Title: 3rd Quiz, Name, date, email
13rd 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?
2Emergent diseases3 exotic pathogens
- 99 of times human responsible for their
introduction
3Like 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
4California 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
5How 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
6The 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.
7What 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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9Girdling aerial cankers removed from roots
10Big Sur 2006 K. Frangioso
11Wickland et al., unpublished
12P. ramorum growing in a Petri dish
13Organism new to science
- Origin unknown
- Biology unknown
- Symptoms caused unknown
- Immediately though highly regulated
14Rhododendron In EU mostly a nursery issue, but
also present in nurseries in US and Canada
Stem canker
Leaf necrosis
15Phytophthora ramorum
Sporangia
Chlamydospores
16Is 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
17Where 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
18Lets 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?
19- 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
20The 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
21Mating Type A1 A2 A2
Growth Rate Fast Slow Fast
22Terminology Genotype Lineage Population
23Results 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
24Was the pathogen first in US forests or in US
nurseries?
Slide 12
25Was the pathogen first in US forests or in US
nurseries?
Slide 12
nurseries
forests
26Where was it introduced?
- First reports mid 90s
- Pathogen identified in 2000
- By then, the pathogen was widespread
- CLUES severity of symptoms and anedoctal stories
27We found same genotypes in nurseries and forests
proving origin of wild outbreak
28Introduction 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
29What 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
30Bay/Oak association
Bay
Coast Live Oak (no sporulation)
Canker margin in phloem
Bleeding canker
Sporangia
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33Infectious diseases spread not randomly but
around initial infections
34Mantel 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
35Synchrony pathogen-host
Susceptibility of oaks (lesion size)
36Wetness gt 12 h
Temp gt19 C
37Bay Laurel / Tanoak SOD Spore Survey
Temp (C)
Rain (mm)
Date
38How 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
39Forest pathogens can never be eradicated
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41PREVENT Diagnose
Symptoms relatively generic, very variable, and
pathogen not always culturable
LAB CULTURES
DNA TESTS
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43AgriFos and PentraBark Topical Application
44Agrifos vs. Azomite Treatments (efficacy 1 - 24
months)
a
a
Canker Size (mm)
b
45Why 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 -
46Why 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
47Why 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
48New host pathogen combinations
- Pathogen stays/Plant moves invasive plant
- Pathogen moves/Plant stays exotic epidemic
- Pathogen moves/Plant moves biological control
49Success. 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
50- Invasion driven by ecological conditions
- Enemy release hypothesis
-
- Resource availability (pathogenicity/virulence)
51Pathogenicity
- Qualitative ability to cause disease
- Often regulated by a single gene
- Avr genes in pathogen and resistance genes in
host
52Gene for gene
- Resistance in host is dominant
- Virulence is recessive
- ar aR
- Ar AR
53Gene for gene
- Resistance in host is dominant
- Virulence is recessive
- ar aR
- Ar AR
Resistance no disease
54Functions 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)
55Avr/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
56Can 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
57Plants 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
58Virulence quantitative response
- Multiple genes controlling
- Phenotypic traits conferring virulence
- Production of plant detoxifying enzymes
- Production of plant toxins
59CAN 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
60CAN 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
61CAN 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