3rd Quiz, Name, date, email

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3rd Quiz, Name, date, email

• 1 Pick one of the following two
• A)Explain how environmental changes can increase
  severity of disease
• B)Why is it useful to be able to follow
  individual genotypes (strains) of a microbe?
• 2 Pick one of the following two
• A) What is the likleihood of a host shift for an
  exotic pathogen?
• B)- What are R and avr genes?

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Emergent diseases3 exotic pathogens

• 99 of times human responsible for their
  introduction

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Like the conquistadores brought diseases that
were lethal to those who had never been exposed
to them, so do exotic diseases cause true
devastation in plant communities because of lack
of coevolution between hosts and microbes
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California invaded 1849 A.D.
Port Orford Cedar Root Disease 1950s
New hybrid root pathogen 1990s
Manzanita/madrone die-back
Sudden Oak Death 1990s
White pine blister rust 1930s
Canker-stain of Sycamores 1980s
Dutch Elm Disease 1960s
Pitch canker disease 1980s
Oak root canker 2000
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How can people transport pathogens

• By transporting plants and plant parts
• Crops, and seeds
• Raw food
• Ornamental plants
• Untreated lumber
• Soil
• Insects vectoring fungi
• Military activity

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The Irish Potato Famine

• From 1845 to 1850
• Phytophthora infestans
• Resulted in the death of 750,000
• Emigration of over 2 million, mainly to the
  United States.

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What favors invasion of exotic fungi ?

• Density of host increases severity of disease
• _ Presence of related hosts phylogenetic signal)
• Corridors linking natural habitats
• Synchronicity between host susceptibility and
  pathogen life cycle
• Ecological and environmental conditions
• Disturbances
• Capacity of pathogen to survive in unfavorable
  conditions
• Transmission rate

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Girdling aerial cankers removed from roots
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Big Sur 2006 K. Frangioso
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Wickland et al., unpublished
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P. ramorum growing in a Petri dish
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Organism new to science

• Origin unknown
• Biology unknown
• Symptoms caused unknown
• Immediately though highly regulated

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Rhododendron In EU mostly a nursery issue, but
also present in nurseries in US and Canada
Stem canker
Leaf necrosis
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Phytophthora ramorum
Sporangia
Chlamydospores
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Is it exotic?

• Our studies have indicated that California
  population is extremely simplified, basically two
  strains reproducing clonally as expected of an
  introduced organism
• Many hosts appear to have no resistance at all
• Limited geographic distribution

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Where does it come from?

• It is unknown where pathogen originally comes
  from, but previous studies have shown that
  California forest population is derived from a
  relatively genetically diversified US nursery
  population, indicating ornamental nurseries were
  the most likely avenue for pathogen introduction

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Lets look at its genetic structure

• Need a number of independent and neutral DNA
  markers
• Used AFLP, a technique that scans the entire
  nuclear genome
• Are our isolates the same as the European ones?
• Is the genetic structure suggestive of an
  introduced or native species?

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• US forest isolates clearly distinct from EU
  nursery isolates, also have different mating type
• Isolates from nurseries in WA, OR, BC both of
  the US and EU types
• Potential for XXX sex and recombination in US
  nurseries
• US forest population is genetically very
  homogeneous, trademark of an introduced species

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The entire genome was sequenced in less than 3
years since discovery of organism
12 SSR loci (di- and tri- repeats identified)
Loci selected to be polymorphic both between
and within continental populations 500
representative isolates analyzed
CCGAAATCGGACCTTGAGTGCGGAGAGAGAGAGAGACTGTACGAGCCCGA
GTCTCGCAT
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Mating Type A1 A2 A2
Growth Rate Fast Slow Fast
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Terminology Genotype Lineage Population
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Results of 1st microsatellite study

• There actually three distinct (genotypically and
  phenotypically) lineages of P. ramorum
• Very low diversity in US forests (microsats
  cannot discriminate among individuals, clonality
  confirmed), only one lineage
• Several genotypes but only one lineage in EU
  nurseries
• Three lineages in US nurseries

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Was the pathogen first in US forests or in US
nurseries?
Slide 12
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Was the pathogen first in US forests or in US
nurseries?
Slide 12
nurseries
forests
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Where was it introduced?

• First reports mid 90s
• Pathogen identified in 2000
• By then, the pathogen was widespread
• CLUES severity of symptoms and anedoctal stories
  

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We found same genotypes in nurseries and forests
proving origin of wild outbreak
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Introduction phase 1- Escape of pathogen
from Infected nursery plants at two locations
Mount Tamalpais (Marin County), and
Scotts Valley (Santa Cruz County) 2- Nurseries
and two sites have identical strain composition,
but distance between sites is impossible for
natural spread of organism
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What favors invasion of exotic fungi ?

• Density of host increases severity of disease
• Corridors linking natural habitats
• Synchronicity between host susceptibility and
  pathogen life cycle
• Ecological and environmental conditions

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Bay/Oak association
Bay
Coast Live Oak (no sporulation)
Canker margin in phloem
Bleeding canker
Sporangia
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Infectious diseases spread not randomly but
around initial infections
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Mantel test among all individuals. Morans I vs
ln (geographic distance)
Site ID Correlation coeff. (r) P-value (1000,000 perm)
ALL -0.2153 lt0.000001
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Synchrony pathogen-host
Susceptibility of oaks (lesion size)
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Wetness gt 12 h
Temp gt19 C
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Bay Laurel / Tanoak SOD Spore Survey
Temp (C)
Rain (mm)
Date
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How to control emergent exotic diseases

• PREVENT THEIR INTRODUCTION
• LIMIT THE HUMAN-SPREAD OF PATHOGENS (infected
  plants, plant parts, dirty tools)
• EMPLOY HOST RESISTANCE
• CHEMICAL AND OTHER MITIGATION STRATEGIES

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Forest pathogens can never be eradicated
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PREVENT Diagnose
Symptoms relatively generic, very variable, and
pathogen not always culturable
LAB CULTURES
DNA TESTS
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AgriFos and PentraBark Topical Application

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Agrifos vs. Azomite Treatments (efficacy 1 - 24
months)
a
a
Canker Size (mm)
b
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Why emphasis on molecular analyses?

• As a way to identify and quantify microbes in
  the environment
• As a way to understand microbial biology how do
  microbes reproduce and infect hosts
• As a way to determine epidemiology follow the
  movement of a strain

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Why emphasis on molecular analyses?

• As a way to determine potential for spread use
  genes as markers for individuals
• As a way to determine whether population of
  microbes is exotic or native
• As a way to identify source of a pathogen and
  migration patterns

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Why emphasis on molecular analyses?

• As a way to determine the size of the gene pool
  of a pathogen, Important to scale management
  options
• As a way to determine rapid evolutionary changes
  linked to an introduction
• As a way to determine epigenetic effects

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New host pathogen combinations

• Pathogen stays/Plant moves invasive plant
• Pathogen moves/Plant stays exotic epidemic
• Pathogen moves/Plant moves biological control

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Success. The 110 rule

• Can exotic withstand new environment
• 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

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• Invasion driven by ecological conditions
• Enemy release hypothesis
• Resource availability (pathogenicity/virulence)

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Pathogenicity

• Qualitative ability to cause disease
• Often regulated by a single gene
• Avr genes in pathogen and resistance genes in
  host

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Gene for gene

• Resistance in host is dominant
• Virulence is recessive
• ar aR
• Ar AR

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Gene for gene

• Resistance in host is dominant
• Virulence is recessive
• ar aR
• Ar AR

Resistance no disease
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Functions of avr/R genes

• Avr genes may help detoxify plant enzymes, secure
  necessary aminoacids or proteins, plant toxins,
  promoting pathogen growth. Normally they are
  mobile, wall-bound products
• R genes normally recognize multiple avr genes and
  start hypersensitive response (programmed cell
  death)

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Avr/R genes matches are specific

• Race of the pathogen (avr1) matched by variety of
  the crop (R1).
• At the base of crop breeding science
• If R genes target avr genes linked to important
  housekeeping functions, they are more durable

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Can be R genes accumulated?

• There is a cost associated with R genes
• Mostly R genes initiate costly defense processed,
  often even when challenged by innocuous microbes
• Some evidence that in absence of specific avr, R
  are lost

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Plants immune response

• Plants do not possess an immune system such as
  that of animals
• They do recognize pathogens
• Recognition initiates secondary metabolic
  processes that produce chemicals that will stop
  or slow microbial infections thickening of cell
  wall, premature cell death (HR response),
  systemic resistance

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Virulence quantitative response

• Multiple genes controlling
• Phenotypic traits conferring virulence
• Production of plant detoxifying enzymes
• Production of plant toxins

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CAN WE PREDICT

• Success of an exotic microbe?
• Survival structures such as cysts, spores, etc
• Saprotrophic ability (ability to feed on dead
  matter)
• Degree of host specialization, the more
  specialized the harder it may be to establish
• Phylogenetic distance of hosts (the closertive
  and new hosts are, the easier the establishment)
• Similar ecology

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CAN WE PREDICT

• Levels of the epidemic?
• Density dependence abundance of susceptible
  hosts
• Genetic variation in host. In general it is
  assumed that genetic variation in host
  populations slows down epidemics, however backing
  data from natural ecosystems is missing. It could
  be that low genetic diversity associated with
  widespread presence of resistance may be more
  beneficial than genetic variability

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CAN WE PREDICT

• Selection of increased R in host?
• Host R to exotic may be significantly present
  because it identifies native pathogen.
• R may be absent.
• R may be present at low frequency. If host does
  not exchange genes long distance, but only in
  areas already infested there is a stronger
  selection process. Otherwise locally selected R
  genes may be swamped by genes coming from outside
  the area of infestation
• Shorter generation times favor pathogen