest Pathogens in CA
Port-Orford Cedar root disease
Phytophthora lateralis
White Pine Blister Rust
Cronartium ribicola
Pitch canker
Fusarium circinatum
Phytophthora root rot
Phytophthora cinnamomi
Sudden Oak Death
Phytophthora ramorum
Marin County, CA
June 2000
Gypsy moth
Lymantria dispar
Golden spotted oak borer
Agrilus coxalis
Laurel Wilt
Raffaelea lauricola sp. nov. consistently isolated from
affected tissue...
& from exotic boring beetle:
Xyleborus glabratus
(an ambrosia beetle)
Pesticide resistance
• Late blight of potato, caused by Phytopthora infestans
• 1845-1849 caused the Irish famine, potato was like the
rubber tree. Moved from its native range, but without the
pathogen (ERH). Then pathogen was introduced in
Europe with dire consequences on crop production
• More recently, introduction in Europe and North America
of different mating type allowed pathogen to reproduce
sexually and overcome effect of pesticide methalaxyl with
50% drop in potato production
Environment
Disease
Pathogen
Host
Environment
• Logging
• Fire suppression
• Pollution
• Climate change
Disease
Pathogen
Host
Armillaria spp
Heterobasidion spp.
Change in land use (stress).
Logging as pathogen
establishes itself through
stumps
Dothiostroma needle blight: fire
exclusion
New host pathogen
combinations
• Pathogen stays/Plant moves: invasive
plant
• Pathogen native/plant introduced
• Pathogen moves/Plant stays: exotic
epidemic
• Pathogen moves/Plant moves:
biological control
Success. The “1:10” rule
•
•
•
•
•
Can exotic be transported ( where will it survive: resting structures, soil,
insect, wood, live plants)
What pathways are in place: single event not likely to be successful but
repeated event increases chances
Can exotic withstand new environment (obviously the more similar the
environment in the native and invaded area, the more likely its success)
Can it withstand attacks of predators
•
Can it outcompete similar native organisms by accessing resources
– Can a pathogen be pathogenic
– Can a pathogen be sufficiently virulent
– Can a pathogen use a saprobic stage to enhance its success
How will it survive when conditions are unfavorable?
•
How effectively can it reproduce: two strategies
–
–
r selection (reproduce constantly because spectrum of conditions favorable to
reproduction are broad)
K selection: large reproductive potential in specific condition
• Invasion driven by ecological conditions
• Enemy release hypothesis
• Resource availability
(pathogenicity/virulence): lack of
coevolution