Course Powerpoint (FFV).pptx

HARAMAYA UNIVERSITY
COLLEGE OFAGRICULTURE AND ENVIRONMENTAL SCIENCES
SCHOOL OF PLANT SCIENCES
MSc PROGRAMS IN AGRONOMYAND PLANT BREEDING
Compiled Lecture Notes on Plant Pathology (PLCP 521)
First Semester of the 2021/2022 Academic Year
By
Abu Jambo (PhD in Plant Pathology)
Haramaya, Ethiopia

 This course contains four major chapters:
1. Introduction
2. Physiology of Host-Pathogen Interactions
3. Genetics of Host-Pathogen Interactions
4. Plant Disease Epidemiology
Course Contents

What is Plant Pathology?
Plant pathology is the science of plant diseases and their
management.
Study of the causes, nature, development and management of
plant diseases.
Study plant disease and attempt to improve the chances for
survival of plant.
What does it involve?
Study of the causes (pathogens) of plant disease
The mechanisms by which the causes produce a disease
Interactions between the causal agents and the host plant
The methods of preventing or controlling diseases
3
Chapter 1: Introduction

Branches of Plant Pathology
Mycology – science of fungi
Bacteriology – science of bacteria
Virology – science of viruses
Nematology – science of nematodes
What is disease?
Malfunctioning of host cells and tissues by pathogens that
leads to symptom development
4
Introduction…

Is abnormal change in physiological process which disturb the
normal activity of an organism.
Most conclusive definition
Plant disease is a deviation from the normal physiological
and morphological development of a susceptible host plant and
is brought about by a virulent pathogen or by unfavorable
environmental factors and is manifested by external signs
called symptoms
5
Introduction…

The concept of disease in plant
Healthy Plant is a plant that can carry out its
physiological activities (cell division, water
absorption, photosynthesis, etc.) to the best of its
genetic potential.
When plants are diseased, one or more of the
above functions are disturbed.
6
Introduction…

How do pathogens cause disease in plants?
Weakening the host by continually absorbing food from the
host for their own use.
Disturbing the metabolism of the host cells through
production of toxin, enzymes or growth regulators .
Blocking the transportation of food, nutrients and water by
closing the conductive tissues.
Consuming the contents of host cells upon contact.
7
Introduction…

Disease development
For a disease to occur there should be:
Host – susceptible
Pathogen – virulent and
Environment – conducive to the
pathogen
The interaction b/n the three disease
elements is called Disease triangle.
8
Introduction…

Such a situation with
all three elements
equally favorable to
disease rarely occurs
The shape of the
triangle varies
depending on each
element’s degree of
suitability to disease
development
9
Introduction…

Plant diseases are of paramount importance to humans b/c they damage
plants.
a) Causes starvation/limit quantity and quality of crops
e.g. Late blight of potato
It destroyed potato crop in Ireland around 1845.
Resulted in death and migration of millions.
 It has also forced man to:
- Understand the importance of plant disease
- Make scientific investigations
- Brought the science of plant pathology into sight
- Played role for the begin of agricultural extension
10
Introduction…
Importance of Plant Diseases

b) Increases cost of production
 Plant Diseases May Cause Financial Losses
Cost for chemicals,
equipment for spray,
laborers
c) Limits kinds of crops to be grown
only resistance crop species will be selected
11
Introduction…

d) Plant Diseases May Make Plants Poisonous to Humans and
Animals
– Production of toxic fungal metabolites
Mycotoxin -ochratoxins, aflatoxins, ergotism
mycotoxins are proven to cause carcinogens
disrupt the immune system
retard the growth of animals or humans
Causes paralysis, disorders, gangrenous,
convulsiveness
e.g. Ergot (Calviceps purpurea) of rye
12
Introduction…

Role of Plant Pathology
• Preserve the environment
• Secure global food security more importantly in developing
country
• Help grow healthy crops
• Ensure an adequate food supply
• Maintain the beauty of ornamental plants
• Invent new ways to control/manage plant diseases
• Have rewarding professional careers
• Enjoy lifelong learning and world travel
Introduction…

Classification is very important for communication about the
disease.
Depending on purpose we have two types of classification
1. Traditional approaches
2. Scientific approaches
1. Traditional approaches
Based on perpetuation mechanism of the pathogen
Soil born disease
Air born disease
seed born disease
17
Chapter 2: Classification of Plant Diseases

Based on the type of the plant affected
Cereal disease
Fruit disease
Vegetable disease
Based on organ of the plant affected
Foliar disease
Root disease
Fruit disease
Stem disease
Based on sign and symptom of the disease
Rust disease
Root rot disease
Mildews
Wilt disease
18
Classification of Plant Diseases …

2. Scientific classification
Infectious plant disease
External causal agent is associated
Can be transmitted from infected to healthy plant
Non-Infectious plant disease
No external agent/organism is associated
Do not transmitted from infected to healthy.
19

Infectious causes of plant diseases
What are the causes of plant disease?
The causal agents of plant disease can be categorized as:
Infectious causes
Fungi
Bacteria
Virus
Nematode
Mycoplasmas like organisms
Parasitic higher plants
Non- infectious causes
Unfavorable weather conditions
Unfavorable soil conditions
Improper agricultural practices
Environmental pollution
20

Fungi: 8,000 known pathogenic species causing
100,000 diseases
Viruses: 1000 different viruses causing 10,000 or
more diseases
Nematodes: 500 species
Bacteria: 275 species
Parasitic plants: only 5-6 plants that are of concern
21

Small, microscopic
Usually filamentous,
Eukaryotic – cell contain a nucleus
Has cell walls, multicellular (except yeast)
Yeast: single celled fungus reproduce by budding or fission.
Heterotrophic-devoid of chlorophyll (can’t make their own
food)- feed by absorbing their food
Reproduce by spores,
Need moist, warm places to grow.
What is fungi?
22

Morphology of fungi
Most fungi have a filamentous vegetative
body called a mycelium/thallus.
The individual branches of the mycelium are
called hyphae
23

Hyphae have cross walls called septa
Hyphae with septa is called septate, and with
out septa is called aseptate /coenocytic.
Some lower fungi lack true mycelium and
instead produce a rhizomycelium.
24

Morphology of fungi
25

Morphology of fungi
Types of hyphae and growth of hyphae from spore
26

…
27

28
Fungi have both asexual (anamorphic) and sexual
(teleomorphic) reproduction
Asexual Reproduction
Fragmentation/breakage of somatic hyphae
Fusion of the somatic cell
Budding
production of spores by modified hyphae
Sexual reproduction
Spore produced as the result of sexual
fertilization

29
Schematic presentation of the generalized fugal life cycles

30
Fungi reproduce chiefly by means of spore,
Spores are specialized propagative or reproductive
bodies.
Help the fungi disseminate, or spread to new
sites.
Help the fungi survive stress periods, when there
is no food source
spores are grouped into
exogenous spores - that develop without sac-like
structure
endogenous spores - that develop within a body
fruiting

31

Sporangiospores are borne in a sac called a sporangium. Which may be motile by
means of flagella and are called Zoospores or non-motile, the Aplanospore.
The sporangium is borne on a specialized hypha known as a sporangiophore.
A conidium is borne on the tip or side of a specialized hypha known as a
conidiophore.
Occasionally there is very little or no difference between the
shape of spores and structure of the hyphae producing it.
32
Asexual reproduction

33

34
Asexual spores include:
Aeciouspores: exogenous spore produced in aecium
Blastospores: exogenous spores that develop by budding
of parent cell, from end or side of the parent cell; also
called thallospores
Oidia: exogenous spores formed by fragmentation of
vegetative hyphae
Chlamydospores: exogenous thick-walled usually
resting asexual spores that develop directly from hyphae
cells

Teliospores: exogenous spores produced on telia
Urediospores: binucleate exogenous spores of
uredinales
Pycniospores: endogenous spores produced in cup
of flask-shaped receptacles on hyphae; also called
stylospores or spermatia
Zoospores: endogenous motile unicellular spores;
also called swarm spores
35

36

38
- The different types of sexual spore includes:
Ascospores: endogenous sexual spores borne within a sack-
like cell called ascus in the class Ascomycetes
Basidiospores: Exogenous spores produced on the fruiting
body called basidium of the class Basidiomycetes
Ascospores
Basidiospores

Oospore
Zygospore
39
Zygospores: exogenous spores formed by a union of
similar
sex cells (gametes)
- Oospores: exogenous spores formed by fertilization of a
large female cell (oogonium) by a small male cell
(anthridium); i.e. fusion of dissimilar sex cells

40
Lack chlorophyll and hence they can not prepare their own
food.
They obtain their nutrition either through infecting living
organisms as parasites or depend on dead organic matter as
saprophytes.
Mode of nutrition
Absorb food through hyphae that grow in to the food
source.
Enzyme(s) released from the hyphae to act on Insoluble
food.
Break-down (digestion) of food.
Fungi “absorb” digested food.
– If food is soluble, digestion is not necessary.
Nutrition of fungi

42
Fungi can be:
Obligate parasites or biotrophs: - grow and multiply only in
association with their host plants.
Hemibiotrophs: pass part of their lives on the host as parasites
and part on dead tissues of the same host on the ground.
Nonobligate parasites: - can grow and multiply on dead
organic matter as well as on living plants.
Nonobligate parasites can be either facultative saprophytes
(primarily saprophytes) or facultative parasites (primarily
parasites).

43
Facultative saprophytes: grow parasitically on the hosts, but they
continue to live, grow, and multiply on the dead tissues of the host
after its death.
Facultative parasites: can live perfectly well in the soil or
elsewhere as saprophytes, but if they happen to come in contact
with a plant organ, they have the ability to parasitize and cause
disease on the plant.

Dissemination of fungi
Fungi are disseminated primarily in the form of spores.
Fragments of hyphae and hard masses of mycelium
known as sclerotia may also be disseminated.
The agents for spread include wind, water, birds, insects,
and other animals and humans.
Zoospores are the only fungus structures that can move
by themselves, but very short distances.
–Myxomycetes, Oomycetes, and
Chytridiomycetes produces zoospor.
44

Identification of fungi
The most significant fungus characteristics used for
identification are
Spores, spore-bearing structures, and to some extent,
the characteristics of the fungus body (mycelium).
Shape, size, colour, and manner of arrangement of
spores on the sporophores or in the fruiting bodies,
and
Shape and colour of the sporophores or fruiting bodies
45

Classification of fungi
The taxonomy of fungi has been based on
Morphology. sexual and asexual spore,
secondary considerations such as hyphal and colony
characteristics (the fungus in culture),
and now a days, molecular techniques
Currently fungi can be classified into two:
fungal-like organisms and
the true fungi.
46

I. Fungal-like organisms
Often referred as lower fungi
Two major Kingdoms
1. Kingdom Protozoa
- Unicellular, plasmodial, colonial, or phagotrophic Mos.
- There are two major Phyla: Myxomycota and Plasmodiophoromycota.
i. Phylum Myxomycota: Produce a plasmodium or plasmodium-like structure (mass
of cytoplasm)
Class: Myxomycetes - slime molds
- May grow on and may cover parts of low-lying plants but do not infect
them
Order: Phyrales:
Genus: Fuligo, Mucilago, and Physarum)
47

Turfgrass leaves covered with fructifications (sporangia) of
the slime mold Physarum
48

ii. Phylum Plasmodiophoromycetes -endoparasitic slime molds
Order: Plasmodiophorales. Plasmodia produced within cells of
roots and stems of plants.
- They are obligate parasites
Genus: Plasmodiophora (e.g. Polymyxa, P. graminis parasitic
on wheat and other cereals
49

2. Kingdom Chromista (Stramenopiles): Unicellular or multicellular,
filamentous or colonial, primarily phototrophic.
This Kingdom contains brown algae, diatoms, oomycetes, and some other
similar organisms.
Phylum: Oomycota - have Biflagellate zoospores
Class: Oomycetes (water molds, white rusts, and downy mildews)
Order: Saprolegniales (root rot of peas), Peronosporales
Genus: Pythium, Plasmopara, e.g. Phytophthora infestans
50

potato late blight caused by
Phytophthora infestans.
51

Damping off disease caused by pythium spp
52

53
II. True Fungi
True fungi belongs to the kingdom fungi.
- Produce mycelium, they luck chloroplasts
hence no photosynthesis.
Phylum:
- Four major Phyla including
Chytridiomycota, Zygomycota,
Ascomycota, and Basidiomycota. The
fifth phyla, Deuteromycota
- Named for the appearance of their
fruiting body (spore-producing
reproductive structures).

…Damping-off of Seedlings
Damping-off of seedlings

55
• A) Chytridiomycota: Produce zoospores that
have a single posterior flagellum
• Class: Chytridiomycetes – have round or
elongated mycelium that lacks cross walls
• Genus:
- Olpidium: O. brassicae – parasitic in roots of
cabbage and other plants. They can transmit
plant viruses.
- Physoderma: P. maydis – cause brown spot of
maize
- Synchytrium: S. endobioticum – cause potato
wart

56
B) Zygomycota: Produce nonmotile
asexual spores in sporangia,
• Class: Zygomycetes (bread molds).
They are saprophytic or parasites of
plants, humans, and animals.
• Order: Mucorales & Glomales

57
i) Mucorales: Nonmotile, asexual spores formed in terminal sporangia
• Genus:
– Rhizopus: Causing bread mold and soft rot of fruits and Vegetables.
– Choanephora: C. cucurbitarum – cause soft rot of squash
– Mucor: Causing bread mold and storage rots of fruits and Vegetables.
ii) Order Glomales:
• Also known as endomycorrhizae. Arbuscules produced in host root.
Chlamydospore-like produced singly in soil, in roots, or sporocarps. Sexual
reproduction rare with spores
• Genus: Glomus, Acaulospora, Gigaspora, Scutellospora

Choanephora wet rot of squash.
59

C) Ascomycota: - sac fungi.
• Most have a sexual stage (teleomorph) and an asexual stage (anamorph).
• Produce sexual spores called ascospores in ascus,and asexual spores (conidia)
on free hyphae.
Three classes:
• i) Archiascomycetes: A group of diverse fungi, difficult to characterize
Order: Taphrinales – Asci arising from binucleate ascogenous cells
Genus: Taphrina – causing peach leaf curl, plum pocket, oak leaf blister, etc.
• ii) Saccharomycetes: Asci naked, no ascocarps produced. They are mostly
unicellular fungi that reproduce by budding.
Genus:
• Galactomyces – causing citrus sour rot
• Saccharomyces – S. cerevisiae (the bread yeast)
60

Sometimes called cup fungi
because of the shape of their
reproductive structures
The ascocarp carries asci within
cups Nuclear fusion
61

iii) Filamentous ascomycetes:
• Order: Erysiphales (the powdery mildew fungi).
- Asci in fruiting bodies completely closed (cleistothecia).
- Mycelium, conidia, and cleistothecia formed on surface of
host plant.
- They are obligate parasites
• Genus:
• Blumeria –causing powdery mildew of cereals & grasses
• Erysiphe - causing powdery mildews of herbaceous plants
• Leveillula - causing powdery mildew tomato
62

D) Basidiomycota: - the club or mushroom fungi.
- Sexual spores called basidiospores are
produced externally on a club-like, spore
producing structure called a basidium.
Order:
i) Ustilaginales (the smut fungi): Basidium has cross walls
/non septate. Only teliospores and basidiospores are
produced; e.g. genus Ustilago (U. maydis – cause smut
of maize).
63

ii) Uredinales (the rust fungi): Basidium with cross walls.
- Produce two or several types of spores: teliospores,
basidiospores,
aeciospores, and uredospores.
- They are obligate parasites; e.g. genus Hemileia (H.
vastatrix – causing
coffee leaf rust).
iii) Exobasidiales: Basidiocarp lacking: basidia produced on
surface of parasitized tissue.
– Genus: Exobasidium - causing leaf, flower and stem galls on several ornamentals
64

iv) Ceratobasidiales: Basidiocarp is web-like, inconspicuous.
- Basidia without cross walls; e.g. genus Athelia causing southern blight
of
many plants.
v) Agaricales (the mushrooms): Basidium without cross walls,
- produced on radiating gills or lamellae. Many are myccorhizal fungi;
e.g. genus
Armillaria (A. mellea – causing root rots of trees such as tea).
vi) Aphyllophorales: Basidia without cross walls produced on hymenium-
forming hyphae and lining the surfaces of small pores or tunes; e.g.
genus Corticium, one species causing the red thread disease of turf
grasses.
65

Bacteria
Bacteria is prokaryotes
Not organized into a nucleus
single-celled microorganisms
Genetic material (DNA) is not bound by a
membrane
Their cytoplasm is surrounded by a cell
membrane and a cell wall.
66

67

Shape of bacteria may be spherical, rod shaped,
ellipsoidal, spiral, comma shaped, or threadlike
(filamentous).
Almost all plant pathogenic bacteria are rod-shaped,
the only exception being Streptomyces which is
filamentous.
68

Most plant pathogenic
bacteria are equipped with
delicate, threadlike flagella.
hence can move
through liquid media.
Others lack flagella and can
not move by themselves.
The bacteria body consists
of cell wall and its
appendages, plasma
membrane and protoplasm.
69

Average size: 0.2 -1.0 µm  2 - 8 µm
Basic shapes:

Cocci (singular - coccus) - spherical
Bacilli (singular - bacillus) - rod-shaped
Spirilli (singular - spirillum) - spiral-shaped
Vibrio – comma shape

Unusual shapes
Star-shaped Stella
Square Haloarcula
Most bacteria are monomorphic
A few are pleomorphic
Figure 4.5

Arrangements
Pairs: diplococci, diplobacilli
Clusters: staphylococci
Chains: streptococci, streptobacilli

• Unusual shapes
– Star-shaped Stella
– Square Haloarcula
• Most bacteria are monomorphic
• A few are pleomorphic
Figure 4.5

When a single bacterium is allowed to grow
(multiply) on the surface of or in a solid medium,
its progeny soon produces a visible mass called a
colony.
Shapes may be circular, oval, or irregular.
Edges may be smooth, wavy, or angular.
Elevation may be flat, raised, or wrinkled
75

Colony – macroscopically visible collection of
millions of bacteria originating from a
single bacterial cell.
Colony morphology: gives important clues as to
the identity of their constituent microorganisms.
Important classes of characteristics include:
 Size
 Type of margin
 Colony elevation
 Colony texture
 Light transmission
 Colony pigmentation

Classification of bacteria
Criteria
The rigidity of the cell and mode of division
Their general shape and type of morphological
aggregation
The possession of flagella and their location
Gram staining reaction
The presence of motile spores
Environmental or growth requirements
77

Bacteria may be classified based on number and arrangement of
flagella
A- Monotrichous- having a single
flagellum at one end
B- Lophotrichous: possessing two or
more flagella at one or both ends of
the cell
C- Amphitrichous: having one
flagellum at each end
D-Peritrichous: possessing large
number of flagella surrounding the
cell
E- Atrichous: bacterial cells without
any flagellum, non motile
78

The most common plant pathogenic genera of bacteria
include:
Agrobacterium
Clavibacter (Corynebacterium)
Erwinia
Pseudomonas
Ralstonia
Xanthomonas
Streptomyces
Xylella
79

Reproduction
Bacteria reproduce chiefly by binary fission, or
fission.
The cells are divided by a simple division into two
halves, the process being repeated every 20 to 50
minutes.
At this rate, one bacterium could produce one
million progeny bacteria in less than a day.
80

Bacterial involves binary fission

Nutrition of bacteria
Bacteria are unicellular and entire cell is capable of
absorbing dissolved nutrients - holophytic feeding.
Certain species can not utilize organic matter, but
synthesize complex compounds from simple organic
salts – autotrophic bacteria.
In other species organic matter is the sole source of food
– obligate heterotrophic bacteria.
82

Environmental requirement
The life processes of bacteria are affected by
temperature,
moisture,
pH,
oxygen, and other factors like pressure and light.
Bacteria are more aquatic than terrestrial and thrive on
the presence of high water
83

Based on growth temperature range bacteria can be:
Thermophiles – Grow up to 70 C
Mesophiles – 20-42 C Most plant pathogenic bacteria.
Psychrophiles – Optimal growth rates below 20 C
– Many plant pathogenic bacteria
PH range
Neutrophiles: PH 7.0 (Most plant pathogenic bacteria)
Acidophiles: <PH 7
Alkaliphiles: > PH 7
84

Oxygen requirement
Obligatory aerobic
require O2 for growth
Most plant pathgoenic bacteria
Facultative aerobes
prefer aerobic growth but can live without O2
e.g. Erwinia
Obligate anaerobes
They are an able to grow in the presence of O2
e.g. Clostridium species associated with soft rot on potato
85

Common features of phytopathogenic bacteria include:
All except Corynebacterium and Streptomyces are gram
negative
All are non-spore forming rods except Streptomyces
Prevalence of water is the key factor of the environment
that influences disease development
Bacterial cells have a passive entry into host through
stomata, lenticles, wounds, insect bites, or through
implements
They colonize the intercellular spaces, vascular bundles and
spaces formed by dead cells
86

Table 2.2: Important characteristics of phytopathogenic genera of bacteria
Genus Gram stain Colony colour Motility
Agrobacterium - White Motile
Corynebacterium + White Non motile
Erwinia - White Motile/Non motile
Pseudomonas - Characteristic pigment Motile/Non motile
Xanthomonas - Yellow Motile
Ralstonia - Do not produce
characteristic pig.
Motile/Non motile
Streptomyces + Wide variety of pigments Non motile
Xylella - Non pigmented Non motile
87

Gram staining
Gram's Stain is a widely used method of staining
bacteria as an aid to their identification.
It was originally devised by Hans Christian Joachim
Gram, a Danish doctor.

procedure
Using heat fix the specimen onto the slide
Flood the slide with crystal violet.
Allow to remain 60 seconds. Rinse with water
Flood the slide with Gram’s iodine.
Allow to remain 60 seconds, and then rinse with water.
Decolorize the slide with acetone, alcohol, or a mixture of
the two for 30 seconds. Rinse with water
Flood the slide with safranin for 60 seconds.
Rinse gently with water.
89

The Gram + ve bacteria, the purple crystal violet stain is
trapped by the layer of peptidoglycan
The Gram – ve bacteria, the outer membrane prevents the
stain from reaching the peptidoglycan layer in the
periplasm.
Results:Gram +: Retains crystal violet and appears purple
Gram - : Decolorizes and retains the counterstain,
safranine, thus appearing red/pink
90

Gram Staining : Gram +’ve

Gram Staining – Gram -’ve

Reagent used at eat step
Reagents
Color of
Gram +
cells
Color of
Gram –
cells
Primary stain:
Crystal violet Purple Purple
Mordant:
Iodine Purple Purple
Decolorizing agent:
Alcohol-acetone Purple Colorless
Counterstain:
Safranin Purple Red

Virus
General characteristics
An infectious agent too small to be seen directly with a
light microscope.
They are not made of cells and can only replicate inside
the cells of another organism.
The study of viruses is known as virology.
The disease caused by viruses is called virosis.
The first plant virus disease discovered TMV.
94

Viruses consist of two or three parts:
All viruses have genes made from either DNA or
RNA, that carry genetic information;
They are mostly Rod-shaped (TMV), Flexuous
thread like (SMV), Isometric/spherical or
polyhedral, Cylindrical or Bacillus-like virus in
shape.
95

(A) Rod-shaped virus (TMV) (B) Flexuous thread virus (SMV) (C)
Isometric/spherical or polyhedral virus (D) Cylindrical or Bacillus-like virus
96

97
Viruses
Figure 13.1
JUCAVM,2012
12/20/2022

Viruses cause three major symptoms in plants:
Reduced growth rate
Mosaics: light green, yellow or white areas
intermingled with the normal green colour of the
leaves or fruits
Ring spots: appearance of chlorotic or necrotic rings
on the leaves, stems or fruits
98

Tobacco Mosiac Virus: ss RNA virus

Grouping (“classification”) of
viruses
12/20/2022 JUCAVM,2012 100
How are they classified?
Criteria used :
Type of Nuclic acid;
Type of Symetry(Structure);
Host range;
Present or absence of envelope

Life cycle
There are six basic stages in the life cycle of viruses:
Attachment: a specific binding between viral capsid
proteins and specific receptors on the host cellular
surface
Penetration: viruses enter the host cell through
receptor mediated endocytosis or membrane fusion.
Uncoating: a process in which the viral capsid is
degraded by viral enzymes or host enzymes thus
releasing the viral genomic nucleic acid
101

Replication: viral protein synthesis and assembly of
viral proteins and viral genome replication
Post-translational modification: of viral proteins
Viruses are released from the host cell by lysis—a
process that kills the cell by bursting its membrane
102

Transmission
Viruses can be transmitted from diseased to healthy plant by
several means.
Vegetative propagation,
Mechanically through sap
Seeds
Pollen
Insect vectors, mite, nematode, fungus, and
Dodder.
103

104

105

Aphids Leafhoppers
Whiteflies Thrips
106

Mycoplasma-like organisms (MLOs)
Mycoplasmas are pleomorphic in shape and have
no cell wall other than a surrounding membrane.
They range in size from 0.1 to 1.0 µM.
They are usually confined to the phloem or xylem
cells.
They can be transmitted by leafhoppers and other
sucking insects.
107

Rickettsia-like organisms (RLOs)
Rickettsia-like organisms resemble MLOs to
some extent but they do possess a cell wall.
They are between 0.4 µM in diameter with a
length of about 3 µM. can be observed with the
electron microscope.
Are vector transmitted mainly by leafhoppers
108

Nematodes
Belongs to the kingdom Animalia.
Wormlike in appearance but quite distinct taxonomically
from the true worms.
Live freely in fresh or salt waters or in the soil.
Feed on living plants obtaining their food with spears or
stylets and causing variety of plant diseases
Nematodes are small in size, ranging
- 300 to 1,000 µM,
- with some up to 4 mm long by 15 to 35 mm wide.
109

They are eel shaped, and
round and with out legs
or other appendages.
Its body is transparent
and is covered by
colourless cuticle,
Reproduce by eggs.
110

Life cycle
The life cycle includes:
Eggs,
four larvae stages
(juveniles) and
the adult form.
- Both the larvae and
adult stages are
infective
111

Ecology and spread
All plant pathogenic nematodes live part of their lives in the
top 15 to 30 cm of soil
Feeding superficially on roots and underground stems.
Survival & movement of nematodes in the soil is affected by:
- soil temperature, moisture, and aeration (oxygen).
Spread through the soil slowly under their own power or can
spread in local areas by farm equipment, water, animal feet,
birds, and dust storms.
Can spread Long distance with farm produce and nursery
plants.
112

Nematode classification
Nematodes can be classified as:
• Kingdom Animalia
• Phylum Nematoda
• Order Tylenchida (few in Dorylaimida)
• Suborder Tylenchina
• Superfamily Tylenchoidea
• Family Heteroderidae
• Genus Meloidogyne (Root-knot nematode)
113

The most important genera of plant parasitic nematodes
include:
Meloidogyne: Root-knot nematode
Heterodera: Cyst nematode
Anguina: Wheat or seed-gall nematode
Pratylenchus: lesion nematode
Longidorus: needle nematode
Tylenchulus: Citrus nematode
114

Nematodes can be:
Ectoparasites: do not completely enter the host but
thrust their
spears into the outer cells.
- Their complete life cycle takes place near the
host surface.
Endoparasites: move freely inside the host and remain
there for some part of their life cycle
115

Parasitic seed plants
They are also called Phanerogamic plants
They parasitize other plants and cause harmful
physiological and morphological changes called
disease.
116

Characteristics
• They parasitize and get their nourishment from their host.
Parasitism can be partial or complete.
– Partial (hemi- or semi-parasites) are
partially depend on their host.
Lack true root system and are dependent on the host for
water and mineral nutrients
possess chlorophyll and can prepare their own food
Possess haustoria which associate with vascular organs.
117

• Total (true/strict/complete parasites)
Are totally dependent for their existence on the host plant.
They do not possess chlorophyll and cannot prepare their
own food.
They are considered as obligate parasites.
Parasitic seed plants can be:
1. Root parasites: 2. Stem parasites:
- Entirely dependent; e.g. Orobanche - Entirely dependent; e.g. Cuscuta
- Partially dependent; e.g. Striga - Partially dependent; e.g. Loranthus
118

Classification
Major families and generas containing parasites include:
• Loranthaceae: mistletoes ~ more than 900 species
• Phoradendron spp. – American mistletoes
• Viscum spp. - European mistletoes
• Dendrophthae spp. – Giant mistletoes
• Arceuthobium spp. – Dwarf mistletoes
• Convolvulaceae: Dodders contain more than 42 species
• Cuscuta spp. – dodder
122

• Scrophulariaceae: Witch weed – of the 50 species, five species of witch weed
are common
• Striga hermonthica
• Striga asiatica
• Striga lutea
• Striga gesnerioides
• Striga euphrasioides
• Orobanchaceae: Broom rape - over 150 species are known
• Orobanche ramose
• Orobanche cernua
• Orobanche minor
• Non-infectious (abiotic) causes of plant diseases (reading assignment)
123

Environmental Factors
Environmental conditions in air & soil affect disease
development
The environmental factors that affect disease dev’t are:
Temperature
Moisture
Light
Soil nutrients
Soil PH….

Their effects on disease dev’t may be through their
influence on:
Growth or susceptibility of the host
Multiplication & activity of the pathogen or
The interaction of host & pathogen

Temperature
Plants & pathogens have their own optimum temp. to grow and
multiply
Under low temp. diseases are not initiated &
those in progress come to stop
When higher temperatures start to come,
pathogens become active and start to infect and
cause disease.
Generally, pathogens differ in their preference for temperature;
but more disease are favored by high temp. & RH

Moisture
Moisture helps:
Germination of spore & penetration of the host by germ
tube
Activates the pathogens
Dissiminates the pathogen ( as splash, running water)
Increases succulence of host plants and susceptibility to
diseases
liberate spores from sporophore

Particularly, in under ground diseases there is positive
correlationbetweensoilmoistureand disease severity
e.g. root rots, damping off, seed decays
Note: Virus infections are inhibited by free moisture.
B/c, moisture removes ions, mainly P ions, which are necessary
for binding of virus particles on plant surface

wind
Effect of wind:
Wind plays role in disease development through:
spread of pathogens
Release of spores (zoospores, conidia, etc)
Injuring plant surfaces or parts (this facilitates penetration)

light
Effect of light:
Insufficient light reduces vigorosity & increases susceptibility
to diseases
i.e. it predisposes plants to infection
E.g. powdery mildew, leaf spots, root rots
Reduced light intensity increases susceptibility of plants to
infections

Nutrients
Effect of nutrients:
Nitrogen:
N abundance results in;
Production of young succulent growth
Prolonged vegetative period and delayed maturity
Makes plants susceptible to pathogens
N deficiency results in:
Weaker, slow growing, fast aging, & susceptible plants

Phosphorus and Potassium
Both nutrients reduce severity of some diseases. B/c:
They increase resistance by accelerating maturity and
allowing to escape from infection
Hasten tissue maturation
Harden cell wall
Promoting wound healing
e.g. K reduces severity of stem rust of wheat & blight of potato

133
What is Koch’s postulates?
A standard method to prove pathogencity of an
organism
Pathogenecity: the ability of the pathogen to cause a
disease
The pathogencity of an organism is determined by
successful completion of Koch’s postulates.
Chapter 3: KOCH’S POSTULATES AND PLANT
DISEASE SYMPTOMS

134
Koch’s postulates
The suspected pathogen must be consistently associated with
diseased plants
The pathogen needs to be isolated from diseased tissue and
identified
Healthy tissue of the same species needs to get the same disease
symptoms after inoculation with the isolated pathogen
The same pathogen characterized in step 2 must be isolated from
the inoculated tissue/plant.
Isolation Culturing Inoculation Re-isolation
KOCH’S POSTULATES AND PLANT DISEASE
SYMPTOMS …

135
Symptom - reaction of the host plant to the living organism or
nonliving agents or a visible response of a plant to a causal agent
over time (e.g., leaf spots, wilting, galls on roots)
Alternaria blotch on apple Crown galls on peach
SYMPTOMS …
Disease symptoms and signs

136
Definition of symptoms and sign
Signs - are structures or products of a pathogen on or in diseased
plants (e.g., mold or fungal spores, bacterial ooze)
Bacterial ooze on
crabapple (fire blight)
Green mold on orange
(Penicillium)
SYMPTOMS …

137
Different diseases are recognized initially by the different sign and
symptoms which they produce
Diagnosis is the first step in addressing the challenge of plant
diseases
Symptoms and sing are helpful in disease diagnosis
Diagnosis aims to determine the cause(s) of a disease & goes
beyond identification of the pathogen
It depends up on an adequate understanding of what a disease is
and how it is caused.
Hence, correct diagnosis is important for effective management
of plant diseases and pests.
SYMPTOMS …

138
Similar symptoms can be invoked by different causal organisms
Same pathogen can cause different symptoms depending on
host plant cultivars
Environment, and
pathogen strain
Hence, symptoms alone are not enough for accurate diagnosis of
many plant diseases
Biotic pathogen often produce signs, which are evidence of their
presence and can aid in diagnosis
There are no signs of abiotic factors
SYMPTOMS …

Disease symptoms and sign
To know the healthy plant
Knowledge of the epidemiology of the disease
- Pattern of occurrence/spread of the disease, previous
history of the location, source of planting material,
agronomic and environmental factors…)
Checking pathogenicity of an organism (Koch’s postulate).
Fundamentals important in diagnosis
SYMPTOMS …

140
Major categories of symptoms
Types of morphological symptoms
Necrosis
Hyperplasia/hypertrophy
Hypoplasia/atrophy
Necrosis: symptoms that results from death of cells, tissues and organs
of plants as a result of the parasitic activity
Hyperplasia: the abnormal increase in the size of a plant organ due to
increase in the number of cells------ excessive cell division
Hypertrophy: an abnormal increase in the size of plant organ due to
increase in the size of cells---- cell enlargement
Hypoplasia/Atrophy: Inhibition of growth resulting in stunting or
dwarfing.
In this cases the whole plant may be dwarfed or only certain organs may
be so affected
KOCH’S POSTULATES AND PLANT DISEASE SYMPTOMS …

141
Common plant disease symptoms
1. Systemic symptoms: affect all or most of the plant parts
Chlorosis- yellowing of foliage due to inhibition of chlorophyll
production in the leaves
it often showing a characteristic pattern
Etiolation- extended growth (like plants grown in shade), due to
production of plant hormones by pathogens
Stunting- a very general symptom
Wilting- water loss from tissues exceeding water supply
2. Localized symptoms:
Necrosis- death of areas of plant tissue
Hyperplasia- excessive, distorted growth of tissues
KOCH’S POSTULATES AND PLANT DISEASE SYMPTOMS
…

142
Common types of necrotic diseases
Anthracnose: darken, sunken, necrotic spots or patches sometimes
with raised borders
xtensive shriveling and death of certain areas of the plant. Eg.
Leaf blight of potato (Phytophthora infestans)
Canker: localized areas of necrotic tissue producing a sunken lesion
a raised margin & usually on woody stems
SYMPTOMS …

143
Necrotic diseases…
Damping-off : necrosis of seedling hypocotyls resulting in a
basal rot of seedlings causing them to collapse and die
Dieback: a necrosis of stems and young twigs which affects
the youngest tissues first and progresses down the site
Gummosis: a necrotic lesion or swelling associated with the
exudation of gum
Leaf spots: many consists of limited areas of necrotic tissue
Rots: involves the necrosis of large areas of tissue, often
complete organs

144
Rot can be:
Soft rot: caused by the dissolution of cell walls and the content of
which leak out. Eg. Erwinia carotovora
Sclerotina spp cause significant rots of flowers & vegetables,
while
Fusarium spp are major root rot pathogens
Dry rots: involve the absorption of cell contents by the parasite
without loss of cell wall structure
These are often caused by Basidiomycete fungi
…

145
Hyperplastic disease symptoms
Galls and knots: local swellings due to excessively disrupted tissue
growth, caused by the presence of a pest or pathogens.
Examples,
Crown gall of young fruit trees (Agrobacterium tumefaciens),
Root knot nematodes (Meloidogyne species)
Leaf blisters and curls: malformation of the leaf lamina by irregular
growth induced by a pest or pathogens.
Scabs: patches of raised deformed tissue often with some necrosis
which occur on herbaceous tissue. Eg Citrus scab
Witches’ brooms: caused by proliferation of lateral buds to produce a
bunch of stems
…

146
3. Symptoms characterized by growth of the pathogen
Mildews: diseases where there is a visible mould growth over the plant
surface
Downy mildews [Peronospora spp]: where the fungal growth
consists of long condiophores growing from the diseased tissue
Powdery mildews [Podosphearia spp]: growth is characterized by
the proliferation of a surface mycelium
Rusts- powdery sporing pustuls on the leaves or stems, usually yellow, orange
or brown in color Eg.
Maize rust, Puccinia polysora
Coffee leaf rust, Hemileia vastatrix
…

147
Smuts: black, powdery spore masses are produced involving the
transformation of some part of the plant
Maize smut, Ustilago zeae
Sooty moulds: black fungal growth on leaves and stems caused by
saprobic fungi growing on exudates;
often associated with sucking pests such as aphids and scale insects
SYMPTOMS …

148
Disease syndrome
• The sum total of all symptoms and signs OR
• The totality of effects produced in a plant by one disease whether
all at one time or successively and including effects not directly
detectable to the unaided eye
Why it is important to study disease syndrome?
• Disease may show various morphological & physiological
symptoms of disturbance from time of infection up to the death of
the attacked plant
• Hence, the occurrence of different symptoms & sign at various
stages while the pathogen is one and the same throughout allure
SYMPTOMS …

149
Fungal disease symptoms
Leaf spots or blotches
Blight
Cankers
Root rot
Wilt
Reduced growth, death
Trunk rot
Abnormal growth or galls
…

150
Bacterial disease symptoms
• Leaf spots or blotches
• Blight
• Cankers
• Root rot
• Wilt, reduced growth, death
• Abnormal growth or galls
…

151
Reduced growth, death
Color deviation
Mosaic: green and yellow color intermingled
Mottling : diffusely bordered variegation
Chlorosis: evenly distributed color change
Blanching: disappearance of color from affected leaves
or tissues
Dead areas on leaves (necrosis)
Phloem necrosis
Vein necrosis
Streaking: Necrosis on petioles and stems
Viral disease symptoms

152
• Water deficiency
• Wilting / withering
• Etching: desiccation of superficial tissues( epidermal cells)
• Abnormal growth
• Leaf curling
• Leaf narrowing
• Enation: small over growths on leaves especially veins or stems
• Phyllody: transformation of floral parts in to leafy structures

153
Viroids
Piece of genetic material
Has no protein coat
Divert plant metabolism to produce more viroids
Spread by vegetative propagation
• Example
• Potato spindle tuber viroid : causing short, upright, stunted
growth

154
Mycoplasmas
• Similar to bacteria
• Have no cell wall
• Found in the infected plant’s water and food conducting vessels
• Leaf hoppers transmit mycoplasmas
They causes:
• Growth abnormalities
• Yellowing
• Short internodes
• Distortion of leaf and flower tissue

155
• Examples:
1. Stubborn disease of citrus (
spiroplasma)
• Uneven fruit size (reduction)
2. Carrot aster yellows
(phytoplasm)
• Yellowing of foliage, hairy roots
and internal root necrosis
SYMPTOMS …

156
Nematodes
• Microscopic worms
• Found in the soil
Nematodes cause:
• Abnormal growth or galls
• Reduced growth, death
• Root lesion
• Excessive root branching

157
Parasitic vascular plants
• Gain nutrients by parasitizing seed-bearing plants
Dodder mistletoe Witch weed

158
Summary of plant disease symptoms
Wilts
Rots
Root rot
Blights
Cankers
Growth or galls
Leaf abnormality

159
Wilt
• Vascular system affected. Eg. tomato

160
Rot
Internally affecting plants
May be wet or dry
– Eg. Fruits, vegetables, trees

161
Root rot
Affects the fine feeder roots
Disease agent enters the crown with above ground symptoms

162
Blights
• General death of a plant part or plant
Fire blight
Late blight

163
tomato dogwood

164
Cankers
Sunken areas in wood
Fungal structures associated
Death of plant parts
Rose

165
Growth or galls
Cell enlargement and division
Bacteria, fungi, virus, nematodes
Bacterial gall

167
Dieback, rust, damping off, smut, etc
Dieback Leaf rust
Damping-off Leaf smut
Downy mildew
Scab

168
General key for identification of symptoms
Insects and nematodes
Feeding or sucking marks, excrements, larval skins, webs,
cocoons or slime on the plant
Sometimes curling, blistering, spotting or galls presents
Usually the organism can be found on or near the plant

169
Fungal pathogens
Signs: mycelial mats, fructification
Symptoms: chlorosis, necrotic spots, rots, premature ripening,
stunting, cankers
Microscope: mycelium, fruiting bodies, spores, sclerotia ( after
incubation or isolation)
Bacterial pathogens
Symptoms: water-soaked spots (later necrotic), often
surrounded by a light-colored halo, stripes, wet rots, stunting,
cankers, malformation
Microscope: profuse oozing of small rods from affected tissue
in to water

170
Viruses and phytoplasmas
Symptoms:
Yellowing, chlorosis or other discolorations,
mottling or mosaic- like patterns on leaves;
deformation of organs;
stunting,
tissue proliferation

Characteristics of Fungal Leaf Spots
Circular-to-irregular shape
Brown-to black in color
May have a chlorotic “halo”
Random distribution across leaf

Bacteria often cause “angular”
lesions because the lesion tends to
be confined between the leaf veins
Square, angular, or
“blocky” lesion shape

Some viruses cause chlorotic or
Necrotic “ring spots’ that are
Highly diagnostic
Tomato spotted
wilt virus
Barnes-TPDDL
Impatiens necrotic spot virus
Barnes-TAMU

Although most plant parasitic nematode problems
occur in the plant’s root zone, leaf infection resulting
from foliar nematode Infection can also occur.
The resulting foliar lesion can be confused with a
bacterial lesion.
Check for the presence of
plant parasitic nematodes
within the lesion
Stylet in mouthpart

PARASITISM AND PATHOGENICITY
An organism that obtains its food from the other
organism is called a parasite.
The removal of food by a parasite from it
pathogenicity- the ability of a pathogen to cause
disease s in host is called parasitism.
biotrophs, i.e., they can grow and reproduce in
nature only in living hosts, and they are called
obligate parasites.
175
Chapter 4: Parasitism and Disease Development

Host range of pathogens
Pathogens differ with respect to
The kinds of plants that they can attack,
With respect to the organs tissues that they can
infect, and
With respect to the age of the organ or tissue of
the plant on which they can grow
176
Parasitism and Disease Development …

Development of disease in plants
A plant becomes diseased in most cases when it is
attacked by a pathogen….
Pathogen can grow and multiply rapidly on
diseased plants,
It can spread from diseased to healthy plants, and
It can cause additional plants to become
diseased, thereby leading to the development
epidemic.
177

What is disease cycle?
Whenever a pathogen attacks a plant, symptom is not seen overnight
B/c in disease development there are several events/steps.
The chain of events in disease development is said to be disease cycle.
The primary events in disease cycle are:
Inoculation
Penetration
Infection
Incubation
Invasion
Reproduction & growth
Dissemination
Overwintering or oversummering

Inoculation: coming in contact of pathogen with the host or
landing of the pathogen on the host
inoculum
Inoculum- the pathogen or pathogen parts that land on the
host

Examples of inoculum:
Fungi: – spores, mycelia, sclerotia
Nematodes:- adult nematodes, larvae, or egg
Parasitic higher plants- seeds or plant fragments
Bacteria, viruses, mycoplasmas – individual microbe

Types of Inoculum
Two types;
1. primary inoculum - survives dormant in the
winter or summer and causes infections in the
new season and the infections it causes are called
primary infections.
2. secondary inoculums - inoculum produced from
primary infections.

Sources of inoculums
seed,
soil,
crop residues,
Tubers &
Other propagative materials
-

Penetration: entrance of pathogens into the
host or the initial invasion of a host by pathogen.
Mechanisms of penetration:
Natural openings: stomata, lenticles
Wounds mechanical injury
Direct penetration: by their own force

Mechanisms of penetration:
Fungi – natural openings, direct penetration,
Bacteria – wounds, natural openings
Viruses, mycoplasmas – wound
Nematodes – direct penetration, natural openings

Infection – the establishment of a pathogen within a host
plant or the colonization of the host by the pathogen
Pathogens start to obtain nutrients from the host
Release biologically active substances (enzymes, toxins,
growth regulators) in the host
Symptom develops on the host
Thus, successful infection leads to symptom development
symptom

incubation -the time interval between inoculation and the
appearance of disease symptom is called incubation period.
Incubation period is affected by:
Pathogen- host combination
Stage of development of the host
Temperature in the environment

Invasion- the spread of pathogen within the host
How pathogens invade the host?
Fungi – growing from one end to the other &
releasing spores through the plant
parasitic higher plants - growing from one end to
the other
Viruses, bacteria, viroids, mycoplasmas – by
multiplying rapidly and increasing their numbers

Dissemination
Dissemination- the transfer of inoculum from its
source to health plants
Methods of dissemination:
Active method: by movement of pathogens by their
own force
e.g. nematodes, zoospores, some bacteria,
sporangiospore
Passive method: dissemination of pathogens by
wind, water, insects, animals, human being, etc
- major means of pathogen dissemination

Overwintering/oversummering
Overwintering/oversummering: surviving the low temperatures
of winter or the hot weather of summer.
- passing the harsh conditions when hosts are absent (in
summer or winter)
Where do pathogens overwinter/oversummer?
In soil
Crop residues
Seeds, tubers, etc
On infected plant parts
In vectors

Pathogens overwinter/oversummer in different forms:
Fungi- as spore, mycelium or sclerotium on infected plant parts, in soil,
seed, plant debris
Nematodes- as eggs or nematodes in the soil, in plant roots or in plant
debris
Parasitic plants- as seeds in soil, or in vegetative form on their host
Bacteria- as bacteria in infected plants, seeds, plant debris, tubers etc.
Viruses- as virus in only plant tissues or in vectors

Disease Cycle of late blight of potato

Pathogens depend on the substances manufactured by the host
plants for survival
Many substances are contained in the protoplast of the plant
cells
- Must first penetrate the outer barriers formed by the
cuticle and/or cell walls
- penetration of more cell – for further invasion
The plant cell contents are not always found in forms
immediately utilizable by the pathogen
- Must be broken down to units that the pathogen can
absorb and assimilate.
HOW Do PATHOGENS ATTACK PLANTS
Chapter 5: Defense Mechanisms of Plants against Pathogens

Moreover the plant:-
Produces structures and chemical substances that interfere
with the advance or existence of the pathogen
Pathogen must be able to overcome, such obstacles
(Neutralize) the defense reactions of the plant to survive.
- Through secretions of chemical substances that affect
certain components or metabolic mechanisms of their hosts.
Defense Mechanisms of Plants against Pathogens …

Successful Attack
Penetration
Neutralize Defense Reactions
Convert Cell Components into Food
Generally, pathogens attack plants through mechanical forces and
chemical weapons

Mechanical forces exerted by pathogens
Plant pathogens are, tiny microorganisms that cannot
apply a “voluntary” force to a plant surface.
Only some fungi, parasitic higher plants, and
nematodes appear to apply mechanical pressure to
the plant surface to penetrate.
Pre-softening of a plant surface by enzymatic
secretions of the pathogen.

For fungi and parasitic higher plants to penetrate a plant surface, they
must, first adhere to it.
- Hyphae (fungi) and
-radicles (parasitic higher plants)
Spore forms adhesion pad and release cutinase and cellulase
enzymes which help the spore adhere to the plant surface.
Spores of some fungi carry adhesive substances at their tips

After contact is established, the diameter of the tip of the hypha
or radicle increases and forms the flattened, bulb-like structure
called the appressorium.
- This increases the area of adherence between the two
organisms.
A fine growing point, penetration peg arises from
appressorium and advances into and through the cuticle and
cell wall
Penetration is assisted by enzymes secreted by the pathogen
at the penetration site, resulting in the softening of the
barrier.

Generally, penetration can be:- direct, through natural openings and
through natural wounds

Nematodes penetrate plant surfaces by means of the stylet,
- Exerts mechanical pressure on the cell wall
Nematode first adheres to the plant surface by bringing its fused
lips in contact with the plant
Brings its body, or at least the forward portion of its body, to a
position vertical to the cell wall
Then thrusts its stylet forward
After several consecutive thrusts of the stylet, the cell wall is
pierced, and the stylet or the entire nematode enters the cell

All bacteria, most fungi, some viruses, and all viroids can enter plants
through various types of wounds

Chemical weapons of pathogens
Although some pathogens may use mechanical force to
penetrate plant tissues the activities of pathogens in plants are
largely chemical in nature
The effects caused by pathogens on plants are almost entirely
the result of biochemical reactions
Enzymes, toxins, growth regulators, and polysaccharides
(plugging substances)– are the major substrates secreted by
the pathogen.

The relative importance of these substrates may be different
from one disease to another
For example
- Soft rots - enzymes seem to be by far the most important
- Crown gall - growth regulators are the main substances
Among the plant pathogens, all except viruses and viroids can
probably produce enzymes, growth regulators, and
polysaccharides

Enzymes in plant disease
Large protein molecules that catalyze organic reactions in
living cells
These enzymes can be constitutive (already presented
in cells) or induced (produced only when they are
needed)
Plant pathogenic enzymes
Disintegrate the structural components of host cells,
Break down inert food substances in the cell, or
Affect components of its membranes and the protoplast
directly

Enzymatic degradation of cell wall substances
The penetration is facilitated by the breakdown of the internal
cell walls, which consist of cuticle, cellulose, pectins, etc
Pathogen secretes:
Cutinase
Cuticle made of cutin
Cutin = Waxes on top, Pectin & Cellulose on Bottom
Cutinases Hydrolyze Cutin Molecules into smaller Pieces
Pectinase
Pectinases liquefy Pectin - Middle Lamella
Cellulase – liquefy cellulose

Enzymatic degradation of substances contained in plant cells
pathogens obviously derive nutrients from the protoplast
Some of the nutrients, e.g., sugars and amino acids, can be easly
absorbed by the pathogen directly.
But starch, proteins, and fats, can be utilized only after degradation
by enzymes secreted by the pathogen.
proteases or proteinases or peptidases - involved in
protein degradation
Amylases – involved in synthesizing starch
The end product of starch breakdown is glucose and it
is used by the pathogens directly.

Microbial Toxins in plant disease
Pathogens release/produce toxins which disturb the metabolic reactions
of a plant cell.
- Seriously damage or kill the cells of the plant.
Extremely poisonous
Effective in low concentrations
Weapon of destruction
- Interfere with membrane permeability
- Interfere with Cell Functions

Some toxins act as general protoplasmic
poisons and affect many species of
plants(non-host-specific)
Others are toxic to only a few plant species
or varieties and are completely harmless to
others(host-specific).

Growth regulators in plant disease
Growth Regulators- Increase or Decrease Ability to Divide &
Enlarge
- Auxins, Gibberellins, and Cytokinins
Powerful at Low Concentrations
- Slight Deviation from Normal may Cause Strikingly
different Plant Growth Patterns
Plant pathogens may produce the same growth regulators or the
same inhibitors of the growth regulators as those produced by
the plant

pathogens often cause an imbalance in the hormonal
system of the plant and bring about abnormal growth,
such as
- Stunting, overgrowths, rosetting, excessive
root branching, stem malformation, leaf epinasty,
defoliation, and suppression of bud growth.

Polysaccharides
Pathogens constantly release varying amounts of mucilaginous
substances
- Coat their bodies and provide the interface between the
outer
surface of the microorganism and its environment.
Used by Vascular Pathogens to Block Translocation of Water
In wilt diseases, large polysaccharide
molecules is released by the pathogen
in the xylem & block vascular bundles
- initiate wilting

213

How do plants defend themselves against pathogens
• Each plant species is affected by different kinds of pathogens
• Many survive all these attacks and grow well and produce
appreciable yields.
• Plants defend themselves against pathogens by a combination of
two groups of weapons
(1) Structural characteristics - act as physical barriers
- Inhibit entrance or spread of pathogen
(2) Biochemical reactions - produce substances that are
- Toxins
- Pathogen Growth Inhibitors
Defense Mechanisms of Plants against Pathogens

Plant defense or resistance controlled by its genes
• Resistance in plant is ultimately controlled by the genetic
material (genes) of the host plant
Non-host resistance
- Brought in contact with a pathogenic biotic agent to
which the plant is not a host
- Common form of resistance in nature

Horizontal resistance - Partial, polygenic, quantitative
- Slows down the development of individual infection by slowing
down the spread of the disease and the development of
epidemics in the field.
Vertical resistance - Race-specific, monogenic
- Inhibits the development of epidemics by limiting the initial
inoculums or by limiting reproduction after infection.
- Varieties with this resistance generally show complete
resistance to a specific pathogen

Pre-existing structural and biochemical defenses
Pre-existing defense structures
–Structural Barriers
- Inhibit Entrance or Spread of Pathogen
- A thick cuticle may increase resistance
Pre-existing biochemical defense
•Toxins
•Pathogen Growth Inhibitors

Inhibitors present in plant cells before infection
• Several phenolic compounds, tannins, and some fatty acid-like
compounds such as dienes, presented in cells of young fruits,
leaves, or seeds,
Inhibitors released by the plant in its environment
• Plants exude a variety of substances – which will inhibit the
growth and survival of pathogens

Defense through lack of essential factors
1. Lack of recognition between host and pathogen
- Plants may not become infected by a pathogen if their surface
cells lack specific recognition factors (specific molecules /
structures) that can be recognized by the pathogen.
- Molecules or structures involved in the recognition of plants and
pathogens include oligosaccharides and polysaccharides, and
proteins or glycoproteins.

2. Lack of host receptors and sensitive sites for toxins
- Pathogen (usually a fungus) produces a host-specific toxin -
react with specific receptors or sensitive sites in the cell.
3. Lack of essential substances for the pathogen
- If plant do not produce one of the substances essential for the
survival of an obligate parasite, or for development of infection
by any parasite, would be resistant to the pathogen that requires it.

Induced structural and biochemical defenses
The induction process
1. Recognition of the pathogen by the host plant
- Early recognition of the pathogen by the plant is very important
to protect itself from the pathogen
- The plant begins to receive signal molecules, i.e., molecules
that indicate the presence of a pathogen, as soon as the
pathogen establishes physical contact with the plant

• pathogen elicitor- a variety of substances released by the
pathogen in their immediate environment.
• Such nonspecific elicitors include toxins, glycoproteins,
carbohydrates, fatty acids, peptides, and extracellular
microbial enzymes, such as proteases and pectic enzymes.
• Host plant receptors- it induces the expression of all defense-
related genes and resistance to subsequent attacks

Mobilization of defenses
• Once a particular plant molecule recognizes and reacts with a
molecule (elicitor) derived from a pathogen, it is assumed that the
plant “recognizes” the pathogen.
• Then, a series of biochemical reactions and structural changes
are set in motion in the plant cell(s) in an effort to defend off the
pathogen and its enzymes, toxins, etc.

Signal transduction - Transmission of the alarm signal to host
defense providers
• Once the pathogen-derived elicitors are recognized by the host, a
series of alarm signals are sent out to host cell proteins and to
nuclear genes
- causing them to become activated, to produce substances
inhibitory to the pathogen, and to mobilize themselves or
their products toward the point of cell attack by the
pathogen.
• Several types of molecules have been implicated in intracellular
signal transduction

Induced structural defenses
• Plants usually respond by forming one or more types of structures
that are more or less successful in defending the plant from further
pathogen invasion.
• Some of the defense structures formed involve the cytoplasm of
the cells under attack, and the process is called cytoplasmic
defense reaction
• Others involve the walls of invaded cells and are called cell wall
defense structures

• Others involve tissues ahead of the pathogen (deeper into the
plant) and are called histological defense structures.
• The invaded cell die and protect the plant from further invasion.
This is called the necrotic or hypersensitive defense reaction.

Cytoplasmic defense reaction
In a few cases of slowly growing, weakly pathogenic fungi
– Cytoplasm Surrounds Hyphae
– Cell Nucleus Stretches, Breaks
– Cytoplasm and nucleus enlarge and becoms Dense, Granular
Cytoplasm Full of New Particles, Structures
– Mycelium of the pathogen disintegrates and the invasion
stops.

Cell wall defense structures
Involve morphological changes derived from the cell wall of the host
1. The outer layer of the cell wall swells and produces an
amorphous, fibrillar material that surrounds and traps the bacteria
and prevents them from multiplying.
2. Cell walls thicken in response to several pathogens by producing
a cellulosic material, and further increase its resistance to
penetration.
3. Celullose papillae are deposited on the inner side of cell walls in
response to invasion by fungal pathogens.

Histological defense structures
• Formation of cork layers- form several layers of cork cells
beyond the point of infection
- The cork layers inhibit further invasion by the pathogen
and also block the spread of any toxic substances that the
pathogen may secrete.
- Stop the flow of nutrients and water from the healthy to the
infected area and deprive the pathogen of nourishment
• Formation of abscission layers- consists of a gap formed between
two circular layers of leaf cells surrounding the locus of infection

Figure 8.5: Schematic formation of an abscission layer around a
diseased spot of a Prunus leaf
Figure 8.6: Development of tyloses in xylem vessels. Longitudinal (A) and cross section (B) views
of healthy vessels (left) and of vessels with tyloses.
Figure 8.3: Formation of a cork layer (CL) between infected (I) and healthy (H)
areas of leaf.
Figure 8.4: Formation of a cork layer on a potato tuber following infection with
Rhizoctonia.

Gum Deposition
• Anatomical & Physiological Responses of Bark Tissues to
Mechanical Injury
• Deposition of phenolic polysaccharide material in the wall.
These substances, usually referred to as gum, & are produced in
response to wounds or infections
• Surrounding the locus of infection, thus forming an
impenetrable barrier that completely encloses the pathogen. The
pathogen then becomes isolated, starves, and sooner or later dies.

Hypersensitive Response
• Necrotic defense reaction
• The invaded cell die and protect the plant from further invasion
• Biochemical response with visible cellular responses
• In Fungal invasions, cell suicide/destraction occurs
• In bacterial invasions, Cell Membranes Destroyed, Followed By
Desiccation & Necrosis of Invaded Leaf Tissues

Figure 8.7: Stages in the development of the necrotic defense reaction in a cell of a very
resistant potato variety infected by Phytophthora infestans. N, nucleus; PS, protoplasmic
strands; Z, zoospore; H, hypha; G, granular material; NC, necrotic cell.
Figure 8.8: Tobacco leaf showing typical hypersensitive responses (white areas)
24 hours after injection with water (A) or with preparations of bacterial strains B,
C, and D. Strain (B), which does not infect tobacco, and (C), which carries a hrp
(hypersensitive response and pathogenicity) gene, both induced the
hypersensitive response, whereas the third strain (D), a mutant of C that lacked
the hrp gene, did not.

Population Dynamics- fluctuations in the numbers of individuals within
populations & the moving forces behind those fluctuations
* Plant pathologists try to prevent the rise and accelerate the fall of populations
of pathogens
Time
Popula
tion
Chapter 6: Population Dynamics of Plant Pathogens

Con’t…
If a population is kept indefinitely in an environment optimal to its growth &
reproduction (if no limitation)
• a population would increase exponentially
• Population growth assumes J- shape
J- shaped curve
This is hypothetical (unreal). B/c there are factors that suppress a population in
an ecosystem.
E.g. - Adverse environmental conditions
- Biological antagonism/parasitism.

Con’t…
Thus in nature population enlarges more slowly than its potential
rate. Thus it assumes S-shape, not J-shape.
S-shaped
curve

Con’t…
• Census of unseen plant pathogens is impossible
• An indirect measure of plant pathogens is the disease
progress curve by depicting disease severity or incidence
against time
• The resulting sigmoid curve is an indirect measure of increase
in numbers of plant pathogens.

Con’t…
Lag
phase
Diseas
e
severit
y (%)
Time
Log/exponential
phase
Stationary
phase
Deat
h
pha
se

Con’t…
Lag phase- infection has taken place but amount of inoculum is small
Logarthmic phase- disease progresses at maximum rate permitted by the
environment
- There is abundance of inoculum for secondary infection
Stationary phase- rate of increase of disease becomes low b/c of limited
amount of healthy tissues
Death phase- population of pathogens declines because of food deficit

The impact of plant disease and the losses that it causes are the
function of disease progress
To keep disease development to below acceptable level one
has to know the ff.
– The progress of disease& factors that influence disease
progress in quantitative terms
– What kind of diseases lead to linear disease progress and
what factors affect the slope of the line (the rate of disease
progress)?
– What kinds of diseases tend to produce exponential disease
progress curves and how we can reduce both the starting
level of disease and the rate of epidemic dev’t
– Why epidemic sometimes level off & what impose limits to
their dev’t?

Factors affecting epidemic dev’t
• The amount of disease that develops in a plant community is
dependent on properties of the host, the pathogen and the
environment.
• For those environmental factors affecting the development of
epidemics, please refer to previous chapter of this course

Host factors that affect dev’t of epidemics
• Level of genetic resistance or susceptibility
• Degree of genetic uniformity of host plants
• Type of crop (annual, perennial )
• Age of host plants

Pathogen factors that affect dev’t of epidemics
• Level of virulence
• Quantity of inoculum near host
• Type of reproduction of the pathogen or ecology of the
pathogen
• Mode of spread of the pathogen

Effect of human cultural practices and control measures
on dev’t of epidemics
• Site selection and preparation
• Selection of propagative material
• Cultural practices
• Disease control measures
• Introduction of new pathogens

Plant disease epidemics
• Plant disease epidemics are cyclical phenomenon : they consists of
repeated cycles of pathogen development

Types of epidemics:
• Monocyclic epidemics: one pathogen cycle per cropping season
• Polycyclic epidemics: many pathogen cycles per cropping season
• Polyetic epidemics: build-up of disease intensity over years eg.
forest pathogen
• Monocyclic epidemics: • Polycyclic epidemics
• Soil-borne diseases • Most air borne diseases
• Post-harvest disease
• Rusts without an uredospore stage

Con’t…
Polycyclic disease- diseases that complete many cycles per
season. E.g. late blight, rusts, powdery mildews
- Has one or more secondary cycles
- The curve increases exponentially at an accelerating rate
demonstrated by a sharp upward curving line of progress
Monocyclic disease- has a single cycle per season
- The curve increases arthimetically (i.e. linearly)

Con’t…
Polycyclic disease
Monocyclic disease
Disease
severity (%)
Time

Con’t…
The sigmoid curve is logarthmic and can be depicted as straight
line by plotting
y = ln x/1-x = loge x/1-x = logit x,
Where, x is disease severity in percentage
y = ln x/1-x
Disease
severity
(loge x/1-x
)
Time

Con’t…
The slope of the straight line plot (angle at which it meets the x-
axis) gives the average rate of infection.
r =
0.65
r =
0.45
r =
0.34
Disease
severity
(loge x/1-x )
Time

Con’t…
Disease severity or incidence can also be presented in the form of
area under progress curves (AUDPC)
AUDPC- expresses the dynamics of an epidemic as a single value
Dise
ase
seve
rity
(%)
Time

Con’t…
AUDPC = ∑ ( xi + Xi+1) (ti+1 – ti)
2
Where,
n - number of observations
ti – days after planting for the ith disease assessment
xi – disease severity (incidence) in percent
n
i=
1

Con’t…
e.g. Bean angular leaf spot severity was measured at 40, 60 & 80
days after planting and severity was found to be 20, 47, & 60%,
respectively. Calculate AUDPC.
AUDPC = ∑ ( xi + Xi+1) (ti+1 – ti)
2
AUDPC = (20 + 47) (60 - 40) + (47 + 60) (80 - 60)
2 2
= 670 + 1070 = 1740

Disease Monitoring- periodic observation of diseases or pathogens
in the field.
Objectives:
- To identify most significant pathogens
- To discover conditions under which epidemics is likely to occur
- Find cultivars which are most susceptible to a pathogen
- Observe change in pathogen’s virulence
Chapter 7: Disease Monitoring, Forecasting &
Measurement

Disease Forecasting- is predicting the occurrence of disease to notify the
growers of a community about the occurrence of the disease.
Objectives:
• To notify growers that a disease can cause significant damage
• To tell the time of occurrence of a disease
• To indicate growers the economical control measures
• To provide the weather-disease relationship for epidemiology

Bases for forecasting
• Weather condition during the crop season
• Weather conditions during the intercrop period
• Amount of disease in the young crop
• Amount of inoculums in air, soil or planting material

Measurement of Plant Disease
This helps to have quantitative data. The importance of
quantitative data is to:
- judge the relative importance of diseases so that research
& extension can be directed towards the most harmful
ones
- Lessen unnecessary expenditure
- Determine the value of control measures

Methods of disease measurement
- Disease incidence
- Disease severity
- Yield loss

Disease incidence- is the percentage of plants within a crop showing disease or
number of plants infected
Number of infected plant units
Disease incidence (I) = -------------------------------------------------------- x 100
(Frequency) Total number (healthy and infected)
of units assessed
I = 4/10 x 100 = 40%

Disease severity- the proportion of area or amount of plant tissue that is diseased
Area of plant tissue affected by disease
Disease severity (S) = ---------------------------------------------------------- x 100
(Area) Total area
S = 300cm2 / 1000 cm2 x 100 = 30%

Methods of assessing disease severity
a) Descriptive key- describes plants with different levels of disease and
assigns category, scale, number, index, grade or percentage to each
description
1 2 3 4 5
6 7 8 9

Standard area diagram: uses standard area diagrams which
typify the development of disease on a whole plant or part
of a plant
10
%
50
%
75
%

Mostly scales are used to rate plant diseases. The scales can
be 1-5 or 1-9.
e.g. ICRISAT 1-5 scale for disease measurement on sorghum
Numerical category %age infection
1 0-5%
2 5-25%
3 25-50%
4 50-75%
5 75-100%

CIAT 1-9 scale for disease measurement on beans
Numerical category %age infection
1 no symptom/immune
3 2% of the leaf damaged
5 5% of the leaf “
Note: 0 is reserved for situation where a rating cannot be
made.

The severity grades obtained will be converted into disease
index (DI) by the formula:
Sum of individual ratings 100
Disease index (DI) = --------------------------------------- X ----------------------
Number of plants assessed Maximum scale

Potato late blight severity was measured on 6 sample plants in a
plot using 1-9 scale. Calculate DI.
Sample plant severity
1 7
2 4
3 1
4 5
5 3
6 9

Sum of individual ratings 100
Disease index (DI) = --------------------------------------- X ----------------------
Number of plants assessed Maximum scale
7 + 4 + 1 + 5 + 3 + 9 100
DI = --------------------------------------- X -----------------
6 9
29 100
DI = ----------- X ------------ = 53.70%
6 9

Yield loss: the proportion of the yield that the grower will not
be able to harvest because the disease destroyed it.
- It is difference between mean yield of fungicide sprayed
(protected) & unsprayed (unprotected) plot.
Yield of protected (YP) – Yield of
unprotected (YUP)
Yield Loss (YL) =
X 100
Yield of protected (YP)

Course Powerpoint (FFV).pptx

More Related Content

What's hot

Similar to Course Powerpoint (FFV).pptx

More from dawitg2

Recently uploaded

Course Powerpoint (FFV).pptx