AGR514

CROP DISEASE MANAGEMENT

Chapter 2: Plant-Pathogen-Environment
Interactions
 PLANT-PATHOGEN-
ENVIRONMENTINTERACTIONS
1. For an infectious disease to develop
there must be a;
i. Susceptible host.
ii. Pathogen capable of causing disease.
iii. Favorable environment for pathogen
development.
2. Collectively, these three aspects are
known as the ‘Disease Triangle’.
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INTERACTIONS (CONT’D)

A disease caused factors by a biotic agent (pathogen). A

susceptible host, virulent pathogen and environment
conditions that favor the pathogen must be present in the
right mix to yield disease. If any of these components is
missing or minimized, disease will not occur. Abbreviation:
E, environment; P, pathogen and H, host.
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(CONT’D)

3. The interaction of components of plant

disease can be expanded to include
time and humans. Why…..?
i. Disease does not occur
instantaneously, even in situations
where a conducive environment.
Time is required for the pathogen to
infect the plant.
ii. Humans factor into the disease
triangle because the influence of
human activity on disease is
pervasive in agriculture and,
perhaps to a lesser degree (represent
special case application only).
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Host factors
1. All plants can be considered hosts.
2. Degree of genetic uniformity-crop plants-
inbred lines.
3. Age – affect disease development depending
on plant-pathogen relationship.
4. There are three levels of susceptibility, which
include;
i. Immune – cannot be infected.
ii. Susceptible – can be infected.
iii. Resistant – may or may not be infected, and is
the plant able to prevent the pathogen from
killing it. i.e. producing defense compounds.
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Pathogen factors
1. Amount of inoculum.
2. Pathogen genetics.
3. Virulence of the pathogen.
4. Type of reproduction;
i. Monocyclic.
ii. Polycyclic.
5. Ecology and mode of spread;
i. Air.
ii. Soil.
iii. Seed.
iv. Vector dependency.
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Environmental factors
1. Moisture.
2. Temperature.
3. Effect of human culture practice;
i. Monoculture.
ii. Amount of inoculum: seed quality,
disease residues, rotation, alternate
host.
iii. Introduction of new pathogens.
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The plant disease cycle

The primary disease cycle general events: 1) come in contact with a susceptible host
(attachment/inoculation), 2) gain entrance or penetrate the host through either a wound, a
natural opening (stomates, lenticels, hydrathodes) or via direct penetration of the host, 3)
establish itself within the host (produce symptom), 4) grow reproduce within or on the host
and 5) be able to spread to other susceptible plants (dissemination).
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Relation of environment to disease development

1. Two types of environment, the aerial environment and The soil
(edaphic) environment.
i. The aerial environment.
a. Moisture is particularly important to pathogenic bacteria and fungi.
– Rain splash plays an important role in the dispersal of some fungi and nearly
all bacteria.
– leaf wetness is necessary for the germination of most airborne spores.
– By using water for propagules.
b. Temperature also affects the incubation or latent period (the time
between infection and the appearance of disease symptoms), the
generation time (the time between infection and sporulation), and
the infectious period (the time during which the pathogen keeps
producing propagules).
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Relation of environment to disease development (cont’d)

c. Air pollution
− In extreme cases (high concentration of pollutants),
damage the plants directly by causing acid rain.

ii. The soil (edaphic) environment.

― Affects soil-borne diseases through;
• Moisture content available to pathogens for germination,
survival and motility
• The fertility and organic matter content of the soil can
affect the development of disease.
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Host-pathogen interactions
1. The defence barrier induced by plants are a co-ordinated
system of molecular, cellular and tissue-based responses to
pathogen attack.
2. Types of plant defenses;
i. Constitutive/passive
― The defense is always present in the plant.
ii. Inducible/active
― The defenses that are produced when a plant is injured or detects
foreign pathogen.
iii. Resistance
― Hosts prevent or slow the development and reproduction of the
majority of pathogen propagules that they come into contact with it.
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Constitutive/passive defences
− Mode of protection by physical and chemical barriers.
• Physical barriers largely involve properties of the plant
surface, that is, the cuticle, stomata, cell walls and etc.
• Chemical barriers by producing antimicrobial
compounds, such as phytoanticipins, phenols, quinones
and etc.
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Inducible/active defenses
– Plants use a vast array of signals originating from micro-
organisms and the environment to recognise pathogens and
elicit plant defence responses.
– Non-specific elicitors of biotic and abiotic origin induce host
defences in a broad range of host species. Abiotic elicitors such
as heavy metal ions or UV light , biotic elicitors include cell
wall fragments released from fungi and bacteria, hydrolytic
enzymes of plant or pathogen origin, some peptides,
glycoproteins and polyunsaturated fatty acids.
– Specific elicitors enable defence against a very specific
pathogen, and are conditioned by avirulence genes in that
pathogen.
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Inducible/active defenses (cont’d)

− Inducible/active defense mechanisms by;
• Producing toxic secondary chemical compounds.
 These compounds usually belong to one of three large
chemical classes: terpenoids, phenolics and alkaloids.
 Have negative impacts on herbivores and pathogens.
• Producing volatile organic compounds (VOCs) such as
quisqualic acid synthesized by Geraniums could
paralyses insects when they feed on the plant.
• Producing pathogen degrading enzymes.
• Deliberate cell suicide.
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Arsenal    
Defence Pre-existing structural defences Pre-existing biochemical defences
mechanism
Passive The structural characteristics that i. Inhibitors released by the plant in its
already present in plant even before the environment such as plant exudates.
pathogen comes in contact with the ii. Inhibitors present in plant cells
plant such as: before infection such as
i. Wax and cuticle that cover the phytoanticipins.
epidermal cells. iii. Defence through deficiency in
ii. Tough and thick epidermal cells. nutrients essential for pathogen.
iii. Nature of natural opening.
iv. Internal structural barriers.

Arsenal    
Defence Induced-structural defences Induced-biochemical defences
mechanism
Active Usually not present in the plants but are i. Inhibitors produced by plants in
produce in response to invading response to microorganism or to
pathogens such as: mechanical and chemical injuries
i. Cork layers formation. such as phenolics and phytoalexins.
ii. Formation of abscission layers. ii. Defence through production of
iii. Formation of tyloses. substances that inhibit effect of
iv. Deposition of gums. enzymes produced by pathogens.
iii. Defence through detoxification of
pathogen toxins.
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Resistance defenses
− The specificity of plant responses to pathogens can be classified into two
broad categories. Non-specific resistance (general, non-host or basic
resistance) is a response to all races of a particular pathogen, and occurs in
all cultivars of a host plant species. In contrast, specific resistance is
dependent upon the presence of a particular pathogen race, a particular host
plant cultivar, or both.
− Host-parasite specific resistance is determined by the interaction of between
products of pathogen avirulence genes, specific elicitors and products of host
resistance genes.
− Non-specific plant disease resistance is relying upon a foundation of passive
plant defences plus involving the activation of active defences by non-specific
elicitors of biotic origin. While specific plant disease resistance appears to be
governed by a single gene or a small number of related genes(are found in
particular subpopulations of the pathogen, plant host, or both interacting
organisms, which encode proteins capable of altering the outcome of an
otherwise compatible plant-pathogen interaction.
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− Communal resistance;
• Plant can communicate with their neighboring
plant through the production of volatile
compound such as methyle jasmonate and
methyle salicylate by activation of defense gene
in their neighboring plant.
• i.e.: Methyle jasmonate from Big sagebrush
(Artemisia tridentate) induce production of
protease inhibitor in adjacent tomato plant.
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Pathogen attack strategies

1. Three main attack strategies is deployed;
i. Necrotrophs – kill host cells and obtain their nutrient from the dead tissue.
ii. Biotrophs – obtain their nutrients from living host cells.
iii. Hemibiotrophs – the pathogen initially keeps cells alive but kills them at later
stages of infection.
 Saprophytes are parasites but different ones.  Saprophytes are living organisms
that feed on dead organic matter, unlike parasites that live on living organisms.
2. Several main factors contribute to widespread of plant pathogens;
i. Rapid and high rate of reproduction during the main growing season for plants.
ii. Efficient dispersal mechanism by wind, water or vector such as insects.
iii. Different types of reproduction (often sexual) toward the end of each plant
growing season to produce a second type of structure (spore, propagule) allowing
long-term survival.
iv. High capacity to generate genetic diversity.
v. Monoculture of crop plants versus well-adapted pathogen genotypes.
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1. Fungi
i. Less than 2% of the approximately 100,000 known fungal
species are able to colonize plants and cause disease.
ii. Necrotrophic species that produce cell wall-degrading
enzymes tend to attack a broad range of plant species.
Botrytis cinerea, the gray mold fungus,
sporulating on grapes. This necrotroph
secretes large numbers of cell wall-degrading
enzymes and thereby destroys plant tissue in
advance of the colonizing hyphae.

Plants respond to the degradation of cell wall

by mounting defense responses that include
enzymes that, in turn degrade fungal cell wall.
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iii. Some necrotrophs produce host-selective toxins that are active

in only a few plant species.
iv. Each toxin has a high-specific mode of action, inactivating just
a single plant enzyme.
v. Other fungi produce non-host-selective toxins.
The maize pathogen Cochliobus carbonum
secretes HC-toxin.
1. The fungus secretes the HC-toxin.
2. HC-toxin inhibits histone deacetylase activity;
this is believed to interfere with transcription
of maize defense genes and thus favor fungal
growth and disease development.
3. Hm1-resistant maize plants produce an HC-
toxin reductase which detoxifies the HC-toxin.
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vi. Biotrophic fungi keep host cells alive and usually exhibit a high degree of
specialization for individual plant species.
Magnaporthe grisea, agent of the rice blast disease

1 2 3 4 5

1. In nature, M. grisea conidia (also called spores) are dispersed by wind or rain and 6
deposited on the leaves of susceptible plants.
2. When the deposited conidia are in an environment with a ready supply of water (for example, a dew drop),
they germinate to produce elongated cells named germ tubes, that are the precursors to hyphae.
3. If the germ tube senses contact with an appropriate 'inductive' surface, it ceases growth and hooks itself.
4. A specialised structure, the appressorium, acquires water from the dew drop by accumulating glycerol
and other compatible solutes. Eventually, the appressorial glycerol concentration exceeds 3 M and, as a
result, extremely high turgor pressure is generated.
5. Using this high turgor pressure, the penetration plug and secondary germ tube produced by the
appressorium exert sufficient force to breach the cuticle of the plant or, in vitro, to push through inert
non-biological materials such as Teflon.
6. Once within the epidermal cells of the plant, 'infection hyphae' grow intracellularly and spread from
cell to cell, producing the characteristic lesions of rice blast.
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vii. To utilize the living plant cells as a food substrate, biotrophic

fungi, after penetration of the rigid cell wall form an haustorium,
which causes invagination of the plasma membrane.
viii. This specialised feeding structure increases the surface contact
between the two organisms, thus maximizing nutrient and water
flow to favor fungal growth.
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ix. Hemibiotrophic fungi sequentially deploy a biotrophic and then a

necrotrophic mode of nutrition.
x. the switch is usually triggered by increasing nutritional demands as
fungal biomass increases.
For example, Phytophtora infestans, which
causes late blight disease of potato, was
responsible for the devastating blight disease
epidemic in Ireland in 1846 and 1847, resulting
in the Irish famine and emigration of more
than one million people to the United States
and other countries. Today this fungus still
causes large losses in annual yields.

xi. The hemibiotrophic lifestyle of this pathogen facilitates its

progress from leaf infection to sporulation in only three days.
xii. If moist, cool conditions prevail, the entire foliage of a potato field
can be destroyed within two weeks.
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2. Bacterial pathogens of plants (phytobacteria)

i. Phytopathogenic bacteria specialize in
colonizing the apoplast (the free diffusional
space outside the plasma membrane) to cause
spots, vascular wilts, and blights.
ii. most are Gram-negative rod shaped bacteria
from the genera Pseudomonas, Xanthomonas,
and Erwinia.
iii. Two features characterize bacteria-plant
relationships;
1. during their parasitic life, most bacteria
reside within the intercellular spaces of
the various plant organs or in the xylem.
2. Second, many cause considerable plant
tissue damage by secreting either toxins,
extracellular polysaccharides (EPSs), or
cell wall-degrading enzymes at some stage
during pathogenesis.
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iv. The particular case of Agrobacterium tumefaciens.

− Ethiological agent of the “crown gall” disease,
characterized by the development of tumors on roots and
lower part of the stems (the crown).

Agrobacterium
tumefaciens as they Agrobacterium tumefaciens gall at the
begin to infect a root of Carya illinoensis.
carrot cell.
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Agrobacterium T-DNA transfer as a natural case of genetic engineering

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3. Plant viruses (phytoviruses)

i. More than 40 families of DNA and RNA plant
viruses exist, most are single-stranded (ss) positive-
sense RNA viruses.
ii. Far fewer plant viruses have DNA genomes but they
are among the most economically important, such as
Geminiviruses, with circular, single-stranded DNA
genome.

Tobacco
mosaic
virus
(TMV)
Geminivirus
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(CONT’D)

iii. Symptoms of viral infection include tissue yellowing (chlorosis) or browning

(necrosis), mosaic pattern and plant stunting.
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iv. Spreading of virus infection.

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4. Plant pathogenic nematodes

i. More than 20 genera of plant nematodes cause plant diseases.
Infections by these round worms (ca. 1 mm long) are nearly always
confined to the plant root system.
ii. Some use their amphidal
secretions to digest the
plant cell wall and
penetrate the host cell
with their stylet.

iii. Effector proteins delivered

into host cells induce cell
division and gigantism,
transforming dividing
cells into a feeding factory.
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(CONT’D)

iv. Four different life styles are found among plant

parasitic nematodes;
− Migratory ectoparasites: move throughout their life and
stay outside the plant while feeding.
− Migratory endoparasites: enter the plant and move
inside its tissues throughout their life while they feed.
− Sedentary ectoparasites: stop moving and establish a
permanent feeding site where the remain outside tissues.
− Sedentary endoparasites: establish a permanent feeding
site within plant tissues and stop moving once
established.
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5. Feeding arthropods not only damage plants directly but

also facilitate colonisation by viral, bacterial, and fungal
pathogens
i. Many of insect species feed, reproduce, and shelter on plants.
Two broad categories of herbivorous insects are recognized: a)
chewing and b) sap sucking.
The 1915 locust plague (March to October), was a
plague of locusts that stripped areas in and around
Palestine of almost all vegetation GFP-
tagged
virus

Colorado SE: phloem sieve elements

potato beetle CC: companion cells
(Leptinotarsa BSC: bundle sheath cell
MC: mesophyll cell
decemlineata)
EC: epidermal cell
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Disruption of
plant function
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(CONT’D)

Disruption of plant function

1. Disease causes changes in plant structure and function in
the ways listed below;
i. Reduced photosynthesis. The green plant manufactures its own food using
sunlight, water, and carbon dioxide. If a disease reduces the amount of light
reaching the leaf, or if part of the leaf is killed, or if the leaf falls off
prematurely, photosynthesis is inhibited. Leaf spots, powdery mildew,
anthracnose, damage due to air pollution or pesticide toxicity, and twig
blights reduce photosynthesis.
ii. Root disease. Roots, especially root tips, absorb nutrients and water while
structurally supporting the plant. Browning, blackening, and limpness of
roots are typical symptoms of root damage or root disease. Damage to roots
results in yellowing, leaf scorching, slowing of growth, wilt, and dieback of
above ground portions of the plant. Fungi, bacteria, and nematodes, as well
as excessive soil moisture, soil compaction, and excavation around the roots,
cause root diseases.
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(CONT’D)

iii. Inhibited water and nutrient transport. Water and nutrients absorbed by

roots are transported to the trunk, branches, and leaves through vascular
tissue. Water moves up the plant even to the tips of the leaves through the
xylem. The food produced by the leaves moves back to supply the root cells by
a parallel path down the plant through the phloem. If water and nutrient
transport is disrupted, leaf tips and margins burn, leaves wilt, and roots
die. Inhibition of nutrient and water transport is caused by stem rots, vascular
wilts, cankers, galls, and mechanical girdling.
iv. Destroyed food reserves. Perennial plants must have a food reserve to
overwinter and energy to resume growth in the spring. Nutrients are stored in
roots and stems. Destruction of food reserves is caused by root rots and stem
rots.
v. Root diversion. Diversion of food from plant growth to pathogen growth
occurs when galls, mildews, nematodes, rusts, and viruses develop on and in
the plant.
vi. Inhibited reproduction. Plant reproduction is inhibited in flower blights, stem
blights, and many abiotic diseases.