CROP PESTS (ACE1022)
Disease Lecture Outlines
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Contents
Introduction: Potato Late Blight
Caused by fungus Phytophthora infestans.
It is estimated that in the Irish potato famine (1845-1849):
- 600,000 people died (starvation or disease).
- 1,000,000 emigrated.
1841: population 8,200,000.
1851: population 6,600,000
What is a Plant Disease?
Abnormal and injurious condition, in which a causal agent, the
pathogen, brings about continuous irritation.
Pathogens can be
A. abiotic (non-living)
B. biotic (living organisms)
A. Abiotic pathogens: 'stress'
- Extremes of temperature, moisture,
nutrient supply, pH
- Pollutants (gases, heavy metals)
B. Biotic pathogens: living organisms
Asterisks give a rough indication of relative importance.
- Viroids: nucleic acid (RNA) only
- Viruses**: nucleic acid + protein
- Prokaryotes:
- Bacteria*
- Spiroplasmas, mycoplasmas (intracellular)
- Eukaryotes:
- Fungi***
- higher plants
The common feature of biotic pathogens is that they obtain
their nutrients from the host plant. Typically, the pathogen grows inside the host.
Impact of Plant Diseases
- Robigus or Robigo – Roman god of plant diseases.
- Irish potato famine due to potato late blight (1840s).
Potato late blight is still a problem.
- Switch from coffee to tea
production in Sri Lanka was a consequence of coffee rust (1870s).
- Brown spot disease of rice contributed to the Bengal famine of 1943.
- Losses of over $1,000,000,000 from Southern corn leaf
blight, a new disease, in 1970.
Plant diseases can:
- reduce yield;
- reduce quality of produce.
Some diseases are post-harvest diseases. Associated problems:
Aims of Plant Pathology
Control: needs to meet three criteria (the 3 "E's"):
- Effective
- Economic – benefit has to be greater than cost
- Environmentally acceptable – minimal effect on non-target organisms
Management
- Trade-offs between criteria for 'optimal' control
- Limitations: pathogens evolve to overcome control measures
- Durability/sustainability – lasting effectiveness
Understanding
- How diseases develop
- Necessary for effective management
How Diseases Affect Plants
Infection cycle
Growth and reproduction occur inside or on the surface of the
infected plant. Pathogens damage their host plants while growing and
reproducing.
Symptoms and signs
Diseased plants are usually visibly different from healthy ones. Two aspects:
- Symptoms: reactions of the plant. Examples:
- abnormal development (for example
crown gall, smut [illustration only accessible from Newcastle University], mosaic)
- yellowing (chlorosis)
- cell death (necrosis)
- wilting (as in Dutch elm disease)
- rotting
Symptoms can be:
- local to where the pathogen is growing
- systemic
- Signs. Examples:
- Fungus: hyphae and spores
- Bacterium: cells in mass
- Virus: particles (with electron microscope!). Some viruses
are rod-shaped,
others are isometric (icosahedral).
The combination of symptoms and signs is characteristic of a disease. Disease diagnosis is based on observation of symptoms and signs. Symptoms and signs do not necessarily allow unambiguous diagnosis: further study may be necessary.
Pathogen nutrition
Pathogens can be divided into:
- Biotrophs: obtain their nutrients from living host cells. Examples: Blumeria (Erysiphe) graminis, Puccinia species.
- Necrotrophs: kill host cells and obtain their nutrients from the dead tissue. Examples:
Septoria tritici,
Rhynchosporium secalis.
- Hemibiotrophs: initially biotrophic but eventually
kill host cells. Example: Phytophthora infestans
Biotrophic pathogens
- Host cells must stay alive as long as possible: pathogen avoids killing plant.
- Viruses are always biotrophic – because dependent on host cells.
- Biotrophic fungi tend to be specialised pathogens, with limited host range.
Many biotrophic pathogens obtain their
nutrients by forming haustoria
(singular haustorium): ingrowths of pathogen into host cells.
Biotrophic pathogens may:
- Divert nutrients from host
- Interfere with host metabolism and development:
- replacement of host structures with pathogen structures
- abnormal growth (galls, witches brooms, etc.)
- yellowing, mosaic
- stunting
- premature senescence, leaf drop
Necrotrophic pathogens
Examples: Septoria
tritici, Rhynchosporium
secalis
- Tend to be less specialised than biotrophs
- Plant cells die around around where the pathogen is growing (whole plant may not be killed).
- Have to compete with saprophytes to grow in dead tissues
Necrotrophic pathogens may:
- Produce enzymes that damage the plant, especially cell walls. Examples:
- cellulases: degrade cellulose
- pectinases: degrade pectic substances, etc.
High production of these enzymes leads to rotting.
- Produce toxins: small molecules toxic to host
- Interfere with host metabolism.
- Often cause necrosis (cell death).
- Structures and modes of action are diverse.
- Some only affect specific plants ('host-selective'),
others have broad toxicity.
When Are Diseases Serious?
Epidemics are exceptional.
Factors promoting epidemics
- Favourable environment.
- Presence of inoculum (source of pathogen).
- Host
uniformity – so if pathogen can attack one plant, can attack
all. Contrast: agricultural uniformity vs. natural diversity.
- Introduction of exotic
pathogens – so host lacks resistance. The most devastating
epidemics are generally caused by introduced pathogens.
Patterns of epidemic development
Two variables summarise:
- Amount of initial inoculum, to start disease out
- Rate at which disease spreads
Both can be influenced by:
- Environment.
- Resistance of plants to pathogen.
- Control measures.
An infection cycle can take as little as 4 days. Many diseases are polycyclic: have many cycles per growing season. Allows exponential
build-up of disease until build-up of disease becomes limited by availability of plant material:
logistic growth.
Some diseases are monocyclic: only have one cycle per season, and so
spread more slowly. Common with diseases where pathogen infects through roots.
Reproduction and spread
Typically, inefficient.
Most fungi form specialised structures, spores:
- One to a few cells.
- More or less resistant to adverse conditions, especially
desiccation.
Mechanisms of dispersal
- Wind – mostly fungal
spores.
Examples: Blumeria
(Erysiphe) graminis, Puccinia
species, Phytophthora infestans.
Allows long-distance dissemination if spores are
sufficiently resistant to adverse conditions.
- Water, especially rain splash. Local.
- Vectors:
- Most viruses. Vectors are most commonly insects, especially aphids.
- Some bacteria and fungi, such as the Dutch elm disease pathogen (a fungus).
Effect of
environment on disease severity
- Physical:
- Temperature. For any
disease, there will be an optimum temperature.
- Moisture
- Most fungal pathogens require free water (rain, dew)
for spore germination and infection.
- Fungi require high relative humidity to produce spores.
- Dissemination of
pathogens that are spread by water.
- Chemical: soil fertility and pH.
- Biological:
- Availability of vectors.
- Presence of organisms that are antagonistic to the pathogen.
- Human activity!
Prediction
Knowledge of factors affecting disease severity makes it possible
to predict:
- How severe a disease outbreak is likely to be.
- How bad losses will be.
Can use prediction to make decisions about control
(especially whether chemical control is necessary), but prediction is
imperfect, and so involves risk.
How to Control Plant Diseases
Methods:
- Exclusion of the pathogen
- Avoidance of the pathogen
- Cultural practices
- Chemical control
- Disease resistance
- 'Novel' methods: biological control, biotechnology.
Ideally, use combination (integrated disease management).
Exclusion of the pathogen
If main source of pathogen is seed or vegetative
propagating material (cuttings, potatoes, etc.) – ensure they
are free of pathogen.
Eliminates initial inoculum.
With vegetative propagation especially, viruses can build up
progressively from one generation to the next.
Certification: quality standards for seeds and propagating
material, to ensure freedom from pathogens.
Stringent example (for seeds): lettuce
mosaic virus on lettuce seed in California. Must have 0 seeds
infected out of 30,000.
Avoidance of the pathogen
Grow plants where pathogen is absent or conditions are
unfavourable for it. Especially useful for production of seed or
vegetative propagating material.
Example: seed potatoes. In UK, produced in Scotland and
northern England:
- away from major production areas
- unfavourable for aphids
- usually unfavourable to late blight
Cultural practices
How crop is grown; very diverse. Most useful to reduce initial
inoculum. Examples:
- Hygiene/sanitation: remove
infected plants.
- Crop rotation: many
pathogens are specific to one kind of plant, and can't survive for
long in the absence of their host
- Destroy crop residues, if pathogen can survive on them
between growing seasons.
Chemical control
There has been a substantial increase in use in the last 20 years,
notably in 'high input, high output' systems for growing cereals.
Almost entirely for control of fungi: fungicides.
Fungicides go back over 100 years.
First to be widely adopted was Bordeaux mixture (copper-based;
1885).
Fungicides can be divided into two main categories:
1.
Protectant
2. Systemic
Organic protectant fungicides
Developed since 1930s.
Remain on surface of plant, and protect against infection.
- Relatively non-specific
- Need frequent applications and
relatively large amounts (kilograms per hectare)
- Thus, expensive to use, so restricted to high value crops
Examples: mancozeb (old), fluazinam (new), both used
against late blight.
Systemic fungicides
Developed since 1960s. Taken up by plants, and so kill pathogens
after infection.
Example: ergosterol biosynthesis inhibitors inhibit
biosynthesis of membrane lipid ergosterol (the fungal equivalent of
cholesterol).
Characteristics of systemic fungicides:
- Specific (relatively) in action,
so
- relatively non-toxic to other
organisms
- probably less hazardous to the
environment than protectant fungicides
- Are inside plant and translocated
to new growth so can be applied infrequently.
- Low doses (~50 - 200 g ha-1)
- Thus, economical. Can be used, for example, on cereals.
Fungicide resistance
Major problem with systemic fungicides is that pathogens
evolve resistance to them.
Example: benomyl was used to control grey mould in
vineyards; control failed in 2 years.
Strategies to 'manage'
resistance:
- Don't over-use fungicide
- Use different fungicides at
different times
- Use mixtures of fungicides at any one application
Disease resistance
'Most plants are resistant to most pathogens'.
See illustrations
of different degrees of resistance of wheat to rusts
(only accessible from Newcastle University).
Mechanisms
Plants respond actively to threat of infection. Components
of response:
- Produce chemicals toxic to
microorganisms called phytoalexins.
- Produce enzymes that attack
pathogen directly. Example: chitinase degrades chitin in
fungal cell walls.
- Structural barriers: strengthen
cell walls. Especially increases in lignin, protein.
- Hypersensitive response:
localised cell death (may be one cell only)
- Others, still unknown!
Genetic
control of disease resistance
- Major-gene: a single gene determines whether plant is
resistant or susceptible. Resistance is often complete (associated
with hypersensitive response).
Advantages:
- Resistance can be complete
- Easy to breed
Disadvantage: Pathogens can
evolve to overcome resistance (requires only a single mutation in
the pathogen).
- Polygenic: due to many genes, each with small effect,
effects cumulative.
Advantage: Pathogen evolves very slowly to overcome
resistance, so resistance is durable.
Disadvantages:
- Resistance is usually only
partial
- Breeding difficult (slow)
Biological control
Use of microorganisms (mostly bacteria or fungi) that are
antagonistic to pathogen.
41 products available in September 2000. Most are for soil-borne
diseases, especially of seedlings.
Major problem is lack of reliability, mainly due to the
difficulty of getting biocontrol organisms established in association
with plants.
Some organisms produce antibiotics. Amount can be <1 g
ha-1.
Biotechnology
Application of molecular biology and gene cloning and
manipulation.
Uses in disease control:
- Rapid detection of pathogens
- Genetic modification (genetic engineering): transfer of
specific new genes into plants.
Current application in plant
pathology: resistance to viruses.
The plant pathogen Agrobacterium tumefaciens (causes crown
gall) is a natural genetic engineer and can be used to introduce
DNA into plants.
Viruses
Structure
of tobacco mosaic virus
Viral nucleic acid (usually RNA) has genes for:
- coat protein
- viral replication
- aphid transmission
- movement in plants
Genetically engineered virus resistance
Most important use of genetic modification in plant pathology.
Genetic engineering process:
- Copy viral RNA to DNA.
- Introduce DNA into plant.
Consequence: plant is resistant to virus.
Works with many different viruses. Coat protein gene used
most commonly, but other viral genes can work too.
Examples
- First discovery: tobacco
resistant to tobacco mosaic virus
- A squash cultivar with coat
protein genes giving resistance to two important viruses. One of the
first genetically modified plants to be grown commercially (released
1964).
- Resistance of papaya to
papaya
ringspot virus has saved papaya production in Hawaii.
- Potatoes with resistance to potato leafroll virus and
to potato virus Y.
Integration
Use different methods together. Examples:
- Use lower chemical doses on plant
with partial disease resistance
- Combine cultural practices with fungicides or disease
resistance
Fungal Pathogens
Major groups:
- 'True fungi'
- Ascomycetes (largest
number)
- Basidiomycetes (includes
mushrooms/toadstools)
- Oomycetes. Look similar to 'true fungi', but not
closely related.
Features
distinguishing fungal groups
1. Characteristics of hyphae (especially cross-walls:
septa)
2. Biochemistry (cell walls,
membranes)
|
Ascomycetes
|
Basidiomycetes
|
Oomycetes
|
Hyphae
|
Septate
|
Coenocytic
|
Principal CW polysaccharide
|
Chitin
|
Cellulose
|
Ergosterol in membranes
|
+
|
-
|
Motile cells
|
None
|
Zoospores
|
3. Reproduction
- Asexual: commonly, usual
means of dispersal. Offspring genetically identical to
parents.
- Sexual: tends to occur under adverse conditions
(e.g. cold, dry, nutrients in plant used up). Offspring have new
combinations of genes.
Diseases Caused by
Ascomycetes
Powdery mildews
Examples:
Barley
powdery mildew (only accessible from Newcastle University)
Apple
powdery mildew
Key properties:
- Only grow on leaf surface
(unusual)
- Biotrophic
- Cause serious diseases in cereals,
especially barley. Most serious cereal disease in UK at present.
- Specialised: different kinds for different plant species.
Example:
Causal organism
|
Host
|
family Erysiphaceae
|
most plants
|
Blumeria (Erysiphe) graminis
|
grasses
|
B. graminis forma specialis (f.sp.) tritici
|
wheat
|
B. graminis f.sp. hordei
|
barley
|
Interaction with host
- Growth pattern: hyphae
growing on surface form haustoria
in epidermis.
- Effect on host
- Transfer of nutrients
- Shading by hyphae reduces photosynthesis
Plants rarely killed, but can have yield losses of up to 20-25%.
Life cycle
Conidia
form in chains on leaf surface; spread by wind. Fungus produces new
conidia 7-10 days after infection.
Requires:
- moderate temperatures
- high humidity
- not free water (unusual)
As plants senesce, ascospores form in cleistothecia,
which look like tiny
black dots embedded in the mycelium. Allows pathogen to survive
over summer.
Control
A. Cultural practices
- Minimise initial inoculum:
- remove 'green bridge' of living
plants: eradicate volunteers, isolate autumn, spring-sown cereals
- dispose of stubble and debris (remove cleistothecia)
Imperfect, because conidia can spread
long distances (e.g. European continent to England)
- Avoid excess fertiliser, especially N.
B. Chemical control
Use systemic fungicides, e.g.
ergosterol biosynthesis inhibitors.
Resistance of B. graminis to chemicals is a significant
problem.
2 to 3 treatments during growing season:
- Seed treatment – protects
seedling, which takes up chemical as seed imbibes
- Spring treatment of winter barley,
especially if:
- variety is highly susceptible
- lush growth because high N
fertiliser
- mildew present
- Spray at flag leaf emergence. Flag leaf is major contributor
to yield, so essential to protect it.
C. Disease resistance
Usefulness limited. Most important: mlo resistance
gene (barley) – recessive. No evidence of pathogen virulence to
plants with this gene, despite widespread use in spring barley.
Leaf spotting
diseases of cereals
Necrotrophic pathogens – kill
areas of cells in leaves.
Septoria (or speckled leaf) blotch of wheat
Illustration
(only accessible from Newcastle University)
Causal organism: Septoria tritici
Symptoms: elongated
lesions with chlorotic edges
Signs: black dots –
pycnidia,
which exude
highly elongated conidia in wet conditions.
Stagonospora (formerly Septoria) nodorum
causes a similar disease.
Leaf scald of barley
Illustration
Causal organism: Rhynchosporium secalis
Symptoms: irregular
lesions with dark edges around tan-coloured area of dead cells
Common features
- Spread by rain splash (not
wind) – local. Upward spread from leaf to leaf important.
- Overwintering in crop
debris. Septoria tritici forms ascospores, which can
be carried by wind, in the spring.
- Control mainly by systemic
fungicides (similar to powdery
mildew). Also:
- removal of crop debris
- some disease resistance
Take-all disease
Major root disease of wheat (not barley).
Causal organism: Gaeumannomyces graminis
Symptoms:
- Patches of yellow or stunted
plants; grain may fail to develop (hence 'take-all')
Illustration
- Roots blackened ('dry rot'), stunted
Illustration
(only accessible from Newcastle University)
Signs: may see dark
mycelium (illustration)
Control
- Chemical – little use.
- Resistance – little available.
- Cultural practices:
- Fungus doesn't live long in
absence of living host. Thus, can use crop rotation:
alternate cereal with other crop.
- Take-all decline.
Take-all decline
Natural biological control.
Major organisms responsible for decline are probably strains of the
bacterium Pseudomonas fluorescens. Deliberate addition of
biocontrol bacteria to soil has given inconsistent results in the
past, but recently strains that provide useful control have been
identified.
Diseases Caused
by Basidiomycetes
Example: rusts
General characteristics of rusts:
- Biotrophic.
Grow intercellularly and form haustoria.
- Most plants have their 'own' rust
pathogen.
- Many have complex life cycles, with more than one host.
Three cereal rusts important in UK:
- Puccinia hordei causes
brown or leaf rust of barley.
Illustration
(only accessible from Newcastle University)
- Puccinia recondita causes
brown or leaf rust of wheat (similar in
appearance to brown rust of barley).
- Puccinia striiformis causes yellow or stripe
rust (mainly wheat).
Illustration
Life cycle
Cereal rusts, caused by several Puccinia species, can
reproduce asexually on cereal host by
uredospores,
as long as living host leaves are present. Uredospores form in
pustules
called uredia (singular: uredium).
Uredospores are spread by wind.
Sexual reproduction requires an
alternate host, a different plant species. Alternate hosts are not
important for cereal rusts in UK.
Control
Similar to powdery mildew,
but resistance is more effective.
See illustrations
of different degrees of resistance of wheat to rusts (only accessible
from Newcastle University).
Diseases Caused by
Oomycetes
Example: late blight
Causal organism: Phytophthora infestans
Main hosts: potatoes, tomatoes,
The American Phytopathological Society has an excellent web
site dealing with late blight, including illustrations of
symptoms and of Phytophthora infestans.
Effects on host
Pathogen spreads by wind-blown sporangia.
Tuber infection occurs when sporangia are washed off leaves
and fall on ground. Penetration occurs through lenticels or wounds.
Can have post-harvest infection by sporangia contaminating
tubers.
Severe disease favoured by:
- moisture (free water for
infection; sporulation requires high relative humidity)
- moderate temperatures
Under favourable conditions, 1 cycle
takes as little as 4 days (infection to sporulation).
Control
1. Exclusion
Plant pathogen-free potatoes.
2. Cultural practices
- Sanitation to minimise initial
inoculum
- destroy potato dumps (cull piles)
- kill sprouts or prevent sprouting
- destroy volunteer plants
- Kill vines before harvest, to minimise tuber infection
3. Disease resistance
- Major-gene
no use as pathogen overcomes rapidly.
- Polygenic
- not sufficient for complete
control but
- useful as supplement to chemical control; pathogen does not
overcome rapidly.
4. Chemical control
- Protectant
fungicides, e.g. mancozeb, fluazinam. Need
frequent application (every 5 to 14 days).
- Systemic fungicides.
Systemic fungicides for control of oomycetes are different from
those used to control true fungi.
Most important: metalaxyl (introduced in late 1970s). When
introduced, was highly effective and only needed application about
every 21 days. Pathogen rapidly evolved resistance. Is now only sold
in mixtures, e.g. mancozeb + metalaxyl.
5. Integrated control
Main objective is to reduce reliance on fungicide. Make use of:
- Cultural practices, mainly
to minimise initial inoculum.
- Disease resistance: with
partial resistance, need less fungicide.
- Disease forecasting. In UK,
warning of need to spray has been provided by ADAS (Agricultural
Development and Advisory Service) when there is a sufficient period
of:
- Temperature >= 10°C
- Relative humidity >90%
Now available through the world
wide web.
Limited use of advice by farmers, because:
- Risk of mistake (if don't spray
when needed)
- Need for advance planning of
spraying
- Not a large reduction in spray use, because threat of
disease almost always present
Nevertheless, further development expected.