Microbial Disease In Plants

• Negative Interactions can occur in the form of a parasite, virus, fungi or bacteria
entering the plant and causing infection within the plant entering through
different tissues especially openings such as the stomata.
• Many pathogens are of ecological and economical importance.
• Disease of plants cause malfunction that results in reduce capabilities of the
plant to survive in its habitat.
• Sometimes may cause impairment in growth or death of plants.
• Microbial disease may even cause famine.
• 1845 potato blight in Ireland, caused mass starvation and emigration from
Ireland to North America.
• Chestnut an important cash crop of North America destroyed the economy due
to chestnut blight.
• In 1970, leaf blight of maize caused destruction of more than 10 million acres of
corn crops in one yr.
• Disease of plants starts with initial contact, entry, growth of pathogens and
development of disease symptoms.
• Initial contact may be in the rhizoplane or phylloplane.
• Many fungi that disperse spores in air that contacts aerial structures of plants.
• Viral pathogens are carried by vectors at the phylloplanes.
• Bacterial and fungal pathogens can also be carried by insect vectors.
• Soilborne pathogens may be carried by nematodes or other soil animals at the
rhizoplanes.
• Some motile pathogens attack roots by chemotactically attracted to and comes in
contact with plants.
• Fungal Pathogens may enter through wounds or natural openings like stomata.
• Viral pathogens may enter through wounds caused by insect vector.
• Virus can also enter through roots with water.
• Some can enter through plant cuticle directly.
• Pathogens attach to the plant surface through a penetration peg and enter through
• When a specific antibody blocked cutinase of Fusarium solani, no infection
occurred though the spore remained viable.
• Enzymatic attack by pathogens, softens the cuticle and plant tissues so they can
easily enter. Soft rot Fusarium solani, Powdery mildew etc.
• After entrance the pathogens disrupt normal plant activities, by producing
enzymes, toxins, growth regulators etc.
• Soil plant pathogens produce, cellulase, pectinases, hemicellulases, producing
soft rot and lesions.
• Plant growth regulators may be destructed causing dwarfism of plants,
• Production of IAA, gibberillins, cytokinins results in gall formation, or excessive
plant elongation.
• Toxins interfere with normal plant metabolic functions.
• Beta-hydroxy diamino pimelic acid a toxin produced by Pseudomonas tabaci
causes tobacco wildfire disease, due to interference with methionine
metabolism.
• Some pathogenic fungi produce special toxins, like low mol. wt. peptides, linear
polyketols makes them able on causing damage to mitochondria and cell
membranes.
• Cell membrane damage helps in spread of infection.
• Plants may be tolerant to the enzymes due to modified receptors.
• Microbial infections can cause different abnormal morphological and metabolic
abnormalities.
• Some cases plants die very rapidly. Or else a slow death.
• When pathogens attack elicit a morphological response by plants. They form
papillae that helps block the spread of infection.
• Cell walls are modified by swelling or other distortions.
• Disruption of plant cell permeability, causing imbalances in water retention, leads
to leakage and death of plant cells.
• Damage to water conducting tissues.
• Blocking of transport can cause desiccation and wilting as seen in tomatoes by
Fusarium, reduction of water through the xylem.
• Symptoms of Microbial diseases of plants

• Disease Symptoms

• Necrosis Death of Plant cells, may appear as spots in localized

areas
• Canker Localized necrosis resulting in lesions usually stem
• Wilt Droopiness du to loss of turgor
• Blight Loss of foliage
• Chlorosis Loss of photosynthetic capability due to bleaching of
chlorophyll
• Hyperplasia Stunted Growth
• Hypoplasia Excessive Growth
• Gall Tumorous Growth
• Bacterial pathogens cause wilts by blocking stomata that modifies
transpiration and water transport.
• Diseased plants may show changes in respiratory activity due to electron
transport uncoupling or changes in glycolytic pathways of carbohydrate
metabolism.
• Pathogens may Interfere with CO2 fixation.
• Chlorosis prevents plants from carrying out oxidative phosphorylation and
Producing ATP.
• There may be changes in protein synthesis resulting in impaired metabolism.
• Altering in NA function that controls protein synthesis can cause gall
formation, Overgrowth.
• Changes in metabolic pathways and enzyme activities due to changes in
protein synthesis.
• Primary plant pathogens makes plants susceptible to secondary opportunistic
pathogens when plant surfaces and cell walls lose their integrity.
• Plants can produce phytoalexins in response to pathogen attack.
• These are abroad range of inducible polyphenolic flavonoid or proteinaceous
antimicrobial compounds, that can save the plant from further microbial
attacks.
• Known as systemic acquired resistance (SAR).
• Also, rapid local necrosis (death) and desiccation of infected cells helps
contain the invading microbes.
• Plants response to viral infection by Synthesis of antiviral proteins.
• Salicylic acid was in elevated levels after viral infection.
• Viral Disease:
• Plant pathogenic viruses are classified according to the ability to cause a
particular disease.
• Needs vectors to transport virus in soil or in diseased plant tissues..
• Insects, ants and nematodes act as vectors (aphids, leafhoppers, etc).
• Virus must survive outside host until they encounter susceptible living plants.
• These are obligate intracellular parasite. So needs host for replication.
• Outside plants and even in vectors they retain their infective capability.
• In vectors they are protected from soil microbial enzymes.
• Environmental factors that affect the movement and survival of vectors,
determines the distribution patterns of viruses.
• Infected plant structures can also help in transmission. Tobacco rattle virus are
found in pollen infected petunia plants. Disseminated in air through pollen.
• Transmitted through seeds. These ensure that disease are maintained within
susceptible host plants.
• Bacterial disease:
Common genera Mycoplasma, Corynebacterium, Agrobacterium, Pseudomonas,
Xanthomonas, Streptomyces, Spiroplasma and Erwinia.
Widely distributed and cause several disease, like hypertrophy, wilts, rots, blights and galls.
These do not form any resting stages and so remains in contact with plant tissues.
Many can remain viable in seeds, and on other tissues as they are resistant to desiccation.
Some are obligate parasites and cannot compete soil saprophytes.
Few opportunistic pathogens are able to reproduce in soil after sufficient population.
Some do not have any soil phase.
During winter Erwinia amylovora that cause fire blight in fruit trees remains dormant
within infected tissue of stems and branch.
In spring when rain and insects distribute it to other new plants.
• Bacteria that have a permanent soil phase like Pseudomonas sp.
Cause soft rots infects plant through roots.
• They are abundant and exist as saprophytes in rhizosphere.
• Seed borne bacterial pathogens survive in soil for a short time.
• Usually found on seed surface or micropyle.
• Pseudomonas phaseolicola causes halo blight of beans are found in
micropyle.
• Xanthomonas malvacearum cause blight of cotton are found on
surface.
• As they are externally located these are much affected by soil
texture, pH, moisture, temp etc.
One most interesting interaction is Crown gall a plant
disease caused by the soil-inhabiting bacterium,
Agrobacterium tumefaciens.
The bacterium causes abnormal growths or galls on
roots, twigs, and branches of shrubs primarily in the
rose family.
The bacterium stimulates the rapid growth of plant
cells and transform it into tumor like galls of uneven
size.
The bacteria enters the plant through roots or
wounded surface of susceptible dicot plants usually at
the soil stem interface of sugar beet, fruit trees and
other broad leaf plants.
Tumor cells use plant metabolites to form nutrients for
bacterial growth.
 Disease is caused by Agrobacterium- Two major disease caused by
Agrobacterium in plants.
• 1. Crown Gall 2. Hairy Root
Crown gall Symptoms :
 Symptoms: roundish, rough-surfaced overgrowths appearing as tumor like
growth (galls) on roots and at the base or "crown" of woody plants galls,
several inches or more in diameter, usually at or near the soil line, or on
roots and lower stems
 The galls, at first cream coloured or greenish, later turn brown or black.
 These growth first appears as whitish pustules and later starts to increase
in size.
 These galls becomes hard and woody as it matures.
 Plant growth is retarded and slow growth.
 Plant becomes weak and may affect on yield of crop
• This bacterium can survive in the free-living state in many soils with good
aeration where crown gall diseased plants have grown.
• The bacterium can also survive on the surface of roots of many orchard weeds.
• Characteristics are Gram-negative, strictly aerobic, bacilliform rods measuring 1
x 3 µm, and whose nutritional requirements are non-fastidious.
• The rods bear flagella that are arranged sub-polarly around the cylindrical
circumference of the cell.
• Bacterium is passive invader.
• Entry of pathogen through wound by insect injury, pruning, wind damage, etc.
• Bacteria multiply in galls in large number then insect, fungi or other organism
breaks the gall and pieces of gall fall on ground which have millions of bacterial
cells in them.
• Bacteria can move from field to field through runoff water.
• Pathogenicity
• Pathogenicity/Virulence and the host-range of A. tumefaciens are
conferred by a large extrachromosomal DNA element designated as
the Ti plasmid (for tumor-inducing) that resides in all virulent strains
of this pathogen.
• The interesting feature of the Ti plasmid is T-DNA (transfer DNA)
which is actually transferred from bacterium to the plant genome.
• The ability of Agrobacterium tumefaciens to cause crown gall disease
depends on the Ti-plasmid.
• The Ti plasmid a megaplasmid is approximately 200 kilobases in
length and is comprised of a covalently closed, double-stranded DNA
circular molecule.
• Analysis of the nuclear DNA in the plant tumor indicated the
presence of the bacterial plasmid DNA which was integrated into the
Important regions on Ti plasmid

Ti plasmid consists of the following regions;

Origin of replication. (which enable plasmid to replicate independent of the

bacterial chromosome).

Plasmid conjugative transfer region (which decide to compatibility with

other strain)

Vir region (consist of Vir genes).

Opine catabolism region (that breaks down opine to provide nutrition and
energy for bacterial proliferation).

T DNA region (transfer to the host plant cell).

• Ti plasmid

• T-DNA enter in the plant cell and integrate into the plant genome thus
genetically modify the plant.
• T-DNA region which is transferred to the host plant is bounded by the left &
right border which consists of an imperfect direct repeat sequence of 25bp.
• Within the border, a gene involved in auxin & cytokinin biosynthesis called
oncogenes and genes involved in opine synthesis are present.
• All the genes in T-DNA have eukaryotic promotors since they are express in the
plant.
• The oncogenes lead to change in the level of auxin & cytokinin in transformed cell
& cause rapid growth/multiplication of plant cell leading to tumor formation.
• Tumor cells synthesize opines.
• Also referred as nature’s smallest genetic engineer.
• A. tumefaciens genetically engineers the plant cell for its own purposes.
• When cells perceive plant phenolic compounds, the virulence genes that
are located in the resident Ti (tumour-inducing) plasmid are expressed,
resulting in the formation of a long flexuous filament called the T pilus.
• Bacterium gets attached to the plant cell and transfer its Ti plasmid into
the plant cell.
• The products of the vir genes carry out the processing of the T-DNA and
functions for T-DNA transfer to the plant cell.
• Also, perception of the plant phenolic compounds by VirA switches off A.
tumefaciens cell motility.
• In addition, certain chromosomal genes (e.g., chv, att genes) of A.
tumefaciens are also involved in virulence.
• Most of them have a role in the attachment of A. tumefaciens to plant
cells, in promoting signal molecule recognition, and in the regulation of
certain vir and T-DNA genes.
• The T-DNA is integrated into the plant chromosome as evidenced by in
situ hybridization using the T-DNA as the probe.
• The T-DNA genes are expressed by plant transcriptional machinery.
• The products of the T-DNA genes catalyze the formation of auxin,
cytokinin and opines.
• Profuse production of auxin and cytokinin in the transformed cells results
in abnormal cell division, cell enlargement, and uncontrolled growth of
the infected plant tissues.
• Opines are utilized as specific nitrogen and carbon sources by A.
tumefaciens.
• The opines produced by the transformed plant cells provide unique
nutritional sources for the pathogen, and certain opines serve as inducers
and promote transfer of the Ti plasmid between conjugative
Agrobacterium strains.
• Induction of Vir operon
• Vir region determine the pathogenicity of the bacterium in response to phenolic
(p-hydroxybenzoic acid and vanillin) signals from wounded damaged plant cells.
• The Vir A protein present in the bacterial membrane is auto-phosphorylated
and then transfer the phosphate signal to Vir G protein, both Vir A & Vir G are
expressed in Agrobacterium, the activated Vir G binds to the promotors of the
other Vir gene in the Vir operon.
• The Vir D protein nicks Ti plasmid DNA adjacent to the T DNA.
• The Vir E protein binds to the single stranded DNA of T DNA region.
• The VirE-T DNA region complex is transmitted to the plant cell as in conjugation.
• The VirB protein acts like a sex pilus and is involved in the transfer of the single
stranded DNA into the plant cell.
• Opines
• Secondary amine derivatives formed by condensation of an amino acid
(arginine) and sugar/keto acid.
• More than 30 opines have been identified in Agrobacterium strains and
the most common opines are octopine, mannopine, nopaline, agropine.
• Opines cannot be metabolized by plants.
• Agrobacterium Ti plasmid has an opine catabolism gene that codes for
an enzyme that metabolizes opines.
• Opines provide building blocks and energy for bacterial growth and
proliferation.
• Some of the plant photosynthate are diverted towards production of
these opine.
• Agrobacterium uses these opines as their sole source of C, N and energy.
• Cause of Death

• Uncontrolled cell proliferation at the infection site leads to tumors or

galls.
• Poor cell differentiation in root gstunting of growthalls leads to
decreased uptake of water and nutrients for the plant, eventually
leading to plant death.
• Galls may fall off after plant death, exposing surrounding plants to A.
tumefaciens.
• A. tumefaciens may also be transferred by biting insects or harvesting
equipment.
• Treatment of disease
• 1- Plant  A. Tumefaciens Resistant Crops.
• 2- Use biochemical agents.
• Spray antibiotics such as agrocin on the entire field.
• Agrocin structurally resembles the opine agrocinopine A, taken up by A. tumefaciens.
• Agrocin inhibits nucleic acid and protein synthesis by obstructing the intake of amino
acid residues by pathogenic A. tumefaciens.
• Prevention-Replant the entire field with cereal crops for a long period of time.
• Cereal crops are not in the host range of A. tumefaciens.
• Lack of hosts significantly decreases A. tumefaciens  population.
• Removing severely infected plants (including as many roots as possible);
• Protecting plants against injury;
• Keeping down weeds;
• Controlling root-chewing insects and nematodes;
• Cutting away large galls on trees, and disinfecting the wounds
• Hairy root Symptoms :

• In India, occurrence of hairy root caused by A. rhizogenes was first

reported in 1943 from Kumaon Hills of Uttar Pardesh.
• Hairy root disease is characterized by an overabundant growth of
adventitious roots at the site of infection (usually on the stems of plants
near and immediately below the soil surface).
• Symptoms of hairy root disease may also include wrinkled leaves.
• The roots are unable to absorb proper amount of water and nutrients, so
plant remains stunted and weak.
• In sever cases plant is unable to produce flowers and fruits.
• Hairy root disease symptoms have been divided into 2 categories, ‘simple
or fibrous hairy-root’ and ‘woolly-knot form of hairy root.’
• The woolly-knot form is characterized by the initial formation of a
smooth tumour on the plant stem followed by an outgrowth of
adventitious roots from the tumour surface.
• Causal organism : Previously known as Agrobacterium rhizogenes
• Now known as Rhizobium rhizogenes .
• Host : The plant families Solanaceae, Rosaceae, Fabaceae,
Crassulaceae, Caesalpinaceae, Brassicaceae, Polygonaceae, and
Asteraceae are susceptible to hairy root caused by R. rhizogenes.
• Laboratory experiments have shown that many plants can serve as
hosts including monocots and primitive dicots.
• R. rhizogenes has a world-wide distribution but it cannot grow
above 30°C in culture.
• Biology : Agrobacterium rhizogenes had small rod, capsulate non-
spore forming, motile by one polar flagellum.
• However, on certain media, Agrobacterium formed star shaped
arrangements which have been considered as stages in sexual
processes of these bacteria.
• Optimum growth occurs at pH above 4 and temp. 20-28°C.
• Many live their entire lives as saprophytes (non-pathogenic) and do
not cause damage to plants.
• They can exist as biofilms on plant root surfaces.
• The strains which contain Ri-plasmids with virulence genes are
considered plant pathogens
• It is a soil born bacteria and can remain in soil for a long time in absence of host
on dead plant debris.
• Pathogen enters in host through injuries and wounds.
• When a plant is wounded it releases phenolic compounds which are sensed by
the bacterium in the soil.
• R. rhizogenes is attracted towards the plant wound and it can transfer its DNA
into the host cell via transfer of a portion of the root-inducing (Ri) plasmid.
• The transferred DNA (T-DNA) is integrated into the plant cell genome.
• After integration the plant produces an abundance of growth hormones and
opines which are beneficial for growth of R. rhizogenes.
• It is thought that the virulence genes of R. rhizogenes are activated by the lignin
forming compounds in some plant cell walls.
• Pathogen can travel to a long distance in runoff water.
• Fungal Disease : Most important economic disease are caused by-
• RUST More than 2000 sp. Require two unrelated host to complete their
• life cycle.
• SMUT More than 1000 sp. Loose smut of oats, corn smuts, bunt or
• stinking smut of wheat, and onion smut

• These are of the family Basidiomycota. Causes millions of dollars in crop

damage every year.
• Spores produced by fungi remains viable outside plants and permit aerial
transmission between plants.
• Many plant pathogenic fungi exhibit complicated life, part of it in plant
infection and part of it is accomplished outside plant.
• Some lives on plants and part on soil or plant litter as saprophytes.
• These fungi always remain in close contact with both live and dead tissues.
• Survival and infectivity depends on the environmental conditions like
temperature and moisture.
• Mycelial germination is between -5^0C to +45^0C provided
appropriate moisture is present.
• Spores can survive and viability for long periods under conditions
that do not permit germination.
• Changes in environment may affect the pathogen, the host or both.
• Pathogens may cause disease during warm months that favors them,
but can be inactive during winter season or unfavorable conditions.
• In some cases, optimum temperature for disease development may
be very different than the optimum growth temperature of
pathogens and or plants.
•
• Theilaviopsis basicola causes black root of tobacco, has an optimal
growth temp. higher than the optimal temp for disease.
• So host is less able to resist pathogens at temp of 17-23^0C.
• But some fungi like, Typhula and Fusarium that cause snow mold of
cereals and grasses survive in cool seasons or cold regions.
• Gibberella zeae causing root rots of corn and wheat, has an optimum
temp for disease higher than the optimum growth temp. of both
pathogen and host.
• Moisture also influence the initiation and development of infectious
plant disease.
• Some plant pathogens are dispersed by rain drops and comes in close
contact with susceptible plants.
• Distribution of rainfall in some regions is closely associated with
occurrence of plant disease.
• Downey mildew of grapes and fire blight of pears, are more severe in
heavy rainfall or high humidity during their growing season.
• Soil pH also has marked effect on the infectivity for soil borne plant
pathogens.
• Plasmodiphora brassiceae causes club foot of crucifers at pH about
5.7 but the disease is inhibited at pH 7.8