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Phytopathology (Phyton : plant) Greek - Pathos (suffering) + Logos
(study) = The study of the suffering plant
Plant pathology is that branch of agricultural, botanical or biological
sciences which deals with the study of:
-cause of the disease (Etiology/aetiology)
-mechanism of disease development
-host-pathogen interaction in relation to environmnet
-Resulting losses and
-Control and management of plant diseases
Plant pathology is both science (of Learning and understanding
the nature of disease ) and Art (of diagnosing and controlling/managing
the disease)
WHAT IS PLANT PATHOLOGY?
OBJECTIVES OF PLANT PATHOLOGY
1. Study of origin, causes or reasons. Study of living, non-living and
other causes of disease or disorder in plants- Etiology
2.Study of mechanism of disease development i.e. processes of
infection and colonization of the host by the pathogen. This phase
involves complex host-pathogen interactions- Pathogenesis
3.study the interaction between the causal agent and the diseased
plants in relation to environmental conditions. Generally at the
population level- Epidemiology
4.Development of management systems of the diseases and reduction
of losses caused by them- Control/ Management.
WHAT IS PLANT HEALTH?
The ability to carry out normal physiological
functions at a acceptable level consistent to
genetic potential.
Normal physiological functions include:
 Normal cell division, differentiation, and development,
 Absorption of water and minerals from the soil and translocation;
 Photosynthesis and translocation of photosynthates;
 Utilization and storage of photosynthates;
 Metabolism of metabolites and synthates;
 Reproduction;
 Storage of reserves for overwintering or reproduction
CONCEPT OF DISEASE
 Plant is healthy, or normal, when it can carry out
its physiological functions to the best of its genetic
potential.
Any deviation- Disease
The kinds of cells and tissues that become
affected determine the type of physiological
function that will be affected/altered
-For example, infection of roots may cause roots to
rot and make them unable to absorb water and
nutrients from the soil;
-Infection of xylem vessels, interferes with the
translocation of water and minerals to the crown of
the plant;
-Infection of the foliage, (leaf spots, blights, rusts,
mildews, mosaics etc.), interferes with
photosynthesis
Disease can be defined as the result of interaction between host, pathogen
and environment
DEFINING DISEASE
Disease is the process in which a pathogen interferes with one or more essential
plant cell functions
Disease is as physiological disorder or structural abnormality that is deleterious to
the plant or its part or product, that reduces the economic value of the plant
e.g., wilt, potato blight, Loose smut of wheat, Karnal bunt of wheat (Stakman &
Harrar, 1957)
Disease is a malfunctioning process that is caused by continuous irritation, which
results in some suffering producing symptoms. ( Accepted by both American
Phytopathological Society and British Mycological Society)
Horsfall & Diamond (1957): Disease can be defined as a physiological disorder or
structural abnormality that is deleterious or harmful to the plant or its part or
product that reduces its economic value.
How Pathogens affect Plants?
-By utilizing host cell contents
-By killing host or by interfering with its metabolic processes through their
enzymes, toxins etc.
–By weakening the host due to continuous loss of the nutrients.
–By interfering with the translocation of the food, minerals and water.
–They can suppress the chlorophyll content.
–They can reduce the leaf area.
–They can curb the movement of solutes and water through
the stems.
–They sometimes reduce the water-absorbing capacity of the
roots.
–They suppress the translocation of photosynthates away
from the leaves.
–They sometimes promote wasteful use of the products of
photosynthesis as in the formation of galls.
IMPORTANCE OF PLANT DISEASES
-Late blight of potato-1841-51 (Irish famine) –Phytophthora
infestans.
-Bengal Famine 1942 (India)- Bipolaris/Helminthosporium
oryzae
-Coffee rust 1867-1870 (Srilanka) –Hemileia vastatrix
-Downy mildew of grapes (1880s) (France)- Plasmopara
viticola
-Outbreak of Black stem Rust (Ug99) in wheat (1999)-
Puccinia graminis f. sp. tritici
-Bacterial Blight of Rice 1963 (Bihar)- Xanthomonas oryzae
pv. oryzae
-Southern corn leaf blight -1970 (USA) –Bipolaris maydis
Out of 36.5% agriculture
yield loss:
Disease cause: 14.1%
Insects cause: 10.2%
Weed causes 12.2%
-Plant pathology deals with different
aspects of plant diseases and has wide
scope than human pathology which only
deal with only one aspect
-In recent years plant pathologists have
begun to specialize in particular
aspect. The field in which notable
advances have been made are:
–Interaction between host and
pathogen at chemical, molecular and
genetic level
–Plant virology, chemistry of
fungitoxicity
–Disease forecasting
-Breeding for resistance
What is Disorder?
Iron deficiency
Abnormal physiological change due to non-parasitic agent or is a non-parasitic
physiological malfunctioning due to either excess or deficiency in environmental
factors or nutrients.
e.g. Physiological wilt, sun scald, Nutrient deficiency
SOME FUNDAMENTAL TERMINOLOGIES
 Pathogen
 Parasite
 Various levels of Parasitism
 Symbiosis
 Obligate parasite (Biotrophs)
 Facultative parasite
 Facultative saprophyte
 Saprohytes
 Hemibiotrophs
 Perthotrophs/Necrotrophs/Perthopy
te
 Pathogenicity
 Pathogenesis/Disease Cycle
 Virulence
 Infection
 Colonization
 Inoculum
 Invasion
 Inoculum Potential
 Symptoms
 Signs
 Syndromes
 Incubation period
 Alternate host
 Collateral host
 Inoculation
 Isolation
 Etiology
 Epidemiology
 Pre-dispostion
 Resistance
 Susceptibility
 Tolerance
 Hypersensitivity
 Physiologic race
 Biotype
 Mutualism
 Antagonism
 Mutation
 Crop Damage
 Deficiency
 Pathogen: An entity, usually a micro-organism that can cause the disease. (Fungus,
Bacteria, virus, Phytoplasma, Viroids, RLO’s, Parasitic Plants, Nematodes )
 Parasite: An organism living upon or in another living organism (the host) and obtaining
the food from the invading host.
 Obligate parasite (Biotrophs): A plant pathogenic fungus that requires living host cells
i.e. an obligate parasite. E.g. Smuts, Rusts, Powdery mildew, Downy mildew.
 Hemi-biotroph: A plant pathogenic fungus that initially requires living host cells but
after killing the host cell grows on the dead and dying cells. E.g. leaf spotting fungi
 Necrotroph/Perthotrophs A pathogenic fungus that kills the host tissues in advance of
penetration and then live saprohytically. E.g. Sclerotium rolfsii
 Saprophyte: They are those organisms that secure their nutrients from dead organic
tissues or from available inorganic materials.
 Facultative parasite (weak Parasite/ strongly saprophytic): They are ordinarily
saprophytic but under certain conditions they may become parasitic. E.g. Pythium,
Rhizoctonia,
 Facultative saprophyte (Weak saprophyte/ strongly parasitic) : They ordinarily have a
life cycle similar to that of obligate parasite but under certain conditions, may subsist
as saprophyte. E.g. Smut fungi, Taphrina, Protomyces, Phytophthora infestans etc.
Pathogenicity: The relative capability of a pathogen to cause disease.
Pathogenesis: It is a process caused by an infectious agent (pathogen) when it comes in
contact with a susceptible host.
Disease cycle: A series of events involved in disease development including stages of
development of pathogen and the effect of pathogen on the host (inoculation, penetration,
infection, invasion, colonization, growth and reproduction , dissemination of pathogen,
survival of pathogens)
Virulence: It is a qualitative component of pathogenicity expressed vertically. The degree of
infectivity of a given pathogen
OR It is a measure of degree of pathogenicity of a given pathogen
Aggressiveness: It is a quantitative component of pathogenicity expressed horizontally. It is
the capacity of the pathogen to invade and colonize the host and to reproduce/survive on or in
it.
Features Vertical resistance/ Qualitative
resistance/R-Gene Resistance/
Monogenic resistance/Race-
specific resistance/Major gene
resistance/Differential rsistance
Horizontal resistance/ Partial
resistance/ Polygenic
resistance/Minor gene
resistance/Non-differential
resistance/Race-non-
specific/Adult/ Field resistane
Pathotype specificity Specific Non specific
Nature of gene action monogenic or sometimes oligogenic Polygenic
Effectivity Generally biotrophs Generally necrotrophs
Efficiency Against specific races Variable, but operate against all races
Risk of boom and bust Present Absent or Minimal
Stage of expression Seedling to maturity Expression increase as plant matures
HORIZANTAL AND VERTICAL RESISTANCE
Introductory Plant Pathology Class Slides.pdf
BOOM AND BUST CYCLE
Inoculation: It is the process of landing the pathogenic spore on the host
surface naturally or transferring the pathogenic propagules artificially
Infection: It is establishment of parasitic relationship between two organisms
following entry or penetration or initiation and establishment of a parasite
within the host
Invasion: The penetration and spread of a pathogen in the host.
Colonization: The growth and reproduction of a pathogen, particularly a
fungus, in the host after infection is called colonization.
Inoculum: It is the infectious material can cause disease, and it is that
portion of individual pathogens that is brought into contact with host.
Inoculum Potential: Garret (1956) defined it as the energy of fungal parasite
available for infection of a host at the surface of the host organ to be
affected.
Symptoms and Signs
Symptom – are the internal and external expression of the disease
caused by the manifestation of the physiological reaction of the plant
due to harmful activity of the pathogen
• Sign - physical evidence of the presence of disease agent (e.g., mold
or fungal spores, bacterial ooze, sclerotia, exudates)
Syndrome
• Defined as sequential appearance of disease symptoms on a plant during
the development of the disease
• or sum total of symptoms exhibited by a disease
Fleck or necrotic spot
Blight
Fungal growth
Death of organ or plant
Incubation period: The period of time between penetration of a
pathogen to the host and the first appearance of symptoms on the
plant.
Host: An organism that harbors or supports the activities of parasite
Alternate host (wild host of different families): Plants not related
to the main host of parasitic fungus, where it produces its different
stages to complete one cycle (heteroecious).
Collateral host: The wild host of same families of a pathogen is
called as collateral host.
Isolation: It is process of taking out/separating the pathogenic part
from diseased sample for disease diagnosis
Pre-disposition: The effect of one or more environmental factors
which makes a plant vulnerable to attack by a pathogen.
Susceptibility: Inability of the host to resist the attack of the
pathogen
Tolerance: is a type of defense that minimises crop losses with
out restricting the disease development.
Resistance: Ability of the host to resist the attack of the
pathogen. (Horizontal/Vertical resistance)
Immunity: It implies exemption from infection by pathogen
Hypersensitivity: The hypersensitive response (HR) is a type of
programmed cell death, which is part of the plant’s defense
response against pathogen attack. It is defined as a rapid,
localized necrosis of cells at the infection site and it occurs in
resistant plants in response to pathogen attack
Gene-for-gene Hypothesis
• Postulated by Harold Henry Flor in
1951
• Based on his work on Linseed rust
caused by Melampsora lini.
“For each gene conditioning avirulence in the
pathogen, there is a corresponding gene
conditioning resistance in the host and vice-
versa”
“For each gene conditioning resistance in host,
there is a corresponding gene conditioning
avirulence in pathogen and vice-versa”
OR
Molecular basis for gene-for-
gene relationship
Gene-for-gene relationship is the consequence of specific interaction
between product of host genes governing resistance and pathogen genes
specifying virulence.
 on the basis of molecular interaction involved in producing
resistance/susceptible response in host gene-for-gene relationship may
be classified to:
1. Incompatible reaction (Resistant)
2. Compatible reaction (susceptible)
Introductory Plant Pathology Class Slides.pdf
Eg- peptide encoded by Avr9 gene of fungal pathogen
Cladosporium fulvum induce HR in tomato strain
carrying resistance gene cf9
RESISTANCE GENE
VIRULENCE
R1 Resistance Susceptible
r1 Susceptible Susceptible
Avr1 avr1
Primary infection: The first infection of a plant by the over wintering or over
summering structure (resting/ survival structure) of the pathogen
Primary inoculum: The propagules coming from survival structures or
neighbouring field that cause primary infection.
Secondary inoculum: The inoculum that develops subsequestly after primary
infection or primary symptoms
Secondary infection: The infection caused by secondary inoculum is known as
secondary infection.
Epidemiology : Epidemiology of disease is study of factors affecting the outbreak
of an infectious disease. It is science of disease in population (deals with
population of host and pathogens under varying environment)
Pathodeme: Pathodeme is that population of a host in which all individual have a
stated resistance in common.
 Formae speciales (Pl.Forma specialis)- f. sp.- individuals with in the spp. Of a
pathogen that morphologically similar but difffer with respect to their
pathogenecity on particular host genera • E.g. Puccinia graminis f.sp. tritici, oats
(P. graminis f. sp. avenae) and rye (P. graminis f. sp. secalis)
Formae speciales of
Puccinia graminis
Host plant
tritici Wheat,
secalis Rye,
avenae Oats
phleipratensis Timothy
agrostidis Redtop
poae Kentucky blue grasses,
Physiologic race: individuals with in the species of a pathogen that
are morphologically similar but differ with respect to their
pathogenicity on particular set of host varieties (differential host)
Mutualism: Symbiosis of two organisms that are mutually helpful or
that mutually support one another.
Antagonism: The counteraction between organisms or groups of
organisms.
Mutation: An abrupt appearance of a new characteristic in an
individual as a result of an accidental change in genes present in
chromosomes.
Crop Damage: It is defined as any reduction in the quality or
quantity of yield or loss of revenue resulting from crop injury.
Deficiency: Abnormality or disease caused by the lack or subnormal
level of availability of one or more essential nutrient elements.
RACE/PATHOTYPE IDENTIFICATION (Puccinia graminis f.sp.
tritici)
• To identify the races of Puccinia graminis f.sp. tritici , the isolate is inoculated on twelve
standard differentials and the symptoms produced are noted and classified in to infection
type.
• These are then compared with the existing records and race is identified.
• Key numbers are given each on the basis of its identity.
Standard differentials
REACTION CLASSES OF TWO RACE OF P. graminis f.sp.
tritici
Terms describing microbial habitats related to
plants
Epiphytic: organisms growing on the surface of photosynthetic
organisms
Endophytic: organisms growing inside the host
Phylloplane: leaf surface
Phyllosphere: area surrounding the leaf and impacted by it
Rhizoplane: root surface
Rhizosphere: area surrounding the root and impacted by it
HISTORY OF PLANT PATHOLOGY
 Greek Philosopher Theophrastus (300 BC) recorded some
observations on the plant diseases in his book “Enquiry into plants”
PIER ANTONIO MICHELLI (Italian) botanist in 1729 published a book
“Nova Plantarum Genera”- FOUNDER AND FATHER OF MYCOLOGY
BENEDICT PREVOST proved that diseases are caused by micro-
organisms and in 1807, published his findings in the paper “memoir
on the immediate cause of bunt or smut of wheat and of several
other diseases and on preventives of bunt”
CHRISTIAN HENDRICK PERSOON published Mycologica Europa in
1822 and gave the name to rust pathogen of wheat as “Puccinia
graminis”
PERSON AND FRIES first time introduced binomial system of
nomenclature to classify the fungal organisms
 HEINRICH ANTON De BARY (German botanist) in 1863, studied the
epidemics of late blight of Potato and renamed the causal organism as
Phytophthora infestans- FOUNDER AND FATHER OF MODERN PLANT
PATHOLOGY
ROBERT KOCH (1881) developed plate method for isolation of bacteria –
Father of Modern bacteriology
PIERRE-MARIE-ALEXIS MILLARDET- discovered Bordeaux mixture for the
control of Downey Mildew of Grape Vine
 M.W. BEIJERINCK (Dutch)- a Dutch microbiologist and founder of virology
proved that the virus inciting tobacco mosaic is not a microorganism. He
believed it to be contagium vivum fluidum (infectious living fluid). He was
the first to use the term virus, which is the Latin word for poison.- FOUNDER
OF VIROLOGY
IWANOWSKI (1888)- demonstrated filtrable nature of virus
W.H. STANLEY in 1953- proved the crystalline nature of viruses.
J.F. DUSTUR: First Indian plant pathologist credited for his detailed studies
on fungi and plant diseases
CAUSES OF PLANT DISEASES
Animate/Biotic Causes
Fungi
Bacteria
Nematodes
Algae
Protozoa
 Mollicutes
-Phytoplasma (MLOs)
-Spiroplama
Rickettsia like
organism/bacteria
(RLOs/RLBs/Fastidious
bacteria)
Phanerogamic parasites/
parasitic higher plants
Insects
Mesobiotic Causes
Viruses
Viroids
Inanimate/Abiotic Causes
1. Soil condition
a) Moisture-
b) Structure
c) Soil Oxygen
d) Soil nutrients (N, P, K, Ca,
Mo, B, Zn)
2. Meteorological factors
a) Light
b) Temperature
c) Wind
d) Atmospheric humidity
3. Agriculture practices
Eg. Herbicides
4. Industrial contaminants
Eg. Peroxyacetyl Nitrate,
SO2
FUNGUS (PL. FUNGI)
 eukaryotic,
 spore-bearing,
 Achlorophyllous organisms
 generally reproduce sexually and
asexually
 whose usually filamentous,
branched somatic structures are
typically surrounded by cell walls
containing chitin or cellulose, or
both of these substances, together
with many other complex organic
molecules.
 May be either saprophytic or
parasitic
SOME DISEASES CAUSED BY FUNGI
Bean Anthracnose (Colletotrichum
lindemuthianum)
Brown spot of rice (Bipolaris oryzae)
Downy mildew of Pumpkin
(Pseudoperonspora cubensis)
Powdery mildew of Cucumber
(Podosphaera xanthii)
Stripe/Yellow rust of Wheat
(Puccinia striiformis f. sp. tritici)
Late blight of Potato (Phytophthora
infestans)
BACTERIUM (PL. BACTERIA)
 are microscopic, unicellular prokaryotes, which lack
chlorophyll.
are with a primitive nucleus lacking a clearly defined
membrane.
70 S ribosome
Cell wall made up of peptidoglycan (murein), lipo
proteins and lipopolysaccharides
are smaller than fungi and measure about 0.5 to 1.0 x 2.0
to 5.0 μm in size.
are equipped with delicate, thread like flagella
(locomotory organ)
Most of plant pathogenic bacteria are rod shaped except
Streptomyces (filamentous) and Cornyebacterium (club)
Reproduction by binary fission and budding
Important plant pathogenic
bacterial Genera
Agrobacterium,
Clavibacter(Cornyebacterium),
Erwinia,
Pseudomonas,
Ralstonia,
Xanthomonas,
Streptomyces,
Xyllela
Acidovorax
SOME DISEASES CAUSED BY BACTERIA
Bacterial leaf blight of Rice
(Xanthomonas oryzae pv. oryzae
Bacterial wilt /Brown rot of
Potato (Ralstonia solanacearum)
Black rot of crucifers
(Xanthomonas campestris )
Citrus canker (Xanthomonas
axonopodis pv. citri
Crown Gall of Apple
(Agrobacterium tumefaciens )
Potato Scab ( Streptomyces
scabies)
Nematodes
• Microscopic roundworm like animals
• Barely visible with naked eye
• Triploblastic, bilaterally symmetrical
• Unsegmented, pseudocoelomate
• Bisexual, Vermiform
• 300nm-100nm but Up to 4mm long
• Free living to parasitic
• Almost all plant parasitic nematodes are
obligate parasite and are soil inhabitants
• Reproduction- sexual and parthenocarpic
Important Plant Pathogenic nematode
Meloidogyne (Root-knot nematode)
Heterodera and Globodera (Cyst nematode)
Ditylenchus (stem and bulb nematode)
Pratylenchus (lesion nematode)
Anguina (seed gall nematode)
Aphelenchoides ( Foliar nematode)
Xiphinema (Dagger nematode)
Longidorus and Paralongidorus (Needle nematode)
Trichodorus and Paratrichodorus (Stubby-root
nematodes)
SOME PLANT DISEASES CAUSED BY NEMATODES
Ditylenchus dipsaci (Stem and
bulb nematode) in onion
Root knot of Tomato
(Meloidogyne incognita)
White tip of rice
(Aphenchoides besseyi)
Golden cyst of Potato
(Globodera rostochiensis)
Ear cockle of wheat (Anguina
tritici)
ALGAE
Algae are eukaryotic, unicellular or multicellular
organisms and mostly occur in aquatic
environments. Many algae thrive as terrestrial or
subterranean algae.
The size of algae ranges from 1.0mm to many
centimetres in length.
They contain chlorophyll and are
photosynthetic/autotrophs
They reproduce by asexual and sexual processes.
The study of algae is called phycology or algology.
Spread by wind borne sporangia and produces
zoospores.
Enter into plant cell through natural openings and
grow as a chain of algal cells
E.g.Cephaleuros mycoides/virescens (Red rust of
mango, litchi, guava, tea, coffee, Avocado, etc)
FLAGELLATE PROTOZOAN (PL. PROTOZOA)-
PHYTOMONAS
Protozoa derived from Greek word Protos
(first) and zoon (animal)
They are eukaryotic protists
Generally Single celled
Distinguished from other eukaryotic
protists by their ability to move at some
stage of their life cycle and lack of cell
wall
Members of family Trypnosomatidae
(Kingdom Protista) are know to be plant
parasitic
Phytomonas
leptovasorum (Phloem
necrosis of coffee)
P. francai (Empty root
rot of Cassava
MYCOPLASMA LIKE ORGANISMS (PHYTOPLASMA)
Resembles mycoplasmas – animal pathogens
Highly pleomorphic, non-motile, non-spore forming,
unicellular , filterable, extremely small.
Generally ovoid but filamentous forms are also reported
are obligate bacterial parasites of plant phloem tissues and of
the insect vectors that are involved in plant to plant
transmission
Lack cell wall however, have specialized triple layered
membrane, lack cell wall.
Sensitive to tetracycline and insensitive/resistant to penicillin
Mostly transmitted by Phloem feed insects such as hoppers
and psyllids.
They have not been grown in an artificial nutrient medium so
far
Important diseases
caused by Phytoplasma
 Aster yellows
 Apple proliferation
 European stone fruit
yellows
 Coconut lethal
yellowing
 Elm yellows
 Ash yellows
 Pear Decline
 Little leaf of brinjal
 Sandal Spike
 Sesamum phyllody
 Grassy Shoot disease
 Peach X
Aster yellows Coconut lethal yellowing Sesamum Phyllody
Peach X disease
SPIROPLASMA
Similar to Phytoplasma in many regards
except that they can be cultured and are
motile and helical in structure
Small helical mollicutes
Are motile. Can somehow use their
corkscrew shape to propel themselves
Lack cell wall but have specialized triple
layered membrane
Require sterol for growth
Resistant to penicillin but sensitive to
tetracycline and neomycin
Can be cultured in artificial medium
Colonies on nutrient medium give fried
egg appearance
Generally transmitted by insect vectors
(leaf hoppers)
Important plant diseases
caused by Spiroplasma
Citrus Stubborn
Corn Stunt
Carrot purple leaf
disease
Citrus Stubborn Corn stunt
FASTIDIOUS VASCULAR BACTERIA- (RLOs/RLBs)
Formerly known as Rickettsia like organisms
Generally Gram negative bacteria, straight rod
shaped, smaller than MLOs
Have cell wall unlike MLOs and Spiroplasma
Develop within both xylem and phloem
Categorized into xylem-, phloem and non-
tissue limited (meristematic and parenchyma)
Very difficult to grow artificially as they have
specific nutritional requirements (Xylem
limited RLB has been more successfully
cultured)
Dependent on insect vectors and nematodes
for transmission
Sensitive to tetracycline and penicillin (*Xylem
limited insensitive to penicillin)
Xylem limited:
• Pierce’s disease of Grape vine
• Almond leaf scorch
• Phony disease of peach (Xyllela fastiodosa)
Pholem limited:
• Citrus greening (Candidatus liberibacter)
• Clover club leaf
• White clover disease
• Clover rugose leaf curl
Non-tissue limited:
• Aspermy of wheat
• Yellows of grapevine
Pierce’s disease of Grape Phony disease of Peach
Citrus greening/Huanglongbing (HLB) /yellow dragon disease
VIRUSES
Strictly intracellular, ultramicroscopic,
nucleoprotein entities, which are
infectious agents
obligately parasitic pathogens, which are
less than 200 mμ in size.
They can only replicate themselves
within a host's cell.
Possess only one type of nucleic acid
either DNA and RNA but never both
are devoid of enzymes and depend on the
host protein synthesis machinery
(ribosomes).
Most of plant pathogenic viruses are RNA-
viruses
Need mechanical, insects, seeds,
nematodes, propagation, grafting, etc. or
their entry into host
RNA Viruses:
Tobacco Mosaic virus
Barley stripe mosaic
Potato mop-top virus
Tobacco rattle virus
DNA Virus:
• Cauliflower mosaic virus,
• banana bunchy top virus,
• maize streak virus
• sugar beet curly top
virus.
Tobacco Mosaic Virus Tobacco Rattle virus Tomato leaf curl
Okra yellow vein
mosaic
VIROIDS
are small low molecular weight
ribonucleic acids (RNA) that can infect
plant cells
replicate themselves and cause disease.
They are also called as mini viruses.
are devoid of outer protein coat (capsid)
 Although it has no protein of its own, a
viroid's RNA affects a plant's ability to
produce essential proteins.
Depends entirely on the host cell for
replication
Diseases caused by
Viroids
Potato spindle tuber,
 Chrysanthemum
stunt,
 Coconut Cadang
cadang.
Potato Spindle tuber Coconut cadang cadang
Phanerogamic Plant Parasites
Some flower and seed bearing higher
plants (phanerogams) live parasitically on
other living plants
can cause important diseases on
agricultural crops and also in forest trees.
They may semi or partial or total parasite
(Holo parasite)
Holo parasite- absence of chlorophyll,
depend entirely on the host plants for
their food materials.
Spread in various ways including animals,
wind and forcible ejection of seeds
Cuscuta, the dodder (stem
parasite)- Aakash beli
 Orobanche , the broomrapes (root
parasite/holoparasite)- Neerjhar
 Striga (the witchweeds-root
parasite)
Inanimate/ abiotic/ nonliving causes of plant
diseases
1. Soil conditions:
A. Soil moisture:
Low moisture-physiological wilting
Excess moisture- Reduced O2, CO2
accumulation, accumulation of toxic
metabolites by anaerobic bacteria,
accumulation of soluble salts around roots
and stem –
Damping off of seedlings, Root rots,
Fusarium and Verticillium wilts are more
severe in wet soils
Potato scab (Streptomyces scabies),
Charcoal rot (Macrophomina phaseoli) are
severe in dry soil
Charcoal Rot of Bean
Verticillium wilt of tomato
(V. alboatrum)
B. Soil structure:
-affects moisture holding capacity and aeration
-Hard and compact soil retards root growth, results
in stunted growth and predisposes the plant to
parasitic diseases
-Hard pan results in withering, yellowing die back
symptoms
C. Soil aeration
• Limited supply of oxygen coupled with poor
ventilation causes several post harvest disease in
storage e.g. Black heart of Potato
D. Soil pH:
• Club root of crucifers (Plasmodiophora brassicae) is
serious at pH 5.7 and controlled at pH 7.8
• Likewise Potato scab is also more prevalent in
alkaline soil, inhibited below pH 5.2
Black heart of Potato
Club root of Crucifer
Potato Scab
E. Nutritional Imbalance (Deficiencies and Abundance)
Nitrogen:
Abundance of N makes the plant succulent and predisposes
the plant to pathogen e. fire blight of Pear (Erwinia
amylovora) and Wheat Rust (Puccinia graminis).
Deficiency of nitrogen leads stunting and yellowing
symptoms following reddening of leaf blade E.g. Red leaf
of cotton
Phosphorus:
Leaves of Phosphorus deficient plants are generally bluish-
green with purple tints
Deficiency in Cotton causes dwarfing and excessively dark
green foliage
Potassium:
K deficiencies are particularly important in potatoes,
tobacco. cotton, forage legumes and other crops
which require high K.
E.g. Brown spot of cotton and little spot of alfa alfa
High K increases the severity of rice blast
P deficiency in Guava
P deficiency in
Maize
K deficiency in cotton Rice leaf blast
Boron:
-Soil with high lime content are deficient in Boron
-Deficiency of B cause Heart rot of Beet, Internal cork of apple, Brown
heart of cabbage and turnip, Hollow stem of Brassica, Internal browning
of Cauliflower
Calcium:
Deficiency cause Blossom end rot of tomato, black heart of celery, wither tip
of flax
Molybdenum:
Deficiency cause whiptail disease of cauliflower
Zinc:
Deficiency results in mottling/foliocellosis, little leaf, rosette of citrus;
yellow streak in corn; Khaira disease of rice
Khaira disease of rice
Internal browning of
Cauliflower
(Boron deficiency)
Internal cork of apple (Boron
deficiency)
Blossom end rot of tomato
(Ca deficiency)
Whiptail of Cauliflower
(Mo Deficiency)
METEOROLOGICAL FACTORS
Temperature:
Low temperature- frost of Pigeon Pea
High temperature- sun scald of tomato
Light :
No direct effect, yet, reduced light cause etiolation
Balanced light decreases susceptibility to obligate parasites like Puccinia
Wind:
 Helps in spread of propagules of pathogens and in initiation of epidemics
 Wind-blown rain help release fungal and bacterial spores and disseminate
them over long distance
Atmospheric humidity:
 High humidity favours most of the disease caused by fungi and bacteria
Industrial Contaminants:
Sulphur dioxide released from the Brick kilns cause black tip of mango when the
orchards are near to 15 km
Ozone concentration exceeding above 0.035 ppm for 4 hours may cause water soaked
spots on leaves
Peroxyacetyl Nitrate (PAN) produce visible symptoms when sensitive plants are
exposed for 4 hours to about 14 ppb.
Characteristically, injury from PAN appears as glazing or bronzing of the lower leaf
surface but the symptom syndrome may also include tissue collapse, chlorosis, and
leaf drop.
Agricultural Practice:
High dose of Agrochemicals causes phytotoxicity. E.g., 2,4-D kills Chenopodium but high dose
will affect the wheat also.
Faulty and improper application of fungicides and insecticides causes injuries to the plants.
E.g. cucurbits are very sensitive to chlorinated hydrocarbon group of insecticides,
 Copper ion is toxic to plants so high dose application of copper fungicide may cause injury
Sulphur toxicity in tropical areas
Black tip of Mango
Ozone phytotoxicity in musk
melon
PAN phytotoxicity on lettuce 2, 4-D damage on tomato
CLASSIFICATION OF PLANT DISEASES
BASED ON CAUSE OF DISEASE/ETIOLOGY:
A. INFECTIOUS/PARASITIC DISEASE
Fungi, bacteria, virus, viroid, phytoplasma, RLBs, nematodes, higher
parasitic plants etc.
Contagious, are transmitted from diseased to healthy plants via various
agencies.
B. NON-INFECTIOUS/NON-PARASITIC/PHYSIOLOGICAL/ABIOTIC DISEASE
nutritional deficiencies e.g. Khaira disease of rice due to Zn deficiency,
unfavourable environment e.g. frost injury, physiological wilt, etc.
BASED ON TYPE OF INFECTION:
A. LOCALIZED DISEASES:
These diseases are limited to a definite area of an organ or
part(s) of a plant.
Localized effect of pathogen
E.g. leaf spots and Anthracnoses caused by different fungi.
B. SYSTEMIC DISEASES:
In these diseases the pathogen spreads from a single infection
point so as to infect all or most of the host tissues.
 E.g. Fungal and bacterial wilt, Downy mildews caused by fungi;
mosaics and leaf curls caused by viruses.
Tikka disease of Ground nut (Cercospora
personata/arachidicola)
Tan spot of Wheat
(Pyrenophora tritici-repentis)
C. BASED ON NATURAL PERPETUATION AND MODE OF INFECTION
1. Soil borne diseases
 caused by pathogens which persist (survive) in the soil matrix and in residues on
the soil surface
 soil is the reservoir of primary inoculum of these pathogens
 E.g. Damping off of seedlings
2.Seed borne disease :
Seed-borne pathogens typically survive for a long period in or on contaminated or infected seed.
 be admixed with the seed during harvesting/threshing
(Concomitant contamination) e.g. sclerotia (Sclerotinia sclerotium) in sunflower
 externally seed borne pathogen : Covered smut of barley (Ustilago hordei), Anthracnose of Chilli (Colletotrichum
capsici)
 Internally seed borne: Loose smut of barley (Ustilago nuda) and wheat (Ustilago tritici), Soyabean mosaic virus,
 Both internally and externally seed borne. Black arm of Cotton (Xanthomonas malvacearum)
3.Air borne disease:
foliar pathogens causing foliar diseases.
In this case pathogen survives in weed hosts (alternate or collateral hosts) during off season and the wind-borne
inoculum of pathogen is carried to the crop plants and cause diseases in crops.
E.g. Wheat Rust (Puccinia sp.) , Brown spot of rice (H. oryzae or Bipolaris oryzae)
D. BASED ON SYMPTOMS
D. BASED ON
SYMPTOMS
Rusts
Smuts
Leaf spot
Septoria leafspot of tomato
(Septoria lycopersici)
Angular leafspot of beans
(Pseudocercospora griseola)
Black/Stem Rust
Puccinia graminis f.sp. tritici
Brown/Leaf Rust (P. recondita) Stripe/ Yellow rust (P. striiformis f.sp.
tritici)
Loose smut of Wheat (Ustilago tritici)
Rots
Blight
Canker
 Wilt
Buckeye rot of tomato (Phytophthora parasitica)
Foot rot of Papaya (Pythium
aphanidermatum)
Late blight of Potato (Phytophthora
infestans)
Citrus Canker (Xanthomonas axonopodis pv. citri)
Bacterial Wilt of Tomato
(Ralstonia solanacearum )
Browning of vascular tissues
Downy mildews
Powdery
mildew
Anthracnose
Die-back Downy mildew of Pumpkin
(Pseudoperonospora cubensis)
Powdery mildew of Pea
(Erysiphe pisi)
Powdery mildew of Grapes (Uncinula necator)
Bean anthracnose
(Colletorichum lindemuthianum)
Die back symptoms in Chilli anthracnose
(Colletotrichum capsici)
Blotch
Tumour/Gall
Atropy/Stunting/
Dwarfing
Shot holes
Purple Blotch of Onion (Alternaria porii)
Shot hole of Cherry
(Coccomyces hiemalis)
Crown Gall on apple (Overgrowth) Corn Stunt (Spiroplasma kunkelii)
Crown gall on peach
(Agrobacterium tumefaciens)
Mummification
Enation
Witches’ broom
Mummification of Peach (Monilinia fructicola) Enation (Pea enation mosaic virus)
Potato witches’ broom (Phytoplasma) Groundnut witches’ broom (Phytoplasma) Enation in cotton (Cotton leaf curl Virus)
Gummosis
Rosette
Mosaic
Scab Rosette (Groundnut rosette umbravirus) Potato scab (Streptomyces scabies) Apple scab (Venturia inaequalis)
Citrus Gummosis (Phytophthora nicotianae
var. parasitica) Bean common mosaic virus
Bean yellow mosaic virus
Damping off
Vein clearing
Vein banding
Epinasty
Damping off (Pythium, Rhizoctonia,
Phytophthora)
Vein clearing (Okra yellow vein mosaic)
Vein banding (Bean common mosaic virus) Epinasty in mustard (Beet curly top
virus)
Epinasty in tomato (due to exposure to
ethylene)
Ergot
Leaf Curl
Mold
Phyllody
Leaf gall
Tomato leaf curl Ergot of Bajra (Claviceps purpurea)
White mold of bean (Sclerotinia sclerotiorum) Sesamum Phyllody (Phytoplasma) Leaf gall
 Albication
 Chlorosis
Club root
Root knot
Rugosity
Broad bean stain virus in pea Chlorosis
Club root of crucifers (Plasmodiophora brassicae) Root knot (Meloidogyne)
Potato Virus Y (Rugosity)
E. BASED ON HOST PLANTS
• Cereal diseases
• Vegetable diseases
• Fruit diseases
• Forest diseases
• Ornamental diseases
F. BASED ON CROP
• Diseases of Wheat
• Diseases of maize etc
G. BASED ON ORGAN THEY ATTACK
• Root diseases
• Shoot diseases
• Fruit diseases
• Foliage diseases
Mango anthracnose
Colletotrichum gloeosporioides
Brown Spot of rice
(Bipolaris oryzae)
Northern Leaf blight of maize
(Exserohilum turcicum)
Gray leaf spot of Maize
(Cercospora zeae-maydis)
H. BASED ON OCCURRENCE AND DISTRIBUTION
A. ENDEMIC :
When a disease is more or less constantly prevalent from year to year in a moderate to
severe form in a particular country. E.g., Wart disease of potato (Synchytrium endobioticum)
is endemic to Darjeeling,
B. EPIDEMIC OR EPIPHYTOTIC:
A disease occurring periodically but in a severe form involving major area of the crop. it may
be constantly present in locality but assume severe form occasionally e.g. Rust, Late blight,
Mildews
C. SPORADIC:
Diseases which occur at very irregular interval and location in a moderate to severe form
e.g., leaf blights, wilt, Angular leaf spot of cotton(Pseudomonas lachrymans)
D. PANDEMIC:
Diseases occurring throughout the continent or sub-continent resulting in mass mortality
and devastating damage in short period of time e.g., Late blight of potato
BASED ON EPIDEMIOLOGY/PATHOGEN GENERATION
A. SIMPLE INTEREST/ MONOCYCLIC DISEASES
Those diseases the increase of which is analogous of increase
in money due to simple interest
Those diseases which have only generation in one cropping
season e.g. loose smut of wheat, vascular wilts, Black leg of
potato (Erwinia caratovora), Verticillium wilt, Cereal cyst
nematode
B. COMPOUND INTEREST/ POLYCYCLIC DISEASES
Those diseases which have more than one generation in a
cropping season. e.g. late blight of potato, Downy mildews,
Powdery mildews, Rusts, Aphid borne viruses.
C. POLYETIC DISEASES (MULTI-YEAR DISEASE)
These are also polycyclic diseases but they complete their
disease cycle in more than one year or over years e.g. Cedar
Apple Rust. Disease Progress Curve
Symptoms due to change in host plant
Hyperplasia: Increase cell division
(Increase in cell no.) plant overgrowth
Hypertrophy: Cell enlargement plant
overgrowth
 Gall: Swelling or overgrowth of plant
parts
Leaf Curl:Twisted leaves due to
overgrowth of tissue
Witches broom: Broom like clustering of
leafs
Hypoplasia:Decrease cell division
Hypotrophy: Decrease Cell
enlargement
Leaf curl of tomato
Crown Gall of Rose
Witches’ broom on woody plants
Symptoms due to visible pathogen
1) Mildew:
 Powdery mildew: Superficial growth giving
dusty or powdery appearance
 Downy mildew: Cottony downy growth like a
day old chicken
2) Rust: Spores breaking through the epidermis
giving rusty appearance
3) Smuts: Sooty or charcoal like powder usually
on floral parts
4) White blisters: Blister like pustules exposing
powdery white mass
Symptoms due to visible pathogen
5) Sclerotia: Compact mass of dormant mycelium (resting structure)
6) Scab: Rough or crust like lesion which are scabby
Symptoms due death of cells or tissues
1)Spot: Localized lesion on host surface (Cercospora
capsici)
2) Anthracnose: Necrotic and sunken ulcer like lesions
(Colletotrichum lindemuthianum)
3) Canker: Necrotic lesion sunken or raised beneath or
over the surface (Xanthomonas axonopodis pv. citri)
4) Blight: Rapid burning of leaves and other succulent
parts leading death (Late blight of Potato)
5) Damping off: Stem near the soil surface of
seedling becomes constricted and weak
and unable to bear load of upper parts
and topples down (Pythium)
6) Rots: Maceration and disintegration of tissue
Root rot (Rhizoctonia solani, Pythium, Phytophthora)
7) Shot-hole: A perforated appearance of a leaf as the
dead areas of local lesions drop out leaving a shot hole
(shot hole of Cherry-Coccomyces hiemalis )
Cercospora leaf spot
Anthracnose of Chilli
Late Blight of Potato
Citrus canker
Damping off of tomato
Papaya foot rot
Cherry shot hole
Some symptoms associated to virus infection
1) Stunting: Reduced growth
2) Local lesions: Necrotic lesion at the point of entry
3) Mosaic: Alternate patches of green, light green and yellow
4) Ringspot: Distinct chlorotic or necrotic ring
5) Rosette: Short branching habit
6) Enation: Over growth
7) Stem pitting: shrunken pits on the stem
Citrus Ring spot Virus
Rosette
Mosaic
Enation Citrus tristeza virus
Some symptoms associated to virus infection
8) Puckering:Distortion in shape of leaf
9) Vein banding: Chlorosis of interveinal space
10) Vein clearing: Chlorosis of vein
11) Shoe string : Excessive reduction of leaf
lamina a. Shoe string b. Ring Spot
(Papaya Ring spot Virus)
Shoe String
Puckering Vein Clearing Vein banding
Miscellaneous disease symptoms
Blast:tissues, young buds and fruits are killed rapidly
Blotch: irregular discolored area
Dieback: Progressive death of plant starting from tip
Wilting: Loss of turgidity of plant
Sooty mould : Dark coating on foliage by fungal hyphae
Chlorosis: yellowing of normal green tissue
Die back of Chilli Wilting
Neck Blast Leaf Blast
Nodal Blast Septoria leaf blotch Sooty mould of mango
IMPORTANCE OF FUNGI
A. Beneficial Effect
Decomposition of plant debris with the help of cellulase
Biocontrol agents. Trichoderma sp.
 Organic acid production- Gibberella fujikori
(Gibberillin)
Mushrooms are appreciated for nutritional and delicious
food value e.g. Agaricus, Pleurotus, Lentinula edodes
Use in genetic research E.g. Neurospora
Industrial use-value particularly in fermentation (Bread,
wines, Beers, cheese)
Source of medicine E.g. Penicillin from Penicillium
digitatum and P. crysogenus
Soil inhabitants such as Fusarium, Chaetomium,
Aspergillus, Mucor improve soil structure by formation of
soil aggregates
Entomogenous fungi helps in controlling insect pests. Eg.
Beauveria bassiana, Metarhizium anisopliae
HARMFUL EFFECTS OF FUNGI
Saprophytic fungi are responsible for destruction
of food, fabrics, leather and other good
manufactured for raw material
Many fungal group of mushroom are poisonous
and cause serious health hazards e.g. Coprinus
comatus, Amanita muscaria
Post harvest disease in citrus by Penicillium
digitatum
Member of Mucorales, Yeasts, Moniliales are
responsible for food spoilage
Green and blue mould of
orange
Amanita muscaria
Coprinus comatus
Peniciliium digitatum
GENERAL CHARACTERISTICS OF FUNGI
All are eukaryotic - Possess membrane-bound
nuclei (containing chromosomes) and a range
of membrane-bound cytoplasmic organelles
(e.g. mitochondria, vacuoles, endoplasmic
reticulum)
 Generally Extra cellular digestion is the way in
which fungi feeds
Most are filamentous - Composed of individual
microscopic filaments called hyphae, which
exhibit apical growth and which branch to form
a network of hyphae called a mycelium.
 some are unicellular - e.g. yeasts.
Protoplasm of a hypha or cell is surrounded by
a rigid cell wall - Composed primarily of chitin
and glucans, although the walls of some species
contain cellulose.
Many reproduce both sexually and asexually -
Both sexual and asexual reproduction often
result in the production of sexual and asexual
spores.
Their nuclei are typically haploid and hyphal compartments are
often multinucleate – Although the Oomycota and some yeast
possess diploid nuclei.
All are achlorophyllous - They lack chlorophyll pigments and are
incapable of photosynthesis.
All are chemoheterotrophic (chemo-organotrophic) - They utilize
pre-existing organic sources of carbon in their environment and the
energy from chemical reactions to synthesize the organic
compounds they require for growth and energy.
 Possess characteristic range of storage compounds - e.g.
trehalose, glycogen, sugar alcohols and lipids.
May be free-living or may form intimate relationships with other
organisms i.e. may be free living, parasitic or mutualistic
(symbiotic)
Most of the fungi grow well at 20 to 30*C
EUCARPIC Vs HOLOCARPIC THALLUS
Thallus/Thalli
The body of the fungus is called as 'thallus’.
Eucarpic thallus
The thallus is differentiated into vegetative part, which absorbs
nutrients, and a reproductive part, which forms reproductive structure.
Such thalli are called as Eucarpic. e.g. Pythium aphanidermatum.
Holocarpic thallus
The thallus does not show any differentiation on vegetative and
reproductive structure.
Such thalli are called as 'holocarpic' e.g. yeast, Synchytrium
endobioticum
HYPHAE (PL. HYPHA)
Hyphae is a tubular, transparent
filament, usually branched, composed of
an outer cell wall and a cavity (lumen)
lined or filled with protoplasm including
cytoplasm.
divided into compartments or cells by
cross walls called septa and are generally
called as septate
(with cross wall)-septate or coenocytic
(aseptate -without cross wall).
Hyphae of most of the fungi measures 5-
10 μm in diameter
DOLIPORE SEPTUM
Each septum is pierced by a narrow
septal pore.
The pore is surrounded by a barrel-
shaped thickening or septal swelling.
The septal pore is over arched with a
perforated cap (extension of
endoplasmic reticulum
MYCELIUM
• The hyphal mass or network of hyphae constituting the body (thallus) of the
fungus is called as mycelium.
• The mycelium of parasitic fungi grows on the surface of the host and spread
between the cells and it is called intercellular mycelium.
• The mycelium of parasitic fungi, which grows on the surface of the host and
penetrates into the host cells and is called intracellular mycelium.
HAUSTORIA???
HAUSTORIUM/HAUSTORIA
Haustoria (sing. haustorium; L. haustor =
drinker) are special knob-like or root like
hyphal structures or outgrowths of somatic
hyphae sent into the host cell to
absorb/derive nutrients.
The hyphae of obligate parasites of plants
like downy mildew, powdery mildew or
rust fungi, late blight fungus etc., produce
haustoria
Monokaryotic mycelium (uninucleate)
 Mycelium contains single nucleus that usually forms part of
haplophase in the life cycle of fungi.
Dikaryotic mycelium (binucleate)
 Mycelium contains pair of nuclei (dikaryon), which denotes
the diplophase in the life cycle of fungi.
Homokaryotic mycelium
 The mycelium contains genetically identical nuclei.
Heterokaryotic mycelium
 The mycelium contains nuclei of different genetic
constituents.
Multinucleate
 The fungal cell contains more than 2 nuclei.
Homothallism:
 The thalli are monoecious and both male and female sex
organs occur on the same thallus
Heterothallism:
 Thalli are dioecious and male and female sex-organs occur in
different thalli
SPECIALIZED SOMATIC STRUCTURES
Rhizoid
A rhizoid (Gr. rhiza = root + oeides = like)
is a short, root-like filamentous
outgrowth of the thallus
Rhizoid serves as anchoring or
attachment organ to the substratum and
also as an organ of absorption of
nutrients from substratum.
E.g. Rhizopus, Cladochytrium
APPRESSORIUM /APPRESSORIA
(L. apprimere = to press against) is a simple or
lobed or bulbous structure of hyphal or germ
tube and a pressing organ from which a minute
infection peg usually grow and enter the
epidermal cell of the host.
It helps germ tube or hypha to attach to the
surface of the host or substrates.
These appressoria are formed from germ
tubes of Uredinales (rust fungi), Erysiphales
(powdery mildew fungi) and other fungi in
their parasitic or saprophytic stages.
These are organ of attachment and anchorage
FUNGAL TISSUE (PLECTENCHYMA)
Plectenchyma ( Gr. Plekein= to weave +
encyma (infusion i.e. woven tissue)
A. Prosenchyma: Mycelium is present in form of
loosely woven tissues in which the
component hypha lie more or less parallel to
one another and their typically elongated
cells are distinguishable and the individuality
of the cells is not lost.
B. Pseudoparenchyma: consist of closely packed
more or less isodiametric or oval cells
resembling parenchyma of vascular plants.
Individuality of hyphae is lost
C. Pseudosclerenchyma: consists of closely
packed, thick walled and dark coloured cells.
AGGREGATION OF HYPHAE
A. MYCELIAL STRANDS
Mycelial strands are aggregates of parallel or
interwoven undifferentiated hyphae, which
adhere closely and are frequently
anastomosed or cemented together.
They are relatively loose compared to
rhizomorph.
E.g. (e.g. Sclerotium rolfsii growth on
culture medium)
ANASTOMOSIS
• involves fusion of hyphae of some species,
movement of one or more nuclei into one
or the other of the fused cells,
• and the establishment of a compatible
heterokaryotic state.
• Important phenomena for heterokaryosis
B. RHIZOMORPHS
Rhizomorph (Gr. rhiza=root + morphe =
shape) is the aggregation of highly
differentiated hyphae with a well defined
apical meristem, which are often darkly
pigmented.
Root like aggregations of somatic hyphae
E.g. Honey fungus/ Honey agric ,
Armillariella mellea
C. Stroma (Pl. stromata):
Compact somatic structure much like cushion or
mattress on which or in which fruiting bodies are
usually formed
E.g. various type of ascocarps, basidiocarps,
pycnidia, acervuli, sporodochia
D. Sclerotium (Pl. Sclerotia):
is a hard resting body formed by aggregation of
somatic hyphae into dense, rounded,
flattened, elongated or horn-shaped dark masses.
 are thick-walled resting structures, which contain
food reserves.
Sclerotia are hard structures resistant to
unfavourable physical and chemical conditions.
They may remain dormant for longer periods of
time, sometimes for several years and germinate
on the return of favourable conditions. Sclerotia of Rhizoctonia solani
Sclerotia of Sclerotinia
MYCORRHIZAE
• Mycorrhiza (pl. mycorrhizae; Gr. mykes =
mushroom + rhiza = root) is the symbiotic
association between higher plant roots and
fungal mycelia.
• Many plants in nature have mycorrhizal
associations.
REPRODUCTION IN FUNGI
Asexual/Vegetative
Reproduction
Sexual
Reproduction
1. Fragmentation
2. Fission
3. Budding
4. Production of asexual spores
(mitospores)
a. Sprangiospores
b. Conidia
c. Chlamydospores
1. Planogametic copulation
2. Gametangial contact
3. Gametangial copulation
4. Spermatization
5. Somatogamy
Asexual Reproduction
Fragmentation
The septate hyphae break up into their
component cell, and each fragment may
grow into new individuals under suitable
conditions.
They are known as Oidium (Pl. Oidia) or
arthrospores
They do not store reserve food and hence
cannot survive under unfavorable conditions.
 E.g. Erysiphe, Rhizopus
Fission (Transverse cell division)
 simple splitting of cells into two daughter
cells by constriction and formation of a cell
wall.
E.g Yeast (Schizosaccharomyces spp)
SEM of Erysiphe
(Oidia)
BUDDING
Production of a small outgrowth (bud) from a
parent cell
As the bud is formed, the nucleus of the
parent cell divides and one daughter nucleus
migrates into the bud.
The bud increases in size, while still attached
to the parent cell and eventually breaks off
and forms a new individual.
common in yeasts.(Saccharomyces sp. )
Spores formed by process of budding of
somatic cells or conidiospores are called
Blastospores ( E.g. Taphrina)
SEM of budding yeast
PRODUCTION OF ASEXUAL SPORES
A. SPORANGIOSPORES:
They are produced inside globose or
sac like structure known as
Sporangia.
 are of two kinds:
a. Motile (Planospores/zoospores)
E.g. Pythium, Phytophthora
b. non-motile (aplanospore)
E.g. Mucor, Rhizopus
The structure that bear sporangia is
known as Sporangiophore
CONIDIOSPORE/CONIDIUM (PL. CONIDIA)
Non motile asexual spore usually formed at
the tip or side of a Conidiophore
 May be borne singly or in chains or in
cluster.
They vary from
• unicellular (Penicillium, microconidia of
Fusarium, Colletotrichum)
• Bicellular (Diplodia, Lasiodiplodia)
• multicellular (Pestalotiopsis, Cercospora).
Common in Ascomycotina, Basidiomycotina
and Deuteromycotina
Conidia of Colletotrichum
Micro and macro-conidia Cercospora
CHLAMYDOSPORES
Chlamydospore (Gr. Chlamys =
mantle + spora = seed, spore) is a
thick walled asexual spore or
conidium that generally function as a
resting spore.
Terminal or intercalary segments or
mycelium may become packed with
food reserves and develop thick
walls.
The walls may be colourless or
pigmented with dark melanin
pigment.
E.g. Mucor racemosus, Saprolegnia,
Protomyces, Fusarium
Chlamydospore of
Fusarium
Chlamydospore of
Protomyces
Sexual Reproduction in Fungi
Three distinct phases of Sexual
Reproduction
1) Plasmogamy (fusion of cytoplasm)
2) Karyogamy (fusion of nuclei)
3) Karyokinesis/Meiosis
(haploidisation)
PLANOGAMETIC COPULATION
Isogamy:
 Morphologically similar but
compatible mating type of gametes
unite to form a motile zygote. e.g.
Synchytrium.
Anisogamy:
 involves union of one larger gamete
with another smaller gamete.
Heterogamy:
 In this type, a non-motile female
gamete (oosphere) lying on oogonium
is fertilized by a motile male gamete. Isogamy Anisogamy Heterogamy
GAMENTANGIAL CONTACT
The male gametangia (antheridium) and
the female gametangia (oogonium) come
in contact
one or more nuclei from the male
gamete enter the female gamete through
a pore/ fertilization tube
In no case, the gametangia actually fuse
or lose their identify during the sexual
act.
 E.g.Pythium, Phytophthora
GAMETANGIAL COPULATION
This is a process of fusion of entire
contents of the two mating gametangia.
A. Mixing of entire protoplasm of male and female
gametangia
 Two gametangia meet and their entire contents fuse in
the female gametangium leading to formation of a
zygote.
 The zygote forms a resting sporangium.
 e.g. Aquatic fungi (Chytridiomycetes).
B. Isogamous copulation:
 Two morphologically similar gametangial hyphae come in
contact, the wall at the point of contact dissolves and
the contents mix in the cell thus formed.
 This results in the formation of Zygospore.
 E.g. Mucor, Rhizopus, Phycomyces.
SPERMATIZATION
• Some fungi like Puccinia (Rust) bear
numerous, minute, uninucleate, spore-
like male structure called spermatia
• These are carried to female
gametangial specialized receptive
hyphae to which it is attached
(Trichogyne)
• Pore develops and the content of
spermatia pass on to the receptive
hyphae
SOMATOGAMY
somatic cells function as gametes
hypha anastomose and the nuclei of
opposite mating type are brought together
in one cell.
The post-fertilization changes result in the
production of a fruiting body which is called
ascocarp in Ascomycetes and basidiocarp in
Basidiomycetes.
 common in members of Ascomycotina and
Basidiomycotina.
TYPES OF FRUITING BODIES
ASEXUAL FRUITING BODIES
Synemma (PL. Synemmata) or
Coremium
Sporodochium (Pl.
Sporodochia)
Pycnidium (Pl. Pycnidia)
Acervulus (Pl. Acervuli)
SEXUAL FRUITING BODIES
A. ASCOCARP
Cleistothecium
(Pl.Cleistothecia)
Perithecium (Pl. Perithecia)
Apothecium (Pl. Apothecia)
Ascostroma(Pl.Ascostromata) or
Pseudothecium(Pl.Pseudothecia)
B. BASIDIOCARP
ASEXUAL FRUITING BODIES
SYNEMMA:
A group of conidiophore held together
and forming an elongated spore
bearing structure
E.g. Graphium, Stilbella, Isariopsis
(Stilbellaceae)
SPORODOCHIUM/SPORODOCHIA:
An asexual fruiting structure consisting of
cluster of conidiophores woven together
on a mass of hyphae
E.g. Fusarium, Myrothecium, Tubercularium
PYCNIDIUM/PYCNIDIA:
 A flask shaped or spherical asexual
fruiting body containing conidia and
conidiophores
E.g. Ascochyta, Septoria, Diplodia,
Phoma
ACERVULUS/ACERVULI
• Flat or saucer or disc shaped bed of
short of conidiophores that grow side
by side within the host tissue and
beneath the epidermis or cuticle
• E.g. Colletotrichum, Pestalotia,
Sphaceloma
SEXUAL FRUITING BODIES
CLEISTOTHECIA/CLEISTOTHECIUM
Globular or spherical completely
closed ascocarp containing asci
and ascospores
Asci are irregularly arranged
are provided with different kind
of appendages
E.g. Erysiphe, Talaromyces,
Eurotium
A. ASCOCARP
PERITHECIUM/PERITHECIA
A flask shaped ascocarp having an
opening or pore (ostiole) and
paraphyses in the neck
Asci are arranged in a hymenium
(fertile) layer or parallel series or a
basal tuft
E.g. Claviceps, Venturia inequalis
APOTHECIUM/APOTHECIA
An open cup or saucer shaped
ascocarp which bears asci and
ascocarp
E.g. Sclerotinia, Cup fungi
(Pyronema, Ascobolus, Peziza,
Morchella)
ASCOSTROMA/PSEUDOTHECIUM
 just like perithecium ( flask-
shaped ascocarp provided with an
ostiole)
 asci are directly formed in a cavity
(locule) within the stroma.
The ascus is bitunicate (ascus wall
is double)
E.g. Cochliobolus, Pyrenophora,
Ophiobolus, Pleospora,
BASIDIOCARP
 Sexual fruiting body that consists
basidium and basidiospores
• Basidia are borne on the under
surface of fruit body.
• Basidia bear basidiospores
exogenously usually on projections
called sterigmata.
• Most fungi in Basidiomycotina
except smuts (Ustilaginales) and
rusts (Uredinales) form
basidiocarps.
ASEXUAL SPORES
(Mitospores)
Sporangispores
Conidium
Chlamydospores
Blastospores
Arthrospores (Oidia)
 Oospore
 Zygospore
 Ascospores
 Basidiospores
SEXUAL SPORES
(Meiospores)
OOSPORE
 Sexual spore produced by union of two
morphologically different gamentangia
(gamentangial contact)
Found in member of Oomycetes
E.g. Pythium, Phytophthora
ZYGOSPORE
Sexual spore formed by fusion of two
morphologically similar gametes
(gametangial copulation)
Are formed in members of Zygomycetes
E.g. Rhizopus, Mucor
ASCOSPORE:
Sexual spores produced in members of
Ascomycotina
Produced inside an ascus
E.g. Eurotium, Claviceps
BASIDIOSPORE:
Sexual spores produced in members of
Basidiomycotina
Borne on basidium
E.g. Agaricus, Pleurotus
CLASSIFICATION OF FUNGI (AINSWORTH, 1973)
MYCOTA (FUNGI)
MYXOMYCOTA (SLIME MOLD)
(Plasmodium or
Pseudoplasmodium present)
EUMYCOTA (TRUE FUNGI)
(Plamodium/Pseudoplasmodium absent,
assimilative phase, typically filamentous)
KINGDOM
DIVISION
SUBDIVISION
CLASS
ORDER
FAMILY
MASTIGOMYCOTINA
Motile cells (zoospores
present; perfect state
spores typically oospores
ZYGOMYCOTINA
Motile cells absent,
perfect state spores,
zygospores
ASCOMYCOTINA
Motile cells absent
perfect state spore
ascospore
BASIDIOMYCOTINA
Motile cells absent,
perfect state spores
basidiospores
DEUTEROMYCOTINA
Motile cells absent, perfect
state absent
-MYCETES
-ALES
- ACEAE
GENUS
SPECIES
Sub-division Mastigomycotina Zygomycotina Ascomycotina Basidiomycotina Deuteromycotina
Hyphae Aseptate
(coenocytic)
Aseptate Septate Septate Septate
Cell wall Cellulose +
Glucans
Cellulose-
chitosan
Chitin and
Glucans
Chitin Chitin
Asexual spore Motile
(zoospores/Plano
spores)
Aplanospore
(non-motile
sporangiospore)
All asexual spore
except zoospore
and aplanospore
(Conidia,
Blastospores,
Arthrospores)
Blastospores and
Chlamydospores
All asexual spore
except zoospore
and aplanospore
Asexual fruiting
body
Absent Absent Present Absent Present
Sexual spores Oospore Zygospore Ascospore Basidiospore Absent
Sexual fruiting
body
Absent Absent Ascocarp Basidiocarp Absent
MYXOMYCOTA
MYXOMYCETES
(Plasmodium saprobic or free
living)
PLASMODIOPHOROMYCETES
(Plasmodium parasitic within
cells of the host plant)
PLASMODIOPHORALES
PLASMODIOPHORACEAE
E.g. Plasmodiophora,
Spongospora, Polymyxa
CLASS
ORDER
FAMILY
DIVISION
EUMYCOTA
MASTIGOMYCOTINA
Chytridiomycetes
Zoospore posteriorly
uniflagellate, whiplash type
Hyphochytridiomycetes
Zoospores anteriorly uniflagellate,
tinsel type
Oomycetes
Zoospores biflagellate,
posterior whiplash,
anterior tinsel;
cellulosic cell wall
Chytridiales
Synchytriaceae
(Synchytrium)
Saprolegniales Leptomitales Lagenidiales Peronosporales
Pythiaceae
(Pythium,
Phytophthora )
Albuginaceae
(Albugo)
Peronosporaceae
(Peronospora, Plasmopara,
Pseudoperonospora,
Sclerospora, Bremia, etc.)
ASCOMYCOTINA
Hemiascomycetes
(Ascocarps and
ascogenous hyphae
lacking; thallus mycelial
or yeast like)
Plectomycetes
(Asci scattered
irregularly in
Cleistothecium
Loculoascomycetes
Ascostroma
(Pseudothecium);
bitunicate ascus
Discomycetes
Ascocarp:
Apothecium
Pyrenomycetes
Asci arranged in
perithecium; not a
exoparasite
Endomycetales Protomycetales Taphrinales
Spermopthoraceae
(Spermopthora,
Nematospora)
Protomycetaceae
(Protomyces)
Taphrinaceae
(Taphrina)
Erysiphales Sphaeriales
Erysiphaceae
(Erysiphe,
Uncinula,
Podosphaera, )
Clavicipitaceae
(Claviceps)
Helotiales
Sclerotiniaceae
(Sclerotinia,
Monilinia)
Laboulbeniomycetes
Asci arranged in
perithecia;
exoparasite of
arthropods
ZYGOMYCOTINA
Zygomycetes
(Saprobic or if parasitic
having mycelium
immersed in host tissue)
Trichomycetes
(Entomogenous fungi and
associated with arthropods and
attached to the digestive tract of
arthropods by a holdfast and not
immersed in host tissue)
Mucorales
Mucoraceae
(Rhizopus, Mucor)
BASIDIOMYCOTINA
Teliomycetes
Basidiocarp lacking and
replaced by teliospores;
parasitic on vascular plants
Hymenomycetes
(Basidiocarp well
developed)
Gasteromycetes (No
plant pathogen)
Uredinales
(Rust Fungi)
Ustilaginales
(Smut Fungi)
Pucciniaceae
(Puccinia,
Hemileia,
Uromyces,
Phragmidium)
Melampsoraceae
(Melampsora,
Phakopsora)
Ustilaginaceae
(Smut fungi)
(Ustilago,
Tolyposporium,
Sphacelotheca)
Tilletiaceae
(Bunt fungi)
(Tilletia,
Neovossia,
Urocystis)
DEUTEROMYCOTINA
Hyphomycetes
(mycelia sterile or sporephores
aggregated but not in pycnidia or
acervuli)
Coelomycetes
(sporophore aggregated in
acervuli or pycnidia)
Agonomycetales
(Mycelia Sterilia/zno
spore produced)
(Rhizoctonia,
Sclerotium)
Moniliales
Moniliaceae
(Monilia,
Aspergillus,
Penicillium,
Trichoderma,
Verticillium)
Dematiaceae
(Alternaria,
Helminthosporium,
Cercospora,
Stemphylium
Pyricularia,
Curvularia, Botrytis)
Stillbellaceae
(Isariopsis,
Graphium,
Stilbella)
Tuberculariaceae
(Fusarium,
Myrothecium,
Tubercularium)
Melanconiales
(conidia in acervuli)
Sphaeropsidales
(Conidia in
pycnidia)
Melanconiaceae
(Colletotrichum,
Pestalotia,
Marssonina,
Cylindrosporium)
Sphaeropsidaceae
(Ascochyta, Diplodia,
Macrophoma,
Phoma, Septoria,
Phomopsis)
Blastomycetes
(budding yeast like
with or without
pseudomycelium; true
mycelium lacking)
ASPERGILLUS
Colonies are usually fast growing,
white, yellow, yellow-brown, brown
to black or shades of green, mostly
consisting of a dense felt of erect
conidiophores.
Conidiophores terminate in a vesicle
covered with either a single
palisade-like layer of phialides
Conidia are one-celled, smooth or
rough-walled, hyaline or pigmented,
are produced in long dry chains
PENICILLIUM
 Phialides brush like; upright –Penicillium
 Colonies are usually fast growing, in
shades of green, sometimes white, mostly
consisting of a dense felt of
conidiophores.
 Microscopically, chains of single-celled
conidia are produced in basipetal
succession from a specialised
conidiogenous cell called a phialide.
TRICHODERMA
Colonies are fast growing, at first white and
downy, later developing yellowish-green to deep
green
Conidiophores are repeatedly branched,
irregularly verticillate, bearing clusters of
divergent, often irregularly bent, flask-shaped
phialides.
Conidia are mostly green, sometimes hyaline,
with smooth or rough walls and are formed in
slimy conidial heads (gloiospora) clustered at the
tips of the phialides.
RHIZOPUS
 The genus Rhizopus is characterised by
the presence of stolons and pigmented
rhizoids, the formation of
sporangiophores, singly or in groups
from nodes directly above the rhizoids,
and apophysate, columellate,
multispored, generally globose
sporangia.
 After spore release the apophyses and
columella often collapse to form an
umbrella-like structure.
 Sporangiospores are globose to ovoid,
one-celled, hyaline to brown and
striate in many species.
MUCOR
 Sporangiophores are erect, simple or branched,
forming large (60-300 µm in diameter), terminal,
globose to spherical, multispored sporangia,
without apophyses and with well-developed
subtending columellae.
 Sporangiospores are hyaline, grey or brownish,
globose to ellipsoidal, and smooth-walled or
finely ornamented
Thallus is plasmodium
Plasmodium is holocarpic
Zoospore are anteriorly biflagellate,
heterokont and uninucleate
Flagella are of whiplash type
Resting spores occur singly or held
together in groups-cystosori
Obligate parasite
Plasmodiophora brassicae (Club root
of Crucifers)
PLASMODIOPHORA
Kingdom: Mycota
Division: Myxomycota
Order: Plasmodiophorales
Family: Plasmodiophoraceace
Genus: Plasmodiophora
SPONGOSPORA
Cystosorus sponge like
 Obligate parasite
 Heterokont zoospore
 Tuber infection near to the eyes
 Secondary zoospore of similar size
 Resting spores on spongy balls
 Sexual reproduction via isogamy
and turns resting spore
Kingdom: Mycota
Division: Myxomycota
Order: Plasmodiophorales
Family: Plasmodiophoraceace
Genus: Plasmodiophora
EUMYCOTA
MASTIGOMYCOTINA
Chytridiomycetes
Zoospore posteriorly
uniflagellate, whiplash type
Hyphochytridiomycetes
Zoospores anteriorly uniflagellate,
tinsel type
Oomycetes
Zoospores biflagellate,
posterior whiplash,
anterior tinsel;
cellulosic cell wall
Chytridiales
Synchytriaceae
(Synchytrium)
Saprolegniales Leptomitales Lagenidiales Peronosporales
Pythiaceae
(Pythium,
Phytophthora )
Albuginaceae
(Albugo)
Peronosporaceae
(Peronospora, Plasmopara,
Pseudoperonsopora,
Sclerospora, Bremia, etc.)
SYNCHYTRIUM
Obligate, holocarpic, endobiotic parasite
 long cycled chytrid
Unicellular thallus
Does not develop any mycelium through out
its life cycle
Thin walled summer sporangia and resting
spores are formed
Sporangia produce zoospores
E.g. Synchytrium endobioticum (Potato
wart)
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Chytridiomycetes
Order: Chytridiales
Family: Synchytriaceae
Genus: Synchytrium
Mature sporangia
PYTHIUM
Facultative parasite and mostly
homothallic
Are common as soil inhabitants
Mycelium is hyaline coenocytic ,
inter or intracellular
Sporangia are filamentous or oval or
globose which arise on unspecialized
branches.
Zoospore formation occur in
spherical vesicle and liberated after
burst
Zoospores are reniform and laterally
biflagellate
Oospores are colourless,
unornamented and often plerotic
Cause damping off of seedling
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Pythiaceae
Genus: Pythium
Introductory Plant Pathology Class Slides.pdf
PHYTOPHTHORA
• Mycelium endophytic, coenocytic,
hyaline, branched and inter-cellular
• Haustoria club shaped
• Sporangiophore easily distinguishable
from somatic hypha
• Sporangiophore indeterminate,
branched , hyaline
• Renewed growth of sporangiophore
give a sympodial shape
• Sporangia are lemon shaped with
distinct papilla at the apex
• Zoospores are reniform and
biflagellate. (anterior tinsel and
posterior whiplash)
• Zoospore formation occurs in the
sporangium itself
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Pythiaceae
Genus: Phytophthora
PYTHIUM Vs PHYTOPHTHORA
PYTHIUM PHYTOPHTHORA
Sporangia are produced on somatic hyphae
indistinguishable from the other hyphae
Sporangia are produced on special aerial reproductive hyphae
called sporangiophore
Global to oval sporangia either terminal or
intercalary
The papillate lemon shaped sporangia always terminal in
origin but subsequently shifted to the side
Differentiation of zoospore take place in vesicle.
They are liberated by sudden bursting of vesicle wall
Zoospore are differentiated in sporangium and liberated by
bursting of special papilla. No vesicle are formed
Haustoria absent Haustoria present
Germ tube enters the host tissue through stomata or
by puncturing of epidermal wall
Germ tube enters the host through epidermal cells by
infection peg that grows from appresorium
ALBUGO
Obligate parasite
Thallus is eucarpic and mycelial
Mycelium is inter cellular with coenocytic
hypha
Haustoria are knob-like or globular
Sporangiophore is club-shaped, short, erect
giving rise to chains of spherical sporangia
in basipetal succession
Sporangia are globose and germinate by
producing biflagellate zoospores
Albugo candida (White Blister/Rust of
Crucifer)
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Albuginaceae
Genus: Albugo
PLASMOPARA
Obligate parasite
Sporangiophore hyaline, intercellular
with branches at right angle to the axis
and irregularly spaced
Sterigmata are blunt with single
sporangium at its tip
Sporangia are elliptical, hyaline and
germinate to produce egg shaped zoo
spores
E.g. Plasmopara viticola (DM of Grapes)
Key feature of Family: Peronosporaceae
 Mycelium is coenocytic and inter-cellular
 Sporangiophore of determinate growth and
emerge singly or in tuft, thorough the stomata
on the lower surface of leaves
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Peronosporaceae
Genus: Plasmopara
SCLEROSPORA
Sporangiospore are stout with heavy
branches clustered at the apex and
dichotomously branched
Sporangia may be papillate or non-
papillate and germinate by forming
zoospore
Oospore smooth with thick walls and
plerotic.
E.g. Sclerospora philippinensis, S.
sacchari, S. maydis, S. sorghi (DM of
Maize)
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Peronosporaceae
Genus: Sclerospora
PERONOSPORA
Sporangiophore hyaline, aseptate and
dichotomously branched at acute angle
The terminal branches known as
sterigmata are sharply pointed
Sporangia germinate directly through
germtube i.e. zoospores are not formed
Oospore is yellow green in colour and its
wall is very tough with reticulations.
Kingdom: Mycota
Division: Eumycota
Subdivision: Mastigomycotina
Class: Oomycetes
Order: Peronosporales
Family: Peronosporaceae
Genus: Peronospora
ASCOMYCOTINA
Hemiascomycetes
(Ascocarps and ascogenous
hyphae lacking)
Plectomycetes
Asci scattered
irregularly in
Cleistothecium
Loculoascomycetes
Ascostroma; bitunicate
ascus
Discomycetes
Ascocarp: Apothecium
Pyrenomycetes
Asci arranged in
perithecium; not a
exoparasite
Endomycetales Protomycetales Taphrinales
Spermopthoraceae
(Spermopthora)
Protomycetaceae
(Protomyces)
Taphrinaceae
(Taphrina)
Erysiphales Sphaeriales
Erysiphacea
e
(Erysiphe,
Uncinula,
Podosphaera
, etc.)
Clavicipitacea
e
(Claviceps)
Helotiales
Sclerotiniaceae
(Sclerotinia,
Monilinia)
Laboulbeniomycetes
Asci arranged in
perithecia;
exoparasite
TAPHRINA
True endoparasite strictly confined to definite
host
Ascus not formed in a synascus
Asci arise from binucleate “ Ascogenous cells”
Asci lie in a palisade like layer parallel to one
another but without enclosing sheath
Parasitic on higher plants causing galls and
deformation
Mycelium is septate constituting typically of
binucleate cells, may ne intercellular or sub-
cuticular
Asexual reproduction by budding
E.g. Taphrina deformans (Peach Leaf curl)
Kingdom: Mycota
Division: Eumycota
Subdivision: Ascomycotina
Class: Hemiascomyctes
Order: Taphrinales
Family: Taphrinaceae
Genus: Taphrina
PROTOMYCES
• Ascospore formed in a spore sac- synascus
• Parasitic on higher plants causing lesion and
galls.
• Mycelium is filamentous and septate
• Diploid mycelium spreads intercellularly in the
host and produces thick walled resting spores
which germinate and form a vesicle called
synascus
• E.g. Protomyces macrosporus (Stem Gall of
coriander)
Ascogenous cell of
Protomyces
Stem gall of coriander
Kingdom: Mycota
Division: Eumycota
Subdivision: Ascomycotina
Class: Hemiascomyctes
Order: Protomycetales
Family: Protomycetaceae
Genus: Protomyces
ERYSIPHE
• Obligate parasite
• Mycelium is hyaline and mostly
ectophytic/superficial
• Have globular to pyriform haustoria
• Asexual reproduction takes place through
conidia on condiophores
• Sexual reproduction through ascospores in
ascus in enclosed ascocarp (Cleistothecia)
• Asci are persistent, globose to pyriform
and explodes at the time of release of
ascospore
• Cleistothecia contains more than one ascus
with myceloid/simple appendages
Kingdom: Mycota
Division: Eumycota
Subdivision: Ascomycotina
Class: Pyrenomycetes
Order: Erysiphales
Family: Erysiphaceae
Genus: Erysiphe
CLAVICEPS
Intercellular, hyaline and septate mycelium
Perithecia are deeply immersed in stroma which
develops an apical head on an erect stalk arising
from dark colored sclerotium
It has three stages:
1. Sphacelia stage: bears apical hyaline aseptate,
oblong-oval conidia in succession. They are embedded
in sticky fluid known as honey dew
2. Sclerotial stage: hard purple or brown coloured
slightly curved like horn sclerotia replace the ovary
3. Perithecial stage: Sclerotium on germination
produces several columnar structures( stalks/stipes).
On stipes, rugh, rounded orange or pink coloured
small perithecial stroma are produced
Hard sclerotium yields an alkaloid known as ergotin
(ergotism)
Kingdom: Mycota
Division: Eumycota
Subdivision: Ascomycotina
Class: Pyrenomycetes
Order: Sphaeriales
Family: Claviciptiaceae
Genus: Claviceps
SCLEROTINIA
Cup shaped apothecia which are usually yellowish
brown
Asci contains 8 ascospores
Ascospores are hyaline one celled and ovate
Apothecia arise from a seed like sclerotium formed
in host tissue
Mycelium is septate, cottony, white and turn
brown with age
Sclerotia are brown to black, spherical to irregular,
smooth/wrinkled
Kingdom: Mycota
Division: Eumycota
Subdivision: Ascomycotina
Class: Discomycetes
Order: Helotiales
Family: Sclerotiniaceae
Genus: Sclerotinia
BASIDIOMYCOTINA
Teliomycetes
Basidiocarp lacking and
replaced by teliospores;
parasitic on vascular
plants
Hymenomycetes Gasteromycetes (No plant
pathogen)
Uredinales (Rust
Fungi)
Ustilaginales
(Smut Fungi)
Pucciniaceae
(Puccinia, Hemileia,
Uromyces)
Melampsoraceae
(Melampsora,
Phakopsora)
Ustilaginaceae
(Ustilago,
Tolyposporium)
Tilletiaceae
(Tilletia,
Neovossia)
PUCCINIA
Some are autoecious (P. melanocephala-Brown rust
of sugarcane); some are heterocious, macrocyclic
which need more than one host to complete their
life cycle.
Important species: P. graminis, P. recondita,
P.striifromis
Pedicillate or stalked two celled teliospore
Promycelium is septate
Urediospore borne singly, echinulate
Polymorphic fungus: 5 different type of spores
Stage O- Pycniospore
Stage I- Aeciospore
Stage II- Urediospore
Stage III- Teliospore
Stage IV-Basidiospore
Kingdom: Mycota
Division: Eumycota
Subdivision: Basidiomycotina
Class: Teliomycetes
Order: Uredinales
Family: Pucciniaceae
Genus: Puccinia
Introductory Plant Pathology Class Slides.pdf
MELAMPSORA
Mycelium is inter cellular, septate, branched and
dikaryotic
Teliospores are sessile, cylindrical, one celled
reddish brown in colour and are borne in crusts
of laterally arranged adherent spores
Uredospores are ellipsoidal or obovoidal and
echinulate. Hyaline, capitate paraphyses are
abundant in the uredia
Kingdom: Mycota
Division: Eumycota
Subdivision: Basidiomycotina
Class: Teliomycetes
Order: Uredinales
Family: Melampsoraceae
Genus: Melampsora
UROMYCES
An autoceous (U. fabae)/heteroecious rust (U.
pisi)
Teliospores are brown, single celled with one
apical germ pore, binucleate and thickened at
the apex.
Urediospores are round to ovate, light brown,
echinulate with 3-4 equatorial germ tube
Teliospore
Urediospore
Kingdom: Mycota
Division: Eumycota
Subdivision: Basidiomycotina
Class: Teliomycetes
Order: Uredinales
Family: Pucciniaceae
Genus: Uromyces
USTILAGO
Teliospores are round or semi round, yellowish
brown to olivaceous brown with one side
lighter in colour covered with minute spikes
The mycelia of Ustilago has two distinct phase
Primary mycelia which is hyaline, slender,
septate with single haploid nucleus in each cell
and formed by germination of Basidiospores
Secondary mycelia which is formed by primary
mycelia by diploidisaton
E.g. U. tritici (Loose smut of wheat)
Kingdom: Mycota
Division: Eumycota
Subdivision: Basidiomycotina
Class: Teliomycetes
Order: Ustilaginales
Family: Ustilaginaceae
Genus: Ustilago
TILLETIA
Teliospore produced singly, medium to large
sized usually sculptured, rarely smooth,
commonly encased in a hyaline gelatinous
sheath.
Teliospores germinate by the means of
continuous promycelium, terminally bearing
basidiospores (6-16) which usually copulate in
situ, giving rise to secondary sporidia.
Tilletia differ from Ustilago in the method of
teliospore germination . Promycelium remains
aseptate and 4 basidiospores are formed on the
promycelium .
Kingdom: Mycota
Division: Eumycota
Subdivision: Basidiomycotina
Class: Teliomycetes
Order: Ustilaginales
Family: Tilletiaceae
Genus: Tilletia
DEUTEROMYCOTINA
Hyphomycetes Coelomycetes
Agonomycetales
(Mycelia Sterilia)
(Rhizoctonia,
Sclerotium)
Moniliales
Moniliaceae
(Monilia,
Aspergillus,
Penicillium)
Dematiaceae
(Alternaria,
Helminthosporium,
Cercospora,
Pyricularia,
Curvularia)
Stillbellaceae
(Isariopsis,
Graphium,
Stilbella)
Tuberculariaceae
(Fusarium,
Myrothecium,
Tubercularium)
Melanconiales
(conidia in acervuli)
Sphaeropsidales
(Conidia in
pycnidia)
Melanconiaceae
(Colletotrichum,
Pestalotia, Marssonina,
Cylindrosporium)
Sphaeropsidaceae
(Ascochyta,
Diplodia,
Macrophoma,
Phoma)
HELMINTHOSPORIUM
Grow both inter cellularly and intracellularly
The hyphae are typically dark bearing conidia
on simple erect, septate, conidiophore
The conidia are obclavate, brown, thick
walled with 8-10 transverse septa and a basal
scar indicating the point of attachment on the
conidiophore
Conidiophores are determinate, ceasing
growth with the production of the apical
conidia , relatively short and simple of if,
sparingly brancehed, the branching is not
dichotomous
E.g. Helminthsporium graminearum (Stripe
disease of barley ), H. oryzae (Brown spot of
rice), H. maydis (Southern leaf blight of
maize), H. turcicum (Northern leaf blight of
maize)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Moniliales
Family: Dematiaceae
Genus: Helminthosporium
PYRICULARIA
Perfect state: Magnoporthe grisea
Conidiophore are simple, erect, septate and
hyaline or grey
Hyaline or pale grey, pyriform/pear shaped
conidia produced singly at the tip of the
conidiophore and it successive growing points.
Sympodial branching habit
 Mostly two septa and three cells in conidia
Produces pyricularin
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Moniliales
Family: Dematiaceae
Genus: Pyricularia
Introductory Plant Pathology Class Slides.pdf
RHIZOCTONIA
Mostly soil inhabitants
Sclerotia formed of loosely woven hyphae; irregular
in shape but of uniform texture brown or black
Under suitable conditions they cause diseases like
damping off and root rots.
The cells of the hyphae are barrel shaped,
anastomosing frequently, branching more or less at
right angles, and pale brown to brown in colour.
(Constriction near branching)
 Rhizoctonia bataticola (damping off, Dry root rot
of Pulse, cotton, etc.) (Pycnidial stage-
Macrophomina phaseoli)
Rhizoctonia solani (Sheath blight of cereals) –
Thanatephorus cucumeris (Teleomorph)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Agonomycetales
Family: Agonomycetaceae
Genus: Rhizoctonia
SCLEROTIUM
characterized by hard, brown to black, fairly
large sclerotia with pseudoparenchymatous rind.
These are produced on sterile, cotton, white
mycelium provided with clamp connections.
The perfect states of Sclerotium are Pellicularia
(Hymenomycetes)
Sclerotium cepivorum -White rot of onion
S. oryzae-Stem rot of rice (Perfect state:
Magnaporthe salvinii, Conidial state: Nakataea
sigmoidea)
S. rolfsii - Root rot of soybean, black pepper
groundnut, cotton, cabbage tomato etc. (Perfect
State: Corticium rolfsii(syn. Pellicularia rolfsii)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Agonomycetales
Family: Agonomycetaceae
Genus: Sclerotium
COLLETOTRICHUM
Perfect stage: Glomerella
Acervuli subcuticular, subepidermal or
peridermal, hyaline to dark brown, thin or
thick walled, dehiscence irregular
Setae are brown, smooth, septate, acutely
pointed at the apex
Conidiophore simple of branched only at the
base, aseptate or septate, hyaline to brown
Conidia hyaline, aseptate, straight to falcate,
smooth, thin-walled, sometimes guttulate
E.g Bean anthracnose (C. lindemuthianum),
Red rot of Sugarcane (C. falcatum) Mago
anthracnose (C. gloesporiodes)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Coelomycetes
Order: Melanconiales
Family: Melanconiaceae
Genus: Colletotrichum
ALTERNARIA
• Mycelium is intercellular but later becomes
intracellular
• Conidiophore are pale yellow to dark
brown, simple or irregularly and loosely
branched bearing conidia at the apex
• Conidia are dark brown, muriform typically
obclavate with distinct oval body and a
beak
• Conidia may have longitudinal, transverse
or oblique septa
• Produce Alternarin
• E.g. Early blight of Potato (A. solani), Leaf
spot of Crucifers (A. brassicicola), A.
triticina (Alternaria blight of wheat).
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Moniliales
Family: Dematiaceae
Genus: Alternaria
CERCOSPORA
Perfect stage: Mycosphaerella
Conidiophores are septate and dark coloured
Conidia are long, slender, narrow, tapering
and contains many transverse septa
Conidia develop sympodially on clustered
dark conidiphore
Conidia leave scar at the place of
attachment
Produce cercosporin
E.g. C. capsici (Cercospora leaf spot of
Chilli)
C. personata and C. arachidicola (Tikka
disease of Groundnut)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Moniliales
Family: Dematiaceae
Genus: Cercospora
FUSARIUM
Mycelium is branched, septate and hyaline
Reproduces asexually by three kinds of spores viz.,
macroconidia, microconidia and chlamydospores
Macroconidia are sickle shaped with well marked
marked foot cells at the attachment end of spore
Microconidia are small, usually unicellular
spherical or oval bodies
Chlamydospores are round or oval thick walled
terminal or intercalary cells of old hyphae. They
develop singly or in short chains
E.g. Fusarium oxysporum f.sp. ciceri (Wilt of
Chickpea)
Kingdom: Mycota
Division: Eumycota
Subdivision: Deuteromycotina
Class: Hyphomycetes
Order: Moniliales
Family: Tuberculariaceae
Genus: Fusarium
MORPHOLOGY OF BACTERIA
Surface adherents: Flagella and Pilli
Capsule: protecting layer
Cell wall: made of mucopeptide (murein)
Cytoplasm: dense and contains granules of glycogen, proteins ,
fats but lack mitochondria and endoplasmic reticulum
Ribosome: 70 S
Mesosome: Energy production (respiration), DNA replication, cell
division, nitrogen fixation and endo-sporulation
Most of the plant pathogenic bacteria are gram negative except
Streptomyces (Gram +ve) and Clavibacter (Gram +ve)
SHAPE OF BACTERIA
1. Rod shaped/Bacilliform: Most of the plant pathogenic bacteria are rod
shaped except Streptomyces (filamentous) and Cornyebacterium (Club-
shaped)
2. Spherical: Coccus, Diplococus, Streptococcus, Tetracoccus,
Staphylococcus
3. Helical: a. Spirilla: Spirillium undulum b. Vibrio: Vibrio comma
GRAM’S STAINING
GRAM –VE Vs GRAM +VE BACTERIA
Gram positive Gram negative
Appear bluish or purplish under
microscope after staining and do retain
crystal violet dye
Appear pinkish or reddish under
microscope after staining; do not retain
gram’s stain
gram positive (85% or more mucopeptide
and rest is polysaccharide
Only 3-12% mucopepetide and rest are
lipo-proteins and lipo-polysaccharides
Techoic acid present Techoic acid absent
Mesosomes are prominent Mesosomes are less prominent
Outer membrane absent Outer membrane present
2 rings in basal body of flagellum 4 rings in basal body of flagellum
LOCOMOTION OF BACTERIA
1. Monotrichous: A single flagellum at one end
of cell. E.g. Xanthomonas
2. Amphitrichous: A single flagellum at
each(both) end: E.g. Nitrosomonas
3. Cephalotrichous: Two or more flagella at
one end .E.g. P. fluorescens
4. Lophotrichous: Two or more polar flagella
at both end of cell. E.g. Spirillum
5. Peritrichous: Large number of flagella
surrounding the cell. E.g. Erwinia
6. Atrichous: No flagella at either side e.g
Clavibacter
REPRODUCTION IN BACTERIA
A. ASEXUAL REPRODUCTION
 Binary Fission
Budding
 Sporulation (Endospore)
B. SEXUAL REPRODUCTION
 Conjugation
VARIABILITY IN BACTERIA
 CONJUGATION
TRANSFORMATION
TRANSDUCTION
Introductory Plant Pathology Class Slides.pdf
CLASSIFICATION OF BACTERIA
KINGDOM: PROKARYOTE
GRACILICUTES
 Gram –ve;
 thin cell wall
 Generally, no
endospore formation
FIRMICUTES
 Mostly Gram +ve
 Thick cell wall;
 Some produce
endospore
TENERICUTES
 Lack cell wall
 Mollicutes(MLOs/
Phtyoplasma)
MENDOSICUTES
 Faulty cell wall
(no murein in
cell wall)
PROTEOBACTERIA
(mostly single-celled,
non-photosynthetic)
DIVISION
GENUS:
 Agrobacterium,
 Erwinia,
 Pseudomonas,
 Xanthomonas,
 Xyllela,
 Acidovorax,
 Ralstonia
FIRMIBACTERIA
(Simple gram +ve
bacteria)
GENUS:
 Bacillus
 Clostridium
THALLOBACTERIA
(Gram +ve, branching
bacteria)
GENUS:
 Streptomyces
 Clavibacter,
 Arthrobacteria
MOLLICUTES (soft
bodied
prokaryote)
GENUS:
 Phytoplasma
 Spiroplasma
ARCHAEBACTERIA
 Methanogens
(Methanobacterium,
Methanothermococcu
s)
 Halophiles
(Halobacterium)
 Thermoacidophil
es
(Thermomyces)
CLASS
KEY CHARACTERISTICS OF SOME IMPORTANT GENERA
GENERA MOTILITY SHAPE Gram’s reaction Cultural Characteristics
Xanthomonas Single polar
flagellum
Rod -ve Non-spore forming, non-capsulated
and usually yellow water soluble
pigment in culture
Pseudomonas One or many polar
flagella
Rod -ve Green/Brown diffusible pigment or
no pigment
Erwinia Peritrichous Rod -ve Non-spore forming and non-
capsulated; no pigment in culture
Agrobacterium Peritrichous or
sub polar
Rod -ve White colonies (rarely yellow)
Clavibacter Generally Non-
motile
Club-
shaped
or rod
+ve Usually non-pigmented
Streptomyces Atrichous Filament
ous
+ve Colonies are first white and smooth
and later become velvety due to
weft of aerial mycelium
Ralstonia Single polar
flagellum
Rod -ve Creamy white colonies
Xanthomonas Pseudomonas Erwinia
Streptomyces
Uncoating
Translation
Replication
Assembly
Cell entry
(vector)
+
Cell-to-cell
movement
.
systemic
movement
Virus Infection Process
Vector mediated
spread
Infected
Healthy
1.Cell entry (Penetration)
2.Uncoating
3.Translation
4.Replication
5.Virion assembly
6.Release of new
infectious virus
7.Cell to cell movement
8.Long distance (systemic
movement)
1.Disassembly
2. Translation
3. Viral movement
complex assembly
Cell-to-Cell Movement of Virus
viral RNA
Virus assembly
coat protein
virus particles
Viral movement protein
Movement of virus particle
through modified plasmodesmata
Assembly of viral
movement complex
Disassembly of viral
movement complex
Virus disassembly
Viral RNA replication,
translation, etc
Plasmodesmata = junction between plant cells
More cell-to-cell
movement
Host proteins
VIRAL MULTIPLICATION AND TRANSMISSION
Plant viruses enter cells only through the
wounds made mechanically or made by vectors,
or are deposited into an ovule by an infected
pollen grains.
In a RNA replication of an RNA virus, the nucleic
acid (RNA) is first freed from the protein coat.
It induces the host cell to form the viral RNA
polymerase.
The RNA polymerase utilizes the viral RNA as a
template and forms complementary RNA.
The first new RNAs produced are not the viral
RNAs but are the mirror images (complementary
copies) of that RNA.
As the complementary RNA is formed, it is
temporarily connected to the viral strand. Thus,
the two form a double-stranded RNA that soon
separates to produce the original virus RNA and
the mirror image (-) strand, with the latter then
serving as a template for more virus (+) strand
RNA synthesis.
In dsDNA viruses, the viral ds DNA enters the cell nucleus and appears
to become twisted and supercoiled and forms a mini-chromosome.
The latter is transcribed into two single-stranded RNAs (RNA
Polymerase II)
The smaller RNA is transported to the cytoplasm, where it is
translated into virus-coded proteins (Inclusion bodies).
The larger RNA is also transported to the same location in the
cytoplasm, but it becomes encapsidated by coat protein subunits and
is used as a template for the reverse transcription into a complete
virion dsDNA.
REPLICATION OF dsDNA viruses
VIRAL TRANSMISSION
HORIZONTAL TRANSMISSION:
 Horizontal transmission is by vectors, human pruning shears and
tools, and other direct, external contamination.
VERTICAL TRANSMISSION:
 Vertical transmission occurs when a plant gets it from its parent
plant. Either through asexual propagation (cuttings) or in sexual
reproduction via infected seeds.
MEANS OF VIRAL TRANSMISSION
A. MECHANICAL TRANSMISSION:
Easiest method of experimental inoculation
Sap of infected plant is manually transferred to the healthy plant
E.g. TMV, Potato Virus X, etc.
B. GRAFT TRANSMISSION/ VEGETATIVE PROPAGATION
Scion- Root stock or vice-versa .
E.g. Mosaic and leaf roll of Potato, Sugarcane viruses, etc
C. DODDER TRANSMISSION
Cuscuta used in laboratory for transmission
D. SEED AND POLLEN TRANSMISSION
Seed transmission: Muskmelon mosaic virus in watermelon, barley
stripe mosaic virus, Tobacco ring spot virus in soybean, common bean
mosaic virus.
Pollen transmission: Prunus necrotic ring spot virus in Cherry
E. VECTOR TRANSMISSION:
Insect:
 Aphid: Cucumber mosaic Virus, Papaya ring
spot virus, Potato leaf roll virus, Potato virus Y,
etc
 White flies: Begomo viruses (Tomato yellow
leaf curl, Bean Golden mosaic virus, Okra
yellow vein mosaic virus)
 Leaf hoppers: Rice tungro virus, Beet curly top
virus
 Plant hoppers: Maize mosaic, Maize rough
dwarf virus
 Thrips: Tomato spotted wilt
Nematodes:
 Longidorus and Xiphinema species are shown to
transmit several polyhedral viruses-
NEPO(Cherry leaf roll virus and Tomato ring
spot virus) and tubular viruses-NETU (Pea early
browning and tobacco rattle virus)
Fungi:
 Olpidium brassicae- Tobacco Necrosis Virus
 Polymyxa graminis- Oat Mosaic, Wheat
Mosaic
 Polymyxa betae- Beet necrosis yellow vein
 Spongospora subterranea- Potato mop top
virus
PRIMARY EVENTS IN PATHOGENESIS/DISEASE CYCLE
Inoculation
Penetration
Infection
Invasion
Growth and Reproduction of
Pathogen (Colonization)
Dissemination
 Production of dormant/ resting
structure and Survival of (Over-
seasoning) of the pathogen
Infection
Invasion
Colonization
Symptom
develop
ment
Disseminatio
n
Production of
survival/resting
structures
Dormancy and
survival
Inoculation
Penetration
PATHOGENESIS/DISEASE CYCLE
MONOCYCLIC VS POLYCYCLIC DISEASE
1. Primary inoculum (Sclerotia, dormant mycelium, oospore, chlamydospores, teliospore)
2. Secondary inoculum (conidia, uredospores, zoospores)
INOCULATION
Inoculation is the initial contact of the pathogen with the site of the
plant where infection is possible.
Primary inoculum -The inoculum that survives dormant in the winter
or summer and brings about original infections in the spring and
autumn is called primary inoculum, and the infections it cause are
called primary infections.
Secondary inoculum- The inoculum produced from primary infections
is called secondary inoculums, and it, in turn causes secondary
infections.
Generally, inoculum density, inoculum potential and prevalence of
favourable environmental conditions determine the success of
infection.
Two groups of zoospores of the grape downy mildew oomycete have
gathered over two leaf stomata.
Uredospores of rust.
Mitospores (conidia) of a fungus that causes a corn leaf spot disease.
Pseudomonas syringae that causes bacterial spot and canker of
stone fruits are seen in and surrounding a stoma of a cherry leaf.
PENETRATION
PRE PENETRATION
PENETRATION
POST PENETRATION
PRE-PENETRATION:
Differs in different host pathogen combinations
 Attachment of the pathogen to the host
 Spore germination in fungi, multiplication in bacteria and hatching of nematode
eggs
 Perception of the host surface (Host Pathogen recognition)
ATTACHMENT OF PATHOGEN TO THE HOST
Some of the pathogens like Viruses, phytoplasma, viroid, RLOs, etc.
are directly placed in side their host by different agencies.
Almost all fungi, bacteria, parasitic plants, nematodes, first come in
contact with the host surface and must get attached to the external
surface.
This is done through some kind of adhesive material present on the
propagules surface consisting of water soluble polysaccharides,
glycoproteins, lipids or fibrillar material which, when moistened,
become sticky and help the pathogen adhere to the plant.
 In some fungi, hydration of the spore by moist air or dew causes the
extrusion of preformed mucilage at the tip of the spore that serves for
the immediate adherence of the spore to the hydrophobic plant surface
and resistance to removal by flowing water.
Pre-penetration
SPORE GERMINATION
Spores of different fungi germinate according to the
nature of spore & environmental conditions
Resting spores: (Asexual; sclerotia, chlamydospores,
Sexual- teliospores, Oospore, ascospores)
–Propagative spores (conidia, zoospores)
Spore may germinate soon after formation or need
dormancy
Moisture is one of the important factor, followed by
temperature, light, O2
Pre-penetration
INFECTION STRUCTURES
Germtube
Appressorium
Infection hyphae/peg
Haustoria
Rhizomorph
SPORE GERMINATION AND PERCEPTION OF HOST SURFACE
It seems that stimulation by the contact with the host
surface, hydration and absorption of low molecular weight
ionic material from the host surface and availability of the
nutrients plays an important role in spore germination.
Stimulations received by the spore, mobilizes their food
reserves (like lipids, polysaccharides and CHO) or spore
contents, and direct them to the cell membrane and cell wall
for the formation of germ tube and its extension.
Germ tube also perceives the host surface and if it does not
receive the appropriate external stimuli, it remains
undifferentiated and when the nutrients are exhausted it stop
growing and dies.
Appropriate physical and chemical signals (like host surface
hardiness, its topography, hydrophobicity, and plant signals)
leads to germ tube extension and differentiation.
RECOGNITION BETWEEN HOST AND PATHOGEN
It is still unclear how pathogens recognize their hosts and vice versa.
Host components acting as signals for recognition by and activation of pathogens
are numerous.
They may include
 fatty acids of the plant cuticle that activate production of the cutinase enzyme,
by the pathogen which breaks down cutin;
 galacturonan molecules of host pectin, which stimulate the production of pectin
lyase enzymes by the fungus or bacterium;
 certain phenolic compounds, such as strigol, which stimulate activation and
germination of propagules of some pathogens;
 isoflavones and other phenolics, amino acids, and sugars released from plant
wounds that activate a series of genes in certain pathogens leading to infection.
 A host plant may also send cues for recognition by some of its pathogens by
certain of its surface characteristics such as ridges or furrows, hardiness, or
release of certain ions such as calcium.
INTERACTION BETWEEN HOST AND PATHOGEN
PENETRATION
Direct penetration
Indirect penetration
 Fungi may penetrate in either
way
 Bacteria mostly enter through
wounds and some time by natural
openings (Stomata, lenticels,
hydathodes, natural cracks)
 Viruses, viroids, phytoplasma,
RLOs etc. by mechanical means
(wounds) and by vectors
INFECTION
Infection is the process by which pathogens establish contact with
susceptible cells or tissues of the host and procure nutrients from
them.
Successful infection evident as: Symptoms
Infection is of different types
 Local infection
 Systemic infection
 Latent infection
Invasion and reproduction are the two concurrent stages that occur
during infection as pathogen invade different cells, grow & multiply
INVASION
Pathogens enters to variable extents
inside the host
Different pathogens invade their host
as:
Ectoparasite e.g. powdery mildew
Endoparasites e.g. wilts, viruses etc.
 Sub-cuticular pathogens (Apple scab-
Venturia inequalis)
 Sub-epidermal pathogens (wheat rust
)
 Vascular pathogens (Pseudomonas
solanacearum)
 Ecto-endo parasites e.g. potato
canker (Corticium solani)
Ectoparasite: Powdery
mildew
Apple scab: Venturia
Sub-epidermal: Wheat Rust
Endoparasite: bacteria in
xylem vessels
GROWTH AND REPRODUCTION (COLONIZATION)
Different pathogens grow intercellulary & intracellularly inside their
host
Growth & reproduction rate depends upon invasion behaviour of the
pathogen
Method of reproduction
 Asexual
 Sexual
 Replication in case of majority of sub-microscopic pathogens
(viruses/viroids)
Growth and reproduction of the pathogen is affected by pathogen
aggressiveness, susceptibility of the host tissue and environmental
factors
DISSEMINATION/DISPERSAL OF PLANT PATHOGENS
Autonomous/Direct/ Active
Dispersal
Passive or Indirect dispersal
Energy of pathogen is used No energy of pathogen is used
Through soil, seed and planting
materials
Through water, air, man,
machinery, insects, phanerogamic
plants, nematodes and other
animals
The knowledge of dispersal is essential for effective control and
management of disease
SEED AS SOURCE OF AUTOMONOUS DISPERSAL
 Externally Seed Borne:
 Stinking smut/Hill Bunt/Common bunt of Wheat (Tilletia caries/T. foetida)
 Covered smut of barley (Ustilago hordei), Anthracnose of Chilli (Colletotrichum capsici)
Internally seed borne disease:
 Loose smut of Wheat and barley (Ustilago tritici and U. nuda)
Concomitant contamination:
 Ear cockle of Wheat, Ergot of Bajra, Smuts, Seeds of Cuscuta mixed with seeds of host
PLANT AND PLANT ORGANS AS SOURCE OF AUTONOMOUS DISPERSAL
 Vegetative parts helps in dispersal of plant pathogens especially virus and viroid diseases of
vegetatively propagated plants
 Late Blight of Potato was introduced in Europe and North America through seed tubers from South
America
SOIL AS SOURCE OF AUTONOMOUS DISPERSAL
Dispersal in Soil:
 occur in case of soil borne pathogens (facultative parasite or saprophyte)
 Pathogens persists in the soil as dormant structures such as oospore,
chlamydospores, Smut spores or sclerotia
Dispersal of pathogens by soil during cultural operations through agricultural
implements, irrigation water, workers feet, etc.
NEMATODE AS SOURCE OF PASSIVE DISPERSAL
Bacteria causing Yellow ear rot of Wheat (Rathyibacter tritici) is dispersed by
Anguina tritici (Ear cockle of Wheat)
Longidorus and Xiphinema species are shown to transmit several polyhedral
viruses-NEPO(Cherry leaf roll virus and Tomato ring spot virus) and tubular viruses-
NETU (Pea early browning and tobacco rattle virus)
FUNGI AND PHANEROGAMIC PLANTS AS SOURCE OF PASSIVE DISPERSAL
 Olpidium brassicae- Tobacco Necrosis Virus, Lettuce big vein virus
 Polymyxa graminis- Oat Mosaic, Wheat Mosaic, White Spindle Streak Mosaic,
Barley Yellow dwarf mosaic
 Polymyxa betae- Beet necrosis yellow vein
 Spongospora subterranea- Potato mop top virus
 Cuscuta transmits many plant viruses
WATER AS AGENT OF PASSIVE DISPERSAL (HYDROCHORY)
Facilitate short distance and long distance dispersal of fungi, bacteria and
nematodes
Mycelial fragments, spores or sclerotia of fungi are dispersed mainly through
surface running water and rain splash. E.g. Colletotrichum, Fusarium, Pythium,
Phytophthora, Sclerotium,etc.
WIND AS AGENT OF PASSIVE DISPERSAL (AEROCHORY)
Wind act as a potent carrier of propagules of fungi, bacteria and viruses
E.g. Powdery mildew, Downey mildew, Rusts, Smuts, etc.
DISPERSAL BY OTHER ANIMALS
Birds help in dispersal od phanerogamic parasitic plants such as Cuscuta and
Dendrophthae
 Conidia of Colletotrichum falcatum (Red rot of Sugarcane) and Sclerotia of many
fungi have been detected in Cattle dung.
KOCH’S POSTULATE/PATHOGENECITY TEST
Pathogen must be invariably found in the
affected plant or it must be associated with in
some forms
The pathogen should be separated from infected
host and grown in artificial culture
The pathogen from artificial culture should be
able to reproduce the disease when inoculated on
a healthy plant of some kind from which it was
isolated.
The symptom produced should be identical with
those seen on the plant from which isolation was
made
The artificially produced disease should yield the
same pathogen of re-isolation
SURVIVAL OF PLANT PATHOGENS
A. INFECTED HOST AS RESERVOIR OF INOCULUM
Collateral Hosts (wild hosts of same families)
 Pyricularia grisea can infect the grass weeds like Brachiara mutica, Dinebra
retroflexa, Leersia hexandra, Panicum repens, etc. and survive during off-
season
Alternate hosts (Wild hosts of other families)
 Puccinia graminis fsp. tritici survive on Barberry (Alternate Host)
Self sown crops:
 Self sown, voluntary and early sown crops serve as reservoir of plant
pathogens such as Rice tungro virus
Ratoon Crops (Sugarcane mosaic)
Survival by latent Infection
 Xyllela fastidiosa (Pierce’s disease of Grape Vine) infect weeds without
developing visible symptoms
Soil inhabitants:
 Those which survive indefinitely in soil as saprophyte (obligate or facultative) even in
absence of host
 E.g. Pythium and Rhizoctonia survive as oospore and sclerotia for longer period in soil in
active form
Soil invaders/Root inhabitants:
 Survive in soils in close association with hosts.
 The saprophytic phase continues as long the host is not completey decomposed.
 E.g. Fusarium species, Verticillium species, etc.
Rhizosphere colonizers:
 Colonize the dead substrate in the root region and continue to live for longer period
 Are more tolerant to soil antagonism
 E.g. Cladosporium fulvum (Leaf mould in tomato)
B. SAPROPHYTIC SURVIVAL OUTSIDE THE HOST
Plant viruses: no resting stage; transmitted through continuous infection
chain
Bacteria: no resting spores; continually live in their active parasitic stage in
living host or as active saprophyte
Nematode: survive in form of active parasitic phase on living host and also
survive through dormant structures such as eggs, cysts, galls
Phanerogamic parasites: survive in dormant state through seeds.
 Fungi
 Soil Borne: Oospores, sclerotia, Chlamydospores, thickened hypha,
microsclerotia, Rhizomorphs
 Seed Borne:
 Dormant fungal structures on dormant or active host:
 Survival in association with insects, nematodes and fungi:
 Corn flea beetle carries the corn wilt pathogen inside its body (Xanthomonas
stewartii)
 Fungi like Polymyxa and Spongospora transmit viruses
C. SURVIVAL AS DORMANT SPORES OR SPECIALIZED RESTING STRUCTURES
CRITERIA FOR PATHOTOXIN
A pathotoxin should produce all characteristic symptoms of the
disease when applied in low concentration
Toxin production by the pathogen should be directly related to its
ability to cause disease
Toxin and pathogen should have same host range; same resistance
and susceptibility spectrum
MICROBIAL TOXINS AND ENZYMES
BASED ON THE ROLE IN PATHOGENESIS:
 Pathotoxin
 Vivotoxins
 Phytotoxins
A. PATHOTOXINS (Wheeler and Luke, 1963)
These are the toxins which play a major role in disease production and
produce all or most of the symptoms characteristic of the disease in
susceptible plants.
Most of these toxins are produced by pathogens during pathogenesis.
E.g. Victorin: Cochliobolus victoriae (Helminthosporium victoriae), the
causal agent of Victoria blight of oats. This is a host specific toxin.
SELECTIVE PATHOTOXIN (HOST- SPECIFIC) NON-SELECTIVE PATHOTOXIN (NON-HOST SPECIFIC)
T-toxin: H. maydis (Race T) Tentoxin: Alternaria alternata
HC-toxin- H. carbonum Tabtoxin/wild fire toxin: Pseudomonas tabaci
HS-toxin- H. sacchari Phaseolotoxin: Pseudomonas syringae pv.
phaseolicola
Phytoalternarin: Alternaria kikuchiana
PC-toxin: Periconia circinata
VIVOTOXIN (Diamond & Waggoner, 1953)
 These are the substances produced in the infected host by the
pathogen and / or its host which functions in the production of the
disease, but is not itself the initial inciting agent of the disease.
 Generally non-host specific
 Ex:-Fusaric acid – Wilt causing Fusarium sp.
Piricularin- Pyricularia oryzae
Lycomarasmin- F
. oxysporum f.sp. lycopersici
 Vivotoxin is always isolated from diseased plants and it should not be present in
healthy plants
 Such toxin should be chemically characterized
 When introduced in its pure form, it must be able to produce characteristics
symptoms or a part of disease syndrome in question.
PHYTOTOXIN (Wheel and Luke, 1963)
These are the substances produced in the host plant due to host-
pathogen interactions for which a causal role in disease is merely
suspected rather than established.
These are the products of parasites which induce few or none of
the symptoms caused by the living pathogen.
They are non-specific and there is no relationship between toxin
production and pathogenicity of disease causing agent.
• Eg. Alternaric acid – Alternaria solani,
ENZYMES
Substrate Effect Enzymes Pathogen Involved
Pectic substance Breakdown in the
chain of linkage
Pectin methyl esterase
Pectin lyase
Polygalacturonase
Transeliminase
Phytophthora
Rhizopus
Erwinia caratovora
Rhizoctonia solani
Sclerotinia
sclerotiorum
Cellulose Turns to glucose
Softening/
disintegration of
cell wall
Cellulase/Gluconase Fungal, bacterial,
nematodes and
Phanerogamic plants
Hemicellulose Turns into simple
sugar
Hemicellulase
β-Manosidase
α-galctoriodose
Sclerotinia fructigena
S. sclerotiorium
Lignin Breakdown Lignanease
Ligase
Oxidase
Alternaria
Cephalosporium
Fusarium
EPIDEMICS AND EPIDEMIOLOGY/EPIPHYTOLOGY
Epidemic???
Epidemiology:
The study of epidemics and factors influencing
them is called epidemiology.
Epidemiology is concerned simultaneously with
populations of pathogens and host plants as
they occur in an evolving environment, i.e., the
classic disease triangle.
It deals with outbreaks and spread of diseases
in a population or at population level
Slow epidemic (Tardive epidemic)
 Occurs in monocyclic diseases
 On perennial plants
 E.g. Dutch elm disease, Chestnut blight
Fast epidemic (Explosive epidemic)
 In polycyclic diseases
 Annual crops
 E.g. rice blast, potato blight
Epidemics in the past
The Irish potato famine of 1845–1846 was caused by the Phytophthora
late blight epidemic of potato,
The Bengal famine of 1943 was caused by the Cochliobolus
(Helminthosporium) brown spot epidemic of rice.
Questions in one’s mind during outbreak of disease
What will happen over the next few weeks?
Will all the plants die, leaving nothing to harvest ? Or
Will only currently infected plants will yield less?
Are all the plants infected and only few showing symptoms?
Is the pathogen air/water/wind/vector dispersed?
Can this crop be planted next season etc.?
 Epidemiology helps in answering entire questions by describing
disease development pattern during the single season and from
year to year.
DISEASE PYRAMID/TETRAHEDRON
DISEASE
SUSCEPTIBLE HOST  Susceptible host
 Virulent pathogen
 Favourable environment
 Development of disease is affected by
 Duration & frequency of each element of
over time,
 Timing, Duration & frequency of
favourable environment
 Human activities such as training/pruning
ELEMENTS OF AN EPIDEMIC
IN FUNGAL & BACTERIAL DISEASES:
The Host (susceptible)
The Pathogen (virulent)
Environment (favourable)
Human activity
IN VIRUS & VIRUS LIKE DISEASES
The Virus
The Host
The Vector
Environment
FACTORS AFFECTING DEVELOPMENT OF EPIDEMICS
A. HOST FACTORS
Levels of Genetic Resistance or Susceptibility of the Host
 Highly resistant
 Moderately resistant
 Susceptible
Degree of Genetic Uniformity of Host Plants
 Monoculture (vertical/ horizontal resistance) e.g.
 Cochliobolus (Helminthosporium) blight on Victoria oats and
 in southern corn leaf blight on corn carrying Texas male-sterile cytoplasm.
Type of Crop
 Annual
 Perennial
Age of Host Plants
 Plants change in their reaction (susceptibility or resistance) to disease with age.
The change of resistance with age is known as Ontogenic resistance.
B.PATHOGEN FACTORS
Levels of Virulence/aggressiveness
Quantity of Inoculum near Hosts
Type of Reproduction of the Pathogen
 Sexual (oospores, ascospores)
 Asexual (conidia, zoospores)
Ecology of the Pathogen
 Ectoparasites
 Endoparasites
Mode of Spread of the Pathogen
 Active dispersal
 Passive dispersal
ENVIRONMENTAL FACTORS
Temperature
Light
Moisture
Dew duration
HUMAN FACTORS- A KEY PLAYER
 Site selection
 Selection of Propagative material
 Cultural practices
 Disease control measures
 Introduction of new pathogen
MATHEMATICAL MODEL FOR DISEASE SPREAD
Vander Plank in 1963 in his historical book "Plant Diseases-
Epidemics and Control” suggested a model based on the
infection rate 'r’.
The equation for describing a epidemic is:
X= Xo
ert
Where,
Xo= Amount of critical inoculum
r= average infection rate
t= time during infection has occurred
X= Proportion of disease at any one time
e= base of natural logarithm
MEASUREMENT OF PLANT DISEASE AND YIELD LOSS
The disease is measured in term of :
Disease incidence ( disease prevalence)
Disease severity (extent of damage to host)
Yield loss (the yield loss is the difference between attainable yield and
actual yield)
AREA UNDER DISEASE PROGRESS CURVE
(AUDPC)
useful quantitative summary of disease intensity over time, for
comparison across years, locations, or management tactics.
The most commonly used method for estimating the AUDPC, the
trapezoidal method, is to discretize the time variable (hours, days,
weeks, months, or years) and calculate the average disease
intensity between each pair of adjacent time points (Madden et al.
2007).
Where, Yi = disease severity on the ith date,
ti= time on which Yi was recorded and
n = number of times observations were taken.
Severity: 5, 10, 30,60, 80, 90, 100
Days of observation: 7, 14, 21, 28, 35, 42, 49
Calculate AUDPC???
CLASSIFICATION OF DISEASE BASED ON EPIDEMIOLOGY
Monocyclic disease
Polycyclic disease
Polyeptic disease
APPLICATION OF DISEASE EPIDEMIOLOGY FOR DISEASE MANAGEMENT
A. Disease forecasting on the basis of primary inoculums and
environmental conditons
B. Fixing strategies to reduce the final disease
 Control measures to reduce initial inoculum (Xo): Rouging, Soil
fumigation, hot water treatment, Sanitation, Insect vector
control, summer deep ploughing, Resistant varieties, Soil
solarization
 Control measure to reduce infection rate (r): Use of horizontal
resistance, Modification of cultural practices, Proper crop
geometry
 Control measure to reduce time during infection (t): Early or late
planting, Early or late maturing varieties
CRITERIA FOR PATHOTOXIN
A pathotoxin should produce all characteristic symptoms of the
disease when applied in low concentration
Toxin production by the pathogen should be directly related to its
ability to cause disease
Toxin and pathogen should have same host range; same resistance
and susceptibility spectrum
MICROBIAL TOXINS AND ENZYMES
BASED ON THE ROLE IN PATHOGENESIS:
 Pathotoxin
 Vivotoxins
 Phytotoxins
A. PATHOTOXINS (Wheeler and Luke, 1963)
These are the toxins which play a major role in disease production and
produce all or most of the symptoms characteristic of the disease in
susceptible plants.
Most of these toxins are produced by pathogens during pathogenesis.
E.g. Victorin: Cochliobolus victoriae (Helminthosporium victoriae), the
causal agent of Victoria blight of oats. This is a host specific toxin.
SELECTIVE PATHOTOXIN (HOST- SPECIFIC) NON-SELECTIVE PATHOTOXIN (NON-HOST SPECIFIC)
T-toxin: H. maydis (race T) Tentoxin: Alternaria alternata
HC-toxin- H. carbonum Tabtoxin/wild fire toxin: Pseudomonas tabaci
HS-toxin- H. sacchari Phaseolotoxin: Pseudomonas syringae pv.
phaseolicola
Phytoalternarin: Alternaria kikuchiana
PC-toxin: Periconia circinata
VIVOTOXIN (Diamond & Waggoner, 1953)
 These are the substances produced in the infected host by the
pathogen and / or its host which functions in the production of the
disease, but is not itself the initial inciting agent of the disease.
 Generally non-host specific
 Ex:-Fusaric acid – Wilt causing Fusarium sp.
Piricularin- Pyricularia oryzae
Lycomarasmin- F
. oxysporum f.sp. lycopersici
 Vivotoxin is always isolated from diseased plants and it should not be present in
healthy plants
 Such toxin should be chemically characterized
 When introduced in its pure form, it must be able to produce characteristics
symptoms or a part of disease syndrome in question.
PHYTOTOXIN (Wheel and Luke, 1963)
These are the substances produced in the host plant due to host-
pathogen interactions for which a causal role in disease is merely
suspected rather than established.
These are the products of parasites which induce few or none of
the symptoms caused by the living pathogen.
They are non-specific and there is no relationship between toxin
production and pathogenicity of disease causing agent.
• Eg. Alternaric acid – Alternaria solani,
ENZYMES
Substrate Effect Enzymes Pathogen Involved
Pectic substance Breakdown in the
chain of linkage
Pectin methyl esterase
Pectin lyase
Polygalacturonase
Transeliminase
Phytophthora
Rhizopus
Erwinia caratovora
Rhizoctonia solani
Sclerotinia
sclerotiorum
Cellulose Turns to glucose
Softening/
disintegration of
cell wall
Cellulase/Gluconase Fungal, bacterial,
nematodes and
Phanerogamic plants
Hemicellulose Turns into simple
sugar
Hemicellulase
β-Manosidase
α-galctoriodose
Sclerotinia fructigena
S. sclerotiorium
Lignin Breakdown Lignanease
Ligase
Oxidase
Alternaria
Cephalosporium
Fusarium
EPIDEMICS AND EPIDEMIOLOGY/EPIPHYTOLOGY
Epidemic???
Epidemiology:
The study of epidemics and factors influencing
them is called epidemiology.
Epidemiology is concerned simultaneously with
populations of pathogens and host plants as
they occur in an evolving environment, i.e., the
classic disease triangle.
It deals with outbreaks and spread of diseases
in a population or at population level
Slow epidemic (Tardive epidemic)
 Occurs in monocyclic diseases
 On perennial plants
 E.g. Dutch elm disease, Chestnut blight
Fast epidemic (Explosive epidemic)
 In polycyclic diseases
 Annual crops
 E.g. rice blast, potato blight
Epidemics in the past
The Irish potato famine of 1845–1846 was caused by the Phytophthora
late blight epidemic of potato,
The Bengal famine of 1943 was caused by the Cochliobolus
(Helminthosporium) brown spot epidemic of rice.
Questions in one’s mind during outbreak of disease
What will happen over the next few weeks?
Will all the plants die, leaving nothing to harvest ? Or
Will only currently infected plants will yield less?
Are all the plants infected and only few showing symptoms?
Is the pathogen air/water/wind/vector dispersed?
Can this crop be planted next season etc.?
 Epidemiology helps in answering entire questions by describing
disease development pattern during the single season and from
year to year.
DISEASE PYRAMID/TETRAHEDRON
DISEASE
SUSCEPTIBLE HOST  Susceptible host
 Virulent pathogen
 Favourable environment
 Development of disease is affected by
 Duration & frequency of each element of
over time,
 Timing, Duration & frequency of
favourable environment
 Human activities such as training/pruning
ELEMENTS OF AN EPIDEMIC
IN FUNGAL & BACTERIAL DISEASES:
The Host (susceptible)
The Pathogen (virulent)
Environment (favourable)
Human activity
IN VIRUS & VIRUS LIKE DISEASES
The Virus
The Host
The Vector
Environment
FACTORS AFFECTING DEVELOPMENT OF EPIDEMICS
A. HOST FACTORS
Levels of Genetic Resistance or Susceptibility of the Host
 Highly resistant
 Moderately resistant
 Susceptible
Degree of Genetic Uniformity of Host Plants
 Monoculture (vertical/ horizontal resistance) e.g.
 Cochliobolus (Helminthosporium) blight on Victoria oats and
 in southern corn leaf blight on corn carrying Texas male-sterile cytoplasm.
Type of Crop
 Annual
 Perennial
Age of Host Plants
 Plants change in their reaction (susceptibility or resistance) to disease with age.
The change of resistance with age is known as Ontogenic resistance.
B.PATHOGEN FACTORS
Levels of Virulence/aggressiveness
Quantity of Inoculum near Hosts
Type of Reproduction of the Pathogen
 Sexual (oospores, ascospores)
 Asexual (conidia, zoospores)
Ecology of the Pathogen
 Ectoparasites
 Endoparasites
Mode of Spread of the Pathogen
 Active dispersal
 Passive dispersal
ENVIRONMENTAL FACTORS
Temperature
Light
Moisture
Dew duration
HUMAN FACTORS- A KEY PLAYER
 Site selection
 Selection of Propagative material
 Cultural practices
 Disease control measures
 Introduction of new pathogen
MATHEMATICAL MODEL FOR DISEASE SPREAD
Vander Plank in 1963 in his historical book "Plant Diseases-
Epidemics and Control” suggested a model based on the
infection rate 'r’.
The equation for describing a epidemic is:
X= Xo
ert
Where,
Xo= Amount of critical inoculum
r= average infection rate
t= time during infection has occurred
X= Proportion of disease at any one time
e= base of natural logarithm
MEASUREMENT OF PLANT DISEASE AND YIELD LOSS
The disease is measured in term of :
Disease incidence ( disease prevalence)
Disease severity (extent of damage to host)
Yield loss (the yield loss is the difference between attainable yield and
actual yield)
AREA UNDER DISEASE PROGRESS CURVE
(AUDPC)
useful quantitative summary of disease intensity over time, for
comparison across years, locations, or management tactics.
The most commonly used method for estimating the AUDPC, the
trapezoidal method, is to discretize the time variable (hours, days,
weeks, months, or years) and calculate the average disease
intensity between each pair of adjacent time points (Madden et al.
2007).
Where, Yi = disease severity on the ith date,
ti= time on which Yi was recorded and
n = number of times observations were taken.
Introductory Plant Pathology Class Slides.pdf
CLASSIFICATION OF DISEASE BASED ON EPIDEMIOLOGY
Monocyclic disease
Polycyclic disease
Polyeptic disease
APPLICATION OF DISEASE EPIDEMIOLOGY FOR DISEASE MANAGEMENT
A. Disease forecasting on the basis of primary inoculums and
environmental conditons
B. Fixing strategies to reduce the final disease
 Control measures to reduce initial inoculum (Xo): Rouging, Soil
fumigation, hot water treatment, Sanitation, Insect vector
control, summer deep ploughing, Resistant varieties, Soil
solarization
 Control measure to reduce infection rate (r): Use of horizontal
resistance, Modification of cultural practices, Proper crop
geometry
 Control measure to reduce time during infection (t): Early or late
planting, Early or late maturing varieties
PLANT DISEASE FORECASTING
Plant disease forecasting is an applied
epidemiology and involves:
all the activities in ascertaining and notifying the farmer in
an area/community that the conditions are sufficiently
favourable for certain diseases,
that application of control measures will result in economic
gain or
that the amount of disease expected is unlikely to be enough
to justify the expenditure of time, money and energy for its
control.
PLANT DISEASE FORECASTING
 requires complete knowledge of epidemiology
 is made more reliable if the reasons for a particular
disease developing under certain conditions are
known.
 Experimental investigation is necessary to show that
exactly what stage during the disease development
is critical for variable incidence or intensity of
disease.
 A timely and reliable forecast gives the farmer
many options to choose from that he/she can weigh
the risks, costs and benefits of his possible
decisions.
CONDITIONS OF DISEASE FORECASTING
The disease must be causing economically significant damage in terms
of loss of quantity and quality of the produce in the area concerned.
The onset, speed of spread and destructiveness of the disease is
variable mostly due to dependence on the weather which is variable.
Control measures are known and can be economically applied by the
farmer when told to so.
Information on weather- disease relationship is fully known.
SOME SUCCESSFUL EXAMPLES OF DISEASE FOREASTING
LATE BLIGHT OF POTATO
Holland pioneered the development of forecasting and spray
warning services for the control of late blight of potato.
Van Everdingen (1926) analyzed the combined effect of several
weather conditions on the development of Phytophthora
infestans and evolved four rules, popularly known as Dutch
rules, on which the appearance of blight was observed to
depend.
Dutch Rule:
i) Night temperature below dew point at least for 4 hours
ii) A minimum temperature of 10 C or above
iii) A mean cloudiness on the next day of 0.8 or more, and
iv) At least 0.1mm rainfall during the next 24 hours.
When all these four conditions were obtained in Holland, potato
blight was expected after the next 7 days and therefore the
control measures were immediately recommended to the farmers.
RICE BLAST:
In India, forecasting rice blast ( Pyricularia ozyzae) is done by
correlative information method.
It is predicted on the basis of minimum night temperature 20 to
26°C in association with high relative humidity of 90% or above.
EARLY AND LATE LEAF SPOTS OF GROUNDNUT
When the groundnut foliage remains wet for a
period greater than or equal to 10 h and
the minimum temperature is 21°C or higher for
two consecutive days or nights, the disease
development is forecasted in USA
DISEASE FORECASTING METHODS
EMPIRICAL FORECASTING :
Derived based upon pathogen development and its life cycle, effected by various environmental
conditions
VAN DER PLANK MODEL :
Based on information of initial inoculum of disease (Xo), the rate of the disease increase (r) in
particular time (t) and estimated the final disease as their magnitude i.e. X= Xo
ert
COMPUTER BASED DISEASE FORECASTING:
Utilizes quantitative data regarding the effects of weather variables on pathogenesis and
production of primary and secondary inocula, pathogen and vector activities, antagonists as well as
genetic variation in the pathogen and host
EPIDEM- first model for early blight of potato
BLITECAST-late blight of potato
SYMPHYT- late blight of potato
EPIMAY-Southern Corn leaf blight
EPIPRE- Yellow rust of Wheat
Introductory Plant Pathology Class Slides.pdf
METHODS OF LOSS ASSESSMENT
Survey method:
Based on study over large area about disease incidence and its
impact
Experimental method:
REMOTE SENSING
• Remote sensing refers to noncontact
measurements of radiation reflected or
emitted from agricultural fields, which are
based on the interaction of electromagnetic
radiation with soil or plant material.
• Based on aerial photography or satellite
photography
The electromagnetic spectrum of greatest interest to use in remote
sensing is the optical wavelengths, which extend from 0.3–15 μm.
This is divided into part:
i) 0.38-3 μm (reflective part),
ii) 0.38-0.72 μm (visible part),
iii) 0.72-3 μm (infrared),
iv) 0.72-1.3 μm (near infrared),
v) 1.3-3.0 μm (middle infrared)
vi) emissive part: 7-15 μm far infrared (emissive/ thermal infrared).
WHEAT RUST MONITORING USING REMOTE SENSING
In recent years, significant progress is made in remote
sensing technologies for monitoring wheat rust at
following four levels
 Single Leaf scale (ground based)
 Canopy scale (ground based)
 Field crop scale (aerial)
 Countries/regional scale (satellite based)
Remote sensing data at single leaf, canopy and field crop
scale levels provide local and limited experimental
information.
While satellite based remote sensing can provide a
sufficient and inexpensive data base for rust over large
wheat regions or at spatial scale. It also offers the
advantage of continuously collected data and availability
of immediate or archived data sets.

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Introductory Plant Pathology Class Slides.pdf

  • 1. Phytopathology (Phyton : plant) Greek - Pathos (suffering) + Logos (study) = The study of the suffering plant Plant pathology is that branch of agricultural, botanical or biological sciences which deals with the study of: -cause of the disease (Etiology/aetiology) -mechanism of disease development -host-pathogen interaction in relation to environmnet -Resulting losses and -Control and management of plant diseases Plant pathology is both science (of Learning and understanding the nature of disease ) and Art (of diagnosing and controlling/managing the disease) WHAT IS PLANT PATHOLOGY?
  • 2. OBJECTIVES OF PLANT PATHOLOGY 1. Study of origin, causes or reasons. Study of living, non-living and other causes of disease or disorder in plants- Etiology 2.Study of mechanism of disease development i.e. processes of infection and colonization of the host by the pathogen. This phase involves complex host-pathogen interactions- Pathogenesis 3.study the interaction between the causal agent and the diseased plants in relation to environmental conditions. Generally at the population level- Epidemiology 4.Development of management systems of the diseases and reduction of losses caused by them- Control/ Management.
  • 3. WHAT IS PLANT HEALTH? The ability to carry out normal physiological functions at a acceptable level consistent to genetic potential. Normal physiological functions include:  Normal cell division, differentiation, and development,  Absorption of water and minerals from the soil and translocation;  Photosynthesis and translocation of photosynthates;  Utilization and storage of photosynthates;  Metabolism of metabolites and synthates;  Reproduction;  Storage of reserves for overwintering or reproduction
  • 4. CONCEPT OF DISEASE  Plant is healthy, or normal, when it can carry out its physiological functions to the best of its genetic potential. Any deviation- Disease The kinds of cells and tissues that become affected determine the type of physiological function that will be affected/altered -For example, infection of roots may cause roots to rot and make them unable to absorb water and nutrients from the soil; -Infection of xylem vessels, interferes with the translocation of water and minerals to the crown of the plant; -Infection of the foliage, (leaf spots, blights, rusts, mildews, mosaics etc.), interferes with photosynthesis
  • 5. Disease can be defined as the result of interaction between host, pathogen and environment DEFINING DISEASE Disease is the process in which a pathogen interferes with one or more essential plant cell functions Disease is as physiological disorder or structural abnormality that is deleterious to the plant or its part or product, that reduces the economic value of the plant e.g., wilt, potato blight, Loose smut of wheat, Karnal bunt of wheat (Stakman & Harrar, 1957) Disease is a malfunctioning process that is caused by continuous irritation, which results in some suffering producing symptoms. ( Accepted by both American Phytopathological Society and British Mycological Society) Horsfall & Diamond (1957): Disease can be defined as a physiological disorder or structural abnormality that is deleterious or harmful to the plant or its part or product that reduces its economic value.
  • 6. How Pathogens affect Plants? -By utilizing host cell contents -By killing host or by interfering with its metabolic processes through their enzymes, toxins etc. –By weakening the host due to continuous loss of the nutrients. –By interfering with the translocation of the food, minerals and water. –They can suppress the chlorophyll content. –They can reduce the leaf area. –They can curb the movement of solutes and water through the stems. –They sometimes reduce the water-absorbing capacity of the roots. –They suppress the translocation of photosynthates away from the leaves. –They sometimes promote wasteful use of the products of photosynthesis as in the formation of galls.
  • 7. IMPORTANCE OF PLANT DISEASES -Late blight of potato-1841-51 (Irish famine) –Phytophthora infestans. -Bengal Famine 1942 (India)- Bipolaris/Helminthosporium oryzae -Coffee rust 1867-1870 (Srilanka) –Hemileia vastatrix -Downy mildew of grapes (1880s) (France)- Plasmopara viticola -Outbreak of Black stem Rust (Ug99) in wheat (1999)- Puccinia graminis f. sp. tritici -Bacterial Blight of Rice 1963 (Bihar)- Xanthomonas oryzae pv. oryzae -Southern corn leaf blight -1970 (USA) –Bipolaris maydis Out of 36.5% agriculture yield loss: Disease cause: 14.1% Insects cause: 10.2% Weed causes 12.2%
  • 8. -Plant pathology deals with different aspects of plant diseases and has wide scope than human pathology which only deal with only one aspect -In recent years plant pathologists have begun to specialize in particular aspect. The field in which notable advances have been made are: –Interaction between host and pathogen at chemical, molecular and genetic level –Plant virology, chemistry of fungitoxicity –Disease forecasting -Breeding for resistance
  • 9. What is Disorder? Iron deficiency Abnormal physiological change due to non-parasitic agent or is a non-parasitic physiological malfunctioning due to either excess or deficiency in environmental factors or nutrients. e.g. Physiological wilt, sun scald, Nutrient deficiency
  • 10. SOME FUNDAMENTAL TERMINOLOGIES  Pathogen  Parasite  Various levels of Parasitism  Symbiosis  Obligate parasite (Biotrophs)  Facultative parasite  Facultative saprophyte  Saprohytes  Hemibiotrophs  Perthotrophs/Necrotrophs/Perthopy te  Pathogenicity  Pathogenesis/Disease Cycle  Virulence  Infection  Colonization  Inoculum  Invasion  Inoculum Potential  Symptoms  Signs  Syndromes  Incubation period  Alternate host  Collateral host  Inoculation  Isolation  Etiology  Epidemiology  Pre-dispostion  Resistance  Susceptibility  Tolerance  Hypersensitivity  Physiologic race  Biotype  Mutualism  Antagonism  Mutation  Crop Damage  Deficiency
  • 11.  Pathogen: An entity, usually a micro-organism that can cause the disease. (Fungus, Bacteria, virus, Phytoplasma, Viroids, RLO’s, Parasitic Plants, Nematodes )  Parasite: An organism living upon or in another living organism (the host) and obtaining the food from the invading host.  Obligate parasite (Biotrophs): A plant pathogenic fungus that requires living host cells i.e. an obligate parasite. E.g. Smuts, Rusts, Powdery mildew, Downy mildew.  Hemi-biotroph: A plant pathogenic fungus that initially requires living host cells but after killing the host cell grows on the dead and dying cells. E.g. leaf spotting fungi  Necrotroph/Perthotrophs A pathogenic fungus that kills the host tissues in advance of penetration and then live saprohytically. E.g. Sclerotium rolfsii  Saprophyte: They are those organisms that secure their nutrients from dead organic tissues or from available inorganic materials.  Facultative parasite (weak Parasite/ strongly saprophytic): They are ordinarily saprophytic but under certain conditions they may become parasitic. E.g. Pythium, Rhizoctonia,  Facultative saprophyte (Weak saprophyte/ strongly parasitic) : They ordinarily have a life cycle similar to that of obligate parasite but under certain conditions, may subsist as saprophyte. E.g. Smut fungi, Taphrina, Protomyces, Phytophthora infestans etc.
  • 12. Pathogenicity: The relative capability of a pathogen to cause disease. Pathogenesis: It is a process caused by an infectious agent (pathogen) when it comes in contact with a susceptible host. Disease cycle: A series of events involved in disease development including stages of development of pathogen and the effect of pathogen on the host (inoculation, penetration, infection, invasion, colonization, growth and reproduction , dissemination of pathogen, survival of pathogens) Virulence: It is a qualitative component of pathogenicity expressed vertically. The degree of infectivity of a given pathogen OR It is a measure of degree of pathogenicity of a given pathogen Aggressiveness: It is a quantitative component of pathogenicity expressed horizontally. It is the capacity of the pathogen to invade and colonize the host and to reproduce/survive on or in it.
  • 13. Features Vertical resistance/ Qualitative resistance/R-Gene Resistance/ Monogenic resistance/Race- specific resistance/Major gene resistance/Differential rsistance Horizontal resistance/ Partial resistance/ Polygenic resistance/Minor gene resistance/Non-differential resistance/Race-non- specific/Adult/ Field resistane Pathotype specificity Specific Non specific Nature of gene action monogenic or sometimes oligogenic Polygenic Effectivity Generally biotrophs Generally necrotrophs Efficiency Against specific races Variable, but operate against all races Risk of boom and bust Present Absent or Minimal Stage of expression Seedling to maturity Expression increase as plant matures HORIZANTAL AND VERTICAL RESISTANCE
  • 15. BOOM AND BUST CYCLE
  • 16. Inoculation: It is the process of landing the pathogenic spore on the host surface naturally or transferring the pathogenic propagules artificially Infection: It is establishment of parasitic relationship between two organisms following entry or penetration or initiation and establishment of a parasite within the host Invasion: The penetration and spread of a pathogen in the host. Colonization: The growth and reproduction of a pathogen, particularly a fungus, in the host after infection is called colonization. Inoculum: It is the infectious material can cause disease, and it is that portion of individual pathogens that is brought into contact with host. Inoculum Potential: Garret (1956) defined it as the energy of fungal parasite available for infection of a host at the surface of the host organ to be affected.
  • 17. Symptoms and Signs Symptom – are the internal and external expression of the disease caused by the manifestation of the physiological reaction of the plant due to harmful activity of the pathogen • Sign - physical evidence of the presence of disease agent (e.g., mold or fungal spores, bacterial ooze, sclerotia, exudates)
  • 18. Syndrome • Defined as sequential appearance of disease symptoms on a plant during the development of the disease • or sum total of symptoms exhibited by a disease Fleck or necrotic spot Blight Fungal growth Death of organ or plant
  • 19. Incubation period: The period of time between penetration of a pathogen to the host and the first appearance of symptoms on the plant. Host: An organism that harbors or supports the activities of parasite Alternate host (wild host of different families): Plants not related to the main host of parasitic fungus, where it produces its different stages to complete one cycle (heteroecious). Collateral host: The wild host of same families of a pathogen is called as collateral host. Isolation: It is process of taking out/separating the pathogenic part from diseased sample for disease diagnosis Pre-disposition: The effect of one or more environmental factors which makes a plant vulnerable to attack by a pathogen.
  • 20. Susceptibility: Inability of the host to resist the attack of the pathogen Tolerance: is a type of defense that minimises crop losses with out restricting the disease development. Resistance: Ability of the host to resist the attack of the pathogen. (Horizontal/Vertical resistance) Immunity: It implies exemption from infection by pathogen Hypersensitivity: The hypersensitive response (HR) is a type of programmed cell death, which is part of the plant’s defense response against pathogen attack. It is defined as a rapid, localized necrosis of cells at the infection site and it occurs in resistant plants in response to pathogen attack
  • 21. Gene-for-gene Hypothesis • Postulated by Harold Henry Flor in 1951 • Based on his work on Linseed rust caused by Melampsora lini. “For each gene conditioning avirulence in the pathogen, there is a corresponding gene conditioning resistance in the host and vice- versa” “For each gene conditioning resistance in host, there is a corresponding gene conditioning avirulence in pathogen and vice-versa” OR
  • 22. Molecular basis for gene-for- gene relationship Gene-for-gene relationship is the consequence of specific interaction between product of host genes governing resistance and pathogen genes specifying virulence.  on the basis of molecular interaction involved in producing resistance/susceptible response in host gene-for-gene relationship may be classified to: 1. Incompatible reaction (Resistant) 2. Compatible reaction (susceptible)
  • 24. Eg- peptide encoded by Avr9 gene of fungal pathogen Cladosporium fulvum induce HR in tomato strain carrying resistance gene cf9 RESISTANCE GENE VIRULENCE R1 Resistance Susceptible r1 Susceptible Susceptible Avr1 avr1
  • 25. Primary infection: The first infection of a plant by the over wintering or over summering structure (resting/ survival structure) of the pathogen Primary inoculum: The propagules coming from survival structures or neighbouring field that cause primary infection. Secondary inoculum: The inoculum that develops subsequestly after primary infection or primary symptoms Secondary infection: The infection caused by secondary inoculum is known as secondary infection. Epidemiology : Epidemiology of disease is study of factors affecting the outbreak of an infectious disease. It is science of disease in population (deals with population of host and pathogens under varying environment) Pathodeme: Pathodeme is that population of a host in which all individual have a stated resistance in common.  Formae speciales (Pl.Forma specialis)- f. sp.- individuals with in the spp. Of a pathogen that morphologically similar but difffer with respect to their pathogenecity on particular host genera • E.g. Puccinia graminis f.sp. tritici, oats (P. graminis f. sp. avenae) and rye (P. graminis f. sp. secalis)
  • 26. Formae speciales of Puccinia graminis Host plant tritici Wheat, secalis Rye, avenae Oats phleipratensis Timothy agrostidis Redtop poae Kentucky blue grasses,
  • 27. Physiologic race: individuals with in the species of a pathogen that are morphologically similar but differ with respect to their pathogenicity on particular set of host varieties (differential host) Mutualism: Symbiosis of two organisms that are mutually helpful or that mutually support one another. Antagonism: The counteraction between organisms or groups of organisms. Mutation: An abrupt appearance of a new characteristic in an individual as a result of an accidental change in genes present in chromosomes. Crop Damage: It is defined as any reduction in the quality or quantity of yield or loss of revenue resulting from crop injury. Deficiency: Abnormality or disease caused by the lack or subnormal level of availability of one or more essential nutrient elements.
  • 28. RACE/PATHOTYPE IDENTIFICATION (Puccinia graminis f.sp. tritici) • To identify the races of Puccinia graminis f.sp. tritici , the isolate is inoculated on twelve standard differentials and the symptoms produced are noted and classified in to infection type. • These are then compared with the existing records and race is identified. • Key numbers are given each on the basis of its identity. Standard differentials
  • 29. REACTION CLASSES OF TWO RACE OF P. graminis f.sp. tritici
  • 30. Terms describing microbial habitats related to plants Epiphytic: organisms growing on the surface of photosynthetic organisms Endophytic: organisms growing inside the host Phylloplane: leaf surface Phyllosphere: area surrounding the leaf and impacted by it Rhizoplane: root surface Rhizosphere: area surrounding the root and impacted by it
  • 31. HISTORY OF PLANT PATHOLOGY  Greek Philosopher Theophrastus (300 BC) recorded some observations on the plant diseases in his book “Enquiry into plants” PIER ANTONIO MICHELLI (Italian) botanist in 1729 published a book “Nova Plantarum Genera”- FOUNDER AND FATHER OF MYCOLOGY BENEDICT PREVOST proved that diseases are caused by micro- organisms and in 1807, published his findings in the paper “memoir on the immediate cause of bunt or smut of wheat and of several other diseases and on preventives of bunt” CHRISTIAN HENDRICK PERSOON published Mycologica Europa in 1822 and gave the name to rust pathogen of wheat as “Puccinia graminis” PERSON AND FRIES first time introduced binomial system of nomenclature to classify the fungal organisms
  • 32.  HEINRICH ANTON De BARY (German botanist) in 1863, studied the epidemics of late blight of Potato and renamed the causal organism as Phytophthora infestans- FOUNDER AND FATHER OF MODERN PLANT PATHOLOGY ROBERT KOCH (1881) developed plate method for isolation of bacteria – Father of Modern bacteriology PIERRE-MARIE-ALEXIS MILLARDET- discovered Bordeaux mixture for the control of Downey Mildew of Grape Vine  M.W. BEIJERINCK (Dutch)- a Dutch microbiologist and founder of virology proved that the virus inciting tobacco mosaic is not a microorganism. He believed it to be contagium vivum fluidum (infectious living fluid). He was the first to use the term virus, which is the Latin word for poison.- FOUNDER OF VIROLOGY IWANOWSKI (1888)- demonstrated filtrable nature of virus W.H. STANLEY in 1953- proved the crystalline nature of viruses. J.F. DUSTUR: First Indian plant pathologist credited for his detailed studies on fungi and plant diseases
  • 33. CAUSES OF PLANT DISEASES Animate/Biotic Causes Fungi Bacteria Nematodes Algae Protozoa  Mollicutes -Phytoplasma (MLOs) -Spiroplama Rickettsia like organism/bacteria (RLOs/RLBs/Fastidious bacteria) Phanerogamic parasites/ parasitic higher plants Insects Mesobiotic Causes Viruses Viroids Inanimate/Abiotic Causes 1. Soil condition a) Moisture- b) Structure c) Soil Oxygen d) Soil nutrients (N, P, K, Ca, Mo, B, Zn) 2. Meteorological factors a) Light b) Temperature c) Wind d) Atmospheric humidity 3. Agriculture practices Eg. Herbicides 4. Industrial contaminants Eg. Peroxyacetyl Nitrate, SO2
  • 34. FUNGUS (PL. FUNGI)  eukaryotic,  spore-bearing,  Achlorophyllous organisms  generally reproduce sexually and asexually  whose usually filamentous, branched somatic structures are typically surrounded by cell walls containing chitin or cellulose, or both of these substances, together with many other complex organic molecules.  May be either saprophytic or parasitic
  • 35. SOME DISEASES CAUSED BY FUNGI Bean Anthracnose (Colletotrichum lindemuthianum) Brown spot of rice (Bipolaris oryzae) Downy mildew of Pumpkin (Pseudoperonspora cubensis) Powdery mildew of Cucumber (Podosphaera xanthii) Stripe/Yellow rust of Wheat (Puccinia striiformis f. sp. tritici) Late blight of Potato (Phytophthora infestans)
  • 36. BACTERIUM (PL. BACTERIA)  are microscopic, unicellular prokaryotes, which lack chlorophyll. are with a primitive nucleus lacking a clearly defined membrane. 70 S ribosome Cell wall made up of peptidoglycan (murein), lipo proteins and lipopolysaccharides are smaller than fungi and measure about 0.5 to 1.0 x 2.0 to 5.0 μm in size. are equipped with delicate, thread like flagella (locomotory organ) Most of plant pathogenic bacteria are rod shaped except Streptomyces (filamentous) and Cornyebacterium (club) Reproduction by binary fission and budding Important plant pathogenic bacterial Genera Agrobacterium, Clavibacter(Cornyebacterium), Erwinia, Pseudomonas, Ralstonia, Xanthomonas, Streptomyces, Xyllela Acidovorax
  • 37. SOME DISEASES CAUSED BY BACTERIA Bacterial leaf blight of Rice (Xanthomonas oryzae pv. oryzae Bacterial wilt /Brown rot of Potato (Ralstonia solanacearum) Black rot of crucifers (Xanthomonas campestris ) Citrus canker (Xanthomonas axonopodis pv. citri Crown Gall of Apple (Agrobacterium tumefaciens ) Potato Scab ( Streptomyces scabies)
  • 38. Nematodes • Microscopic roundworm like animals • Barely visible with naked eye • Triploblastic, bilaterally symmetrical • Unsegmented, pseudocoelomate • Bisexual, Vermiform • 300nm-100nm but Up to 4mm long • Free living to parasitic • Almost all plant parasitic nematodes are obligate parasite and are soil inhabitants • Reproduction- sexual and parthenocarpic Important Plant Pathogenic nematode Meloidogyne (Root-knot nematode) Heterodera and Globodera (Cyst nematode) Ditylenchus (stem and bulb nematode) Pratylenchus (lesion nematode) Anguina (seed gall nematode) Aphelenchoides ( Foliar nematode) Xiphinema (Dagger nematode) Longidorus and Paralongidorus (Needle nematode) Trichodorus and Paratrichodorus (Stubby-root nematodes)
  • 39. SOME PLANT DISEASES CAUSED BY NEMATODES Ditylenchus dipsaci (Stem and bulb nematode) in onion Root knot of Tomato (Meloidogyne incognita) White tip of rice (Aphenchoides besseyi) Golden cyst of Potato (Globodera rostochiensis) Ear cockle of wheat (Anguina tritici)
  • 40. ALGAE Algae are eukaryotic, unicellular or multicellular organisms and mostly occur in aquatic environments. Many algae thrive as terrestrial or subterranean algae. The size of algae ranges from 1.0mm to many centimetres in length. They contain chlorophyll and are photosynthetic/autotrophs They reproduce by asexual and sexual processes. The study of algae is called phycology or algology. Spread by wind borne sporangia and produces zoospores. Enter into plant cell through natural openings and grow as a chain of algal cells E.g.Cephaleuros mycoides/virescens (Red rust of mango, litchi, guava, tea, coffee, Avocado, etc)
  • 41. FLAGELLATE PROTOZOAN (PL. PROTOZOA)- PHYTOMONAS Protozoa derived from Greek word Protos (first) and zoon (animal) They are eukaryotic protists Generally Single celled Distinguished from other eukaryotic protists by their ability to move at some stage of their life cycle and lack of cell wall Members of family Trypnosomatidae (Kingdom Protista) are know to be plant parasitic Phytomonas leptovasorum (Phloem necrosis of coffee) P. francai (Empty root rot of Cassava
  • 42. MYCOPLASMA LIKE ORGANISMS (PHYTOPLASMA) Resembles mycoplasmas – animal pathogens Highly pleomorphic, non-motile, non-spore forming, unicellular , filterable, extremely small. Generally ovoid but filamentous forms are also reported are obligate bacterial parasites of plant phloem tissues and of the insect vectors that are involved in plant to plant transmission Lack cell wall however, have specialized triple layered membrane, lack cell wall. Sensitive to tetracycline and insensitive/resistant to penicillin Mostly transmitted by Phloem feed insects such as hoppers and psyllids. They have not been grown in an artificial nutrient medium so far Important diseases caused by Phytoplasma  Aster yellows  Apple proliferation  European stone fruit yellows  Coconut lethal yellowing  Elm yellows  Ash yellows  Pear Decline  Little leaf of brinjal  Sandal Spike  Sesamum phyllody  Grassy Shoot disease  Peach X
  • 43. Aster yellows Coconut lethal yellowing Sesamum Phyllody Peach X disease
  • 44. SPIROPLASMA Similar to Phytoplasma in many regards except that they can be cultured and are motile and helical in structure Small helical mollicutes Are motile. Can somehow use their corkscrew shape to propel themselves Lack cell wall but have specialized triple layered membrane Require sterol for growth Resistant to penicillin but sensitive to tetracycline and neomycin Can be cultured in artificial medium Colonies on nutrient medium give fried egg appearance Generally transmitted by insect vectors (leaf hoppers) Important plant diseases caused by Spiroplasma Citrus Stubborn Corn Stunt Carrot purple leaf disease
  • 46. FASTIDIOUS VASCULAR BACTERIA- (RLOs/RLBs) Formerly known as Rickettsia like organisms Generally Gram negative bacteria, straight rod shaped, smaller than MLOs Have cell wall unlike MLOs and Spiroplasma Develop within both xylem and phloem Categorized into xylem-, phloem and non- tissue limited (meristematic and parenchyma) Very difficult to grow artificially as they have specific nutritional requirements (Xylem limited RLB has been more successfully cultured) Dependent on insect vectors and nematodes for transmission Sensitive to tetracycline and penicillin (*Xylem limited insensitive to penicillin) Xylem limited: • Pierce’s disease of Grape vine • Almond leaf scorch • Phony disease of peach (Xyllela fastiodosa) Pholem limited: • Citrus greening (Candidatus liberibacter) • Clover club leaf • White clover disease • Clover rugose leaf curl Non-tissue limited: • Aspermy of wheat • Yellows of grapevine
  • 47. Pierce’s disease of Grape Phony disease of Peach Citrus greening/Huanglongbing (HLB) /yellow dragon disease
  • 48. VIRUSES Strictly intracellular, ultramicroscopic, nucleoprotein entities, which are infectious agents obligately parasitic pathogens, which are less than 200 mμ in size. They can only replicate themselves within a host's cell. Possess only one type of nucleic acid either DNA and RNA but never both are devoid of enzymes and depend on the host protein synthesis machinery (ribosomes). Most of plant pathogenic viruses are RNA- viruses Need mechanical, insects, seeds, nematodes, propagation, grafting, etc. or their entry into host RNA Viruses: Tobacco Mosaic virus Barley stripe mosaic Potato mop-top virus Tobacco rattle virus DNA Virus: • Cauliflower mosaic virus, • banana bunchy top virus, • maize streak virus • sugar beet curly top virus.
  • 49. Tobacco Mosaic Virus Tobacco Rattle virus Tomato leaf curl Okra yellow vein mosaic
  • 50. VIROIDS are small low molecular weight ribonucleic acids (RNA) that can infect plant cells replicate themselves and cause disease. They are also called as mini viruses. are devoid of outer protein coat (capsid)  Although it has no protein of its own, a viroid's RNA affects a plant's ability to produce essential proteins. Depends entirely on the host cell for replication Diseases caused by Viroids Potato spindle tuber,  Chrysanthemum stunt,  Coconut Cadang cadang.
  • 51. Potato Spindle tuber Coconut cadang cadang
  • 52. Phanerogamic Plant Parasites Some flower and seed bearing higher plants (phanerogams) live parasitically on other living plants can cause important diseases on agricultural crops and also in forest trees. They may semi or partial or total parasite (Holo parasite) Holo parasite- absence of chlorophyll, depend entirely on the host plants for their food materials. Spread in various ways including animals, wind and forcible ejection of seeds Cuscuta, the dodder (stem parasite)- Aakash beli  Orobanche , the broomrapes (root parasite/holoparasite)- Neerjhar  Striga (the witchweeds-root parasite)
  • 53. Inanimate/ abiotic/ nonliving causes of plant diseases 1. Soil conditions: A. Soil moisture: Low moisture-physiological wilting Excess moisture- Reduced O2, CO2 accumulation, accumulation of toxic metabolites by anaerobic bacteria, accumulation of soluble salts around roots and stem – Damping off of seedlings, Root rots, Fusarium and Verticillium wilts are more severe in wet soils Potato scab (Streptomyces scabies), Charcoal rot (Macrophomina phaseoli) are severe in dry soil Charcoal Rot of Bean Verticillium wilt of tomato (V. alboatrum)
  • 54. B. Soil structure: -affects moisture holding capacity and aeration -Hard and compact soil retards root growth, results in stunted growth and predisposes the plant to parasitic diseases -Hard pan results in withering, yellowing die back symptoms C. Soil aeration • Limited supply of oxygen coupled with poor ventilation causes several post harvest disease in storage e.g. Black heart of Potato D. Soil pH: • Club root of crucifers (Plasmodiophora brassicae) is serious at pH 5.7 and controlled at pH 7.8 • Likewise Potato scab is also more prevalent in alkaline soil, inhibited below pH 5.2 Black heart of Potato Club root of Crucifer Potato Scab
  • 55. E. Nutritional Imbalance (Deficiencies and Abundance) Nitrogen: Abundance of N makes the plant succulent and predisposes the plant to pathogen e. fire blight of Pear (Erwinia amylovora) and Wheat Rust (Puccinia graminis). Deficiency of nitrogen leads stunting and yellowing symptoms following reddening of leaf blade E.g. Red leaf of cotton Phosphorus: Leaves of Phosphorus deficient plants are generally bluish- green with purple tints Deficiency in Cotton causes dwarfing and excessively dark green foliage Potassium: K deficiencies are particularly important in potatoes, tobacco. cotton, forage legumes and other crops which require high K. E.g. Brown spot of cotton and little spot of alfa alfa High K increases the severity of rice blast P deficiency in Guava P deficiency in Maize K deficiency in cotton Rice leaf blast
  • 56. Boron: -Soil with high lime content are deficient in Boron -Deficiency of B cause Heart rot of Beet, Internal cork of apple, Brown heart of cabbage and turnip, Hollow stem of Brassica, Internal browning of Cauliflower Calcium: Deficiency cause Blossom end rot of tomato, black heart of celery, wither tip of flax Molybdenum: Deficiency cause whiptail disease of cauliflower Zinc: Deficiency results in mottling/foliocellosis, little leaf, rosette of citrus; yellow streak in corn; Khaira disease of rice
  • 57. Khaira disease of rice Internal browning of Cauliflower (Boron deficiency) Internal cork of apple (Boron deficiency) Blossom end rot of tomato (Ca deficiency) Whiptail of Cauliflower (Mo Deficiency)
  • 58. METEOROLOGICAL FACTORS Temperature: Low temperature- frost of Pigeon Pea High temperature- sun scald of tomato Light : No direct effect, yet, reduced light cause etiolation Balanced light decreases susceptibility to obligate parasites like Puccinia Wind:  Helps in spread of propagules of pathogens and in initiation of epidemics  Wind-blown rain help release fungal and bacterial spores and disseminate them over long distance Atmospheric humidity:  High humidity favours most of the disease caused by fungi and bacteria
  • 59. Industrial Contaminants: Sulphur dioxide released from the Brick kilns cause black tip of mango when the orchards are near to 15 km Ozone concentration exceeding above 0.035 ppm for 4 hours may cause water soaked spots on leaves Peroxyacetyl Nitrate (PAN) produce visible symptoms when sensitive plants are exposed for 4 hours to about 14 ppb. Characteristically, injury from PAN appears as glazing or bronzing of the lower leaf surface but the symptom syndrome may also include tissue collapse, chlorosis, and leaf drop. Agricultural Practice: High dose of Agrochemicals causes phytotoxicity. E.g., 2,4-D kills Chenopodium but high dose will affect the wheat also. Faulty and improper application of fungicides and insecticides causes injuries to the plants. E.g. cucurbits are very sensitive to chlorinated hydrocarbon group of insecticides,  Copper ion is toxic to plants so high dose application of copper fungicide may cause injury Sulphur toxicity in tropical areas
  • 60. Black tip of Mango Ozone phytotoxicity in musk melon PAN phytotoxicity on lettuce 2, 4-D damage on tomato
  • 61. CLASSIFICATION OF PLANT DISEASES BASED ON CAUSE OF DISEASE/ETIOLOGY: A. INFECTIOUS/PARASITIC DISEASE Fungi, bacteria, virus, viroid, phytoplasma, RLBs, nematodes, higher parasitic plants etc. Contagious, are transmitted from diseased to healthy plants via various agencies. B. NON-INFECTIOUS/NON-PARASITIC/PHYSIOLOGICAL/ABIOTIC DISEASE nutritional deficiencies e.g. Khaira disease of rice due to Zn deficiency, unfavourable environment e.g. frost injury, physiological wilt, etc.
  • 62. BASED ON TYPE OF INFECTION: A. LOCALIZED DISEASES: These diseases are limited to a definite area of an organ or part(s) of a plant. Localized effect of pathogen E.g. leaf spots and Anthracnoses caused by different fungi. B. SYSTEMIC DISEASES: In these diseases the pathogen spreads from a single infection point so as to infect all or most of the host tissues.  E.g. Fungal and bacterial wilt, Downy mildews caused by fungi; mosaics and leaf curls caused by viruses.
  • 63. Tikka disease of Ground nut (Cercospora personata/arachidicola) Tan spot of Wheat (Pyrenophora tritici-repentis)
  • 64. C. BASED ON NATURAL PERPETUATION AND MODE OF INFECTION 1. Soil borne diseases  caused by pathogens which persist (survive) in the soil matrix and in residues on the soil surface  soil is the reservoir of primary inoculum of these pathogens  E.g. Damping off of seedlings 2.Seed borne disease : Seed-borne pathogens typically survive for a long period in or on contaminated or infected seed.  be admixed with the seed during harvesting/threshing (Concomitant contamination) e.g. sclerotia (Sclerotinia sclerotium) in sunflower  externally seed borne pathogen : Covered smut of barley (Ustilago hordei), Anthracnose of Chilli (Colletotrichum capsici)  Internally seed borne: Loose smut of barley (Ustilago nuda) and wheat (Ustilago tritici), Soyabean mosaic virus,  Both internally and externally seed borne. Black arm of Cotton (Xanthomonas malvacearum) 3.Air borne disease: foliar pathogens causing foliar diseases. In this case pathogen survives in weed hosts (alternate or collateral hosts) during off season and the wind-borne inoculum of pathogen is carried to the crop plants and cause diseases in crops. E.g. Wheat Rust (Puccinia sp.) , Brown spot of rice (H. oryzae or Bipolaris oryzae)
  • 65. D. BASED ON SYMPTOMS D. BASED ON SYMPTOMS Rusts Smuts Leaf spot Septoria leafspot of tomato (Septoria lycopersici) Angular leafspot of beans (Pseudocercospora griseola) Black/Stem Rust Puccinia graminis f.sp. tritici Brown/Leaf Rust (P. recondita) Stripe/ Yellow rust (P. striiformis f.sp. tritici) Loose smut of Wheat (Ustilago tritici)
  • 66. Rots Blight Canker  Wilt Buckeye rot of tomato (Phytophthora parasitica) Foot rot of Papaya (Pythium aphanidermatum) Late blight of Potato (Phytophthora infestans) Citrus Canker (Xanthomonas axonopodis pv. citri) Bacterial Wilt of Tomato (Ralstonia solanacearum ) Browning of vascular tissues
  • 67. Downy mildews Powdery mildew Anthracnose Die-back Downy mildew of Pumpkin (Pseudoperonospora cubensis) Powdery mildew of Pea (Erysiphe pisi) Powdery mildew of Grapes (Uncinula necator) Bean anthracnose (Colletorichum lindemuthianum) Die back symptoms in Chilli anthracnose (Colletotrichum capsici)
  • 68. Blotch Tumour/Gall Atropy/Stunting/ Dwarfing Shot holes Purple Blotch of Onion (Alternaria porii) Shot hole of Cherry (Coccomyces hiemalis) Crown Gall on apple (Overgrowth) Corn Stunt (Spiroplasma kunkelii) Crown gall on peach (Agrobacterium tumefaciens)
  • 69. Mummification Enation Witches’ broom Mummification of Peach (Monilinia fructicola) Enation (Pea enation mosaic virus) Potato witches’ broom (Phytoplasma) Groundnut witches’ broom (Phytoplasma) Enation in cotton (Cotton leaf curl Virus)
  • 70. Gummosis Rosette Mosaic Scab Rosette (Groundnut rosette umbravirus) Potato scab (Streptomyces scabies) Apple scab (Venturia inaequalis) Citrus Gummosis (Phytophthora nicotianae var. parasitica) Bean common mosaic virus Bean yellow mosaic virus
  • 71. Damping off Vein clearing Vein banding Epinasty Damping off (Pythium, Rhizoctonia, Phytophthora) Vein clearing (Okra yellow vein mosaic) Vein banding (Bean common mosaic virus) Epinasty in mustard (Beet curly top virus) Epinasty in tomato (due to exposure to ethylene)
  • 72. Ergot Leaf Curl Mold Phyllody Leaf gall Tomato leaf curl Ergot of Bajra (Claviceps purpurea) White mold of bean (Sclerotinia sclerotiorum) Sesamum Phyllody (Phytoplasma) Leaf gall
  • 73.  Albication  Chlorosis Club root Root knot Rugosity Broad bean stain virus in pea Chlorosis Club root of crucifers (Plasmodiophora brassicae) Root knot (Meloidogyne) Potato Virus Y (Rugosity)
  • 74. E. BASED ON HOST PLANTS • Cereal diseases • Vegetable diseases • Fruit diseases • Forest diseases • Ornamental diseases F. BASED ON CROP • Diseases of Wheat • Diseases of maize etc G. BASED ON ORGAN THEY ATTACK • Root diseases • Shoot diseases • Fruit diseases • Foliage diseases Mango anthracnose Colletotrichum gloeosporioides Brown Spot of rice (Bipolaris oryzae) Northern Leaf blight of maize (Exserohilum turcicum) Gray leaf spot of Maize (Cercospora zeae-maydis)
  • 75. H. BASED ON OCCURRENCE AND DISTRIBUTION A. ENDEMIC : When a disease is more or less constantly prevalent from year to year in a moderate to severe form in a particular country. E.g., Wart disease of potato (Synchytrium endobioticum) is endemic to Darjeeling, B. EPIDEMIC OR EPIPHYTOTIC: A disease occurring periodically but in a severe form involving major area of the crop. it may be constantly present in locality but assume severe form occasionally e.g. Rust, Late blight, Mildews C. SPORADIC: Diseases which occur at very irregular interval and location in a moderate to severe form e.g., leaf blights, wilt, Angular leaf spot of cotton(Pseudomonas lachrymans) D. PANDEMIC: Diseases occurring throughout the continent or sub-continent resulting in mass mortality and devastating damage in short period of time e.g., Late blight of potato
  • 76. BASED ON EPIDEMIOLOGY/PATHOGEN GENERATION A. SIMPLE INTEREST/ MONOCYCLIC DISEASES Those diseases the increase of which is analogous of increase in money due to simple interest Those diseases which have only generation in one cropping season e.g. loose smut of wheat, vascular wilts, Black leg of potato (Erwinia caratovora), Verticillium wilt, Cereal cyst nematode B. COMPOUND INTEREST/ POLYCYCLIC DISEASES Those diseases which have more than one generation in a cropping season. e.g. late blight of potato, Downy mildews, Powdery mildews, Rusts, Aphid borne viruses. C. POLYETIC DISEASES (MULTI-YEAR DISEASE) These are also polycyclic diseases but they complete their disease cycle in more than one year or over years e.g. Cedar Apple Rust. Disease Progress Curve
  • 77. Symptoms due to change in host plant Hyperplasia: Increase cell division (Increase in cell no.) plant overgrowth Hypertrophy: Cell enlargement plant overgrowth  Gall: Swelling or overgrowth of plant parts Leaf Curl:Twisted leaves due to overgrowth of tissue Witches broom: Broom like clustering of leafs Hypoplasia:Decrease cell division Hypotrophy: Decrease Cell enlargement Leaf curl of tomato Crown Gall of Rose Witches’ broom on woody plants
  • 78. Symptoms due to visible pathogen 1) Mildew:  Powdery mildew: Superficial growth giving dusty or powdery appearance  Downy mildew: Cottony downy growth like a day old chicken 2) Rust: Spores breaking through the epidermis giving rusty appearance 3) Smuts: Sooty or charcoal like powder usually on floral parts 4) White blisters: Blister like pustules exposing powdery white mass
  • 79. Symptoms due to visible pathogen 5) Sclerotia: Compact mass of dormant mycelium (resting structure) 6) Scab: Rough or crust like lesion which are scabby
  • 80. Symptoms due death of cells or tissues 1)Spot: Localized lesion on host surface (Cercospora capsici) 2) Anthracnose: Necrotic and sunken ulcer like lesions (Colletotrichum lindemuthianum) 3) Canker: Necrotic lesion sunken or raised beneath or over the surface (Xanthomonas axonopodis pv. citri) 4) Blight: Rapid burning of leaves and other succulent parts leading death (Late blight of Potato) 5) Damping off: Stem near the soil surface of seedling becomes constricted and weak and unable to bear load of upper parts and topples down (Pythium) 6) Rots: Maceration and disintegration of tissue Root rot (Rhizoctonia solani, Pythium, Phytophthora) 7) Shot-hole: A perforated appearance of a leaf as the dead areas of local lesions drop out leaving a shot hole (shot hole of Cherry-Coccomyces hiemalis ) Cercospora leaf spot Anthracnose of Chilli Late Blight of Potato Citrus canker Damping off of tomato Papaya foot rot Cherry shot hole
  • 81. Some symptoms associated to virus infection 1) Stunting: Reduced growth 2) Local lesions: Necrotic lesion at the point of entry 3) Mosaic: Alternate patches of green, light green and yellow 4) Ringspot: Distinct chlorotic or necrotic ring 5) Rosette: Short branching habit 6) Enation: Over growth 7) Stem pitting: shrunken pits on the stem Citrus Ring spot Virus Rosette Mosaic Enation Citrus tristeza virus
  • 82. Some symptoms associated to virus infection 8) Puckering:Distortion in shape of leaf 9) Vein banding: Chlorosis of interveinal space 10) Vein clearing: Chlorosis of vein 11) Shoe string : Excessive reduction of leaf lamina a. Shoe string b. Ring Spot (Papaya Ring spot Virus) Shoe String Puckering Vein Clearing Vein banding
  • 83. Miscellaneous disease symptoms Blast:tissues, young buds and fruits are killed rapidly Blotch: irregular discolored area Dieback: Progressive death of plant starting from tip Wilting: Loss of turgidity of plant Sooty mould : Dark coating on foliage by fungal hyphae Chlorosis: yellowing of normal green tissue Die back of Chilli Wilting Neck Blast Leaf Blast Nodal Blast Septoria leaf blotch Sooty mould of mango
  • 84. IMPORTANCE OF FUNGI A. Beneficial Effect Decomposition of plant debris with the help of cellulase Biocontrol agents. Trichoderma sp.  Organic acid production- Gibberella fujikori (Gibberillin) Mushrooms are appreciated for nutritional and delicious food value e.g. Agaricus, Pleurotus, Lentinula edodes Use in genetic research E.g. Neurospora Industrial use-value particularly in fermentation (Bread, wines, Beers, cheese) Source of medicine E.g. Penicillin from Penicillium digitatum and P. crysogenus Soil inhabitants such as Fusarium, Chaetomium, Aspergillus, Mucor improve soil structure by formation of soil aggregates Entomogenous fungi helps in controlling insect pests. Eg. Beauveria bassiana, Metarhizium anisopliae
  • 85. HARMFUL EFFECTS OF FUNGI Saprophytic fungi are responsible for destruction of food, fabrics, leather and other good manufactured for raw material Many fungal group of mushroom are poisonous and cause serious health hazards e.g. Coprinus comatus, Amanita muscaria Post harvest disease in citrus by Penicillium digitatum Member of Mucorales, Yeasts, Moniliales are responsible for food spoilage Green and blue mould of orange Amanita muscaria Coprinus comatus Peniciliium digitatum
  • 86. GENERAL CHARACTERISTICS OF FUNGI All are eukaryotic - Possess membrane-bound nuclei (containing chromosomes) and a range of membrane-bound cytoplasmic organelles (e.g. mitochondria, vacuoles, endoplasmic reticulum)  Generally Extra cellular digestion is the way in which fungi feeds Most are filamentous - Composed of individual microscopic filaments called hyphae, which exhibit apical growth and which branch to form a network of hyphae called a mycelium.  some are unicellular - e.g. yeasts. Protoplasm of a hypha or cell is surrounded by a rigid cell wall - Composed primarily of chitin and glucans, although the walls of some species contain cellulose. Many reproduce both sexually and asexually - Both sexual and asexual reproduction often result in the production of sexual and asexual spores.
  • 87. Their nuclei are typically haploid and hyphal compartments are often multinucleate – Although the Oomycota and some yeast possess diploid nuclei. All are achlorophyllous - They lack chlorophyll pigments and are incapable of photosynthesis. All are chemoheterotrophic (chemo-organotrophic) - They utilize pre-existing organic sources of carbon in their environment and the energy from chemical reactions to synthesize the organic compounds they require for growth and energy.  Possess characteristic range of storage compounds - e.g. trehalose, glycogen, sugar alcohols and lipids. May be free-living or may form intimate relationships with other organisms i.e. may be free living, parasitic or mutualistic (symbiotic) Most of the fungi grow well at 20 to 30*C
  • 88. EUCARPIC Vs HOLOCARPIC THALLUS Thallus/Thalli The body of the fungus is called as 'thallus’. Eucarpic thallus The thallus is differentiated into vegetative part, which absorbs nutrients, and a reproductive part, which forms reproductive structure. Such thalli are called as Eucarpic. e.g. Pythium aphanidermatum.
  • 89. Holocarpic thallus The thallus does not show any differentiation on vegetative and reproductive structure. Such thalli are called as 'holocarpic' e.g. yeast, Synchytrium endobioticum
  • 90. HYPHAE (PL. HYPHA) Hyphae is a tubular, transparent filament, usually branched, composed of an outer cell wall and a cavity (lumen) lined or filled with protoplasm including cytoplasm. divided into compartments or cells by cross walls called septa and are generally called as septate (with cross wall)-septate or coenocytic (aseptate -without cross wall). Hyphae of most of the fungi measures 5- 10 μm in diameter
  • 91. DOLIPORE SEPTUM Each septum is pierced by a narrow septal pore. The pore is surrounded by a barrel- shaped thickening or septal swelling. The septal pore is over arched with a perforated cap (extension of endoplasmic reticulum
  • 92. MYCELIUM • The hyphal mass or network of hyphae constituting the body (thallus) of the fungus is called as mycelium. • The mycelium of parasitic fungi grows on the surface of the host and spread between the cells and it is called intercellular mycelium. • The mycelium of parasitic fungi, which grows on the surface of the host and penetrates into the host cells and is called intracellular mycelium. HAUSTORIA???
  • 93. HAUSTORIUM/HAUSTORIA Haustoria (sing. haustorium; L. haustor = drinker) are special knob-like or root like hyphal structures or outgrowths of somatic hyphae sent into the host cell to absorb/derive nutrients. The hyphae of obligate parasites of plants like downy mildew, powdery mildew or rust fungi, late blight fungus etc., produce haustoria
  • 94. Monokaryotic mycelium (uninucleate)  Mycelium contains single nucleus that usually forms part of haplophase in the life cycle of fungi. Dikaryotic mycelium (binucleate)  Mycelium contains pair of nuclei (dikaryon), which denotes the diplophase in the life cycle of fungi. Homokaryotic mycelium  The mycelium contains genetically identical nuclei. Heterokaryotic mycelium  The mycelium contains nuclei of different genetic constituents. Multinucleate  The fungal cell contains more than 2 nuclei. Homothallism:  The thalli are monoecious and both male and female sex organs occur on the same thallus Heterothallism:  Thalli are dioecious and male and female sex-organs occur in different thalli
  • 95. SPECIALIZED SOMATIC STRUCTURES Rhizoid A rhizoid (Gr. rhiza = root + oeides = like) is a short, root-like filamentous outgrowth of the thallus Rhizoid serves as anchoring or attachment organ to the substratum and also as an organ of absorption of nutrients from substratum. E.g. Rhizopus, Cladochytrium
  • 96. APPRESSORIUM /APPRESSORIA (L. apprimere = to press against) is a simple or lobed or bulbous structure of hyphal or germ tube and a pressing organ from which a minute infection peg usually grow and enter the epidermal cell of the host. It helps germ tube or hypha to attach to the surface of the host or substrates. These appressoria are formed from germ tubes of Uredinales (rust fungi), Erysiphales (powdery mildew fungi) and other fungi in their parasitic or saprophytic stages. These are organ of attachment and anchorage
  • 97. FUNGAL TISSUE (PLECTENCHYMA) Plectenchyma ( Gr. Plekein= to weave + encyma (infusion i.e. woven tissue) A. Prosenchyma: Mycelium is present in form of loosely woven tissues in which the component hypha lie more or less parallel to one another and their typically elongated cells are distinguishable and the individuality of the cells is not lost. B. Pseudoparenchyma: consist of closely packed more or less isodiametric or oval cells resembling parenchyma of vascular plants. Individuality of hyphae is lost C. Pseudosclerenchyma: consists of closely packed, thick walled and dark coloured cells.
  • 98. AGGREGATION OF HYPHAE A. MYCELIAL STRANDS Mycelial strands are aggregates of parallel or interwoven undifferentiated hyphae, which adhere closely and are frequently anastomosed or cemented together. They are relatively loose compared to rhizomorph. E.g. (e.g. Sclerotium rolfsii growth on culture medium)
  • 99. ANASTOMOSIS • involves fusion of hyphae of some species, movement of one or more nuclei into one or the other of the fused cells, • and the establishment of a compatible heterokaryotic state. • Important phenomena for heterokaryosis
  • 100. B. RHIZOMORPHS Rhizomorph (Gr. rhiza=root + morphe = shape) is the aggregation of highly differentiated hyphae with a well defined apical meristem, which are often darkly pigmented. Root like aggregations of somatic hyphae E.g. Honey fungus/ Honey agric , Armillariella mellea
  • 101. C. Stroma (Pl. stromata): Compact somatic structure much like cushion or mattress on which or in which fruiting bodies are usually formed E.g. various type of ascocarps, basidiocarps, pycnidia, acervuli, sporodochia D. Sclerotium (Pl. Sclerotia): is a hard resting body formed by aggregation of somatic hyphae into dense, rounded, flattened, elongated or horn-shaped dark masses.  are thick-walled resting structures, which contain food reserves. Sclerotia are hard structures resistant to unfavourable physical and chemical conditions. They may remain dormant for longer periods of time, sometimes for several years and germinate on the return of favourable conditions. Sclerotia of Rhizoctonia solani Sclerotia of Sclerotinia
  • 102. MYCORRHIZAE • Mycorrhiza (pl. mycorrhizae; Gr. mykes = mushroom + rhiza = root) is the symbiotic association between higher plant roots and fungal mycelia. • Many plants in nature have mycorrhizal associations.
  • 103. REPRODUCTION IN FUNGI Asexual/Vegetative Reproduction Sexual Reproduction 1. Fragmentation 2. Fission 3. Budding 4. Production of asexual spores (mitospores) a. Sprangiospores b. Conidia c. Chlamydospores 1. Planogametic copulation 2. Gametangial contact 3. Gametangial copulation 4. Spermatization 5. Somatogamy
  • 104. Asexual Reproduction Fragmentation The septate hyphae break up into their component cell, and each fragment may grow into new individuals under suitable conditions. They are known as Oidium (Pl. Oidia) or arthrospores They do not store reserve food and hence cannot survive under unfavorable conditions.  E.g. Erysiphe, Rhizopus Fission (Transverse cell division)  simple splitting of cells into two daughter cells by constriction and formation of a cell wall. E.g Yeast (Schizosaccharomyces spp) SEM of Erysiphe (Oidia)
  • 105. BUDDING Production of a small outgrowth (bud) from a parent cell As the bud is formed, the nucleus of the parent cell divides and one daughter nucleus migrates into the bud. The bud increases in size, while still attached to the parent cell and eventually breaks off and forms a new individual. common in yeasts.(Saccharomyces sp. ) Spores formed by process of budding of somatic cells or conidiospores are called Blastospores ( E.g. Taphrina) SEM of budding yeast
  • 106. PRODUCTION OF ASEXUAL SPORES A. SPORANGIOSPORES: They are produced inside globose or sac like structure known as Sporangia.  are of two kinds: a. Motile (Planospores/zoospores) E.g. Pythium, Phytophthora b. non-motile (aplanospore) E.g. Mucor, Rhizopus The structure that bear sporangia is known as Sporangiophore
  • 107. CONIDIOSPORE/CONIDIUM (PL. CONIDIA) Non motile asexual spore usually formed at the tip or side of a Conidiophore  May be borne singly or in chains or in cluster. They vary from • unicellular (Penicillium, microconidia of Fusarium, Colletotrichum) • Bicellular (Diplodia, Lasiodiplodia) • multicellular (Pestalotiopsis, Cercospora). Common in Ascomycotina, Basidiomycotina and Deuteromycotina Conidia of Colletotrichum Micro and macro-conidia Cercospora
  • 108. CHLAMYDOSPORES Chlamydospore (Gr. Chlamys = mantle + spora = seed, spore) is a thick walled asexual spore or conidium that generally function as a resting spore. Terminal or intercalary segments or mycelium may become packed with food reserves and develop thick walls. The walls may be colourless or pigmented with dark melanin pigment. E.g. Mucor racemosus, Saprolegnia, Protomyces, Fusarium Chlamydospore of Fusarium Chlamydospore of Protomyces
  • 109. Sexual Reproduction in Fungi Three distinct phases of Sexual Reproduction 1) Plasmogamy (fusion of cytoplasm) 2) Karyogamy (fusion of nuclei) 3) Karyokinesis/Meiosis (haploidisation)
  • 110. PLANOGAMETIC COPULATION Isogamy:  Morphologically similar but compatible mating type of gametes unite to form a motile zygote. e.g. Synchytrium. Anisogamy:  involves union of one larger gamete with another smaller gamete. Heterogamy:  In this type, a non-motile female gamete (oosphere) lying on oogonium is fertilized by a motile male gamete. Isogamy Anisogamy Heterogamy
  • 111. GAMENTANGIAL CONTACT The male gametangia (antheridium) and the female gametangia (oogonium) come in contact one or more nuclei from the male gamete enter the female gamete through a pore/ fertilization tube In no case, the gametangia actually fuse or lose their identify during the sexual act.  E.g.Pythium, Phytophthora
  • 112. GAMETANGIAL COPULATION This is a process of fusion of entire contents of the two mating gametangia. A. Mixing of entire protoplasm of male and female gametangia  Two gametangia meet and their entire contents fuse in the female gametangium leading to formation of a zygote.  The zygote forms a resting sporangium.  e.g. Aquatic fungi (Chytridiomycetes). B. Isogamous copulation:  Two morphologically similar gametangial hyphae come in contact, the wall at the point of contact dissolves and the contents mix in the cell thus formed.  This results in the formation of Zygospore.  E.g. Mucor, Rhizopus, Phycomyces.
  • 113. SPERMATIZATION • Some fungi like Puccinia (Rust) bear numerous, minute, uninucleate, spore- like male structure called spermatia • These are carried to female gametangial specialized receptive hyphae to which it is attached (Trichogyne) • Pore develops and the content of spermatia pass on to the receptive hyphae
  • 114. SOMATOGAMY somatic cells function as gametes hypha anastomose and the nuclei of opposite mating type are brought together in one cell. The post-fertilization changes result in the production of a fruiting body which is called ascocarp in Ascomycetes and basidiocarp in Basidiomycetes.  common in members of Ascomycotina and Basidiomycotina.
  • 115. TYPES OF FRUITING BODIES ASEXUAL FRUITING BODIES Synemma (PL. Synemmata) or Coremium Sporodochium (Pl. Sporodochia) Pycnidium (Pl. Pycnidia) Acervulus (Pl. Acervuli) SEXUAL FRUITING BODIES A. ASCOCARP Cleistothecium (Pl.Cleistothecia) Perithecium (Pl. Perithecia) Apothecium (Pl. Apothecia) Ascostroma(Pl.Ascostromata) or Pseudothecium(Pl.Pseudothecia) B. BASIDIOCARP
  • 116. ASEXUAL FRUITING BODIES SYNEMMA: A group of conidiophore held together and forming an elongated spore bearing structure E.g. Graphium, Stilbella, Isariopsis (Stilbellaceae)
  • 117. SPORODOCHIUM/SPORODOCHIA: An asexual fruiting structure consisting of cluster of conidiophores woven together on a mass of hyphae E.g. Fusarium, Myrothecium, Tubercularium
  • 118. PYCNIDIUM/PYCNIDIA:  A flask shaped or spherical asexual fruiting body containing conidia and conidiophores E.g. Ascochyta, Septoria, Diplodia, Phoma
  • 119. ACERVULUS/ACERVULI • Flat or saucer or disc shaped bed of short of conidiophores that grow side by side within the host tissue and beneath the epidermis or cuticle • E.g. Colletotrichum, Pestalotia, Sphaceloma
  • 120. SEXUAL FRUITING BODIES CLEISTOTHECIA/CLEISTOTHECIUM Globular or spherical completely closed ascocarp containing asci and ascospores Asci are irregularly arranged are provided with different kind of appendages E.g. Erysiphe, Talaromyces, Eurotium A. ASCOCARP
  • 121. PERITHECIUM/PERITHECIA A flask shaped ascocarp having an opening or pore (ostiole) and paraphyses in the neck Asci are arranged in a hymenium (fertile) layer or parallel series or a basal tuft E.g. Claviceps, Venturia inequalis
  • 122. APOTHECIUM/APOTHECIA An open cup or saucer shaped ascocarp which bears asci and ascocarp E.g. Sclerotinia, Cup fungi (Pyronema, Ascobolus, Peziza, Morchella)
  • 123. ASCOSTROMA/PSEUDOTHECIUM  just like perithecium ( flask- shaped ascocarp provided with an ostiole)  asci are directly formed in a cavity (locule) within the stroma. The ascus is bitunicate (ascus wall is double) E.g. Cochliobolus, Pyrenophora, Ophiobolus, Pleospora,
  • 124. BASIDIOCARP  Sexual fruiting body that consists basidium and basidiospores • Basidia are borne on the under surface of fruit body. • Basidia bear basidiospores exogenously usually on projections called sterigmata. • Most fungi in Basidiomycotina except smuts (Ustilaginales) and rusts (Uredinales) form basidiocarps.
  • 125. ASEXUAL SPORES (Mitospores) Sporangispores Conidium Chlamydospores Blastospores Arthrospores (Oidia)  Oospore  Zygospore  Ascospores  Basidiospores SEXUAL SPORES (Meiospores)
  • 126. OOSPORE  Sexual spore produced by union of two morphologically different gamentangia (gamentangial contact) Found in member of Oomycetes E.g. Pythium, Phytophthora ZYGOSPORE Sexual spore formed by fusion of two morphologically similar gametes (gametangial copulation) Are formed in members of Zygomycetes E.g. Rhizopus, Mucor
  • 127. ASCOSPORE: Sexual spores produced in members of Ascomycotina Produced inside an ascus E.g. Eurotium, Claviceps BASIDIOSPORE: Sexual spores produced in members of Basidiomycotina Borne on basidium E.g. Agaricus, Pleurotus
  • 128. CLASSIFICATION OF FUNGI (AINSWORTH, 1973) MYCOTA (FUNGI) MYXOMYCOTA (SLIME MOLD) (Plasmodium or Pseudoplasmodium present) EUMYCOTA (TRUE FUNGI) (Plamodium/Pseudoplasmodium absent, assimilative phase, typically filamentous) KINGDOM DIVISION SUBDIVISION CLASS ORDER FAMILY MASTIGOMYCOTINA Motile cells (zoospores present; perfect state spores typically oospores ZYGOMYCOTINA Motile cells absent, perfect state spores, zygospores ASCOMYCOTINA Motile cells absent perfect state spore ascospore BASIDIOMYCOTINA Motile cells absent, perfect state spores basidiospores DEUTEROMYCOTINA Motile cells absent, perfect state absent -MYCETES -ALES - ACEAE GENUS SPECIES
  • 129. Sub-division Mastigomycotina Zygomycotina Ascomycotina Basidiomycotina Deuteromycotina Hyphae Aseptate (coenocytic) Aseptate Septate Septate Septate Cell wall Cellulose + Glucans Cellulose- chitosan Chitin and Glucans Chitin Chitin Asexual spore Motile (zoospores/Plano spores) Aplanospore (non-motile sporangiospore) All asexual spore except zoospore and aplanospore (Conidia, Blastospores, Arthrospores) Blastospores and Chlamydospores All asexual spore except zoospore and aplanospore Asexual fruiting body Absent Absent Present Absent Present Sexual spores Oospore Zygospore Ascospore Basidiospore Absent Sexual fruiting body Absent Absent Ascocarp Basidiocarp Absent
  • 130. MYXOMYCOTA MYXOMYCETES (Plasmodium saprobic or free living) PLASMODIOPHOROMYCETES (Plasmodium parasitic within cells of the host plant) PLASMODIOPHORALES PLASMODIOPHORACEAE E.g. Plasmodiophora, Spongospora, Polymyxa CLASS ORDER FAMILY DIVISION
  • 131. EUMYCOTA MASTIGOMYCOTINA Chytridiomycetes Zoospore posteriorly uniflagellate, whiplash type Hyphochytridiomycetes Zoospores anteriorly uniflagellate, tinsel type Oomycetes Zoospores biflagellate, posterior whiplash, anterior tinsel; cellulosic cell wall Chytridiales Synchytriaceae (Synchytrium) Saprolegniales Leptomitales Lagenidiales Peronosporales Pythiaceae (Pythium, Phytophthora ) Albuginaceae (Albugo) Peronosporaceae (Peronospora, Plasmopara, Pseudoperonospora, Sclerospora, Bremia, etc.)
  • 132. ASCOMYCOTINA Hemiascomycetes (Ascocarps and ascogenous hyphae lacking; thallus mycelial or yeast like) Plectomycetes (Asci scattered irregularly in Cleistothecium Loculoascomycetes Ascostroma (Pseudothecium); bitunicate ascus Discomycetes Ascocarp: Apothecium Pyrenomycetes Asci arranged in perithecium; not a exoparasite Endomycetales Protomycetales Taphrinales Spermopthoraceae (Spermopthora, Nematospora) Protomycetaceae (Protomyces) Taphrinaceae (Taphrina) Erysiphales Sphaeriales Erysiphaceae (Erysiphe, Uncinula, Podosphaera, ) Clavicipitaceae (Claviceps) Helotiales Sclerotiniaceae (Sclerotinia, Monilinia) Laboulbeniomycetes Asci arranged in perithecia; exoparasite of arthropods
  • 133. ZYGOMYCOTINA Zygomycetes (Saprobic or if parasitic having mycelium immersed in host tissue) Trichomycetes (Entomogenous fungi and associated with arthropods and attached to the digestive tract of arthropods by a holdfast and not immersed in host tissue) Mucorales Mucoraceae (Rhizopus, Mucor)
  • 134. BASIDIOMYCOTINA Teliomycetes Basidiocarp lacking and replaced by teliospores; parasitic on vascular plants Hymenomycetes (Basidiocarp well developed) Gasteromycetes (No plant pathogen) Uredinales (Rust Fungi) Ustilaginales (Smut Fungi) Pucciniaceae (Puccinia, Hemileia, Uromyces, Phragmidium) Melampsoraceae (Melampsora, Phakopsora) Ustilaginaceae (Smut fungi) (Ustilago, Tolyposporium, Sphacelotheca) Tilletiaceae (Bunt fungi) (Tilletia, Neovossia, Urocystis)
  • 135. DEUTEROMYCOTINA Hyphomycetes (mycelia sterile or sporephores aggregated but not in pycnidia or acervuli) Coelomycetes (sporophore aggregated in acervuli or pycnidia) Agonomycetales (Mycelia Sterilia/zno spore produced) (Rhizoctonia, Sclerotium) Moniliales Moniliaceae (Monilia, Aspergillus, Penicillium, Trichoderma, Verticillium) Dematiaceae (Alternaria, Helminthosporium, Cercospora, Stemphylium Pyricularia, Curvularia, Botrytis) Stillbellaceae (Isariopsis, Graphium, Stilbella) Tuberculariaceae (Fusarium, Myrothecium, Tubercularium) Melanconiales (conidia in acervuli) Sphaeropsidales (Conidia in pycnidia) Melanconiaceae (Colletotrichum, Pestalotia, Marssonina, Cylindrosporium) Sphaeropsidaceae (Ascochyta, Diplodia, Macrophoma, Phoma, Septoria, Phomopsis) Blastomycetes (budding yeast like with or without pseudomycelium; true mycelium lacking)
  • 136. ASPERGILLUS Colonies are usually fast growing, white, yellow, yellow-brown, brown to black or shades of green, mostly consisting of a dense felt of erect conidiophores. Conidiophores terminate in a vesicle covered with either a single palisade-like layer of phialides Conidia are one-celled, smooth or rough-walled, hyaline or pigmented, are produced in long dry chains
  • 137. PENICILLIUM  Phialides brush like; upright –Penicillium  Colonies are usually fast growing, in shades of green, sometimes white, mostly consisting of a dense felt of conidiophores.  Microscopically, chains of single-celled conidia are produced in basipetal succession from a specialised conidiogenous cell called a phialide.
  • 138. TRICHODERMA Colonies are fast growing, at first white and downy, later developing yellowish-green to deep green Conidiophores are repeatedly branched, irregularly verticillate, bearing clusters of divergent, often irregularly bent, flask-shaped phialides. Conidia are mostly green, sometimes hyaline, with smooth or rough walls and are formed in slimy conidial heads (gloiospora) clustered at the tips of the phialides.
  • 139. RHIZOPUS  The genus Rhizopus is characterised by the presence of stolons and pigmented rhizoids, the formation of sporangiophores, singly or in groups from nodes directly above the rhizoids, and apophysate, columellate, multispored, generally globose sporangia.  After spore release the apophyses and columella often collapse to form an umbrella-like structure.  Sporangiospores are globose to ovoid, one-celled, hyaline to brown and striate in many species.
  • 140. MUCOR  Sporangiophores are erect, simple or branched, forming large (60-300 µm in diameter), terminal, globose to spherical, multispored sporangia, without apophyses and with well-developed subtending columellae.  Sporangiospores are hyaline, grey or brownish, globose to ellipsoidal, and smooth-walled or finely ornamented
  • 141. Thallus is plasmodium Plasmodium is holocarpic Zoospore are anteriorly biflagellate, heterokont and uninucleate Flagella are of whiplash type Resting spores occur singly or held together in groups-cystosori Obligate parasite Plasmodiophora brassicae (Club root of Crucifers) PLASMODIOPHORA Kingdom: Mycota Division: Myxomycota Order: Plasmodiophorales Family: Plasmodiophoraceace Genus: Plasmodiophora
  • 142. SPONGOSPORA Cystosorus sponge like  Obligate parasite  Heterokont zoospore  Tuber infection near to the eyes  Secondary zoospore of similar size  Resting spores on spongy balls  Sexual reproduction via isogamy and turns resting spore Kingdom: Mycota Division: Myxomycota Order: Plasmodiophorales Family: Plasmodiophoraceace Genus: Plasmodiophora
  • 143. EUMYCOTA MASTIGOMYCOTINA Chytridiomycetes Zoospore posteriorly uniflagellate, whiplash type Hyphochytridiomycetes Zoospores anteriorly uniflagellate, tinsel type Oomycetes Zoospores biflagellate, posterior whiplash, anterior tinsel; cellulosic cell wall Chytridiales Synchytriaceae (Synchytrium) Saprolegniales Leptomitales Lagenidiales Peronosporales Pythiaceae (Pythium, Phytophthora ) Albuginaceae (Albugo) Peronosporaceae (Peronospora, Plasmopara, Pseudoperonsopora, Sclerospora, Bremia, etc.)
  • 144. SYNCHYTRIUM Obligate, holocarpic, endobiotic parasite  long cycled chytrid Unicellular thallus Does not develop any mycelium through out its life cycle Thin walled summer sporangia and resting spores are formed Sporangia produce zoospores E.g. Synchytrium endobioticum (Potato wart) Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Chytridiomycetes Order: Chytridiales Family: Synchytriaceae Genus: Synchytrium Mature sporangia
  • 145. PYTHIUM Facultative parasite and mostly homothallic Are common as soil inhabitants Mycelium is hyaline coenocytic , inter or intracellular Sporangia are filamentous or oval or globose which arise on unspecialized branches. Zoospore formation occur in spherical vesicle and liberated after burst Zoospores are reniform and laterally biflagellate Oospores are colourless, unornamented and often plerotic Cause damping off of seedling Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Pythiaceae Genus: Pythium
  • 147. PHYTOPHTHORA • Mycelium endophytic, coenocytic, hyaline, branched and inter-cellular • Haustoria club shaped • Sporangiophore easily distinguishable from somatic hypha • Sporangiophore indeterminate, branched , hyaline • Renewed growth of sporangiophore give a sympodial shape • Sporangia are lemon shaped with distinct papilla at the apex • Zoospores are reniform and biflagellate. (anterior tinsel and posterior whiplash) • Zoospore formation occurs in the sporangium itself Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Pythiaceae Genus: Phytophthora
  • 148. PYTHIUM Vs PHYTOPHTHORA PYTHIUM PHYTOPHTHORA Sporangia are produced on somatic hyphae indistinguishable from the other hyphae Sporangia are produced on special aerial reproductive hyphae called sporangiophore Global to oval sporangia either terminal or intercalary The papillate lemon shaped sporangia always terminal in origin but subsequently shifted to the side Differentiation of zoospore take place in vesicle. They are liberated by sudden bursting of vesicle wall Zoospore are differentiated in sporangium and liberated by bursting of special papilla. No vesicle are formed Haustoria absent Haustoria present Germ tube enters the host tissue through stomata or by puncturing of epidermal wall Germ tube enters the host through epidermal cells by infection peg that grows from appresorium
  • 149. ALBUGO Obligate parasite Thallus is eucarpic and mycelial Mycelium is inter cellular with coenocytic hypha Haustoria are knob-like or globular Sporangiophore is club-shaped, short, erect giving rise to chains of spherical sporangia in basipetal succession Sporangia are globose and germinate by producing biflagellate zoospores Albugo candida (White Blister/Rust of Crucifer) Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Albuginaceae Genus: Albugo
  • 150. PLASMOPARA Obligate parasite Sporangiophore hyaline, intercellular with branches at right angle to the axis and irregularly spaced Sterigmata are blunt with single sporangium at its tip Sporangia are elliptical, hyaline and germinate to produce egg shaped zoo spores E.g. Plasmopara viticola (DM of Grapes) Key feature of Family: Peronosporaceae  Mycelium is coenocytic and inter-cellular  Sporangiophore of determinate growth and emerge singly or in tuft, thorough the stomata on the lower surface of leaves Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Peronosporaceae Genus: Plasmopara
  • 151. SCLEROSPORA Sporangiospore are stout with heavy branches clustered at the apex and dichotomously branched Sporangia may be papillate or non- papillate and germinate by forming zoospore Oospore smooth with thick walls and plerotic. E.g. Sclerospora philippinensis, S. sacchari, S. maydis, S. sorghi (DM of Maize) Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Peronosporaceae Genus: Sclerospora
  • 152. PERONOSPORA Sporangiophore hyaline, aseptate and dichotomously branched at acute angle The terminal branches known as sterigmata are sharply pointed Sporangia germinate directly through germtube i.e. zoospores are not formed Oospore is yellow green in colour and its wall is very tough with reticulations. Kingdom: Mycota Division: Eumycota Subdivision: Mastigomycotina Class: Oomycetes Order: Peronosporales Family: Peronosporaceae Genus: Peronospora
  • 153. ASCOMYCOTINA Hemiascomycetes (Ascocarps and ascogenous hyphae lacking) Plectomycetes Asci scattered irregularly in Cleistothecium Loculoascomycetes Ascostroma; bitunicate ascus Discomycetes Ascocarp: Apothecium Pyrenomycetes Asci arranged in perithecium; not a exoparasite Endomycetales Protomycetales Taphrinales Spermopthoraceae (Spermopthora) Protomycetaceae (Protomyces) Taphrinaceae (Taphrina) Erysiphales Sphaeriales Erysiphacea e (Erysiphe, Uncinula, Podosphaera , etc.) Clavicipitacea e (Claviceps) Helotiales Sclerotiniaceae (Sclerotinia, Monilinia) Laboulbeniomycetes Asci arranged in perithecia; exoparasite
  • 154. TAPHRINA True endoparasite strictly confined to definite host Ascus not formed in a synascus Asci arise from binucleate “ Ascogenous cells” Asci lie in a palisade like layer parallel to one another but without enclosing sheath Parasitic on higher plants causing galls and deformation Mycelium is septate constituting typically of binucleate cells, may ne intercellular or sub- cuticular Asexual reproduction by budding E.g. Taphrina deformans (Peach Leaf curl) Kingdom: Mycota Division: Eumycota Subdivision: Ascomycotina Class: Hemiascomyctes Order: Taphrinales Family: Taphrinaceae Genus: Taphrina
  • 155. PROTOMYCES • Ascospore formed in a spore sac- synascus • Parasitic on higher plants causing lesion and galls. • Mycelium is filamentous and septate • Diploid mycelium spreads intercellularly in the host and produces thick walled resting spores which germinate and form a vesicle called synascus • E.g. Protomyces macrosporus (Stem Gall of coriander) Ascogenous cell of Protomyces Stem gall of coriander Kingdom: Mycota Division: Eumycota Subdivision: Ascomycotina Class: Hemiascomyctes Order: Protomycetales Family: Protomycetaceae Genus: Protomyces
  • 156. ERYSIPHE • Obligate parasite • Mycelium is hyaline and mostly ectophytic/superficial • Have globular to pyriform haustoria • Asexual reproduction takes place through conidia on condiophores • Sexual reproduction through ascospores in ascus in enclosed ascocarp (Cleistothecia) • Asci are persistent, globose to pyriform and explodes at the time of release of ascospore • Cleistothecia contains more than one ascus with myceloid/simple appendages Kingdom: Mycota Division: Eumycota Subdivision: Ascomycotina Class: Pyrenomycetes Order: Erysiphales Family: Erysiphaceae Genus: Erysiphe
  • 157. CLAVICEPS Intercellular, hyaline and septate mycelium Perithecia are deeply immersed in stroma which develops an apical head on an erect stalk arising from dark colored sclerotium It has three stages: 1. Sphacelia stage: bears apical hyaline aseptate, oblong-oval conidia in succession. They are embedded in sticky fluid known as honey dew 2. Sclerotial stage: hard purple or brown coloured slightly curved like horn sclerotia replace the ovary 3. Perithecial stage: Sclerotium on germination produces several columnar structures( stalks/stipes). On stipes, rugh, rounded orange or pink coloured small perithecial stroma are produced Hard sclerotium yields an alkaloid known as ergotin (ergotism) Kingdom: Mycota Division: Eumycota Subdivision: Ascomycotina Class: Pyrenomycetes Order: Sphaeriales Family: Claviciptiaceae Genus: Claviceps
  • 158. SCLEROTINIA Cup shaped apothecia which are usually yellowish brown Asci contains 8 ascospores Ascospores are hyaline one celled and ovate Apothecia arise from a seed like sclerotium formed in host tissue Mycelium is septate, cottony, white and turn brown with age Sclerotia are brown to black, spherical to irregular, smooth/wrinkled Kingdom: Mycota Division: Eumycota Subdivision: Ascomycotina Class: Discomycetes Order: Helotiales Family: Sclerotiniaceae Genus: Sclerotinia
  • 159. BASIDIOMYCOTINA Teliomycetes Basidiocarp lacking and replaced by teliospores; parasitic on vascular plants Hymenomycetes Gasteromycetes (No plant pathogen) Uredinales (Rust Fungi) Ustilaginales (Smut Fungi) Pucciniaceae (Puccinia, Hemileia, Uromyces) Melampsoraceae (Melampsora, Phakopsora) Ustilaginaceae (Ustilago, Tolyposporium) Tilletiaceae (Tilletia, Neovossia)
  • 160. PUCCINIA Some are autoecious (P. melanocephala-Brown rust of sugarcane); some are heterocious, macrocyclic which need more than one host to complete their life cycle. Important species: P. graminis, P. recondita, P.striifromis Pedicillate or stalked two celled teliospore Promycelium is septate Urediospore borne singly, echinulate Polymorphic fungus: 5 different type of spores Stage O- Pycniospore Stage I- Aeciospore Stage II- Urediospore Stage III- Teliospore Stage IV-Basidiospore Kingdom: Mycota Division: Eumycota Subdivision: Basidiomycotina Class: Teliomycetes Order: Uredinales Family: Pucciniaceae Genus: Puccinia
  • 162. MELAMPSORA Mycelium is inter cellular, septate, branched and dikaryotic Teliospores are sessile, cylindrical, one celled reddish brown in colour and are borne in crusts of laterally arranged adherent spores Uredospores are ellipsoidal or obovoidal and echinulate. Hyaline, capitate paraphyses are abundant in the uredia Kingdom: Mycota Division: Eumycota Subdivision: Basidiomycotina Class: Teliomycetes Order: Uredinales Family: Melampsoraceae Genus: Melampsora
  • 163. UROMYCES An autoceous (U. fabae)/heteroecious rust (U. pisi) Teliospores are brown, single celled with one apical germ pore, binucleate and thickened at the apex. Urediospores are round to ovate, light brown, echinulate with 3-4 equatorial germ tube Teliospore Urediospore Kingdom: Mycota Division: Eumycota Subdivision: Basidiomycotina Class: Teliomycetes Order: Uredinales Family: Pucciniaceae Genus: Uromyces
  • 164. USTILAGO Teliospores are round or semi round, yellowish brown to olivaceous brown with one side lighter in colour covered with minute spikes The mycelia of Ustilago has two distinct phase Primary mycelia which is hyaline, slender, septate with single haploid nucleus in each cell and formed by germination of Basidiospores Secondary mycelia which is formed by primary mycelia by diploidisaton E.g. U. tritici (Loose smut of wheat) Kingdom: Mycota Division: Eumycota Subdivision: Basidiomycotina Class: Teliomycetes Order: Ustilaginales Family: Ustilaginaceae Genus: Ustilago
  • 165. TILLETIA Teliospore produced singly, medium to large sized usually sculptured, rarely smooth, commonly encased in a hyaline gelatinous sheath. Teliospores germinate by the means of continuous promycelium, terminally bearing basidiospores (6-16) which usually copulate in situ, giving rise to secondary sporidia. Tilletia differ from Ustilago in the method of teliospore germination . Promycelium remains aseptate and 4 basidiospores are formed on the promycelium . Kingdom: Mycota Division: Eumycota Subdivision: Basidiomycotina Class: Teliomycetes Order: Ustilaginales Family: Tilletiaceae Genus: Tilletia
  • 167. HELMINTHOSPORIUM Grow both inter cellularly and intracellularly The hyphae are typically dark bearing conidia on simple erect, septate, conidiophore The conidia are obclavate, brown, thick walled with 8-10 transverse septa and a basal scar indicating the point of attachment on the conidiophore Conidiophores are determinate, ceasing growth with the production of the apical conidia , relatively short and simple of if, sparingly brancehed, the branching is not dichotomous E.g. Helminthsporium graminearum (Stripe disease of barley ), H. oryzae (Brown spot of rice), H. maydis (Southern leaf blight of maize), H. turcicum (Northern leaf blight of maize) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Moniliales Family: Dematiaceae Genus: Helminthosporium
  • 168. PYRICULARIA Perfect state: Magnoporthe grisea Conidiophore are simple, erect, septate and hyaline or grey Hyaline or pale grey, pyriform/pear shaped conidia produced singly at the tip of the conidiophore and it successive growing points. Sympodial branching habit  Mostly two septa and three cells in conidia Produces pyricularin Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Moniliales Family: Dematiaceae Genus: Pyricularia
  • 170. RHIZOCTONIA Mostly soil inhabitants Sclerotia formed of loosely woven hyphae; irregular in shape but of uniform texture brown or black Under suitable conditions they cause diseases like damping off and root rots. The cells of the hyphae are barrel shaped, anastomosing frequently, branching more or less at right angles, and pale brown to brown in colour. (Constriction near branching)  Rhizoctonia bataticola (damping off, Dry root rot of Pulse, cotton, etc.) (Pycnidial stage- Macrophomina phaseoli) Rhizoctonia solani (Sheath blight of cereals) – Thanatephorus cucumeris (Teleomorph) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Agonomycetales Family: Agonomycetaceae Genus: Rhizoctonia
  • 171. SCLEROTIUM characterized by hard, brown to black, fairly large sclerotia with pseudoparenchymatous rind. These are produced on sterile, cotton, white mycelium provided with clamp connections. The perfect states of Sclerotium are Pellicularia (Hymenomycetes) Sclerotium cepivorum -White rot of onion S. oryzae-Stem rot of rice (Perfect state: Magnaporthe salvinii, Conidial state: Nakataea sigmoidea) S. rolfsii - Root rot of soybean, black pepper groundnut, cotton, cabbage tomato etc. (Perfect State: Corticium rolfsii(syn. Pellicularia rolfsii) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Agonomycetales Family: Agonomycetaceae Genus: Sclerotium
  • 172. COLLETOTRICHUM Perfect stage: Glomerella Acervuli subcuticular, subepidermal or peridermal, hyaline to dark brown, thin or thick walled, dehiscence irregular Setae are brown, smooth, septate, acutely pointed at the apex Conidiophore simple of branched only at the base, aseptate or septate, hyaline to brown Conidia hyaline, aseptate, straight to falcate, smooth, thin-walled, sometimes guttulate E.g Bean anthracnose (C. lindemuthianum), Red rot of Sugarcane (C. falcatum) Mago anthracnose (C. gloesporiodes) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Coelomycetes Order: Melanconiales Family: Melanconiaceae Genus: Colletotrichum
  • 173. ALTERNARIA • Mycelium is intercellular but later becomes intracellular • Conidiophore are pale yellow to dark brown, simple or irregularly and loosely branched bearing conidia at the apex • Conidia are dark brown, muriform typically obclavate with distinct oval body and a beak • Conidia may have longitudinal, transverse or oblique septa • Produce Alternarin • E.g. Early blight of Potato (A. solani), Leaf spot of Crucifers (A. brassicicola), A. triticina (Alternaria blight of wheat). Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Moniliales Family: Dematiaceae Genus: Alternaria
  • 174. CERCOSPORA Perfect stage: Mycosphaerella Conidiophores are septate and dark coloured Conidia are long, slender, narrow, tapering and contains many transverse septa Conidia develop sympodially on clustered dark conidiphore Conidia leave scar at the place of attachment Produce cercosporin E.g. C. capsici (Cercospora leaf spot of Chilli) C. personata and C. arachidicola (Tikka disease of Groundnut) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Moniliales Family: Dematiaceae Genus: Cercospora
  • 175. FUSARIUM Mycelium is branched, septate and hyaline Reproduces asexually by three kinds of spores viz., macroconidia, microconidia and chlamydospores Macroconidia are sickle shaped with well marked marked foot cells at the attachment end of spore Microconidia are small, usually unicellular spherical or oval bodies Chlamydospores are round or oval thick walled terminal or intercalary cells of old hyphae. They develop singly or in short chains E.g. Fusarium oxysporum f.sp. ciceri (Wilt of Chickpea) Kingdom: Mycota Division: Eumycota Subdivision: Deuteromycotina Class: Hyphomycetes Order: Moniliales Family: Tuberculariaceae Genus: Fusarium
  • 176. MORPHOLOGY OF BACTERIA Surface adherents: Flagella and Pilli Capsule: protecting layer Cell wall: made of mucopeptide (murein) Cytoplasm: dense and contains granules of glycogen, proteins , fats but lack mitochondria and endoplasmic reticulum Ribosome: 70 S Mesosome: Energy production (respiration), DNA replication, cell division, nitrogen fixation and endo-sporulation Most of the plant pathogenic bacteria are gram negative except Streptomyces (Gram +ve) and Clavibacter (Gram +ve) SHAPE OF BACTERIA 1. Rod shaped/Bacilliform: Most of the plant pathogenic bacteria are rod shaped except Streptomyces (filamentous) and Cornyebacterium (Club- shaped) 2. Spherical: Coccus, Diplococus, Streptococcus, Tetracoccus, Staphylococcus 3. Helical: a. Spirilla: Spirillium undulum b. Vibrio: Vibrio comma
  • 178. GRAM –VE Vs GRAM +VE BACTERIA Gram positive Gram negative Appear bluish or purplish under microscope after staining and do retain crystal violet dye Appear pinkish or reddish under microscope after staining; do not retain gram’s stain gram positive (85% or more mucopeptide and rest is polysaccharide Only 3-12% mucopepetide and rest are lipo-proteins and lipo-polysaccharides Techoic acid present Techoic acid absent Mesosomes are prominent Mesosomes are less prominent Outer membrane absent Outer membrane present 2 rings in basal body of flagellum 4 rings in basal body of flagellum
  • 179. LOCOMOTION OF BACTERIA 1. Monotrichous: A single flagellum at one end of cell. E.g. Xanthomonas 2. Amphitrichous: A single flagellum at each(both) end: E.g. Nitrosomonas 3. Cephalotrichous: Two or more flagella at one end .E.g. P. fluorescens 4. Lophotrichous: Two or more polar flagella at both end of cell. E.g. Spirillum 5. Peritrichous: Large number of flagella surrounding the cell. E.g. Erwinia 6. Atrichous: No flagella at either side e.g Clavibacter
  • 180. REPRODUCTION IN BACTERIA A. ASEXUAL REPRODUCTION  Binary Fission Budding  Sporulation (Endospore) B. SEXUAL REPRODUCTION  Conjugation
  • 181. VARIABILITY IN BACTERIA  CONJUGATION TRANSFORMATION TRANSDUCTION
  • 183. CLASSIFICATION OF BACTERIA KINGDOM: PROKARYOTE GRACILICUTES  Gram –ve;  thin cell wall  Generally, no endospore formation FIRMICUTES  Mostly Gram +ve  Thick cell wall;  Some produce endospore TENERICUTES  Lack cell wall  Mollicutes(MLOs/ Phtyoplasma) MENDOSICUTES  Faulty cell wall (no murein in cell wall) PROTEOBACTERIA (mostly single-celled, non-photosynthetic) DIVISION GENUS:  Agrobacterium,  Erwinia,  Pseudomonas,  Xanthomonas,  Xyllela,  Acidovorax,  Ralstonia FIRMIBACTERIA (Simple gram +ve bacteria) GENUS:  Bacillus  Clostridium THALLOBACTERIA (Gram +ve, branching bacteria) GENUS:  Streptomyces  Clavibacter,  Arthrobacteria MOLLICUTES (soft bodied prokaryote) GENUS:  Phytoplasma  Spiroplasma ARCHAEBACTERIA  Methanogens (Methanobacterium, Methanothermococcu s)  Halophiles (Halobacterium)  Thermoacidophil es (Thermomyces) CLASS
  • 184. KEY CHARACTERISTICS OF SOME IMPORTANT GENERA GENERA MOTILITY SHAPE Gram’s reaction Cultural Characteristics Xanthomonas Single polar flagellum Rod -ve Non-spore forming, non-capsulated and usually yellow water soluble pigment in culture Pseudomonas One or many polar flagella Rod -ve Green/Brown diffusible pigment or no pigment Erwinia Peritrichous Rod -ve Non-spore forming and non- capsulated; no pigment in culture Agrobacterium Peritrichous or sub polar Rod -ve White colonies (rarely yellow) Clavibacter Generally Non- motile Club- shaped or rod +ve Usually non-pigmented Streptomyces Atrichous Filament ous +ve Colonies are first white and smooth and later become velvety due to weft of aerial mycelium Ralstonia Single polar flagellum Rod -ve Creamy white colonies
  • 186. Uncoating Translation Replication Assembly Cell entry (vector) + Cell-to-cell movement . systemic movement Virus Infection Process Vector mediated spread Infected Healthy 1.Cell entry (Penetration) 2.Uncoating 3.Translation 4.Replication 5.Virion assembly 6.Release of new infectious virus 7.Cell to cell movement 8.Long distance (systemic movement) 1.Disassembly 2. Translation 3. Viral movement complex assembly
  • 187. Cell-to-Cell Movement of Virus viral RNA Virus assembly coat protein virus particles Viral movement protein Movement of virus particle through modified plasmodesmata Assembly of viral movement complex Disassembly of viral movement complex Virus disassembly Viral RNA replication, translation, etc Plasmodesmata = junction between plant cells More cell-to-cell movement Host proteins
  • 188. VIRAL MULTIPLICATION AND TRANSMISSION Plant viruses enter cells only through the wounds made mechanically or made by vectors, or are deposited into an ovule by an infected pollen grains. In a RNA replication of an RNA virus, the nucleic acid (RNA) is first freed from the protein coat. It induces the host cell to form the viral RNA polymerase. The RNA polymerase utilizes the viral RNA as a template and forms complementary RNA. The first new RNAs produced are not the viral RNAs but are the mirror images (complementary copies) of that RNA. As the complementary RNA is formed, it is temporarily connected to the viral strand. Thus, the two form a double-stranded RNA that soon separates to produce the original virus RNA and the mirror image (-) strand, with the latter then serving as a template for more virus (+) strand RNA synthesis.
  • 189. In dsDNA viruses, the viral ds DNA enters the cell nucleus and appears to become twisted and supercoiled and forms a mini-chromosome. The latter is transcribed into two single-stranded RNAs (RNA Polymerase II) The smaller RNA is transported to the cytoplasm, where it is translated into virus-coded proteins (Inclusion bodies). The larger RNA is also transported to the same location in the cytoplasm, but it becomes encapsidated by coat protein subunits and is used as a template for the reverse transcription into a complete virion dsDNA. REPLICATION OF dsDNA viruses
  • 190. VIRAL TRANSMISSION HORIZONTAL TRANSMISSION:  Horizontal transmission is by vectors, human pruning shears and tools, and other direct, external contamination. VERTICAL TRANSMISSION:  Vertical transmission occurs when a plant gets it from its parent plant. Either through asexual propagation (cuttings) or in sexual reproduction via infected seeds.
  • 191. MEANS OF VIRAL TRANSMISSION A. MECHANICAL TRANSMISSION: Easiest method of experimental inoculation Sap of infected plant is manually transferred to the healthy plant E.g. TMV, Potato Virus X, etc. B. GRAFT TRANSMISSION/ VEGETATIVE PROPAGATION Scion- Root stock or vice-versa . E.g. Mosaic and leaf roll of Potato, Sugarcane viruses, etc C. DODDER TRANSMISSION Cuscuta used in laboratory for transmission D. SEED AND POLLEN TRANSMISSION Seed transmission: Muskmelon mosaic virus in watermelon, barley stripe mosaic virus, Tobacco ring spot virus in soybean, common bean mosaic virus. Pollen transmission: Prunus necrotic ring spot virus in Cherry
  • 192. E. VECTOR TRANSMISSION: Insect:  Aphid: Cucumber mosaic Virus, Papaya ring spot virus, Potato leaf roll virus, Potato virus Y, etc  White flies: Begomo viruses (Tomato yellow leaf curl, Bean Golden mosaic virus, Okra yellow vein mosaic virus)  Leaf hoppers: Rice tungro virus, Beet curly top virus  Plant hoppers: Maize mosaic, Maize rough dwarf virus  Thrips: Tomato spotted wilt Nematodes:  Longidorus and Xiphinema species are shown to transmit several polyhedral viruses- NEPO(Cherry leaf roll virus and Tomato ring spot virus) and tubular viruses-NETU (Pea early browning and tobacco rattle virus)
  • 193. Fungi:  Olpidium brassicae- Tobacco Necrosis Virus  Polymyxa graminis- Oat Mosaic, Wheat Mosaic  Polymyxa betae- Beet necrosis yellow vein  Spongospora subterranea- Potato mop top virus
  • 194. PRIMARY EVENTS IN PATHOGENESIS/DISEASE CYCLE Inoculation Penetration Infection Invasion Growth and Reproduction of Pathogen (Colonization) Dissemination  Production of dormant/ resting structure and Survival of (Over- seasoning) of the pathogen Infection Invasion Colonization Symptom develop ment Disseminatio n Production of survival/resting structures Dormancy and survival Inoculation Penetration PATHOGENESIS/DISEASE CYCLE
  • 195. MONOCYCLIC VS POLYCYCLIC DISEASE 1. Primary inoculum (Sclerotia, dormant mycelium, oospore, chlamydospores, teliospore) 2. Secondary inoculum (conidia, uredospores, zoospores)
  • 196. INOCULATION Inoculation is the initial contact of the pathogen with the site of the plant where infection is possible. Primary inoculum -The inoculum that survives dormant in the winter or summer and brings about original infections in the spring and autumn is called primary inoculum, and the infections it cause are called primary infections. Secondary inoculum- The inoculum produced from primary infections is called secondary inoculums, and it, in turn causes secondary infections. Generally, inoculum density, inoculum potential and prevalence of favourable environmental conditions determine the success of infection.
  • 197. Two groups of zoospores of the grape downy mildew oomycete have gathered over two leaf stomata. Uredospores of rust. Mitospores (conidia) of a fungus that causes a corn leaf spot disease. Pseudomonas syringae that causes bacterial spot and canker of stone fruits are seen in and surrounding a stoma of a cherry leaf.
  • 198. PENETRATION PRE PENETRATION PENETRATION POST PENETRATION PRE-PENETRATION: Differs in different host pathogen combinations  Attachment of the pathogen to the host  Spore germination in fungi, multiplication in bacteria and hatching of nematode eggs  Perception of the host surface (Host Pathogen recognition)
  • 199. ATTACHMENT OF PATHOGEN TO THE HOST Some of the pathogens like Viruses, phytoplasma, viroid, RLOs, etc. are directly placed in side their host by different agencies. Almost all fungi, bacteria, parasitic plants, nematodes, first come in contact with the host surface and must get attached to the external surface. This is done through some kind of adhesive material present on the propagules surface consisting of water soluble polysaccharides, glycoproteins, lipids or fibrillar material which, when moistened, become sticky and help the pathogen adhere to the plant.  In some fungi, hydration of the spore by moist air or dew causes the extrusion of preformed mucilage at the tip of the spore that serves for the immediate adherence of the spore to the hydrophobic plant surface and resistance to removal by flowing water. Pre-penetration
  • 200. SPORE GERMINATION Spores of different fungi germinate according to the nature of spore & environmental conditions Resting spores: (Asexual; sclerotia, chlamydospores, Sexual- teliospores, Oospore, ascospores) –Propagative spores (conidia, zoospores) Spore may germinate soon after formation or need dormancy Moisture is one of the important factor, followed by temperature, light, O2 Pre-penetration
  • 202. SPORE GERMINATION AND PERCEPTION OF HOST SURFACE It seems that stimulation by the contact with the host surface, hydration and absorption of low molecular weight ionic material from the host surface and availability of the nutrients plays an important role in spore germination. Stimulations received by the spore, mobilizes their food reserves (like lipids, polysaccharides and CHO) or spore contents, and direct them to the cell membrane and cell wall for the formation of germ tube and its extension. Germ tube also perceives the host surface and if it does not receive the appropriate external stimuli, it remains undifferentiated and when the nutrients are exhausted it stop growing and dies. Appropriate physical and chemical signals (like host surface hardiness, its topography, hydrophobicity, and plant signals) leads to germ tube extension and differentiation.
  • 203. RECOGNITION BETWEEN HOST AND PATHOGEN It is still unclear how pathogens recognize their hosts and vice versa. Host components acting as signals for recognition by and activation of pathogens are numerous. They may include  fatty acids of the plant cuticle that activate production of the cutinase enzyme, by the pathogen which breaks down cutin;  galacturonan molecules of host pectin, which stimulate the production of pectin lyase enzymes by the fungus or bacterium;  certain phenolic compounds, such as strigol, which stimulate activation and germination of propagules of some pathogens;  isoflavones and other phenolics, amino acids, and sugars released from plant wounds that activate a series of genes in certain pathogens leading to infection.  A host plant may also send cues for recognition by some of its pathogens by certain of its surface characteristics such as ridges or furrows, hardiness, or release of certain ions such as calcium.
  • 204. INTERACTION BETWEEN HOST AND PATHOGEN
  • 205. PENETRATION Direct penetration Indirect penetration  Fungi may penetrate in either way  Bacteria mostly enter through wounds and some time by natural openings (Stomata, lenticels, hydathodes, natural cracks)  Viruses, viroids, phytoplasma, RLOs etc. by mechanical means (wounds) and by vectors
  • 206. INFECTION Infection is the process by which pathogens establish contact with susceptible cells or tissues of the host and procure nutrients from them. Successful infection evident as: Symptoms Infection is of different types  Local infection  Systemic infection  Latent infection Invasion and reproduction are the two concurrent stages that occur during infection as pathogen invade different cells, grow & multiply
  • 207. INVASION Pathogens enters to variable extents inside the host Different pathogens invade their host as: Ectoparasite e.g. powdery mildew Endoparasites e.g. wilts, viruses etc.  Sub-cuticular pathogens (Apple scab- Venturia inequalis)  Sub-epidermal pathogens (wheat rust )  Vascular pathogens (Pseudomonas solanacearum)  Ecto-endo parasites e.g. potato canker (Corticium solani) Ectoparasite: Powdery mildew Apple scab: Venturia Sub-epidermal: Wheat Rust Endoparasite: bacteria in xylem vessels
  • 208. GROWTH AND REPRODUCTION (COLONIZATION) Different pathogens grow intercellulary & intracellularly inside their host Growth & reproduction rate depends upon invasion behaviour of the pathogen Method of reproduction  Asexual  Sexual  Replication in case of majority of sub-microscopic pathogens (viruses/viroids) Growth and reproduction of the pathogen is affected by pathogen aggressiveness, susceptibility of the host tissue and environmental factors
  • 209. DISSEMINATION/DISPERSAL OF PLANT PATHOGENS Autonomous/Direct/ Active Dispersal Passive or Indirect dispersal Energy of pathogen is used No energy of pathogen is used Through soil, seed and planting materials Through water, air, man, machinery, insects, phanerogamic plants, nematodes and other animals The knowledge of dispersal is essential for effective control and management of disease
  • 210. SEED AS SOURCE OF AUTOMONOUS DISPERSAL  Externally Seed Borne:  Stinking smut/Hill Bunt/Common bunt of Wheat (Tilletia caries/T. foetida)  Covered smut of barley (Ustilago hordei), Anthracnose of Chilli (Colletotrichum capsici) Internally seed borne disease:  Loose smut of Wheat and barley (Ustilago tritici and U. nuda) Concomitant contamination:  Ear cockle of Wheat, Ergot of Bajra, Smuts, Seeds of Cuscuta mixed with seeds of host PLANT AND PLANT ORGANS AS SOURCE OF AUTONOMOUS DISPERSAL  Vegetative parts helps in dispersal of plant pathogens especially virus and viroid diseases of vegetatively propagated plants  Late Blight of Potato was introduced in Europe and North America through seed tubers from South America
  • 211. SOIL AS SOURCE OF AUTONOMOUS DISPERSAL Dispersal in Soil:  occur in case of soil borne pathogens (facultative parasite or saprophyte)  Pathogens persists in the soil as dormant structures such as oospore, chlamydospores, Smut spores or sclerotia Dispersal of pathogens by soil during cultural operations through agricultural implements, irrigation water, workers feet, etc.
  • 212. NEMATODE AS SOURCE OF PASSIVE DISPERSAL Bacteria causing Yellow ear rot of Wheat (Rathyibacter tritici) is dispersed by Anguina tritici (Ear cockle of Wheat) Longidorus and Xiphinema species are shown to transmit several polyhedral viruses-NEPO(Cherry leaf roll virus and Tomato ring spot virus) and tubular viruses- NETU (Pea early browning and tobacco rattle virus) FUNGI AND PHANEROGAMIC PLANTS AS SOURCE OF PASSIVE DISPERSAL  Olpidium brassicae- Tobacco Necrosis Virus, Lettuce big vein virus  Polymyxa graminis- Oat Mosaic, Wheat Mosaic, White Spindle Streak Mosaic, Barley Yellow dwarf mosaic  Polymyxa betae- Beet necrosis yellow vein  Spongospora subterranea- Potato mop top virus  Cuscuta transmits many plant viruses
  • 213. WATER AS AGENT OF PASSIVE DISPERSAL (HYDROCHORY) Facilitate short distance and long distance dispersal of fungi, bacteria and nematodes Mycelial fragments, spores or sclerotia of fungi are dispersed mainly through surface running water and rain splash. E.g. Colletotrichum, Fusarium, Pythium, Phytophthora, Sclerotium,etc. WIND AS AGENT OF PASSIVE DISPERSAL (AEROCHORY) Wind act as a potent carrier of propagules of fungi, bacteria and viruses E.g. Powdery mildew, Downey mildew, Rusts, Smuts, etc. DISPERSAL BY OTHER ANIMALS Birds help in dispersal od phanerogamic parasitic plants such as Cuscuta and Dendrophthae  Conidia of Colletotrichum falcatum (Red rot of Sugarcane) and Sclerotia of many fungi have been detected in Cattle dung.
  • 214. KOCH’S POSTULATE/PATHOGENECITY TEST Pathogen must be invariably found in the affected plant or it must be associated with in some forms The pathogen should be separated from infected host and grown in artificial culture The pathogen from artificial culture should be able to reproduce the disease when inoculated on a healthy plant of some kind from which it was isolated. The symptom produced should be identical with those seen on the plant from which isolation was made The artificially produced disease should yield the same pathogen of re-isolation
  • 215. SURVIVAL OF PLANT PATHOGENS A. INFECTED HOST AS RESERVOIR OF INOCULUM Collateral Hosts (wild hosts of same families)  Pyricularia grisea can infect the grass weeds like Brachiara mutica, Dinebra retroflexa, Leersia hexandra, Panicum repens, etc. and survive during off- season Alternate hosts (Wild hosts of other families)  Puccinia graminis fsp. tritici survive on Barberry (Alternate Host) Self sown crops:  Self sown, voluntary and early sown crops serve as reservoir of plant pathogens such as Rice tungro virus Ratoon Crops (Sugarcane mosaic) Survival by latent Infection  Xyllela fastidiosa (Pierce’s disease of Grape Vine) infect weeds without developing visible symptoms
  • 216. Soil inhabitants:  Those which survive indefinitely in soil as saprophyte (obligate or facultative) even in absence of host  E.g. Pythium and Rhizoctonia survive as oospore and sclerotia for longer period in soil in active form Soil invaders/Root inhabitants:  Survive in soils in close association with hosts.  The saprophytic phase continues as long the host is not completey decomposed.  E.g. Fusarium species, Verticillium species, etc. Rhizosphere colonizers:  Colonize the dead substrate in the root region and continue to live for longer period  Are more tolerant to soil antagonism  E.g. Cladosporium fulvum (Leaf mould in tomato) B. SAPROPHYTIC SURVIVAL OUTSIDE THE HOST
  • 217. Plant viruses: no resting stage; transmitted through continuous infection chain Bacteria: no resting spores; continually live in their active parasitic stage in living host or as active saprophyte Nematode: survive in form of active parasitic phase on living host and also survive through dormant structures such as eggs, cysts, galls Phanerogamic parasites: survive in dormant state through seeds.  Fungi  Soil Borne: Oospores, sclerotia, Chlamydospores, thickened hypha, microsclerotia, Rhizomorphs  Seed Borne:  Dormant fungal structures on dormant or active host:  Survival in association with insects, nematodes and fungi:  Corn flea beetle carries the corn wilt pathogen inside its body (Xanthomonas stewartii)  Fungi like Polymyxa and Spongospora transmit viruses C. SURVIVAL AS DORMANT SPORES OR SPECIALIZED RESTING STRUCTURES
  • 218. CRITERIA FOR PATHOTOXIN A pathotoxin should produce all characteristic symptoms of the disease when applied in low concentration Toxin production by the pathogen should be directly related to its ability to cause disease Toxin and pathogen should have same host range; same resistance and susceptibility spectrum MICROBIAL TOXINS AND ENZYMES BASED ON THE ROLE IN PATHOGENESIS:  Pathotoxin  Vivotoxins  Phytotoxins
  • 219. A. PATHOTOXINS (Wheeler and Luke, 1963) These are the toxins which play a major role in disease production and produce all or most of the symptoms characteristic of the disease in susceptible plants. Most of these toxins are produced by pathogens during pathogenesis. E.g. Victorin: Cochliobolus victoriae (Helminthosporium victoriae), the causal agent of Victoria blight of oats. This is a host specific toxin. SELECTIVE PATHOTOXIN (HOST- SPECIFIC) NON-SELECTIVE PATHOTOXIN (NON-HOST SPECIFIC) T-toxin: H. maydis (Race T) Tentoxin: Alternaria alternata HC-toxin- H. carbonum Tabtoxin/wild fire toxin: Pseudomonas tabaci HS-toxin- H. sacchari Phaseolotoxin: Pseudomonas syringae pv. phaseolicola Phytoalternarin: Alternaria kikuchiana PC-toxin: Periconia circinata
  • 220. VIVOTOXIN (Diamond & Waggoner, 1953)  These are the substances produced in the infected host by the pathogen and / or its host which functions in the production of the disease, but is not itself the initial inciting agent of the disease.  Generally non-host specific  Ex:-Fusaric acid – Wilt causing Fusarium sp. Piricularin- Pyricularia oryzae Lycomarasmin- F . oxysporum f.sp. lycopersici  Vivotoxin is always isolated from diseased plants and it should not be present in healthy plants  Such toxin should be chemically characterized  When introduced in its pure form, it must be able to produce characteristics symptoms or a part of disease syndrome in question.
  • 221. PHYTOTOXIN (Wheel and Luke, 1963) These are the substances produced in the host plant due to host- pathogen interactions for which a causal role in disease is merely suspected rather than established. These are the products of parasites which induce few or none of the symptoms caused by the living pathogen. They are non-specific and there is no relationship between toxin production and pathogenicity of disease causing agent. • Eg. Alternaric acid – Alternaria solani,
  • 222. ENZYMES Substrate Effect Enzymes Pathogen Involved Pectic substance Breakdown in the chain of linkage Pectin methyl esterase Pectin lyase Polygalacturonase Transeliminase Phytophthora Rhizopus Erwinia caratovora Rhizoctonia solani Sclerotinia sclerotiorum Cellulose Turns to glucose Softening/ disintegration of cell wall Cellulase/Gluconase Fungal, bacterial, nematodes and Phanerogamic plants Hemicellulose Turns into simple sugar Hemicellulase β-Manosidase α-galctoriodose Sclerotinia fructigena S. sclerotiorium Lignin Breakdown Lignanease Ligase Oxidase Alternaria Cephalosporium Fusarium
  • 223. EPIDEMICS AND EPIDEMIOLOGY/EPIPHYTOLOGY Epidemic??? Epidemiology: The study of epidemics and factors influencing them is called epidemiology. Epidemiology is concerned simultaneously with populations of pathogens and host plants as they occur in an evolving environment, i.e., the classic disease triangle. It deals with outbreaks and spread of diseases in a population or at population level
  • 224. Slow epidemic (Tardive epidemic)  Occurs in monocyclic diseases  On perennial plants  E.g. Dutch elm disease, Chestnut blight Fast epidemic (Explosive epidemic)  In polycyclic diseases  Annual crops  E.g. rice blast, potato blight
  • 225. Epidemics in the past The Irish potato famine of 1845–1846 was caused by the Phytophthora late blight epidemic of potato, The Bengal famine of 1943 was caused by the Cochliobolus (Helminthosporium) brown spot epidemic of rice.
  • 226. Questions in one’s mind during outbreak of disease What will happen over the next few weeks? Will all the plants die, leaving nothing to harvest ? Or Will only currently infected plants will yield less? Are all the plants infected and only few showing symptoms? Is the pathogen air/water/wind/vector dispersed? Can this crop be planted next season etc.?  Epidemiology helps in answering entire questions by describing disease development pattern during the single season and from year to year.
  • 227. DISEASE PYRAMID/TETRAHEDRON DISEASE SUSCEPTIBLE HOST  Susceptible host  Virulent pathogen  Favourable environment  Development of disease is affected by  Duration & frequency of each element of over time,  Timing, Duration & frequency of favourable environment  Human activities such as training/pruning
  • 228. ELEMENTS OF AN EPIDEMIC IN FUNGAL & BACTERIAL DISEASES: The Host (susceptible) The Pathogen (virulent) Environment (favourable) Human activity IN VIRUS & VIRUS LIKE DISEASES The Virus The Host The Vector Environment
  • 229. FACTORS AFFECTING DEVELOPMENT OF EPIDEMICS A. HOST FACTORS Levels of Genetic Resistance or Susceptibility of the Host  Highly resistant  Moderately resistant  Susceptible Degree of Genetic Uniformity of Host Plants  Monoculture (vertical/ horizontal resistance) e.g.  Cochliobolus (Helminthosporium) blight on Victoria oats and  in southern corn leaf blight on corn carrying Texas male-sterile cytoplasm. Type of Crop  Annual  Perennial Age of Host Plants  Plants change in their reaction (susceptibility or resistance) to disease with age. The change of resistance with age is known as Ontogenic resistance.
  • 230. B.PATHOGEN FACTORS Levels of Virulence/aggressiveness Quantity of Inoculum near Hosts Type of Reproduction of the Pathogen  Sexual (oospores, ascospores)  Asexual (conidia, zoospores) Ecology of the Pathogen  Ectoparasites  Endoparasites Mode of Spread of the Pathogen  Active dispersal  Passive dispersal
  • 231. ENVIRONMENTAL FACTORS Temperature Light Moisture Dew duration HUMAN FACTORS- A KEY PLAYER  Site selection  Selection of Propagative material  Cultural practices  Disease control measures  Introduction of new pathogen
  • 232. MATHEMATICAL MODEL FOR DISEASE SPREAD Vander Plank in 1963 in his historical book "Plant Diseases- Epidemics and Control” suggested a model based on the infection rate 'r’. The equation for describing a epidemic is: X= Xo ert Where, Xo= Amount of critical inoculum r= average infection rate t= time during infection has occurred X= Proportion of disease at any one time e= base of natural logarithm
  • 233. MEASUREMENT OF PLANT DISEASE AND YIELD LOSS The disease is measured in term of : Disease incidence ( disease prevalence) Disease severity (extent of damage to host) Yield loss (the yield loss is the difference between attainable yield and actual yield)
  • 234. AREA UNDER DISEASE PROGRESS CURVE (AUDPC) useful quantitative summary of disease intensity over time, for comparison across years, locations, or management tactics. The most commonly used method for estimating the AUDPC, the trapezoidal method, is to discretize the time variable (hours, days, weeks, months, or years) and calculate the average disease intensity between each pair of adjacent time points (Madden et al. 2007). Where, Yi = disease severity on the ith date, ti= time on which Yi was recorded and n = number of times observations were taken.
  • 235. Severity: 5, 10, 30,60, 80, 90, 100 Days of observation: 7, 14, 21, 28, 35, 42, 49 Calculate AUDPC???
  • 236. CLASSIFICATION OF DISEASE BASED ON EPIDEMIOLOGY Monocyclic disease Polycyclic disease Polyeptic disease
  • 237. APPLICATION OF DISEASE EPIDEMIOLOGY FOR DISEASE MANAGEMENT A. Disease forecasting on the basis of primary inoculums and environmental conditons B. Fixing strategies to reduce the final disease  Control measures to reduce initial inoculum (Xo): Rouging, Soil fumigation, hot water treatment, Sanitation, Insect vector control, summer deep ploughing, Resistant varieties, Soil solarization  Control measure to reduce infection rate (r): Use of horizontal resistance, Modification of cultural practices, Proper crop geometry  Control measure to reduce time during infection (t): Early or late planting, Early or late maturing varieties
  • 238. CRITERIA FOR PATHOTOXIN A pathotoxin should produce all characteristic symptoms of the disease when applied in low concentration Toxin production by the pathogen should be directly related to its ability to cause disease Toxin and pathogen should have same host range; same resistance and susceptibility spectrum MICROBIAL TOXINS AND ENZYMES BASED ON THE ROLE IN PATHOGENESIS:  Pathotoxin  Vivotoxins  Phytotoxins
  • 239. A. PATHOTOXINS (Wheeler and Luke, 1963) These are the toxins which play a major role in disease production and produce all or most of the symptoms characteristic of the disease in susceptible plants. Most of these toxins are produced by pathogens during pathogenesis. E.g. Victorin: Cochliobolus victoriae (Helminthosporium victoriae), the causal agent of Victoria blight of oats. This is a host specific toxin. SELECTIVE PATHOTOXIN (HOST- SPECIFIC) NON-SELECTIVE PATHOTOXIN (NON-HOST SPECIFIC) T-toxin: H. maydis (race T) Tentoxin: Alternaria alternata HC-toxin- H. carbonum Tabtoxin/wild fire toxin: Pseudomonas tabaci HS-toxin- H. sacchari Phaseolotoxin: Pseudomonas syringae pv. phaseolicola Phytoalternarin: Alternaria kikuchiana PC-toxin: Periconia circinata
  • 240. VIVOTOXIN (Diamond & Waggoner, 1953)  These are the substances produced in the infected host by the pathogen and / or its host which functions in the production of the disease, but is not itself the initial inciting agent of the disease.  Generally non-host specific  Ex:-Fusaric acid – Wilt causing Fusarium sp. Piricularin- Pyricularia oryzae Lycomarasmin- F . oxysporum f.sp. lycopersici  Vivotoxin is always isolated from diseased plants and it should not be present in healthy plants  Such toxin should be chemically characterized  When introduced in its pure form, it must be able to produce characteristics symptoms or a part of disease syndrome in question.
  • 241. PHYTOTOXIN (Wheel and Luke, 1963) These are the substances produced in the host plant due to host- pathogen interactions for which a causal role in disease is merely suspected rather than established. These are the products of parasites which induce few or none of the symptoms caused by the living pathogen. They are non-specific and there is no relationship between toxin production and pathogenicity of disease causing agent. • Eg. Alternaric acid – Alternaria solani,
  • 242. ENZYMES Substrate Effect Enzymes Pathogen Involved Pectic substance Breakdown in the chain of linkage Pectin methyl esterase Pectin lyase Polygalacturonase Transeliminase Phytophthora Rhizopus Erwinia caratovora Rhizoctonia solani Sclerotinia sclerotiorum Cellulose Turns to glucose Softening/ disintegration of cell wall Cellulase/Gluconase Fungal, bacterial, nematodes and Phanerogamic plants Hemicellulose Turns into simple sugar Hemicellulase β-Manosidase α-galctoriodose Sclerotinia fructigena S. sclerotiorium Lignin Breakdown Lignanease Ligase Oxidase Alternaria Cephalosporium Fusarium
  • 243. EPIDEMICS AND EPIDEMIOLOGY/EPIPHYTOLOGY Epidemic??? Epidemiology: The study of epidemics and factors influencing them is called epidemiology. Epidemiology is concerned simultaneously with populations of pathogens and host plants as they occur in an evolving environment, i.e., the classic disease triangle. It deals with outbreaks and spread of diseases in a population or at population level
  • 244. Slow epidemic (Tardive epidemic)  Occurs in monocyclic diseases  On perennial plants  E.g. Dutch elm disease, Chestnut blight Fast epidemic (Explosive epidemic)  In polycyclic diseases  Annual crops  E.g. rice blast, potato blight
  • 245. Epidemics in the past The Irish potato famine of 1845–1846 was caused by the Phytophthora late blight epidemic of potato, The Bengal famine of 1943 was caused by the Cochliobolus (Helminthosporium) brown spot epidemic of rice.
  • 246. Questions in one’s mind during outbreak of disease What will happen over the next few weeks? Will all the plants die, leaving nothing to harvest ? Or Will only currently infected plants will yield less? Are all the plants infected and only few showing symptoms? Is the pathogen air/water/wind/vector dispersed? Can this crop be planted next season etc.?  Epidemiology helps in answering entire questions by describing disease development pattern during the single season and from year to year.
  • 247. DISEASE PYRAMID/TETRAHEDRON DISEASE SUSCEPTIBLE HOST  Susceptible host  Virulent pathogen  Favourable environment  Development of disease is affected by  Duration & frequency of each element of over time,  Timing, Duration & frequency of favourable environment  Human activities such as training/pruning
  • 248. ELEMENTS OF AN EPIDEMIC IN FUNGAL & BACTERIAL DISEASES: The Host (susceptible) The Pathogen (virulent) Environment (favourable) Human activity IN VIRUS & VIRUS LIKE DISEASES The Virus The Host The Vector Environment
  • 249. FACTORS AFFECTING DEVELOPMENT OF EPIDEMICS A. HOST FACTORS Levels of Genetic Resistance or Susceptibility of the Host  Highly resistant  Moderately resistant  Susceptible Degree of Genetic Uniformity of Host Plants  Monoculture (vertical/ horizontal resistance) e.g.  Cochliobolus (Helminthosporium) blight on Victoria oats and  in southern corn leaf blight on corn carrying Texas male-sterile cytoplasm. Type of Crop  Annual  Perennial Age of Host Plants  Plants change in their reaction (susceptibility or resistance) to disease with age. The change of resistance with age is known as Ontogenic resistance.
  • 250. B.PATHOGEN FACTORS Levels of Virulence/aggressiveness Quantity of Inoculum near Hosts Type of Reproduction of the Pathogen  Sexual (oospores, ascospores)  Asexual (conidia, zoospores) Ecology of the Pathogen  Ectoparasites  Endoparasites Mode of Spread of the Pathogen  Active dispersal  Passive dispersal
  • 251. ENVIRONMENTAL FACTORS Temperature Light Moisture Dew duration HUMAN FACTORS- A KEY PLAYER  Site selection  Selection of Propagative material  Cultural practices  Disease control measures  Introduction of new pathogen
  • 252. MATHEMATICAL MODEL FOR DISEASE SPREAD Vander Plank in 1963 in his historical book "Plant Diseases- Epidemics and Control” suggested a model based on the infection rate 'r’. The equation for describing a epidemic is: X= Xo ert Where, Xo= Amount of critical inoculum r= average infection rate t= time during infection has occurred X= Proportion of disease at any one time e= base of natural logarithm
  • 253. MEASUREMENT OF PLANT DISEASE AND YIELD LOSS The disease is measured in term of : Disease incidence ( disease prevalence) Disease severity (extent of damage to host) Yield loss (the yield loss is the difference between attainable yield and actual yield)
  • 254. AREA UNDER DISEASE PROGRESS CURVE (AUDPC) useful quantitative summary of disease intensity over time, for comparison across years, locations, or management tactics. The most commonly used method for estimating the AUDPC, the trapezoidal method, is to discretize the time variable (hours, days, weeks, months, or years) and calculate the average disease intensity between each pair of adjacent time points (Madden et al. 2007). Where, Yi = disease severity on the ith date, ti= time on which Yi was recorded and n = number of times observations were taken.
  • 256. CLASSIFICATION OF DISEASE BASED ON EPIDEMIOLOGY Monocyclic disease Polycyclic disease Polyeptic disease
  • 257. APPLICATION OF DISEASE EPIDEMIOLOGY FOR DISEASE MANAGEMENT A. Disease forecasting on the basis of primary inoculums and environmental conditons B. Fixing strategies to reduce the final disease  Control measures to reduce initial inoculum (Xo): Rouging, Soil fumigation, hot water treatment, Sanitation, Insect vector control, summer deep ploughing, Resistant varieties, Soil solarization  Control measure to reduce infection rate (r): Use of horizontal resistance, Modification of cultural practices, Proper crop geometry  Control measure to reduce time during infection (t): Early or late planting, Early or late maturing varieties
  • 258. PLANT DISEASE FORECASTING Plant disease forecasting is an applied epidemiology and involves: all the activities in ascertaining and notifying the farmer in an area/community that the conditions are sufficiently favourable for certain diseases, that application of control measures will result in economic gain or that the amount of disease expected is unlikely to be enough to justify the expenditure of time, money and energy for its control.
  • 259. PLANT DISEASE FORECASTING  requires complete knowledge of epidemiology  is made more reliable if the reasons for a particular disease developing under certain conditions are known.  Experimental investigation is necessary to show that exactly what stage during the disease development is critical for variable incidence or intensity of disease.  A timely and reliable forecast gives the farmer many options to choose from that he/she can weigh the risks, costs and benefits of his possible decisions.
  • 260. CONDITIONS OF DISEASE FORECASTING The disease must be causing economically significant damage in terms of loss of quantity and quality of the produce in the area concerned. The onset, speed of spread and destructiveness of the disease is variable mostly due to dependence on the weather which is variable. Control measures are known and can be economically applied by the farmer when told to so. Information on weather- disease relationship is fully known.
  • 261. SOME SUCCESSFUL EXAMPLES OF DISEASE FOREASTING LATE BLIGHT OF POTATO Holland pioneered the development of forecasting and spray warning services for the control of late blight of potato. Van Everdingen (1926) analyzed the combined effect of several weather conditions on the development of Phytophthora infestans and evolved four rules, popularly known as Dutch rules, on which the appearance of blight was observed to depend. Dutch Rule: i) Night temperature below dew point at least for 4 hours ii) A minimum temperature of 10 C or above iii) A mean cloudiness on the next day of 0.8 or more, and iv) At least 0.1mm rainfall during the next 24 hours. When all these four conditions were obtained in Holland, potato blight was expected after the next 7 days and therefore the control measures were immediately recommended to the farmers.
  • 262. RICE BLAST: In India, forecasting rice blast ( Pyricularia ozyzae) is done by correlative information method. It is predicted on the basis of minimum night temperature 20 to 26°C in association with high relative humidity of 90% or above. EARLY AND LATE LEAF SPOTS OF GROUNDNUT When the groundnut foliage remains wet for a period greater than or equal to 10 h and the minimum temperature is 21°C or higher for two consecutive days or nights, the disease development is forecasted in USA
  • 263. DISEASE FORECASTING METHODS EMPIRICAL FORECASTING : Derived based upon pathogen development and its life cycle, effected by various environmental conditions VAN DER PLANK MODEL : Based on information of initial inoculum of disease (Xo), the rate of the disease increase (r) in particular time (t) and estimated the final disease as their magnitude i.e. X= Xo ert COMPUTER BASED DISEASE FORECASTING: Utilizes quantitative data regarding the effects of weather variables on pathogenesis and production of primary and secondary inocula, pathogen and vector activities, antagonists as well as genetic variation in the pathogen and host EPIDEM- first model for early blight of potato BLITECAST-late blight of potato SYMPHYT- late blight of potato EPIMAY-Southern Corn leaf blight EPIPRE- Yellow rust of Wheat
  • 265. METHODS OF LOSS ASSESSMENT Survey method: Based on study over large area about disease incidence and its impact Experimental method:
  • 266. REMOTE SENSING • Remote sensing refers to noncontact measurements of radiation reflected or emitted from agricultural fields, which are based on the interaction of electromagnetic radiation with soil or plant material. • Based on aerial photography or satellite photography
  • 267. The electromagnetic spectrum of greatest interest to use in remote sensing is the optical wavelengths, which extend from 0.3–15 μm. This is divided into part: i) 0.38-3 μm (reflective part), ii) 0.38-0.72 μm (visible part), iii) 0.72-3 μm (infrared), iv) 0.72-1.3 μm (near infrared), v) 1.3-3.0 μm (middle infrared) vi) emissive part: 7-15 μm far infrared (emissive/ thermal infrared).
  • 268. WHEAT RUST MONITORING USING REMOTE SENSING In recent years, significant progress is made in remote sensing technologies for monitoring wheat rust at following four levels  Single Leaf scale (ground based)  Canopy scale (ground based)  Field crop scale (aerial)  Countries/regional scale (satellite based) Remote sensing data at single leaf, canopy and field crop scale levels provide local and limited experimental information. While satellite based remote sensing can provide a sufficient and inexpensive data base for rust over large wheat regions or at spatial scale. It also offers the advantage of continuously collected data and availability of immediate or archived data sets.