PLANT PATHOLOGY

Principles of Crop Protection

Plant Pathology  Also known as Phytopathology

 It is the study of the organisms and of

Etymology
the environmental factors that cause
“Pathos” – suffering
disease in plants; of the mechanisms
“Logos” – to study by which these factors induce disease
in plants; and of the methods of
preventing or controlling disease and
reducing the damage it causes.
  As a science
It looks into the characteristics of diseases,
their causes, plant-pathogen interactions, factors
affecting disease development in individual plants and
in populations, the various means of controlling
diseases.
PLANT
PATHOLOGY  As an art
It deals with the application of the
knowledge gained from studying the science.
1. diagnosis or recognition of a particular
disease
2. disease assessment and forecasting
3. control measures
Ultimate objective of Phytopathology

 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
The economic importance of plant diseases

 Plant disease epidemics have caused human sufferings, deaths and upheavals.
 Potato late blight disease (1845-1846)
- caused famine and death of more than a million people in Ireland
 Coffee rust in Ceylon (now Sri Lanka)
- destroyed vast coffee plantations; tea was planted instead
 Ergot poisoning in Europe (875 AD)
- acquired from eating bread made from infected rye grains; caused by the
fungus Caviceps purpurea which produces sclerotia containing alkaloids that impede blood
circulation.
Examples of plant diseases in the Philippines
that caused enormous economic losses
1. Cadang-cadang disease of coconut – first observed in 1918; have caused the country a loss
of $200 million
2. Downy mildew of corn – the nemesis of corn
- loss can be as high as 95% amounting to over PhP170 million annually
- now controlled by chemical seed treatment using metalaxyl
- caused by the fungus Peronosclerospora philippinensis
3. Rice tungro disease – affected 70,000 hectares in 1971; 1.22 M cavans, an estimate of rice
lost was valued at PhP30, 357,000
4. Coffee rust – destroyed the coffee industry in Batangas
5. Citrus decline – destroyed citrus plantations in Batangas
Types of crop losses due to plant diseases
 Reduction in yield
- leaf spots/blights reduce photosynthetic capacity of plants
- root pathogens
- fruit rots and fruit spots – reduce quantity of harvestable and marketable fruits
 Losses from deterioration during storage, marketing, or transport
- The amount of food lost daily is enough to feed the world’s population
 Reduction in quality of produce
- citrus fruits with scabs
- moldy cereals and other commodities
- reduced strength and undesirable discoloration in wood pulp
- poor germination of infected seeds
 Losses from produce contaminated with toxins that cause various disorders and/or death to
animals including man
 aflatoxin – produced by Aspergillus flavus
- carcinogenic to animals and man
- commonly found in stored corn, sorghum, copra, root crops, etc.
 Ochratoxin – a mycotoxin produced by A. ochraceous
- causes cancer of the liver
 Yellow rice toxins – formed by Penicillium spp.
- caused several deaths in Japan
 estrogenic factor in corn – produced by Fusarium graminearum
- causes testes of young male pigs to enlarge and abort
 Fumonisms – formed by Fusarium spp. In corn grains
- caused esophageal cancer in man and toxic to animals like horses
 Losses due to predisposition of host to attack by other pathogens
- nematode injuries on roots serve as ports of entry for other pathogens
- leaf pathogens weaken plants which can become a host susceptible to root-rotting
pathogens
- severely defoliated trees can be readily attacked by Armillaria mellea and other
fungi

 Losses from increased cost of production and handling

- Cost of disease control is an added cost
- Cost of culling diseased commodities for marketing and processing
- Infected and stained wood chips need longer time to bleach to obtain white paper
product.
History of Plant Pathology
 Mycology
1675 - Dutch worker Anton von Leeuwenhoek developed the first microscope.
1729 - Italian botanist P. A. Micheli proposed fungi comes from spores; father of Mycology.
1755 - French botanist Tillet published a paper on bunt or stinking smut of wheat; discovered
bunt is a disease of wheat.
1807 - French scientist I. B. Prevost showed bunt of wheat is a fungus and showed evidence
that a disease is caused by a microorganism.
1821 - E. M. Fries published Systema Mycologicum for naming of fungi; he was named as
Linnaeus of Mycology.
1821 - Robertson of England stated that sulphur is effective against peach mildew.
1845 - Irish Potato famine due to Phytophthora infestans caused starvation of million and
immigration of 1.5 million people.
1858 - J. G. Kuhn published first textbook in Plant Pathology – The Diseases of Cultivated
Crops, their Causes and their Control.
1861 -Anton de Bary (Germany) worked out the life cycle of potato late blight and first to
prove experimentally Phytophthora infestans is the cause of potato late blight. He proved that
fungi are causes but not the results of diseases. He is the Father of Modern Plant Pathology.
1865 – Anton de Bary reported heteroecious nature of wheat stem rust.
1869 – England loses coffee production to coffee rust, forced to grow tea.
1874 - Robert Hartig published a book entitled, “Important Diseases of Forest Trees”.
1875-1912 - Brefeld discovered the methods of artificial culture of microorganisms; he also
illustrated the complete life cycles of cereal smut fungi and diseases caused by them.
1877 – M. S. Woronin discovered and named the Club root of Cabbage pathogen as
Plasmodiophora brassicae.
1878 – M. S. Woronin found out the life cycle of potato wart disease.
1878 -Downy mildew of grapevine was introduced into Europe from America. The disease
almost ruined the wine industry.
1881 - H.M. Ward worked out the life cycle of coffee leaf rust. He is called as Father of
Tropical Plant Pathology.
1882 -Robert Hartig published a textbook -Diseases of Trees. He is called as "Father of Forest
Pathology".
1885 -Pierre Marie Alexis Millardet accidentally discovered the Bordeaux mixture for the
control of downy mildew of grapevine.
1885 – A. B. Frank defined and named mycorrhizal associations in plant roots.
1887 -Burgundy mixture was introduced by Mason of France.
1894 -Swedish scientist Eriksson described the phenomenon of physiologic races in cereal rust
fungus, Puccinia graminis.
1899 – W. A. Orton selected and bred water-melon, cowpea and cotton for resistance to
Fusarium wilt diseases. He is considered as a pioneer worker in the development of disease
resistant varieties.
1904 – A. F. Blakeslee, American Geneticist founded heterothallism in Rhizopus
1904 – R. H. Biffen was the first to show that resistance to pathogens in plants can be inherited
as a Mendelian character; pioneer in genetics of plant disease resistance.
1912 – H. Burgeff reported that within a cell of a fungus, fusion between dissimilar nuclei can occur. He
called this phenomenon as heterokaryosis.
1917 -E. C. Stakman demonstrated physiologic forms in stem rust of wheat.
1918 - E. J. Butler published book on Fungi and Disease in Plants; he made exhaustive study on Indian
fungi and the diseases caused by them. He is called as the Father of Modern Plant Pathology in India;
He joined as the first Director of Imperial Bureau of Mycology (Commonwealth Mycological Institute,
CMI) now CAB International Mycological Institute in Kew, England in 1920. He began the journal
Review of Applied Mycology; with S.G. Jones he wrote, 'Plant Pathology' in 1949.
1929 -Sir Alexander Fleming isolated the antibiotic, Penicillin from the fungus, Penicillium notatum.
1932 – H. N. Hansen and R. E. Smith were the first to demonstrate the origin of physiologic races
through heterokaryosis.
1934 -W. H. Tisdale and I. Williams studied the organic fungicides by discovering alkyl
dithiocarbamates.
1938 – H. N. Hansen found out dual phenomenon in Fungi Imperfecti.
1942 – H. H. Flor developed gene-for-gene hypothesis in flax rust.
1943 – Great Bengal Famine due to Helminthosporium oryzae caused death of 2 million
people in India.
1943 - Dimond, Heuberger and Horsfall discovered the ethylene bis dithiocarbamates.
1945 - J. G. Horsfall explored the mechanism of fungicidal action.
1948 - B. B. Mundkur started Indian Phytopathological Society with its journal Indian
Phytopathology. He has written a book ‘Fungi and Plant Diseases’ in 1949, which is the
second, book in plant pathology in India.
1951-57 - E. A. Gaümann was one of the first to investigate the physiology of the wilts caused
by Fusarium spp. He put forth the involvement of toxin (toxin theory) in wilt diseases.
1952 - N.F. Jensen suggested blending of different resistant genotypes of similar agronomic
characters in fields of oats to reduce the spread of rust and losses from rust.
1953 - N. E. Borlaug and associates developed multiline cultivars for wheat
1953 – Pontecorvo and his associates demonstrated parasexualism in fungi.
1956 - J. G. Horsfall published a book entitled "Principles of Fungicidal action“
1957 – E. C. Stakman with J. G. Harrar wrote a book Principles of Plant Pathology.
1963 - J. E. Van der Plank found out vertical and horizontal
types of resistance in crop plants.
1966 -van Schmeling and Marshall Kulka were the first to
find out systemic fungicides (oxathiin compounds – carboxin
and oxycarboxin).
1970 -S. D. Garrett investigated the management of root
diseases and he is the pioneer worker in the field of
biological control.
1972 – G. Rangaswami wrote a book on Diseases of Crop
Plants in India.
 Plant Bacteriology
1683 – Anton von Leeuwenhoek first observed bacteria.
1876 - Louis Pasteur and Robert Koch -They proved that anthrax disease of cattle was caused by specific
bacterium.
1876 - Robert Koch of Germany described the theory called "Koch's postulates." He established the
principles of pure culture technique.
1876 - Robert Koch and Pasteur disproved the theory of spontaneous generation of diseases and propose
germ theory in relation to the diseases of man and animal.
1882 - American Plant Pathologist -T. J. Burrill first time proved that fire blight of apple and pear was
caused by a bacterium (now known as Erwinia amylovora).
1901-1920 - E. F. Smith of U.S.A gave the final proof of the fact that bacteria could be incitants of plant
diseases. He also worked on the bacterial wilt of cucurbits and crown gall disease. He is also called as
"Father of Phytobacteriology". Chilton and his coworkers demonstrated that crown gall bacterium
transforms plant cell to tumour cell by introducing into them a plasmid.
 Plant Virology
1886 - Adolf Mayer described a disease of tobacco called mosaic kranheit (tobacco mosaic).
Adolf Mayer demonstrated the sap transmission of Tobacco Mosaic Virus disease.
1892 - Dimitri Ivanowski demonstrated that the causal agent of tobacco mosaic could pass
through bacterial filter.
1895 - E.F. Smith of U.S.A. showed the peach yellows was a contagious disease.
1898 - M.W. Beijerinck -a Dutch microbiologist and founder of virology proved that the virus
inciting tobacco mosaic is not a microorganism. He believed it to be contagium vivum fluidum
(infectious living fluid). He was the first to use the term virus, which is the Latin word for
poison.
1929 - F. O. Holmes provided a tool by which the virus could be measured by showing that the
amount of virus present in a plant sample preparation is proportional to the number of local
lesions produced on appropriate host plant leaves rubbed with the contaminated sap.
1935 - W. M. Stanley proved that viruses can be made as crystals. He got Nobel Prize in 1946.
1910 - C. O. Jensen related crown gall of plants to cancer of animals.
1952 - J. Lederberg coined the term plasmid
1952 – S. A. Waksman won Nobel prize for the discovery of streptomycin.
1952 – Zinder and J. Lederberg discovered transduction in bacteria
1962 – H. Stolp discovered bellovibrios.
1972 – P. B. New and A. Kerr success in biological control of A. radiobacter strain K.
1972 – I. M. Windsor and L. M. Black observed a new kind of phloem inhabiting bacterium
causing clover club leaf disease.
1974 – I. Zanen et al. demonstrated Ti plasmid in Agrobacterium tumefaciens.
1980 – D. W. Dye et al. introduced the pathovar in the taxonomy of plant pathogenic bacteria
1936 - F. C. Bawden and, N.W. Pirie (Britain) found that the crystalline nature of the virus
contains nucleic acid and protein.
1939 - Kausche and colleagues first time saw the TMV virus particles with the help of
Electron microscope.
1956 - Gierer and Schramm proved that the nucleic acid fraction of the virus is actually the
infectious agent.
1959 - Munday succeeded in inducing TMV mutations.
1966 - Kassanis discovered the satellite viruses.
1971 - T. O. Diener discovered viroids, which only consist of nucleic acids. Smaller than
viruses, caused potato spindle tuber disease (250-400 bases long of single-stranded circular
molecule of infectious RNA).
 Phytoplasma
1967 – Doi et al and Ishiie et al, the Japanese scientists found that mycoplasmalike organisms
(MLO) could be responsible for the disease of the yellows type. Doi observed that MLO's are
constantly present in phloem while Ishiie observed MLO's temporarily disappeared when the
plants are treated with tetracycline antibodies.

 Spiroplasma
1972-Davies et al., observed that a motile, helical wall-less microorganism associated with
corn stunt diseases, which could be cultured and characterized and they named it as
spiroplasma.
Concepts of Plant Disease
 A ”physiological malfunctioning caused by animate agents” (Whetzel, 1929). He called
malfunctioning caused by non-living or inanimate agents as “physogenic disease”.
 “Any deviation from normal growth or structure of plants that is sufficienty pronounced
and permanent to produce visible symptoms or to impair quality or economic value”
(Stakman and Harrar, 1957)
 A “malfunctioning process caused by continuous irritation” (Horsfall and Dimond). The
authors emphasize the difference between disease and injury. A disease progresses over a
period of time while injury is an instantaneous action such as the breaking of a twig.
 “A dynamic interaction between an organism and its environment which results in
abnormal physiological and often morphological or neurological changes in the organism”
(Merril, 1980)
 “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 effected plant changes in appearance and yields less than a normal healthy
plant of the same variety” (Agrios, 1978).
 “Any malfunctioning of host cells and tissues that results from continuous irritation by a
pathogen or an environmental factor and leads to the development of symptoms” (Agrios,
1998)
Characteristics of Plant Disease

1. A malfunctioning process that results in suffering

2. Generally harmful/detrimental
3. Produces symptoms – histological and morphological abnormalities
4. Caused by an agent
Vital processes of plants affected by disease

1.Root absorption
2.Uptake of water and minerals
3.Photosynthesis
4.Respiration
5.Transport of photosynthates
6.Reproduction
 Importance of Plant Diseases
1. Plant diseases endanger food supply
2. Reduce the quality and quantity of plant produce
3. Cause financial losses
4. Limit the kinds of plants and industries in an area
5. Make plants poisonous to humans
6. Increase cost of production due to control measures
Definitions of terminology
 Pathogen – any agent that causes disease especially the biotic or living agent
 Parasite – an organism that depends wholly or partly on another organism for its food
 Obligate parasite – subsist on living organisms and attacks only living tissues (ex. Virus,
rust fungi, downey mildew fungi, etc.)
 Facultative parasite – an organism, which has the ability to become a parasite but is
ordinarily a saprophyte
 Saprophyte – an organism that lives on dead organic or inorganic matter
 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 is implied.
 Suscept – is a plant that is susceptible to a disease whether or not the pathogen is parasitic.
 Pathogenecity – is the capacity of an organism to cause disease.
 Pathogenesis – refers to series of events that lead to disease development in the plant.
 Virulence – refers to the quantitative amount of disease that an isolate (the pathogen) can
cause in a group of plants. A characteristic of a pathogen.
 Aggressiveness – measures the rate at which virulence is expressed by a given pathogenic
isolate.
 Disease resistance – inherent ability of an organism to overcome in any degree the effects
of a pathogen.
 Susceptibility – opposite of resistance; the inability to overcome the effects of a pathogen.
 Tolerance – ability of plant to withstand the severe effects of the pathogen without
experiencing a severe reduction in yield.
 Plant disease diagnosis – defined as identification of diseases based on symptoms and
signs
 Sign – a pathogen or a part of a pathogen found on a host
 Symptom – manifestation or expression of a plant as a result of a disease; evidences of
disease in the plant
 Symptom complex – different symptoms exhibited by the plant
 Syndrome – symptom + sign
 Masked symptoms – symptoms not expressed due to unfavourable condition.
 Symptomless carrier - host that do not show symptom irrespective of environment.
 THE DISEASE TRIANGLE

It illustrates that the following are requisites

for disease development to occur: Pathogen

1. Susceptible plant
2. The pathogen
3. Favorable environment Disease

Host Environment

*The absence of one or more of these factors

will produce no disease.
 Plant Disease Diagnosis
 It is defined as identification of diseases based on symptom and signs.
 Correct plant disease diagnosis is necessary for recommending appropriate
control measures, and in plant disease surveys.
 Diagnoses based on symptoms alone are not reliable because some disease
exhibit the same symptom although their pathogens are different.
 The presence of signs of the disease increases the reliability of the diagnosis
 Secondary invaders and saprophytic microorganisms may be found on or in
invaded tissues and may be mistaken for the primary pathogen.
 Classification of Plant Diseases
 A rational grouping of plant diseases is helpful in the identification and subsequent of a particular
disease.

1. According to affected plant organ

- related to the physiological processes affected
Ex. Root diseases, foliage diseases, fruit diseases, stem diseases
2. According to symptom
Ex. Leaf spots, rusts, smuts, anthracnoses, mosaics, wilts, fruit rots
3. According to type of affected plant
Ex. Vegetable diseases, diseases of forest trees, diseases of field crops, diseases of ornamentals
4. According to type of pathogen that cause the disease
a. Infectious diseases
Ex. diseases caused by:
fungi, mycoplasmas, bacteria, viruses, viroids, protozoa, parasitic
flowering plants, nematodes
b. non-infectious diseases
Ex. Diseases caused by non-parasitic or abiotic agents such as
extremely high or excessively low temperatures
unfavourable oxygen relations
unfavourable moisture conditions
nutrient deficiencies
mineral toxicities
air pollution
toxicity of pesticides, etc.
 Symptoms of Plant Diseases
 They are the evidences of disease in the plant by which a particular plant
disease may be distinguished from the other.
 Include visible response by the suscept as well as any measurable host
response to infection, such as, increased respiration, increased leaf
temperature.
 Symptoms vary according to the environment, the host variety, and the
race of the pathogen involved.
 Different pathogens may cause the formation of identical symptoms.
 The different symptoms exhibited by the plant is known as symptom
complex.
Classification of Symptoms

a. Local or Systemic
b. Primary or Secondary
c. Microscopic or Macroscopic
Local or Systemic Symptoms

 Local symptom – expressed as physiological or structural changes in a

limited area of the tissues of the host (ex. galls, spots, cankers)

 Systemic symptom – expressed as the reaction of a greater part of or all

of the plants (ex. Dwarfing, wilting, yellowing)
Primary or Secondary Symptoms (caused by
the same disease)

 Primary symptom – the direct result of pathogen activity on the

invaded tissues

 Secondary symptom – the physiological effects on distant and

uninvaded organs
Microscopic or Macroscopic Symptoms

 Microscopic symptom– expressions of disease in cell structure or arrangement

that can be studied only under the microscope
Examples: abnormality in cell content, structure or arrangement;
cell enlargement and vascular discoloration

 Macroscopic symptom – expressions of the disease in the plant or in its parts

that can be studied with unaided eye.
Types of macroscopic symptom
pre-necrotic – stage preceding death of cells
necrotic – characteristics of dead cells and tissues
General types of symptoms

 Plesionecrotic symptoms
 Necrotic symptoms
 Hypoplastic symptoms
 Hyperplastic symptoms
Plesionecrotic symptom

 Stage preceding death of cells or pre-necrotic

 It changes before actual death of protoplast or cell
 Involves protoplasmic disorganization and degeneration
Examples: silvering, yellowing, and wilting
Necrotic symptom

 Involves the death of protoplast, cells or tissues

Examples: spot blight scorch, canker, and die-back

Hypoplastic symptom

 Inhibition or failure in the differentiation/development of some aspect of

plant growth

Examples: stunting, chlorosis, mosaic, curling and rosetting

Hyperplastic symptoms

 Expressed with excessive multiplication, enlargement or overdevelopment of plant

organs
 Prolonged retention of green color
Examples: gall formation, scab, knots

Hypertrophy – overdevelopment due to the increase in the size of the cell

Hyperplasia – abnormal increase in the number of cells
SYMPTOMS & DISEASES
 Abscission – premature falling of leaves, fruits or flowers due to the early laying down of
the abscission layer.
 Blast – term applied to the sudden death of young buds, inflorescence or young fruits.
 Bleeding – flow of plant sap from wounds.
 Blight – an extensive, usually sudden, death of host tissue, such as leaf blight.
 Blotch – large, irregular spots on leaves or fruits with necrotic injury of epidermal cells.
 Callus – an overgrowth of tissue formed in response to injury in an effort of the plant to
heal the wound.
 Canker – an often sunken necrotic area with cracked border that may appear in leaves,
fruits, stems and branches.
 Chlorosis – yellowing caused by some factors other than light, such as infection by a virus
or a mycoplasma.
 Curling – abnormal bending or curling of leaves caused by over-growth on one side of the
leaf or localized growth in certain portions.
 Damping off – rotting of seedlings prior to emergence or rotting of seedling stems at an
area just above the soil line.
 Die-back – a drying backward from the tip of twigs or branches.
 Etiolation – yellowing of normally green tissues caused by inadequate light.
 Fasciculation or fasciation – clustering of roots, flowers, fruits, or twigs around a common
focus.
 Flecks – extremely tine spots on leaves, fruits, stems, etc.
 Gumming or gummosis – oozing out of viscid gum from wounds in bark.
 Leak – the host’s juices exude or leak out from soft-rotted portions.
 Mosaic – the presence, usually on leaves, of variegated patterns of green and yellow
shades with sharply defined borders.
 Mottling – the variegation is less defined than mosaic and the boundaries of light and dark
variegated areas are more defused.
 Mummification – an infected fruit is converted to a hard, dry shrivelled mummy.
 Phyllody – metamorphosis of sepals, petals, stamens, or carpels into leaf-like structures.
 Pitting – defined depressions or pits are found on the surface of fruits, tubers and other
fleshy organs resulting in a packed appearance.
 Rosetting – shortening of the internodes of shoots and stems forming a crowding of the
foliage in a rosette.
 Rotting – the disintegration and decomposition of host tissues. A dry rots 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, etc.
 Russeting – a superficial brownish roughening of the skin of fruits, tubers or other fleshy
organs usually due to the suberization of epidermal or subepidermal tissues following
injury to epidermis.
 Sarcody – abnormal swelling of the bark above wounds due to the accumulation of
elaborated food materials.
 Savoying – the cupping or pocketing of parts of the leaf; also curling or puckering; due to
underdevelopment of veins of leaf margins.
 Scab – slightly raised, rough, ulcer-like lesions due to the overgrowth of epidermal and
cortical tissue accompanied with rupturing and suberization of cell walls.
 Shot-hole – a perforated appearance of a leaf as the dead areas of local lesions drop out.
 Spot – a localized necrotic area also referred to as a lesion, may be circular, angular or
irregularly shaped. Several spots may run together or coalesce forming large necrotic
areas.
 Streak or stripe – long, narrow necrotic lesions on leaves or stems.
 Vein clearing – the leaf veins are translucent or pale while the rest of the leaf is in its
normal color.
 Virescence or greening – development of chlorophyll in tissues or organs where it is
normally absent.
 Wilting – may be due to an infectious agent or to lack of water. Wilting caused by the latter
is often temporary and 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.
Abscission
Blast
Bleeding
Bacterial blight
Purple blotch lesions on onion leaf
Canker of apple stem caused by Nectria
galligena
Chlorosis and necrosis on leaf tip due to
fluoride toxicity (abiotic)
Scorching of alfalfa leaves due to sulphur
dioxide injury (abiotic)
Callus
Crown gall caused by Agrobacterium tumefaciens
(proliferation of cells is called a callus growth)
Curling
Damping-off on soybean seedlings
Damping-off
Dieback of a pine tree
Dieback
Etiolation
Fasciculation
Flecks
Gumming or gummosis
Leak oozing from a cactus plant
Mosaic on leaf Ring spots on peanut
Mosaic on yellow Ringspot on peach
crookneck squash
Rice yellow mottle virus
Mummification (mummy berry disease)
Phyllody
Pitting and chlorosis
Rosetting
Sheath rot Stem rot
Fruit rot of peach caused by Monilinia
fructicola
Black rot of cabbage
Russeting
Rust diseases
Stem rust on barley caused by Puccina
graminis
chrysanthemum white rust
Sarcody
Savoying
Scab
Bacterial spot/shot-hole
Fungal spot Bacterial leaf spot
Leaf scald
Bacterial leaf streak
Rice stripe virus Red stripe
Stunting on chrysanthemum infected with
Fusarium oxysporum
Stunt Rice tungro
Vein clearing (damaged by frost)
Vein banding – a band of yellow tissues along
the larger veins of the leaf
Virescence
Wilting (Verticillium wilt of cucumber caused
by Verticillium dahlia)
SIGNS OF PLANT DISEASES

 Structures of the pathogen found associated with the

infected plant part.
 Some of these structures may not always be present in
diseased plants because their formation depends on
environmental conditions.
 Most of the signs are best seen and distinguished under a
microscope
Three General Categories of Signs
1. Vegetative structures – function primarily in absorption and storage
of nutrients.
a. Felt – a densely woven mat of mycelium
b. Haustorium – an absorbing organ of a fungus which penetrates a
host cell without penetrating the plasma membrane
c. Mycelium – a mass of fungal threads or hyphae
d. Pathogen cells – masses of bacterial cells
e. Plasmodium – naked mass of protoplasm
f. Rhizomorph – cordlike strand of fungal hyphae
g. Sclerotium – a hard, compact, resting body composed of fungal
hyphae
Felt Mycelium
HAUSTORIUM
Pathogen cells
2. Reproductive structures – those pathogen structures that function in
reproduction of the organism.
a. Acervulus – a mat of hyphae, generally associated with a host,
forming lesions with short densely packed conidiophores.
b. Apothecium – open, cuplike, ascus-containing fruiting body.
c. Ascus – sac-like structure containing ascosphores formed as a
result of karyogamy and meiosis.
d. Basidium – characteristically club-shaped structure on which
basidiospores are produced as a result of karyogamy and meiosis.
e. Cleistothecium – a closed ascus-containing fruiting body.
f. Conidiophore – a specialized hyphal branch on which conidia are
produced.
g. Conk – woody shelf-like structure characteristic of many woody-
rotting fungi.
h. Mildew – cobwebby or powdery growth usually on leaves.
i. Mold – wooly of furry surface growth of mycelium.
j. Mushroom (toadstool) – umbrella-shaped fruiting structure of many
Basidiomycetes.
k. Perithecium – charatistically flask-shaped, ascus-containing fruiting
body with a small opening (ostiole) and a wall of its own kind.
l. Pseudothecium – fruiting body bearing asci in locules within a
stroma.
Basidium
Powdery
mildew
Mold
Mushrooms
m. Pycnidium – asexual, hollow fruiting body containing conidia.
n. seed-bearing plants – higher plants that parasitize trees.
o. Sorus – mass or cluster of spores borne on short stalks.
p. Sporangium – enlarged tip of specialized hyphal branch in which sporangiospores are borne.
q. Spore – general name for a single to several celled propagative unit in fungi and other lower
plants. Examples of spores with specific names are: conidia, ascospores, basidiospores, zoospores,
oospores, sporangiospores, aeciospores, urediospores, chlamydospores and teliospores.
r. Sporodochium – cushion-shaped stroma covered with conidiophores.
s. Stroma – compact mass of fungal hyphae on or within which fruiting structures are formed.
t. Worms – generally nematodes which are microscopic, wormlike animals that can cause disease.
Spore Conidia
3. Disease products – gases and exudation products resulting from disease.
a. Odor – characteristic smell associated with some host-pathogen interactions.
b. Ooze- viscid mass made up of plant juices and often pathogen cells.
Signs of fungal diseases – mycelia, spores, fruiting bodies, etc.
Signs of bacterial diseases – bacterial cells, bacterial ooze
Signs of nematode diseases – eggs, juveniles, adult nematodes
Signs of virus diseases – virus particles, inclusion bodies
Signs of viroid diseases – RNA fragments
Signs of diseases caused by parasitic flowering plants – seeds and the plant
itself.
White mycelia of Armillaria growing under bark of
peach tree
Bacterial ooze from tomato stem infected with
Ralstonia solanacearum
 Koch’s Postulate
 Criteria used to confirm the identity of the causal agent
of a new or unknown disease.
 It is a set of rules used to prove the pathogenicity of
facultative parasites
 The steps involved in Koch’s Postulate are:
ASSOCIATION
ISOLATION
INOCULATION
RE-ISOLATION
Step 1: Association – the pathogen or signs of the pathogen must be found
associated with the disease in all diseased plants examined.

Step 2: Isolation – the pathogen must be isolated and grown in pure culture on
nutrient media, and its characteristics described. Obligate parasites must be
isolated and grown on a healthy but susceptible host plant. The characteristics of
the obligate parasite must also be described.

Step 3: Inoculation – the pathogen from the pure culture must be inoculated on
healthy plants of the same species or variety on which the disease appears, and it
must produce the same disease on the inoculated plants

Step 4: Re-isolation – the pathogen must be re-isolated from the inoculated plants
and grown once more in pure culture. Its characteristics must be exactly like those
observed in steps 1 and 2.
CAUSES OF PLANT DISEASES
Non-parasitic Agents of Plant
diseases
ABIOTIC/NON-PARASITIC/NON-LIVING FACTORS

Plants that grow normally only within certain
ranges of various environmental factors such as
light, temperature, moisture, air, nutrients, etc.
 Diseased caused by non-parasitic agents have been
referred to as physiological disorders.
 Plants are weakened/stressed by biotic agents of
diseases are more prone to infection by parasitic
pathogens.
Abiotic diseases or injury
1. Injury caused by too low temperatures
 Freezing injury – when temperature is below 0 degree Celsius, ice crystals
form within or in-between cells
 Chilling injury – low temperatures slightly above freezing (below 12.5
degree Celsius causes many tropical fruits and vegetables to have a pitted
and water-soaked symptoms
2. Injury caused by too high temperature
 Sunscald – tissues are light-colored and blistered due to prolonged
exposure to high temperature and bright sunlight
 Heat necrosis of potato – potatoes grown in soils where it is hot and dry
exhibit yellow or brown discoloration in the vascular system.
3. Stress caused by lack of oxygen
 At oxygen below 2%, normal respiration cannot proceed
which results in anaerobiosis
 Blackheart disease of potato
4. Too much or too little light
 Too much light scorches or scalds leaf tissues; too little
light produces plants that are etiolated.
5. Injury caused by adverse meteorological conditions
 Strong winds, heavy rains, lightning can also cause
various disorders in plants
6. Injury caused by air pollutants
 Mainly gases and particulates (soots, dusts, ashes)
 Ethylene – essential plant hormone, also from vehicle emissions
 Nitrogen oxides – from automobile emissions, also produced from the
combustion of coal, gasoline, natural gas and fuel oil
 Peroxyacetyl nitrates (pans) – formed from nitrogen oxides undergoing a
phytochemical reactions with gaseous hydrocarbons
 Ozone – constituent of smog, also formed in the same way as pans
 Particulates – lime and cement dusts, ash and soot
 Other air pollutants like chlorine, sulphur dioxide, flourides, hydrogen
chloride, etc.
7. Mineral deficiencies/mineral excesses
8. Unfavorable soil pH
9. Excessive pesticide levels
10. Improper agricultural practices
11. Lack or excess of soil moisture
12. Naturally occurring toxic chemicals
Example: hydrogen sulphide at toxic levels may be
formed in the presence of ferrous ion in flooded rice fields
under anaerobic conditions causing disease of rice.
Parasitic or Biotic Agents of
Plant Diseases
VIRUS
 More than 2,000 types of viral diseases of plants are known, and together
they account for an estimated annual loss of $15 billion worldwide due to
their destruction of agricultural and horticultural crops.

 Characteristics of virus

 Obligate parasites of submicroscopic size

 Consists of segments of double or singe-stranded RNA or DNA encased
in protein structures
 Lack the machinery for the production of energy through respiration, and
for at least some viruses the isolated nucleic acid genome is infective.
Viruses replicate only in host cells
 Viruses lack metabolic enzymes and equipment for making proteins,
such as ribosomes.
 The are merely packaged sets of genes in transit from one host cell
to another.
 Each particular virus can infect cells of only a limited number of
host species, called the host range of the virus. This host specificity
results from the evolution of recognition systems by the virus.
 Viruses usually identify host cells by “lock-and-key” fit between
viral surface proteins and specific receptor molecules on the outside
of cells.
 Components:
> protein coat (capsid)
- provide a protective sheath for the nucleic acid
- facilitate movement of virus from cell to cell
- for transmission of viruses
- determines the kinds of symptoms it causes
> nucleic acid – infective component
 Most plant viruses have single-stranded RNA genomes
 Satellite virus – a virus that must be associated with an autonomous virus
before it can cause infection
 Bacteriophages – viruses that attack bacteria
 Bacteriophages can replicate by two alternative mechanisms: the
lytic cycle and the lysogenic cycle
 Common symptoms of viral infection
 One or more symptoms may appear on diseased plants.
 Virus infected plants are generally stunted; the yield is less and the produce is of
poor quality.
 A plant may appear healthy without apparent external symptoms though infected by
a virus.
 The common viral symptoms are:
- mosaic - stunting
- ring spot - chlorosis
- excessive branching-witches’ broom - leaf curling
- vein clearing
- color breaking
Entry of virus into plants
 Virus enters through wounds made mechanically or by
vectors (horizontal transmission)

 Virus enters by deposition into an ovule of an infected

pollen grain (vertical transmission). It can also occur in
asexual propagation or in sexual reproduction via seeds.
Means of virus transmission

 Infected pollen, seeds and other planting materials

 Grafting
 Mechanical
 Via vectors
- nematodes
- soil-borne fungi
- mites
- insects – these are the major means of virus spread
 Virus-vector relationship
1. Non-persistent (stylet-borne) – transmit the virus within seconds or minutes
after acquisition then losses the ability to transmit it
2. Semi-persistent (foregut-borne) – viruses can stay in the vector for days
3. Persistent – insect transmits the virus after a latent period has elapsed after
acquisition; vector capable of transmission for days
a. stylet-borne – for viruses that adhere to and are borne on stylet of an
insect that feeds on infected plant
b. circulative – viruses are swallowed by an insect, passed thru the blood
and are returned to the salivary glands before they can be transmitted by the insect
c. propagative – viruses multiply in the body of the vector. Transmission
may take hours to days after acquisition but once infective, it can transmit the
virus for life
 Methods of identifying viruses
1. Transmission studies using indicator hosts (local lesion hosts)
2. Electron microscopy – for virus morphology (size and shape)
3. Serological tests – for virus relationships; done by mixing
antibodies with an antigen. Example: ELISA - enzyme-linked
immunosorbent assay
4. Microscopy for the presence of inclusion bodies in young infected
tissues
5. Symptomatology and host range
  ELISA – is a test that uses antibodies and color
ELISA change to identify a substance
 It uses a solid-phase enzyme immunoassay (EIA)
to detect the presence of a substance, usually an
antigen, in a liquid sample or wet sample.
 Antigens from the sample are attached to a surface.
 Then, a further specific antibody is applied over
the surface so it can bind to the antigen. This
antibody is linked to an enzyme.
 Finally, a substance containing the enzyme’s
Microtiter plate being used in ELISA
substrate is added.
 The subsequent reaction produces a detectable
signal, most commonly a color change in the
substrate
6. Physical properties
a. Thermal inactivation point (tip) – exposure of the
viruses for 10 minutes to a specific temperature; the
lowest temperature at which virus is inactivated
b. longevity of the virus in vitro (liv)
c. dilution end point (dep) – the dilution of a virus in
crude extract at which it can still cause infection
 Control of virus diseases
1. Preventive measures – key to control of virus diseases
a. Quarantine
b. Certification
c. Use of virus-free seeds and planting materials
2. Eradicative measures
a. rouging and destruction of infected plants
b. cut and burn diseased plants
c. hot water treatment of plant propagative organs – the temperature must inactivate the
virus but should not destroy host tissues
3. Protective measure
a. control of vectors – nematodes and insects
4. cross-protection – inoculation of healthy plant with a mild strain of a
virus to protect it from infection of a more virulent strain that can
cause a more severe symptom

5. Genetic engineering – confers resistance through the introduction of

the pathogen’s coat protein gene – interferes with the infection process

6. Early detection and subsequent destruction of infected plants.

 VIROIDS

 These are circular RNA molecules, only a few hundred nucleotides long, that
infect plants.
 They do not encode proteins but can replicate in host plant cells using host
cell enzymes.
 These small RNA molecules seem to cause errors in the regulatory systems
that control plant growth.
 The typical signs of viroid diseases are abnormal development and stunted
growth.
 One viroid disease, called CADANG-CADANG, has killed more than 10
million coconut palms in the Philippines
Coconut Cadang-cadang viroid
Characteristics of viroids

 Stable “naked (no protein coat)” RNA that infect plant

 Smaller than viruses
 Closely associated with nuclei of infected cells especially
the chromatin
Symptoms of viroid-infected plants

1. Yellowing of leaves – cadang-cadang disease of coconut

2. Stunting – chrysanthemum stunt disease
3. Rolling and twisting of leaves – potato spindle tuber
4. Mottling and chlorosis – chrysanthemum chlorotic mottle
5. Vertical breaking of bark – Citrus exocortis
Transmission and spread of viroids:

 Through infected sap in contaminated tools and

hands or by alighting and chewing insects

 Through vegetative propagating materials

Control of viroids:
 Prevention is the best means to control viroids
 Generally resistant to heat. Hot water treatment is not
applicable
a. Thorough washing and disinfestations of tools used in
handling infested plants
b. Use of viroid-free seedlings and other planting
materials
c. Early detection and destruction of infected plants
BACTERIA

 General characteristics:
 Prokaryotic microorganisms; largest group; no
well-defined nucleus and nuclear membrane
 Typically one-celled
 Have unit membrane and rigid cell wall
 Reproduce asexually by binary fission
 Gene transfer is accomplished through:
-Transformation: change in cell through uptake and expression
of additional genetic material

- Transduction: transfer of genetic material from one bacterium

to another by means of a bacteriophage

- Conjugation: transfer of genetic material from a donor cell to

a recipient cell through direct cell-to-cell contact.
 Some with plasmids
-extracellular, closed, circular genetic components
-Self-replicating; can be integrated into the bacterial
chromosomes and replicated with it
-Cells may express new genetic characteristics through
plasmids
 Advantages imparted by plasmids to bacteria:
-Carry determinants for: drug resistance, phage resistance,
UV resistance, survival in secondary habitats, and for
pathogenesis
 shapes:
-Spherical (cocci)
-Rod-shaped (bacilli)
-Spiral-shaped (spirilla)
-Some rods and spirilla possess flagella
 Types of flagellation:
-Monotrichous
-Lophotrichous
-Amphitrichous
-Peritrichous
 Characteristics of plant pathogenic bacteria:

 Most plant pathogenic bacteria are:

- rod-shaped
- Aerobic
- Flagellated
- Gram negative
- Non-spore forming
 Exceptions
- Streptomyces spp. - filamentous like a mold but their biochemical and
physiological properties like bacteria
- Genus Corynebacterium id Gram positive
- Clostridia is anaerobic and spore-forming
 Gram staining
 Developed by the 19th century Danish physician Hans Christian Gram.
 Used to categorize many bacterial species according to differences in cell wall
composition.
 Samples are first stained with crystal violet dye and iodine, then rinsed in alcohol,
and finally stained with a red dye such as safranin.
 The structure of a bacterium’s cell wall determines the staining response.
 Gram-positive bacteria have simpler walls with a relatively large amount of
peptidoglycan.
 Gram-negative bacteria have less peptidoglycan and are structurally more complex,
with an outer membrane that contains lipopolysaccharides (carbohydrates bonded to
lipids).
 Genera and specie of plant pathogenic bacteria

 There used to be only 5 major genera:

- Pseudomonas
- Xanthomonas
- Agrobacterium
- Corynebacterium
- Erwinia
 Now, there are 29 known genera of plant pathogenic bacteria:
- Acetobacter - Curtobacterium -
Rhibacter
- Acidovorax - Enterobacter -
Rhodococcus
- Agrobacerium - Erwinia -
Sphingomonas
- Arthrobacter - Gluconobacter (Rhozomonas)
- Bacillus - Nocardia
- Serratia
- Brenneria - Pantoea
- Spiroplasma
- Burkholderia - Pectobacterium -
Streptomyces
- Clavibacter - Pseudomonas -
Symptoms caused by bacteria:
1. leaf-spot – examples: Xanthomonas campestris pv.vesicatoria (leaf spot of
tomato and pepper)
- Pseudomonas syringae pv. Mori (leaf pot of mulberry)
2. soft-rot – example: Pectobacerium carotovorum subsp. carotovorum (bacterial
soft rot of vegetables)
3. Blight – examples: Pseudomonas syringae pv. tabaci (tobacco wildfire)
- Xanthomonas axonopodis pv. dieffenbachiae (bacterial blight of
anthurium)
- Xanthomonas oryzae pv. oryzae (bacterial leaf blight of rice)
4. Gall – due to hypertrophy and hyperplasia of meristematic and
parynchematous tissues. Example: Agrobacterium tumefaciens (crown gall of
roses)
5. Canker – phloem and parenchyma tissues become sunken, dry and die.
Example: Xanthomonas axonopodis pv. citri (citrus canker)
6. Wilting – a result of vascular disorders; bacteria multiply and block normal
flow of water. Examples: Ralstonia solanacearum (wilt of solanaceous and
non-solanaceous plants
- Pantoea stewartii subsp. stewartii (bacterial wilt of corn)
7. Scab
8. Chlorosis
9. Streak – Example: Xanthomonas oryzae pv. oryzicola (bacterial leaf streak of
rice)
 Control of bacterial diseases
1. Cultural – sanitation to reduce inoculum levels; crop rotation for
bacterial pathogens that do not have a wide host range; proper
watering and drainage to inhibit infection and disease.
2. Seed treatment – soak seeds in weak acid solution or sodium
hypochlorite
3. Use antibiotics – examples are streptomycin, oxytetracycline.
Disadvantage would be bacteria soon develop resistance to
chemicals
4. Use resistant cultivars
 MOLLICUTES
 Characteristics:
 Prokaryotic
 No cell wall but have a unit plasma membrane; 9-12 nm thick
 Pleomorphic – due to absence of cell wall, hence, sensitive to
osmotic change
 Contain both RNA and DNA
 Pathogenic on plants, arthropods, other animals including man
 Cause diseases in plants in several ways:
a. blocking translocation in the phloem
b. interfering with plants’ hormonal balance
 Common symptoms of plant diseases caused by mollicutes:
- yellows
- phyllody
- virescence
- stunting
- production of axillary shoots and adventitious roots
 Resistant to penicillin but sensitive to tetracycline and
chloramphenicol
 CLASS MOLLICUTES
 Order Mycoplasmatales

2 plant pathogenic taxa:

1. Phytoplasmas
2. Spiroplasmas
1. Phytoplasmas
> formerly called mlo’s or mycoplasma-like organisms
> generally found in phloem
> varied shape but generally spherical or ovoid; may also appear
mucoid of filamentous
> nutritionally fastidious; very difficult to culture in artificial media
> reproduce by budding and by binary transverse fission of cells
2. Spiroplasmas
> helical or spiral-shaped during certain phases of growth
> relatively easy to grow
> require sterol for growth
> larger than phytoplasma
Transmission of Mollicutes

 By insect vectors
 Mainly by leafhoppers, planthoppers, psyllids
 Insect acquire the mollicutes in the phloem sieve tubes of
the plant
 Incubation period from acquisition of feeding: 10-45 days

 Mechanical transmission
e.g. budding and grafting
 Diseases caused by Mollicutes
 1967 – Doi and co-workers observed mollicutes to be associated with aster
yellows, mulberry dwarf and potato witche’s broom.
 Example of disease:
- lethal yellowing of coconut trees – phytoplasma causes death of
flowers and leaves; blight kills trees in 6 months or less.
- citrus stubborn disease – spiroplasma `affects leaves, fruits and stems;
stunting, die-back, bunchy growth of twigs and branches, mottling, leaf
chlorosis.
- corn stunt – spiroplasma causes leaf chlorosis, stunting, and bunchy
top appearance
 Management of Diseases caused by Mollicutes

1. Use of resistant cultivars or hybrids

2. Proper control of insect vectors
3. Use of mollicute-free planting materials
4. Eradication of alternative hosts – example: weeds
5. Use of tetracycline antibiotic – if economically feasible and
no danger of residue on edible plant parts
6. Sanitation – cutting and burning diseased plant parts during
early stages of infection
FASTIDIOUS VASCULAR BACTERIA
(RICKETTSIA-LIKE ORGANISM OR RLO)
 Cannot be grown on simple culture media in absence of host cells
 Fastidious phloem-limited bacteria – observed in 1972 in phloem of
clover and periwinkle plants affected with clover club leaf disease.
Later observed in citrus plants affected with the greening disease.
 Fastidious xylem-limited bacteria – observed in 19773 in xylem
vessels of grape plants affected with Pierce’s disease (Xyllela
fastidiosa) and alfalfa affected with alfalfa dwarf
Characteristics of FVB
 Generally rod-shaped
 Measures 0.2 to 0.5 um in diameter by 1 to 4 um in length
 Bounded by a cell membrane and cell wall
 No flagella
 Cell is usually undulated or rippled
 Nearly all fastidious vascular bacteria are gram negative
 Several xylem-limited bacteria are placed in the recently created
genus Xyllela.
 Only xylem-limited – inhabiting bacteria causing sugarcane ratoon
stunting and Bermuda grass stunting are gram positive
 None of the phloem-inhabiting bacteria (cause of clover
club leaf and citrus greening) has been grown in culture.
 All xylem-inhabiting fastidious bacteria can be grown in
culture in complex nutrient media; growth is slow and
colonies produced are tiny (1-2 mm)
 All fastidious vascular bacteria are unable to grow on
conventional bacteriological media.
 Fastidious vascular bacteria are sensitive to tetracycline
and penicillin and to high temperature.
Important disease caused by FVB
1. Fastidious xylem-limited gram negative bacteria: (caused by forms of the
bacterium Xylella fastidiosa)
a. Pierce’s disease of grapes
b. Citrus variegation chlorosis
c. Phony peach disease
d. Almond leaf scorch
e. Plum leaf scald
2. Fastidious xylem-limited gram positive bacteria
a. Ratoon stunting disease of sugarcane – caused by Clavibacter xyli
subsp. Xyli
3. Fastidious phloem-limited bacteria – cause of the important citrus
greening disease and minor diseases of clover and periwinkle
PLANT PATHOGENIC PROTISTS

 They are not considered as fungi anymore but protozoa-like or

fungi-like
 Their cell walls are not made up of chitin but not of cellulose and
other glucans
I. protozoa-like protists – unicellular, plasmodia, or very simple
multicells, phagotrophic (feeding by engulfing food)
A. Phylum Myxomycota or slime molds – from naked, amorphous
plasmodia
Genera: Fuligo, Mucilago, Physarum
B. Phylum Plasmodiophoromycota or endoparasitic slime molds
fungal-like
Examples:
Plasmodiophora brassicae – clubroot of cabbage and
other crucifers
Sporongospora subterranea – powedery scab of potato
tubers

C. Flagellate protozoa – reported in laticiferous plants particularly in

the sieve tubes
Examples:
Phytomonas leptovasorum – phloem necrosis of coffee in
Surinam
Heart rot disease of coconut and oil palm
II. Fungal-like protists – have mycelia and conidia but cell walls are made up of
cellulose and glucans, not chitin as true fungi would have.

Phylum Oomycota
Class Oomycetes
Order Peronosporales
Families:
A. Pythiaceae – causes damping-off, root rots of vegetables
a. genus: Pythium (damping-off, rots of vegetables,
turf disease)
b. genus: Pytophthora (root rots, rots of fleshy tissues)
B. Peronosporaceae – downey mildews
C. Albuginaceae – white rust
NEMATODES
 Etymology: Greek words “nema/nematos” = thread
“edos” =
resembling or likeness
CHARACTERISTICS
thread-like unsegmented worms which are usually
elongated and cylindrical in chape
May be saprophagous, predaceous or plant-parasitic
depending on their sources of food
 Saprophagous nematodes – feed on other nematodes and on other minute
animals
 Phytonematology – deals with nematodes that parasitize plants
 Tubatrix aceli – wheat gall nematode; the first plant parasitic nematode
described
 Caenorhabdilisi elegans – used as a model organism for genetic and
physiological studies
 Plant parasitic nematodes (ppn) – feed on all forms of plant life
including seed plant and algae; some feed on fungi and bacteria
 Mostly are obligate parasites; dependent on the living host for survival as
they feed and reproduce only in their hosts.
 Most ppn have a stylet – a hollow, needle-like spear; others have a
modified solid spear.
Nematode Biology
females laying eggs in the
host plant or in the soil

Sexually mature adult males/ the eggs hatched into

Females after the last molt larvae or juveniles

4 larval stages; molting

after each stage

LIFE CYCLE OF A NEMATODE

1. Life Cycle: Zygote – Juvenile Stage – Adult
2nd Juvenile (J2) – the feeding or infective stage
2. Reproductive stage:
a. Amphimixis – mode of reproduction where males
are needed
b. Parthenogenesis – mode of reproduction wherein
only females are produced and offsprings are clone of the
female
c. Sex reversal – observed in juvenile stage of
parthenogenetic species of Meloidogyne during
unfavourable condition
3. Survival Strategy
Dormancy – lowered metabolism
Types of Dormancy
a. Diapause – state of arrested development which persist
until specific requirements for development are satisfied
even if favourable condition return
b. Quiescence – spontaneous reversible response to
unpredictable unfavourable condition
Egg stage – the survival stage of nematodes
Groups of plant parasitic nematodes
1. According to feeding position
a. Ectoparasites
> feed from the outside and only the stylet enters the plant
> they do not enter the roots
> feed mainly on root hairs and root tips; resulting to roots may form many lateral
branches and stop growing
Ex. The genera Xiphinema, Trichdorous, and Tylenchorynchus

b. Semi endoparasites
> feed by burying the front part of the body into the host cells while the posterior
portion is outside the host
Ex. Rotylenchulus reniformis (reniform nemas), Tylenchulus semipenetrans (citrus
nemas), and Helicotylenchus (spiral nemas)
c. Endoparasites
> the entire nematode body enters the plant cells while it feeds
Ex. Meloidogyne (root knot nematode), Heterodera (cyst nematode), and
Pratylenchus (lesion nematode) which feed on the root cortex of many plants)
2. According to movement while feeding
a. migratory
> move from one part of the plant to another portion of the host
> move from the plant to the soil and back
Ex. Radopholous (burrowing nematode), Pratylenchus, Ditylenchus dipsaci (stem
and bulb nematodes), and Aphelenchoides (foliar and seed nematodes)
b. sedentary
> attach themselves to the roots or burrow into the root; in each case they
remain sedentary
Ex. Meloidogyne, Rotylenchulus, and Tylenchulus
Stylet of nematodes

 Is a protrusible in the mouth of nematodes which distinguishes plant

parasitic from living forms.
 It is the structure they use for puncturing plant cells and
withdrawing their contents.
 Three types:
1. stomato – with distinct cone, shaft and knobs, inside is
hallow (Order Tylenchida)
2. Odontostylet – hallow spear (Order Dorylaimida)
3. Onchiostylet – bent solied needle-like stylet (Order
Triplonchida)
Sampling Theories

1. Spatial Distribution – nematode distribution within the

field is generally patchy owing to their small size and slow
rate of active movement.
2. Vertical Distribution – refers to the dispersal of nematodes
in a soil profile
3. Temporal/seasonal Distribution – influenced by climatic
pattern (wet and dry) and availability

* Nematode density is highest during near harvest stage of

crop.
Extraction techniques
 Motility-dependent/active methods: extract slender and active stages
of nematodes
Ex. Baermann funnel and its modification and water incubation
method
 Motility-independent/passive methods: extracts even sluggish (slow
moving nematodes)
Ex. Wet sieving method (by nematode size)
Maceration sieving (by nematode size)
Elutriation method (by sedimentation difference of
nematode and soil profile)
Centifugal flotation (by specific gravity)
Nematode diseases important in the Philippines

 Slow decline of citrus – Tylenchulus semipenetrans

 Spreading decline of citrus – Radophulus similis
 Toppling disease of banana – Radopholus similis
 Root knot – Meloidogyne spp.
 False root knot – Naccibus spp.
 Ufra disease of rice – Aphelenchoides besseyi
 Rice root knot – Hirschmaniella oryzae
 Yellow dwarf disease of black pepper – Radopholus similis
 Red ring disease of coconut – Radinaphelenchus cocophilus
FUNGI
 Characteristics:
 Form a mycelium
 Cell walls contain chitin and glucan
 No chloroplast
 Nutrition: by absorption; heterotrophic; depend upon other living
plants for food (food derived from organic matter)
 Reproduction: usually by means of spores, which are very small
seed-like structures (germinate and produce threadlike filaments
through the plant’s natural opening like the stomates, hydathodes,
and lenticels)
 Has a specialized structure, appresorium, used for
attachment and penetration to an intact host
 Has a structure called haustoria which takes food needed
for its growth
 Survival: in the form of spores or threadlike p[arts
(mycelia or fruiting bodies) in some dead parts of plants or
decaying materials
 Primary stored carbohydrate: Glycogen
The Four Phyla with Plant Pathogens

1. CHYTRIDIOMYCOTA
2. ZYGOMYCOTA
3. ASCOMYCOTA
4. BASIDIOMYCOTA
 Phylum CHYTRIDIOMYCOTA
 Have zoospores with one posterior flagellum
 Only member of fungi that form motile cells (zoospores or
gametes)

a. Class Chytridiomycetes
ex. Physoderma maydis – causes brown spot of corn
Synchytrium psopocarpi – causes orange galls
of winged bean Olpidium brassicae – root disease of
crucifers
Phylum ZYGOMYCOTA
 No zoospores
 Have asexual spores in sporangis
 Produce zoospores which are non-motile sexual resting spores
a. Order Mucorales
> Rhizopus – Ex. Rhizopus nigricans, R. stolonifer – causes soft rot
of fruits and vegetable
> Mucor
> Choanephora – Ex. Choanephora cucurbitarum – causes soft rot of
squash
b. Order Glomales (mycorrhiza)
> Glomus
> Gigaspora
Phylum BASIDIOMYCOTA
 The club and mushroom fungi
 Sexual spores called basidiospores or sporadia, are produced externally
on one or four-celled structure called a basidium
a. Order Ustilaginales (the smut fungi)
Ex. Ustilago maydis – causes corn smut
Urocystis cepulae – causes smut of onion
b. Order Uredinales – (the obligate rust fungi)
- attacks mostly leaves and stems; some form swellings and even
galls
- most rust fungi are very specialized; attack only certain genera or
varieties
Formae speciales
Ex. Puccinia graminis f. sp. tritici – attacks wheat
only
Puccinia graminis f. sp. hordei – attacks barley
only
Pathogenic (physiologic) race – P. f. sp. tritici attacks some
varieties of wheat (within crop species)
Examples of rust diseases
Uromyces phaseoli – causes rust of beans
Hemileia vastatrix – causes coffee rust
Puccinia polysora – peanut rust
c. Order Agaricales (mushrooms)
Phylum ASCOMYCOTA
 The sac fungi
 Produce sexual spores called ascospores in groups of eight within a sac known as ascus
a. Class ARHIASCOMYCETES
b. Class SACCHAROMYCETES – ex. Galactomycetes sp. - causes sour rot of citrus fruits
c. Class PLECTOMYCETES
d. Class PYRENYMYCETES – ex. Claviceps purpurea – causes ergot of rye; Ceratocystis
paradoxa – causes pineapple black rot; Ceratocystis fimbriata – causes root rot of sweet
potato; Magnaporthe grisea – causes rice blasts
e. Class LOCULOASCOMYCETES – ex. Mycosphaerella fijiensis – causes black sigatoka
leafspot of banana; Capnodium sp. – sooty mold fungi on a variety of crops; Blumeria
graminis – causes powdery mildew of grasses
f. Class DISCOMYCETES – ex. Diplocarpon rosae – causes black spot of roses

Teleomorph – the sexual or perfect stage of ascomycetes

Anamorph – the asexual or conidial or imperfect stage
Deuteromycetes or Imperfect Fungi
 The imperfect stage of Phylum Ascomycota
 Sexual reproduction and sexual structures are lacking or unknown
 3 groups of Deuteromycetes or imperfect fungi
1. Hypomycetes – fungi that produce conidia on free conidiophores or groups of conidiophores
a. Alternaria – cause of leaf spots and blights on many crop plants
b. Bipolaries – leaf spots in cereal plants
2. Coelomycetes – fungi that produce acervuli or pycnidia that bear conidia and conidiophores
a. Diplodia – fruit rots
3. Mycelia sterilia –no asexual nor sexual spores
a. Rhizoctonia – rotting of leaves, stems and roots
b. Sclerotium – seed, root and stem rots and seedling diseases
Fungicides
 Kinds of fungicides
1. Protective fungicides – as foliage and fruit sprays or dusts to keep
disease causing fungi from penetrating plants. Ex. Zineb
2. Eradicant fungicides – kills or inhibit fungi after they have
penetrated the plants. Ex. Mercury chloride
3. Protective and eradicant fungicides – controls foliage and fruit
diseases; as seed treatment. Ex. Captan
4. Systemic and curative fungicides – absorbed by roots and
distributed within the plants to control certain diseases; applied to
seeds or soil. Ex. Benlate, Apron 35
PARASITIC HIGHER PLANTS
 Classification:
1. Hemiparasites – contains chlorophyll but without roots so it depends
on host for water and minerals
Examples: Witchweeds
True mistletoe and leafy mistletoe
Loranthus sp.
2. True parasites – have little or no chlorophyll and no roots either so
entirely dependent on host for water and minerals
Examples: Dodder
Broomrapes
Bunga ng tubo (Aeginetia indica)
Variability in Plant Pathogens
General Concepts
 Plant pathogenic microorganisms like other organisms, continually
undergo changes
 The shorter the generation time and the larger the numbers of
reproductive units formed in each generation, the greater are the
chance of producing genetic changes over a given period of time.
 Bacterial populations – can double their numbers every 20 minutes
during favourable environmental conditions
 Fungus – can form millions of spores within a few days
 The changes that a pathogen undergoes may involve an increase or
decrease in its pathogenicity. Thus, new races capable of attacking
new host varieties may be formed; or some races may lose their
virulence.
 Terms used in grouping organisms below the species level:
A. Biotype
 Populations of life forms that is identical in all inheritable traits;
genetically homogenous.
 If an organism from one biotype mates with one from another
biotype, a different group is formed as a result of hybridization.
B. Pathovar
 Among bacterial plant pathogen, a strain or group of strains at the
infrasubspecies level, with identical or similar characteristics based
on pathogenicity, symptoms, or signs and host range.
C. Pathogenic race
 Another subdivision of the subspecies level which is made up of one or more
biotype with morphologically identical members. The development of pathogeneic
races is enhanced by the following:
1. absence of susceptible varieties
2. presence of resistant varieties
3. sexual reproduction of pathogen
4. obligate parasitism
5. narrow host range
D. Formae speciales or special form
 Based on the ability to attack different genera of crop plants
 Example is Puccinia graminis with members that infect different cereal crops with
forma speciales tritici attacking wheat only and f.sp. avenae attacking oat only.
 Each forma speciales may contain different races that attack different varieties of
the host.
Mechanism of Variation

 Microorganisms naturally undergo

genetic changes through hybridization,
mutation, and a variety of sexual-like
and asexual processes
 Sources of Variation in the Fungi
1. Heterokaryosis
 The presence of different nuclei in the same mycelium
 Each nucleus in a heterokaryon is independent of the other nuclei although the behaviour and
phenotype of the microorganism are controlled by the kinds of genes present and by the
proportion of each kind.
 It is an important method of producing new fungal strains or races with a concomitant change
in pathogenicity
2. Parasexual process
 Parasexuality was first observed by Pontecorvo and Roper while working with Aspergillus
nidulans.
 It mimics sexual reproduction in that genetic recombination occurs but it is mitotic
recombination with vegetative heterokaryotic hyphae.
 It starts with the formation of a heterokaryon, followed by karyogamy or diploidization of
nuclei, the multiplication of these nuclei and finally, the restoration to the haploid state .
3. Mutation
 A discontinuous heritable change of the genetic material which may
arise spontaneously or through the action of mutagenic agents.
4. 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 extrachromosomal particulate elements can multiply and be
transmitted asexually through hyphal anastomosis or sexually.
5. Sexual reproduction
 This results in hybridization through segregation and genetic
recombination.
Sources of Variation in Bacteria
1. Mutation
2. Transformation
 A sexual-like process through which bacterial cells absorb and incorporate in
their own cells heritable genetic materials that are released by other bacteria.
 The agent is believed to be DNA which the recipient bacteria aquire from the
growth filtrate of the donor bacteria
3. Transduction
 Occurs when a bacteriophage transfers genetic material from its former host
bacterium to its next host
4. Conjugation
> There is transfer of genetic material from one bacterium to another when two
compatible cells come in contact with each other.
Sources of Variation in Nematodes

 Nematodes form new pathogenic races

through hybridization and mutation.
Pathogenicity varies according to the degree
of resistance/susceptibility of the host.
Disease Cycle
Parts of the disease cycle

A.Dissemination of inocula
B.Inoculation
C.Penetration or ingress
D.Infection
E. Colonization/Invasion
F. Incubation
G.Survival
A. Dissemination of Inocula
Inoculums – signs of pathogens or the pathogen structures
found on the surface of the host
 By wind –major means of spreading air-borne pathogens such
as fungal spores of leaf, stem, and fruit pathogens.
- take-off: inoculum gets into the air
- flight: inoculum move with the wind
- deposition: settling of the inoculum from the atmospheres
Not disseminated by wind
- viruses, viroids and mycoplasmas, nematodes (occasional),
bacteria (via soil particles)
 By rain – fungal spores and bacterial cells are carried to short
distances by rain splashes.
 feed on a plant, the inoculum that they carry is deposited and is left
on the injured portions where the insects had just fed on.
 B seed and planting materials – infected planting materials posses
viruses, viroids, mycoplasmas and many bacteria internally. Infested
planting materials carry fungal spores, bacterial cells or nematodes
externally or on the surface.
 By man – man is a major long-distance disseminator of plant
pathogens by carrying of infected ad infested planting materials and
shipping crates and equipment used for agricultural products usually
carry all kinds of inocula.
 By insects – plant to plant via insects: viruses, bacteria and fungi.
As insects
B. Inoculation
 Contact of the pathogen with the host
 Deposition of inoculum into an infection court
Infection court – the susceptible part which could be natural opening (stomata, lenticels,
hydathode, growth crack), a wound or intact plant surface
Inoculum - is composed of pathogen structures capable of initiating disease production.

Types of inoculum:
Fungi – asexual or sexual spores, mycelia fragments, sclerotial bodies, rhizomorphs, and
dormant mycelia in seed
Nematodes – eggs, larvae and adults
Bacteria – phytoplasma cells, protozoan cells
Others – bacteria and mycoplasmas, rickettsia, virus particles, viroid entities and seeds of
parasitic flowering plants
 Sources of inocula:
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
 Pathogens may survive over adverse conditions by:
1. Surviving as saprophyte in dead plant debris in the soil
2. Forming thick-walled resistant structures for survival
3. Surviving in weeds and other hosts
4. Surviving in vectors
5. Surviving in the seed
C. Penetration or Ingress
 Entrance of pathogen into the host
 Penetration does not imply successful infection
 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.
 Entry points
1. natural openings
2. intact host surface
3. wounds
*Direct penetration is through intact epidermis. Bacteria and viruses
cannot penetrate directly.
 2 types of penetration
1. Passive – if the pathogen plays no active part in it, as
when bacterial cells are carried by a film of water through
the stomata into the host tissues.
2. Active – when the pathogen directly participates as when
the fungal spore germinates, forms a germ tube, an
appresorium for attachment, and penetrates through the
intact host surface by forming an infection hypha or
penetration peg.
D. Infection – occurs when the pathogen has become
established in the plant tissues after penetration and obtains
nutrients from the host.

 Latent infection – the state in which the host is infected

with the pathogen but does not show any symptoms.
 Following infection – the pathogen continues to grow and
colonize the host.
E. Colonization/Invasion
 Colonization – is the growth or movement of the pathogen through the
host tissues.
 It can be active or passive movement:
- active: when the pathogen does something as when a fungal
pathogen, for instance, grows as it passes from cell to cell;
- passive: if the pathogen is merely carried through the transpirational
stream, as are some viruses.
 Produce harmful chemicals like enzymes, toxins, hormones, etc.
 Colonization by viruses, viroids and molicutes: they are intracellular
parasites, they colonize the epidermal cells, the palisade cells, the spongy
mesophyll, and the vascular system.
 Colonization by bacteria:
intracellular – in xylem and phloem vessels, ex. Gall formations,
vascular wilts.
intracellular – in between cells
 Colonization by nematodes – sedentary endoparasites, migratory
endoparasite
 Colonization by phytoplasma – binary fission, budding, etc. to produce
more cells
 Colonization by fungi
– colonization on the host surface
- external colonization with haustoria inside the host cells
- intercellular colonization without haustoria
- intercellular colonization with intracellular haustoria
- intercellular colonization
- intercellular and intracellular colonization
F. Incubation
 Incubation period has been used to mean the time from
inoculation to the production of visible symptoms.
 Also, refers to the time from the first response of the plant
to the formation of visible symptoms.

G. Survival
> Some pathogen structures may not land on a susceptible
plant and certain environmental factors may not favour their
continued growth and development
Epidemiology of Plant Disease
 Definitions of terms
 Epidemiology – study of epidemics or study of the increase of
diseae in a population and the factors that influence them
 Epidemic – any increase of disease in a population; it occurs when a
pathogen spread to and affects many individuals within a population
over a relatively large area and within a relatively short time
 Epiphytotics – refers to epidemics of plant disease
 Endemic disease – one that is native or introduced from some other
area
 Pandemic disease – bone or worldwide or widespread occurrence
throughout a continent or a region
 Sporadic disease – one that occurs at irregular interval
Elements of an Epidemic
 Plant disease epidemic develop as a result of the timely combination
of the same elements that result in plant diseases:
1. susceptible host
2. virulent pathogen
3. favourable environment
4. intervention by man
 Humans may help to initiate and develop epidemics through some
of their activities, e.g., topping or pruning plants in wet weather;
introduction of new pathogen from other areas through
contaminated planting materials, etc.
 Factors that affect the development of epidemics
1. Host factors
a. levels of genetic resistance or susceptibility of the host
- host plants carrying major or minor genes for resistance less likely to develop an epidemic
than host plants with no genes of resistance.
b. degree of uniformity of host plants
- when genetically uniform host plants, particularly with regard to the genes associated with
disease resistance, are grown over large areas, a greater likelihood exists that a new pathogen race will
appear that can attack other genome and result in an epidemic.
c. type of crop
- in annual crops such as corn, vegetables, rice, etc.; epidemics generally develop mush more
rapidly (usually in a few weeks) than they do in diseases or perennial woody plants.
d. age of host plants
- younger plants are generally more susceptible than adults (adult resistance)
2. Pathogen factors
a. Level of virulence – virulent pathogens capable of rapidly infecting the host ensure faster production
of larger amounts of inoculum.
b. Quantity of inoculum near host – amount of initial inoculum
c. Ecology of the pathogen – pathogens that produce inoculum on the surface of the aerial parts of the
plants can disperse with ease and are more responsible for epidemics than internal pathogens.
d. Mode of spread of the pathogen – aerially dispersed pathogen cause more of the epidemics
3. Environmental factors
e. Moisture
f. Temperature
4. Human factors
g. Site selection and preparation
h. Selection of propagative materials
i. Cultural practices
j. Disease control measure
k. Introduction of new pathogens
Analysis of Epidemics
 The increase in the amount of disease at any one time is dependent on the
following:
 The initial amount of disease or initial inoculum
 The rate of disease increase
 The duration of disease increase or the period of time involved
Compound interest disease – those wherein the pathogens are readily spread
from plant to plant during the disease cycle
- repeating cycles occur with several generations of the pathogen
Simple interest disease – those where no plant to plant spread occurs during
the primary cycle
- only one generation occurs during the growing season
Van der Plank
 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 until the
remaining uninfected plant population decreases
 If disease incidence is plotted against time, one gets the sigmoid curve
 Epidemic starts at that point where the sigmoid curve begins to leave the
horizontal line and to approach the vertical line;
 Soon after the onset of the epidemic, disease incidence becomes logarithmic until
the amount of susceptible plant tissues decreases;
 Epidemic ends when all infection courts have been eliminated or some factor in
the environment prevents further increase in the amount of disease;
 The sigmoid curve levels off at this stage.
Principles and Methods of Plant Disease
Control
 Four general principles in plant disease control

CONTROL AIMED AT
SUSCEPT
PATHOGEN
1. Protection –shield suscept with 1. Exclusion – kept pathogen out
chemical or physical barrier
2. Immunization – change suscept’s2. Eradication – destroy or elimi-
reaction to disease
nate the pathogen
 Protection – a susceptible plant can be shielded by a chemical or
physical barrier which prevents the pathogen from invading the
plant.
 Immunization – geneticists and plant breeders often change the
disease reaction of a plant to make it resistant to a pathogen.
 Exclusion – aiming out sights now at the pathogen, it is sometimes
possible to keep pathogens out of a country, province, farm or field
by employing practices based on the principles of exclusion.
 Eradication – if the pathogen has unfortunately eluded us and has
become established in a field, on a farm, etc., it is sometimes
practical to destroy, remove or eliminate it by adopting measures
based on the principles of eradication.
Exclusion Principle
 Prevention of a “new pathogen” from being introduced
into s locality where it is currently unknown.
 Methods of plant disease control
a. quarantine – regulatory actions to prevent the
introduction or dispersal of non-native organism (exotic)
diseases), legal methods
b. inspection and seed certification
c. use of pathogen-free propagating materials
Eradication Principle
 Elimination of pathogen that have become established within the plant or
in an area.
A. physical
a. heat treatment (hot air, hot water, soil sterilization, soil
solarisation)
b. irradiation – UV rays, X-rays, and Gamma rays
c. light wavelengths that prevent sporulation
d. drying stored grain
B. Chemical
a. systemic chemicals
b. soil fumigants
c. disinfestation of warehouse
d. control of insect vectors
 Issues related to use of chemicals
- pathogen resistance
- risk of poisoning humans and animals
- contamination of livestock products
- harm beneficial insects and miclofora
- contamination of food products, waterways and soil
C. Biological
 Mechanism of biological control
a. Parasitism
b. Predation
c. Competition
d. Induced resistance
e. Production of antimicrobial substance
D. Cultural
a. Roguing or removal
b. Removal of alternate host
c. Sanitation
d. Crop rotation
e. Creating unfavourable conditions
Protection Principle
 Prevention of infection through
1. Chemical barrier
2. Biological control
3. Crop management
4. Manipulation of environment
 Putting chemical barrier between the pathogen and the host
1. Before inoculation
2. To prevent spore germination
3. Or kill germinating spores
Resistance/Immunization Principle
 Involve modifying certain physiological or physical features of the host so that it can repel
infection
 Resistance – is the relative ability of the plant to overcome the effects of a pathogen.
 Methods in resistance
1. Improving the growing conditions of plants (cultural management)
2. Use of resistant varieties
vertical resistance (few major genes)
horizontal resistance (many minor genes)
Resistant varieties developed by or used in:
3. Selection
4. Gene pyramiding – involves incorporation of several resistance genes in one host variety
5. Multiline varieties – a mixture of several lines with similar agronomic characteristics but with
different genes for resistance