Agro-Technical and Technology College

Department of Agro-Ecology

Course title: Plant Pathology Semester: I

Course #: CPS-2101 Academic year: 2019/20

Credit hours: 3 Program: BSc in Crop Production

Instructors: Dr Habtamu Terefe

Course Material

Course objectives:
1. Introduce the basic principles of plant pathology
2. Introduce techniques and methods used in plant pathology
3. Identify the major causes of plant diseases
4. Familiarize the role of environmental factors in disease development
5. Recognize plant diseases and management principles
6. Realize the importance and application of biotechnology in plant pathology
7. Introduce economically important plant diseases

Topical Outlines:
1. Introduction
1.1. Disease in plants: Definitions
1.2. Plant pathology and its role

2. Classification of Plant Diseases

2.1. Infectious Plant Diseases (Structures and Reproduction of plant pathogens including)
2.1.1 Fungi as plant pathogens
2.1.2 Bacteria as pathogens
2.1.3 Virus and viroids as pathogens
2.1.4 Nematodes as pathogens
2.1.5 Parasitic higher plants
2.2. Non-infectious plant diseases
2.2.1 Unfavourable metrological factors

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 2.2.2 Status of moisture contents
2.2.3 Nutritional disorders
2.2.4 Atmospheric impurities
2.2.5 Improper cultural practices
3. Koch’s Postulates and Plant Disease Symptoms
3.1. Koch’s postulates
3.2. Morphological symptoms of plant diseases
3.2.1. Necrotic symptoms
3.2.2. Hypoplasia
3.2.3. Hyperplasia
3.3. Effects of plant pathogens on plant physiology
3.4. Diagnosis of plant diseases

4. Host-Pathogen Relations: Parasitism and Disease Development

4.1. Disease development: Disease triangle/disease pyramid
4.2. Plant disease cycle
4.2.1. Inoculum and inoculation
4.2.2. Pre-penetration/penetration process
4.2.3. Infection/invasion and establishment
4.2.4. Reproduction
4.2.5. Dissemination
4.2.6. Survival of pathogens

5. Defense Mechanisms of Plants against Pathogens

5.1. Mechanisms of attack by pathogens
5.2. Structural defense mechanisms
5.2.1. Pre-existing defense structures
5.2.2. Post-infectional defense structures
5.3. Biochemical defense mechanisms
5.3.1. Pre-existing biochemical defense
5.3.2. Induced biochemical defense

6. Genetics of Plant Diseases

6.1. Variability of pathogens and mechanisms
6.2. Genetics of virulence and resistance
6.3. Gene-for-gene concept

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6.4. Types of plant resistance to pathogens
6.5. Breakdown of plant disease resistance

7. Epidemiology of Plant Diseases

7.1 Different factors affecting epiphytotics
7.1.1. Host factors
7.1.2. Pathogen factors
7.1.3. Environmental factors
7.1.4. Human factors
7.2. Measurement of plant diseases
7.3. Simple and compound interest plant diseases
7.4. Monitoring and forecasting of plant disease epidemics and bases for forecasting

8. General Management Methods of Plant Diseases

8.1. Regulatory methods: quarantine, sanitation, exclusion of plant pathogens.
8.2. Cultural methods/eradication of plant pathogens
8.3. Mechanical/physical methods
8.4. Host plant resistance (HPR)
8.5. Biological control of plant diseases
8.6. Chemical protection of plants
8.7. Integrated Disease Management of plant diseases

9. Biotechnology and Plant Pathology

9.1. Application of biotechnology
9.2. Tissue culture techniques of significance to pathology
9.3. Prospectus of biotechnology in pathology

10. Introduction to Major Plant Diseases

10.1. Root rots and damping-off
10.2. Stem and branch diseases
10.3. Foliar diseases
10.4. Floral and seed diseases
10.5. Fruit diseases and soft rots
10.6. Vascular wilts

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Laboratory Practicals:
 List practicals to be covered by the course will be well identified, sorted out and made
ready for the students.

Mode of Delivery:
 Lecture, classroom discussions, peer teaching and lab studies

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1. Introduction (2 Hrs)
1.1. Disease in Plants: Definitions

Definitions of terms
 Disease = any deviation from the normal physiological activities or that results in
morphological abnormalities caused by continuous (constant) irritation of the plant by a
primary agent or pathogen. It is a malfunctioning process, interruption or disturbance of
the normal metabolism of the plant. If the disturbance is a temporary phase, it is an injury,
eg. cutting leaves.
 Pathogen = any living or non-living entity that brings about or incites a disease by its
persistent association with the host plant.
 Parasite = an organism which lives on or in another organism obtaining its sustenance
from the latter called a host. Can a parasite cause disease to a host?
 Host = an organism that supports a parasite.
 Pathogenicity = the capacity of the pathogen to cause disease.
 Virulence = successful expression of pathogenicity; it expresses the degree of
pathogenicity.
 Pathogenesis = the chain of metabolic events that bring about the disease; involves action
of the pathogen, susceptibility of the plant and the impact of the environment.
 Sign = manifestation of the pathogen, eg. Some structural parts of the pathogen.
 Symptoms = visible external expressions of the host’s response to infection.
 Disease syndrome = the sum total of all symptoms and signs.
 Predisposition = the environmental effects that make plants more susceptible to
infection.

1.2. Plant Pathology and Its Role

The word ‘pathology’ is derived from two Greek words: pathos = disease, suffering; Logos =
word, study, discourse. Therefore, it can be defined as:
Pathology = science of diseases or the study of the suffering organism. It is the study of a disease
and all its manifestations, especially of the functional and structural changes caused by it. It
also investigates the responsible causal agent(s) for the disease.
Plant pathology (Phytopathology) is the study of:
(1) The living entities and environmental conditions that cause disease in plants  etiology
(2) The mechanisms by which these factors produce disease in plants
(3) The interactions between the disease-causing agent and the diseased plant

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 (4) The methods of preventing or controlling (managing) disease and alleviating the damage
it causes

Two major objectives of phytopathologists

(1) To minimize crop losses through application of principles of plant disease prevention
(2) To develop a deeper understanding of biological science through knowledge of the
principles of plant disease

Relations of Plant Pathology with Other Disciplines

Phytopathology uses the fundamental knowledge and techniques of:

(1) Bacteriology (10) Molecular biology

(2) Biochemistry (11) Mycology
(3) Biotechnology (12) Nematology
(4) Botany (13) Physics
(5) Chemistry (14) Plant anatomy & morphology
(6) Forestry (15) Plant physiology
(7) Genetics (16) Soil science
(8) Horticulture (17) Virology
(9) Meteorology (18) Other branches of sciences

Major Divisions of Phytopathology

1. Bacteriology 3. Nematology
2. Mycology 4. Virology

Summary
 Plant pathology increases our knowledge of causes and development of plant diseases.
 Phytopathology attempts to develop controls for all plant diseases to save the produce that
today is destroyed by plant diseases and to make it available to human beings.

2. Classification of Plant Diseases

Various schemes of classifying plant diseases have been presented in plant pathology in a
logical system, depending on the purpose of treatment. The following are the bases of plant
disease classifications:
1. Host plants or crops affected: (Crop category or taxonomic approach)

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 E.g., Cereal diseases, truck crop diseases, legume diseases, forest diseases, maize diseases,
and others.
2. Organs of the affected plants: (Histological approach)
E.g., Root diseases stem diseases, leaf diseases, floral diseases, fruit diseases, seed rots, and
others.
3. Physiology of diseased plants (Physiological approach)
The seven physiological processes (according to G.L. McNew, Boyce Thompson Institute
for Plant Research) and the corresponding diseases based on the vital functions affected are:
 A) Storage of food  Soft rots and seed-decays
 B) Hydrolysis and utilization of stored food  Damping-off and seedling blights
 C) Absorption and accumulation of water and minerals  Diebacks
 D) Growth (meristematic activity) and reproduction  Galls and smuts
 E) Conduction of water and transpiration  Vascular wilts
 F) Photosynthesis  Diseases affecting photosynthesis (spots, mildews, blights, rusts)
 G) Translocation of elaborated food materials  Diseases interfering with translocation
4. Based on symptoms/effects (Symptomatological approach)
This classification properly directs attention to studies of the diseased plant. It is a
classification of the conditions of the disease and varies with different environments. It is
useful for disease diagnosis. E.g., Rots, mildews, wilts, blights, and others.
5. Based on occurrence of plant diseases (Epidemiological approach)
a) Endemic diseases – The diseases are more or less constantly present from year to year in a
moderate to severe form. Pathogens survive from crop season to the next in soil, on crop
residue or in wild plants for a long persistence. They cause regular crop losses. E.g.,
Potato scab (Streptomyces scabies), and brown rust (Puccinia recondita).
b) Epidemic/epiphytotic diseases - Diseases that occur widely but periodically. This depends
on the environment favourable to disease development that occurs only periodically. E.g.,
Late blight of potato (Phytophthora infestans). Disease phases: lag phase (exponential
phase), logistic phase and terminal phase.
c) Sporadic diseases - Diseases that occur at very irregular fitful intervals and locations and
in relatively few instances (also called spasmodic diseases). They cause incidental (minor)
crop losses. E.g., Stem rust (Puccinia graminis).
d) Pandemic diseases - Diseases that result in wide devastation and starvation (famine)
leading to death of human beings. E.g., Late blight of potato (Phytophthora infestans) in
Ireland in 1845.

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6. Based on source of inoculum/spread. E.g., Air-borne (wind-borne), soil-borne, seed-borne,
insect-borne, water-borne, animal-borne, man-borne, etc. For instance, stem rust of wheat is
an air-borne disease.
7. Taxonomy of the pathogen – Causal factor (Etiological or classical approach). This is the
most useful. It unravels the various causal factors and is the most satisfactory classification
method.
a) Parasitic/pathogenic causes. E.g., Fungi, bacteria, viruses, nematodes, and others.
b) Non-parasitic (non-infectious) causes

3. Infectious Causes of Plant Diseases/Etiology…4 hrs

Under this subtopic, the structure, reproduction and classification of the major plant pathogens
shall be treated.
3.1. Fungi as Pathogens

There are about 260,000 fungus species in the world. More than 8,000 fungal species cause
diseases in plants, each attacking one or many kinds of plants. Thus fungi cause about 100,000
plant diseases. The fungi are generally microscopic and lack chlorophyll (achlorophyllous).
They could be obligate (biotrophs) or non-obligate parasites.

Structure/Morphology

The body of the fungus is known as mycelium (thallus) and the individual branches (filaments)
are called hyphae (0.5 – 100 m thick or more). The mycelial strands may extend several meters
long, e.g., rhizomorphs of Armillaria mellea. The mycelium consists of many cells
(multicellular). The cells of the true fungi possess cell wall. Each cell contains one, two or
many nuclei, i.e. the mycelium could be coenocytic – contains many nuclei. The mycelium may
be one continuous tubular, branched, or un-branched multinucleate cell or it is partitioned by
several cross-walls (septa).

Habitat of Fungi/Ecology
Fungi are found in the soil, in air (as spores), in water, in or on plants and animals. Some can
grow near 0 oC, others at 40 – 50 oC or higher. Fungi may require dry or moist ecology. For
example, Powdery mildew fungal spores can germinate at very dry conditions  can survive
under varied situations.

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Reproduction of Fungi
The fungi mainly reproduce by sporulation - spores. The process is known as cryptogamy. The
spores are specialized propagative or reproductive bodies of one or a few cells. They may be
produced in a sac-like container and such spores are known as endogenous spores, while others
develop as naked and called exogenous spores. The spores could be sexual or asexual spores:
Asexual spores
1. Zoospores – motile spores with flagella produced in sporangium (endogenous).
2. Pycniospores/pycnidiospores – endogenous spores produced in the pycnia/ pycnidia.
3. Conidia – conidiospores produced by cutting off the hyphae called conidiophores
(exogenous spores). The process is known as conidiogenesis and conidia are released from
the conidiogenous cells, e.g., phialides.
4. Chlamydospores – modified hyphal cells with a thick wall (exogenous spores). These
could be apical or intercalary chlamydospores.
Sexual spores
1. Zygospores – product of two similar sex gametes fusing together to produce a zygote –
exogenous.
2. Oospores – product of fusion of unequal sex cells (dissimilar gametes) – exogenous.
3. Ascospores – sexual and endogenous spores produced in an ascus.
4. Basidiospores – produced externally on the basidium and are exogenous spores.
 When both female and male gametes are produced on the same mycelium –
Hermaphroditic fungi.
 When the male gametes can fertilize the female ones of the same mycelium – Homothallic
fungi (Isogamy)
 When the male gametes fertilize only the female gametes of another, sexually compatible
mycelium – Heterothallic fungi (Heterogamy)

Classification of Plant Pathogenic Fungi

The fungi that cause diseases on plants are diverse group. Some fungi, often referred to as the
lower fungi, are now considered to belong to the kingdom Protozoa (e.g., the Myxomycetes
and Plasmodiophoromycetes) or to the kingdom Chromista (e.g., the Oomycetes). The true
fungi, however, (i.e. Chytridiomycetes, Zygomycetes, Ascomycetes, Basidiomycetes, and
Deuteromycetes) belong to the kingdom Fungi (earlier called Eumycotina or Mycetae).

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Fungilike Organisms or Pseudofungi (The Lower Fungi)

KINGDOM: PROTOZOA – Microorganisms that may be unicellular, plasmodial, colonial,

very simple multicells, or phagotrophic, i.e. feeding by engulfing their food. The kingdom
contains many microorganisms in addition to fungallike organisms (classes) of Myxomycetes
and Plasmodiophoromycetes.
Phylum: MYXOMYCOTA – Produce a plasmodiumlike structure.
CLASS: MYXOMYCETES (slime moulds) – Their body is naked, amorphous
plasmodium. They produce zoospores (swarm cells). May grow on and over parts of
low-lying plants but do not infect plants.
Order: Physarales – Saprophytic plasmodium that gives rise to crusty
fructifications containing spores. They produce zoospores that have flagella.
Genus: Fuligo, Mucilago, and Physarum cause slime molds on low-lying plants.
Phylum: PLASMODIOPHOROMYCOTINA (the Plasmodiophoromycetes –
endoparasitic slime moulds).
Order: Plasmodiophorales – Plasmodia produced within cells of roots and stems
of plants. They produce zoospores that have two flagella. Obligate parasites.
Genus: Plasmodiophora, P. brassicae causing clubroot of crucifers.
Polymyxa, P. graminis parasitic in wheat and other cereals. Can transmit plant
viruses. Spongospora, S. subterranean causing powdery scab of potato tubers.
KINGDOM: CHROMISTA – Unicellular or multicellular, filamentous or colonial, primarily
phototrophic (micro-) organisms, some with tubular flagellar appendages or with chloroplasts
inside the rough endoplasmic reticulum, or both. Contains the brown algae, diatoms, oomycetes,
and some other similar organisms.
Phylum: OOMYCOTA – Have biflagellate zoospores, with longer tinsel flagellum directed
forward and a shorter whiplash flagellum directed backward. Diploid thallus, with meiosis
occurring in the developing gametangia. Gamentagial contact produces thick-walled sexual
oospore. Cell walls composed of glucans and small amounts of hydroxyproline and cellulose.
CLASS: Oomycetes (the water moulds, white rusts, and downy mildews) – Have non-
septate elongate mycelium. Produce zoospores in zoosporangia. Zoospores have two
flagella. Sexual resting spores (oospores) produced by the union of morphologically
different gametangia called antheridia (male) and oogonia (female).
Order: Saprolegniales – Have well-developed mycelium. Zoospores produced in
long, cylindrical zoosporangia attached to mycelium. Usually several oospores in an
oogonium.

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 Genus: Aphanomyces, A. euteiches causing root rot of peas.
Order: Peronosporales – Mycelium well-developed, nonseptate, branching, inter-
or intracellular, often with haustoria. Zoosporangia oval or lemon-shaped, borne on
ordinary mycelium or on sporangiophores. Sporangia in most species germinate by
producing zoospores, but in some they germinate directly and produce a germ tube.
Sexual reproduction is by characteristic oogonia and anthridia that fuse and produce an
oospore. Oospores germinate by giving rise to zoospores or to a germ tube which soon
produces a sporangium, depending on the species.
Family: Pythiaceae – Sporangia, usually zoosporangia, produced along somatic
hyphae or at tips of hyphae of indeterminate growth and set free. Oogonia thin-
walled. Facultatve parasites.
Genus: Pythium, causing damping-off of seedlings, seed decay, root rots, and
cottony blight of turf grasses.
Phytophthora, P. infestans causing late blight of potato, others causing mostly
root rots.
Family: Peronosporaceae (the downy mildews) – Sporangia borne on
sporangiophores of determinate growth. Sporangia wind-borne. Obligate parasites.
Genus: Plasmopara, P. viticola causing downy mildew of grape.
Peronospora, P. tabacina causing downy mildew (blue mould) of tobacco.
Bremia, B. lactucae causing downy mildew of lettuce.
Pseudoperonospora, P. cubensis causing downy mildew of cucurbits.
Peronosclerospora causing downy mildews of corn (P. philippinensis), of
sugarcne and corn (P. sacchari), of sorghum (P. sorghi), and others.
Sclerophthora causing the crazy top downy mildew of corn.
Sclerospora causing downy mildew of pearl millet and many other grasses.
Family: Albuginaceae (the white rusts) – Sporangia borne in chains.
Albugo, A. candida causing white rust of crucifers.

The True Fungi

KINGDOM: FUNGI – Produce mycelium, the walls of which contain glucans and chitin. Lack
chloroplasts.
Phylum: CHYTRIDIOMYCOTA: Produce zoospores that have a single posterior
flagellum.

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 CLASS: CHYTRIDIOMYCETES – Have round or elongated mycelium that lacks cross
walls.
Genus: Olpium, O. brassicae being parasitic in roots of cabbage and other
plants. Can transmit plant viruses.
Physoderma, P. maydis causing brown spot of corn.
Synchytrium, S. endobioticum causing potato wart
Urophlyctis, U. alfalfae causing crown wart of alfalfa
Phylum: ZYGOMYCOTA – Produce nonmotile asexual spores in sporangia. No
zoospores. The resting spore is a zygospore, produced by the fusion of two
morphologically similar gametes.
CLASS: ZYGOMYCETES (the bread moulds) – Saprophytic or parasites of plants,
humans and animals.
Order: Mucorales – Nonmotile asexual spores formed in terminal sporangia
Genus: Rhizopus, causing bread moulds and soft rot of fruits and vegetables.
Choanephora, C. Cucurbitarum causing soft rot of squash.
Mucor, causing bread mould and storage rots of fruits and vegetables.
Order: Glomales – Fungi causing vesicular-arbuscular mycorrhizae, also known as
endomycorrhizae. Arbuscules produced in host roots. Chlamydosporelike spores
produced singly in soil, in roots, or in sporocarps. Sexual reproduction rare.
Genus: Glomus, Acaulospora, Gigaspora, Scutellospora.
Phylum: ASCOMYCOTA (ascomycetes, the sac-fungi) – Most have a sexual stage
(teleomorph) and an asexual stage (anamorph). Produce sexual spores, called ascospores,
generally in groups of eight within an ascus. Produce asexual spores (conidia) on free hyphae or
in asexual fruiting structures (pycnidia, acervuli, etc.).
I. CLASS: ARCHIASCOMYCETES – A group of diverse fungi, difficult to characterize.
Order: Taphrinales – Asci arisng from binucleate ascogenous cells.
Taphrina, causing peach leaf curl, plum pocket, oak leaf blister, etc.
II. CLASS: SACCHAROMYCETES (the yeast fungi) – Asci naked, no ascocarps produced.
Mostly unicellular fungi that reproduce by budding.
Genus: Galactomyces, causing citrus sour rot.
Saccharomyces, S. cervisiae, the bread yeast.
III. CLASS: FILAMENTOUS ASCOMYCETES
A. ASCOMYCETES WITH CLEISTOTHECIA - Mycelium, conidia, and cleistothecia
on surface of host plant. Obligate parasites.

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 Order: Erysiphales (the powdery mildew fungi) – Asci in fruiting bodies completely
closed (cleistothecia).
Genus: Blumeria, causing powdery mildew of cereals and grasses.
Erysiphe, causing powdery mildews of many herbaceous plants.
Leveillula, causing powdery mildew of tomato and pepper.
Microsphaeria, one species causing powdery mildew of apple.
Sphaerotheca, S. pannosa causing powdery mildew of roses and peach.
Uncinula, U. necator causing powdery mildew of grape.
B. PYRENOMYCETES: ASCOMYCETES WITH PERITHECIA – Perithecia or,
occasionally, cleistothecia in a stroma, immersed in a loose hyphal mat, or free. Asci have
one wall.
Order: Hypocreales – Stromata pale to blue, purple or brightly colored. Asci ovoid
to cylindrical with apical pore. Conidia produced from phialidic conidiophores. Some
produce substances toxic to humans and animals. Some produce growth regulators.
Some are antagonistic or parasitic on other fungi and some are systemic parasites
(endophytes) of many grain crops and make them poisonous to grazining animals.
Genus: Hypocrea, some species of which produce anamorphs like Trichoderma
and Gliocladium, which are used as biocontrol agents against several plant
pathogenic fungi.
Melanospora, of which its anamorphs Phialophora and Gonatobotrys parasitize
the mycelium of many fungi, including the important plant pathogens
Ophiostoma, Ceratocystis, Fusarium, and Verticillium.
Nectria, causing twig and stem cankers of trees.
Gibberella, causing foot or stalk rot of corn and small grains.
Claviceps, C. purpurea causing ergot of rye, which is poisonous to humans and
animals.
Epichloe, endophytic in grasses and sedges.
Atkinsonella, endophytic in grasses and sedges.
Myriogoeenospora, endophytic in grasses and sedges
Order: Microascales – Lack stromata. Most have perithecia but some have
cleistothecia. Asci are globoid or ovoid, disintegrating. Ascospores one-celled.
Genus: Ceratocystis, causing oak wilt (C. fagacearum); cankers in stone fruit
and other trees and root rot of sweet potato (C. fimbriata); butt rot of pineapple (C.
paradoxa); sapstain or blue stain of cut wood surfaces (C. coerulescens and
others).

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Order: Phyllachorales – Perithecia in stroma, asci oblong to cylindrical, with
pores at their tips. Ascospores of vaying shapes, hyaline or dark.
Genus: Glomerella, G. cingulata causing many anthracnose diseases and
bitter rot of apples; its anamorphic stage is Colletotrichum gloeosporioides
Phyllachora, P. graminis causing lead spots on grasses.
Order: Ophiostomatales – Perithecia without paraphyses. Asci globose to ovoid,
disintegrating. Several species are dispersed by beetles. Some species cause
sapstain (blue stain) in wood.
Genus: Ophiostroma, O. (formely Ceratocystis) ulmi, causing the Dutch
elm disease; O. novo-ulmi, causing a more severe form of Dutch elm disease, is
replacing O. ulmi in nature (anamorphs are Sporothrix and Graphium).
Order: Diaporthales – Perithecia in a substrate of either fungal and substrate
tissue, or of hyphae on substrate. Asci cylindrical with pores. Ascospores have
one to several septa and may be hyaline to brown.
Genus: Diaporthe, causing citrus melanose (D. citri), eggplant fruit rot
(D. vexans), soybean pod and stem rot (D. phaseolorum); their anamorphs are
species of Phomopsis.
Gnomonia, causing anthracnose and leaf spot diseases.
Gaeumannmyces, G. graminis causing the take-all disease of grain crops
(wheat, rice, oats) and grasses.
Magnaporthe, M. grisea causing the very important rice blast disease; its
anamorph is Pyricularia oryzae.
Cryphonectria (formerly Endothia), C. parasitica causing the chestnut
blight disease.
Leucostoma (formerly Valsa), causing canker diseases of peach and other
trees.
Order: Xylariales – Perithecia dark, leathery, hard, sometimes embedded in a
stroma. Asci cylindrical to subglobose. Ascospores one to a few-celled, hyaline
or dark.
Genus: Hypoxylon, H. mammatum causing a severe canker on poplars.
Roselinia, R. necatrix causing root diseases of fruit trees and vines.
Xylaria, causing tree cankers and wood decay.
Eeutypa, E. armeniacae causing serious canker diseases of fruit trees and
vines.

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 C. LOCULOASCOMYCETES: ASCOMYCETES WITH ASCOSTROMATA –
Produce asci within locules (cavities) preformed in stroma. Ascostroma may be
monolocular (pseudothecium ) or multilocular. Asci have a double wall.
Order: Dothideales – Locules lack sterile hyphae and open by an apical pore,
Asci ovoid t cylindrical, in fasciles. Ascospores one to several celled, hyaline to brown.
Genus: Mycosphaerella, causing leaf spots on many plants, such as the Sigatoka
diseases of banana (M. musicola and M. fijiensis), and leaf spot of strawberry
(M. fragariae); its anamorphs may be Cercospora, Septoria, and others.
Elsinoë, causing citrus scab (E. faucetii), grape anthracnose (E. ampelina), and
raspberry anthracnose (E. veneta).
Order: Capnodiales – Ascocarps superficial, produced in a loose mat of dark
hyphae.
Genus: Capnodium, being one of several fungi causing sooty moulds on plants.
Order: Pleosporales – Asci surrounded by pseudoparaphyses. Ascostroma
variable
Genus: Cochliobolus, whose anamorphs are Bipolaris or Curvularia, causes leaf
spots and root rots on grain crops and grasses.
Pyrenophora, whose anamorph is Drechslera, causing leaf spots on cereals and
grasses.
Septosphaera (anamorph is Exserohilum), causing leaf spots on cereals and
grasses
Pleospora (anamorph is Stemphylium), causing black mould rot of tomato.
Leptosphaeria (anamorph is Phoma), causing black and foot rot of cabbage.
Venturia (anmorph is Spilocaea), causing black rot of grapes.
Guignardia (anamorph is Phyllosticta), causing black rot of grapes.
Dibotryon, D. morbosum causing black rot of cherries and plums.
D. DISCOMYCETES: ASCOMYCETES WITH APOTHECIA – Ascocarps shaped as
cups, saucers, or cushions and called apothecia. Asci cyndrical to ovoid, often interspersed
with paraphyses. Ascospores discharged forcibly.
Order: Rhytismales – Ascocarps are black, spherical, discoid, or elongate, and are
produced in stromata. Asci variable. Ascospores hyaline or brown, ovoid to filiform.
Genus: Hypoderma, causing pine leaf spot (needle cast) diseases.
Lophoderminum, causing pine needle blight.
Rhabdocline, causing pine cast disease.
Rhytisma, R. ascerinum causing tar spot of maple leaves.

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 Order: Helotiales – Apothecia cup– or disk-shaped. Asci with only slightly thicked
apices. Ascospores are spherical, elongate, to filiform, and have one to several septa.
Genus: Monilinia, causing the brown rot disease of stone fruits.
Sclerotinia, S. sclerotiorum causing the white mould or watery soft rot of
vegetables.
Stromatinia, S. gladioli causing corm rot of gladiolus.
Pseudopeziza, P. trifolii causing alfalfa leaf spot
Diplocarpon, D. maculatum causing black spot of quince and pear, and black
spot of roses (D. rosae).
Sclerotium, S. cepivorum causing the white rot of onions.
Phylum: DEUTEROMYCOTA (DEUTEROMYCETES, Imperfect or asexual fungi) –
Mycelium well-developed, septate, branched. Sexual reproduction and structures rare,
lacking, or unknown. Asexual spores (conidia) formed on conidiophores existing singly,
grouped in specialized structures such as sporodochia and synemata, or produced in
structures known as pycnidia and acervuli.

Anamorphic stage Certain or likely

teleomorphic group

Genus: Geotrichum, G. candidum causing sour rot rot of fruits and vegetables Saccharomycetales
Cleistothecial
ascomycetes
Penicillium, causing blue mould rot of fruits Talaromyces
Aspergillus, causing bread mould and seed decays Eurotium
Paecilomyces, used as biological control agent against white flies Byssochlamys
Oidium, causing the powdery mildews Erysiphe, Etc.
Perithecial
ascomycetes
Chalara, causing oak wilt, tree cankers Ceratocystis
Acremonium, endophytic in grasses Epichloe
Sporothrix and Graphium, causing the Dutch elm disease Ophiostoma
Trichoderma, used as biocontrol agent against other fungi Hypocrea
Verticillium, causing vascular wilts in many plants Hypocrea
Fusarium, causing vascular wilts, root rots, stem rots, seed infections Gibberella
Colletotrichum, causing anthracnoses in many plants Glomerella
Loculoascomycetes
Cercospora, causing Sigatoka disease of bananas Mycosphaerella
Septoria, causing leaf spots on many crops Mycosphaerella
Phyllosticta, causing black rot of grape Guignardia
Alternaria, causing many leaf spots, blights Lewia
Stemphylium, causing fruit rots on tomato Pleospora
Bipolaris, causing leaf spots and root rots in grasses Cochliobolus
Drechslera, causing leaf spots on grasses Pyrenophora
Exserohilum, causing leaf spots on grasses Setosphaera
Curvularia, causing leaf spots on grasses Cochliobolus
Cladosporium, causing leaf moulds on tomato (C. fulvum), and scab of peach Fulvia, Venturia
and almond (C. carpophilum)
Sphaeropsis, causing black rot on apple Physalospora

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 Apothecial
ascomycetes
Botrytis, B. cinerea causing gray mould rots on many plants Botryotinia
Monilia, causing the brown rot of stone fruits Monilinia
Marssonina, causing the black spot of rose Diplocarpon
Entomosporium, causing a leaf and fruit spot on pear Diplocarpon
Cylindrosporium, causing leaf spots on many kinds of plants Mycosphaerella
Melanconium, causing the bitter rot of grape Greeneria
Basidiomycetes
Rhizoctonia, R. solani causing root and stem rots Thanatephorus
Rhizoctonia binucleate forms Ceratobasidiales
Sclerotium, S. rolfsii causing southern blight of many crops Aethalium_____

Phylum: BASIDIOMYCOTA (basidiomycetes, the club and mushroom fungi) – Sexual

spores, called basidiospores, are produced externally on a clublike, one- or four-celled spore-
producing structure called a basidium.
Order: Ustilaginales (the smut fungi) – Basidium has cross-walls or is nonseptate. It is
the promycelium of the teliospore. Teliospores single or united into clusters or columns,
remaining in host tissue or bursting through the epidermis. Fertilization by union of
compatible spores, hyphae, etc. Only teliospores and basidiospores are produced.
Genus: Ustilago, causing smut of corn (U. maydis), loose smuts of oats (U.
avenae), of barley (U. nuda) and wheat (U. tritici).
Tilletia, causing covered smut or bunt of wheat (T. caries), and kernel bunt
(partial bunt) of wheat (T. indica).
Urocystis, U. cepulae causing smut of onion.
Sporisporium, causing covered kernel smut of sorghum (S. sorghi) and loose
smut sorghum smut (S. cruentum).
Sphacelotheca, causing head smut of sorghum.
Order: Uredinales (the rust fungi) – Basidium with cross-walls. Sperm cells called
spermatia fertilize special receptive hyphae in spermogonia. Produce two to several
types of spores: teliospores, basidiospores, aeciospores, and uredospores. Uredospores
can be repeating spores. Obligate parasites.
Genus: Cronartium, several species causing stem rusts of pines.
Gymnosporangium, G. juniperi-virginianae causing cedar-apple rust.
Hemeleia, H. vastatrix causing coffeee rust disease.
Melampsora, M. lini causing rust of flax.
Phakopsora, P. pachyrrhizi causing rust of soybeans.
Phragmidium, one species causing rust of roses
Puccinia, several species causing severe rust diseases of cereals and other plants.
Uromyces, U. appendiculatus causing rust of beans.

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 Order: Exobasidiales – Basidiocarp lacking: basidia produced on surface of parasitized
tissue.
Genus: Exobasidium, causing leaf, flower, and stem galls on several
ornamentals.
Order: Ceratobasidiales – Basidiocarp is weblike, inconspicuous. Basidia without cross-
walls, with four prominent sterigmata.
Genus: Thenatephorus, T. cucumeris is the teleomorph of Rhizoctonia solani,
causing root and stem rots, damping-off and fruit rots in many plants.
Typhula, causing typhula blight (snow mould) of turf grasses.
Order: Agaricales (the mushrooms) – Basidium without cross walls, produced on
radiating gills or lamellae. Many are mycorrhizal fungi.
Genus: Armillaria, A. mellea causing root rots of forest and fruit trees.
Crinipellis, C. perniciosus causing witches’-broom of cocoa in Central and South
America.
Marasmius, causing the fairy ring disease of turf grasses.
Pleurotus, causing white rot on logs, tree stumps, and living trees.
Pholiota, causing brown wood rot in deciduous forest trees.
Order: Aphyllophorales (the polypores) – Basidia without cross walls produced on
hymenia-forming hyphae and lining the surfaces of small pores or tubes.
Genus: Aethaliumi (Sclerotium), causing root and stem rots of many plants.
Chondrostereum, C. purpureum causing the silver leaf diseases of trees
Corticium, one species causing the red thread disease of turf grasses.
Heterobasidion, H. annosum causing heart rot of many trees.
Ganoderma, causing root and basal stem rots in many trees.
Inonotus, causing a heart rot of living trees and rot of dead trees and logs
Postia, causing wood and root rots of forest trees.
Phellinus, (Poria) causing tree root rots and cubical rots in buildings.
Peniophora, causing decay in coniferous logs and pulpwood.
Polyporus, causing heart rot of living trees & rot of dead trees or logs.

3.2. Bacteria as Pathogens

There are about 1600 bacterial species in the world. The majority are saprophytic bacteria.
About 180 species of bacteria cause diseases in plants. Most phytopathogenic bacteria are
facultative saprophytes and grow on synthetic media.

14
Morphology and physiology of bacteria
Bacteria differ in morphology and physiology: size, shape, motility, colour, Gram reaction, etc.

Shape: Almost all plant pathogenic bacteria are rod-shaped (Bacillus-type), except
filamentous (Streptomyces). Other shapes include: spherical (Cocci), ellipsoidal,
spiral (Spirilla), comma-shaped (Vibrio).
Size: The rod-shaped bacteria of young cultures range 1.0 – 4.0 x 0.5 –1.0 m. The
Streptomyces = 0.5 – 2 m in diameter. (NB. 1mm = 1000 m; 1 m = 1000 nm; 1 nm =
10 Å).
Motility: Motile or non-motile. Motile bacteria possess thread-like flagella, 10 – 15  long
(average 12 m long), usually longer than the cells (10 times longer than the bacterial
length) and about 20 nm thick; flagella consist of 2 - 30000 molecules of protein
polymers.
a) Atrichous: Possess no flagella on bacterial cells. E.g., some Agrobacterium. ,
Streptomyces
b) Monotrichous: With a single flagellum at the polar end. E.g., Xanthomonas,
Vibrio.
c) Lophotrichous: With more than one flagellum at one or both polar ends. E.g.,
Spirillium.

d) Amphitichous – With a tuft of flagella at each polar end. E.g., Pseudomonas.

e) Peritrichous – With several flagella distributed around the rod-shaped bacteria. Eg.,
Erwinia

Bacterial Colony

The spherical (cocci) bacteria may occur in different colonies:

a) Diplococci – When cells occur in pairs.
b) Streptococci – Occur in chains.
c) Tetrad – Occur in fours
d) Staphylococci – Occur in irregular bunches.
e) Sarcinnae – In cubical and rectangular forms.

Colony margin: Colony’s margin may be smooth, wavy, or angular

Elevation of colony: May be flat, raised, dome-shaped or wrinkled.
Colony colour: Whitish, grayish, but some are yellow, red or other colours.

15
Cytology:
Bacteria possess rigid cell-wall, cytoplasmic membrane, slime layer (capsule), protoplast,
protoplasmic membrane, cytoplasm [proteins, lipids, CHO, organic compounds, minerals, H 2O,
nuclear material (chromosome), and plastid].

Slime layer (capsule)

Ribosomes Cytoplasmic membrane
Plasma
membrane Cytoplasm
(Protoplasmic
membrane) Cell-wall

Vacuole

Nucloid Mesosome Flagella arise here

Reproduction of Bacteria
Phytopathogenic bacteria reproduce by the asexual process, binary fission. Bacteria reproduce
by dividing every 20 minutes. One bacterium could produce one million bacteria in 10 hours.

Ecology of Bacteria
Phytopathogenic bacteria live in the host plant as parasites and partly in the soil/host as
saprophytes. Agrobacterium tumefaciens, Pseudomanas solanacearum (syn.: Ralstonia
solanacearum), and Streptomyces scabies are soil inhabitants.

Classification of Phytopathogenic Bacteria

The bacteria belong to the prokaryotes – generally single-celled microorganisms that have a cell
wall, cell membrane, cytoplasm, ribosomes and genetic material (DNA) not bound by a
membrane, i.e., not organized into a nucleus. Thus:
Kingdom: Prokaryotae
Part I: Gram-negative aerobic rods and cocci
Family: Pseudomonadaceae
Genera: Pseudomonas – Rod-shaped with one or several polar flagella,
colonies white/yellow. Dimension: (0.5 – 1.0 x 1.5 – 4.0 µm)
Xanthomonas – Rod-shaped, with one polar flagellum, colonies
yellow. Dimension: (0.4 – 1.0 x 1.2 – 3.0 µm)
Family: Rhizobiaceae.
Genus: Agrobacterium – Rod-shaped, sparse lateral flagella, white
colony, rarely yellow. (0.8 x 1.5 – 3.0 µm)

16
 Genus: Rhizobium: (0.5 – 0.9 x 1.2 – 3.0 µm)
Part II: Gram-negative facultative anaerobic rods.
Family: Enterobacteriaceae.
Genus: Erwinia – Peritrichous flagella, colonies white/yellow. (0.5–1.0 x 1.0–3.0 µm)
Part III: Irregular, Gram-positive, non-sporing rods. A few phytopathogenic
Corynebacterium spp. (Clavibacter) (0.5 – 0.9 x 1.5 – 4.0 µm)
Part IV: Actinomycetes – Bacteria forming branching filaments.
Genus: Streptomyces – Gram-positive, aerial mycelium with chains of non-
motile conidia (without flagella). (0.5 – 2.0 µm)

3.3. Viruses and Viroids

Viruses
There are over 2000 viruses. Plant viruses are known to cause more than 600 plant diseases.
Viruses are sub-microscopic particles that are obligate intercellular and intracellular pathogens.
Viruses cause diseases not by consuming cells or killing them with toxins, but by utilizing
cellular substances, taking up space in cells, and by disrupting cellular components and
processes which, in turn, upset the metabolism of cells and lead to the development by the cell
of abnormal substances and conditions injurious (deleterious, detrimental) to the functions and
the life of the cell or the organism. E.g., TMV.

Morphology, physiology and chemistry: Viruses vary in size, shape, chemical composition,
physical structure, infection method, multiplication, translocation, dissemination, and
symptoms. Viruses have no cytoplasm, no ribosomes, no nuclear membrane, no
mitochondria, no cell membrane, and no other organelles.
Shape: Viruses are usually elongate (rigid rods or flexuous threads), rhabdovirus (Bacillus-like)
and spherical (isometric and polyhedral or icosahedral).
Size: Most of the elongated viruses range in length: 480 – 2000 x 10 – 13 nm. E.g., Potato virus
X: 480 x 10 – 13 nm. The citrus tristeza virus: 2000 nm x 10 – 13 nm. Spherical viruses:
17 – 60 nm in diameter.
Composition: Viruses consist of nucleic acid and protein, with the protein forming a protective
coat, called a capsid, around the nucleic acid. There is always only RNA or only DNA in
each virus and in most plant viruses, only one kind of protein. The proportion of nucleic
acid and protein vary with each virus, nucleic acid making up 5 – 40% of the virus and
protein making up the remaining 60 – 95%.

17
Multiplication: Viruses multiply by duplication or replication within the host cells, where the
RNA and protein subunits are formed separately in the host cells and combine to form the full
particles. Viruses lack enzyme system (Lipman system).

Classification of Viruses (Cryptogram)

Naming (grouping) viruses is based on the most remarkable symptom they cause on the host.
Eg. Tobacco mosaic virus (TMV). All viruses belong to:
Kingdom: VIRA
Division I: DNA viruses (helical/cubical)
Division II: RNA viruses (helical/cubical)
26 groups exist.

Question: Can we control viruses with chemicals, if no, why not?

Viroids
Viroids are small, low molecular weight ribonucleic acids (RNA) that can infect plant cells,
replicate themselves and cause plant diseases. Viroids are circular, single-stranded RNA
molecules. Viroids are 50 nm thick. They are associated with the cell nuclei. Differences
between viroids and viruses include:
1) Low molecular weight of 110,000 to 130,000 in viroids versus 10,000,000 in
viruses.
2) Viroids are devoid of a protein coat-free RNA.
Diseases due to viroids include:
1) Potato spindle tuber
2) Citrus exocortis
3) Chrysanthemum stunt
4) Chrysanthemum chlorotic mottle
5) Tomato bunchy top
6) Avocado sun blotch
7) Hop stunt
8) Coconut cadang-cadang
9) Cucumber pale fruit

3.4. Nematodes
Several hundred species of nematodes are known to feed on living plants, causing a variety of
plant diseases (about 1000 species of nematodes attack plants).

18
Morphology of Nematode
Nematodes are worm-like in appearance and are transparent.
Size: Parasitic nematodes 300 – 1000 x 15 – 35 m, some are up to 4 mm long.
Shape: Eel-shaped, round in cross-section, with smooth, un-segmented bodies without legs or
other appendages. In Meloidogyne species, mature females are pear-shaped.
Stylet: Spear used to puncture plant cells.
Life cycle: Eggs  larvae (four larval stages)  adult males and females (4 or 3 weeks).
Reproduction: Parthenogenetically or through fertilization by sperm produced in the individual
(hermaphroditic) or through mating.
Ecology of Nematodes
Nematodes survive in soil, plant roots, stems, kernels, etc. Abundance of nematodes 0 – 15 cm
depth; sometimes 30 – 150 cm or more deep in the soil.
Stylet
Musceles
Median bulb
Nerve ring
Salivary gland
Intestine Eggs
Ovary Spermatheca

Vulva
Annus
Female nematode

Uterus Phasmid

Testis

Sperm

Male nematode

Spicule Bursa

Classification of Nematodes

Nematodes could be ectoparsites, endoparasites, migratory or sendentary parasites.

Kingdom: Animalia
Phylum: Nematoda with 25 genera.
Order 1: Tylenchida
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 Genera: 14 most important and 7 less important genera are known = 21 genera.
Order 2: Dorylaimida
Genera: 4 genera known.
For example, Meloidogyne, Anguina, Pratylenchus, Heterodera, Ditylenchus, Radopholus,
Longidorus, Xiphinema, and others.

Genera of Nematodes

A. Tylenchida order

1. Anguina = Wheat or seed-gall nematode (eg. Anguina tritici)

2. Aphelenchoides = Foliar nematode of Chrysanthimum, strawberry, begonia, rice, coconut,
and others.
3. Belonolaimus = Sting nematode of cereals, legume, cucumber, and others.
4. Bursaphelenchus = The pine wood-nematode.
5. Criconemella = Ring nematode of wood plants.
6. Ditylenchus = Stem/bulb nematode of alfalfa, onion, and others.
7. Globodera = Cyst nematode of potato.
8. Helicotylenchus = Spiral nematode.
9. Hemicycliophora = Sheath nematode of various plants.
10. Heterodera = Cyst nematode of tobacco, soybean, sugar beets, cereals, and others.
11. Hoplolaimus = Lance nematode of corn, sugarcane, cotton, alfalfa, and others.
12. Meloidogyne = Root knot nematode of almost all plants.
13. Naccobus = False root knot nematode.
14. Paratylenchus = Pin nematode of various plants.
15. Pratylenchus = Lesion nematode of almost all crop plants and trees.
16. Radopholus = Burrowing nematode of banana, Citrus, coffee, sugarcane, and others.
17. Rhadinaphelenchus = The coconut red ring nematode.
18. Rotylenchulus = Reniform nematode of cotton, papaya, tea, tomato, and othrs.
19. Rotylenchus = Spiral nematode of various plants.
20. Tylenchorhynchus = Stunt nematode of tobacco, corn, cotton, and others.
21. Tylenchulus = Citrus nematode of Citrus, grapes, olive, lilac, and others.
Dorylaimida order
22. Longidorus = Needle nematode of some plants
23. Paratrichodorus = Stubby root nematode of cereals, vegetables, cranberry, apple.
24. Trichodorus = Stubby root nematode of sugar beet, potato, cereals, apple.

20
25. Xiphinema = Dagger nematode of trees, woody vines, and of many annuals.

3.5. Mycoplasma-like Organisms (MLOs) and Related Pathogens

3.5. 1. Mycoplasma-like Organisms (MLOs)
MLOs were first seen under the electronmicroscope in 1967. They are susceptible to antibiotics
(such as tetracycline, etc), but not to penicillin. They cause about 200 plant diseases. E.g., Corn
stunt. They are wall-less, have no flagella and cannot grow on artificial nutrient media 
obligate pathogens.

Morphological Characteristics
MLOs lack cell wall, are bound by a triple layered “unit” membrane, and have cytoplasm,
ribosomes, and strands of nuclear material.
Shape: Spherical to ovoid or irregularly tubular to filamentous. MLOs are present in the sap of
a small number of phloem sieve tubes. They are transmitted by leafhoppers, psyllids and
planthoppers. Yellow-type diseases are due to MLOs.

Size: 175 – 250 nm; fully developed or mature ones: up to 150 µm.

Classsification

Division: Tenericutes
Class: Mollicutes
Order: Mycoplasmatales
Family: 1. Mycoplasmataceae
Genus: Mycoplasma
Family: 2. Acholeplasmataceae
Genus: Acholeplasma
Family: 3. Spiroplasmataceae
Genus: Spiroplasma

3.5.2. Rickettsia-like Organisms (RLOs)

These are recently known as “fastidious vascular bacteria” and are considered to be parasitic
bacteria that cannot be cultivated on simple culture media in the absence of the host cells 
obligate pathogens. They are both xylem and phloem limited bacteria found in 1972. They are
rod-shaped (1 – 4 x 0.2 – 0.5), bound by a cell membrane and cell wall, without flagella,
nearly all Gram-negative.
Example, phloem-limited: club disease (clover); xylem-limited: Pierce’s disease (grape)

21
3.6. Parasitic Higher Flowering Plants: Phanerogamic Plant Parasites
More than 2500 species of higher plants are known to live as parasites on host plants. They
produce seeds and flowers. They are partially (semi-parasites) or totally dependent on hosts. For
example, Striga (commonly known to parasitisize sorghum in eastern parts of Ethiopia). The
most common and serious parasites are:

1. Cuscutaceae:
Genus: Cuscuta (dodders; strangle weed, pull-down; hell-bind); serve as vectors for viruses,
etc.; have no true roots; no chlorophyll; distributed in N America and Europe.
2. Viscaceae: Have chlorophyll but no true roots; use absorbed water and minerals - to
manufacture food.
Genera a) Arceuthobium (dwarf mistletoes of conifer)
b) Phoradendron (American true mistletoes of broad-leaved trees)
c) Viscum (European true mistletoes)
3. Orobanchaceae: Favoured by dry and warm regions; can attack herbaceous dicot; remain
dormant for more than 10 years.
Genus: Orobanche (Broomrapes; witchs’-broom).
4. Scrophulariaceae: Absorb organic matter, water and minerals - to manufacture food.
Genus: Striga (Witch-weeds of monocot); have no root-hairs; produce 50,000 to 500,000
seeds per plant; complete their life cycles within 90 to 120 days. For example, Striga
asiatica and Striga hermonthica.

4. Non-infectious Plant Diseases (2 lecture hours)

4.1. Unfavourable Meteorological Factors

High and low temperature effects

There are three cardinal points of temperature.
Minimum: at which growth first resumes.
Optimum: at which growth is most rapid
Maximum: at which growth ceases.

Low temperature
It affects green plants adversely in two ways:
 It limits the rates of metabolic chemical reactions.

22
  Temperatures below zero degrees may kill plants (ice formation in intra- and inter-cellular
spaces). Frost (freezing) results in foliage distortion and death of plants before maturation.
For example, months of October and November at Haramaya University best describes frosting
in the region.

High temperature
High temperature accelerates rate of evapo-transpiration and wilting of seedlings. Sunscald of
vegetables and heat injury to fruits is the result of high temperature.
Light
Weak light results in etiolation, long internodes, and succulent growth of foliage. The status of
light depends on light intensity, light quality and photoperiodic variation.
Wind
Strong wind results in desiccation and breakage or uprooting of plants. Example, Slovak was hit
by harsh wind or storm with speed of 180 km/hr on 26/11/04 and 26,000 ha forest area
demolished.
Humidity
Low humidity leads to plant wilting due to high evapo-transpiration and loss of soil water as
vapour. Also, high humidity may favour the development of certain diseases.
Oxygen relations
Atmospheric nitrogen = 78.00%
Atmospheric Oxygen = 21.00%
Atmospheric CO2 = 0.03%
Others (inert gases) = 0.97%
100.00%
Blackheart of potato is a disease brought on by the inaccessibility of the tuber tissues to oxygen
when the tubers are at high temperatures.

Lightening

Lightening, hail and wind-blown rain may cause injury to plants particularly leaves and stems.

4.2. Status of Soil Moisture

Insufficient and excessive amounts of water

Plants affected by drought may suffer from chlorosis, if the drought is severe  permanent
wilting of the foliage. Firing and scorching are common leaf symptoms of plants that do not
receive sufficient moisture. On the other hand, concentrations of toxic substances, such as

23
nitrites, build up in waterlogged soils. Plants grow poorly in soils with excessive water and
typically show a general yellowing of foliage. Excessive soil moisture results in the wilting of
herbaceous plants and roots become blackened and decayed. Suffocation results in under
waterlogged conditions. Roots become thirsty since they are not able to absorb water without
O2 .

4.3. Nutritional Disorders

Nutritional disorders include deficiencies and excesses of nutrients or imbalances.

Nutrient Deficiencies
When any of the elements in the soil are deficient, the plants show symptoms of deficiency
(hunger signs). For example, N, P, K, B, Ca, Cu, Fe, Mg, Mn, Mo, Al, Na, Cl, S, Zn, and Co.
For instance, deficiency of N on maize seedlings shows yellowing of leaves though common to
other crops. P deficiency  Purplish.

Nutrient Excessive
Plant nutrients, especially in trace amounts, sometimes accumulate to toxic concentrations in
plant tissues.

4.4. Atmospheric Impurities

Air pollutants are categorized into four groups:
1) Naturally occurring pollutants. For example, Ozone (O3), CO, CFC (chlorofluorocarbon)
2) Toxic gases released from green plants. For example, Ethylene
3) Photochemical reaction products from combustion products and natural chemicals in the
air. For example, Smog (smoke + fog)
4) Specific industrial processes. For example, SO2

4.5. Improper Cultural Practices

The incorrect use of fertilizers, fungicides, insecticides, and herbicides can cause serious
damage. For instance, the herbicide 2,4-D, when drifted to broad-leaf crops, can damage much;
ecessive application of N fertilizers cause vegetative growth that results in succulence and
logding in plants, and even prone the crop to infection by pathogens. Therefore, improper
agronomic practices can damage the roots, stems and leaves opening avenues to infection by
pathogens.

24
5. Koch’s Postulates and Disease Symptoms (3 lecture hours)

5.1. Koch’s Postulates (Rules) – Procedures

Robert Koch (German bacteriologist who lived b/n 1843-1910) presented three rules for
pathogenicity test in 1883 and Erwin Frink Smith (1854 – 1927) added a fourth rule in 1905.
These are known as the “Koch’s Postulates”. These are:

1) The suspected organism must be found associated with the disease in all the diseased
plants examined.
2) The organism must be isolated and grown in pure culture on nutrient media, and its
characteristics described (nonobligate parasites), or on a susceptible host plant (obligate
parasites), and its appearance and effects recorded.
3) The suspected organism from pure culture must be inoculated on healthy plants of the
same species or variety on which the disease appears, and it must produce the same
disease on the inoculated plants.
4) The suspected organism must be isolated in pure culture again, and its characteristics must
be exactly like those observed in step 2.

5.2. Morphological Symptoms of Plant Diseases

Symptoms refer to manifestations of physiological reactions of plants to the harmful activities of

pathogens. Disease symptoms are of two types:

1) Histological symptoms (pathological anatomy) – detectable only by microscopic

examinations.
2) Morphological symptoms externally detectable.

Necroses
Morphological symptoms Hypoplases
Hyperplases
5.2.1. Necrotic Symtoms

These symptoms are characterized by degeneration of protoplasts, followed by death

(necrosis) of cells, tissues, organs, and whole plants. Examples: Damping-off, leaf and fruit
spots (shot-holes), flecks (specks), streak, stripe, blight, scorch, scald, canker, diebacks,
gummosis, blast (sudden death of buds and inflorescence).

25
5.2.2. Hypoplastic Symptoms (Atrophy)
Hypoplasia refers to the under-development of cells, tissues or organs due to decreased cell
division or slow growth. E.g., dwarfing, rosetting (absence of internode enlongation and
clustering of leaves). Chlorosis (etiolation) is also another example.

5.2.3. Hyperplastic Symptoms (Hypertrophy)

Hyperplasia is due to over-development in size or colour of plants or plant organs, or the

abnormal early development of plant organs. This could be due to an excessive increase in size
of a cell, a tissue, and organ, or an entire plant. E.g., galls, root-knots, tumour.

5.3. Effects of Plant Pathogens on Plant Physiology

Different effects of plant pathogens befall on hosts:

(1) Effects of pathogens on photosynthesis

Any interference by pathogens with photosynthesis results in a diseased condition in the plant.
Chlorosis, necrotic lesions on leaves, reduced growth and amounts of fruits could be results of
affected photosynthesis. E.g., leaf spot, blight, rusts, and other diseases of defoliation 
Reduced photosynthesis.

Toxins produced by some fungi and bacteria can inhibit enzymes involved in photosynthesis. In
vascular pathogens, stomata close, chlorophyll is reduced, photosynthesis stops before final
wilting.

Generally, in diseased plants, photosynthesis rate is reduced by more than one-fourth the normal
rate.

(2) Effect of pathogen on translocation of nutrients and water

When a pathogen interferes with the upward movement of inorganic nutrients and water or with
the downward movement of organic substances, diseased conditions will result in the parts of
the plant denied these materials. The diseased parts, in turn, will be unable to carry out their
own functions and will deny the rest of the plant their services or other products, thus causing
disease of the entire plant.

Examples

1. Damping-off fungi  Roots

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 2. Agrobacterium tumefaciens  Translocation
3. Fusarium, Verticillium, Ceratocystis, Pseudomonas, Erwinia  Wilts
4. Some viruses
5. Nematodes (root knot)
6. Others

(3) Effects of pathogens on host plant respiration

When plants are infected by pathogens, the rate of respiration generally increases, i.e., affected
tissues use up their reserve carbohydrates faster than healthy tissues would. This happens
shortly after infection (after visible symptoms) and rises during sporulation of the pathogens,
then declines, even below the healthy ones. The respiration is higher in the resistant varieties
than in the susceptible ones.

Increased respiration is accompanied by accelerated production of phenolic compounds

(phytoalexins), fermentation, and others.

(4) Effect of pathogens on permeability of cell membranes

Disruption or disturbance of the cell membrane by chemical or physical factors alters (usually
increases) the permeability of the membrane with subsequent uncontrollable loss of useful
substances as well as inability to inhibit the inflow of undesirable substances or excessive
amounts of any substances. The loss of electrolytes (small water soluble ions and molecules)
from the cell is the most commonly observed effect of changes in the cell membrane
permeability.

(5) Effects of pathogens on translation and transcription

Disturbance of any of these processes by pathogens or environmental factors may, by its effect
on the expression of genes, cause drastic unfavourable changes in the structure and function of
the affected cells. (Note: rRNA = Ribosomal RNA; mRNA = Messenger RNA; tRNA =
Transfer RNA).
5.4. Diagnosis of Plant Diseases
Diagnosis refers to the recognition (determination) of the nature of a disease from its
symptoms. It is wise to first determine whether the disease is caused by a pathogen or an
environmental factor. Detailed examination of the symptoms and injury may be required for
correct diagnosis. Diagnosis can help us suggest correction of crop production problems.

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Procedures in diagnosis of plant diseases include:

1. Field Observations

Fields must be visited frequently to observe disease developments at all stages of plant growth.
Observations must also be made in different seasons, under different agronomic and cultural
practices.

 Field observations: Field observations involve a careful look at plants in the field.
Attention should also be paid to: distribution of the disease in the field to hint at whether it
is air-borne or soil-borne: Small circular infected areas imply lightening or soil-borne
diseases, e.g., nematodes; scattered diseased plants imply air-borne diseases. If the edges of
fields are infected, it implies the disease(s) is (are) vector-transmitted.
 History of the disease in the field: Informs whether the disease is introduced, due to
herbicides, etc. Interviews with the growers are useful to determine the history of the field
and the crops grown in it in the preceding years (seasons). Interviews include information
on source of seed, cultural practices, variety, rainfall, temperature, and others.

2. Plant Diagnosis

Necessary equipment: Hand lens, paper bags, a vasculum for carrying specimens, budding
knife, spatula, pruning knife, scissors, hoe, soil auger, sterile containers, pH kit, plant press, and
others.

Plant diagnosis includes making observations of individual plants. Symptoms should be noted.
Careful examination should consider:

 Obvious physical damage/injury

 Location of the symptoms on the plant (Vascular wilt? soil-borne? air-borne?)
 Signs of pathogens or agents (insects, sclerotia, mycelia, conidia, bacterial exudates). You
may need dissecting microscope and magnifying glasses for closer observation of the signs.
 Description of the disease symptom: shape, colour, margin, leaf-surface (under, upper, or
both sides); taking pictures too.
3. Laboratory Examination
 Collect samples of flowers, fruits, stem, leaves, roots, bark, soil, and othhers.
 Spread out samples on sheets of paper/blotters and press and change blotters at frequent
intervals.
 Label specimen and store dry.

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  Examine the organism under a stereoscopic and/or compound microscope. Identify the
causal agent.
Summary of Disease Diagnosis
1) Diseases caused by pathogens (fungi, bacteria, viruses, mycoplasma-like organisms,
protozoa) are characterized by the presence of these pathogens on the surface of the
diseased plants.
A) Look for additional symptoms and, especially, for pathogens inside the diseased plant 
Margins of affected tissues, vascular tissues, or base of the plant, and on or in its roots.
B) Diseases caused by parasitic higher plants are characterized by the presence of the parasitic
plants growing on a plant. E.g., dodders, mistletoes, witchweeds, broomrapes, and others.
C) Nematode diseases are recognized by the presence of the organisms in or on the host
plants.
2) If no pathogen can be found, cultured from or transmitted from a diseased plant, then the
causal factor should be assumed as a non-living, environmental factor.
3) Follow the Koch’s postulates for pathogenicity test  Pathogenic, saprophytic.

Note: Use indicator plants for pathogenicity tests.

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6. Host Parasitic Relations (Host-parasite Relationship) (3 lecture hours)
6.1. Disease Development: Disease Triangle and Disease Pyramid (Disease Tetrahedron)

Previously the phrase ‘disease triangle’ was used to express the disease development as a result
of concurrent actions of pathogen (P), host plant (H) and environment (E). G.L. McNew
formalized it in the 1960s.
E
Disease

H P
A) Disease Triangle

Man

Pathogen Environment

Host
B) Disease Pyramd

The base of the disease tetrahedron symbolizes the interaction of the host, pathogen, and
environment. On each of these, man has various effects that are important to the development
and control of epidemics.

Epidemiology deals with plant disease development and depends on four factors:

1) Pathogen population
2) Host plant population
3) Environment
4) Human (man) factor

6.2. Plant Disease Cycle

Disease cycle = a chain or series of more or less distinct events occurring in succession and
leading to the development of the disease and perpetuation of the causal pathogen. The disease
cycle includes: inoculation, prepenetration, penetration, infection, invasion, reproduction,
dissemination and survival.

6.2.1. Inoculum and Ioculation

Inoculum = The pathogen(s) that lands on or comes into contact with the plant. E.g.,
Spores, sclerotia, fragments of mycelia of fungi or whole individuals of bacteria,

30
 viruses, MLOs, RLOs, protozoa, viroids, eggs of nematodes, larvae, or their adults.

Primary inoculum
Inoculum
Secondary inoculum

Sources of Inoculum

 Plant debris or soil in the field, seed, transplants, tubers, propagative organs (cuttings, etc.).
 Nearby infected plants, perennial weeds or alternate hosts (Volunteer plants, left-over
plants, ratoons, collaterals, etc.). N.B. Inocula may live on or in the hosts.

Inoculation = The coming in contact of the pathogen with the host.

6.2.2. Pre-penetration and Penetration Process

Pre-penetration process includes germination of spores (e.g., Fungi) and seeds (dodders),
hatching of eggs, pathogen anchorage through haustoria (e.g., parasitic plants), etc. Pathogens
penetrate host plants through various mechanisms:
(a) Direct penetration: E.g., Fungi (penetration peg) and nematodes (stylet)
Spore  germ tube  appressoria (cushion)  infection peg (penetration peg, needle)
(b) Natural openings: via stomata, hydathodes, nectarthodes, and lenticels. E.g., fungi
and bacteria.
(c) Wounds: E.g., All bacteria, most fungi, some viruses, all viroids, MLOs and RLOs.
Viruses, viroids, MLOs and RLOs penetrate via wounds produced by vectors.

6.2.3. Infection and Establishment

Infection: The process by which pathogens establish contact with the susceptible cells or
tissues of the host and procure nutrients from them. Successful infections result in the
appearance of discoloured, malformed, or necrotic areas on the host plant called symptoms.
There are two types of infection:  active and latent. (Latent = not able to produce
symptoms right away; Active = able to produce disease symptoms immediately after
inoculation or in short incubation period).

Incubation period = The time interval between inoculation and the appearance of disease
symptom. This depends on pathogen-host combination, stage of host, temperature, and others.

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Invasion

It is the spread of the pathogen into the host. Most pathogens spread into all the tissues of the
plant organs (roots, leaves, stems, and fruits) they infect intercellularly (most fungi and
nematodes) and/or intracellularly (bacteria, viruses, viroids, MPLOs, and RLOs). The
invasion could be local or systemic. E.g., Wilt fungi in xylem vessels (systemic diseases).

6.2.4. Reproduction of Pathogens

Fungi reproduce by spores (cryptogamy), spores could be produced on or in host tissues; fungi
also grow by means of mycelium (endophytic or epiphytic); parasitic seed plants by seeds;
bacteria, MPLOs, and protozoa, by binary fission. Bacteria divide every 20 – 30 minutes.
Viruses and viroids are replicated, and MLOs and RLOs are reproduced inside cells. Viruses
duplicate in cells until as many as 100,000 to 10,000,000 viral particles/ cell are synthesized.
Nematodes are reproduced through eggs. Female nematodes can lay 300 – 600 eggs each,
with 2 – 12 generations a year.

6.2.5. Dissemination/Spread of Pathogens/Dispersal/Transmission

Autonomous movement by pathogens are limited. Only a few pathogens move in this way.
E.g., Nematodes, fungal spores, bacteria (via flagella), fungal hyphae, rhizomorphs, parasitic
plants, and fruits (through shattering) are means of autonomous movement. Passive movement
occurs through air, water, insects, humans and animals, mites, nematodes and other vectors.
So the pathogens could be:
a) Anemochorous = wind-borne
b) Anthropochorous = man-borne
c) Entomochorous = insect-borne
d) Hydrochorous = water-borne
e) Zoochorous = animal-borne
f) Caryopochorous = seed-borne???
g) Edaphochorous = soil-borne???

6.2.6. Survival of Pathogens (perennation, overseasoning, overwintering,

oversummering)
 Pathogens can survive, as mycelium in tissues and as spores on plant surface and bud scales,
on perennial hosts, on plant debris, fruits, seed, and leaves; as mycelium, common spores,
resting spores (chlamydospores), sclerotia, seeds and tubers, in the soil. Soil-borne
pathogens (soil-invaders) can be:

32
 a) Soil transients (live for shorter period)
b) Soil inhabitants (live for longer period)

 Nematodes as eggs in soil, adults (larvae) in plant tissues, in debris, seeds, or in bulbs for
many months/years.
 Parasitic higher plants as seeds in soil e.g. Striga, Orobanche
 Parasitic higher plants as vegetative form on the hosts; e.g., Dodders, mistletoes,
Arceuthobium.

7. Defense Mechanisms of Plants against Pathogens (2 lecture hours)

7.1. Mechanisms of Attack by Pathogens

How do pathogens attack plants?

Plant diseases can affect any or all tissues, organs, and functions of a plant. G.L. McNew of the
Boyce Thompson Institute for Crop Research has provided a classification of diseases based
mainly on the seven plant functions that are affected.

These disturbed functions are as follows:

1) Destruction of food reserves

2) Prevention of seedling metabolism (respiration)
3) Interference with procurement of nutrients (absorption)
4) Interference with upward transport or conduction (both water and minerals)
5) Increased transpiration
6) Interference with photosynthesis and food manufacturedisruption of photosynthesis
7) Interference with translocation of food
8) Diversion of food stuff to abnormal use
9) Interference with reproduction

Why do pathogens attack plants?

 Pathogens attack plants to obtain their nutrients from the host plants to survive on the
substances.

How do pathogens penetrate plant tissues?

 Pathogens mostly attack plants through chemical substances and mechanical forces.

33
Each plant species is affected by several different kinds of pathogens including fungi, bacteria,
MLOs, RLOs, viruses, viroids, and nematodes. However, resistant plants defend themselves
against pathogens through:

1. Structural defense mechanisms serving as physical barriers

2. Biochemical reactions that produce toxic substances that inhibit the growth of the
pathogens
3. Combination of both mechanisms

7.2. Structural Defense Mechanisms

7.2.1. Pre-existing Defense Structures (Passsive Mechanisms)

These are defense structures that are present in the plant even before the pathogen is inoculated.
These include:

a) Amount and quality of wax and cuticle covering epidermis

b) Structure of epidermal cell walls
c) The size, location, and shapes of stomata and lenticels; and time of stomatal opening
d) Thickness and toughness of cell walls

Waxes and trichomes of leaf and fruit surfaces repel film of water that may be required for
germination and multiplication of pathogens. Thick cuticles may prevent penetration by
pathogen. Thickness and toughness of outer cell-wall of epidermal cells may make penetration
difficult. Stomata that may open late in the day or very narrow stomata or broad but elevated
stomata surrounded by guard cells prevent penetration. Thickness and toughness of cell walls
composed of sclerenchyma cells can make penetration hard/difficult.

7.2.2. Post-infectional Defense Structures (Active Mechanisms)

Plants may defend themselves against pathogens even after penetration by pathogens. This
could be by forming one or more types of structures that prevent further pathogen invasion.
These include:

a) Histological defense structures (via formation of tissues ahead of pathogens)

b) Cellular defense structures (via cell walls of invaded cells)
c) Cytoplasmic structures (via cytoplasm of invaded cells)
d) Necrotic/hypersensitive structures (via death of invaded cells)

34
Histological Defense Structures

a) Formation of Cork Layers:

By inducing plants to form several layers of cork cells beyond the point of infection by
stimulating host through secretion of pathogens (elicitors). The layers block spread of toxins
and spread of pathogens, i.e. restrict pathogens. E.g., Fungi, bacteria, viruses and
nematodes.

b) Formation of Abscission Layers:

This is formed on young and active leaves of stone fruit trees after infection by any of
several fungi, bacteria, or viruses. It is a gap between two circular layers of cells of a leaf
surrounding the locus of infection. The middle lamella between the two layers of lignified
cells dissolves, cutting off the infected area. Generally the area shrivels, dies, and sloughs
off, carrying the pathogen with it. There could be shot-hole formation. E.g., Cercospora
beticola.

c) Formation of Tyloses

These are formed in xylem vessels of most plants during infection by vascular pathogens.
They are overgrowths of parenchymatous cells and clog the vessels (lumen), block
advancement of pathogens.

d) Deposition of Gums:

Different gums form around infection sites, Eg. Stone fruit trees, and deposited in the
intercellular spaces and within the cells, serving as impenetrable barrier and enclose the
pathogen  isolated, starved and dies.

Cellular Defence Structures

This is a result of morphological changes in the cell wall of the invaded cell by pathogen. The
mechanisms involved here include:
a) Swelling of the outer layer of the cell wall of parenchyma cells producing fibrillar material
that traps bacteria and prevents multiplication.
b) Thickening of cell wall in response to viral and fungal infection. Phenolic compounds may
be produced too.
c) Callose papillae deposition on the inner side of cell walls in response to fungal infection
 Prevents penetration by pathogens.
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Cytoplasmic Defense Reaction

Here the cytoplasm surrounds the clump of hyphae and the nucleus is stretched to the point
where it breaks in two. The cytoplasm becomes granular and dense, various structures appear.
Eventually the pathogen disintegrates.

Necrotic Defense Reaction (Hypersensitivity)

When the pathogen penetrates the cell wall, the nucleus approaches the pathogen in the
protoplast; it disintegrates, produces brown resin-like granules in the cytoplasm, the cell
disintegrates and pathogen degenerates. E.g., by obligate fungal parasites, viruses and
nematodes infection.

7.3. Biochemical Defense Mechanisms (Metabolic)

7.3.1. Pre-existing Biochemical Defence (Passive Resistance)

The various mechanisms involved in this category:

a) Inhibitors/Fungitoxic Exudates Released into the Plant Environment

Inhibitors of pathogens are secreted by the plants and exuded through the plant surface (aerial
and roots). For example, fungitoxic exudes are released on leaves of tomatoes against Botrytis
and on sugar beets against Cercospora species to inhibit spore germinations on the respective
plants. Colletotrichum circinans (onion smudge) is defended by the two phenolic compounds
protocatechuic acid and catechol contained in the red scales. Onions with white-scales are
susceptible to the same pathogen.

b) Inhibitors present in plant cells before infection.

Several phenolic compounds have been proposed to be present in high concentrations in cells of
young fruits and leaves. As the plants become older, the contents of the inhibitors decrease and
resistance lowers too.

c) Lack of Essential Factors

This includes:

i) Lack of recognition between host and pathogen

This occurs (a) if the plant lacks recognition factors (specific molecules or structures) such
as oligosaccharides, polysaccharides, proteins or glycoproteins (lectins); and (b) if the

36
 plant fails to produce replicase (enzyme) whose absence prevents viral infection. For
example, sorghum varieties that do not produce Strigol are resistant to Striga species.
ii) Lack of host receptors and sensitive sites for toxins
Lack of receptors/ sensitive sites for pathogen toxins prevents their attachment and
reactions in the cells. To this effect, there will be no disease symptom development.
iii) Lack or low concentration of essential nutrients for pathogen
(1) Plants lacking essential substances (growth factors) for the pathogen become resistant to
infection. E.g., no hyphal cushion (appressoria) in Rhizoctonia forms in the absence of such a
substance. (2) Lower concentration of growth factors also inhibits pathogen development.

7.3.2. Induced Biochemical Defence (Active Resistance)

This is an active resistance mechanism and is performed in any one or more of the following
responses.

a) Biochemical inhibitors produced in plants due to infection

When plant cells and tissues are injured by pathogens, chemical agents or mechanical means,
they produce fungitoxic substances around the sites of injury such as chlorogenic and caffeic
acids, oxidation products of phenolic compounds and phytoalexins  inhibit the growth of
fungi and bacteria.

b) Hypersensitive reaction
This occurs in incompatible combinations of hosts and pathogens (fungi, bacteria, viruses and
nematodes).

In the resistant varieties, a number of physiological changes occur in the infected cells and in
the cells surrounding them (loss of turgor, browning, death, loss of permeability of cell
membranes, increased respiration, accumulation of phenolic compounds, synthesis of
phytoalexins, etc.). The pathogens within the operation area are isolated by necrotic tissue and
die quickly; thus the pathogen spread is restricted.

c) Increase in phenolic compound concentration

There are two groups of phenolics:

(i) Common phenolics: Phenolics found in healthy as well as diseased (resistant and
susceptible) hosts; their concentration may vary (usually increase) after infection. Examples,
Chlorogenic and caffeic acids, scopoletin.

37
(ii) Phytoalexins: Toxic substances produced in appreciable amounts in plants only after
stimulation by the various types of phytopathogenic microorganisms, chemical or
mechanical injury. They are toxic to most fungi, a few bacteria, nematodes, and other
pathogens. Phenolics are produced (stimulated) after infection in diseased plants only.
Examples, phaseollin and kieviton in bean, pisatin in pea, glyceollin in soybean, alfalfa and
clover, rishitin in potato, gossypol in cotton, and capsidiol in pepper.

N.B. Elicitors = Pathogen substances that stimulate phytoalexins production.

Suppressors = Pathogen substances that prevent phytoalexin production.

d) Fungitoxic phenolics released from non-toxic phenolic complexes.

Several fungi are able to liberate some phenolic molecules (toxic phenolics that can kill the
pathogens) from non-toxic glycosides (sugars) through an enzyme called glycosidase.

e) Phenol-oxidizing enzymes (polyphenoloxidases)

The activity of the enzymes is higher in resistant varieties than in the susceptible ones 
Quinones.
Peroxidase  Oxidizes phenolics and increases the rate of polymerisation of such compounds
into lignin-like substances to be deposited in cell walls and papillae (preventing pathogens’
growth and development).

f) Induced synthesis of enzymes

Phenylalanine ammonia lyase (PAL) is a key enzyme in the production of phytoalexins and
lignin. The synthesis of PAL is stimulated (accelerated) after infection.

g) Formation of substances resisting pathogen enzymes

Complexes between pectins and proteins, and polyvalent cations of calcium and magnesium
near the infection sites result in formation of pectin salts or other complexes that resist
degradations by the pathogen enzymes  prevent tissue maceration and restrict pathogen.

h) Inactivation of pathogen enzymes

Polyphenols have inhibitory action on pectolytic and pectinolytic enzymes of the pathogen.
E.g., resistance of apple to Monilinia, grape to Botrytis.

i) Release of Fungitoxic Cyanides from Nontoxic Complexes

Hydrolytic enzymes of pathogens can liberate, upon plant infection, hydrogen cyanide (HCN)
(that is toxic to most micro-organisms) from cyanogenic glycosides contained in sorghum.

38
j) Detoxification of Pathogen Toxins
Detoxification of toxins, such as fusaric acid and pyricularin, is known to occur in plants
through metabolization or combination with other substances and formation of less toxic or
non-toxic compounds.

k) Induced Resistance
In plants, induced resistance is a resistance type that develops after pre-inoculation treatment of
plants with various biotic agents or after pre-treatment with various chemical or physical agents.
It is a non-specific resistance against fungi, bacteria, viruses and even insects. E.g., TMV
induces a systemic resistance to itself, to several other viruses, to fungi (Phytophthora), to
bacteria (Pseudomonas tabaci), and to aphids.
Local induced resistance
Induced resistance
Systemic induced resistance
N.B. Refer to “Cross-protection”. (Refer to explanation by Bos).

8. Genetics of Plant Diseases (3 lecture hours)

8.1. Variability of Pathogens and Mechanisms

8.1.1. Variability in Organisms

All individuals produced as a result of a sexual process are expected to be different from each
other and from their parents in a number of characteristics, although they retain most
similarities with them and belong to the same species. This is true of fungi produced from
sexual spores (oospores, ascospores, basidiospores), and seeds of parasitic higher plants, and of
nematodes produced from fertilized eggs.

When individuals are produced asexually, the frequency and degree of variability among the
progeny are reduced greatly but even then certain individuals among the progeny will show
different characteristics. This is the case in asexual reproduction of fungi (by conidia,
zoospores, sclerotia, uredospores), bacteria, mycoplasmas, and viruses.

8.1.2. Mechanisms of Variability

There are two main categories of mechanisms of variability:
I. General mechanisms of variability

39
II. Specialized mechanisms of variability

I. General Mechanisms of Variability

A) Mutations
Mutation is a more or less abrupt change in the genetic material of an organism, which is then
transmitted to the progeny in a hereditary fashion. Mutations occur spontaneously in nature in
all living organisms that reproduce through: (1) only sexually; (2) only asexually; and (3) both
sexually and asexually. Actually, mutations represent changes in the sequence of bases
[Adenine (A), Guanine (G), Cystocine (C), Thymine (T) and Uracil (U)] in the DNA through:

1) Substitution of one base pair for another

2) Addition of one or many base pairs
3) Deletion of one or many base pairs
4) Amplification of particular segments of DNA to multiple copies
5) Insertion of a movable DNA segment into a coding or regulatory sequence of a gene
6) Inversion of a DNA segment

Mutations can take place in nuclear DNA or extranuclear DNA (cytoplasmic inheritance), i.e.
nuclear chromosomes or extrachromosomal DNA. Mutations in single-celled organisms
(bacteria and haploid mycelia of fungi) and in viruses are expressed immediately after their
occurrence. Since most mutant factors are usually recessive, in diploid or dikaryotic organisms,
mutations can remain unexpressed until they are brought together in a hybrid. Example: AA →
Aa (heterozygous mutant); crossing Aa x Aa →AA, Aa, Aa, aa, where the homologous ‘aa’
individual is a recessive mutant obtained after crossing of the heterozygous ‘Aa’ individuals.
Causes for mutations include radiations (ultra-violet, x-rays), high temperature, chemical
treatments, such as treatment with colchicine, etc. Factors favouring mutations include: (1) great
number of progeny produced by pathogens; (2) monocultural cropping system; and (3) planting
only a few genetically homogenous varieties of each crop continuously over enormous land
expanses for a number of years.

B) Recombination
Recombination occurs during the sexual reproduction of plants, fungi, and nematodes whenever
two haploid (1N) nuclei, containing slightly different genetic material, unite to form a diploid
(2N) nucleus, called a zygote. Recombination occurs during the meiotic division of the zygote
as a result of genetic crossovers in which parts of chromatids (and the genes they carry) of the
one chromosome of the pair are exchanged with parts of chromatids of the other chromosome of

40
the pair. In this way, recombinations of the genes of the two parental nuclei or gametes resulting
after meiosis are different both from gametes that produced the zygote and from each other. In
the fungi, the haploid nuclei or gametes often divide mitotically to produce haploid mycelium
and spores, which results in genetically different groups of relatively homogenous individuals
that may produce large populations asexually until the next sexual cycle.

II. Specialized Mechanisms of Variability in Pathogens

Specialized mechanisms of variability are sexuallike or parasexual processes and include
heterokaryosis, parasexualism, and heteroploidy in fungi; conjugation, transformation and
transduction in bacteria, and genetic recombination in viruses.

A) Sexual-like Processes in Fungi

(1) Heterokaryosis
It is the condition in which, as a result of anastomosis, cells of fungus hyphae or parts of hyphae
contain two or more nuclei that are genetically different. E.g. in Basidiomycetes, the dikaryotic
state differs drastically from the haploid mycelium and spores of the fungus. In Puccinia
graminis, for example, haploid basidiospores infect barberry (Berberis vulgaris) and haploid
mycelium grow only on barberry too, while the dikaryotic aeciospores and uredospores can
infect wheat only and dikaryotic mycelium (possessing two nuclei) can grow on both barberry
and wheat.

(2) Parasexualism
It is the process by which genetic recombination can occur within fungal heterokaryosis. This
occurs by the occasional fusion of the two nuclei and the formation of a diploid nucleus (two
chromosomes). During multiplication, crossing over occurs in a few mitotic divisions and
results in the appearance of genetic recombinants by the occasional separation of the diploid
nucleus into its haploid components.
(3) Heteroploidy
Heteroploidy is often associated with cellular differentiation and represents a normal situation in
the development of most eukaryotes. It is the existence of cells, tissues, or whole organisms
with a number of chromosomes per nucleus that are different from the normal 1N or 2N for the
particular organism. Heteroploids may be haploids, diploids, triploids, or tetraploids, or they
may be aneuploids, that is, they have 1, 2, 3, or more extra chromosomes or are missing one or
more chromosomes from the normal euploid number. In several studies, spores of the same
fungus were found to contain nuclei with extra chromosome numbers ranging from 2 to 12 per

41
nucleus and also diploids and polyploids. Heteroploidy affects the growth rate, spore size, rate
of spore production, hyphal color, enzyme activities, and pathogenicity.

Sectoring (Saltation)
It is the appearance of morphologically distinct sectors in fungus colonies and is a common
occurrence when most fungi are cultured on nutrient media. Sectors show morphological and
pathogenicity differences. Mutation`, heterokaryosis, parasexualism and heteroploidy might
have involved in sectoring.

B) Sexuallike Processes in Bacteria

There are three sexuallike processes in bacteria:
1. Conjugation:- Two compatible bacteria come in contact with each other and a small
portion of the chrosomal or non-chrosomal (plasmid) genetic material of one bacterium is
transferred to the genetic material of the other.
2. Trasformation:- Bacteria are transformed genetically by absorbing and incorporating
genetic materials secreted by or released during rupture of another compatible bacteria
into their own genetic materials.
3. Transduction:- A bacterial virus (bacteriophage) transfers genetic material from the
bacterium in which the phage was produced to the bacterium it infects next.

C) Genetic Recombination in Viruses

When two strains of the same virus are inoculated into the same host plant, one or more new
virus strains are recovered with properties (virulence, symptomatology, etc) different from those
of either of the original strains inoculated into the host. The new strains probably are
recombinants or mutants. In multipartite viruses of 2, 3, or more nucleic acid components, new
virus strains may also arise in host plants or vectors from recombination of the appropriate
components of two or more strains of such viruses.

8.1.3. Stages of Variation in Pathogens

The entire population of a particular organism on earth, for example, a fungal pathogen, has
certain morphological characteristics in common and makes up the species of pathogen, such as
Puccinia graminis, the cause of stem rust of cereals. Some individuals of this species, however,
attack only wheat, only barley, or only oats, and these individuals make up groups that are
called varieties or special forms (formae specialis, abbreviated as f.sp.) such as P. graminis f.
sp. tritici, P.g. f.sp. hordei, and P.g. f. sp. avenae. But even within each special form, some
individuals attack some of the varieties of the host plant but not the others, some attack another

42
set of host plant varieties, and so on, each group of such individuals making up a physiological
race. Thus, there are more than 200 races of Puccinia graminis tritici (race 1, race 15, race 59,
and so on).

Occasionally, one of the offspring of a race can suddenly attack a new variety or can cause
severe symptoms on a variety that it could barely infect before. This individual is called a
variant. The identical individuals produced asexually by the variant make up a biotype. Each
race consists of one or of several biotypes (race 15A, 15B, and so on). The change in the variant
pathogen enables it to infect a plant variety cultivated because of its resistance to the parental
strain, the variant individual, being the only one that can survive on this plant variety, grows
and multiplies on the new variety without any competition and soon produces large populations
that spread and destroy the heretofore resistant variety. This is the way the resistance of a plant
variety is “broken down” although it was the change in the pathogen, and not the host plant, that
brought it about.

Summary of stages of variation in pathogens:

Species = The entire population of a particular pathogen with certain morphological
characteristics in common. E.g., Puccinia graminis.
Varieties, special forms, formae specialis (f.sp.) = Some individuals or groups of the species
that attack only certain plant species (such as only wheat, only barley, or only oats,
etc.). E.g., Puccinia graminis f.sp. tritici.
Physiological race = Group of individuals within each formae specialis that attack some of the
crop varieties of the host plant but not others, while some others attack another set of
host plant varieties, and so on. E.g., Puccinia graminis f.sp. tritici (race1, race15,
etc.). Differential varieties are used for distinguishing the physiological races that
exist in a locality or country.
Variant = An individual or offspring of a physiological race that can suddenly attack a new
crop variety or can cause severe symptoms on a variety that it could barely infect
before.
Biotype = The individuals produced asexually by the variant. Each physiological race consists
of one or of several biotypes. E.g. Race 15A, 15B, and so on.

43
8.2. Genetics of virulence and resistance

8.2.1. Understanding the genetics of plant disease and host resistance

The genetic information of all organisms is encoded in their DNAs (deoxyribose nucleic acid).
DNA is usually present in the chromosome. In RNA viruses and viroids, genetic information is
encoded in RNA (ribose nucleic acid). In Eukaryotes (and in all other organisms) there are
several chromosomes in the nucleus. Similarly, all cells of Eukaryotes carry DNA in their
mitochondria. Plants also carry DNA in their chloroplasts. In prokaryotes, (such as bacteria and
mycoplasmas), there is only one chromosome in the cytoplasm. However, many prokaryotes
and some lower Eukaryotes carry smaller circular molecules of DNA (plasmids, which are
about 0.5 to 2% of DNA) in the cytoplasm.

The stretches of DNA include:

1. Introns = non-coding stretches of DNA
2. Promoters = act as signals for production of RNAs and proteins that themselves act as
inducers and enhancers of gene expression.
3. Terminators = act as represssors and terminators of gene expression.

Genetic information in DNA is encoded in a linear fashion, in the order of four bases (A =
adenine, C = cystosine, G = guanine, and T = thymine). A gene is a stretch of a DNA
molecule, usually of about one hundred to five hundred or more adjacent triplets, that codes
for one protein molecule, or in a few cases, one RNA molecule. When a gene is active, one of
its DNA strands is copied (transcribed) into RNA. There are 3 RNA types, namely:

1. rRNA = ribosomal RNA  Consists up to 80% of RNA and carries the four bases
2. tRNA = transfer RNA  Brings amino acids (20 in number) and transcribes RNA.
(tRNA and rRNA are determinants for RNA).
3. mRNA = messanger (exon)  Carries ribosomes and codes for protein synthesis. (It is
structural RNA).

The mRNA becomes attached to ribosomes, which with the help of tRNA, translate the base
sequence of the rRNA into a specific sequence of amino acids and eventually construct a
particular protein. (There are about 2500 proteins in nature).

The proteins thus synthesized can:

1. be part of the structure of cell membranes
2. act as enzymes or toxins

44
 3. give cells and organisms their characteristics such as shape, size, and color
4. determine what kinds of chemical substances are produced by the cell
In many cases of host-pathogen interaction, genes in the one component are triggered and
expressed by a substance produced by the other component. For example, genes for cell-wall-
degrading enzymes (CWDE) in the pathogen are apparently induced by macromolecules,
substrates for these enzymes, present in the host cell wall. Also, genes for defense reactions in
the host, for example, genes for the production of phytoalexins, apparently are triggered to
expression by certain inducer molecules (elicitors) produced by the pathogen.

8.2.2. Genes and Disease

What makes possible for the development of disease in a host is the presence in the pathogen of
one or more genes for specificity and for virulence against the particular host that, in turn, is
thought to have certain genes for specificity and for susceptibility to the particular pathogen.
The gene or genes for virulence in the pathogen are usually specific for one or a few related
kinds of hosts. Also, the genes that make a host plant susceptible to a particular pathogen are
present only in that one host and possibly a few related kinds of host plants. That is, the
concurrent occurrence and interaction of specific genes for virulence in the pathogen and of
specific genes for susceptibility in the host determine the initiation and development of disease.

However, a few pathogens are able to attack many kinds of hosts because they either have many
diverse genes for virulence or because their genes of virulence have a much wider spectrum of
host specificity than those of more specialized pathogens. Similarly, all plants are not attacked
by their pathogens because they have acquired, in addition to their genes for susceptibility, one
or more genes for resistance, which protect them from infection or from severe disease. When a
gene for resistance to a pathogen appears or is introduced into a plant, the plant becomes
resistant to all the previously existing individuals of the pathogen. A partial or complete loss of
virulence in pathogens is sometimes called attenuation (= avirulence). This may happen due to
prolonged or repeated culturing of the pathogen or when it is passed one or more times through
different hosts.
8.3. Gene-for-gene concept

Gene-for-gene concept: ‘For each gene that confers resistance in the host there is a
corresponding gene in the pathogen that confers virulence to the pathogen and vice versa’,
H.H. Flor (1946, 1955 and 1971). In other words, the hypothesis states that, “For every gene for
virulence in the pathogen, there is a corresponding gene for susceptibility in the susceptible
plant species (Flor, 1971)”. The gene-for-gene hypothesis is based on Flor’s 1946 classical

45
experiments with flax rust (Melampsora lini). Experience with diseases other than flax rust
suggests the general truth of the hypothesis, at least for parasitic pathogens and monogenically
resistant plant varieties that react hypersensitively (a reaction of the plant to the pathogen that
results in little or no spread of the pathogen in the tissues and, therefore, only a minor spotting
or flecking). See the following table.

Table 1. Host-pathogen interaction in the gene-for-gene hypothesis in its simplest form

Genes in the plant

R r
Genes of the A-R A-r
pathogen (Resistant) (Susceptible)
A
a a-R a-r
(Susceptible) (Susceptible)

Key: ‘A’ = Represents the dominant gene for avirulence (non-pathogenicity) and ‘a’ = The
recessive gene for virulence (pathogenicity) in the pathogen, and ‘R’ = Represents the
dominant gene for resistance and ‘r’ = The recessive gene for susceptibility in the attacked
plant. Avr = avirulence gene.
Sources: 1) H.H. Flor. 1956. The complementarity genetic system in flax rust. Adv. Genet. 8:
29 - 54.
2) H.H. Flor. 1971. Current status of the gene-for-gene concept. Ann. Rev.
Phytopathol. 9: 275-296.

According to the gene-for-gene hypothesis, only one of the possible gene combinations above,
A-R, would result in resistance (hypersensitivity). In all other combinations, the susceptible
reaction would occur because the host plant is susceptible (r), the parasite is virulent (a), or both
conditions (a-r) are fulfilled in the same host-parasite interaction.

The interactions between corresponding pairs of genes (the A genes of the parasite and the R
genes of the host) are highly specific. This significant aspect of the gene-for-gene concept can
be illustrated only by considering interactions in which the corresponding pairs of genes occur
at two or more different loci on the chromosomes. With two loci, four different gene
combinations are possible. Notations for genes at two loci in the parasite would be A1A2, A1a2,
a1A2, and a1a1. For corresponding genes at two loci in the host, the relations would be R1R2,
R1r2, r1R2, and r1r2. All possible interactions between corresponding pairs of genes, along with
the disease reaction that would result from each interaction, are set forth in the table below.

46
Table 2. Disease reactions following interactions between corresponding genes at two different
loci
_______________________________________________________________
Genes of the Genes of the Disease
pathogen host plant reaction
A1A2 R1R2 Resistant
A1A2 R1r2 Resistant
A1A2 r1R2 Resistant
A1A2 r1r2 Susceptible

A1a2 R1R2 Resistant

A1a2 R1r2 Resistant
A1a2 r1R2 Susceptible
A1a2 r1r2 Susceptible

a1A2 R1R2 Resistant

a1A2 R1r2 Susceptible
a1A2 r1R2 Resistant
a1A2 r1r2 Susceptible

a1 a2 R1R2 Susceptible
a1 a2 R1r2 Susceptible
a1 a2 r1R2 Susceptible
a1 a2 r1r2 Susceptible

Because of the specificity of interaction, resistance (hypersensitivity) is expressed only when

combinations A1-R1ˉor ˉA2-R2 occur in the same parasite-host system. That is, A1“recognizes”
only R1, and A2 “recognizes”only R2.

Finally it is significant that hypersensitivity ensues when a single gene for avirulence (A) at a
given locus (x) in the parasite interacts with a single gene for resistance (R) at the corresponding
locus (x) in the host. The A2-R2 interaction thus overrides any reaction between corresponding
genes at other loci.

8.4. Types of Plant Resistance to Pathogens

(Refer to R.A. Robinson. 1969. Disease resistance terminology, Rev. Appl. Mycol. 48: 593-606).

Plants are resistant to pathogens because:

1. They are immune to these pathogens (non-host resistance)
2. They possess genes for resistance directed against genes of virulence of the pathogen (true
resistance)
3. The plants, for various reasons, escape or tolerate infection by these pathogens (apparent
resistance).

47
The variation in susceptibility or resistance to the pathogen among plant varieties is due to
different kinds and different numbers of genes for resistance that may be present in each variety.
A variety that is very susceptible to a pathogen isolate obviously has no effective genes for
resistance against that isolate. The same variety, however, may (or may not) be susceptible to
another pathogen isolate obtained from infected plants of another variety.

8.4.1. True Resistance

In this resistance, genes are commonly located in cell nucleus. Disease resistance that is
genetically controlled by the presence of one, a few, or many resistance genes in the plant is
known as true resistance. The pathogen and the host are incompatible because of:
1. lack of chemical recognition between the host and the pathogen
2. the host plant can defend itself against the pathogen by the various defense mechanisms
already present, or activated, in response to infection by the pathogen.

There are two kinds of true resistance and are discussed as follows.

A) Horizontal Resistance (HR)

Here, all plants have a certain (but not always the same) level of unspecific resistance that is
effective against each of their pathogens. Also, some degree of HR is present in plants
regardless of the presence of vertical resistance (VR). HR is also called non-specific, general,
quantitative, adult-plant, field, durable resistance, and most commonly horizontal resistance.
HR is controlled by many (dozens and hundreds of) genes and named as polygenic, or multigene
resistance. Each of the genes alone may be ineffective against the pathogen and may play a
minor role in the total horizontal resistance (minor gene resistance). The resistance of a variety
to all races of a pathogen may be greater, or smaller, than those of other varieties to the same
pathogen, but the differences are usually small and insufficient to distinguish varieties by HR
(non-differential resistance). Varieties with general (polygenic) resistance are stable and may
vary in their reaction to the pathogen under different environmental conditions, i.e. HR is
affected by different environmental conditions, but a pathogen will have to undergo many more
mutations to completely breakdown the resistance of the host. Also, HR does not protect plants
from becoming infected, but it slows down the development of individual infection loci on a
plant and slows down the spread of the disease and development of epidemics in the field.

48
B) Vertical Resistance (VR)
Many plant varieties are quite resistant to some races of a pathogen while they are susceptible to
other races of the same pathogen. Such resistance is called specific, qualitative, differential
resistance, and most commonly vertical resistance.

VR is controlled by one or a few genes and called monogenic or oligogenic. These genes play a
major role in the pathogen-host interaction and are called major gene resistance. The host and
pathogen are incompatible, the host responding with a hypersensitive reaction (hr). VR inhibits
the initial establishment of pathogens that arrive at a field from host plants that lack or have
different major genes for resistance. Thus VR inhibits the development of epidemics by limiting
the initial inoculum. Varieties with specific (monogenic or oligogenic) resistance show
complete resistance to a specific pathogen under most environmental conditions, but a single or
a few mutations in the pathogen may produce a new physiological race that may infect the
previously resistant variety.

Complete resistance may be provided by a single gene, for example, R1, R2, and R3, but more
than one resistance gene may be combined (R1R2, R1R3, R1R2R3) in the same plant, which then
is resistant to all the pathogen races to which each of the genes provides resistance. A plant
species may have as many as 20 – 40 resistance genes against a particular pathogen, although
each variety may have only one or a few of these genes. E.g. wheat has 20 – 40 resistance genes
against P. recondita in different varieties in the world.

C) Cytoplasmic Resistance
Here either type of resistance (HR or VR) is controlled by genetic material contained in the
cytoplasm of the cell. E.g. Genes against: (1) Bipolaris (Helminthosporium) maydis, and (2)
Phyllosticta maydis in corn.

8.4.2. Apparent Plant Resistance

Apparent resistance to a disease of plants known to be susceptible is generally a result of
disease escape or tolerance to disease.

(1) Disease Escape

This happens because the three factors (susceptible host, virulent pathogen and favourable
environment) do not coincide and interact at the proper time or for sufficient duration. Seeds
germinate faster, and seedlings harden earlier than others. Plants may be susceptible at a
particular growth stage (young leaves, stems, or fruits, at blossoming, or fruiting; at maturity, or

49
early senescence) when the pathogen is absent or inactive. Other factors that contribute to
disease escape include: isolation distance or spacing; borders (barriers); surface hairs
(trichomes) and wax that repel water and pathogens; erect growth habit; natural openings
(stomata) and their position at high or low levels and which open too early or loo late; absence
of wounds; unattractiveness to vectors; and factors that affect the survival, infectivity,
multiplication and dissemination of pathogens.

(2) Disease Tolerance

This refers to the ability of plants to produce a good crop even when they are infected with a
pathogen. This is made possible through:
a) lack of receptor sites for the pathogen
b) inactivation of the irritant (toxic) excretion or secretion of the pathogen
c) compensating for irritation by pathogens

Tolerance is most commonly observed in many plant-virus interactions. Although tolerant

plants produce a good crop even when they are infected, they can produce an even better crop
when they are not infected.

8.4.3. Sources of Resistance Genes

The sources of plant resistance genes include:
1. Wild plant relatives
2. Older varieties abandoned earlier or discarded breeder’s stock
3. Native or foreign commercial varieties
4. Induced mutationsn (tissue culture, transgenic plants, transgenes)

Resistance genes are present in varieties or species normally grown in the area where the
disease is severe and in which the need for resistant varieties is most pressing. With most
diseases, a few plants remain virtually unaffected by the pathogen, although most or all other
plants in the area may be severely diseased. Such survivors are likely to have remained healthy
because of resistant characteristics present in them.

8.5. Breakdown of Plant Disease Resistance

Varieties with specific (monogenic or oligogenic) resistance show complete resistance to a
specific pathogen under most environmental conditions, but a single or a few mutations in the
pathogen may produce a new race that may infect the previously resistant variety. The
breakdown in vertical resistance can be avoided by the use of multilines- either mixtures of

50
individual varieties (lines or cultivars) that are agronomically similar but differ in their
resistance genes or varieties that contain the mixtures of genes. E.g. Small cereals against rust
fungi.

Horizontal resistance is universally present in wild and domesticated plants but it is at its
highest levels in wild plants and is at its lowest in greatly ‘improved’ varieties. Varieties with
general (polygenic) resistance are also stable and may vary in their reaction to the pathogen
under different environmental conditions, i.e. HR is affected by different environmental
conditions, but a pathogen will have to undergo many more mutations to completely breakdown
the resistance of the host. HR is eroded in the absence of the pathogen because there is no
selection pressure for resistance. HR can be incorporated into cultivated crops by crossbreeding
of existing, genetically different varieties.

Note: As a rule, a combination of major and minor genes for resistance against a pathogen is the
most desirable makeup of any plant variety.

51
9. Epidemiology of Plant Diseases (3 lecture hours)
9.1. Different Factors Affecting Epiphytotics

Considerations in Disease Development

Although the four factors (pathogen, host, environment, and man) are involved in disease
development, there are situations of the factors whereby diseases are developed:

9.1.1. Host Plant Factors

 Susceptible host
 Susceptible stage
 Predisposition
 Others.

9.1.2. Pathogen Factors

 Virulent pathogen
 Infective stage
 Inoculum potential and inoculation method
 Age of inoculum

9.1.3. Environmental Factors

 Favourable temperature, light, humidity, wind, etc. to the pathogen
 Duration of exposure (time)
 Season of the year
 Soil status (nutrient, moisture, pH, etc.)
 Ecology

9.1.4. Human Factors

 Cultivation practices (irrigation, levelling, etc.)
 Source of seed (disease introduction)
 Introduction of susceptible host

52
9.2. Measurement of Plant Diseases
9.2.1. Assessment of Plant Diseases and Crop Losses
9.2.1.1. Disease Assessment Methods

Disease Measurement (Phytopathometry)

Disease and pathogen measurements are used to quantify the development of epidemics in
space and time, for analysis of the factors that affect disease development (e.g., temperature,
surface wetness), as a basis for disease and yield loss prediction, and for definition of disease
action threshold levels for management programs. Several terms have been used to define
aspects of measurement, including prevalence, incidence, severity and intensity.

1. Disease incidence = refers to the number or proportion of plant units (plants, stems, leaves,
and fruits) diseased or that show symptoms. It is a relatively quick, easy, and most common
method in plant epidemiology to measure the spread of disease through a field, region, or
country. In diseases such as cereal loose smuts (where an infected ear represents a total loss of
production) and vascular wilts of annuals, incidence has a direct relationship to disease
severity and crop yield losses. However, in most leaf spots, root lesions, and rusts, disease
incidence has little implication to the severity or yield losses because the mere presence of
symptoms does not mean that proportional crop loss would occur. There are also some related
phrases. Disease density refers to the percentage of plants with disease symptoms, while
disease prevalence refers to the proportion of production units in which at least some disease
or pathogen may be found, i.e., percentage of fields attacked by a disease. Disease intensity
refers to the amount of disease present, often based on incidence and/or severity.

2. Disease severity = Refers to the proportion (fraction) of area or amount of plant tissue that is
diseased or damaged. It is expressed as percentage (or proportion) of plant area or fruit
volume destroyed by a pathogen. Scales from 0 to 5 or 1 to 9 disease scale are often used to
express the relative proportions of affected tissue at a particular point in time. Disease severity
surveys use standard diagrams to represent the proportions of plant tissues infected. Disease
index is calculated as the average of the observations or disease ratings on a specified number
of plants. Refer to the example given for late blight of potato caused by Phytophthora
infestans (Table 3).

53
Table 3. Field key for severity assessment of potato late blight (Phytophthora infestans) Moore
(1943) and British Mycological Society (1947).
___________________________________________________________________________
Disease Percentage (%) Description of disease status on leaves, plants
scale infection or potato field______________________________________
1 0 No disease on plants
2 0.1 Only few plants are affected (1 or 2 spots in 10 metre radius)
3 1 Up to 10 spots per plant or general light spotting occurred
4 5 About 50 spots per plant or up to 1 leaflet in 10 attacked
5 25 Nearly every leaflet with lesions (field may smell of blight)
6 50 Every plant affected and half leaf area destroyed
7 75 About ¾ of leaf area destroyed by blight; severe shoot
infection
8 95 Only a few leaves left green but stems are green
9 100 All leaves are dead, stems dead or dying__________________
3. Yield loss = Refers to the proportion of the yield that the grower will not be able to harvest
(because the disease destroyed it directly or prevented the plants from producing it). Yield
loss due to disease is measured at a specified growth stage or phenology (e.g. Feeke’s scales
for cereals), or from sequential disease assessment at several stages of a crop’s growth, or by
measuring the area under a disease progress curve (AUDPC). Yield loss is always positively
correlated with economic loss from disease.

x 1.0
0.1
0.8 0.05
Disease fraction

0.6

0.4 0.01

0.2
0.0
0
20 30 40 50 10
Time in days (t)
Disease progress curves (x = disease fraction)
Xt = loge 1/(1-xt), when xt<0.05.
Xt = 1-e-rs.t

54
9.2.1.2. Rationale for and Concepts of Crop Loss Assessment

Measuring plant diseases enables us to:

1. obtain quantitative data on occurrence and development of diseases
2. assess the relative importance of different diseases comparing their incidence
3. determine the relationship between disease intensity and crop yield or quality loss
4. calculate the economic losses from surveys conducted to assess the importance of
diseases
5. to distinguish treatment differences, i.e., to test the relative efficacy of fungicides and
their formulations
6. detect differences in disease resistance among varieties

Yields → are categorized as theoretical, attainable, economic, actual and primitive yields. FAO
uses: Crop yield loss = Attainable yield – actual yield.

Crop loss is the reduction in either quantity and/or quality of yield. Crop loss assessment is
based on any or combinations of the following sources.
1. Statement of the authority
2. Enquiries (questionnaires/interviews)
3. Surveys:- which could be regional or national surveys
4. Aerial photography:- Immediate assessment may be required for sudden disaster; terrain
may be inaccessible; or area could be too large.
5. Field experiments:-

The experiments should be conducted at different locations on different varieties with reference
to different diseases. It is important to relate disease severity with individual crop yield losses of
those crops. The experimental field consists of treated and untreated plots with non-host crop
being grown between the plots to prevent disease/chemical transfer or interference. The crop
losses should be compared with the attainable or economic yield. Such trials need to be repeated
for at least 3 or more years. The data so obtained are reliable.

Crop losses could be potential losses (losses that may occur in the absence of control measures)
or actual losses (losses that have already occurred and still are occurring). Crop losses may also
be categorized as primary losses (preharvest or postharvest losses of plant products due to
diseases) or secondary losses (losses in yielding capacity of future crops due to cumulative
effect of soil-, seed-, or tuber-borne diseases in annual crops); regular losses (losses that occur
each season in more or less equal amounts) or incidental losses (losses that occur only once or

55
at irregular intervals); transitional (temporary losses that occur when growers change over from
one farming system to another) or structural losses (losses that are unavoidable in a given
agricultural situation but may be reduced by research findings of new technologies); recognized
losses (readily observable losses caused by the destructive agent) or hidden losses (the extent to
which normal crop falls short of its potential yield, it is unrecognised loss); and direct or
indirect losses (could be farmer’s losses, losses to rural community, consumer’s losses,
exporter’s losses, state/government losses, and environmental losses).

9.3. Simple and Compound Interest Diseases

Some phytopathogens require one growing season or one year to complete their life cycles. That
means they produce only one generation per growing season or per year. Plant diseases caused
by such pathogens are known as simple interest diseases. The amount of inoculum is assumed
to be constant during the vegetation period. Monocyclic epidemics can occur due to simple
interest diseases when the inoculum comes from a reservoir such as soil inhabiting pathogens.
Example: Sclerotial diseases caused by Sclerotium rolfsii. Other plant pathogens can produce
two or more generations (polycyclic) per growing seasons or per year. The plant diseases that
are caused by such pathogens are known as compound interest diseases. Example: Rust diseases
caused by pathogens such as Puccinia graminis (black stem rust of wheat) can have 10 to 30
generations per year. Pathogens that require many years to complete one life or disease cycle
are called polyetic pathogens.

The apparent infection rate (logistic infection rate or simple interest infection rate), rs, which
measures the speed of epidemic process in simple-interest disease is estimated as (according to
Vanderplank, 1963):

rs = 1/(t2 – t1) {loge.[x2/(1-x2)] – loge [x1/(1-x1)]}

or
rs = 1/(t2 –t1) [loge (1 – x1)/(1 – x2)]
or
rs = 1/(t2 – t1) (logit x2 – logit x1)

Similarly: (logitx2 – logit x2)/(t2-t1)

where, r = apparent infection rate

t1 = initial time of disease scoring, in days

56
 t2 = time interval after the initial time
x1 = amount of infection or fraction diseased at time t1
x2 = amount of infection or fraction diseased at time t2
Similarly, the relative growth rate (intrinsic growth rate or exponential infection rate), rl, in
compound interest diseases is expressed as:

rl = 1/(t2 – t1) (loge x2/x1).

Similarly: (loge x2/x1)/(t2-t1)

Source: Van der Plank, J.E. 1963. Plant diseases: Epidemics and control. Academic Press, New
York.

9.4. Monitoring and Forecasting Plant Disease Epidemics, and Bases for Forecasting
A forecast is a prophecy or prediction of a future event or condition. The forecasting of
epidemics is, therefore, simply a prognostication, or foretelling. Forecasting involves all the
activity in ascertaining and notifying the growers of a community that conditions are
sufficiently favourable for certain diseases, that application of control measures will result in
economic gain, or on the other hand, and just as important, that the amount of disease expected
is unlikely to be enough to justify the expenditure of time, energy and money for control.

Disease forecasting allows the prediction of probable outbreaks or increases in intensity of

disease and, therefore, allows us to determine whether, when, and where a particular
management practice should be applied. In managing the diseases of their crops, growers must
always weigh the risks, costs, and benefits of each of the numerous decisions. Most frequently,
farmers need forecasts that will help them determine whether a plant infection is likely to occur
so they can decide whether to spray a crop right away or to wait for several more days before
they spray. If disease forecasting allows them to wait, they can reduce the amounts of chemicals
and labour used without increasing the risk of losing their crop.

To develop a plant disease forecasting system, the particular pathogen, host plant, and
environment must be considered. For monocyclic diseases (e.g., apple scab), assessment of the
amount of initial inoculum is very important. For polycyclic diseases (e.g., potato late blight),
assessment of the rate of occurrence of the infection cycles is useful for forecasting. In cases
where both the amount of initial inoculum and the number of disease cycles are large (rusts up
to 20 generations), e.g., beet yellows, both factors must be assessed for accurate prediction of
disease epidemics.

57
Weather monitoring is useful in the development of a forecasting system. This necessitates for
continuous monitoring of several different factors (temperature, relative humidity, leaf wetness,
rain, wind, and cloudiness) at various locations in the crop canopy or on the plant surfaces in
one or more fields. In modern weather-monitoring systems, the weather sensors are connected
to data-logging devices. The data may be read on a digital display, or transmitted to a cassette
tape recorder or a printer or may be transferred to microcomputer for analysis. Thus accurate
weather information provides the most useful basis to predict sporulation and infection and
therefore provides the best warning to time disease management practices, such as the
application of fungicides.

Bases for Forecasting Plant Diseases

The bases for forecasting include:

1. Amount of initial inoculum (in soil, seed, etc.)
2. Amount of secondary inoculum
3. Weather conditions favouring initial and secondary inoculum or vectors
4. The host plant (degree of susceptibility of varieties)

10. General Control Methods of Plant Diseases (2 lecture hours)

10.1. Regulatory Disease Control Methods

National and state laws regulate the import and distribution of crops between states and
countries. Such regulatory control methods include:
1. Quarantines
2. Inspections of plants in the field/warehouses
3. Compulsory eradication of host plants
4. Exclusion (evasion)

10.1.1. Quarantines and Inspections

Quarantine refers to the control of import and export of plants to prevent (prophylactic
measures) spread of diseases and pests. This method excludes the pathogen from entering into
the area or country. Plant quarantine measures can keep out foreign pathogens by prohibiting by
restricting entry into or passage through the second country, i.e., importing country, via plants,
plant products, soil, and other materials. Quarantine regulations (acts) are enforced in most
countries, e.g. at the entry port to intercept catastrophic diseases. Quarantine is effective against
viruses, bacteria, nematodes and parasitic higher plants carried through seeds and plant
materials. Plant quarantine measures include:
58
 1. Growing plants under observations for certain periods before releasing to the importer.
2. Inspecting the crop fields for the occurrence of potentially dangerous pathogens. If they
are free from diseases, inspection certificates are issued.
3. Controlling the movement and sale of seeds between states (However, they are not
effective against air-borne pathogens).
4. Indexing of crops in the field and storage. Indexing is a procedure to determine whether
a virus can infect a given plant. It involves the transfer of a bud, scion, sap, etc. from one
plant to one or more kinds of (indicator) plants that are sensitive to the virus.

Certification of Planting Materials

Certification is normally offered on the basis of purity, freedom from parasitic weeds, and
germination percentage for which standards are fixed for each crop. Seeds are treated with
pesticides. For vegetative propagative stocks, tubers and other planting materials, plants are
examined in the growing season for freedom from diseases. Heat treatment, meristem, or tuber
indexing are practiced to make such planting materials free of pathogens.

10.1.2. Exclusion/Avoidance/Evasion of Pathogens

This method deals with crop isolation (e.g. perennial crops). This is possible through avoidance.
You may need to create a barrier between the host and the pathogen. Chemicals may be applied
as seed treatment or seed dressing to exclude the pathogen from coming into contact with the
susceptible host plant. Fungicides may be sprayed before the pathogen attacks the host too.

10.1.3. Eradication of Plant Pathogens

It is aimed at the elimination of a pathogen from an area into which it has been introduced.
Pathogens can be eradicated from an area by: (1) the eradication (rouging) of susceptible plants
(alternate or alternative host) that carry the pathogen; (2) crop rotation; (3) heat treatment ( e.g.
seed treatment with hot water at 50 oC for 10 minutes against Xanthomonas campestris of
cabbage); and (4) physical treatment of the soil by dry heat, steam or hot water, flooding, and
fumigation with chemicals, e.g. green-house or pot soils. Nematodes are eradicated by
fumigating with dichloropropane-dichloropropene (DD) mixture with other nematicides.
Pentachloronitrobenzene (PCNB) is effective against Sclerotia-producing pathogens. This is
known as chemotherapy, e.g., use of benomyl. (5) Eradication of plant pathogens is also
possible using biological control against soil-borne diseases.

Historical examples for eradication of pathogens: (1) bacterial canker of citrus (Xanthomonas
citri) in Florida in 1915 (more than 3 million trees uprooted) and in 1984 (millions of nursery

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and trees were uprooted); (2) witch-weed (Striga asiatica) in Carolina in the last quarter
century; and (3) coffee leaf rust (Hemileia vastatrix) in Sri Lanka (the then Ceylon) in 1870.

10.2. Cultural Methods

These methods are intended to reduce inoculum potential of pathogens either by encouraging a
healthy growth of plants or avoiding attack by changing various agronomic practices, i.e., by
adjusting the cropping system. These methods encompass:

1. Field sanitation:- Reduces inoculum and avoids epidemics

2. Clean cultivation:- uses disease free seeds and propagative materials
3. Crop rotation:- To control root diseases or soil-borne diseases
4. Adjustment of sowing/planting dates
5. Adjustment of planting space (spacing)
6. Water and fertilizer management
7. Tillage practices
These must be practiced with efficient management from time of planting to harvesting for high
yield. Normally vigorously growing healthy plants can withstand attack by pathogens and build
up defense mechanisms. For successful results, knowledge of the biology and ecology of the
pathogenic organisms as well as methods of perennation is necessary. Information on
environmental and biotic factors is also useful.

10.2.1. Sanitation, Disease-free Seed, Crop Rotation and Trap Crops

(1) Sanitation
Sanitation deals with destruction of residues, stubbles, and tillers; use of eradicant sprays;
eradication of infected plants or their parts; eradication of alternate or collateral hosts; and
proper tillage practices.

(2) Clean Planting Materials /Use of Pathogen-free Propagating Materials

Use of disease-free materials is useful to control fungi, bacteria, nematodes, viruses, etc. This
suppresses inocula of pathogens. Systemic diseases such as mycoplasma-like organisms,
viroids, and fastidious vascular bacteria are controlled through the use of disease-free
propagative materials. This is practiced through:
1. Use of an area free of pathogen.
2. Growing host plants in areas not suitable to the pathogens.
3. Use of an area free of vectors of the virulent pathogen.

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 4. Use of pathogen-free propagative materials (seeds, tubers, nursery stock, etc).

(3) Crop Rotation

This agronomic practice deals with the rotation of different crops on the same farmland year
after year. The change in sequence of cropping pattern usually reduces disease incidence. It is
effective against soil invaders that survive in the soil for less than 3 to 4 years. It disrupts the
continuity of food supply for the root diseases using (with inclusion of) non-host or non-
susceptible crops, but not effective against soil inhabitors that survive for more than 5 or 6
years. Example: Verticillium spp. Inclusion of leguminous crops in the crop rotation can
augment the soil fertility too.

(4) Trap Crops

This may be effective against nematodes that are trapped in susceptible host roots and are
rogued out of field and burnt together with the roots. Example: Crotalaria spp., Tagetes minuta.

10.2.2. Adjustment in Sowing or Planting

This avoids the coincidence of the active stage of the pathogen and susceptible stage of the host
plant. Early planting may help the susceptible host escape the pathogen. Plants may be grown
where the pathogen is non-existent or its vector is absent. Seed multiplication is often practiced
in dry areas to have low level of seed-borne infection.

10.2.3. Soil Factors (pH, temperature, soil moisture, organic matter, nutrients, texture)
a) High temperature favours flax wilt (Fusarium oxysporum f. sp. lini) and tomato wilt
(Fusarium oxysporum f. sp. lycopersicii).
b) Low temperature favours Rhizoctonia solani, tobacco root rot (Thielaviopsis basicola),
and onion smut (Urocystis cepulae).
c) High moisture favours club root (Plasmodiophora brassicae), Pythium spp., Phytophthora
spp. and Fusarium spp.
d) Low moisture favours smuts (Sphacelotheca spp.) of cereals and potato scab
(Streptomyces scabies).
e) Light soils favour wilts (Fusarium spp.)
f) Acid soils favour Fusarium spp., club root, and powdery scab of potato (Spongospora
subterranea)
g) Alkaline soils favour potato bacterial wilt [Pseudomonas (Ralstonia) solanacearum] and
potato scab.

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 h) Organic matter favours bunt (Tilletia spp.), flag smut (Urocystis agropyri) of wheat and
root rot of tea (Rosellinia spp.). But most diseases are checked by application of organic
matter.

Water management constitutes a very important cultural control method. Example: Flood
fallowing can make the soil free from soil-borne infection such as Fusarium oxysporum f. sp.
cubense (Panama disease of banana).

Application of nitrogen, phosphorus and potassium fertilizers have an effect on plant diseases.
This is because plants receiving adequate balanced nutrients have good growth. Excessive
nitrogen, however, predisposes plants to diseases.

10.2.4. Plant Spaces (Spacings)

Very close spacing results in more humid microclimatic conditions that favour incidence of
foliage blights. Avoidance of planting at close distance may check early spread of black rot of
cabbage (Xanthomonas campestris), which takes place by plant-to-plant contact. N.B. A
balance has to be maintained between planting distance for maximization of crop yields and the
consequent effect on microclimatic conditions favouring diseases.

10.2.5. Tillage Practices

1. Deep planting delays seedling emergence and makes them vulnerable to pre-emergence
damping-off; and
2. Deep ploughing is beneficial for control of chickpea wilt (Fusarium oxysporum f. sp. cicer
arietini).

Stalk rot of grain sorghum (Fusarium moniliforme) has been dramatically reduced by reduced
tillage plus fallow (ecofallow) where herbicides are used during the fallow. Fallow allows
greater heating and drying of soil and marked reduction of nematodes and other pathogens.

10.3. Use of Resistance Genes and Plant Breeding for Resistance

10.3.1. Plant Breeding for Disease Resistance
Plant breeding deals with collection, introduction, selection, and hybridisation. If resistant
plants are found, they are crossed with the cultivated varieties in an effort to incorporate the
resistance genes of the other species into the cultivated varieties.

10.3.1.1. Classical Breeding for Disease Resistance (Conventional Methods)

There are some systems of screening for plant disease resistance and include:

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 1. Precise conditions for inoculating the plants with the virulent pathogen
2. Accurate monitoring and control of the environmental conditions in which the inoculated
plants are kept
3. Accurate assessment of disease incidence (percentage of plant, leaves, or fruits infected)
and disease severity (proportion of the total area of plant tissue affected by disease)

The main plant breeding techniques for disease resistance also include:
1. Mass selection of seed:- This deals with selection of most highly resistant plants
surviving in a field where severe natural infection occurs regularly. It is a simple breeding
method but it is slow and there is no control of pollen source in cross-pollinated plants.
2. Pure line or pedigree selection:- Here, individual highly resistant plants are selected and
their progenies are propagated separately and are inoculated repeatedly to test for
resistance. This is an easy and most effective breeding method with self-pollinated crops
but quite difficult with cross-pollinated ones.
3. Recurrent selection or backcrossing:- It is a breeding method where desirable but
susceptible variety of a crop is crossed with another cultivated or wild relative that carries
resistance to a particular pathogen. The progeny is then tested for resistance, and the
resistant individuals are backcrossed to the desirable variety. This is repeated several times
until the resistance is stabilized in the genetic background of the desirable variety. It is
time-consuming but more easily performed in cross-pollinated crops than in self-
pollinated crops.

4. Other classical breeding techniques:- These include:

a) Use of F1 hybrids of two different but homozygous lines carrying different genes for
disease resistance (heterosis).
b) Use of naturally or artificially induced (x-ray, UV-light, colchicines, radiation, etc.)
mutants with increased resistance.
c) Use of change of number of chromosomes in a plant and production of euploids (4n,
6n), or aneuploids (2n + 1 or 2 chromosomes).

10.3.1.2. Breeding for Resistance Using Tissue Culture and Genetic Engineering
techniques (Contemporary Methods)
Genetic engineering techniques allow the detection, isolation, modification, transfer, and
expression of single genes, or groups of related genes from one organism into another.

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Recent advances in plant tissue culture include:
1. Meristem tip propagation (tissue culture)
2. Callus and single cell culture (somaclonal variation)
3. Haploid plant production
4. Protoplast isolation, culture, transformation, fusion, and regeneration into the whole
plants

10.3.2. Plant Disease Resistance in Practice

Incorporating one, a few, or many resistance genes into a variety can provide plant resistance to
a certain disease. Vertical resistance is easy to manipulate in a breeding programme. VR is most
effective when:
1. It is incorporated in annual crops (small cereals) that are easy to breed.
2. It is directed against pathogens that do not reproduce and spread rapidly. E.g. Fusarium
spp.
3. It consists of ‘strong’ genes that confer complete protection to the plant that carries it.
4. The host population does not consist of a single genetically uniform variety grown over
large acreages, but desirable if multilines are grown.

Horizontal resistance is universally present in wild and domesticated plants but it is at its
highest levels in wild plants and is at its lowest in greatly ‘improved’ varieties. HR is eroded in
the absence of the pathogen because there is no selection pressure for resistance. HR can be
incorporated into cultivated crops by crossbreeding of existing, genetically different varieties.

The breakdown in vertical resistance can be avoided by the use of multilines- either mixtures of
individual varieties (lines or cultivars) that are agronomically similar but differ in their
resistance genes or varieties that contain the mixtures of genes. E.g. Small cereals against rust
fungi.

10.4. Biological Control of Plant Diseases

10.4.1. Mechanisms
Biological control deals with any condition or practice whereby the survival or activity of a
pathogen is reduced through the agency of any other living organism (except man himself)
resulting in a reduction in the incidence of the disease caused by that pathogen. Biological
control has been mostly attempted in case of pathogens operating in the soil where a micro-
biological equilibrium is maintained in relation to a soil agro-ecosystem. Green manuring and
incorporation of organic matter into the soil can alter soil conditions that favour some

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saprophytic micro-organisms which, in turn, control the activities of pathogens and change the
microbiological balance in the soil thereby suppressing soil-borne diseases E.g. Potato scab
(Streptomyces scabies) can be controlled in this way. Weindling (1930) found that Trichoderma
viride served as a parasite on other fungi through production of antibiotics (probably viridin).
Biological control of plant diseases through a living organism mainly operates by its action on
the pathogen, which is commonly designated as antagonism. Antagonistic action is divided into:

1. Antibiosis:- It deals with the suppression of pathogenic organisms through the production of
metabolic agents (antibiotics = having a harmful effect on pathogens) by other micro-
organisms.

It is worth considering the following points in relation to antibiosis. (1) Antibiotics (toxins)
production can take place in suppressive soils in the vicinity of organic substrates, which are
rich carbon sources like straw or seed coats. (2) It is known that antibiotic production is
positively correlated with suppression in disease-causing micro-organisms. (3) The ability to
secrete antibiotic toxin in vitro does not signify antibiosis in the soil. (4) Metabolic products
(antibiotics) connected with antibiosis may be inactivated in a number of ways, e.g. adsorption.
(5) Antibiotics may be slowly released from adsorbed condition or may be extracted from the
soil. (6) Antibiosis may also be due to release of high quantities of CO2 during crop residue
decomposition. E.g. Rhizoctonia and Fusarium oxysporum f.sp. cubense are suppressed in this
way.

2. Competition for food (competitive saprophytic organisms):-This deals with competition

for nutrient supply, i.e., quicker and greater utilization of available nutrients by saprophytic
micro-organisms over the pathogens, which are normally poor competitors leading to lysis or
starvation.

Factors determining good saprophytic ability, i.e. competitiveness with the pathogens include:
1. high growth rate and rapid germinability of reproductive structures, which deplete levels
of carbon, nitrogen and vitamins;
2. good enzymes or antibiotic toxins producing ability; and
3. tolerance to antibiotics produced by other micro-organisms (pathogens)

Many soil organisms, such as strains of Streptomyces, Nocardia, Pseudomonas and Bacillus are
capable of causing lysis of hyphae of Fusarium spp., and Penicillium chrysogenum. For
example, Fusarium solani f. sp. phaseoli is very sensitive to supply of nutrients. Incorporation

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of carbohydrate-rich materials in the soil (E.g. turning under residues of barley crop) reduces
this pathogen by way of encouraging growth of competitive saprophytic microorganisms.

3. Exploitation:- It is the direct parasitism (mycoparasitism) or predation of organisms over

other pathogenic ones.

There are a lot of evidences where exploitation operates in nature. (1) Parasitism by destructive
mycoparasites by their direct penetration into or coiling round the host hyphae has been
observed in Rhizoctonia solani on various other fungi and Penicillium vermicullatum
parasitizing Rhizoctonia solani. (2) Didymella exitialis penetrates and kills hyphal cells of
Ophiobolus graminis (now Gaeumannomyces graminis) that causes ‘take-all’ disease. (3)
Gliocladium roseum parasitizes and destroys conidia of many species of fungi. (4) Dactylaria
species have been noted to be good nematode-trapping fungi. Amendment of soil with organic
manures has been found to be beneficial in suppressing the reproduction of plant parasitic
nematodes. (5) Inoculation of the soil with Trichoderma viride suppresses Rhizoctonia solani
attacking citrus seedlings, Fusarium solani and potato scab, etc. (6) If chitinous cell walls,
laminarin, and polysaccharide are added to the soil, Actinomycets population increases and
suppresses Fusarium wilt of peas and Rhizoctonia stem rot of beans. (7) Early inoculation with
weakly parasite Cephalosporium sp. suppresses later infection by Fusarium oxysporum f. sp.
lycopersicii, the process of which is called ‘cross-protection’ (hypovirulence). (8) Cultivation of
decoy crops:- This refers to conditions where the roots of some plants will stimulate
germination of dormant propagules of pathogens without themselves being sufficiently
susceptible. Examples for (8) are as follow:

(a) Datura stromonium stimulates the cause for potato powdery scab (Spongospora
subterranean).
(b) Papaya seedlings suppress Phytophthora palmivora.
(c) Solanum tuberosum f. sp. andigena suppresses golden nematode (Heterodera
rostochienensis).
(d) Growing a leguminous crop after potato and turning it under whilst it is still green, as green
manuring, can control potato scab (Streptomyces scabies).

4. Volatile substances (e.g., ethylene): Such chemicals produced by plants may be considered
as biological control agents.

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10.4.2. Examples of Biological Control
Among the most common mycoparasitic fungi are Trichodema spp. (e.g. Trichoderma
harzianum) against Rhizoctonia, Sclerotium, Pythium, Fusarium, and Fomes. The following
organisms are also examples for biological control.

 Laetsaria arvalis (Corticium sp.) against Pythium and Rhizoctonia spp.

 Sporidesmium sclerotivrum, Gliocladium virens and Coniothyrium minitants against
Sclerotinia sclerotiorum.
 Chaetomium sp. suppresses Venturia inaequalis (apple scab).
 Tuberculina maxima against white pine blister rust (Cronartium ribicola).
 Darluca filum and Verticillium lecani against several rusts.
 Ampelomyces quisqualis against powdery mildews.
 Tilletiopsis sp. against cucumber powdery mildew (Sphaerotheca fuligena).
 Nectria inventa and Gonatobotrytis simplex against two Alternaria spp.
 Streptomyces and Pseudomonas against Pythium sp. and Gaeumannomyces tritici.
 The nematode Aphalenchus avenae against Rhizoctonia and Fusarium.
 Catenaria auxiliaris, Nematophthora gynophila and Verticillium chlamydosporium (all
fungi) against Heterodera and Globodera (both nematodes).
 Dactylella oviparasitica against Meloidogyne sp.
 Bacillus (Pasteuria) penetrans against Meloidogyne javanica.

10.5. Chemical Protection (Chemotherapy) of Plants

This method deals with use of chemical compounds that are toxic to the pathogens. It is the
most commonly used method of controlling plant diseases in the field, in the storage and in the
greenhouse. The chemical compounds may:

1. inhibit spore/mycelium germination in fungi or interfere with egg hatching in nematodes;

2. inhibit the growth of pathogens;
3. inhibit multiplication or sporulation of pathogens; and
4. be lethal to the pathogens due to their toxicity.

Based on the pathogens controlled, the chemicals could be fungicides, bactericides,

nematicides, viricides, or herbicides for parasitic higher plants. Most chemicals are used to
disinfect and protect from infection of seed, tubers, and bulbs. Some are used to disinfcst the
soil, warehouses, treat tree wounds, or protect stored fruits, vegetables and grains, or control

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pathogen vectors. Chemicals could be contact (local action) or systemic fungicides and
antibiotics (absorbed and translocated) through the plant system.

10.5.1. Uses of Chemical Application

1) Foliar Sprays and Dusts

Fungicides and bactericides are applied in these ways. Most fungicides and bactericides are
protectants and must be present on the surface of the plants in advance of the pathogen to
prevent infection. The chemicals inhibit spore germination or kill bacteria and inhibit
multiplication. Some chemicals act as eradicants [i.e., kill the pathogen inside host (curative) or
suppress sporulation without killing]. Some fungicides have partial systemic action (e.g.,
dodine) and others are clearly systemics (e.g., benomyl, thiabendazole, carboxin, and
metalaxyl). Streptomycin and most antibiotics are also systemics. Some are used as rescue
treatments (effective in post-infection application and serve as sterol inhibitors) e.g.,
triadimefon, fenarimol, and metalaxyl. Lime may be added to fungicides to reduce phytoxicity.
Detergents may be added to fungicides to facilitate spreading on the surface (have surface
tension). Starch and oils are added to increase adherence of fungicides. Systemic and protectant
fungicides may be applied with sprinkler irrigation (fungigation) against foliar diseases.

Apply chemicals by dust or spray before or immediately after every rain. The whole plant part
must be covered to obtain satisfactory results from contact fungicides/bactericides (protectants),
esp. young, expanding leaves, twigs, and fruits. Interval of sprays varies from 7 to 14 days or
longer. This depends on (1) particular disease (2) frequency and duration of rain (3) persistence
(residue life) of fungicide (4) season of year. Optimal number of sprays per season varies from
2 to 15 or more. Dusters, sprayers and fumigators are used for chemical application on seed,
foliage, and soil.

2) Seed Treatment
Seeds, tubers, bulbs, and roots are usually treated with chemicals to prevent their decay after
planting or damping-off of young seedlings by controlling pathogens carried on them or
existing in the soil where they will be planted. Pathogens are inactivated with systemic
fungicides in infected seeds (e.g., carboxin against loose smut) or foliage of developing plants
(e.g., metalaxyl against downy mildews of oats and sorghum; triadimenol against leaf rust and
Septoria of wheat and Pyrenophora net blotch of barley). Chemicals are applied as dusts or as
thick water suspension mixed with the seed. Seeds, tubers, bulbs, corms and roots are also

68
soaked in a water or solvent solution of the chemical and then allowed to dry. (Take care of
phytotoxicity and watch enough chemical has been coated on the seed).

Inorganic copper and zinc compounds and mostly organic protectants (captan, chloroneb,
chloranil, dichlone, hexachloronitrobenzene, maneb, zineb, mancozeb, thiram,
pentachloronitrobenzene (PCNB), and synthetic compounds (carboxin, benomyl, thiabendazole,
metalaxyl, triadimenol, and streptomycin) are used to treat seeds, bulbs, corms, tubers, and
roots. Some chemicals may control many diseases of one or a number of crops.

3) Soil Treatment
Certain fungicides are applied as fumigants (volatile compounds), dusts, drenches, or granules
to control nematodes, fungi, and bacteria by reducing the inoculum. Thus damping-off, seedling
blights, wilts, crown and root rots, and other diseases are controlled. These fungicides include
captan, diazoben, PCNB, chloroneb, metalaxyl, fosetyl-Al, triadimefon, ethazol, and
propamocarb. Many of the systemic fungicides, such as metalaxyl, fosetyl-Al, are so effective
even in small amounts that a single preplant broadcast soil spray followed by disking can
provide a full season’s protection against several pathogens. Fumigation is also possible to
control soil-borne diseases.

4) Treatment of Tree Wounds

Painting tree wounds with shellac or with any other commercial wound dressing prevents the
trees from infection by pathogens. The wood cuts are also sterilized by swabbing them with a
solution of 0.5 – 1.0% NaOCl (10 – 20% chlorox) or with 70% ethyl alcohol. Tree wounds are
also painted with a 10:2:2 lanolin, rosin, and gum mixture (or Cerano), Bordeaux paint, or with
an asphalt varnish tree paint.

5) Control of Post-harvest Diseases

Chemical compounds used as commercial control of post-harvest diseases of Citrus and other
fruits include: borax, biphenyl, sodium o-phenylphenate, benomyl, thiabendazole, and imazalil.
Certain chemicals such as elemental sulfur, SO2, dichloran, captan, and benzoic acid are used
for the control of storage rots of stone and pome fruits, banana, grapes, strawberry, melons, and
potatoes. Preservatives like weal acids are also used. For example, propionic acid.

10.5.2. Chemical Formulations

Formulation determines how a pesticide is used. The following formulations are used in
pesticide applications.

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(1) Powders/Dusts (D)
(2) Wettable powders (WP)
(3) Granules (G)
(4) Solutions (S)
(5) Emulsifiable concentrates (EC)
(6) Aerosols (A)
(7) Fumigants (F)

(i) Powders/Dusts (D)

The particle sizes of the dusts range between 15-25 µm for surface treatment and 25 – 50 µm
(even 70 µm) for aerial treatment, but poorly retained in the soil. They are mechanical mixtures
of fungicide and filler or carrier. They are used at a rate of 10 – 30 kg/ha dust. Talc, chalk,
kaolin, diatomite, silica gel, pyrophyllite and clays are used as carriers. From 3 to 5% mineral
oil may be added to dusts to reduce drift.

(ii) Wettable Powders (WP)

They contain 30 to 80% active ingredients (A.I.), 15 to 60% carriers and 2.5 to 4% others such
as adhesives and surfactants. About 80% of the particles are 3 µm in diameter. When diluted
with water, they give stable suspensions and better adhere on foliage than dusts. Good WPs
must fulfil the following characteristics.
(1) They must be stable in storage and not cake;
(2) They must rapidly form suspensions with slow settling of the solid particles; and
(3) They must wet the leaves of plants very well and be retained.

Wettable powders contain active ingredients (toxicants), carriers, surfactants, and adhesives
(stickers). Carriers include kaolin, bentonite, silica gel, and synthetic calcium metasilicate.

(iii) Granules (G)

The diameters of the particles range between 0.25 and 5 mm, the large ones with 3 to 5 mm and
small ones with 0.25 to 1.5 mm. Granules are incorporated into the soil to control soil fungi and
other pathogens. Granules contain toxicants, carriers, and adhesives. Nematicides are generally
formulated as granules. Granules generally lose their pesticidal action less than other
formulations; can pose less danger to man, and cause less phytotoxicity.

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(iv) Solutions (S)
These formulations are dispersed in water and in organic solvents. They contain surfactants to
reduce surface tension to wet the leaf surfaces well. Petroleum hydrocarbons deodorized
kerosene, diesel fuel, or mineral oils are used to prepare pesticide solutions.

(v) Emulsifiable Concentrates (EC)

These formulations are solutions of pesticide in oil comminuted into fine drops coated with a
emulsions that do not stratify for a long time. Homogenizers are used to prepare EC.
Emulsifiable concentrates are divided into miscible and immiscible concentrates. The miscible
ones contain fungicide, solvent, and emulsifier. They are prepared at 40 - 80 oC temperature.

(vi) Aerosols (A)

The droplet size varies from 0.001 to 50 µm (optimum 20 to 50 µm) in diameter. Aerosols are
defined as suspensions of fine droplets of liquid or solid particles of pesticides in air. Aerosols
can make both mists and solids (smokes). The aerosol particles settle in air very slowly.
Diameter of water droplets, µm………………100 10 0.1
Speed of settling of water drops in air, cm/s…120 1.2 0.00012
Example, Chloropicrin is used for disinfecting of granaries and stores, greenhouses and other
premises.

(vii) Fumigants (F)

These are gases used in the decontamination of objects from insects, their larvae and eggs,
mites, nematodes, and other pests by fumigating them with vapours or gases of poisonous
substances.

10.5.3. Methods of Application and Mechanisms of Action

1) Spraying
This method is a widely used way of applying pesticides in the form of solutions, emulsions, or
suspensions to a surface being treated. Special equipment called sprayer (hand, tractor, and
aerial) is used for spraying pesticides. Spraying is a universal method of pesticide application.
Advantages of spraying:
a) It uses very low active ingredients per unit area;
b) It has very uniform distribution and good coverage of treated surfaces; and
c) There is very good pesticide retention on treated surfaces, especially if wetting agents and
adhesives are contained;

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Spray volumes

a) Orchards and woods…………………2000 litres per hectare

b) Field crops…………………………..400 – 500 litres per hectare

Spray volumes Litres/ha on trees or shrubs Litres/ha on ground crops

Very low volume (ULV) Under 250 Under 60
Low volume (LV) 250 – 600 60 – 250
Medium volume (MV) 600 – 1200 250 – 700
High volume (HV) Over 1200 Over 700_______

Spray Droplet Sizes

a) Up to 50 µm ……………….Aerosol (ULV)
b) 51 – 150 µm ……………….Fine drops (LV)
c) 151 – 300 µm ……………...Ordinary/medium drops (MV)
d) > 300 µm ………… ……….Large drops (HV)

2) Dusting (D)
Dusting is the application of dust formulations to the surface of plants. Dusting can cover dense
cereal crops very well. Disadvantages of dusting include:
1) High dust contact of the air is dangerous to workers.
2) It requires high rate of the formulation.
3) There is drift of dust cloud with wind currents, especially in those having 25µm diameter of
particles.
4) There could be problem of washing off by rain. About 3 – 5% of bonifiers (mineral oils) are
added to dusts to reduce drift, especially in aerial treatments. Drift problem is especially
high if particle size is 25 µm falling from 10 m height. Dust particle sizes of 100 to 200 µm
do not pose drift problems, especially when the height of falling is 5 m.

3) Fumigation (F)
Fumigation is one of the most widespread ways of controlling pests in storage and
transportation, pests and diseases in sheltered ground, planting stock and valuable citrus crops
and tea. Fumigation is very effective method because the toxicant vapours (gases) together with
the air penetrate very well into various porous materials, cracks, and minute openings. The main
kinds of fumigation are:
1) Fumigation of premises (stores, elevators, granaries, grain, etc.). Example, chloropicrin.
2) Chamber fumigation (seeds, fruits, bulbs, planting stocks, etc.). Use gas masks, e.g., to
protect oneself from methyl bromide.
3) Tent fumigation (used for valuable trees and shrubs). Example, hydrogen cyanide in citrus
stock.

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4) Greenhouse fumigation. Example, in sheltered soil structures.
5) Fumigation of the soil to a depth of 18 – 20 cm.

10.5.4. Advantages and Disadvantages of Chemical Control

1) Advantages of Chemical Control

a) Fungicides can inhibit germination, growth, and multiplication of pathogens as contact or
systemic chemicals.
b) Chemicals show very quick results in controlling plant diseases (protectants, eradicants,
fumigants)).
c) Chemicals are used to disinfect stores, soils and are as protectants of planting materials such
as seeds.
d) Fungicides can be employed in prophylactic (preventive) programmes.

2) Disadvantages of chemical control

a) Pesticides are, in general, expensive; their application is also labour and time-consuming.
b) They (pesticides) require trained personnel for application and costs for pesticide applicators
are required.
c) Development of pesticides requires a long time and high resources.
d) Most chemicals used in crop protection are toxic to human beings and animals, i.e., they are
not environment friendly or safe, e.g. residue problems. They pose blastogenesis,
carcinogenesis, mutagenesis, teratogenesis, nephrogenesis, etc.
e) Some chemicals are not convenient for storage, i.e. they could be flammable, corrosive to
metal containers, volatile, or may have short shelf life.
f) Some chemicals have phytotoxicity problems to sensitive plants.
g) Some pathogens and pests can develop resistance to the chemicals and make them useless for
future use.
h) Others.

10.5.5. Safety Precautions

1) Toxicity Classification of Pesticides (Oral Toxicity)

a) Powerful toxicants: LD50 up to 50 mg/kg body weight
b) Highly toxic substances: LD50 equals 50 –200 mg/kg
c) Moderately toxic substances: LD50 equals 200 – 1000 mg/kg
d) Slightly toxic substances: LD50 over 1000 mg/kg

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2) Safety Measures in Storing, Dispensing and Transportation of Pesticides
Chemical pesticides should not be stored closer than 200 m from residence and livestock
buildings, water supply, and not closer than 2000 m from water bodies for fishing. The chemical
stores should be fenced for safe and secure keeping. The roofs of chemical stores should be in
good order and the floors paved with asphalt or cement. The stores should have racks, windows
and forced ventilation. Such a store should have two rooms: one for storing and issuing the
pesticides, and the second for keeping documents, garments, medicine kits, soap, and water.

The stores should be reliably locked. The containers of toxicants must be marked with warning
stripes:
Black = for insectoacaricides and nematicides
Blue = for disinfectants
Green = for fungicides
Red = for herbicides
White = for defoliants
Yellow = for zoocides (rodenticides)

Issuing and receiving toxicants is performed with the use of protective means. It is prohibited to
take food, smoke, or work without protective outer garments, at a store. A toxicant is issued
from the store according to a written order of the head of the farm, his/her deputy, to the person
responsible for performing the work with toxicants. It is strictly forbidden to issue toxicant to
unauthorized persons. The residues of pesticides prohibited for use in agriculture or unfit for use
are destroyed in accordance with special instructions. It is strictly prohibited to store or carry
pesticides together with food products or commodities. Safety measures when using pesticides
are aimed at preventing the poisoning of the workers by the toxicants, contamination of the
environment, and the contact of outsiders and animals with the pesticides. Special attention
must be given to the strict observance of the safety rules when working with virulent, highly
toxic, and volatile pesticides.

3) Personal Hygiene Rules for Workers

a) Workers handling chemical pesticides must perform with great care, special attention and
precision.
b) Strictly observe instructions and personal hygiene rules.
c) Do not drink, eat or smoke while handling or working with pesticides or in the chemical
stores and premises.

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d) The person dealing with chemicals should eat food that is rich in proteins, vitamins, starch,
and gelatin to diminish irritating action of chemicals.
e) Take food before beginning work with toxicants. This reduces the harmful effects of
chemicals substances that may enter the blood system. The breakfast and lunch should
contain an adequate amount of liquid (soup, milk, stewed fruit, tea), not very salty food.
Avoid fats and spicy foods. Use food rich in animal proteins (meat, cheese, fish), calcium
salts, and vitamin B2 (riboflavin), vegetables, fruits, green, porridge, and vitamin C; sugar,
honey, beef, etc. N.B. The kind of food to take or to avoid depends on the type of toxicants.
f) Persons working with toxicants must wash their hands and face with soap and rinse their
mouths before eating. After finishing work, they must take showers.
g) To prevent pesticides from getting into their organs through skin, respiratory organs, and
mucous membranes, all workers must be provided with means for individual protection.
Special clothing, gloves, and boots are used to protect the skin. When working with dusty
substances, one must use overalls of a dustproof fabric with a smooth surface. When
spraying liquid pesticides, one must use clothing made from acid-proof fabrics or dust proof
overalls with a film coated apron and arm sleeves made from a rubberized fabrics. To
prevent the eyes from pesticides, one must use hermetic goggles. Antidust or antigas
(universal) respirators and gas masks are used to protect the respiratory organs.

10.6. Integrated Control of Plant Diseases

An integrated plant disease control is an approach that attempts to use all available methods of
control of a disease or of all the diseases and pests of a crop plant for best control results but
with the least cost and least damage to the environment. Integrated disease control is a
combination or integration of all effective, economical and environmentally safe practices and
includes use of resistant varieties, chemical control, biological control, cultural practices,
regulatory methods and physical methods, maintaining the disease below that causing economic
injury level. Use of resistant varieties, clean planting, materials, eradication measures (seed
treatment, crop rotation) and biological control have important role in integrated control.

The goals of integrated plant disease control includes:

1) Elimination or reduction of the initial inoculum
2) Reduction of the effectiveness of initial inoculum
3) Increase in the resistance of the host
4) Delaying the onset of disease
5) Slowing down of the secondary of secondary cycles

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In an integrated disease control programme, several control methods are employed including:
1) Regulatory inspections for healthy seed or nursery stock production
2) Cultural practices (crop rotation, sanitation, pruning)
3) Biological control (biocontrol agent – antagonism)
4) Physical control (storage temperature)
5) Chemical control (soil fumigation, seed or nursery stock treatment, sprays, disinfestations
of cutting tools, crates, warehouses, and washing solutions)

A) Integrated Control in Annual Crops

1) Use resistant variety (varieties) if available.
2) Start with healthy stock and plant it in a suitable field. Starting with clean, disease-free seed
is of paramount importance. Use of certified seed produced under strict quarantine and
inspection rules is a guarantee for freedom from any pathogens. The healthy seed should be
treated with a fungicide (bio-control agent) and must be planted in a field free of the major
pathogens of the specific crop.
3) Use crop rotation that includes legumes or other unrelated crops (non-host) and reduce the
pathogen populations in the soil.
4) Destroy crop residues that may serve as sources of inocula for the next cropping season. The
residues may be sprayed with effective chemicals. Use disinfected tools and fumigate the soil,
if possible.
5) Adjust your planting time and properly drain the field to reduce diseases such as damping-off
and root rots.
6) Spray the crop with appropriate fungicides as soon as the disease appears or even before, and
continue the sprays throughout the growing season as necessary. If insect vectors are
responsible for the pathogen transmission, you have to spray the appropriate insecticide. Use
weather data to forecast disease appearance and development. This can help you to spray at
the right time without wasting any sprays.
7) Harvest crops carefully avoiding wounding that would allow the development of storage rot
fungi. Sorting may be necessary in some crops to discard damaged ones.
8) Store your harvested crops in clean and disinfected storage rooms. Frequent inspection of the
stores, ventilation of storage and taking any other appropriate measures avoids storage losses.

B) Integrated Control in Perennial Crops

1) First consider the nursery stock to be used and select carefully the location where it is going
to be planted. Both the rootstock and scion must be free of any pathogens if the nursery stock

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 is susceptible to the problematic pathogen(s) in the area. Nursery stock should be inspected
and certified. If nematodes are suspected, heat-treat the stock and plant them in disease free
areas. You may disinfest the soil with fumigants before planting if it is already infested. Use
resistant varieties as scions.
2) Check and improve drainage of the soil. Site selection is very important in this connection.
Do not plant seedlings on sites previously occupied by similar crops, or do not plant seedlings
next to old trees that are heavily infected with a virulent pathogen.
3) Strengthen the newly planted seedlings by fertilizing, irrigating, pruning, and spraying
against diseases, and insects to produce vigorous plants free of infections. Remove or rogue
seedlings infected by systemic diseases.
4) Apply disease control measures starting at fruit harvesting or during pruning operations. This
reduces the inoculum potential. Raking of infected leaves, fruits, or twigs from the orchard
floor can reduce the pathogen. Spraying fungicides or application of bio-control agents can do
the job. Disinfect pruning shears and saws before moving to new trees and avoid
contamination or spread of pathogen. You can spray pruned trees with fungicides such as
benomyl. To protect blossoms and leaves from infection, spray them with appropriate
chemicals such as fungicides, bactericides, or their mixtures. You use systemic fungicides for
more efficacy. In case of contact fungicides, spraying may be repeated every 3 to 5 days. Use
of weather data is very important to schedule the spray programme. Fruit must be sprayed
every 10 to 14 days until harvesting to control fruit rotting fungi.
5) Avoid wounding of fruits during harvesting and handling to prevent fungal infections.
Harvesting baskets should be clean and free of rotten debris that may harbour fruit rotting
fungi. Fumigate the warehouse with formaldehyde, SO2, or another fumigant. Wash the fruit
with solution containing a fungicide or a biological control agent to protect the fruit during
storage and transportation. Sort the fruits and discard injured or infected ones. Keep fruits
under refrigerated conditions during storage, transportation or marketing.

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11. Biotechnology and Plant Pathology (1 lecture hour)

Biotechnology is composed of a continuum of technologies, ranging from traditional

biotechnology to modern biotechnology. In this context, biotechnology is defined as “any
technique that uses living organisms, or substances from those organisms, to make or modify a
product, to improve plants or animals, or to develop micro-organisms for specific uses”.

In modern terms, biotechnology is defined as ‘the manipulation, genetic modification, and

multiplication of living organisms through novel technologies, such as tissue culture and genetic
engineering, resulting in the production of improved or new organisms and products that can be
used in a variety of ways’. Traditional biotechnology covers well established and widely used
technologies based on the commercial use of living organisms. Modern biotechnologies
encompasse the uses more recently developed technologies, particularly those based on the use
of: recombinant DNA technologies; monoclonal antibodies; and new cell and tissue culture
techniques, including novel bio-processing.

Genetic engineering
of plants
Genetic engineering of animals
Genetic engineering to improve
rhizobia
Genetic engineering to develop
animal vaccines

Genetic engineering of biocontrol

agents against plant pests
and diseases
Use of recombinant DNA for diagnostics for plant and
animal diseases
Plant protoplast
fusion Monoclonal antibody production

Plant tissue culture

Biological nitrogen fixation: Collection, selection, and production of
appropriate strains of bacteria

Figure. Biotechnology continuum, from traditional biotechnologies to modern biotechnologies

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Biotechnology as applied to crop production is concerned with:
1. Agricultural microbiology, to produce beneficial to crop production
2. Cell and tissue culture, including the rapid propagation of useful micro-organisms and
plant species
3. New techniques, based on the use of monoclonal antibodies and nucleic acids probes, for
diagnosing plant pests and diseases and detecting foreign chemicals in food
4. Genetic engineering of plant species to introduce new traits
5. New genetic mapping techniques, based on the use of restriction fragment length
polymorphisms (RFLPs), as an aid to conventional plant breeding programmes

11.1. Application of Biotechnology

Plant biotechnology is based on a thorough understanding of plant molecular biology, on the use
of a variety of plant tissue culture techniques, and on our ability to identify, isolate, and transfer
specific genes from one kind of organism (plant) to another plant or organisms.

Plant biotechnology impinges upon plant pathology in several ways. The most obvious of these
ways are discussed in the following paragraphs.
1) Increased production of plants through rapid clonal propagation is likely to result in a greater
need to obtain pathogen-free mother plants and subsequently protect daughter plants from
pathogens.
2) New plant varieties to which genes have been added through genetic engineering are likely
to exhibit greater or unexpected instability toward certain unpredictable sets of
environmental conditions and toward the pathogenic microflora of their habitats.
3) The main vehicles for moving genes from donor plants or other organisms to percipient
plants are plant pathogens, particularly the bacterium Agrobacterium tumefaciens and
cauliflower mosaic virus, while several viruses are being further developed as vectors.
4) The study of plant genes for resistance to disease and of pathogen genes for virulence to
pathogens is already aided considerably by genetic engineering and is expected to be
greatly advanced by it in the future.
5) Control of many plant diseases is likely to come about either by inserting resistance genes
into plants by genetic engineering techniques, or by genetically engineering micro-
organisms that can effectively antagonize or compete with particular pathogens.

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11.2. Tissue Culture Techniques of Significance to Plant Pathology
Almost all tissue culture techniques used by plant scientists are of importance to plant pathology.
Some of them, for example, plant micropropagation, carry with them the danger of disseminating
pathogens, or conversely, they are used to produce pathogen-free plants. More importantly,
however, many of them can be used to study, locate, and isolate the genes of resistance to certain
pathogens, and others are used for modification and transfer of such genes to susceptible plants.

The most important tissue culture techniques and their importance to plant pathology are:
1) Rapid clonal propagation in culture
2) Callus and single-cell culture
3) Plant protoplast
4) Haploids

Genetic Engineering Techniques of Importance to Plant Pathology

These include the following major plant genetic engineering techniques:

1) Plant molecular biology
2) Molecular biology of plant pathogens
3) Gene cloning
a) Cloning complimentary DNA from m RNA
b) Cloning genes from Genome DNA
c) Expression of Cloned Genes
d) Vectors used for Gene Cloning in Plants

11.3. Role of Biotechnology and Information Technology in Plant Pathology

Now numerous laboratories throughout the world are cloning, mapping, and studying the genes
of several plant pathogenic bacteria. Similar studies are revealing the number, kinds, and
regulation of the genes of several plant viruses. Work has just begun to clone genes of plant
pathogenic fungi and to study their physical structures, metabolic functions, and mechanisms of
regulation. Once the genes have been identified and isolated, it will be possible to manipulate
them, modify them, transfer them, study their communication with the host genes, and eventually
inhibit them or neutralize them. Once known and available, genes for virulence or inhibition may
be transferred to micro-organisms antagonistic to pathogens, which then may be used on plant
surfaces to protect plants from the pathogens.

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In addition to the study of the virulence genes of pathogens, knowledge of the nature and
expression of host genes for resistance is likely to produce the greatest dividends of
biotechnology to plant disease control. Plants can be genetically engineered to be resistant to
antibiotics effective against certain pathogens and therefore not injured when treated to control
the disease. Genetically engineered bacteria or viruses (bacteriophage) can be sprayed on plants
to prevent frost injury. All such breakthroughs are just the beginning of biotechnology and we
expect more miraculous advances to follow soon in biotechnology.

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12. Introduction to Major Plant Diseases (7 lecture hours)

12.1. Damping-off and Root Rots (1 lecture hour)

12.1.1. Damping-off
Damping-off diseases are characterized by rapid death and collapse of very young seedlings.
Plant diseases leading to root rots and damping-off are caused by different types of micro-
organisms. The invasion of tissues involves the degradation of the cell wall constituents (mostly
pectic substances and cellulose) of the host. Pathogens capable of forming the pectolytic and
cellulolytic enzymes (especially the former) are, therefore, associated with such diseases.
Damping-off disease results in collapse and death of young seedlings. Damping-off at pre-
emergence stage kills the seedlings before their emergence over the soil surface, with complete
rotting of radicle and plumule when they come out of the seed. High moisture content of soil and
excessive organic matter accompanied by high temperature usually favour such diseases. The
familiar damping-off is the one that manifests its symptoms at post-emergence stage. Infection is
usually initiated at ground level and soft water-soaked areas appear on the young stems. The stem
rots then get constricted and finally collapse.

Generally fungi like Pythium, Phytophthora, Sclerotinia, Thielavia, Glomerella, Fusarium,

Rhizoctonia, Phoma, and Ozonium are responsible for such diseases. Sometimes, species of
Botrytis, Cylindrocladium, and Dipolodia have also been associated with damping-off diseases.

The control measures mainly comprise the use of seed protectants to avoid pre-emergence
infection. Proper aeration of soil and good hygienic conditions are helpful in reducing the post-
emergence infections.

12.1.2. Root Rots

Root rot refers to disintegration or decay of part or all of the root system of a plant. Several
ascomycetous fungi attack primarily the roots and lower stems of plants. Some, such as
Cochliobolus, Gibberella, and Gaeumannomyces, attack only cereals and grasses. A few, such as
Sclerotinia and Diplodia, contain some species that attack cereals and grasses while other species
cause severe diseases on several vegetables and field crops. A third group of soil-borne fungi,
such as Fusarium solani, Leptosphaeria, Phymatotrichum, and Thielaviopsis, cause root and
lower stem rots of many vegetables, ornamentals, field crops, and even trees.

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As a general rule, the root and stem rot diseases caused by these and by other soil-borne
Ascomycetes and Fungi Imperfecti appear on the affected plant organs at first as water-soaked
areas that later turn brown to black. The roots and stems are killed or is killed. The fungi that
cause these diseases are nonobligate parasites that live, grow, and multiply in the organic matter.
These fungi are favoured by high soil moisture and high relative humidity in the air. Most of
them produce conidia, and some produce ascospores occasionally or regularly. Several produce
sclerotia. In all of the above fungi the fungus can over-winter as mycelium in infected plant
tissues or debris, as sclerotia, or as spores. These stages also serve as inoculum that can be spread
and start new infections. Considerable progress has been made in biological control of several
root and stem rot fungi by treating the seed with antagonistic fungi and bacteria.

12.1.3. Galls and Root Knots

Several fungi, bacteria, viruses, nematodes, and insects are capable of stimulating excessive
localized outgrowths in plant cells. Usually, these areas of stimulated growth have richer pools of
metabolites from which the organisms draw materials for their growth and development. Galls
are developed practically on all the plant parts. Formation of galls is accompanied by cell
enlargement as well as by rapid cell division that, in turn, are dependent upon specific substances
that may be synthesized by such cells.

There are different pathogens that produce plant diseases identified by gall formation. Examples:
Club root disease of cabbage (Plasmodiophora brassicae), wart disease of potato (Synchytrium
endobiotricum), stem gall of coriander (Protomyces macrosporus), and crown gall of stone fruits
(Agrobacterium tumefaciens). Galls are also produced on stems and roots of plants infected
primarily by bacteria of the genus Agrobacterium and Rhodococcus. The galls may be
amorphous, consisting of overgrowth of more or less unorganised or disorganized plant tissues,
as are most Agrobacterium and Pseudomonas galls, or they may be proliferations of tissues that
develop into more or less organized, teratomorphic organs, as are some Agrobacterium and
Rhodococcus galls (fasciations or leafy galls). Rhizobacter also causes galls.

All sanitary precautions should be adopted. Clean and healthy stocks should be used. Grafting
knife should be frequently sterilized. Certain antibiotics like penicillin and vancomycin have been
found to be effective in inhibiting the galls.

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Several cultivated and wild plants suffer from root knot disease. This is caused by nematodes
belonging to the genus Meloidogyne. Infection results in reduced growth of the host, sudden
wilting and formation of galls on the roots, which may result in their clubbing. The infection is
initiated by larval penetration in large numbers, due to which, while growth along the pith is
arrested, the cortical cells enlarge considerably to form giant cell. Sometimes, cell walls of
adjacent cortical cells may disintegrate. The mature female nematode is embedded in the plant
tissues while the eggs are commonly found to be clinging to the surface of the roots. When the
eggs hatch, young larvae may again penetrate the young roots just below the growing point. The
enlarged cells of the host contain 6 – 20 nuclei, although in certain plants, the giant cells may
contain up to 500 nuclei. Often the galls may show severe rotting due saprophytic organisms.
Larvae of Meloidogyne may act as vectors for certain soil fungi like Fusarium and Pythium.

The females and the larvae survive in soil and on plant debris. Their concentration decreases with
the depth of the soil. In light sandy soil they may be present up to 20 cm deep. Various biotic and
environmental factors influence their population and action. Root exudates also play a decisive
role in attracting the larvae. Under normal conditions only females are produced and they
reproduce parthenogenetically. When the food supply is scarce, and the concentration of the
larvae in the cells is high, formation of male nematodes takes place.

Some of the important root knots caused by the species of Meloidogyne are as follows:
1. Root knot of potato and tomato (Meloidogyne hapla)
2. Root knot of wheat, barley, groundnut (M. arenaria)
3. Root knot of sugarcane, garden balsam (M. javanica)
4. Root knot of coffee (M. exigna)

The species of Melodogyne have a wide host range; therefore, rotation of crop is not to be of
much advantage for controlling the disease. Application of soil fumigants, after destruction of
root residues, eliminates infection to a considerable degree. Simple ploughing of the fields twice
or thrice during summer months also helps in reducing the incidence of disease. In nature, there is
possibility of some biological interference. Roots of Tagetes have been reported to have toxic
effect on certain species of Meloidogyne. More than fifty predators and parasites of Meloidogyne
that attack pineapples in Hawii have been counted. Majority of them were fungi and other
nematodes.

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12.2. Stem and Branch Diseases (1 lecture hour)

12.2.1. Stem Rusts

Rusts, in general, refer to diseases characterized by many small lesions on leaves or stems,
usually of a rusty colour. Stem rust occurs on many grasses and cereal-grain crops, including
wheat, barley, oats, and rye. The disease is distributed throughout the world wherever susceptible
plants are grown. In diseased cereals, chloranemic flecks develop in leaves, leaf sheaths, and
stems. Soon after the beginning of disease, the fungus produces sori that bear uredospores, which
are red in mass. The stalked uredospores break through the cuticle in the infected areas. These
pustules (uredia) may be a quarter of an inch or more in length and frequently run into one
another. They burst early exposing a brown powder (consisting of the uredospores) and
surrounded by prominent white epidermal fringes. Later, the sori become black, owing to the
production of teliospores, which have dark, thick, walls. The leaves of diseased plants die
prematurely; diseased plants are dwarfed, therefore, their production of grain is reduced.

Stem rust fungi polymorphic (macrocyclic, long-cycle fungi), showing different stages in the life
cycle, each stage being characterized by its spore form as follows:
________________________________________________________________
Stage Spore type Fruiting body
O= Pycniospores (spermatia) (pycnium, spermogonium)
I= Aeciospores (Aecium, aecidium)
II = Uredospores (Uredium, uredosorium)
III = Teliospores (teleutospores) (Telium, teleutosorium)
IV = Sporida (Basidium)____________

The stem rusts of cereals include Puccinia graminis tritici (wheat), P. g. hordei (barley), and P.
g. avenae (oats).
The most effective, and the only practical, means of control of stem rust is through the use of
varieties resistant to infection by the pathogen. A tremendous effort is now directed toward
development of varieties with general or non-specific resistance and toward development of
multilane cultivars. Eradication of the alternate host barberry in the temperate regions reduces
losses from stem rust by eliminating the early season infections on hosts in the areas where
uredospores cannot overwinter.

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Several fungicides, such as sulphur, zineb, and mixtures of zinc ion with maneb, can effectively
control stem rust. Two applications of zinc ion – maneb mixtures, coordinated with forecast of
weather conditions favouring rust epidemics, may reduce damage from stem rust by as much as
75%. These chemicals have both protective and eradicative properties. Certain systemic
fungicides, such as fenapanil, triarimol, and especially triadimefon, also control stem rust when
applied as one or two sprays 1 to 3 weeks apart during the early stages of disease development.
Seed treatment with triadimenol inhibits early but not late season infections.

Damage by the stem rust fungus is usually lower in fields in which heavy fertilization with nitrate
forms of nitrogen and dense seeding have been avoided.

12.2.2. Cankers
Cankers are localized wounds or dead areas in the bark of the stem or twigs of woody plants that
often sunken beneath the surface of the bark. In some cankers, the healthy tissues immediately
next to the canker may increase in thickness and appear than the normal surface of the stem.
Innumerable kinds of pathogens cause cankers on trees. The most common causes of tree cankers
are ascomycetous fungi, although some other fungi, some bacteria, and some viruses also cause
cankers.

The basic characteristic of cankers is that they are visible dead areas that develop in the bark and,
sometimes, in the wood of the tree. Cankers generally begin at a wound or at a dead stub. From
that point, they expand in all directions but much faster along the main axis of the stem, branch,
or twig. Under some environmental conditions, the host may survive the disease by producing
callus tissue around the dead areas and thus limiting the canker. In infections of large limbs,
concentric layers of raised callus tissue may form. If, however, the fungus grows faster than the
host can produce its defensive tissues, either no callus layers form and the cankers appears
diffuse and spreads rapidly, or the fungus invades each new callus layer and the canker growers
larger each year. Young twigs are often girdled by the canker and killed soon after infection, but
on larger limbs and stems cankers may become up to several meters long, although their width
extends to only part of the perimeter of the limb. Eventually, however, the limb or entire tree may
be killed through girdling either by the original canker or by additional cankers that develop from
new infections caused by the spores from the original canker.

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Cankers are generally much more serious on fruit trees such as apple and peach, which they
debilitate and kill. On forest trees, cankers deform but do not kill their hosts. They do, however,
reduce tree growth and the quality of lumber, result in greater wind breakage, and weaken the
trees so that other more destructive wood- or root-rotting fungi can attack the trees.
Although most canker-causing fungi are Ascomycetes, only some of them produce their sexual
stage regularly. The other canker fungi produce primarily conidia, usually in pycnidia embedded
in the bark, and only occasionally do they produce perithecia. Some of the canker-producing
fungi and their most important host plants are as follows:

1) Botrysphaeria dothidea (cankers on apple, peach, etc.)

2) Ceratocystis fimbriata (Cankers on cacao, coffee, stone fruits, etc.)
3) Eutypa armeniacae (Dieback in grapevines)
4) Gremmeniella abietina (Canker on conifers)
5) Nectria galligena (Cankers on apple, pear, and many forest trees)
6) Urnula craterium (Cankers on forest trees)
7) Leucostoma spp. (Vlasa spp., Cytospora spp.) (Cankers on peach, many other
fruits trees, and more than 70 species of hardwood trees).

Bacteria can cause a relatively few canker diseases of plants, but some of them are widespread
and devastating. The bacteria and the most important cankers they cause are the following:
1. Pseudomonas, causing the bacterial canker of stone fruits and pome fruits
2. Xanthomonas, causing the bacterial canker of citrus
3. Clavibacter michiganense, bacterial canker of tomato

Control measures for cankers include good cultural practices: watering and fertilization to keep
the trees in good vigour; avoiding wounding and severe pruning of trees; removing cankers from
trunks and large branches during dry weather and treating the wound and all pruning cuts with a
disinfectant and a wound dressing; removing and burning cankered and dead branches and twigs;
pruning as late in the spring as possible; and spraying with benomyl immediately after pruning
and before it rains.

12.2.3. Diebacks
Diebacks are extensive necrosis of twigs beginning at their tips and advancing towards their
bases. Dieback is characterized by dying back of terminal twigs, almost invariably of those that
have borne inflorescence. Acute dieback manifests by sudden dying back of an entire branch and

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leaves dry up on the trees to a conspicuous russet-red colour. The branches attacked can be of any
size and occasionally the attack can be in the main trunk in which case leads to the death of the
tree. When the branch showing dieback is cut open at the point between the dead and living
tissues, a red-brown discoloration is seen in the affected tissues.

Several factors can cause dieback in plants. They could be organic or inorganic agents.
Unfavourable soil conditions, high temperature, drought or improper cultural practices can
initiate diebacks. Rodents, insect pests such as termites that can attack the roots can be
responsible for the diebacks. Pathogenic micro-organisms including fungi, bacteria, and
nematodes can cause diebacks. Plantation trees usually suffer from dieback. The coffee tree, for
example, usually suffers from diebacks caused by various micro-organisms.

The remedies for dieback depend on the diagnoses of the real cause(s) of the diebacks and taking
appropriate correction measures.

12.3. Foliar Diseases (2 lecture hours)

12.3.1. Downy Mildews
Downy mildew refers to a plant disease in which the sporangiophores and spores of the fungus
appears as a downy growth on the lower surface of leaves and stems, fruits, etc., caused by fungi
in the family Peronosporaceae. All species of this family are obligate parasites of higher plants
and cause downy mildew diseases on a large number of plants including most of the cultivated
grain crops and vegetables, and many field crops, ornamentals, shrubs, and vines.

The downy mildews are primarily foliage blights that attack and spread rapidly in young, tender
green leaf, twig, and fruit tissues. Their development and severity depend greatly on the presence
of a film of water on the plant tissues and on high relative humidity in the air during cool or
warm, but not hot, periods. The downy mildews can cause severe losses in short periods of time.
The best known of the downy mildew epidemics is probably the one caused by the downy
mildew of grapes in 1875, which almost completely destroyed the grape and wine industry in
France and most of the rest of Europe and resulted in the discovery of the first fungicide,
Bordeaux mixture, in 1885.

The downy mildew fungi produce sporangia on sporangiophores that branch in ways distinctive
for the fungus. The sporangia are located at the tips of the branches. The sporangiophores are
usually long, white at first, emerging in groups from the plant tissues through the stomata. Later

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on they appear grayish or light brown and form a visible mat of fungus growth on the lower or
both sides of leaves and on other affected tissues. Each spodrangiophore grows until it reaches
maturity and then produces its crop of sporangia, all at about the same time.

In most downy mildews, the sporangia germinate generally by producing zoospores or, at higher
temperatures, by producing germ tubes. In the genus Bremia, however, the sporangia germinate
most commonly by means of a germ tube, and in genera Peronospora and Peronosclerospora the
sporangia germinate only by means of a germ tube. Whenever sporangia germinate by producing
a germ tube, they are considered spores in themselves rather than sporangia, and in that case they
are often called conidia, which always germinate by germ tubes. The oospores of the downy
mildews usually germinate by germ tubes, but in a few cases they may produce a sporangium that
releases zoospores.

Some of the most common or most serious downy mildews are caused by the following fungi:
1) Bremia lactucae (Downy mildew of lettuce)
2) Peronospora destructor (Downy mildew of onion)
3) Peronospora effusa (Downy mildew of spinach)
4) Peronospora tabacina (Blue mould, downy mildew of tobacco)
5) Peronospora trifoliorum (Downy mildews of alfalfa and clover)
6) Peronosclerospora sorghi (Downy mildew of sorghum)
7) Peronosclerospora maydis (Downy mildew of maize)
8) Peronosclerospora sacchari (Downy mildew of sugarcane)
9) Plansmopara viticola (Downy mildew of grapevines)
10) Pseudoperonospora halstedii (Downy mildew of sunflower)
11) Pseudoperonospora cubensis (Downy mildew of cucumber)
12) Sclephthora macrospora (Downy mildews of cereals: maize, wheat, rice; and
grasses)
13) Sclerospora graminicolla (Downy mildew of grasses and millets)

In most downy mildews, the pathogen routinely causes systemic shoot infection of its host when
it is carried in the seed or bulb, or when infection takes place at the seedling or young plant stage.
When organs of older plants are attacked they may develop localized, although not necessarily
small, infected areas, or they may allow the fungus to spread into young tissues and become
locally systemic. The downy mildews often cause rapid and severe losses of crop plants still in

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the seedbed or in the field. They often destroy from 40 to 90 percent of the young plants or young
shoots in the field, causing heavy or total losses of the crop yields. The amount of losses depends
on the prolonged presence of wet, cool weather during which the downy mildew fungi sporulate
profusely, cause numerous new infections, and spread into and rapidly kill young succulent
tissues. The spread and destructiveness of downy mildews in cool, wet weather are often
uncontrollable, checked only when the weather turns hot and dry.

Since the 1980s, however, several systemic fungicides, such as metalaxyl, propamocarb, and
fosetyl-Al, have improved considerably our ability to control these diseases, although downy
mildews are still very difficult to control.

12.3.2. Powdery Mildews

Powdery mildews are characterized by the appearance of spots or patches of a white to grayish,
powdery, mildewy growth on young plant tissues, or of entire leaves and other organs being
completely covered by the white mildew. Tiny, pinhead-sized, spherical, at first white, later
yellow-brown, and finally black cleistothecia may be present singly or in groups on the white to
grayish mildew in the older areas of infection. Powdery mildew is most commonly observed on
the upper side of the leaves, but it also affects the underside of leaves, young shoots and stems,
buds, flowers, and young fruits.

The fungi causing powdery mildews are obligate parasites: they cannot be cultured on artificial
nutrient media. They produce mycelium that grows only on the surface of plant tissues, never
invading the tissues themselves. They obtain nutrients from the plants by sending haustoria
(feeding organs) into the epidermal cells of the plant organs. The mycelium produces short
conidiophores on the plant surface. Each conidiophore produces chains of rectangular, ovoid, or
round conidia that are carried by air currents. When environmental conditions or nutrition
become unavailable, the fungus may produce cleistothecia containing one or a few asci. The
powdery mildew fungi, although they are common and cause serious diseases in cool or warm,
humid areas, are even more common and severe in warm, dry climates. This happens because
their spores can be released, germinate, and cause infection even when there is no film of water
on the plant surface as long as the relative humidity in the air is fairly high. Once infection has
begun, the mycelium continues to spread on the plant surface regardless of the moisture
conditions in the atmosphere.

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Powdery mildews are so common, widespread, and ever present among crop plants and
ornamentals that the total losses, in plant growth and crop yield, they cause each year on all crops
probably surpass the losses caused by any other single type of plant disease. Powdery mildews
seldom kill their hosts but utilize their nutrients, reduce photosynthesis, increase respiration and
transpiration, impair growth, and reduce yields, sometimes by as much as 20 to 40 percent.
Among the plants most severely affected by powdery mildews are the various cereals, such as
wheat, and barley, primarily because in these crops chemical control of plant diseases in difficult
or impractical. Other crops that suffer common and severe losses from powdery mildew are the
cucurbits, especially squash, and cucumber; sugar beets; strawberries; clovers; many ornamentals
such as rose, begonia; grape; many trees, particularly apple, and oak.

The powdery mildew diseases of the various crops or other plants are caused by many species of
fungi of the family Erysiphaceae grouped into seven main genera. These genera are distinguished
from one another by the number (one versus several) of asci per cleistothecium and by the
morphology of hyphal appendages growing out of the wall of the cleistothecium. The main
genera of powdery mildew fungi and the corresponding diseases caused include:

1) Erysiphe cichoracearum (Powdery mildews of begonia, chrysanthemum, cucurbits, dahlia)

2) Erysiphe polygoni (Powdery mildews of legumes, beets, crucifers, and cucurbits)
3) Blumeria graminis (Powdery mildews of cereals and grasses)
4) Microsphaera alni (Powdery mildews of many shade trees, and woody ornamentals)
5) Phyllactinia sp. (Powdery mildew of shade and forest trees)
6) Podosphaera sp. (Powdery mildew of apple and pear)
7) Podosphaera oxyacanthae (Powdery mildew of peach, etc.)
8) Sphaerotheca macularis (Powdery mildew of strawberry)
9) Sphaerotheca pannosa (Powdery mildew of peach and rose)
10) Uncinula necator (Powdery mildew of grape)

The control of powdery mildews in cereals and several other annual crops has been primarily
through the use of resistant varieties but, more recently, also with systemic fungicides such as
ethirimol, triadimenol, and triforine used as seed treatments, or prochloraz, triadimefon,
tridemorph, and triforine, and others, used as foliar sprays. The same chemicals are used for
control of powdery mildews in other crops and ornamentals, although elemental sulfur and
dinocap have been and still are extensively and effectively. Powdery mildews on trees, such as

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apple, are effectively controlled with sprays of any of several sterol-inhibiting systemic
fungicides such as triadimefon, etaconazole, bitertanol, and triforine. Powdery mildews have also
been controlled experimentally with sprays of phosphate salt solutions and detergents or ultrafine
oils.

12.3.3. Leaf Rusts

The plant rusts, caused by Basidiomycetes of the order Uredinales, are among the most
destructive plant diseases. They have caused famines and ruined the economies of large areas,
including entire countries. They have been most notorious for their destructiveness on grain
crops, especially wheat, oats and barley, but they also attack vegetables such as bean, and
asparagus, field crops, such as cotton, and soybeans, and ornamentals, and have caused
tremendous losses on trees such as apple and coffee.

The rust fungi attack mostly leaves and stems. Rust infections usually appear as numerous rusty,
orange, yellow, or even white-coloured spots that rupture the epidermis. Some form swellings
and even galls. Most rust infections are strictly local spots, but some may spread internally to
some extent. There are about 5000 species of rust fungi (including both stem and leaf rusts). The
most important leaf rusts of crops include:

1) Puccinia recondita (Leaf or brown rust of wheat and rye)

2) Puccinia hordei (Leaf rust of barley)
3) Puccinia coronata (Crown rust of oats)
4) Puccinia sorghi (Maize leaf rust)
5) Puccinic polysora (Southern maize leaf rust)
6) Puccinia purpurea (Sorghum leaf rust)
7) Puccinia sacchari (Sugarcane leaf rust)
8) Puccinia melanocephala (Sugarcane leaf rust)
9) Puccinia stakmani (Leaf rust of cotton)
10) Puccinia asparagi (Rust of asparagus)
11) Hemileia vastatrix (Coffee leaf rust)
12) Phragmidium bulbosum (Leaf rust on rose and yellow rust on raspberry)
13) Uromyces appendiculatus (Leaf rust of legumes)
14) Cronartium ribicola (White blister pine rust on pines)
15) Melampsora lini (Leaf rust of flax)

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16) Gymnoconia sp. (Rust of blackberry and raspberry)
17) Phakopsora pahyrhizi (Soybean rust)
18) Transzchelia sp. (Peach leaf rust)

The rust fungi spread from plant to plant mostly by windblown spores, although insects, rain and
animals may play a role. Some of their spores (uredospores) are transported over long distances
(several hundred kilometres) by strong winds and on landing (being scrubbed from the air by
rain), can start new infections.

Control of rust diseases in some crops, such as grains, is achieved by means of resistant varieties.
In some vegetable, ornamental, and fruit tree rusts, the disease is controlled with chemical sprays.
Removal of alternate hosts may avoid hazards from rusts. Effective systemic fungicides such as
triadimefon, triarimol, and fenapanil, can control rust diseases of annual plants as well as trees,
with the chemicals applied as sprays, seed dressings, soil drenches, or injections. Biological
control of rust diseases has been obtained experimentally by application of antagonistic fungi and
bacteria on the surface of the plants, or by prior systemic inoculation of the plants with certain
viruses that make the plants more resistant to rust infection.

12.3.4. Anthracnose, blights and leaf spots

Anthracnoses are diseases of the foliage, stem, or fruits that typically appear as dark colored spots
or sunken lesions with a slightly raised rim or margin. Some twig or branch dieback. In fruit
infections, anthracnoses often have a prolonged latent stage. In some fruit crops, the spots are
raised and have corky surfaces. Anthracnose diseases of fruit often result in fruit drop and fruit
rot.

Anthracnoses are caused by fungi that produce conidia within black acervuli. Four ascomycetous
fungi, Diplocarpon, Elsinoe, Glomerella, and Gnomonia, are responsible for most anthracnose
diseases. They are found in nature mostly in their conidial stage and can perennate as mycelium
or conidia.

Acervuli producing mitosporic fungi used to make up a separate order (Melanconiales) but are
now included in the group Coelomycetes. The most important plant pathogenic fungi that
produce acervuli are Colletotrichum (Gloeosporium), Coryneum, Cylindrosporium, Marssonina,
Melanconium, and Sphaceloma. The following are some of the important anthracnoses caused
various genera.

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 1) Colletotrichum graminicola (anthracnoses of cereals and grasses)
2) Colletotrichum lagenarium (anthracnose of cucurbits)
3) Colletotrichum phomoides (anthracnose or fruit rot of eggplant and tomato)
4) Colletotrichum acutatum (anthracnose of strawberry)
5) Colletotrichum gloeosporioides (crown rot and wilt of strawberry, mango, sweet orange
(Citrus spp.), papaya, avocado, fig, peach, etc)
6) Colletotrichum falcatum (red rot of sugarcane)
7) Colletotrichum circinans (onion smudge)
8) Colletotrichum lindemuthianum (bean anthracnose)
9) Greeneria uvicola (formerly Melanconium fuligenum)-bitter rot of grapes
10) Coryneum (Stigmina), Coryneum beijerynki (now Wilsonmycetes carpophilus)- coryneum
blight, shot hole, or fruit spot of stone fruits like peaches and apricot
11) Diprocarpon rosae (anthracnose of roses)
12) Elsinoe ampelina (anamorph: Elsinoe Sphaceloma ampelinum)- grape anthracnose (bird’s
eye rot
13) Elsinoe veneta (raspberry anthracnose)
14) Elsinoe fawcettii (anamorph: Sphaceloma fawcettii)- Citrus scab disease
15) Sphaceloma perseae (Avocado scab)
16) Glomerella cingulata (Coffee brown blight) and anamorph: Colletotrichum coffeanum
(now Colletotrichum kahawe)- coffee berry disease
17) Colletotrichum orbiculare (anthracnose of cucurbits)

12.3.5. Streaks and Stripes

Good examples of streak include bacterial streak (Xanthomonas translucens) of wheat and
bacterial streak (Xanthomonas campetris pv. holcicola) of sorghum, while stripe can be
represented by sorghum bacterial leaf stripe cause by the bacterium Pseudomonas andropogonis.

12.3.6. Mosaics and Related Plant Viruses

The most common types of plant symptoms produced by systemic virus infections are mosaics
and ring spots. Mosaics are characterized by light-green, yellow, or white areas intermingled
with the normal green of the leaves or fruits, or of lighter coloured areas intermingled with areas
of the normal colour of flower or fruit. Depending on the intensity or pattern of discolorations,
mosaic-type symptoms may be described as mottling, speak, ring pattern, line pattern, vein-
clearing, vein-banding, or chlorotic spotting.

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Plant viruses do not contain any enzymes, toxins, or other pathogenic substances and yet cause a
variety of symptoms on the host. The mere presence of viral nucleic acid or complete virus in a
plant, even in large quantities, does not always cause disease symptoms, since some plants
containing much concentrations of virus than others may show milder symptoms than the latter or
may even be symptom-less carriers.

Viruses generally cause a decrease in photosynthesis through decreases in chlorophyll per leaf,
chlorophyll efficiency, and leaf area per plant. Viruses usually cause a decrease in the amount of
growth-regulating substances (hormones) in the plant, frequently by inducing an increase in
growth-inhibiting substances. A decrease in soluble nitrogen during rapid virus synthesis is rather
common in virus diseases of plants, and in the mosaic diseases there is a chronic decrease in the
levels of carbohydrates in the plant tissues. Respiration of plants is generally increased
immediately after infection with a virus.

Plant viruses are transmitted from plant to plant in a number of ways. Modes of transmission
include vegetative propagation, mechanically through sap, seed, pollen, dodder, and specific
insects, mites, nematodes, and fungi.

Plant viruses may damage any or all parts of a plant and may cause economic losses by reducing
yields and quality of plant products. Losses may be catastrophic, or may be mild and
insignificant. The virus disease severity may vary with the locality and crop variety, and from one
season to the next.

The best way to control virus disease is by keeping it out of an area through systems quarantine,
inspection, and certification. Eradication of diseased plants to eliminate inoculum from the field
may, in some cases, help to control the disease. Protecting plants against the virus vectors may
protect them against certain viruses. Removing weeds that serve as hosts may help, to some
extent, control viral diseases. Use of virus-free seed, tubers, budwood, etc., is the single most
important measure for avoiding viruses of many crops. Breeding plants for hereditary resistance
to viruses is of great importance, and many plant varieties resistant to certain virus diseases have
already been produced. In some host-virus combinations, the disease caused by severe strains can
be avoided if the plants are inoculated first with a mild strain of the same virus, which then
protects the plant from infection by the severe strain of virus, and the process is known as cross-
protection.

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Once in the plant, some viruses can be inactivated by heat. Dormant, propagative organs, are
usually dipped in hot water at 35-54 oC for a few minutes or hours, whereas actively growing
plants are usually kept in greenhouses or growth chambers at 35 to 40 oC for several days, weeks,
or months, after which the virus in some of them is inactivated and plants are completely healthy.
Plants free of virus may be produced from virus infected ones by culture of short tips (0.1 mm to
1 cm or more) of apical and root meristems, especially at elevated temperatures (28-30 oC). Some
compounds (viricides), such as ribavirin, applied as spray or injected into the plant reduce
symptoms drastically and may eliminate the virus from the treated host plant. Fpliaqr application
of certain growth-regulating substances (hormones), such as gibberellic acid, may overcome the
stunting induced by some viruses and may stimulate growth of virus-suppressed axillary buds in
virus infected trees.

12.4. Floral and Seed Diseases (1 lecture hour)

12.4.1. Smuts and Ergot

Smuts refer to seeds or galls filled with the mycelia or black spores of the smut fungi. The plant
smuts, caused by Basidiomycetes (Ustlaginales), occur throughout the world. There are
approximately 1200 species of smut fungi. The reduction in yield is conspicuous and direct, and
the quality of the remaining yield is drastically reduced by the presence of the black smut spores
on the surface of healthy kernels. In addition to various cereals, smuts also affect sugarcane,
onions, and some ornamentals such carnations.

Table. Seed-borne diseases of selected economic cereal crops in the world

____________________________________________________________________
Causal pathogen Common name Host plant Nature of damage of
disease
Claviceps purpurea Ergot Oats, barley, rye Sclerotia produced
Sphacelotheca cruenta Loose smut Sorghum Smutted kernels
Sphacelotheca reiliana Head smut Sorghum, maize Smutted kernels
Sphacelotheca sorghi Covered smut Sorghum Smutted kernels
Tolyposporium ehrenbergii Long smut Sorghum Smutted kernels
Tilletia caries, T. foetida Bunt Wheat Smutted head
Urocystis agropyri Flag smut Wheat Smutted head
Ustilago hordei Covered smut Barley Smutted head
Ustilago maydis Common smut Maize Smutted parts
Ustilago nuda Loose smut Barley, wheat Smutted head
Ustilago tritici Loose smut Wheat Smutted head

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Most smut fungi attack the ovaries of grains and grasses and develop in them and in fruits, that is,
the kernels of grain crops, which they destroy completely. Several smuts, however, attack the
leaves, stems, or floral parts. Some smuts infect seeds or seedlings before they emerge from the
ground, and they grow internally in seedling until they reach the inflorescence; others cause only
local infections on leaves, stems, and so on. Cells in affected tissues are either destroyed and
replaced by black smut spores, or they are first stimulated to divide and enlarge to produce a
swelling or gall of varying size and are then destroyed and replaced by black smut spores. Smut
fungi rarely kill their hosts, but in some cases infected plants may be severely stunted.

Most smut fungi produce only two kinds of spores: teliospores and basidiospores. The smuts
generally overwinter as teliospores on contaminated seed, in plant debris, or in the soil. Some
smuts overwinter as mycelia inside infected kernels or in infected plants. The teliospores cannot
infect but produce basidiospores, which on germination, either fuse with compatible ones and
then infect, or penetrate the tissue and then fuse to produce dikaryotic mycelium and the typical
infection. Smut fungi have only one generation per year, each infection resulting in one crop of
teliospores per growing season.

Control of smuts is primarily by the use of resistant varieties and seed treatment. The latter may
involve either chemical dusting or dipping, if the fungus is present as teliospores on the seed
surface or in the soil, or hot water if the fungus is present as mycelium inside the seed. The
discovery of carboxin, thiabendazole, etaconazole, and other fungicides that are absorbed and
translocated systematically by seeds and seedlings allows chemical control by seed treatment of
even those smuts present as mycelium inside the seeds. Soil treatments with these and other
chemicals are also useful in the control of smut diseases.

12.4.2. Soft Post-harvest Decays

Some of the most common genera of Ascomycetes or Fungi Imperfecti that cause post-harvest
diseases include Alternaria, Botrytis, Fusarium, Geotrichum, Penicillium, and Sclerotinia.

Various species of Alternaria cause decay on most fresh fruits and vegetables either before or
after harvest. The symptoms appear as brown or black, flat or sunken spots with definite margins,
or as diffuse, large, decayed areas that are shallow or extend deep into the flesh of the fruit or
vegetable. The fungus develops at a range of temperature and may spread into and rot tissues
internally with little or no mycelium appearing on the surface, but with white mat of mycelium
that turns brown to black over time on the surface of rotted area.

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Botrytis causes the gray moulds or gray mould rots of fruits and vegetables, both in the field and
in the storage. Almost all fresh fruits and vegetables, and bulbs are attacked by Botrytis in the
strorage. Some products, such as strawberry, lettuce, onion, grape, and apple, are also attacked in
the field near maturity or while green. The decay appears as well-defined water-soaked, then
brownish area that penetrates deeply and advances rapidly into the tissue. Gray moulds are most
severe in cool, humid environments and continue to develop, even at 0 oC.

Fusarium causes post-harvest pink or yellow moulds on vegetables and ornamentals and
especially on root crops, tubers, and bulbs. Low-lying crops such as cucurbits and tomatoes are
frequently affected. Contamination with Fusarium usually takes place in the field before or
during harvest, but infection may develop in the field or in the storage. Losses are particularly
heavy with crops, such as potatoes, that are stored for long periods. Affected tissues appear moist
and light brown at first, become darker brown later, and dry and sunken with wrinkled skin, and
small tufts of whitish, pink or yellow mould.

Geotrichum causes the sour rots of citrus fruits, tomatoes, carrots, and fruits and vegetables. Sour
rot is one of the messiest and most unpleasant rots of susceptible fruits and vegetables. The ripe
or overripe fruits and vegetables, and those kept in moisture-holding plastic bags and packages,
are particularly susceptible to sour rot. The fungus occurs in soils and decaying fruits and
vegetables and contaminates new ones before or during harvest. The fungus penetrates fruits,
usually after harvest, at wounds of various sorts. Infected areas appear water-soaked and soft and
are easily punctured. The decay spreads rapidly. Later, the skin cracks over the affected area and
is usually filled with a white, cheesy, or scum-like development of the fungus. The whole inside
of the infected product becomes a sour-smelling, decayed, watery mass. Fruit flies that are
attracted by the sour rot further spread the pathogen. The fungus is favoured by high temperature
(24-30 oC).

The various species of Penicillium cause blue mould rots and green mould rots. They are the
most common and most destructive of all post-harvest diseases, affecting most kinds of fruits and
vegetables. On some fruits, such as citrus, some infection may take place in the field, but blue
mould moulds or green moulds are essentially post-harvest diseases and often account up to 90%
of decay in transit, storage, and in the market. Penicillium enters tissues through wounds. Also, it
can spread from infected fruit in contact with healthy ones through uninjured skin. Penicillium
rots appear as soft, watery, slightly discoloured spots of varying size and on any part of the fruit.

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The spots quickly become deeper. At room temperature most or all the fruit decays in a matter of
a few days. Soon a white mould begins to grow on the surface of the fruit, near the centre of the
spot, and starts producing spores. The sporulating area has a blue, bluish-green, or olive-green
colour and is usually surrounded by white mycelium and a band of water-soaked tissue. The
fungus develops on spots of any size as long as the air is moist and warm. In cool, dry air, surface
mould is rare, even when the fruits are totally decayed. Under dry conditions, it may shrink and
become mummified. Under moist conditions, secondary fungi and yeasts also enter the fruit,
which is then reduced to a wet, soft mass. Decaying fruit has a musty odour. Penicillium also
produces several mycotoxins, such as patulin, in fruits and vegetables.

Sclerotinia causes the cottony rot of citrus fruits, especially lemons, and the watery soft rots of
many fruits and practically all vegetables, with the exception of onions.and potatoes. In a moist
atmosphere, a soft rot, watery decay is produced, and the affected tissues are rapidly covered with
a white, cottony growth of mycelium that is characteristic of this decay. In moist air, succulent
decaying products may be completely liquefied, leak, and leave a pool of juice. In dry air, the
water may evaporate as fast as it is liberated by the decay, and the tissues dry down into a
mummy or parchment-like remains. Cottony rot is a rapidly spreading, contact decay that attacks
both green and mature fruits and vegetables. Black sclerotia, 2 to 15 mm long, later develop in
the fungus mat. The activity of the fungus and the severity of the rot increase with temperature up
to 25 oC, but once started, rotting of tissues continues at temperatures as low as 0 oC.

For some post-harvest diseases, control depends on effective control of the pathogens that cause
the same diseases in the field so that the crop will not be contaminated with the pathogens at
harvest and subsequently in the storage. The crop should be harvested and handled carefully to
avoid wounds, bruises, and other injuries that could serve as ports of entry for the pathogen.
Harvesting and handling of the crop should be done when the weather is dry and cool to avoid
further contamination and infection. The crop should be cooled as quickly as possible to prevent
establishment of new infections and the development of existing ones. All fruits and vegetables
showing signs of infection should be removed from the crop that is to be stored or shipped to
avoid further spread of the disease. The storage containers, warehouse, and shipping cars should
be clean and disinfected with formaldehyde, copper sulphate, or other disinfectant before use.
The crop should be stored and shipped at a temperature low enough to slow down development
of infections and the physiological breakdown of the tissues but not so low as to cause chilling
injuries, which then serve as ports of entry for fungi. The crop should be free of surface moisture

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when placed in the storage, and there should be adequate ventilation in the storage to prevent
excessively high relative humidity from building up and condensing on the fruit surface. Avoid
packing in plastic bags. Keep the fruits free of insect pests in the storage. Protect sweet potatoes
and onions from some decay fungi, through suberization or wound periderm formation, by curing
at 28 to 32 oC for 10 to 14 days. Hot air or hot water treatment may help to eradicate incipient
infections at the surface of some fruits.

Controlled atmosphere (CA) storage and transport employing low oxygen (5%) or increased CO 2
(5-20%) have been used to suppress respiration of both the host and the pathogen, thereby
suppressing post-harvest rots. You may improve it by adding 10% CO. Biological control may be
effective too against some fungal and bacterial pathogens. Gamma rays can reduce storage rots of
some crops. Spraying some fruits with calcium chloride seems to reduce post-harvest diseases.

Post-harvest decays of fruits and vegetables can be controlled by chemical treatments. The
commonly used chemicals for such treatments include diphenyl, sodium o-phenyl phenate,
dichloran, 2-aminobutane, thiabendazole, benomyl, thiophanate-methyl, imazalil, chlorothalonil,
cytovirin, triforine, captan, iprodione, vinclozolin, soda ash, and borax. They are usually applied
as fungicidal wash treatments, and are more effective when used hot, that is, at temperatures
between 28 and 50 oC. Periodic fumigation of fruits with sulphur dioxide may also help. Some
fungicides, such as dichloran, biphenyl, acetaldehyde vapours, and some ammonia-emitting or
nitrogen trichloride-forming chemicals, are used as supplementary, volatile in-package fungistats
impregnated in paper sheets during storage and transport.

12.5. Fruit Diseases and Soft Rots (1 lecture hour)

12.5.1. Brown Rot of Stone Fruits

Brown rot occurs wherever stone fruits are grown and there is sufficient rainfall during the
blossoming and fruit ripening periods. It affects peaches, cherries, plums, apricots, and almonds
with about equal severity.

Losses from brown rot result primarily from fruit rotting in the orchard, but serious losses may
appear during transit and marketing of the fruit. Yields may also be reduced by destruction of the
flowers during blossom blight stage of the disease. In severe infections, 50 to 75% of the fruit
may rot in the orchard, and the remainder may become infected before it reaches the market.

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The first symptoms of the disease appear on the blossom and may involve the entire flower and
its stem. In humid, humid weather the infected organs are covered with grayish-brown conidia of
the fungus and later shrivel and dry up, with the rotting mass clinging to the twigs for some time.
At the base of infected flowers, small, sunken, cankers develop on twigs around the flower stem,
which sometimes they encircle and cause twig blight. In humid weather, gum and also gray tufts
of conidia appear on the bark surface.

Fruit symptoms appear when the fruit approaches maturity as small, circular, brown spots that
spread rapidly in all directions. Ash-colored tufts of conidia break through the skin of the infected
areas and appear on the fruit surface. One large or several small rotten areas may be present on
the fruit, which finally becomes completely rotted and either dries up into a mummy and remains
hanging from the tree or falls to the ground, where it also forms a mummy. Some small cankers
also develop on twigs or branches bearing infected fruit.

Brown rot is caused by the pathogen Monilinia (Sclerotinia) fructicola, M. laxa, and M.
fructigena. The mycelium produces chains of elliptical Monilia-type conidia on hyphal branches
arranged intufts (sporodochia). The fungus also produces microconidia (spermatia) in chains on
bottle-shaped conidiophores. The spermatia do not germinate, but seem to be involved in the
fertilization of the fungus. The sexual stage, apothecium, originates from pseudosclerotia formed
in mummified fruit partly or wholly buried in the soil or debris. More than 20 apothecia may
form on one mummy. The inside or upper surface of the surface of the apothecium is lined with
thousands of asci interspersed with sterile hyphae (paraphyses). Each ascus contains eight single-
celled ascospores.

The pathogen overwinters as mycelium in mummified fruit on the tree and in cankers of affected
twigs, or as pseudosclerotia in mummies in the ground. In the spring the mycelium in the
mummified fruit on the tree and in the twig cankers produces new conidia, whereas the
pseudosclerotia in mummified fruit buried in the ground produce apothecia, which form asci and
ascospores. Both conidia and ascospores can cause blossom infections. The conidia are
windblown or may be carried to floral parts by rainwater splashes or insects. Conidia usually
penetrate fruit through wounds made by insects, twigs punctures, or hail, but in some cases they
also gain access through stomata or directly through the cuticle. Fruit infection can also take
place after harvest, in transit, and in storage.

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Brown rot of stone fruits can be controlled best by completely controlling the blossom blight
phase of the disease. This can be done by spraying two to four times with an effective fungicide
from the time the blossom buds show pink until the petals fall. Benomyl, thiophanate-methyl,
triforine, chlorothalonil, iprodione, vinclozolin, captan, and sulphur are the fungicides used for
brown rot control. Twigs bearing infected blossoms or cankers should be removed as clearly as
possible to reduce the inoculum available for fruit infections later in the season and for
overwintering.

To prevent infections at harvest and during storage and transit, fruit should be picked and handled
with the greatest care to avoid punctures and skin abrasions on fruit, which enable the brown rot
fungus to gain entrance more easily. All fruits with brown rot spots should be discarded. Post-
harvest brown rot can be reduced by dipping or drenching the fruit in a dichloran-benomyl
solution before storing, and hydrocooling or cooling fruit in air before refrigeration at 0 to 3 oC.
Biological control of post-harvest brown rot rot has been but is not used commercially.

12.5.2. Soft Rot of Vegetables and Fruits

Rhizopus soft rot of fruits and vegetables occurs throughout the world on harvested fleshy organs
of vegetables, fruits, and flower crops during storage, transit, and marketing of these products.
When conditions are favourable, the disease spreads rapidly throughout the containers, and losses
can be great in a short period. Attacked crops include all cucurbits, peaches, cherries, peanuts,
and several other fruits and vegetables. Bulbs, corms, and rhizomes of flower crops, such as tulip,
and gladiolus, are also susceptible. Corn and some other cereals are affected under fairly high
conditions of moisture.

Infected areas of fleshy organs appear water-soaked at first, and are very soft. If the skin of the
infected organ remains intact, the tissue loses moisture gradually until it shrivels into a mummy.
Fungal hyphae usually grow outward through the wounds and cover the affected portions by
producing tufts of whiskerlike pray sporangiophores and sporangia. The fleshy growth of the
fungus extends to the surface of the infected fruit and affected tissues at first give off a mildly
pleasant smell, but soon yeasts and bacteria move in and a sour odour develops. When loss of
moisture is rapid, infected organs finally dry up and mummify.

Avoid wounding fleshy fruits, roots, tubers, and bulbs during harvest, handling, and
transportation. Discard or pack and store wounded organs separately from healthy ones. Clean
and disinfect storage containers and warehouses with copper sulphate solution, formaldehyde,

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sulphur fumes, or chloropicrin. The temperatures of storage rooms and shipping cars should be
controlled. Pick succulent fruits, such as strawberry, in the morning when it is cool and keep
them at temperatures below 10 oC. Keep sweet potatoes and some other not so succulent organs
at 25 to 30 oC and 90% humidity for 10 to 14 days and subsequently lower the temperature again
to about 12 oC.

12.6. Vascular Wilts (1 lecture hour)

Vascular wilts are widespread, very destructive, spectacular, and frightening plant diseases. They
appear as more or less rapid wilting, browning, and dying of leaves and succulent shoots of plants
followed by death of the whole plant. Wilts occur as a result of the presence and activities of the
pathogen in the xylem vessels of the plant. Entire plants may die within a matter of weeks,
although in perennials death may not occur until several months or years after infection. As long
as the infected plant is alive, the wilt-causing fungi remain in the vascular (xylem) tissues and a
few surrounding cells. Only when the infected plant is killed by the disease do these fungi move
into other tissues and sporulate at or near the surface of the dead plant. There are four genera of
fungi that cause vascular wilts, namely Ceratocystis, Ophiostoma, Fusarium and Verticillium.
Only two of these are discussed below.

12.6.1. Fusarium Wilts

Fusarium wilts affect and cause severe losses on most vegetables and flowers, several field crops
such as cotton and tobacco, plantation crops such as banana, plantain, coffee, and sugarcane, and
a few shade trees. Fusarium wilts are most severe under warm soil conditions and greenhouses.
Most fusarium wilts have disease cycles and develop similar to those of the Fusarium wilt of
tomato discussed below.

Fusarium wilt of tomato is one of the most prevalent and damaging diseases of tomato wherever
tomatoes are grown intensively. The disease is most destructive in warm climates and warm,
sandy soils of temperate regions. The disease causes great losses, especially on susceptible
varieties and under favourable weather conditions. Infected plants become stunted and soon
wilted and finally die. Occasionally entire fields of tomatoes are killed or severely damaged
before a crop can be harvested. The disease does not cause serious losses unless the soil and air
temperatures are rather high during much of the season.

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The first symptoms appear as slight vein clearing on the outer, younger leaflets. Subsequently the
older leaves show epinasty caused by drooping of the petioles. Plants infected at the seedling
stage usually wilt and die soon after appearance of first symptoms. Older plants in the field may
wilt and die suddenly if the infection is severe and if the weather is favourable for the pathogen.
In older plants, plants may stunt, lower leaves may become yellow, plants may form adventitious
roots, young stems and leaves may wilt, leaves may defoliate, and finally the whole plant may die
(mostly on one side of the stem). Fruit may become infected, rot, and drop off without becoming
spotted. Roots are also infected and the smaller side roots rot, with brown ring near the base.
There may be upward discoloration of the stem.

The pathogen is a soil-borne inhabitant. It survives in plant debris in the soil as mycelium and in
all its spore forms, and as chlamydospores in cooler temperate regions. The pathogen is spread
through irrigation water, contaminated farm machinery, infected transplants, or in soils.

Use of resistant varieties is the only practical measure for controlling the disease in the field. Soil
sterilization may be used in greenhouse soils. Use of healthy seed and transplants is mandatory.
Hot-water treatment of suspected seed may precede planting. Use of antagonistic fungi, such as
Trichoderma, may help control the disease. Soil solarization of field soil by covering with
transparent plastic film during summer also reduces disease incidence.

12.6.2. Verticillium Wilts

Verticillium wilts occur worldwide but most important in the temperate regions. Verticillium
attacks more than 200 species of plants including most vegetables, flowers, fruit trees,
strawberries, field crops, and shade and forest trees. Example, potato, eggplant, tomato, etc.
Verticillium is also the main cause of the potato early dying disease.

In many hosts and most areas, Verticillium induces wilt at lower temperatures than Fusarium.
The symptoms develop more slowly and often appear only on the lower or outer part of the plant
or on only a few of its branches. In some hosts, Verticillium develops primarily in seedlings,
which die shortly after infection. Later infections cause upper leaves to droop and other leaves to
develop irregular chlorotic patches that become necrotic. Older plants are usually stunted, and
vascular tissues show discoloration. Verticillium infection may result in defoliation, gradual
wilting, and death of successive branches, or abrupt collase and death of the entire plant.
There are two common species, Verticillium albo-atrum (grows best at 20 to 25 oC and produces
microsclerotia) and Verticillium dahliae (grows best at 25 to 28 oC, common in warmer regions,

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over-winters in the soil and survive for more than 15 years in soil, that cause Verticillium wilts in
most plants. Both produce short-lived conidia. Both can produce conidia and can survive as
mycelia within perennial hosts, in propagative organs, or in plant debris. The pathogen penetrated
directly or through root wounds. Transmission is through contaminated seed, vegetative cuttingd,
and tubers, wind, surface water, soil, etc.

Use of disease-free soils, resistant varieties, and avoidance of susceptible plants can control
Verticillium wilt. Soil fumigation can be used but is expensive. Soil solarization can be used in
areas with high summer temperatures and low rainfall.

The reader is advised to refer to some textbooks on the remaining fungal genera that cause wilt
diseases in cultivated crop plants.

12.6.3. Bacterial Wilts

Vascular wilts caused by bacteria affect mostly herbaceous plants such as several vegetables,
field crops, ornamentals, and tropical plants. The genera of the phytopathogenic wilt bacteria and
the most important vascular wilts they cause include:

1. Clavibacter (Corynebacterium);
a) Clavibacter michiganense subsp. sepedonicum = Ring rot of potato
b) Clavibacter michiganense subsp. michiganense = Bacterial canker and wilt of tomato
2. Curtobacterium (Corynebacterium)
a) Curtobacterium (Corynebacterium) flaccumfaciens = Bacterial wilt of bean
3. Erwinia
a) Erwinia tracheiphila = Bacterial wilt of cucurbits
b) Erwinia stewartii = Stewart’s wilt of corn
c) Erwinia amylovora = Fire blight of pome fruits
4. Pseudomonas
a) Pseudomonas (Ralstonia) solanacearum = Bacterial wilt of solanaceous crops and Moko
disease of banana
5. Xanthomonas
a) Xanthomonas campestris pv. campestris = Black rot of crucifers (cabbages)

In bacterial wilts, the bacteria enter, multiply in, and move through the xylem vessels of the host
plants. In the process, they interfere with the translocation of water and nutrients, and this results

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in the drooping, wilting, and death of the aboveground parts of the plants. Thus they are similar
to fungal wilts caused by Verticillium, Fusarium and Ophistroma.

The bacteria often destroy (dissolve) parts of the cell walls of xylem vessels or cause them to
rupture quite early in the disease development. The bacteria spread and multiply in adjacent
parenchyma tissues at various points along the vessels, kill and dissolve the cells, and cause the
formation of pockets or cavities full of bacteria, gums, and cellular debris. In some bacterial
vascular wilts, once the bacteria reach the leaves, move out of the vascular bundles, spread
throughout the intercellular spaces of the leaf, and may ooze out through the stomata or cracks
onto the leaf surface. The bacteria can also ooze to the surface of stems through cracks formed
over the bacterial pockets or cavities. More commonly, the wilt bacteria are confined to the
vascular elements and do not reach the plant surface until the plant is killed by the disease.

Bacterial vascular wilts can sometimes be determined by cutting an infected stem with a razor
blade and then separating the two parts slowly, in which case a thin bridge of a sticky substance
can be seen between the cut surfaces while they are being separated. Small pieces of infected
stem, petiole, or leaf can also be placed in a drop of water and observed under the microscope, in
which case masses of bacteria will be seen flowing out from the cut ends of the vascular bundles.

The wilt bacteria overwinter in plant debris in the soil, in the seed, in vegetative propagative
material, or, in some cases, in their insect vectors. They enter the plants through wounds that
expose open vascular elements and multiply and spread in the latter. They spread from plant to
plant through soil, through handling tools, through direct contact of plants, or through insect
vectors.

Control of bacterial wilts is possible through crop rotation, resistant varieties, bacteria-free seed
or other propagative material, control of the insect vectors of the bacteria when such vectors
exist, removal of infected plant debris, and proper sanitation.

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