3rd Quiz, Name, date, email - PowerPoint PPT Presentation

1 / 61
About This Presentation
Title:

3rd Quiz, Name, date, email

Description:

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 ... – PowerPoint PPT presentation

Number of Views:131
Avg rating:3.0/5.0
Slides: 62
Provided by: Mat73
Category:

less

Transcript and Presenter's Notes

Title: 3rd Quiz, Name, date, email


1
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?

2
Emergent diseases3 exotic pathogens
  • 99 of times human responsible for their
    introduction

3
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
4
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
5
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

6
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.

7
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

8
(No Transcript)
9
Girdling aerial cankers removed from roots
10
Big Sur 2006 K. Frangioso
11
Wickland et al., unpublished
12
P. ramorum growing in a Petri dish
13
Organism new to science
  • Origin unknown
  • Biology unknown
  • Symptoms caused unknown
  • Immediately though highly regulated

14
Rhododendron In EU mostly a nursery issue, but
also present in nurseries in US and Canada
Stem canker
Leaf necrosis
15
Phytophthora ramorum
Sporangia
Chlamydospores
16
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

17
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

18
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?

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

20
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
21
Mating Type A1 A2 A2
Growth Rate Fast Slow Fast
22
Terminology Genotype Lineage Population
23
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

24
Was the pathogen first in US forests or in US
nurseries?
Slide 12
25
Was the pathogen first in US forests or in US
nurseries?
Slide 12
nurseries
forests
26
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

27
We found same genotypes in nurseries and forests
proving origin of wild outbreak
28
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
29
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

30
Bay/Oak association
Bay
Coast Live Oak (no sporulation)
Canker margin in phloem
Bleeding canker
Sporangia
31
(No Transcript)
32
(No Transcript)
33
Infectious diseases spread not randomly but
around initial infections
34
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
35
Synchrony pathogen-host
Susceptibility of oaks (lesion size)
36
Wetness gt 12 h
Temp gt19 C
37
Bay Laurel / Tanoak SOD Spore Survey
Temp (C)
Rain (mm)
Date
38
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

39
Forest pathogens can never be eradicated
40
(No Transcript)
41
PREVENT Diagnose
Symptoms relatively generic, very variable, and
pathogen not always culturable
LAB CULTURES
DNA TESTS
42
(No Transcript)
43
AgriFos and PentraBark Topical Application

44
Agrifos vs. Azomite Treatments (efficacy 1 - 24
months)
a
a
Canker Size (mm)
b
45
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

46
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

47
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

48
New host pathogen combinations
  • Pathogen stays/Plant moves invasive plant
  • Pathogen moves/Plant stays exotic epidemic
  • Pathogen moves/Plant moves biological control

49
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

50
  • Invasion driven by ecological conditions
  • Enemy release hypothesis
  • Resource availability (pathogenicity/virulence)

51
Pathogenicity
  • Qualitative ability to cause disease
  • Often regulated by a single gene
  • Avr genes in pathogen and resistance genes in
    host

52
Gene for gene
  • Resistance in host is dominant
  • Virulence is recessive
  • ar aR
  • Ar AR

53
Gene for gene
  • Resistance in host is dominant
  • Virulence is recessive
  • ar aR
  • Ar AR

Resistance no disease
54
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)

55
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

56
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

57
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

58
Virulence quantitative response
  • Multiple genes controlling
  • Phenotypic traits conferring virulence
  • Production of plant detoxifying enzymes
  • Production of plant toxins

59
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

60
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

61
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
Write a Comment
User Comments (0)
About PowerShow.com