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 initialinfections

Mantel test among all individuals. [Moran’s I vs ln (geographic

distance)]

Site

IDCorrelation coeff. (r)

P-value (1000,000 perm)

ALL -0.2153 <0.000001

-0.2

-0.1

0

0.1

0.2

0.3

0.4

0.5

10 100 1000 10000 100000

Mean Geographic Distance (m)

Mo

ran

's I

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

Sequential increments

DISEASE TRIANGLEDISEASE TRIANGLE

PathogenPathogenHostHost

EnvironmentEnvironment

DISEASE TRIANGLEDISEASE TRIANGLE

PathogenPathogenHostHost

EnvironmentEnvironment

HIGH DISEASE

PathogenPathogen

Does it need a wound to infect a host?Does it need a wound to infect a host?

Can it survive in the environment without a host?Can it survive in the environment without a host?soil, watersoil, wateron alternate hoston alternate host

How does it move around?How does it move around?airborne/waterborneairborne/waterborneanimal vectorsanimal vectorshumanshumans

Virulence + reproductive potential=transmissionVirulence + reproductive potential=transmission

HostHost

Must be physically present with pathogenMust be physically present with pathogen

Must be physically compatible with pathogenMust be physically compatible with pathogen

Must provide window of opportunity for infection Must provide window of opportunity for infection

ToleranceTolerancelosses where infectedlosses where infectedbut ability to redirect resources but ability to redirect resources

What type of resistance?What type of resistance?simple= one genesimple= one genecomplex=several genescomplex=several genes 0

102030405060708090

100

SimpleComplex

EnvironmentEnvironment

ClimaticClimatic

Climate patterns match pathogen biologyClimate patterns match pathogen biology(high RH, rainfall when needed, temp range for (high RH, rainfall when needed, temp range for growth: thermophilic vs. psychrophilic organisms,growth: thermophilic vs. psychrophilic organisms,Max-min temperatures)Max-min temperatures)

Host phenology: synchrony between pathogen andHost phenology: synchrony between pathogen andhosthost

0

20

40

60

80

0 6 12 18 24 30 36 42 48 54

Time (h)

Ave

rag

e le

sio

n (

mm

_)

0

10

20

30

40

50

15 17 19 21 23 25 27 29Temperature (¡C)

Lesio

n a

rea (

mm

2 )

Wetness > 12 h

Temp >19 C

Bay Laurel / Tanoak SOD Spore Survey

Date

Temp (C)

Rain (mm)

Synchrony pathogen-host

Susceptibility of oaksSusceptibility of oaks(lesion size)(lesion size)

High sporulation by pathogen

Host

Pathogen Environment

• Monocultures• Off site• Exotic• Artificial cross•Enemy Release

HypothesisDisease

Hevea brasiliensis: severely affected by foliar pathogen in South America, but does extremely wellIn Asia where the pathogen has notbeen introduced

Swiss needle cast on Douglas-fir: excessivehomogeneity in plantations

Caused by Phaeocryptopus gaeumannii

Host

Pathogen

Environment

Disease

Host

Pathogen

Environment

•Exotic pathogens•Pesticide resistance

Disease

American chestnut-Castanea dentata

Chestnut blight caused by Cryphonectria parasitica

Stump sprouts

1910

1920

1930

1940

Migration of Cryphonectria parasitica

Modified fromAnagnostakis 1987

Port-Orford Cedar root diseasePhytophthora lateralis

Pitch cankerFusarium circinatum

White Pine Blister RustCronartium ribicola

Phytophthora root rotPhytophthora cinnamomi

Introduced Forest Pathogens in CA

Marin County, CA June 2000

Sudden Oak Death Phytophthora ramorum

Gypsy moth Lymantria dispar

Golden spotted oak borerAgrilus coxalis

Laurel WiltRaffaelea 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

HostPathogen

Environment

Disease

HostPathogen

Environment • Logging • Fire suppression• Pollution• Climate change

Disease

Armillaria spp

Change in land use (stress).

Heterobasidion spp.

Logging as pathogen establishes itself throughstumps

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