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):



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'

B.   Biotic pathogens: living organisms

Asterisks give a rough indication of relative importance.

  1. Viroids: nucleic acid (RNA) only
  2. Viruses**: nucleic acid + protein
  3. Prokaryotes:
    1. Bacteria*
    2. Spiroplasmas, mycoplasmas (intracellular)
  4. Eukaryotes:
    1. Fungi***
    2. 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

Plant diseases can:

Some diseases are post-harvest diseases. Associated problems:

Aims of Plant Pathology

Control: needs to meet three criteria (the 3 "E's"):

Management

Understanding

How Diseases Affect Plants

Infection cycle

infection - growth- reproduction - spread

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:

  1. Symptoms: reactions of the plant. Examples:

    Symptoms can be:

  2. Signs.  Examples:

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:

  1. Biotrophs: obtain their nutrients from living host cells. Examples: Blumeria (Erysiphe) graminis, Puccinia species.
  2. Necrotrophs: kill host cells and obtain their nutrients from the dead tissue. Examples: Septoria tritici, Rhynchosporium secalis.
  3. Hemibiotrophs: initially biotrophic but eventually kill host cells.  Example: Phytophthora infestans
Biotrophic pathogens

Many biotrophic pathogens obtain their nutrients by forming haustoria (singular haustorium): ingrowths of pathogen into host cells.

Biotrophic pathogens may:

  1. Divert nutrients from host
  2. Interfere with host metabolism and development:
Necrotrophic pathogens

Examples: Septoria tritici, Rhynchosporium secalis

Necrotrophic pathogens may:

  1. Produce enzymes that damage the plant, especially cell walls. Examples:

    High production of these enzymes leads to rotting.

  2. Produce toxins: small molecules toxic to host

When Are Diseases Serious?

Epidemics are exceptional.

Factors promoting epidemics

  1. Favourable environment.
  2. Presence of inoculum (source of pathogen).
  3. Host uniformity – so if pathogen can attack one plant, can attack all. Contrast: agricultural uniformity vs. natural diversity.
  4. 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:

  1. Amount of initial inoculum, to start disease out
  2. Rate at which disease spreads

Both can be influenced by:

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:

Mechanisms of dispersal
  1. Wind – mostly fungal spores.
    Examples: Blumeria (Erysiphe) graminis, Puccinia species, Phytophthora infestans.
    Allows long-distance dissemination if spores are sufficiently resistant to adverse conditions.
  2. Water, especially rain splash. Local.
  3. Vectors:

Effect of environment on disease severity

  1. Physical:
  2. Chemical: soil fertility and pH.
  3. Biological:
Prediction

Knowledge of factors affecting disease severity makes it possible to predict:

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:

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:

Cultural practices

How crop is grown; very diverse. Most useful to reduce initial inoculum. Examples:

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.

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:

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:

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:

  1. Produce chemicals toxic to microorganisms called phytoalexins.
  2. Produce enzymes that attack pathogen directly. Example: chitinase degrades chitin in fungal cell walls.
  3. Structural barriers: strengthen cell walls. Especially increases in lignin, protein.
  4. Hypersensitive response: localised cell death (may be one cell only)
  5. Others, still unknown!
Genetic control of disease resistance
  1. Major-gene: a single gene determines whether plant is resistant or susceptible. Resistance is often complete (associated with hypersensitive response).

    Advantages:

    Disadvantage: Pathogens can evolve to overcome resistance (requires only a single mutation in the pathogen).
     

  2. Polygenic: due to many genes, each with small effect, effects cumulative.

    Advantage: Pathogen evolves very slowly to overcome resistance, so resistance is durable.

    Disadvantages:

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:

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:

Genetically engineered virus resistance

Most important use of genetic modification in plant pathology.

Genetic engineering process:

  1. Copy viral RNA to DNA.
  2. 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

  1. First discovery: tobacco resistant to tobacco mosaic virus
  2. 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).
  3. Resistance of papaya to papaya ringspot virus has saved papaya production in Hawaii.
  4. Potatoes with resistance to potato leafroll virus and to potato virus Y.

Integration

Use different methods together. Examples:

  1. Use lower chemical doses on plant with partial disease resistance
  2. Combine cultural practices with fungicides or disease resistance
     

Fungal Pathogens

Major groups:

  1. 'True fungi'
    1. Ascomycetes (largest number)
    2. Basidiomycetes (includes mushrooms/toadstools)
  2. 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


 

Diseases Caused by Ascomycetes

Powdery mildews

Examples:
Barley powdery mildew (only accessible from Newcastle University)
Apple powdery mildew

Key properties:

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
  1. Growth pattern: hyphae growing on surface form haustoria in epidermis.
  2. Effect on host

    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:

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
  1. Minimise initial inoculum:

    Imperfect, because conidia can spread long distances (e.g. European continent to England)
     

  2. 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:

  1. Seed treatment – protects seedling, which takes up chemical as seed imbibes
  2. Spring treatment of winter barley, especially if:
  3. 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

  1. Spread by rain splash (not wind) – local. Upward spread from leaf to leaf important.
  2. Overwintering in crop debris. Septoria tritici forms ascospores, which can be carried by wind, in the spring.
  3. Control mainly by systemic fungicides (similar to powdery mildew). Also:

Take-all disease

Major root disease of wheat (not barley).

Causal organism: Gaeumannomyces graminis

Symptoms:

Signs: may see dark mycelium (illustration)
 

Control
  1. Chemical – little use.
  2. Resistance – little available.
  3. Cultural practices:
    1. Fungus doesn't live long in absence of living host. Thus, can use crop rotation: alternate cereal with other crop.
    2. 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:

Three cereal rusts important in UK:

  1. Puccinia hordei causes brown or leaf rust of barley.
    Illustration (only accessible from Newcastle University)
  2. Puccinia recondita causes brown or leaf rust of wheat (similar in appearance to brown rust of barley).
  3. 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
Life cycle

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:

Under favourable conditions, 1 cycle takes as little as 4 days (infection to sporulation).
 

Control
1. Exclusion

Plant pathogen-free potatoes.
 

2. Cultural practices
3. Disease resistance
  1. Major-gene no use as pathogen overcomes rapidly.
  2. Polygenic
4. Chemical control
  1. Protectant fungicides, e.g. mancozeb, fluazinam. Need frequent application (every 5 to 14 days).
     
  2. 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:

  1. Cultural practices, mainly to minimise initial inoculum.
     
  2. Disease resistance: with partial resistance, need less fungicide.
     
  3. 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:

    Now available through the world wide web.

    Limited use of advice by farmers, because:

    Nevertheless, further development expected.