Plant Pathology: Ronaldo T. Alberto, Ph.D. Professor, Department of Crop Protection

PLANT PATHOLOGY
RONALDO T. ALBERTO, Ph.D.

Professor, Department of Crop Protection
I. INTRODUCTION
1.1 The Science and Art of Plant Pathology
Plant Pathology deals with the nature, causes, and control of plant diseases. Look into the
characteristics of diseases, their causes, plant-pathogen interactions, factors affecting disease
development in individual plants and in populations, and various means of controlling disease.
Deals with the application of the knowledge gained from studying the science to include: (a)
diagnosis or recognizing particular disease by their symptoms and signs, (b) disease assessment
and forecasting, (c) recommendation of appropriate control measures, and (d) field application
of suitable control measures.
The ultimate objective of plant pathology is to prevent or minimize plant diseases not only to
increase food production but also to maintain the quantity and quality of the harvested fresh
commodity until it reaches the consumer.
1.2 The Economic Importance of Plant Diseases
Enormous economic losses. Crop losses are expressed in various ways. A common type of loss
is the reduction in yield of diseased plants. Deterioration of harvested produce during storage,
marketing or transport. Reduction in the quality of the produce.
Poisonous substances or toxins that endanger the health of the consumer. Causes the host plant
to become weak and susceptible to attack by other pathogens. Increase the cost of production
and handling.
1.3 Historical development of plant pathology
A. The Pre-scientific Period
Plant disease had been present on earth long before man appeared on this planet. Bible as well
as the great philosophers of old such as Aristotle, Homer, and Theophrastus recorded a number
of diseases including blights, mildews, rusts, and blasts.
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AGRICULTURIST LICENSURE EXAMINATION REVIEW 2011 (Crop Protection)
Greeks and Hebrews (500 B.C. TO ABOUT 280 B.C.) believed that diseases to their crops were
brought down on them as punishment for their sins by a displeased wrathful god.
They also attributed diseases to bad weather and unfavorable soil conditions.
Romans (320 B.C. to around 475 A.D.) held an annual festival, called Robigalia, to placate their
rusts gods Robigus and Robigo who they believed were responsible for the ravages caused by
various rust diseases on their crops.
Pliny, the Elder, (A Roman philosopher) wrote about blights and rusts in this Historia Natura/is.
He even recommended that early sowing of grains allowed wheat and barley to escape rust in
infection.
Around 875 A.D. and for many years thereafter ergot epidemics in humans swept through
various parts of Europe. Ergot rye is a disease caused by Claviceps purpurea where in the
sclerotium of the fungal pathogen replaces the rye kernel.
All this time hardly any scientific experiment was done. People explained natural phenomena by
deductive reasoning dusted with speculations so that more often than not, reached wrong
conclusions.
B. Beginning and Advances in Scientific Studies
Francis Bacon (1605) advocated inductive reasoning methods, as against deductive reasoning
and speculation, to interpret natural occurrences, and thus propelled the development of
science a step further.
17th century to the mid-19th century early attempts at classifying plant diseases were made by
Tournefort, Zallinger, Fabricius and Unger.
Franz Unger is credited with the "Autogenetic Theory of Disease" which states that when plants
are in the declining phase, the cellular constituents call forth new forms of life by a vital force.
This theory considers the pathogen an outgrowth of the infected host plant Without an
Independent body or life of its own or that the pathogen is the result of the disease, and not the
cause.
Hans and Zaccharias Jansen invented the compound microscope in 1590. 1665 Hooke was the
first to see plant cell in cork and pith and in 1665, in his Micrograhia, was the first to illustrate in
detail a plant pathogenic microscopic fungus.
Leeuwenhoek in 1683 found bacteria, protozoa and other microorganisms in water and other
substrates.
"Germ Theory of Disease" is the foundation of the science of plant pathology was enhanced by
the works of various people.
2 |Plant Pathology
Pier Antonio Micheli (1729) described several genera of fungi complete with illustrations of their
fruiting bodies and spores in hid Nova Plantarium Genera.
Tillet (1755) noted that dust (spores) from smutted wheat when sown on healthy wheat seed
resulted wheat plants. Although he showed that the wheat bunt disease was contagious he
considered the spore dust to be merely the carriers of the
"poisonous entity”.
Targioni - Tozzetti (1766) and Fontana (1767) did some studies on cereal rusts and concluded
that the disease by the rust fungi associated with it.
Prevost (1807) was the first to conclusively demonstrate that the bunt disease of wheat is
caused by a fungous pathogen. He studied the formation of spores and their germination. His
work laid a firm foundation for plant pathology. He also noted that wheat seeds soaked in a
copper bucket resulted in smut-free plants and showed that copper sulfate prevented spore
germination. Pearson and Fries in the 1800's conducted numerous studies on the germination.
The Tulasne brothers made extensive morphological studies with excellent illustrations of rusts,
smuts and ascomycetous fungi. They also confirmed Prevost's observations on spore
germination and the causal role of fungi in plant disease.
Heinrich Anton de Bary published in 1853 his conclusion that from all evidences made by
previous workers on the rusts and smuts of cereals, diseases were caused by parasitic
microorganisms which were separate entities in themselves.
In 1858, Julius Kuhn wrote the first textbook on plant pathology entitled, "Die Kranheiten der
Kulturewachse ihre Ursachen und ihre Verhutung (The Disease of Cultivated Plants, their Causes
and their Prevention). The period from 1850-1900 may be called the etiological period during
which the theory that plant diseases were caused by pathogenic organisms was developed.
Louis Pasteur completed the overthrow of the theory of spontaneous generation in 1860 when
he provide irrefutable evidence that microorganisms arise from pre- existing living entities.
Brefeld, Koch and Petri studied pure culture techniques for the growth of microorganisms. The
role of pollutants in causing plant disease was demonstrated by German scientists as early as
the 1880's.
Burrill showed that fireblight of apple and pear is caused by a bacterium. Walker demonstrated
that the yellow disease of hyacinth is also caused by a bacterium. E. F. Smith studied several
more bacterial plant diseases showing how important these pathogens are.
Ivanowski (1892) and Beijerinck (1898) showed that some plant diseases are caused by very
small entities that could pass through bacteria proof filters. This started the field of virology.
Stanley in 1935 crystallized a virus for the first time (the tobacco mosaic virus), which is
considered as an autocatalytic which is capable of multiplying in the living cells of the host.
Plant Pathology | 3
Bawden and co-workers in 1936 showed that the crystalline virus preparations consisted of
protein and nucleic acid. Kausche and co-workers in 1939 were the first to see virus particles
under an electron microscope.
Gierer and Schramm established in 1956 that the nucleic acid is the infective component of the
virus particle.
Nematodes as plant pathogens were first observed by Needham inside wheat galls (kernels) in
1743. Berkeley noted root knot nematodes in galls formed in roots of cucumber. Cobb
conducted extensive studies on the morphology and taxonomy of plant parasitic nematodes
from 1913 to 1932.
Flagellate protozoa were first observed by Lafont in 1909 in the latex bearing cells of. laticiferous
plants although these organisms parasitized the latex without causing apparent damage to the
plant.
Stahel in 1931 found protozoa causing abnormal phloem formation and wilting of coffee trees
which Vermeulen in 1963 confirmed. Flagellates are also believed to cause the "hart rot disease"
a phloem disorder of coconut trees.
Mycoplasma-like organisms as plant pathogens were first reported by Dol et al to infect aster
yellows in Japan in 1967. Ishiie and co-workers in 1965 observed that treating infected plants
with tetracycline caused a temporary disappearance of the symptoms and the mycoplasma-like
bodies. Diseases in which mycoplasmas have been implicated are lethal yellowing of coconut
palms, potato witches' broom, bunchy top of papaya, rice yellow dwarf, mulberry dwarf, mung
bean withches' broom and aster yellows.
Davis and co-workers observed what they called a spiroplasma in 1972. A motile,
helical'microorganism that caused the stunt disease of corn.
Diener in 1971 observed viroids as plant pathogens of potato causing the spindle tuber disease.
A viroids is an infectious ribonucleic acid molecule which is the smallest agent of plant disease
and is not capable of independent multiplication Cadang-cadang of coconut, citrus exocortis and
potato spindle tuber are believed to be caused by viroids.
Rickettsia-like microorganisms were found by Windsor and Black in 1972 to cause the club leaf
disease of clover. Other diseases such as phony peach and Pierce's of grapes may be caused by
these organisms.
Bordeaux mixture, a fungicide that is being used until today, was discovered by Pierre Marie
Alexis Millardet in October 1882. This formed the foundation for the chemical control of plant
diseases.
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C. Development of plant pathology in the Philippines
The first diseases to be studied in the country are coffee by Hemileia vastatrix and coconut bud
rot caused by Phytophthora palmivora Butler.
Coffee rust was first noted in 1885 in Batangas and five years later (in 1890) it destroyed all the
coffee trees in the province. Coconut bud rot was initially observed in Laguna then spread to
Quezon province causing tremendous damage. Copeland was the first dean of U.P. College of
Agriculture established in 1908. This is where phytopathological work in country all started and
is still going strong today.
Two other diseases that earned early attention were leaf blight of corn reported by C.B.
Robinson in 1911 and downy mildew of corn observed by C. Baker in 1912. Baker also published
in 1914 "The Lower Fungi of the Philippine Islands" (a review of Philippine plant disease) and the
first supplement to the list of lower fungi in the Philippine Islands.
Prof. Reinking assisted by students of plant pathology, published the "Philippine economic Plant
Diseases" in 1918. This work described the symptoms, causes and control measures of various
diseases. He also started the foundation of a herbarium of plant diseases.
G.O. Ocfemia joined the Department in 1918 and became department head from 1933 to 1955.
During this time he made numerous studies notably on the nature and cause of abaca bunchy
top including the vector of the causal agent.
Research studies made during the early years were those of Westin on downy mildew of corn
(1920-23), Ocfemia on bunchy top of abaca and Fiji disease of sugar cane (1920's to 1940's).
From 1950 to 1960 numerous studies on the etiology and control of leaf and seedling diseases
were conducted.
The Philippine Phytopathological Society, an association of plant pathologists, was established in

1963. This society since 1965 has maintained a scientific journal, the Philippine Phytopathology.
In the 1970's, a Surveillance and Early Warming System for Plant Epidemics was established by
the Bureau of Plant Industry. O.R. Exconde and co-workers completely controlled by seed
treatment the corn downy mildew disease in 1978.
2. CONCEPTS OF PLANT DISEASE
Disease a “physiological malfunctioning caused by animate agents, malfunctioning caused by

non-living or inanimate agents in phsyiogenic disease.
Stakman and Harrar in 1957 considered disease as "any deviation from normal growth or
structure of plants that is sufficiently pronounced and permanent to produce visible symptoms
or to impair quality or economic value”.
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Horsfall and Dimond in 1959 stated that disease is “a malfunction process caused by continuous
irritation “. Disease is progressing over a period of time while injuries is instantaneous action
such as the breaking of the twig.
Merill defines disease as "a dynamic interaction between an organism and its environment
which results in abnormal physiological and often morphological or neurological changes in the
organisms”.
Agrios (1978) defined disease as "any disturbance brought about by a pathogen or an
environmental factor which interferes with manufacture, translocation, or utilization of food,
mineral nutrients and water in such a way that the affected plant changes in appearance and/or
yields less than a normal healthy plant of the same variety".
The National Academy of Science, Washington, D.C.) in 1968: defined “Disease as a harmful
alternation of the normal physiological and biochemical development of a plant".
The salient points in most of the definitions of disease are: (a) the presence of physiological
disorders that are generally detrimental and (b) morphological abnormalities result from the
physiological malfunctioning
2.1. Definitions and Terminology in Plant Pathology
A pathogen, is any agent that causes a disease. A parasite is an organism which depends wholly
or partly on another living organism for its food. Most parasites are pathogen.
A parasite may be obligate or facultative. An obligate parasite is an organism that is restricted to

subsist on living organisms and attacks only living tissues. A facultative parasite is an organism
which has the faculty or ability to be a parasite although it is ordinarily saprophyte.
A saprophyte is an organism that lives on dead organic or inorganic matter. A facultative

saprophyte has the ability to become a saprophyte but is ordinarily a parasite
Host, refers to the plant that is being attacked by a parasite. A food relationship between the
host and the parasite (pathogen) is implied, Suscept, on the other hand is a plant that is
susceptible to a specific disease whether or not the pathogen is parasitic.
Pathogenicity is the capacity of a pathogen to cause disease whereas pathogenesis refers to

disease development in the plant.
2.2. Symptoms of Plant Diseases
Symptoms are the expressions by the suscept or host of a pathologic condition by which a
particular plant disease may be distinguished from other diseases. The term “symptom”
however, sometimes take a broader meaning to include any measurable host response to
infection such as increased respiration and increase leaf temperature.
6 |Plant Pathology
Symptoms have been variously described as primary or secondary, localized or systematic, and
histological or morphological.
Primary symptoms are those that are the immediate and direct results of the usual agent's
activities on the invaded tissues whereas secondary symptoms are the effects on the distant and
uninvaded plant parts.
Localized symptoms are characterized by distinct and very limited structural changes usually in
the form of lesions such as canker, leaf spot and gall. Systematic symptoms, on the other hand,
are more generalized pathological conditions such as mottle, mosaic and wilting.
A histological symptom is essentially internal, and seen only upon the dissection of the diseased
plant portion and examination under the microscope. It is expressed as an abnormality in cell
content, structure or arrangement. Cell enlargement and vascular discoloration are histological
symptoms. Morphological symptoms are those malformations and other changes that are visible
to the naked eye.
Symptoms are generally classified into (a) necrotic symptoms, (b) hypoplastic symptoms and (c)
hyperplastic symptoms. Necrotic symptoms involve the death of protoplast, cells or tissues
Examples are spot, blight, scorch, canker, and die-back. Before the actual death of the
protoplast or cell some evidences of protoplasmic disorganization and degeneration may
appear. Examples of these plesionercotic symptoms are silvering, yellowing and wilting.
Hypoplastic symptoms appear when there is an inhibition or failure in the differentiation or

development of some aspect of plant growth. Stunting, chlorosis, mottle, mosaic, curling and
resetting are examples of hypoplastic symptoms.
Hyperplastic symptoms are expressed with the occurrence of excessive multiplication:

enlargement or overdevelopment of plant organs including the abnormal prolonged retention of
the green color. Gall formation, fasciation, scab, premature defoliation of fruit drop, and
greening are examples of hyperplastic symptoms. Overdevelopment may result from an
increase in the size of cells (hypertrophy) or an abnormal increase in the number of cells
(hyperplasia).
The various symptoms were categorized by Kenaga (1974) into (a) abnormal coloration, (b)
wilting, (c) death of host tissue, (d) defoliation and fruit drop, (e) abnormal growth increase of
host, (f) stunting, and (g) replacement of host tissue.
Specific symptoms and their descriptions are given below.
 Etiolation - yellowing of normally green tissues caused by inadequate light

 Chlorosis - yellowing caused by some factor other than light, such as a virus or a
mycoplasma
 Mosaic - the presence usually on leaves of variegated pattern of green and yellow
shades with sharply defined borders.
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 Mottling - the variegated is less defined than mosaic and the boundaries of light and
dark variegated areas are more diffused.
 Veinclearing - the veins are translucent or pale while the rest of the leaf is its normal
color.
 Wilting - may be due to an infectious agent or to lack of water. Wilting caused by the
latter is often temporary and the plant recovers upon the application of enough
moisture unless the drought is prolonged and the plant dies Wilting by an infectious
agent often leads to, death of the plant unless controlled in time.
 Rotting -is the disintegration and decomposition of host tissue. A dry rot is a firm, dry
decay whereas a soft rot is a soft, watery decomposition. Any plant part may suffer from
rot such as fruit rot, stem-end rot, blossom-end rot, stalk rot, root rot.
 Spot - a localized nercotic area also referred to as a lesion. Individual spots may be
circular, angular or irregularly shaped. Several spots may run together or coalesce
forming large nercotic areas.
 Blight - an extensive, usually sudden, death of host tissue, such as leaf blight.
 Shot-hole - a perforated appearance of a leaf as the dead areas of local lesions drop out.
 Canker - an often sunken necrotic area with cracked border that may appear in leaves,
fruits, stems and branches.
 Mummification - an infected fruit is converted to a hard, dry, shriveled mummy.
 Leak - the host's juices exude or leak out from soft-rotted portions. 14. Die-.back - a
drying backward from the tip of twigs or branches.
 Pitting - definite depressions or pits are found on the surface of fruits, tubers and other
fleshly organs resulting in a pocked appearance.
 Rosetting - shortening of the internodes of shoots and stems forming a crowding of the
foliage in a rosette.
 Abscission - premature falling of leaves, fruits of flowers due to the early laying down of
the absciss layer.
 Phyllody - metamorphosis of sepals, petals, stamens or carpels into leaf-like structures.
 Curling - abnormal bending or curling of leaves caused by overgrowth on one side of the
leaf or localized growth in certain portions.
 Scab - slightly raised, rough, ulcer-like lesions due to the over-growth of epidermal an
cortical tissues accompanied with rupturing and suberization of cell walls.
 Damping-off - rotting of seedlings prior to emergence or rotting of seedling stems at an
area just above the soil.
 Sarcody - abnormal swelling of the bark above wounds due to the accumulation of
elaborated food materials.
 Callus - an overgrowth of tissue formed in response to injury in an effort of the plant to
heal the wound. . .
 Fasciculation or fascination - clustering of roots, flowers, fruits, or twIgs around a
common focus.
 Blast - term applied to the sudden death of young buds, inflorescence or young fruits.
 Russeting - a superficial brownish roughening of the skin or fruits. tubers or other fleshy
organs usually due to the suberization of epidermal or sub epidermal tissues following
injury to epidermis
 Streak or stripe - long, narrow necrotic lesions on leaves or stems.
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2.3. Signs of Plant Diseases
Signs of plant disease refer to the structures of the pathogen that are found
associated with the infected plant. Examples sign are fungal mycelia, spores and fruiting bodies,
bacterial ooze, sclerotial bodies, nematodes at various growth stages and plant parts of
phanerogams (parasitic flowering plants).
2.4. Plant Disease Diagnosis
Diagnosis is the identification of specific plant diseases through their characteristics symptoms
and signs including other factors that may be related to the disease process. Correct plant
disease diagnosis is necessary for recommending the appropriate control measures, and in plant
disease surveys.
Studies and work that require actual proof of pathogenicity require that Koch's postulate are
applied, i.e. (1) the suspected pathogen must always be present in the plant when the disease
occurs, (2) the organism which is believed to cause the disease must be isolated and grown in
pure culture, (3) the pure culture of the organism must produce the symptoms and signs of the
disease when inculated into a healthy plant and (4) the suspected causal organism must be
reisolated in pure culture from the inoculated plant and must be identical to the original
organism.
Studies and work that require actual proof of pathogenicity require that Koch's postulate are
applied, i.e. (1) the suspected pathogen must always be present in the plant when the disease
occurs, (2) the organism which is believed to cause the disease must be isolated and grown in
pure culture, (3) the pure culture of the organism must produce the symptoms and signs of the
disease when inculated into a healthy plant and (4) the suspected causal organism must be
reisolated in pure culture from the inoculated plant and must be identical to the original
organism.
Modifications of Koch's rules of proof should be made when dealing with obligate parasites that
cannot be grown in pure cultures, such as the viruses and nematodes, as well as when working
with abiotic or non-living disease agents.
2.5. Classifications of Plant Diseases
 Classification according to the affected plant organ such as root diseases, foliage
diseases, fruit diseases and stem diseases. This can be related to the physiological
processes affected as root diseases affect water and mineral uptake; leaf diseases affect
photosynthesis; fruits diseases affect reproduction; stem diseases affect water
conduction, etc.
 Classification according to the symptoms such as leaf spots, rusts, smuts, anthracnose,
mosaics; wilts, fruit rots, etc.
 Classification according to the type of affected plants such as vegetable diseases,
disease of forest trees, diseases of filed crops, diseases of ornamental, etc.
Plant Pathology | 9
 Classifications according to the type of pathogen that causes the disease. These may be
grouped into infectious diseases such as: (a) diseases caused by fungi, (b) diseases
caused by mycoplasmas, (c) diseases caused by bacteria, (d) diseases caused by viruses,
(e) diseases caused by viroids, (f) diseases caused by protozoa, (g) diseases caused by
parasitic flowering plants and (h) diseases caused by nematodes; and into non-infectious
diseases caused by non-parasitic or abiotic agents such as (a) extremely high or
excessively low temperatures, (b) unfavorable oxygen relations, (c) unfavorable
moisture conditions, (d) nutrient deficiencies, (e) mineral toxicities, (f) air pollution, (g)
toxicity of pesticides etc
3. NON-PARASITIC AGENTS OF PLANT DISEASE

The non-parasitic agents of disease are characteristically non-living and therefore are not spread
from diseased to healthy plants. The diseases that they cause are non-infectious. Diseases
caused by non-parasitic' agents have been also referred to as physiological disorders.
Non-infectious disease are recognized by their symptoms (no signs are present, of course). A
knowledge of the soil conditions, temperature ranges, the weather immediately before and
during disease occurrence, and other environmental factors are often necessary for correct
diagnosis.
The control of these is by avoiding, whenever possible, the causal environmental factor such as
chemical, excessive sunlight, etc. Some may be controlled by providing the lacking factor as in
nutrient deficiency diseases, and disease caused by inadequate moisture, acidic soil, etc.
The more common non-parasitic causes of diseases in plants are:
 excessively low temperatures

 temperatures that are too high
 lack of oxygen
 too much or too little light
 adverse meteorological conditions.
 air pollutants
 mineral deficiencies
 mineral excesses
 unfavorable soil pH
 excessive pesticide levels
 improper agricultural practice
 lack or excess of soil moisture
 naturally occurring toxic chemicals
3.1. Diseases caused by too low temperatures
a. Freezing injury
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This is common in frigid areas where temperatures get down to below O oC. Freezing injury is
caused by ice crystals that form within cells (intercellarly) and/or between cells (intercellarly).
These crystals
damage the cell membrane and eventually kill the cells.
b. Chilling injury
Chilling injury occurs at low temperature that is slightly above freezing. The common symptoms
of this disease are pitting and a water-soaked appearance. Many tropical fruits and vegetables
are sensitive to chilled in a refrigerator are pre-disposed to infection by Alternaria rot and
anthracnose.
3.2. Diseases caused by too high temperatures
a. Sunscald
Sunscald appears on leaves or fruits that undergo prolonged exposure to high temperatures and
bright sunlight. Affected fruits exhibit a light-colored, blistered, sometimes watersoaked area.
Very young leaves often wit and die.
b. Heat necrosis of potato
This occurs in potatoes grown in light soils where it is hot and dry. It is characterized by a yellow
or brown discoloration in the vascular system of affected tubers.
3.3. Disease caused by lack of oxygen
The blackheart disease of potato occurs when oxygen is insufficient so that the oxygen that is
available to the internal tissues of potato is used up faster that it can be ,supplied. The tissue
suffocates and becomes black. The disease is common in waterlogged soils and in ,poorly
aerated storage areas specially during periods of high temperature.
3.4. Disease caused by too much or too little light
Reduced light intensity produces plants that are etiolated. This increases their susceptibility to
infection by non-obligate parasites but decreases their susceptibility to obligately parasitic fungi.
Reduced light often brings about increased susceptibility to virus infections.
Scorching and sun scalding are two diseases caused by too much bright light along with high
temperatures.
3.5. Diseases caused by adverse meteorological conditions
Strong winds and heavy rains can cause- various disorders. The leaves of plants may be ripped,
torn or water-soaked, and are predisposed to bacterial and fungal infections. Entire fields of
crops may be blown down and killed. Lightning injury is quite common on tr.ees which appear
Plant Pathology | 11
after a lightning strike as black, burned poles. Smaller plants that are struck by lightning are
burned within a circular area nearby plants are stunted.
3.6. Air pollutants
Soot, dusts, ashes any factor mediated by the atmosphere that causes an unwanted effect. The
air pollutants that cause plant diseases are mainly gases and particles produced from factories,
smelting and refining plants, automobile exhausts and from other man-related activities. Other
pollutants are, however, produced in nature as much as the ozone from lightning discharges and
ashes from volcanic eruptions.
The more common air pollutants are:
a. Ethylene
Ethylene is a unique pollutant that can cause premature senescence, etiolation, stunting,
flower drop, sepal necrosis, leaf malformations and other symptoms if present at high
concentrations and/or at the wrong stage of plant development. The acute injury threshold is
about .05 ppm for six hours. Ethylene gas is common pollutant in large cities where motor
vehicle exhausts emit the gas.
b. Nitrogen oxides
Automobile exhausts are the main sources of nitrogen oxides. They are produced by the
combustion of coal, gasoline, natural gas and fuel oil.
The symptoms of acute injury from nitrogen dioxide (NO2) are well- defined, irregular brown or
white lesions along leaf margins and between veins. A nitrogen dioxide concentrations of 2.55
ppm for four hours can cause acute damage on young potato and bean plants
c. Peroxyacetyl nitrates (PANs)
Nitrogen oxides undergo a photochemical reaction with gaseous hydrocarbons to form ozone
and PANs which plasmolyze the spongy mesophyll cells and the lower epidermal cells which is
followed by dehydration and the filling up of the empty space with air. This produces the
bronzing, silvering and glazing on the lower leaf surfaces, typical of the silver leaf diseases.
PANs are common constituents of the smog of large cities. A PANs concentration on 0.01 ppm
for six hours may be enough to cause injury to plants.
d. Ozone
12 |Plant Pathology
Ozone is another major constituents of smog. Symptoms of ozone damage include watersoaked
spots on leaves and black flecks along veinlets which eventually bleach out in tobacco as well as
leaf-tip chlorosis and necrosis in conifers. A concentration of 0.035 ppm for four hours may
cause ozone injury in sensitive plants.
3.7. Particulates
Pollutant particulates include lime and cement dusts, ash and soot. The sources of particulates
are burning fields or crash cement factories, lime kiln operations and the combustion of fuel oil
and coal. They cause necrotic lesions where they alight on leaf surfaces. Leaves that are fully
covered by particulates rnay die and falloff. These pollutants may be controlled with the use of
electrostatic precipitators at the source.
There are other air pollutants such as chlorine (CI2), sulfur dioxide (802), fluorides; hydrogen
chloride, etc.
3.8. Diseases caused by mineral deficiencies
Different plants vary in their mineral requirements but they generally require relatively larger
amounts of the macro-element (N, P, K, Ca, S, Mg) and smaller amounts of the microelements
(Fe, Mn, S, Cu, Mo, CI). The typical symptoms of nutrient or mineral deficiencies are indicated
below
 Nitrogen deficiency - chlorotic leaves, dwarfing, premature leaf fall, poor seed and fruit
production. Nitrogen is a cqnstituent of enzymes, proteins and nucleic such as RNA and
DNA. .
 Phosphorus deficiency - subnormal roots, leaves are erect, small, narcotics; in cereals
leaves have reddish or purplish tints. Phosphorus is a constituent of phospholipids,
sugar phosphates, nucleic acids, etc.
 Potassium deficiency - tips of leaves become chlorotic (often starting with older leaves);
tips and margins appear scorched. The leaves may develop bronzing and marginal
scorching, finally turning reddish brown and dying. Potassium is involved in
photosynthesis and respiration
 Magnesium deficiency - chlorosis first appear on the older leaves: necrotic lesions may
develop; the normal green color tending to remain around the veins for sometime as in
the "sand brown" disease of tobacco. Since magnesium is an essential component of
chlorophyll, chlorosis is the primary symptom, typically interveinal chlorosis.
 Iron deficiency - general chlorosis, the leaves becoming almost colorless as in the
pineapple yellow disease. Mottling and dieback of twigs may also occur. Iron deficiency
is common in alkaline soils wherein the iron is not made available for plant use in which
case soil acidification alleviates the problem. Iron is a c0mponent of hemi enzymes and
is involved in chlorophyll synthesis.
 Manganese deficiency - chlorosis and scattered necrotic spots on young leaves,
dwarfing and premature death of plans as in the Paola blight of sugarcane. Manganese
is an enzyme activator in photosynthesis, carbohydrate metabolism and nitrogen
metabolism.
 Sulfur deficiency - yellowing of leaves and dieback. Sulfur is a component of the amino
acids cysteine, cystine and methionine as well as of vitamins such as biotin and
thiamine.
 Boron deficiency - poor growth, young growing parts often become yellowish and the
terminal shoots die as in alfalfa yellows. Boron is involved in sugar transport and in
carbohydrates metabolism.
 Copper deficiency - dieback of leaf tips, wilting, stunting, distortion of certain plant parts
as in dieback of exanthema of citrus. Copper is involved in photosynthesis and is a part
of certain enzymes. .
 Zinc deficiency - mottled chlorosis followed by necrosis and eventual defoliation,
dieback of twigs of fruit trees, and abnormal shortening of growing parts An example of
a disease due to zinc deficiency is the foliocellosis of citrus Zinc is involved in certain
enzyme systems
 Calcium deficiency - leaf mesophyll tissue, stems and flower stalks frequently collapse
and the growing points may be killed resulting in dieback; roots are poorly developed as
in the, wither top disease of flax. Calcium is a component of cell walls and membranes.
It is also an enzyme activator
 Molybdenum deficiency - leaf blades do not develop, leaving the midribs bare.
Molybdenum is an electron carrier in nitrogen metabolism. Deficiency diseases are
corrected by the application of the appropriate chemicals
3.9. Diseases caused by excesses of nutrient elements
Excessively high levels of certain elements affect the solubility and availability of other elements.
A high calcium level reduces the availability of manganese and iron. Too much nitrogen causes a
too luxuriant vegetative growth. Excess boron causes necrosis and dwarfing, Excess copper
results in severe stunting or even death of the plant. Sodium toxicity causes dwarfing of plants,
Excess chloride causes burning of leaf margins and tips, bronzing and premature defoliations.
3.10. Diseases caused by unfavorable soil pH
Alkaline soils with extremely high pH affect the availability of certain minerals required for plant
growth. Acid soils, on the other hand, with very low pH, cause the accumulation in toxic levels of
iron and other elements.
The severity and occurrence caused by Plasmodiophora brassicae is very severe at pH 6-7, and is
virtually controlled at pH 7.8. Scab of potato caused by Streptomyces scabies on the other hand,
is severe from pH 5.2 to 8.0 but is controlled below pH 5.2.
3.11. Disease caused by improper use of pesticides
Pesticides include all chemicals used in crop protection such as fungicides, insecticides,
miticides, herbicides and other chemicals.
14 |Plant Pathology
Pesticides' injuries to plants usually result from the application of excessively high
concentrations of the chemical, from vapor drift to sensitive plants, and from incorrect methods
of applying the pesticide.
3.12. Diseases caused by improper agricultural practices
Aside from the application of too high concentrations of pesticides, other agricultural practices
such as excessive fertilizer application result in plant abnormalities. This may predispose plants
to microbial infection as certain plants fertilized with too much nitrogen are more succulent,
prone to lodge and break, and thus more susceptible to attack by pathogens. Sensitive plants
may respond to spraying with high concentrations of foliar fertilizer by leaf spotting of leaf
burning.
Inadequate or too much watering causes physiological disorders. Too deep cultivation may
injure the roots plants. Potted plants that are in containers which are too small for them may be
stunted and grow poorly as root growth is impaired
3.13. Lack or excess of soil moisture
Inadequate moisture causes temporary or permanent wilting of plants. Prolonged drought will
kill the plant. High temperature, dry winds and bright sunlight make the water shortage and its
effects on plants more acute
An irregular water supply cause blossom-end rot and growth cracks in tomato. These are
brought about by a very rapid growth rate that occurs during a very wet period just a rather long
dry period.
Flooding or excess moisture results in reducing the plant's oxygen supply and weakening the
root system. Moreover, this condition is conducive to the growth of certain moisture-loving
pathogens which multiply rapidly and invade the weakened roots of the plant.
3.14. Diseases caused by naturally occurring toxic chemicals
 Juglone is a compound which is formed by black walnut and is toxic to other plants such
as potato, tomato and apples.
 Hydrogen sulfide at toxic levels may be formed in the presence of ferrous ion in flooded
are fields under anaerobic conditions causing a disease of rice.
4. PARASITIC AGENTS OF PLANT DISEASES
The parasitic agents which cause infectious diseases of plants are viroids, mycoplasmas,
bacteria, fungi, nematodes, parasitic flowering plants or phanerograms, insects and protozoa
4.1 Viroids and Viruses as Plant Pathogens
1. General Characteristics
Viroids are tiny entities composed of stable and free ribonucleic acids (RNA) that can infect plant
cells. They are much smaller than viruses and are "naked" or lacking the protein sheath of
viruses. They appear to be closely associated with the nuclei, specially the chromatin, of the cells
that they infect.
Viruses are ultramicroscopic, obligately parasitic entities that are made up of a nucleic acid core
and a protein coat.
A satellite virus is one that has to be associated with an autonomous virus before it can cause
infection or be replicated in the host plant.
2. Synthesis of viruses and viroids

Viruses or viroids are obligately parasitic and are not capable of independent multiplication
outside the host cells. They are synthesized within the host cells using the synthetic mechanism
of the host.
A virus is synthesized or replicated through the interaction of the virus genome and that of its
host. The virus nucleic acid carries the genetic formation and is the ineffective component. The
initial step in synthetic process is the removal of the protein coat. The nucleic acid, (without the
protein sheath) is carried to a site of synthesis inside the cell where it grains control of the host's
metabolism. The affected host cells then proceed to synthesize viral nucleic acid (not host cells
nucleic acid) and viral protein. This occurs as the genetic information from the virus nucleic acid
is "read" and "copied" by the host cells instead of the host's own genome. The viral protein and
nucleic acid are produced separately and are later combined in a self-assembly process. Some
plant viruses multiply in their insect vectors and are called propagative.
3. Symptoms and diseases caused by viroids and viruses

The symptoms exhibited by viroids-infected plants include stunting as in the chrysanthemum
stunt disease, rolling and twisting of leaves as in potato spindle tuber, mottling and chlorosis as
in chrysanthemum chlorotic mottle, vertical breaking of the bark as in citrus exocortis, and
yellowing of leaves as in cadang- cadang of coconut.
Symptoms brought about by virus infections include mosaic as in tobacco mosaic, ringspot (a
circular pattern of brown and yellow around a green center) as in tobacco ringspot, excessive
branching (witches; broom), vein clearing, color breaking (striping of flowers), stunting chlorosis,
and leaf curling. One or more of these symptoms may appear in a diseased plant. Virus-infected
plants are generally stunted and yield less produce of usually poor quality.
4. Transmission and spread
Viroids are spread from infected to healthy plants by mechanical means through infected sap
that may be carried in contaminated tools and hands, or by alighting and chewing insects. They
also spread through vegetative propagating materials.
16 |Plant Pathology
Viruses are transmitted by mechanical means, by nematodes, by certain soil-borne fungi, by
insects, by mites, through infected seeds and through infected vegetative planting materials.
Viruses require wounds to be able to enter the hosts and are thus called wound pathogens or
wound parasites.
5. Identification of viruses
The precise identification of specific plant viruses necessitates their extraction from the host and
subsequent purification. A study of virus morphology is carried out with an electron microscope
to determine its size and shape. Serological tests are used to determine the relationship among
viruses. This done by mixing antibodies (derived from the blood of a test animal, usually rabbit,
which was injected with a purified virus preparation) with an antigen (purified extract of a virus.
Viruses are usually named according to the major symptom that they cause on the first host
where had been found. Thus, the tobacco mosaic virus (TMV) is called tobacco mosaic virus
whether it is found in tomato or some other host because it was first studied in tobacco.
4.2 Bacteria as Plant Pathogens
1. General characteristics
Bacteria are typically unicellular microorganism that reproduces asexually by binary fission. A
bacterium lacks a well defined nucleus and a nuclear membrane.Bacteria may be spherical
(cocci), rod-shaped) (bacilli), or a spiral- shaped (spirilla). They may occur as single cells, in
couples, in chains, or in clusters.
2. Genera of plant pathogenic bacteria
These bacteria belong to class Schizomycetes and order Eubacteriales. The major bacterial plant
pathogens are rod-shaped, facultative parasites. The plant pathogenic bacteria are
Pseudomonas, Xanthomonas, Erwinia, Corynebacterium, Agrobacterium, and Streptomyces.
Which is insoluble in water. Most species cause tissues necrosis in the form of parenchyma,
vascular or systemic diseases.
3. Symptoms and disease caused by bacteria

a. Leaf spot
b. Soft rot
c. Blight
d. Gall
e. Canker
f. Wilting
4.3 Mycoplasma as Plant Pathogens
Mycoplasmas are non-motile; nonspore-forming, polymorphic microorganisms that lack cell

walls and are bounded by a triple-layered unit membrane. They are very small, often visible
only with an electron microscope. The cells contain cytoplasm, ribosomes and strands of nuclear
material. They may produce by transverse binary fusion. The formation of multinucleate
filaments which later fragment into coccoid cells has been observed.
2. Classification
The mycoplasmas compose the class Mollicutes and the order Mycoplasmatales, a classification
proposed by Edward and Freundt in 1967. The families under the order Mycoplasmataceae with
one genus, Mycoplasma; Acholeplasmataceae with genus Acho/eplasma; and
Spiroplasmataceae with the genus Spirolpasma. Mycoplasma spp. Need sterol for growth is
sensitive to digitonin whereas Acho/eplasma spp. Do not require sterol for growth and are
resistant to digitonin. Spiroplasmas are helical and have been cultured in artificial media.
3. Transmission
Most mycoplasmas are transmitted from diseased to healthy plants by leafhoppers,

planthoppers, treehoppers, aphids, mites and psyllids. Some multiply in the leafhoppers and
psyllid vectors.
4. Symptoms and diseases caused by mycoplasma
Aster yellows causes a general chlorosis and stunting of the plant, malformation of organs and
poor yield. The aster yellows pathogen has a wide host range that includes tomato, potato,
onion, lettuce, carrot, celery and gladiolus The symptoms In the different hosts usually vary.
The lethal yellowing of coconut trees causes premature fruit drop, ' yellowing of leaves starting
from the older to the younger leaves, and finally blighting within 3 to 6 months after the
appearance of initial symptoms.
Plants infected with the corn stunt Spiro plasma exhibit yellowing of
leaves which later turn to red or purple, stunting and excessive formation of sucker shoots
4.4 The Rickettsias as Plant Pathogens
The rickettsias are small, gram-negative microorganisms with a wavy cell wall. Some are
spherical, others are rod-shaped and still others are polymorphic. The rickettsias are generally
transmitted by insects.
18 |Plant Pathology
4.4. Protozoa as Plant Pathogens
Flagellate protozoa of uncertain pathogenicity occur in laticiferous plants. Phytomonas

leptovasorum is believed to cause the phloem necrosis of coffee in Surinam. The hartrot disease
of coconut is reportedly caused by flagellate protozoan.
4.6. Fungi as plant pathogens
Fungi are non-chlorophyll-bearing, spore-forming microorganisms, with branched filamentous

vegetative structures called mycelium. Fungi posses true nuclei and cell walls.
Symptoms and diseases caused by fungi
Symptoms caused by fungi include rots, spots, blights, leaf curl, yellowing, scab, canker,
anthracnose, powdery mildew, downy mildew, leaf streak or stripe, mummification, etc.
4.7. Nematodes as Plant Pathogens
Nematodes are thread like unsegmented worms which are thread like usually elongated and
cylindrical in shape. There is no internal deparation of the organs of the nematode, hence the
term, unsegmented, to describe them.
The nematodes may be saprophagous, predaceous or plant parasitic depending on their sources
of food. Saprophagous nematodes feed on the dead or decaying organic matter, the predaceous
ones feed on other nematodes and on other minute animals, and the plant parasites feed on all
forms of plant life including seed plants, algae, fungi and bacteria.
The plant parasitic nematodes are mostly obligate parasites and thus dependent on the living
host for survival as they feed and reproduce only in their hosts. Most of the plant parasitic
nematodes range from 0.5 to 2.0 mm in length and 0.01 to 0.5 mm in width.
2. Groups of plant parasitic nematodes
The plant parasitic nematodes are grouped according to their feeding position as ectoparasites,
semi-endoparasites and endo-parasites. There are migratory endoparasites and sedentary
endoparasites according to their mobility while feeding.
 Ectoparasite do not enter the roots of the host as they merely feed on root hairs and
tips of roots so that the roots may stop growing and form many lateral branches. Some
genera ofectoparasitic nematodes are:
 Be/ono/aimus - sting nematode of cereals, cucurbits, legumes, etc.
 Paraty/enchus -.pin nematode of many plants.
 Trichodorus - stubby root nematode of field crops and vegetables.
 Xiphinema - dagger nematode of trees and many annuals.
 Longidorus - needle nematode of certain plants.
 Migratory endoparasites migrate within the host and/or between the soil and the host.
 Praty/enchus - lesion nematode feeding on the root cortex of many plants.
 Radopho/us simi/is - burrowing nematode causes lesions in citrus, banana, sugarcane,

etc.
 Hoplolaimus lance nematode
 Helicofylenchus - spiral nematode ,

 Ditylenchus dipsaci - stem and bulb nematode causes deformation of leaves and stems
of onion and other crops
 Aphelencoides - foliar nematodes causing leaf malformations of rice, coconut,

strawberry: etc.
 Sedentary endoparasites may attach themselves to the roots of burrow into the root; in
each case they remain sedentary.
 Meloidogyne, the root knot nematode, and Heferodera, the cyst nematode, completely
enter the root and the adult females s become pear-shaped, lemon-shaped or almost
spherical. The r nematodes attack a very large number of a wide variety of plants
banana, beans, cassava, corn, tomato, papaya, etc.
 Rotylenchulus reniformis, the reniform nematode, and Tyl semipenetrans, the citrus
nematode, bury the front part of the b the host while the posterior portion of the
females swell outside cells. They are semi-endosparasitic.
20 |Plant Pathology
3. Mechanism of the nematode infection and symptoms of nematode damage
As the nematodes feed on the move about the host issues they injure the host mechanically I
but more significantly, the secretions that they inject into the host are toxic in various ways. Cell
division at the tip is inhibited and the root stops growing. Surrounding cells and the tissues are
killed. Giant cells may be formed when cell walls adjacent cells are destroyed and these cells
then coalesce. Other soil borne pathogens may enter through the mechanical injuries and
worsen the root damage.
The symptom if nematode damage is usually related to a malfunctioning of the root system.
 Galls on the roots are usually formed by the root knot nematodes as a result of
hypertrophy and hyperplasia. Galls may also be formed on the leaves, seeds and floral
parts by the leaf and the floral nematodes.
 Stunting of the aboveground parts is a common symptom which is associated with

reduced yield.
 Abnormal foliage coloration.
 The abnormal coloration of the leaves which is typical of mineral deficiency

diseases from root injury and root malfunctioning caused by nematode attack. This
inhibits the uptake of mineral constituents by the plant.
 Wilting results when nematodes injure the roots under conditions of moisture
stress.
 Leaf spots, distortion, twisting and swellings are caused by the stem, bulb and leaf
nematodes.
 Necrotic lesions in the roots and excessive root branching result when nematodes
feed on the root system. The lesion nematode feeds on the cortical root tissues
causing necrotic lesions.
o The salivary secretions of nematodes contain enzymes that may be

responsible for a variety of the host responses such as dissolution of cell
walls and lamellae, necrosis hypertrophy, hyperplasia, and growth
inhibition.
4. Disease complexes
A disease complex is a physiological malfunctioning caused by two or more pathogens.

Nematodes have been involved in disease complexes with fungi, bacteria, viruses, and other
nematodes. This is perhaps to be expected since the soil teems with millions of microorganisms
along with the nematodes. Many of these pathogens invade the host through the injuries made
by the worms. An example is nematode and bacteria and nematodes and fungi.
4.8. Parasitic Flowering Plants as Causes of Plant Diseases
a. The Hemi-parasites
Hemi-parasites depend on their hosts for water and minerals but not for photosynthates
because their leaves contain chlorophyll and can thus food through photosynthesis.
Striga asiatica or witchweed, can cause severe damage in corn, sugarcane, sorghum and other
plants by attaching its roots to the roots of the host, then using up the water and minerals that
are taken up by the host's roots.. The parasitized plants become stunted and yellowish, wilt and
eventually may die.
b. The True Parasites
The dodder, Cuscuta sp., attacks a number of host plants forming yellow
to orange leafless vine strands around the host. After the dodder has established a parasitic
relationship with the host, the basal stem of the dodder dries up and its contact with the soil is
cut. Dodder causes losses in yield and quality.
Broom rapes or Orobanche spp. Appear as clusters of yellowish, brownish or purplish stems
arising form the soil at the bases of host plants. The minute seeds are carried by rain and air
currents and germinate in the soil where suitable host are present. Upon germination, the
broomrape root attaches to the root of its host. New roots and a stem of the parasite fuse with
other host roots and the process is repeated over and over forming a broom rape cluster.
The dwarf mistletoe often parasites conifers trees causing reduced vigor, inhibited growth rate,
and poor timber quality.
4.9. Insects as Plant Pathogens
Insects have been known to cause mechanical injuries in plants with concomitant physiological
malfunctioning in the latter. The insect injury may block or cut off portions of the phloem
and/or xylem thus disturbing the normal transport of plant nutrients.
Insect may also secrete toxic compounds which are harmful to plants. These toxicogenic insects,
usually with piercing-sucking mouth-parts, inject the toxin while feeding on the plant.
22 |Plant Pathology
Insects may cause the formation of local lesions such as leaf spots, or fruit spots at the feeding
area. Scabs, premature defoliation, fruit drop, canker, cork formation, leaf malformations,
rosetting, phyllody, gummosis, and hopper burns may also be produced by insects in susceptible
plants.
5. VARIABILITY IN PLANT PATHOGENS
5.1 General Concepts
 All organisms, including the pathogenic microorganisms, continually undergo changes.

The shorter the generation time and the larger the number of reproductive units formed
in each generation, the greater are the chances of producing changes over a given
period of time. Pathogens such as the bacteria and fungi can grow and multiply rapidly.
Certain bacterial populations can double their numbers in 20 minutes during favorable
environmental conditions. A fungus can form millions of pores within a few days.
 Terms used in the subdivision of organisms
 Biotype as a "population of life forms that are identical in all inheritable traits”. As such,
biotype and are genetically homogeneous If an organism from one biotype mates with
one from another biotype, a different biotype is formed as result of hybridization.
 The next higher subdivision is the physiologic race which is made up of one or more
biotypes with all members morphologically identical. Different physiologic races differ in
the cultivars or host variety that each attacks.
 Next to the physiologic race is the formae speciales which is based on the ability to
attack different genera of crop plants. The classical example is Puccinia graminis with
members that infect different cereal crops with forma specialis triciti attacking wheat
only and f. sp. avenae attacking oat only, etc. Each forma special is may contain different
races that attack different varieties of the host.
 Next to the formae specialis is the species, then the genus, the family, the order, and
the class.
5.2 Mechanism of Variation
Microorganisms undergo genetic changes through hybridization, mutation, and a variety of

sexual-like and asexual processes,
1. Variation in the fungi
Different fungal species have various mechanisms for variation which may include mutation,
heterokaryosis, a parasexual process, cytoplasmic variation and sexual reproduction,
a. Heterokaryosis
Heterokaryosis is the presence of different nuclei in the, same mycelium. Each nucleus in
heterokaryon is independent of the other nuclei although the behavior and phenotype of the
microorganism controlled by the kinds of genes present and by the proportion of each kind.
b. Parasexual process
The parasexual process starts with the formation of a heterokaryon, followed by karyogamy or
dipliodization of nuclei, the multiplication of these nuclei and finally, these restoration to the
haploid state, Haploidization involves non disjunction and the formation of a deficient aneuploid
nucleus which undergoes further loss of chromosomes in successive similarly atypical mitotic
divisions until a haploid nucleus is formed. Mitotic crossing over at chromosome replication
results in the formation of genetically different nuclei after segregation.
c. Mutation
Mutation is a discontinuous heritable change of the genetic material which may arise
spontaneously or through the action of mutagenic agents. Mutation may result form structural
changes in single sites or loci of the DNA brought about by base pair substitution due to U copy
error U during DNA replication (point mutation), through structural alternations in the
chromosomes caused by rearrangement or loss of chromosomes segments (segmental
mutation), or4 through abnormalities occurring during meiosis and/or mitosis resulting in the
formation of polyploids and aneuploids (genome mutation).
d. Cytoplasmic variation
It has long been recognized that the nucleus does not have a monopoly on heredity as the
cytoplasm also carries heredity determinants. These extra chromosomal particulate elements do
multiply and can be transmitted asexually through hyphal anastomosis or sexually. They include
the extra chromosomal factors in the FNA of mitochondria (M-DNA), the particulate
plasmogenes in the cell's cytoplasm, and the mycoviruses which are mostly double-stranded
RNA.
e. Sexual Reproduction
Sexual reproduction in hybridization through segregation and gene recombination. Hybridization

requires the union of two different but compatible haploid nuclei. The nuclear fusion results in
the formation of a diploid nucleus which then undergoes meiosis. During meiosis segregation
and recombination of genes occur. The haploid from either parent as it receives a varying
combination of genes from each parent. Fungi that reproduce sexually produce variants
through hybridization.
24 |Plant Pathology
5.3. Variation in bacteria
Most variations in bacterial plant pathogens are brought about by mutation and transformation.
As in fungi, mutations may come spontaneously or naturally, or through the application of
mutagens.
Other bacterial mechanisms for variation are transduction and conjugation. Transduction occurs
when a bacteriophage (a virus that infects bacteria) transfers genetic material from its next host.
In conjugation there is transfer of genetic material from one bacterium to another when two
compatible cells come in contact with each other.
5.4. Variation in nematodes
Nematodes form a new physiologic races through hybridization and mutation. Pathogenecity
varies according to the degree of resistance! susceptibility of the host plant..
5.5. Variation in other pathogens
All pathogens which reproduce sexually utilize hybridization as a means of variation. Mutation is
also universal among organisms and may occur in the viruses and viroids. Variation are
expressed not only through direct changes in pathogenecity but also through alterations in
growth rate, longevity, host range, optimum temperature or pH, etc.
5.6. Genetics of host Parasite Interactions
The development of infectious plant diseases is dependent on the resistance or susceptibility of

the host plant and the virulence of the pathogen. The host and the pathogen posses their own
distinct genetic determinants. There are number of genes in the plant that determine its
resistance or susceptibility and a number of genes in the pathogen that determine its virulence.
This is the reason for the common observation that various physiologic races of the pathogen
vary in their ability to attack a host variety and that different host cultivars vary in their response
ton a physiological race. When a new resistant variety is developed a new gene for virulence
sooner or later appears, so that the host resistance is said to break down. Plant breeders then
introduce another gene for resistance in the host against the new gene for virulence in the
pathogen.
6. THE DISEASE CYCLES

The disease cycle is the sequence of events that leads to, and is involved in disease production.
The cycle includes the activities of the pathogen while it is away from the suspect as well as
those while the pathogen is on and within the suspect The disease cycle should be distinguished
form the life cycle of the pathogen.
6.1. Parts of a Disease Cycle
a. Inoculation
This is the deposition of inoculum into an infection court. Inoculum is any part of the pathogen
that initiates disease. The infection court may be a natural opening (stomata, lenticel,
hydathode.. growth crack), a wound, or the intact host surface.
b. Penetration
Penetration occurs upon the entrance of the pathogen into the host. Penetration is completed
when the pathogen has passed through the initial cell wall or entered the intercellular areas so
that the pathogen is within the plant.
c. Infection
Infection occurs (after penetration) when the pathogen has become established in the plant
tissues and obtains nutrients from the host.
d. Colonization
Following infection, the pathogen continues to grow and colonize the host. Colonization is the
growth or movement of the pathogen through the host tissues. Incubation .
Incubation period has been used to mean the time from inoculation to the production of visible
symptoms. Others use it to refer to the time from the first response of the plant to the
formation of visible symptoms.
e. Dissemination
After the symptoms have advanced, signs or pathogen structures are formed on the colonized
surface of the host. These structures which can serve as inoculum later are disseminated or
spread by insects, wind, water and other' agents. If the inoculum lands in or on an infection
court, inoculation is effected, penetration may proceed and the disease cycle may continue. The
inoculum produced on a recently diseased plant is called secondary inoculum which initiates the
growing season of a plant.
g. Survival
26 |Plant Pathology
Some pathogen structures may not land on a susceptible plant and certain environmental
factors may not favor its continued growth and development. The pathogen has therefore to
tide over adverse conditions or survive until conditions become once more favorable for
pathogenesis. When favorable conditions occur, inoculation proceeds followed by penetration
and the cycle continues once more.
6.2 Types of Disease Cycles
Different disease caused by various pathogens exhibit disease cycles that vary in detail$. Some
pathogens survive adverse condition$ in the soil and in dead plant refuse, others in weed hosts,
still others in seeds. Some diseases have numerous secondary cycle whereas the secondary cycle
may be significant in certain diseases
7. INOCULUM, INOCULUM SURVIVAL AND INOCULATION
7.1. Types of Inoculum
Fungal pathogens produce asexual or sexual spores that are capable of initiating disease.
Mycelial fragments, sclerotial bodies, rhizomorphs, and dormant mycelia in seeds can also start
disease production.
The eggs, larvae and adults of plant parasitic nematodes may also serve as inoculum.
Other inocula are cells of bacteria and mycoplasmas, rickettsia, virus particles, viroid particles,
viroid entities and seeds of parasitic flowering plants. .
7.2. Sources of Inoculum .
The sources of inoculum are: (1) infected living plants, (2) plant debris, (3) infested soil, (4)
infected seed and vegetative propagating materials, (5) contaminated containers, storage areas
and equipment, (6) insects, nematodes and other living agents that carry inocula.
7.3. Dissemination
Inocula, to be effective, have to reach an infection court. The spread or dissemination of

inoculum may be effected by wind, water, man, insects, mites, nematodes, seeds and other
planting materials.
a. Wind dissemination
 Wind dissemination is the major means of spreading air-borne pat~9gens such as fungal
spores of leaf, stem, and fruit pathogens.
b. Dissemination by rain
 Fungal spores and bacterial cells are carried to short distances by rain splashes. As
raindrops fall on bacterial exudates, the bacterial calls are scattered about and spread to
various infection courts. The energy of raindrops or rain splashes loosen up and disperse
fungal spores from fruiting bodies.
c. Dissemination by insects
 Viruses, as well as some bacteria and fungi, are carried from plant to plant by insect
vectors. As insects feed on a plant, the inoculum that they carry are deposited and are
left on the injured portions where the insects had just fed on.
d. Dissemination by seed and planting materials
 Viruses, viroids, mycoplasmas and many bacteria are often carried internally in infected
seed or vegetative propagating materials. Seeds and other plant materials may also
carry fungal spores, bacterial cells or nematodes externally or on the surface. Such
materials are said to be infested.
e. Dissemination by man
 Man is a major long-distance disseminator of plant pathogens. Many diseases have been
introduced from country to country or between continents by men who carry infected
and infested planting materials and seeds. Shipping crates and various other containers
and equipment used for agricultural products usually carry all kinds of inocula. Man also
inadvertently disseminates and inoculates in the field or garden as he handles diseases
plants then moves on to healthy plants.
7.4 Survival of Inoculum
Pathogens must survive conditions of stress if they are to cause infection at a future date. The
Philippines and other tropical areas like it, are "haven" for plant pathogens as 1here are
practically no environmental extremes for the pathogen has to overcome is the absence of the
host between planting seasons. Even this, however, is not much of a problem for pathogens
with a wide and diverse host range; and with man's help as he practices continuous culture.
Pathogens may tide over adverse conditions by: (1) surviving as saprophyte in dead plant debts
in the soil, (2) forming thick-walled resistant structures for survival, (3) surviving in weeds and
other hosts, (4) surviving in vectors, or (5) surviving in the seed.
28 |Plant Pathology
a. Survival as saprophyte
 Many fungi and bacteria survive as saprophytes in dead organic matter.
 Viruses, viroids, mycoplasmas, nematodes and phanerogams do not survive as

saprophytes as they are obligately parasitic.
b. Production of resistant structures
 Fungi form a variety of specialized resting structures that remain dormant and resist
adverse environmental conditions. The teliospores of the rust and smut fungi, the
oospores of the phycomycetous fungi, . and the ascospores of the ascigerous fungi
remain dormant until conditions become favorable for their germination and continued
growth. Seeds of some phanerogams also remain dormant until a susceptible plant is
available.
c. Survival in weeds and other hosts
 Many pathogens have such a wide host range that in the absence of the one suscept
that infect other host. lf no economic host is present, there are always a number if,
weed host and wild plants which pathogens can infect.
d. Survival in the suscept
 Many viruses, bacteria and fungi survive in various ways in their respective hosts. Such
pathogens remain quiescent or dormant in the suscept until conditions for active
growth once more prevail.
e. Survival in vectors
 Certain viruses, viroids, mycoplasmas and a few bacteria survive in their insect vectors.
7. 5. Inoculation
Inoculation, the deposition of inoculum on or in the infection court, can be carried out in several
ways..
Man often unintentionally, unthinkingly, and unknowingly inoculates. The use of contaminated
agricultural implements (for pruning, trimming, etc.) usually transfers viral, bacterial or fungal
inocula from diseases to healthy plants. The market vendor who trims off soft-rotted portions
from a cabbage head and uses the same knife to trim other cabbage heads is certainly
inoculating.
Cigarette-smoking farmers often inoculate the tobacco mosaic virus to healthy plants as they
handle the plants with contaminated hands.
Insects play an important role in field inoculation specially as they can travel relatively long
distances and find their sucepts
In nature, inoculation by chance is also quite a common occurrence. Some of the spores that are
carried by wind and rain splashes may fa:11 on stomata or some other infection court but the
major proportion of these spores may be deposit~d in way out places. Insects and other animals
that carry inocula in their body parts also deposit these inocula just wherever the happen to
alight or brush against
7.6. Inoculum Potential
Inoculum potential is defined by Kenaga (1974) as the amount of tissues invaded per infection,
and the number of independent infections that may occur in a population of susceptible hosts at
any time or place. It is measured by the ~ymptoms that result from infection. The amount of
tissues invaded per infection may vary from a few cells a$ in some local lesion foliar diseases, to
the entire plant as in many vascular diseases, Since optimally favorable environmental
conditions are required for optimum infection, the inoculum potential is affected by the effect of
the biotic and abiotic factors of the environment on the amount of infection that can occur.
8. PATHOGENS' ENTRY INTO PLANTS
Pathogens may enter their suscepts through wounds, natural openings (Ienticels of stems,
stomata and hydathodes of leaves, nectarines, leaf scars, trichomes), growth cracks, or directly
through the intact host tissue. Many fungi, nematodes, and phanerogams enter their hosts
actively whereas viruses, viroids and mycoplasmas enter passively through their vectors.
Bacteria may penetrate the host passively, or actively by swimming through natural openings.
8.1. Pre-penetration
The inoculum deposited in or near the infection court may be affecteq by various physical,
chemical and biological factors before penetration takes place.
Temperature, moisture, light, pH, oxygen and carbon dioxide relations may variously affect
different pathogens during pre-penetration and subsequent entry into the plant.
8.2. Ports of entry
a. Natural openings
Bacteria enter their hosts through natural openings and through wounds. Bacterial leaf
pathogens usually enter through stomatal openings.
30 |Plant Pathology
Fungi may less frequently enter the host through hydathodes. The spores germinate in the
guttation drops near the lesf tips and penetration hyphae are passed through the hydathodes
into the interior of the host.
Trichomes (hair-like structures found on the surfaces of leaves, some fruits, stems and petioles)
may also serve as avenues for the entrance of bacterial plant pathogens. The cuticle of
glandular trichome may break at the portion where gland secretions have accumulated. The
rupture may be the portal of entry for the bacteria that have found their way in the area Some
trichomes are easily broken by a gentle touch. The broken hairs are readily penetrated by
bacterial cells.
The nectary cells of flowers secreted drops of nectar that are frequented by insects which may
carry bacterial cel1s. !he bacteria are deposited in the remaining nectar wherein they multiply
and later penetrate into the ovary. flower' pedicel and the stem.
Fungi may enter their hosts directly through the intact host surface, through wounds, or through
natural openings.
b. Intact host surface
The uredospore of Phakopsora pachyrhizi (cause of soybean rust) penetrate through the intact
leaf epidermis after forming an appressorium and infection peg which passes through the cuticle
and cell wall. Aerial mycelia are then formed on the host surface which penetrate neighboring
cells and new haustoria for absorbing host nutrients are formed.
8.3 colonization of the Suscept
Colonization is the active or passive movements of the pathogen through the host tissues. It is
active when the pathogen does something as when a fungal pathogen for instance, grows as it
passes from cell to cell; and passive if the pathogen is merely carried through the transpirational
stream as are some viruses. Colonization involves growth the reproduction of the pathogen
such as the formation of new spores, bacterial cells, virus particles, viroid entities, mycoplasma
bodies, nematode stages, or mycelia.
a. Colonization by Viruses, Viroids and Mycoplasma
 Viruses have been found to be moved from cell to cell through the plasmodesmata
(minute passageways between adjacent cells).
b. Colonization of Bacteria
 Movement from cell to cell during mitosis

 Swim actively through the xylem vessels or passively carried into the transpiration
stream
 Production of pectinolytic enzymes which breakdown the middle lamellae between cells
c. Colonization by Fungi
 Fungal colonization may be on the surface or within the host tissues Some get inside the
cells (intracellular) or remain between cells (intercellular). The fungi colonize with
spores and/or mycelia (with or without haustoria). ,
1. Colonization on the host surface
2. External colonization with haustoria inside the host cells
3. Intercellular colonization without haustoria
4. Intercellular colonization with intracellular haustoria
5. Intracellular colonization
6. Intercellular and intracellular colonization
d. Colonization by Nematodes
The fertilized female of a sedentary endoparasite (such as the root knot nematode) slowly
moves into the interior of a susceptible root until the nematode's head is near the middle of the
state. Here, it becomes sedentary while feeding on the cells adjacent to her head. She then lays
an egg mass which breaks through the root surface. After the eggs hatch, the larvae penetrate
the host and later become sedentary, feed, the females lay eggs and so on until a large
population of nematodes is built up.
e. Latent Infection
In certain diseases, colonization of the host is delayed due to latent infection, Verhoeff in 1974
defined latent infection as a quiescent parasitic relationship which can change into an active
one. This phenomenon occurs in certain diseases as the anthracnose of mango, citrus and
banana,
Latent infection is not very well understood. Some theories to explain it )are: (1) the unripe fruit
does not contain the nutrients that the pathogen needs for continued growth (2) the immature
fruit has toxic substances that inhibit colonization or (3) the pathogen lacks the enzymes needed
to colonize the immature fruit.
9. MECHANISMS OF PATHOGENICITY AND HOST RESPONSE
Living green plants need enough water, inorganic elements and carbon dioxide to allow them to
transform the energy from the sun into chemical energy that is required for their cellular
activities. With enough water, minerals and CO2, the plants can manufacture carbohydrates,
proteins, nucleo-proteins, nucleic acids, fats, lipids. vitamins, etc. These are used as sources of
energy, precursors, catalysts. structural materials, and components of the various cell
constituents that function for the plant's normal growth and reproduction. Almost anything that
impairs or interferes with the plant's normal processes causes and abnormal response in the
host.
32 |Plant Pathology
9.1. Interference with the uptake of water and inorganic elements from the soil.
Root-roting microorganisms invade and destroy the roots thereby reducil;l9 their water-
absorbing capacity.
9.2. Interference with translocation of organic compounds
The organic nutrients that are formed in the leaf during photosynthesis are transported through
plasmodesmata to the phloem elements and then to the cell protoplasm where they are used in
various cell reactions or stored in storage organs.
Several virus pathogens cause phloem necrosis which results in the accumulation of starch in
the leaves as phloem transport in impeded. Obligate parasites cause the accumulation of
organic and inorganic nutrients in the portions that they colonize.
9.3. Reduction of the plant's photosynthetic capacity
The role of photosynthesis in the life of the plant is basic to the continued normal functioning of
the suscept. Pathogens that cause leaf abnormalities are guilty of reducing the effective surface
for photosynthesis, such pathogens may cause spotting, blighting, curling, mosaic, mottle, die-
back, canker, scab. chlorosis, little leaf and wilting. Some pathogens destroy the chloroplasts and
reduce the chloroplasts and reduce the chlorophyll needed for photosynthesis Certain viruses,
viroids and mycoplasmas may block the synthesis of chlorophyll resulting in chlorosis. Plants
deprived of adequate photosynthates may be stunted and necrosed.
9.4. Increased transpiration
Leaf pathogens (such as powdery mildews, the downy mildews and the rusts) that destroy the
cuticle and epidermis, as well as increase the permeability of the leaf cells, also bring
detrimental water loss through increased transpiration. If not enough water is absorbed and
translocated 10 make up for the water lost in transpiration, the leaves eventually wilt.
9.5 Changes in growth of the suscept
Normal plant growth involves a series of coherent, well-regulated and coordinated processes as
metabolism is controlled by growth-regulating hormones as well as by compensatory or
feedback mechanisms. Pathogens may adversely affect suscept growth by: (a) producing alien
hormones that cause abnormal host responses, (b) by producing substances that induce the
host to produce too little or too much of the growth hormone, (c) by producing a growth
regulator that is normally produced by the host so that the level of this regulator would be
higher than the normal level, and (d) by .forming metabolites that affect the plant's normal
regulatory system.
9.6. Changes in the reproduction of the host plant
Pathogens may also create changes in the flowers of plants. Some pathogens enter the host
through the nectary cells of flowers and cause blossom blight which reduces the yield of fruits.
From the flower, the pathogen continues to colonize the pedicel, the twig and the branches.
Various pathogens remain dormant in the seed coat and as the seed germinates, invade the
young seedling.
9. 7. Death of cells and tissues
Necrotic diseases brought about by fungi, bacteria, viruses and other pathogens cause a
disintegration of cell walls as well as of protoplasm which resulted to death.
a. Disintegration of the cell wall and middle lamella
The cell wall and middle lamella are made up of complex, high molecular weight compounds
such as cellulose, pectic substances and proteins which pathogens cannot directly absorb.
Hence, these macromolecules have to be degraded to simpler units by hydrolytic enzymes
which the pathogen and/or the host produces during pathogenesis. Cellulose is converted to
glucose, a simple sugar; proteins to amino acids; insoluble pectic substances to soluble pectic
acid. The end product can then be utilized by the pathogens for their growth and reproductive
processes.
Degradation of cellulose in the cell wall
a. Degradation of hemicellulose
Hermicelluloses are polymers of monosaccharides such -as glucose, galactose, mannose, xylose,
and arabinose in varying combinations Hemicellulases break down the hemicelluloses
hydrolytically to the components monosaccharides. Wood-rotting fungi are known to produce
hemicellulases.
Decomposition of pectic substances
a. Breakdown of proteins
Proteolytic enzymes hydrolyze proteinaceous materials in the following manner: (a) proteinases
break down the protein to polypeptides; (b) peptidases break down the polypeptides to amino
acids and smaller peptides. Proteolytic enzymes are known to increase tissue maceration by
pectolytic enzymes.
b. Disintegration of the protoplasm

The decomposition of protoplasmic materials and the consequent cell death may be caused by
pectolytic enzymes that destroy the middle lamella and separate the cells and cause increased
34 |Plant Pathology
permeability and loss of water. Various hydrolytic enzymes attack the cell constituents. The
pathogen may also produce toxins that alter the permeability of the cell membrane causing a
leakage of metabolites and water loss from the cells, coagulate or hydrolyze proteins, or act as
anti-metabolites that deprive the suscept of essential metabolites. The pathogens then obtain
nutrients from the decomposed protoplasmic materials.
"Toxin" is a loose term, used to refer to a compound that is formed by the pathogen or the host
which is detrimental to the host. The toxin may: (1) affect the cell membrane causing changes in
permeability, (2) stimulate abnormal growth of host cells, (3) inhibit or inactive enzymes, (4)
increase respiration, (5) physically block cell and tissue systems and (6) act as an anti metabolite
causing a deficiency for an essential growth factor
10. MECHANISMS OF DEFENSE/DISEASE RESISTANCE
Defense mechanism
 Cuticle
 Waxy layer
 Epidermal wall
 Closing/opening of stomata cells
 Inhibitory compounds
 Secretions (catechal and proto-catecheis acid in dead onion scales)
 Exudates that are toxic and presence of projecting guard
10.1. Passive defense mechanisms to establishment of the pathogen
Many microorganisms manage to penetrate the plant but are unable to progress deeper than a
few cells or are limited only to certain areas. This is due to induced as well as pre-formed
defense mechanisms in the host. The pre- existing mechanisms, (b) presence of toxic
substances, (c) inability of the pathogen to form the enzymes necessary for further invasion, (d)
presence of tissues that block the progress of the would-be pathogen such as lignified and
suberized layers, endodermis, sclerenchyma, and (e) unfavorable factors within the tissues such
as moisture stress, too high or too low pH for the pathogen, unfavorable osmotic concentration,
etc.
10.2. Active defense mechanism to the establishment of pathogen
Active defense mechanism are those resorted to by the host in response to the activities of the
pathogen. In effect, these mechanisms are induced by the pathogen and include mechanical
barriers, hypersensitivity, phytoalexins and other toxic metabolites, and detoxification.
10. EPIDEMIOLOGY OF PLANT DISEASES
1.1.1. Factors affecting the development of epidemics
An epidemic is more likely to occur when a single crop variety is planted over a wide area or
when the plants are predisposed to infection by excessive nitrogen fertilization or by injuries.
The inoculum should. be abundant enough, rapidly formed, vigorous, efficiently liberated,
spread and inoculated. The more numerous and more efficient the vectors are, the more
chances of an explosive disease outbreak
11.2. Analysis of epidemics
The increase in the amount of disease at anyone time is dependent on the following: (a) the
initial amount of disease or initial inoculum, (b) the rate of C disease increases and, (c) the
duration of disease increase or the period of time involved.
Van der Plank has pointed out that an epidemic always starts with the first diseased plant in the
population. During ideal conditions for disease development, the amount of disease in a
susceptible population increases logarithmically in the beginning uninfected plant population
decreases, thereby:, limiting dise~se i~cre~se. I.f disease incidence is therefore plotted against
time, one gets a sigmoid epidemic curve."
Zadoks and Schein (1979) divide an epidemic into 3 phases: exponential or logarithmic phase,
logistic phase and terminal phase.
During the early part of the epidemic when there is a logarithmic increase of disease, the basic
compound interest formula can be used to determine the amount of disease at anyone time: X =
Xoert.
11.3. Relation of epidemiology to control practices
We have seen from the formula X = X oert. that the amount of disease (X) produced is affected by
the initial inoculum (Xo), the rate of disease increase (r.), and the time (t). .
Most control measures are geared towards reducing the initial inoculum and/or the rate of
disease increase. The time factor is less readily manipulated although sometimes one can plant
early enough in the season to escape disease or use early-maturing varieties that could be
harvested before a high level of inoculum has been built up by the pathogen.
11. ASSESSMENT OF DISEASE INCIDENCE AND CROP LOSS
36 |Plant Pathology
The purposes of disease assessment or disease appraisal are to determine the disease severity
and prevalence, relate these to yield loss, and then express yield loss in financial terms and
evaluate its effects on the farm economy.
a. % diseased plant = no of diseased plants X 100

total no. of plants
b. Another method is to measure the diameter or the length and width of lesions from
which the area of infected tissue is calculated.
Some workers prepare percentage disease groups and then determine the number of plants or
organs that fall into each group. A percentage grouping used by Horsfall and Barratt was 0-3, 3-
6,6-12, 12- 25,25-50,50-75,75-88,88-94,94-97,97-100%.
12.1. Use of descriptive disease ratings on a numerical scale
fScales used for rating diseases describe in detail the grades of diseases. The scale used for leaf
blast of rice (caused by Pyricularia oryzae) at the International Rice Research and Institute is as
follows: 0 - no "lesions; 1 - small brown specks of pinhead size; 2 - larger brown specks; 3 - small
roundish to slightly elongated necrotic gray spots, about 1 - 2 mm in diameter; 4 - typical blast
lesions, elliptical, 1 -2 cm long, usually confined to the area of the 2 main veins infecting less
than 2% of the leaf area; 5 - typical blast lesions infecting less than 10% of the leaf area; 6 -
typical blast lesions infecting less than 10-25% of the leaf area; 7 - typical blast lesions infecting
26-50% of the leaf area; 8 - typical blast lesions infecting 51-75% of the leaf area and many dead
leaves; 9 - all leaves dead.
Trait expressions with a score of 3 or less can be used as sources of disease resistance in
breeding work, and for commercial purposes. Scores of 4- 6 may be acceptable for commercial
use in the absence of anything better but should not be used for breeding purposes. Scores of 7-
9 are not desirable at all.
The rating scale used for virus diseases is based on the percentage infected plants per hill: 0 - no
incidence; 1 - less than 1 %; 2 - 1 t05%. 3 - 6 to 10%; 4 - 11 to 20%; 5 - 21 to 30%; 6 - 31 to 40%; 7
-41 to 50.\; 8- 61 to 80%; 9 - 81 to 100%.
Disease severity may also be evaluated by comparison with standard diagrams. These are useful
for leaf diseases such as spots, blights, rusts, mosaics, for fruit rots and spots, and for other
diseases
12.2. Methods of measuring crop losses
After the amount of disease has been determined, the next thing to do is to relative this to crop
or yield loss. Crop loss assessments may be done with survey methods or experimental methods
a. Survey methods
Survey methods involve the gathering of a large number of reports on disease incidence as well
as on crop loss and yield estimates that have been collected through the years. The accuracy of
the method depends on how reliable the data from the assembled reports are.
A comparison of the yield data before and after the application of control measures will give
some idea of crop loss due to the disease.
b. Experimental methods
Experimental methods should be properly designed for sound statistical analysis. Adequate
replicates carried over several different seasons in various places should be provided.
Yield comparisons between diseased and healthy plants will give the amount of crop loss due to
the disease. Diseased plants are obtained by inoculation and healthy plants are kept uninfected
by treating them with protectants or systemic chemicals.
The yield differences between susceptible and resistant or immune varieties in the presence of
disease will also give a pretty good idea of crop loss from the disease. However, the varieties
used should normally yield similarly; otherwise, the innate differences in yield (when there is no
disease) and susceptibility to other diseases and to pests has to be considered and corrected for.
12.3 Plant Disease Surveys
Disease surveys are wide-scale appraisal of the severity and prevalence of disease in a country, a
region or a continent. The objectives are to: (a) determine the geographical distribution of
certain diseases, certain pathogens or certain pathogens or certain physiologic races, (b) detect
and monitor newly introduced pathogens and (c) determine the distribution of alternative and
alternative hosts. All these will and in the evaluation of the relative importance of diseases and
assist in the development of a cooperative control program
13. PRINCIPLES AND METHODS OF PLANT DISEASE CONTROL
13.1 Principles of Plant Disease Control
There are four general principles of plant disease control, namely, exclusion, protection,
eradication and immunization. Each of the available control measures is based on one of these
principles. The purposes of plant disease control are to a) prevent disease development, b)
maintain the tolerable disease incidence and c) minimize yield losses.
38 |Plant Pathology
a. Exclusion
Exclusion is the prevention of a "new pathogen" from being introduced into. locality where it is
currently unknown. This necessarily involves legal methods of control.
Prohibition is the complete prevention of the entry of infected plant materials by quarantine
laws that regulate the movement of plants and plant parts. A plant pathogen may be introduced
into an area through an infected plant, by insects, animals and people on. their bodies, through
contaminated luggage, containers, ships, planes, and even by air currents.
b. Protection
Protection involves the prevention of infection by putting a chemical barrier (protectant spray or
dust) between the pathogen and the suscept, by controlling certain environmental factors that
affect infection, or by crop management practices that prevent or reduce infection.
Protectant chemicals must be applied on the plant surface before inoculum deposition, to
prevent infection. If older plant parts such as leaves are diseased, the uninfective newly
emerged and emerging leaves must be treated at once, before the pathogen's arrival or before
germination and penetration. The protectant prevents spore germination or kills germinating
spores.
A protective measures against the spread of post harvest pathogens is to wrap individual fruits
with paper. This provides a barrier between fruits that may be treated with a fungicide such as
biphenyl for an added measure.
Crop management practices such as choice of planting site and planting date, adjustment of soil
pH (clubroot of cabbage is controlled in slightly alkaline soils, potato crab in acid soils),
fertilization, and irrigation methods may be useful in controlling certain diseases.
c. Eradication
Eradicative measures are intended to eliminate, inhibit or kill the pathogens that have become
established within the plant or in the area.
Eradication by disinfections involves the use of systemic chemicals that are absorbed by plant
tissues in varying degrees and may be translocated through the plant. They can therefore, act on
pathogens that have become established within the host tissues
Disinfections by hot water treatment is an eradicative measure against established infection in

fruits, bulbs and seeds
Heat treatment has been therapeutic against diseased caused by viruses, viroids, mycoplasmas
and rickettsia present in dormant planting materials and growing plants. Soil may be disinfested
by chemical treatment or by heat to kill pathogens.
Rouging or the removal and destruction of infected plants should be done when disease
incidence is still pretty low and when the eradication of diseased plants is economically feasible.
Diseased plant parts may also be removed.
The eradication pf alternate hosts, wild hosts, and weeds that may harbor the pathogen will do
a lot towards eradicating the pathogen.
Crop rotation is quite effective is reduci~ the inoculum level although it may not totally
eradicate the pathogen.
d. Immunization
Immunization involves modifying certain physiological or physical features of the host so that it
can repel infection, as in the breeding for disease resistance.
Resistance is the relative ability of the plant to overcome the effects of a pathogen.
Two recognized types of resistance are vertical resistance (also called major gene resistance,
oligogenic resistance, specific resistance) and horizontal resistance (minor gene resistance,
polygenic, non-specific ~'i resistance, generalized resistance field resistance).
The use of resistant varieties is often the most effective and most economical method of plant
disease control...
13.2. Methods of Plant Disease control
a. Sanitation
 destroying plant refuse or debris (which harbor the pathogens) by burning or burying
them
 cleaning and disinfecting implements used for pruning or trimming
 cleaning, disinfesting, fumigating warehouse before and during storage of produce
b. Cultural Methods
 eradication of diseased plants (or rouging) in greenhouses, nurseries, or in the field to

reduce or eliminate inoculum sources
 crop rotation or planting for a number of year non-hosts of the pathogen
40 |Plant Pathology
 practices that improve the growing conditions of plants such as proper drainage, tillage,
fertilization, irrigation
 providing conditions that are unfavorable to the pathogen such as dry fallowing or
flooding the field for some time to reduce the pathogen population by desiccation,
insufficient oxygen or by starvation
 tissue culture of meristem tips that have not yet been reached by the pathogens as the
plant tissue often grows in advance of the pathogen; used for virus diseases and some
vascular diseases as those caused by Fusarium
c. Physical Methods
 heat treatments of plants, plant parts, soil, containers, etc. using hot water, moist heat
or dry air
 low temperature storage
 controlled atmosphere storage
 irradiation I
d. Chemical Methods
 seed treatment with chemicals 2. fl,jmigation of soil, warehouses

 che.mical control of insect vectors of pathogens
 use of chemical protectants and chemotherapeutants which include copper compounds,
inorganic and organic sulfur compounds, benzene compounds, quinines, heterocyclic
compounds, the systemic biocides, antibiotics, growth regulators and other organic
fungicides.
e. Biological Methods
Biological methods employ the use of microorganisms that compete with, parasitize, or are
antagonistic to the pathogen
1. Cross protection
This refers to the protection of a plant by a mild virus strain, against infection by another strain
of that same virus which is more virulent and causes more severe symptoms.
2. Interference
Roots infected or colonized by mycorrhizae seem to be protected from infection by Fusarium,

Pythium, and other pathogens. The mycorrhizae may provide a barrier to infection by inference.
Crown gall caused by Agrobacterium tumefaciens was found to be effectively controlled if the
seeds, seedlings or rootstocks are treated with a bacterial suspension of a strain of A.
radiobacter.
3. Use of bacteriophages
Laboratory experiments have indicated control of bacterial pathogens by mixing bacterial

inoculum with the phage. Its widespread use as control measure has, however, not been
successful.
4. Use of parasites or antagonists of pathogens
Several mycoparasites have been observed on many pathogenic fungi. Fusarium root rot of corn
can be controlled by treating seeds or dipping seedlings in solutions containing the antagonistic
microorganism. Soil amendments that favor the growth of antagonists may be added to the soil,
thus reducing the numbers of the pathogenic population. Hyperparasitic fungi that attack fungal
pathogens such as rusts, downy mildew, root rotting fungi, etc., viruses, protozoa, and other soil
organisms. Their use to control the nematode population is promising but field application has
not been too successful.
5. Use of resistant varieties
a. Selection
Man, during the early years, developed several resistant varieties simply by planting seeds from
resistant . plants in the field that survived the onslaught of a disease .Selection is still used today
to find sources of resistance for breeding purposes.
b. Gene pyramiding
Gene pyramiding involves the incorporation of several resistance genes in one host variety so
that it would take the pathogen a long time to be able to overcome the resistance. This variety
will reduce the initial effective inoculum (Xo) because chances are that only a very minute
proportion of the pathogen population might infect it. Moreover, all the genes acting together
would mimic horizontal resistance, reducing the rate of infection as it reduces pathogen growth
and development.
c. Multiline varieties
A multilane variety is a mixture of several lines with similar agronomic characteristics but each
with a different gene for resistance. A pathogen would tend to invade only one or two of the
varieties in the multiline.
d. Gene or variety deployment
42 |Plant Pathology
Gene or variety deployment involves the use of different resistance genes or varieties in various
geographical areas instead of the widespread monoculture being practiced today. This would
reduce the chances of epidemics and pandemics occurring. However, its execution presents
great difficulties as it requires the cooperation of growers and governments over an extensive
area.
e. Legislated or regulatory control methods
Now and then, the government enacts laws that regulate, restrict or prohibit the entry or
movements of diseased : plant materials into or within an area. It may also order certain
activities that are intended to contain a disease. Quarantine measures all the ports of entry as
well as post-entry quarantines are regulatory measures.
14. GENETIC ENGINEERING OF PLANTS AND PATHOGENS FOR RESISTANCE TO DISEASE
14.1. Why Use Genetic Engineering Approaches?
To obtain sources of resistance which are not otherwise available:
1. Transferring non-host resistance from other species is the "holy grail" for genetic
engineers. If the resistance in wheat to Phytophthora infestans is under simple genetic
control and can be moved into potatoes by genetic engineering, the hope is that the
resistance will be permanent. But if non-host resistance is polygenic or determined by many
different traits interacting in a complex way, it probably cannot be moved between species
by genetic engineering.
2. When resistance genes cannot be moved between plant species by traditional breeding
practices (which now include species bridges and embryo rescue methods), then genetic
engineering might be useful.
1. When no genetic resistance is known to exist in domesticated germplasm or in wild

relatives.
To accelerate the breeding process, the following can be done:
1. Gene therapy refers to the transfer of resistance genes within species. Genetic
engineering also can be used to make R-gene pyramids or to create new combinations of R-
genes more quickly than by traditional breeding. If R-gene cassettes can be created, then
entire groups of R-genes can be moved among different cultivars easily, facilitating
production of multilines.
2. Wide crosses usually involve the transfer of undesirable linked agronomic traits that come
from the wild relatives. With engineering methods or through marker-assisted selection,
fewer backcrosses are needed to make a resistant variety with good agronomic
characteristics.
3. Quantitative resistance is difficult to work with because many progeny must be

screened and many replications across different environments are needed. Marker-
assisted breeding can be used to identify QTLs and speed movement of quantitative
resistance into good agronomic backgrounds. It remains possible that entire QTL loci can be
cloned and moved within or between species in the future.
14.2. Assessment of the Risk Involved in Genetic Engineering of Plants
Plant breeding practices developed over several thousand years, but only in the last
hundred years have breeders begun using direct manipulations of the genome based on
knowledge of how genetic information is carried and transmitted between generations. For the
first 1000s of years of breeding, all improvement was based on intra-specific hybridization. The
next step was to introduce inter-specific hybridization, sometimes called a wide cross. Next
came direct chromosome manipulation, followed by muta-genesis (chemical/physical), somatic
cell crosses (based on protoplast fusion), and somaclonal variation (tissue culture). The most
recent developments, popularly known as genetic engineering, involve site-directed
mutagenesis (chimeraplasty), and direct gene transfer ("transgenics"). Thus genetic engineering
is only the most recent development in 100 years of progressive increases in technology based
on increasing knowledge of how to manipulate plant genetic material. At each step, the
precision of the genetic manipulations has become more precise. Site-directed mutagenesis can
change a single gene, while protoplast fusions or somaclonal variation involved dozens,
hundreds, or thousands of genes. Traditional intra-specific hybridization affects tens of
thousands of genes at each step.
At the present time, there is lots of hype in genetic engineering, but with the exception
of virus resistance, there is not much success yet in the field setting. All success at this point has
been in growth chambers or greenhouses. Many engineered plants show good resistance in the
lab and greenhouse, but not in the field. This suggests that disease resistance in most cases is
more complicated than simply sticking a new gene into an existing genome.
Most engineered crop plants to date are good "lab pets" that have poor agronomic
characteristics and transgenic plants often perform poorly under field conditions. But, the
potential is enormous and research is vigorous. Resistance packaged in the seed is potentially
the most useful means of control for all plant diseases, and the payoff will be large for
companies that succeed in engineering disease resistance. Public concern about genetic
engineering is high at the moment because the public perception is that the risks involved in
engineering plants are high. What is needed is a scientific evaluation of the actual risks involved
in genetic engineering of plants (risk assessment).
One way to consider risk is to consider what happens when exotic genes are introduced
into a native ecosystem. When Europeans colonized North America, they introduced thousands
of new plant species (and millions of genes within those species) that did not previously exist on
the continent. In addition, many weed species were introduced into North America as a result of
44 |Plant Pathology
trade and travel. By comparison, the number of genes introduced through genetic engineering is
trivial.
Another risk is to human health. One risk to consider when engineering plants for
genetic resistance is that many of the secondary metabolites that are toxic to pathogens (eg.
saponins, lectins) also are toxic to people. It is likely that one of the reasons why agricultural
crops are more susceptible to disease than native plants is that humans selected against
production of toxins during the domestication process. It is probably best not to re-introduce
those toxins into our current agricultural crops, so we must choose the genes to introduce
carefully. Enzymes (e.g. chitinases) that affect only fungal cell walls would be a good target, and
receptors (GFG R-genes) against fungal elicitors already are common. But we probably don’t
want to increase the production of thionins, saponins, etc. in our cultivated crops.
14.3. Creating Transgenic Plants
Three phases are involved in preparing transgenic plants. 1. Transformation: the foreign
gene is introduced into the plant. 2. Gene expression: the introduced gene is expressed, so its
protein product is produced. 3. Selection and regeneration: plant cells expressing the gene are
selected and regenerated to become whole plants (Figure 40).
Two general strategies are used to transform plants. The first strategy is to use
biological systems based on integrative vector systems: e.g. the Ti plasmid of Agrobacterium
tumefaciens. The second strategy is to use direct integration systems e.g. biolistics (particle
bombardment).
For gene expression, it is common to use plant promoters or promoters from plant
viruses to turn on foreign genes in the proper plant tissue (roots vs. leaves vs. fruits). The 35S
promoter from cauliflower mosaic virus (CaMV) is expressed in all plant tissues, and was an early
tool used for expression of foreign genes.
For selection and regeneration, it is most common to use plant tissue culture. Tissue
culture is time-consuming and expensive, and it is associated with high mutation rates
(sometimes exploited as somaclonal variation) that can have deleterious phenotypic effects.
Figure 40. Process of creating transgenic plants.
14.4. Overall Strategies for Genetically Engineered Disease Resistance
1. Add more receptors to plant cells (the major R-genes involved in the gene-for-gene
interaction). Most research at this point is aimed at moving major R-genes within a species
(gene therapy, R-gene cassettes), but some research is oriented toward moving genes
between species (especially looking for non-host resistance).
2. Add enzymes to detoxify pathogen toxins.
3. Add antimicrobial enzymes that attack pathogen cellular infrastructure (chitinases,

glucanases)
4. Add antimicrobial toxins that attack pathogen metabolic pathways or proteins

(phytoalexins, PR-proteins, peroxidases).
5. Interfere with pathogen replication (virus-coat proteins).
6. Engineer non-pathogens in the rhizosphere or phyllosphere to make biocontrol agents.

INA - bacteria to reduce frost damage. Create biocontrol bacteria by adding chitinase.
To increase the number of receptors in a plant. A major genes (receptors) will be moved
between cultivars within a species (gene therapy). The main advantage is that it speeds up the
46 |Plant Pathology
breeding process and allows easier gene pyramiding or other deployment strategies.
Detoxify toxins produced by a pathogen. There are many cases where toxins are needed for a
pathogen to be pathogenic to particular host species. Example: tabtoxin produced by
Pseudomonas syringae is needed to cause wildfire disease on tobacco. The Ttr (tabtoxin
resistance) gene was taken from P. syringae and put into tobacco plants to make them resistant
to this disease.
Increase antimicrobial enzymes produced by the plant. Example: Over expression of chitinase
gene from beans in tobacco to control Rhizoctonia solani (Thanatephorus cucumeris ).
Interfere with replication of the pathogen. Example: Resistance to plant viruses using virus coat
protein genes. Virus replication is a delicate balance between many processes, and any
disruption to those processes can prevent or slow down viral replication. Many commercial
applications are imminent for coat-protein mediated resistance. Already widely used in China.
15. INTEGRATED DISEASE MANAGEMENT
15.1. What is Integrated Management?
Various definitions exist for integrated disease management. It is usually integrated not only for
diseases, but also pests and weed management. An example of such a definition is “‘Integrated
production is an ecologically based, environmentally conscious method that combines, or
integrates, biological and non-biological control techniques to suppress weeds, insects, and
diseases”.
The current definition of IPM accepted by the National Coalition on Integrated Pest
Management is as follows: “A sustainable approach to managing pests (diseases) by combining
biological, cultural, physical, and chemical tools in a way that minimizes economic, health and
environmental risks”.
Integrated disease management is based on knowledge and understanding of economic,

environmental, cultural, genetic, and microbiological factors that determine crop development
and crop use.
How does IP differ from conventional and BIO production? In conventional agriculture,
fungicides have been applied more or less on a calendar basis, either weekly or monthly,
depending on the agricultural system, to control diseases. This is basically a ‘bulldozing
approach’, frequently relying on fungicides as the only means of control. In contrast, IP
integrates all different control and management options providing it is sustainable and
minimizes economic, health and environmental risks. In BIO Production, no fungicides or
chemicals are allowed except for copper. This is also a labeled system and products produced
with BIO production have a higher economic value.
15.2. The Development of Integrated Production
Traditionally, fungicides were applied to control diseases throughout the growing season,
irrespective of whether the disease was present or not. This high load of fungicides had many
negative implications, not only to the environment and the consumer, but also led to the
development of resistance in the targeted pathogens. This meant that certain fungicides could
not be used anymore and led to an increase in other fungicide applications to control of
fungicide resistant pathogens.
Goals of Integrated Management Strategies
Ideally, the integrated management strategy is designed to accommodate several diseases

simultaneously. The goal is to optimize crop yield and economic benefits while minimizing
environmental impacts, leading to a sustainable agricultural ecosystem.
The plant pathologist needs to put together a package of control measures that can be
presented to the farmer, including the use of resistant varieties, choice of best planting dates,
crop rotations, sanitation methods, cultural methods, biological control and chemical controls.
Implications of IP
Management rests on the premise of tolerating diseases and understanding their ecology in
contrast to "bulldozing nature". IP focuses on the combined tactics because these offer longer
term management.
Major Components of Integrated Disease Management
The disease tetrahedron is used to envisage the interaction of diseases with their
environment. The tetrahedron consists of four components, which can all influence each other
and together determine the level of the disease. The four components are the plant pathogen,
the host plant, the environment and human activity (Figure 41). Generally, it can be said that
chemical control is only aimed at influencing the pathogen directly, whereas, integrated control
may reduce the level of disease by influencing any or several of the four components of the
tetrahedron. A thorough knowledge of the influence of different factors on diseases offers the
basis for integrated control.
Figure 41. Disease tetrahedron
15.3. Management Strategies
If action is called for, choose the control strategies that optimize cost and effect, while
minimizing adverse effects. Disease management is an integral component of integrated crop
production. It employs a logical system of technologies, and it requires accurate understanding
of the destructive potential of diseases. First of all, we need to know and understand the
diseases that are important in the crops. Without knowledge of the disease, its life cycle, factors
favoring infection, other epidemiological characteristics of the agroecosystem etc., it is
impossible to apply IP successfully.
Two important precepts result from the integral relation between crop production and disease
development. The first is that disease management will be most successful if it is considered
during all phases of crop production. Effective disease management may require several
approaches, at several times during a crop cycle. For example, if a practitioner relies only on
weekly applications of fungicide to suppress potato late blight, the resulting disease suppression
may be inefficient or inadequate. If irrigation practices, microenvironment of the field, and plant
susceptibility all favour disease development or if there is a large pathogen population
(infections in seed tubers of infections in neighboring potato fields, gardens, in discarded
potatoes), even weekly fungicide applications may not suppress disease adequately. Conversely,
if these factors do not favour disease development, weekly fungicide applications will be
unnecessary. Disease management will be most successful if it is integrated into the crop
production system and if it employs diverse approaches.
The second precept is that changes in crop production will affect disease management. For
example, replacement of tillage by herbicide application is likely to alter the activities of several
pathogens, some may become more prevalent, others less so. Disease management must adjust
to these changes.
The most widely used disease management strategies consist of cultural management
strategies. Some examples are given below:
a. Cultural Management
• Crop rotation
• Tillage: bury infected plant material
• Sowing date
• Cultivar mixtures eg. Blast control in rice
• Intercropping
• Plant density: Especially important in nurseries where humidity is high. Lower plant
density will improve air movement and decrease humidity
• Mulching: Mulches are typically used for control of soil-borne diseases. E.g. a mulch
consisting of composted organic material would be beneficial to the plants in various
ways, depending on the crop. Its mode of action can be: (i) reducing soil pH to
unfavourable levels for the pathogen e.g. Oomycetes, (ii) Prevents splash dispersal
from the soil, iii) Improves soil structure – aeration. However, for some diseases such
as Botrytis cinerea, mulching actually provides organic material for saprophytic
survival of the pathogen and therefore should be avoided in those situations.
• Disinfestation of soil: Solarization, steam sterilization (soil fumigation with e.g. chloropicrin
or methyl bromide – would fit more into chemical control but usually is not allowed in
integrated production)
• Fertility management: Application of ammonium phosphate controls Gaeumannomyces
graminis var. tritici (take all) in wheat
• Irrigation
b. Mechanical Practices
• Removal of infected plant material – sanitation
c.Biological Control
• Suppressive soils
• Microbial antagonists
• Hypovirulence
d. Genetic
• Host plant resistance

• Genetic engineered cultivars
• Multilines and cultivar mixtures
e. Chemical Control
• Fungicides
• Surfactants in irrigation water to control Oomycetes in hydroponics systems
• Soil fumigation – not generally used because of its adverse effects on the
environment
It is important to note that IP consists of both therapeutic and preventative management strategies. In
practice though, it is much easier to prevent diseases than to treat them. Diseases can also be controlled or
managed and both are included in IP.
Control: Reduce pathogen numbers to the limit of our technology.
Management: Reduce pathogen impact to tolerable levels. It is also important to note that each control or
management strategy should be correctly executed in order to obtain maximum profits from IP. For
example, if biological control as a control strategy is opted, the biological control agent should be applied to
the crop which it should protect, at the correct time and place and during conditions that would favour the
establishment of the particular biological control agent.
IP is a dynamic system and can potentially change on a weekly basis. It is therefore extremely important to
re-evaluate the disease situation after every disease control or management action. New judgments might
be required as it is a dynamic system and changes will inevitably occur. This also stresses the point that a
thorough knowledge of the pathogen, environment, production system and crop is required before any
control or management strategy can be undertaken.
15.4. The Decision Making Process
Decision making is the process of selecting and implementing an action with the intention of producing a
favourable outcome. The quality of decisions can be enhanced by applying a structured, analytic
methodology to decision-making. Analytic decision making is based on logic and considers all available data
and alternatives. A valuable decision making tool is forecast systems for specific diseases, such as the apple
scab forecasting system.
The pathogen population, and therefore the degree of damage, will be reduced by applying control
measures which influence the population size of the pathogen.
15.5. Damage and Action Thresholds
In combination with the damage relationship for a given pathosystem, it is important to assess the
damage and action thresholds.
The damage threshold is the maximum level of disease attack below which yield losses do not occur. The
action threshold is the level of disease attack at which control action should be taken to prevent the
epidemic from reaching the damage threshold. Because there are often no fully effective techniques to
control a disease immediately, the action threshold is lower than the damage threshold.
Damage and action thresholds are important tools in integrated control when several control alternatives
are available. Whereas the damage threshold essentially depends on the disease level and yield loss
relationship, the action threshold may vary greatly according to the efficacy of each of the control
alternatives and how long they take to be effective. The action threshold to control a disease will probably
be higher if we choose a quick acting fungicide, than with biological control.

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PLANT PATHOLOGY

RONALDO T. ALBERTO, Ph.D.

1.1 The Science and Art of Plant Pathology

1.2 The Economic Importance of Plant Diseases

1.3 Historical development of plant pathology

A. The Pre-scientific Period

B. Beginning and Advances in Scientific Studies

The Philippine Phytopathological Society, an association of plant pathologists, was established in

2. CONCEPTS OF PLANT DISEASE

Disease a “physiological malfunctioning caused by animate agents, malfunctioning caused by

2.1. Definitions and Terminology in Plant Pathology

A parasite may be obligate or facultative. An obligate parasite is an organism that is restricted to

A saprophyte is an organism that lives on dead organic or inorganic matter. A facultative

Pathogenicity is the capacity of a pathogen to cause disease whereas pathogenesis refers to

2.2. Symptoms of Plant Diseases

Hypoplastic symptoms appear when there is an inhibition or failure in the differentiation or

Hyperplastic symptoms are expressed with the occurrence of excessive multiplication:

Specific symptoms and their descriptions are given below.

 Etiolation - yellowing of normally green tissues caused by inadequate light

2.4. Plant Disease Diagnosis

2.5. Classifications of Plant Diseases

3. NON-PARASITIC AGENTS OF PLANT DISEASE

The more common non-parasitic causes of diseases in plants are:

 excessively low temperatures

3.1. Diseases caused by too low temperatures

3.2. Diseases caused by too high temperatures

b. Heat necrosis of potato

3.3. Disease caused by lack of oxygen

3.4. Disease caused by too much or too little light

3.5. Diseases caused by adverse meteorological conditions

3.6. Air pollutants

The more common air pollutants are:

c. Peroxyacetyl nitrates (PANs)

3.8. Diseases caused by mineral deficiencies

3.9. Diseases caused by excesses of nutrient elements

3.10. Diseases caused by unfavorable soil pH

3.11. Disease caused by improper use of pesticides

3.12. Diseases caused by improper agricultural practices

3.13. Lack or excess of soil moisture

3.14. Diseases caused by naturally occurring toxic chemicals

4. PARASITIC AGENTS OF PLANT DISEASES

4.1 Viroids and Viruses as Plant Pathogens

2. Synthesis of viruses and viroids

3. Symptoms and diseases caused by viroids and viruses

4. Transmission and spread

4.2 Bacteria as Plant Pathogens

2. Genera of plant pathogenic bacteria

3. Symptoms and disease caused by bacteria

4.3 Mycoplasma as Plant Pathogens

Mycoplasmas are non-motile; nonspore-forming, polymorphic microorganisms that lack cell

Most mycoplasmas are transmitted from diseased to healthy plants by leafhoppers,

4. Symptoms and diseases caused by mycoplasma

4.4 The Rickettsias as Plant Pathogens

Flagellate protozoa of uncertain pathogenicity occur in laticiferous plants. Phytomonas

4.6. Fungi as plant pathogens

Fungi are non-chlorophyll-bearing, spore-forming microorganisms, with branched filamentous

Symptoms and diseases caused by fungi

4.7. Nematodes as Plant Pathogens

2. Groups of plant parasitic nematodes