This is a analysis of some collected information of the subject of my M.S. theory semester. Course title was Plant Pathogenesis and Genetics of Plant Pathogens

1. AN ASSIGNMENT
ON
BIO - WARFARE DURING HOST - PATHOGEN
INTERACTIONS IN INDIGENOUS CROP PLANTS
Course No.: P.Path.- 501
Course Title: Plant Pathogenesis and
Genetics of plant pathogens
SUBMITED TO SUBMITED BY
Dr. A. Q. M. Bazlur Rashid Md. Kamaruzzaman
Professor ID No. 11 Ag.P.Path. JJ 07 M
Department of Plant Pathology Reg. No. 33141
Department of Plant Pathology
Bangladesh Agricultural Bangladesh Agricultural University
University Mymensingh
Mymensingh Ph.- +8801722449614
DEPARTMENT OF PLANT PATHOLOGY
BANGLADESH AGRICULTURAL UNIVERSITY
MYMENSINGH

2. Abstract
Plants represent a rich source of nutrients for many organisms including bacteria, fungi,
protists, insects, and vertebrates. Although lacking an immune system comparable to
animals, plants have developed a stunning array of structural, chemical, and protein-based
defenses designed to detect invading organisms and stop them before they are able to
cause extensive damage. Humans depend almost exclusively on plants for food, and
plants provide many important non-food products including wood, dyes, textiles,
medicines, cosmetics, soaps, rubber, plastics, inks, and industrial chemicals.
Understanding how plants defend themselves from pathogens and herbivores is essential
in order to protect our food supply and develop highly disease-resistant plant species.
Plant diseases caused by fungi and oomycetes result in significant economic losses every
year. Although phylogenetically distant, the infection processes by these organisms share
many common features. These include dispersal of an infectious particle, host adhesion,
recognition, penetration, invasive growth, and lesion development. Bacteria pathogenic
for plants are responsible for devastating losses in agriculture. The use of antibiotics to
control such infections is restricted in many countries due to worries over the evolution
and transmission of antibiotic resistance. The advent of genome sequencing has enabled a
better understanding, at the molecular level, of the strategies and mechanisms of
pathogenesis, evolution of resistance to plant defence mechanisms, and the conversion of
non-pathogenic into pathogenic bacteria.
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3. Introduction:
A pathogen is a microorganism that is able to cause disease in a plant, animal or insect.
Pathogenicity is the ability to produce disease in a host organism. Microbes express their
pathogenicity by means of their virulence, a term which refers to the degree of
pathogenicity. Hence, the determinants of virulence of a pathogen are any of its genetic or
biochemical or structural features that enable it to produce disease in a host.
The relationship between a host and a pathogen is dynamic, since each modifies the
activities and functions of the other. The outcome of such a relationship depends on the
virulence of the pathogen and the relative degree of resistance or susceptibility of the
host, due mainly to the effectiveness of the host defense mechanisms.
Plant-interacting micro-organisms can establish either mutualistic or pathogenic
associations. Although the outcome is completely different, common molecular
mechanisms that mediate communication between the interacting partners seem to be
involved. Specifically, nitrogen-fixing bacterial symbiosis of legume plants, collectively
termed rhizobia, and phytopathogenic bacteria have adopted similar strategies and genetic
traits to colonize, invade and establish a chronic infection in the plant host. Quorum-
sensing signals and identical two-component regulatory systems are used by these
bacteria to coordinate, in a cell density-dependent manner or in response to changing
environmental conditions, the expression of important factors for host colonization and
infection. The success of invasion and survival within the host also requires that rhizobia
and pathogens suppress and/or overcome plant defense responses triggered after
microbial recognition, a process in which surface polysaccharides, antioxidant systems,
ethylene biosynthesis inhibitors and virulence genes are involved.
In view of the above facts, the present study was undertaken to achieve the following
objectives –
1. To know about host- pathogen interaction.
2. To get knowledge about bio-warfare and penetration mechanisms.
3. To know about various weapons of fungi, bacteria, viruses and nematodes.
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4. Plant pathogens:
Plant pathology (also phytopathology) is the scientific study of plant diseases caused by
pathogens (infectious diseases) and environmental conditions (physiological factors).
Organisms that cause infectious disease include fungi, oomycetes, bacteria, viruses,
viroids, virus-like organisms, phytoplasmas, protozoa, nematodes and parasitic plants.
Not included are ectoparasites like insects, mites, vertebrate or other pests that affect
plant health by consumption of plant tissues. Plant pathology also involves the study of
pathogen identification, disease etiology, disease cycles, economic impact, plant disease
epidemiology, plant disease resistance, how plant diseases affect humans and animals,
pathosystem genetics, and management of plant diseases. On the other hand, plant
pathogen is an organism that causes a disease on a plant. Although relatives of some plant
pathogens are human or animal pathogens, most plant pathogens only harm plants. Some
plant pathogens make immuno-depressed people also sick. Organisms that cause plant
diseases reduce our ability to produce food and support the economy. All plants from
citrus to grains to ornamental plants are susceptible to plant diseases. Plant diseases cause
billions of dollars’ worth of direct and indirect losses every year (Citrus greening
example). Emerging plant pathogens require preparation and planned, scientifically-based
response to lessen the impact on our farmers and the economy. Management of plant
diseases includes management of overall plant health. Healthy plants are less likely to get
diseases, just like healthy humans. You can help reduce the impact of both emerging and
endemic plant pathogens by remembering not to transport unhealthy plant parts or
products. An endemic pathogen is one that has become established in a new environment
and can no longer be eradicated. At that point, response switches from keeping it out or
eradicating it to managing it through plant health, antimicrobial chemistries and
monitoring production. The major pathogen of plant are as follows-
Fungi:
The majority of phytopathogenic fungi belong to the Ascomycetes and the
Basidiomycetes. The fungi reproduce both sexually and asexually via the production of
spores and other structures. Spores may be spread long distances by air or water, or they
may be soil borne. Many soil inhabiting fungi are capable of living saprotrophically,
carrying out the part of their lifecycle in the soil. These are known as facultative
saprotrophs. Fungal diseases may be controlled through the use of fungicides and other
agriculture practices, however new races of fungi often evolve that are resistant to various
fungicides. A successful infection requires the establishment of a parasitic relationship
between the pathogen and the host, once the host has gained entry to the plant. There are
two broad categories of pathogens –
 Biotrophs:
Those that establish an infection in living tissue. Biotrophs are less dangerous than
necrotrophs.
 Necrotrophs:
Those that kill cells before colonising them, by secreting toxins that diffuse ahead of the
advancing pathogen.
3

5. These two kinds of pathogens are also sometimes known as 'sneaks' and 'thugs', because
of the tactics they use to acquire nutrients from their hosts.
Fig. Powdery mildew (Biotrophic) & Rice blast (necrotrophic)
fungus
 Hemibiotrophic:
Hemibiotrophic begin frist biotrophic phase, then necrotrophic, intermediate host
range e.g., Phytophthora (potato blight disease)
Bacteria:
Bacteria are microscopic, single-celled prokaryotic organisms, without a defined
nucleus, that reproduce asexually by binary fission (one cell splitting into two). They
occur singly or in colonies of cells. Bacteria are classified into two main groups based on
cell wall structure, which can be determined by a simple staining procedure called the
Gram stain. Gram negative bacteria stain red or pink and Gram positive bacteria stain
purple. The difference in color is directly related to the chemical composition and
structure of their cell walls. The cells can be rod-shaped, spherical, spiral-shaped, or
filamentous. Only a few of the latter are known to cause diseases in plants. Most bacteria
are motile and have whip-like flagella that propel them through films of water.. Most
plant pathogenic bacteria are rod shaped (bacilli).
Fig. Crown gall disease caused by Agrobacterium Fig. Infected stem
4

6. Viruses:
Plant viruses are pathogens which are composed mainly of a nucleic acid (genome)
normally surrounded by a protein shell (coat); they replicate only in compatible cells,
usually with the induction of symptoms in the affected plant. Viroids are among the
smallest infections agents known. Their circular, single-stranded ribonucleic acid (RNA)
molecule is less than one-tenth the size of the smallest viruses. There are many types of
plant virus, and some are even asymptomatic. Normally plant viruses only cause a loss of
crop yield. Therefore it is not economically viable to try to control them, the exception
being when they infect perennial species, such as fruit trees.Most plant viruses have
small, single stranded RNA genomesPlant viruses must be transmitted from plant to plant
by a vector. This is often by an insect (for example, aphids), but some fungi, nematodes
and protozoa have been shown to be viral vectors.
Fig. Tobacco mosaic virus
Nematodes:
Nematodes are small, multicellular wormlike creatures. Many live freely in the soil, but
there are some species which parasitize plant roots. They are a problem in tropical and
subtropical regions of the world, where they may infect crops. Potato cyst nematodes
(Globodera pallida and G. rostochiensis) are widely distributed in Europe and North and
South America and cause $300 million worth of damage in Europe every year. Root knot
nematodes have quite a large host range, whereas cyst nematodes tend to only be able to
infect a few species. Nematodes are able to cause radical changes in root cells in order to
facilitate their lifestyle.
5

7. Protozoa:
There are a few examples of plant diseases caused by protozoa. They are transmitted as
zoospores which are very durable, and may be able to survive in a resting state in the soil
for many years. They have also been shown to transmit plant viruses. When the motile
zoospores come into contact with a root hair they produce a plasmodium and invade the
roots.
Fig. Leishmania donovani, (a species of protozoa) in a bone marrow cell
Parasitic plants:
Parasitic plants such as mistletoe and dodder are included in the study of phytopathology.
Dodder, for example, is used as a conduit for the transmission of viruses or virus-like
agents from a host plant to either a plant that is not typically a host or for an agent that is
not graft-transmissible.
Fig. Cuscuta europaea on Sambucus ebulus
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8. Economic significance:
Plant diseases caused by fungi and oomycetes result in significant economic losses every
year. Although phylogenetically distant, the infection processes by these organisms share
many common features. These include dispersal of an infectious particle, host adhesion,
recognition, penetration, invasive growth, and lesion development. Diseases are important
to humans because they cause damage to plants and plant products, commonly with an
associated economic effect, either positive or negative. Negative economic effects include
–
 Germination failure: Basic and primary loss of crop production due to seed
borne pathogen. In diseased seed, pathogen kills the sprouting plumule in the
seed. When farmer sow the seed under favorable condition, it germinates within
24 hours. On the same time pathogen germinate rather than more quickly. This
pathogenic inoculum inhibit the germination ability of the seedlings.
 Seedling diseases: In case of infected seed, when it germinate some seedlings are
found healthy. But after some days this seedlings are infected by diseases.
Infected seeds encourage different pathogen to make diseases. This is the major
reason for destruction of seedlings but sometimes this infection symptom does not
appeared immediately in case of seed borne diseases.
 Adult plant infection: Adult plant are infected by the seed borne pathogen and
almost all times yields are drastically reduced. In rice some pathogens like
Pyricularia, Drechslera, Xanthomonas etc. which causes serious yield loss in other
rice grown areas are common in Bangladesh and assumed to cause severe damage
to the crop here also. Ahmed (1968) reported that stem rot alone damages 5 lakh
bales of jute fibers. The value of five lakh bales of jute is TK. 800 million
approximately at present world market.
 crop failure: Diseases are responsible for the destruction of crop losses, in this
why this is very important to know about all of the responsible causes responsible
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9. for diseases. Ultimate goal of all kinds of diseases are lowering of diseases and we
should try to control the pathogenicity of the pathogens.
 Incremental loss from lower quality or failure to meet market standards:
Diseases infestation results in contamination and loss of quantity in the crops; the
quality losses may be due to relation in nutritional value. Or in marketability
(lowering of grade). Loss is easily overlooked; this is the type of damage done to
stored grain. A more common loss of quantity is the effect of diseases on the
appearance of the crop, for example skeletonized or discolored vegetables or
other crops have a lower market value than intact ones.
Plant diseases are also responsible for the creation of new industries to develop control
methods. Newly developed pesticide, fungicide, bio control agent helps to provide
employment opportunity.
Description of various weapons of fungi, bacteria, viruses and nematodes used in the
bio-warfare:
Biological warfare (BW) also known as germ warfare are bacteria, viruses, fungi, or
biological toxins, used to kill or incapacitate humans, animals or plants as an act of war.
Biological weapons (often termed "bio-weapons" or "bio-agents") are living organisms or
replicating entities (viruses) that reproduce or replicate within their host victims.
Entomological (insect) warfare is also considered a type of BW. Here , the objectives of
pathogen to develop diseases at any cost and plant trying to kill / stop pathogenic
organisms.
Biological weapons may be employed in various ways to gain a strategic or tactical
advantage over an adversary, either by threat or by actual deployment. Like some of the
chemical weapons, biological weapons may also be useful as area denial weapons. These
agents may be lethal or non-lethal, and may be targeted against a single individual, a
group of people, or even an entire population. They may be developed, acquired,
stockpiled or deployed by nation states or by non-national groups
Fig. Logo of bio warfare
Description of various weapons:
Modified hypha:
Hyphae may be modified in many different ways to serve specific functions. Some
parasitic fungi form haustoria that function in absorption within the host cells. The
8

10. arbuscules of mutualistic mycorrhizal fungi serve a similar function in nutrient exchange,
so are important in assisting nutrient and water absorption by plants. Hyphae are found
enveloping the gonidia in lichens, making up a large part of their structure. In nematode-
trapping fungi, hyphae may be modified into trapping structures such as constricting rings
and adhesive nets. Mycelial cords can be formed to transfer nutrients over larger
distances.
Fig. Modified hypha penetrating host cell
Haustoria:
A specialized absorbing structure of a parasitic plant, such as the rootlike outgrowth of
the dodder, that obtains food from a host plant. In parasitic fungi, haustoria are
specialized hyphae that penetrate the cells of other organisms and absorb nutrients
directly from them. Fungi in all major divisions form haustoria. Haustoria take several
forms. Generally, on penetration, the fungus increases the surface area in contact with
host plasma membrane releasing enzymes that break down the cell wall, enabling greater
potential movement of organic carbon from host to fungus. Thus, an insect host a
parasitic fungus such as Cordyceps may look as though it is being "eaten from the inside
out" as the haustoria expand inside of it.
Fig. Haustoria with conidium
Appressorium:
9

11. An appressorium is a flattened, hyphal "pressing" organ, from which a minute infection
peg grows and enters the host, using turgor pressure capable of punching through even
Mylar. Fungi that exhibit appressorial formation include the necrotroph Pyrenophora
teres.
Appressorium are the tube which enters the host, puts out branches between the cells of
the host, and forms a mycelial network within the invaded tissue. The germ tubes of some
fungi produce special pressing organs called appressoria, from which a microscopic,
needlelike peg presses against and punctures the epidermis of the host; after penetration, a
mycelium develops in the usual manner. Many parasitic fungi absorb nutrient through
appressoria from host body.
Fig. Appressoria
Capsules:
The cell capsule is a very large structure of some prokaryotic cells, such as bacterial cells.
It is a layer that lies outside the cell wall of bacteria. It is a well-organized layer, not
easily washed off, and it can be the cause of various diseases. .some bacteria form an
organized glycocalyx called a capsule around their cell walls which increases the
virulence of the species. The capsule helps resist host defenses by interfering with
phagocytosis. If the human body produces antibodies against the capsule, this can allow
destruction of the bacteria by
phagocytosis.
Fig. Bacteria with capsule
10

12. Stylet:
The stylet or stomatostyle, is the primitive mouth-parts of some nematodes and some
nemerteans. It actually presents as a hardened protrusible opening to the stomach.
The stylet is adapted for the piercing of cell walls, providing the operative organism with
access to the nutrients contained within the prey cell. All plant-parasitic nematodes have a
stylet or mouth-spear that is similar in structure and function to a hypodermic needle. The
nematode uses the stylet to puncture plant cells, and then inject digestive juices and ingest
plant fluids through it. All of the plant-parasitic nematodes that are important turfgrass
pests feed on roots.
Fig. stylet of nematode
Toxins:
Pathogens often benefit by producing toxins, which kill the tissue in advance of
enzymatic degradation. In many pathogens, particularly non-obligate pathogens, toxins
cause the majority of damage to the host
Enzymes
Some of the pathogen Produce enzymes that break down key structural components of
plant cells and their walls by soft-rotting bacteria that degrade the pectin ayer that holds
plant cells together.
Mechanism of penetration & host tissue disintegration:
Successful infection of a host plant by a pathogen involves the movement of the pathogen
toward the host, attachment of the pathogen to the plant surface, penetration of the host
by the pathogen, and the proliferation of the pathogen inside the host immediately
following entrance.
Microorganisms have various strategies to establish an infection in a host. Some micro-
organisms recognize molecules on the surface of the host cell, and use these as receptors.
The binding of bacteria or viruses to receptors brings the microorganism in close contact
with the host surface.
11

13. Fig. The mode of penetration by pathogenic organisms
Fungi:
Penetration of a host by an invading fungus gives rise to the potential establishment of
physiological contact between the two organisms. A fungus will usually use a
combination of methods to gain access to host tissue.
Physical mechanisms
Natural Openings: Plants have several types of natural openings utilized by fungi. The
most common are stomates. Some fungi sense the location of openings by chemical or
thigmatropic (touch) stimuli. Other natural openings include lenticels (open pores on
woody stems).
Fig. open stomata
2. Wounds: Damage to a plant surface may result from animal and insect activities,
environmental causes (e.g. hail), and mechanical injury (tree falling against stem,
pruning). These sites provide ideal penetration sites for some types of fungi.
3. Direct Penetration: After contact between a germ tube and the plant surface, the direct
penetration of plant cells requires a combination of mechanical force and enzymatic
12

14. softening of the cuticle. Mechanical force is often achieved by a bulbous appressorium
and penetration peg.
Fig. Direct penetration through penetration peg
Chemical Mechanisms
Enzymatic penetration of cell walls:
During germination and penetration, fungi generally secrete a mixture of hydrolytic
enzymes including cutinases, cellulases, pectinases, and proteases. Although these
enzymes are also required by saprophytes, their structures and biosynthetic regulation
may be adaptated to the specific needs of pathogens. For instance, different cutinase
isozymes are expressed during saprophytic and parasitic stages of Alternaria brassicicola.
Many fungal genes encoding various hydrolytic enzymes have been cloned. Usually,
however, the infection phenotype of gene disruption/replacement mutants does not differ
from wild-type. In particular, enzymatic degradation of cutin, the structural polymer of
the plant cuticle, has been postulated to be crucial for fungal pathogenicity and cutinase to
be a key player in the penetration process.
Bacteria
Bacteria are one of the many harmful germs throughout the body and in the environment.
Germs and bacteria are almost everywhere in the world. Bacteria gets into the body when
there is an open wound or an open patch of skin. When a knee is scraped and a person has
an open wound, it gives bacteria a chance to come directly into the body.
Methods by which bacteria cause disease-
Adhesion: Many bacteria must first bind to host cell surfaces. Many bacterial and host
molecules that are involved in the adhesion of bacteria to host cells have been identified.
Often, the host cell receptors for bacteria are essential proteins for other functions.
Colonization: Some virulent bacteria produce special proteins that allow them to
colonize parts of the host body. Helicobacter pylori is able to survive in the acidic
environment of the human stomach by producing the enzyme urease. Colonization of the
stomach lining by this bacterium can lead to Gastric ulcer and cancer. The virulence of
various strains of Helicobacter pylori tends to correlate with the level of production of
urease.
13

15. Invasion: Some virulent bacteria produce proteins that either disrupt host cell
membranes or stimulate endocytosis into host cells. These virulence factors allow the
bacteria to enter host cells and facilitate entry into the body across epithelial tissue layers
at the body surface.
Immune response inhibitors: Many bacteria produce virulence factors that inhibit the
host's immune system defenses. For example, a common bacterial strategy is to produce
proteins that bind host antibodies. The polysaccharide capsule of Streptococcus
pneumoniae inhibits phagocytosis of the bacterium by host immune cells.
Toxins: Many virulence factors are proteins made by bacteria that poison host cells
and cause tissue damage. For example, there are many food poisoning toxins produced by
bacteria that can contaminate human foods. Some of these can remain in "spoiled" food
even after cooking and cause illness when the contaminated food is consumed. Some
bacterial toxins are chemically altered and inactivated by the heat of cooking.
Most bacterial pathogen damage host cell by in four main ways:
1. By using host's nutrients (mainly iron)
2. By causing direct damage in the immediate area of the invasion
3. By producing toxins that may be transported by blood and lymph to
damage sites far from the original invasion
4. By causing the host to react with a hypersensitivity reaction
Viruses
Viruses require living cells for their replication. Some viruses, such as tobacco mosaic
virus (TMV) and cucumber mosaic virus, are found in many plant species.
The replication of a plant virus appears to proceed according to the following general
scheme: introduction of the virus to a plant through a wound, release of the nucleic acid
from the protein coat, association of viral RNA (or messenger RNA of DNA viruses) with
cellular ribosomes for its translation to the proteins required for virus synthesis,
replication of the nucleic acid and production of coat protein, and assembly of the nucleic
acid and coat protein to form complete virus particles.
Initially, most plant viruses multiply at the site of infection, giving rise to localized
symptoms such as necrotic spots on the leaves. Subsequently, the virus may be distributed
to all parts of the plant either by direct cell-to-cell spread or by the vascular system,
resulting in a systemic infection involving the whole plant. However, the problem these
viruses face in reinfection and recruitment of new cells is the same as they face initially -
how to cross the barrier of the plant cell wall. Plant cell walls necessarily contain
channels called plasmodesmata which allow plant cells to communicate with each other
and to pass metabolites between them.
Fig. Virus replication
14

16. The replication of viroids is not clearly understood at present. Cell-to-cell spread of
viruses usually occurs, and eventually the virus spreads throughout the plant. In some
plants, the cells surrounding the initially infected cells die, and the virus usually does not
spread further.
Nematodes
Plant-parasitic nematodes have evolved diverse parasitic relationships with their host
plants to obtain nutrients that are necessary to support their development and
reproduction. There are different types of plant-parasitic nematodes with characteristic
patterns of plant infestation:
 Ectoparasites feed on the outside of plant roots causing severe moisture stress and
a dramatic reduction in yield, e.g. sting, awl and stubby-root nematodes.
Fig. Ectoparasitic nematode feed outside the host
 Endoparasites enter the plant roots and root hairs resulting in malformation and
yield reduction, e.g. reniform, cyst and root-knot nematodes
Fig. Endoparasitic nematode feed inside the host
Endoparasitic nematode species must penetrate host tissues directly, using
mechanical and/or biochemical methods. Secreted proteases from parasitic
nematodes appear to aid in the penetration and migration through animal tissues. For
plant-parasitic nematodes, a cell wall composed primarily of cellulose poses a
15

17. formidable barrier to penetration. Thrusts of the nematode stylet combined with
esophageal gland secretions mediate penetration and migration through plant
tissues. Plant-parasitic nematodes possess an arsenal of hydrolytic enzymes for
digesting cell wall polymers. Genes encoding secreted cell-wall-modifying enzymes
have been localized to nematode esophageal gland cells including enzymes that
degrade the pectic polysaccharides (pectate lyases and polygalacturonases)
comprising the middle lamella between plant cells and enzymes that degrade the
cellulose (endoglucanases) and hemicellulose (xylanase) structural components of
the cell wall Interestingly, the cell-wall-modifying enzymes appear to be
active only in the subventral gland cells and, in the case of the cyst nematode
endoglucanases, they are only active during nemat ode migration within roots,
whereas plant endoglucanases upregulated in feeding sites probably modify
the walls comprising these specialized cells which named gall.
Disease development:
Pathogenicity is the ability of an organism to enter a host and cause disease. The degree
of pathogenicity, that is, the comparative ability to cause disease, is known as virulence.
The terms pathogenic and nonpathogenic refer to the relative virulence of the organism or
its ability to cause disease under certain conditions. This ability depends not only upon
the properties of the organism but also upon the ability of the host to defend itself (its
immunity) and prevent injury. The concept of pathogenicity and virulence has no
meaning without reference to a specific host.
While necrotrophs have little effect on plant physiology, since they kill host cells before
colonising them, biotrophic pathogens become incorporated into and subtly modify
various aspects of host physiology, such as respiration, photosynthesis, translocation,
transpiration and growth and development. The respiration rate of plants invariably
increases following infection by fungi, bacteria or viruses. The higher rate of glucose
catabolism causes a measurable increase in the temperature of infected leaves. An early
step in the plant's response to infection is an oxidative burst, which is manifested as a
rapid increase in oxygen consumption, and the release of reactive oxygen species, such as
hydrogen peroxide (H2O2) and the superoxide anion (O2-). The oxidative burst is involved
in a range of disease resistance and wound repair mechanisms Link to Rapid Active
Defense. In resistant plants, the increase in respiration and glucose catabolism is used to
produce defence-related metabolites via the pentose phosphate pathway. In susceptible
plants, the extra energy produced is used by the growing pathogen.
Pathogens also affect photosynthesis, both directly and indirectly. Pathogens that cause
defoliation rob the plant of photosynthetic tissue, while necrotrophs decrease the
photosynthetic rate by damaging chloroplasts and killing cells. Biotrophs affect
photosynthesis in varying degrees, depending on the severity of the infection. A
biotrophic infection site becomes a strong metabolic sink, changing the pattern of nutrient
translocation within the plant, and causing net influx of nutrients into infected leaves to
satisfy the demands of the pathogen. The depletion, diversion and retention of
photosynthetic products by the pathogen stunts plant growth, and further reduced the
plant's photosynthetic efficiency. In addition, pathogens affect water relations in the
plants they infect. Biotrophs have little effect on transpiration rate until sporulation
ruptures the cuticle, at which point the plant wilts rapidly. Pathogens that infect the roots
16

18. directly affect the plant's ability to absorb water by killing the root system, thus producing
secondary symptoms such as wilting and defoliation. Pathogens of the vascular system
similarly affect water movement by blocking xylem vessels. Growth and development in
general are affected by pathogen infection, as a result of the changes in source-sink
patterns in the plant. Many pathogens disturb the hormone balance in plants by either
releasing plant hormones themselves, or by triggering an increase or a decrease in
synthesis or degradation of hormones in the plant. This can cause a variety of symptoms,
such as the formation of adventitious roots, gall development, and epinasty (the down-
turning of petioles).
Factors that affect disease development
Pathogen Host Environment
 Presence of pathogen  Susceptibility  Temperature
 Pathogenicity  Growth stage & form  Rainfall / Dew
 Adaptability  Population density &  Leaf wetness period
structure
 Dispersal efficiency  Soil properties
 General health
 Survival efficiency  Wind
 Reproductive fitness  Fire history
 Air pollution
 Herbicide damage
Overall diseases development process includes major steps. They are as follows-
 Enzymatic degradation:
In their most basic form, pathogens secrete enzymes, which catalyze the breakdown of
host tissues, similar to the digestion of food in mammals.
 Toxins:
Pathogens often benefit by producing toxins, which kill the tissue in advance of
enzymatic degradation. In many pathogens, particularly non-obligate pathogens, toxins
cause the majority of damage to the host.
 Growth regulators:
Pathogens often find it advantageous to produce growth regulators (or cause the host to
produce them). The most common are those that cause translocation of nutrients to host
17

19. cells and/or cause host cells to enlarge or divide in the vicinity of the pathogen, thus
providing an increase in food for the pathogen. Obligate pathogens are very good at this
technique because it allows the host to go on living, but still provides extra food for the
pathogen.
 Genetic manipulations:
All viruses plus a few bacteria are able to force the plant to produce pathogen gene
products from pathogen genetic material. This starves plant cells and disrupts their
function.
18

20. Conclusion:
Most of the pathogens can only cause disease on a relatively small group of host plants
because of the slightly different set of specialized genes and molecular mechanisms
required for each host-pathogen interaction. On the other hand, against pathogenicity,
plant show resistance. The cell wall is a major line of defense against fungal and bacterial
pathogens. It provides an excellent structural barrier that also incorporates a wide variety
of chemical defenses that can be rapidly activated when the cell detects the presence of
potential pathogens. All plant cells have a primary cell wall, which provides structural
support and is essential for turgor pressure, and many also form a secondary cell wall that
develops inside of the primary cell wall after the cell stops growing.
Many cell walls also contain lignin, a heterogeneous polymer composed of phenolic
compounds that gives the cell rigidity. Lignin is the primary component of wood, and cell
walls that become “lignified” are highly impermeable to pathogens and difficult for small
insects to chew. Cutin, suberin, and waxes are fatty substances that may be deposited in
either primary or secondary cell walls (or both) and outer protective tissues of the plant
body, including bark. So that biological warfare conduct in indigenous crop plant with
respective wapons. Growth and development in general are affected by pathogen
infection, as a result of the changes in source-sink patterns in the plant. Many pathogens
disturb the hormone balance in plants by either releasing plant hormones themselves, or
by triggering an increase or a decrease in synthesis or degradation of hormones in the
plant. This can cause a variety of symptoms, such as the formation of adventitious roots
and gall development.
Minimizing plant disease requires understanding the mechanisms of survival and spread.
A competitive exclusion mechanism by beneficial organism can be effective in protection
against disease. (Biological Control of Plant Pathogens).
19

21. References:
American Phytopathological Society. 2003. Microbial genomic sequencing. Perspectives
of the American Phytopathological Society (revised 2003). 21 pp.
Anderson RV, Byers JR (1975) Ultrastructure of the esophageal procorpus in the plant
parasitic nematode, Tylenchorhynchus dubius, and functional aspects in relation
to feeding. Can. J. Zool. 53:1581-1595.
Arnold, D.L., Pitman, A., and Jackson, R.W. 2003. Pathogenicity and other genomic
islands in plant pathogenic bacteria. Mol. Plant Pathol. 4:407-420.
Atkinson HJ, Harris PD (1989) Changes in nematode antigens recognized by monoclonal
antibodies during early infections of soya beans with the cyst nematode
Heterodera glycines. Parasitology 98:479-487.
Baum TJ, Hiatt A, Parrott WA, Pratt LH, Hussey RS (1996) Expression in tobacco of a
functional monoclonal antibody specific to stylet secretions of the root-knot
nematode. Mol. Plant-Microbe Interac. 9: 382-387.
Bird AF (1971) Specialized adaptation of nematodes to parasitism. In: Zuckerman BM,
Mai WF, Rohde RA (eds), Plant Parasitic Nematodes Vol. II, pp.35-49. Academic
Press, New York, USA.
Bird AF (1983) Changes in the dimensions of the esophageal glands in root-knot
nematodes during the onset of parasitism. Int. J. Parasitol. 13:343-348.
Bird DMcK (1996) Manipulation of host gene expression by root-knot nematodes. J.
Parasitol. 82:881-888.
Burgess TL, Kelly RB (1987) Constitutive and regulated secretion of proteins. Annu.
Rev. Cell Biol. 3:243-293.
Cao, H., Baldini, R.L. and Rahme, L.G. 2001. Common mechanisms for pathogens of
plants and animals. Annu. Rev. Phytopathol. 39:259-284.
Fire A, Xu S, Montgomery MK, Kostas SA, Driver SE, Mello CC (1998) Potent and
specific genetic interference by double-stranded RNA in Caenorhabditis elegans.
Nature 391:806-811.
Gao B, Allen R, Maier T, Davis EL, Baum TJ, Hussey RS (2001a) Identification of
putative parasitism genes expressed in the esophageal gland cells of the soybean
cyst nematode, Heterodera glycines. Mol. Plant-Microbe Interac. 14:1247-1254.
Glidewell DC, Mims CW. Ultrastructure of the haustorial apparatus in the rust fungus
Kunkelia nitens. Botanical Gazette. 1979;140:148–152. doi: 10.1086/337071.
20

22. Hussey RS, Davis EL, Ray C (1994) Meloidogyne stylet secretions. In: Lamberti F, De
Giorgi C, Bird D Mck (eds), Advances in Molecular Plant Nematology. pp.233-
249. Plenum Press, New York.
Hussey RS, Mims CW (1991) Ultrastructure of feeding tubes formed in giant-cells
induced in plants by the root-knot nematode Meloidogyne incognita. Protoplasma
162:99-107.
Hussey RS, Paguio OR, Seabury F (1990) Localization and purification of a secretory
protein from the esophageal glands of Meloidogyne incognita with monoclonal
antibodies. Phytopathology 80:709-714.
Jaubert S, Laffaire JB, Abad P, Rosso M-N (2002) A polygalacturonase of animal origin
isolated from the root-knot nematode Meloidogyne incognita. FEBS Letters
522:109-112.
Klement, Z., Farkas, G. L. and Lovrekovich, L. 1964. Hypersensitive reaction induced by
phytopathogenic bacteria in the tobacco leaf. Phytopathology 54:474-477.
Lambert KN, Allen KD, Sussex IM (1999) Cloning and characterization of an
esophageal-gland-specific chorismate mutase from the phytoparasitic nematode
Meloidogyne javanica. Mol. Plant-Microbe Interac. 12:328-336.
Lindow, Steven E. 1987. Competitive exclusion of epiphytic bacteria by ice-
Pseudomonas syringae mutants. Appl. Environ. Microbiol. 53:2520-2527.
Mazarei M, Ying Z, Houtz RL (1998) Functional analysis of the rubisco large subunit N-
methyltransferase promoter from tobacco and its regulation by light in soybean
hairy roots. Plant Cell Rep. 17:907-912.
Mitchell HJ, Hardham AR. Characterisation of the water expulsion vacuole in
Phytophthora nicotianae zoospores. Protoplasma. 1999;206:118–130. doi:
10.1007/BF01279258.
Money NP. Why oomycetes have not stopped being fungi. Mycology Research.
1998;102:767–768. doi: 10.1017/S095375629700556X.
Nakai K, Horton P (1999) PSORT: a program for detecting sorting signals in proteins and
predicting their subcellular localization. Trends Biochem. Sci. 24:34-35.Nielsen
H, Engelbrecht J, Brunak S, von Heijne G (1997) Identification of prokaryotic and
eukaryotic signal peptides and prediction of their cleavage sites. Protein Eng.10:1-
6.
Ophel, K.M., Bird, A.F. and Kerr, A. 1993. Association of bacteriophage particles with
toxin production by Clavibacter toxicus, the causal agent of annual ryegrass
toxicity. Phytopathology 83: 676-681.
21

23. Park G, Xue C, Zheng L, Lam S, Xu J-R. MST12 regulates infectious growth but not
appressorium formation in the rice blast fungus Magnaporthe grisea. Mol Plant-
Micro Interact. 2002;15:183–192. doi: 10.1094/MPMI.2002.15.3.183.
Ponciano, G., Ishihara, H., Tsuyumu, S. and Leach, J.E. 2003. Bacterial effectors in plant
disease and defense: keys to durable resistance? Plant Dis. 87:1271-1282.
Popeijus H, Blok V, Cardle L, Bakker E , Phillips MS , Helder J, Smant G , Jones J
(2000a) Analysis of genes expressed in second stage juveniles of the potato cyst
nematodes Globodera rostochiensis and G. pallida using the expressed sequence
tag approach. Nematology 2:567-574.
Popeijus HE, Overmars H, Jones J, Blok V, Goverse A, Helder J, Schots A , Bakker J,
Smant G (2000b). Degradation of plant cell walls by nematodes. Nature 406:36-
37.
Rosso M-N, Piotte C, Favery B, Arthaud L, Hussey RS, de Boer JM, Baum TJ, Abad P
(1999) Isolation of a cDNA encoding a b-1,4-endoglucanase in the root-knot
nematode Meloidogyne incognita during plant parasitism. Mol. Plant-Microbe
Interac. 12:585-591.
Schaad, N. W., Jones, J. B. and Chun, W. (ed.). 2001. Laboratory guide for identification
of plant pathogenic bacteria. 3rd ed. American Phytopathological Society Press.
St. Paul, MN.
Trail F. Fungal cannons: explosive spore discharge in the Ascomycota. FEMS Microbiol
Lett. 2007;276:12–18. doi: 10.1111/j.1574-6968.2007.00900.x.
Urwin PE, Lilley CJ, Atkinson HJ (2002) Ingestion of double-stranded RNA by
preparasitic juvenile cyst nematodes leads to RNA interference. Mol. Plant-
Microbe Interact. 15:747-752.
Vidhyasekaran, P. 2002. Bacterial disease resistance in plants. Molecular biology and
biotechnological applications. 452 pp. The Haworth Press, Binghamton, NY.
Walker SK, Chitcholtan K, Yu YP, Christenhusz GM, Garrill A. Invasive hyphal growth:
An F-actin depleted zone is associated with invasive hyphae of the oomycetes
Achlya bisexualis and Phytophthora cinnamomi. Fungal Genetics and Biology.
2006;43:357–365. doi: 10.1016/j.fgb.2006.01.004.
Williamson VM, Hussey RS (1996) Nematode pathogenesis and resistance in plants.
Plant Cell 8:1735-1745.
Young, J.M., Saddler, G.S., Takikawa, Y., DeBoer, S.H., Vauterin, L., Gardan, L.,
Gvozdyak, R. I. and Stead, D.E. 1996. Names of plant pathogenic bacteria 1864-
1995. Rev. Plant Pathol. 75:721-763.
22

24. Zhao X, Kim Y, Park G, Xu J-R. A mitogen-activated protein kinase cascade regulating
infection-related morphogenesis in Magnaporthe grisea. The Plant Cell.
2005;17:1317–1329.
23