Module 2

Causes of Plant Diseases, Disease Cycle, Epidemiology

and Variability in Plant Pathogens

Non-Parasitic Agents of Plant Disease

• also called as physiological disorders and are therefore non-living factors that causes a
disease.
Examples:
A. Diseases caused by adverse physical factors
• Diseases caused by Too Low Temperatures – i.e. Freezing injury and
Chilling injury
• Diseases caused by too high temperatures – i.e. Sunscald and Heat
necrosis
• Disease caused by lack of oxygen – i.e. black heart
B. Air pollutants as cause of diseases:
Examples of air pollutants:
1. Ethylene 4. Ozones
2. Nitrogen oxides 5. Particulates
3. Peroxyacyl nitrates (PAN’s)

C. Mineral Deficiences – lacks N-P-K, Mg, Fe, Mn, Su, B, Cu, Zi and etc.
D. Disease caused by improper agricultural practices

Examples:
1. Unfavorable soil pH
2. Improper use of pesticides
3. Lack or excess soil moisture

E. Diseases caused by naturall occurring toxic chemicals

Examples:
1. Juglone, amydalin (later converted into hydrogen cyanide) and etc.

Parasitic Agents of Plant Diseases

A. Viruses - are obligate parasites that are ultramicroscopic composed of a nucleic acid (either
RNA or DNA) core surrounded by a protein coat.

Identification of Viruses:
- The precise identification of specific plant viruses necessitates their extraction
from the host and subsequent purification. The infectivity of the purified virus is
 tested usually with the use of an indicator host that will exhibit characteristics
local lesions.
- A study of its morphology is carried out with an electron microscope.
- Serological tests are used to determine the relationship among virues.
- Example of serological test is the Enzyme Linked Immunosorbent Assay (ELISA)
- Virus can also be identified through their typical symptoms (Symptomatology) as
well as its host range.
- Viruses physical properties are also helpful in their identification:
 Thermal inactivation point
 Dilution End Point
 Longevity of the virus in vitro
Transmission and Spread of Viruses:
- viruses may be transmitted through:
 Physical means
 By grafting
 By nematodes (as vectors)
 By certain soil-borne fungi (as vectors)
 By insects (as vectors)
 Through infected seeds
Through infected vegetative planting materials

VIRUSES
B. Bacteria - comprises the biggest group of prokaryotic microorganisms that cause plant
disease. They are typically one-celled, possess a unit membrane and a rigid cell wall. They
reproduce by binary fission. Bacteria lack a nuclear membrane and a well defined nucleus.
Their nuclear material consist of DNA which may appear in the cell as circular, ellipsoidal or
dumbell- shaped. Gene transfer in bacteria may occur through transformation, transduction,
conjugation, lysogenization or phage infection.

Bacteria may be spherical (cocci), rod-shaped (bacilli), or spiral-shaped (spirilla). They

may occur as single cells, in couples, in clusters or in chains.

Some bacteria have a flagella (use for movement) which may be lophotrichous,
amphitrichous, monotrichous or peritrichous.

Bacteria Taxonomy:

* traditional method of bacterial classification was based on the morphological, cultural,

biochemical, physiological, and pathological characteristics of the of the organisms.

Genera and Species of Plant Pathogenic Bacteria:

* Acetobacter * Pectobacterium
* Acidovorax * Pseudomonas
* Agrobacterium * Ralstonia
* Arthrobacter * Rathayibacter
* Bacillus * Rhizobacter
* Brenneria * Rhodococcus
* Burkholderia * Sphingomonas (Rhizomonas)
 * Clavibacter * Serratia
* Clostridium * Spiroplasma
* Corynebacterium * Streptomyces
* Curtobacterium * Xanthomonas
* Enterobacter * Xyllela
* Erwinia * Xylophilus
* Gluconobacter * Pantoea
* Nocardia

Typical Symptoms Caused by Bacteria:

Leaf spot Soft Rot

Leaf Blight Wilting

Control of Bacterial Diseases of Plants:

• Cultural practices
a. sanitation
b. proper watering
c.drainage)
• Seed treatment
• Use of Antibiotic
• Using resistant plants
•
 Shapes: Flagella Location:

Spherical – Cocci Lophotrichous

Rod-shaped – Bacilli Amphitrichous

Spiral-shaped – Spirilla Monotrichous
Peritrichous

C. Plant Pathogenic Mollicutes

• Mollicutes are prokaryotic microorganisms similar to bacteria. Unlike typical

bacteria, however, they have no cell walls but have a unit plasma membrane that
is 9-12 mm. thick. The lack of cell wall makes them pleomorphic and very
sensitive to osmotic change. They contain both RNA and DNA.

• Mollicutes are resistant to penicillin but are sensitive to tetracycline and

chloramphenicol.

Taxonomy of Mollicutes:

• The mollicutes are placed in Class Mollicutes, Order Mycoplamatales with atleast
two plant pathogenic taxa, the Phytoplasmas (former MLO) and the Spiroplasmas.

Detection of Mollicutes:

• Plant mollicutes in host tissues may be detected by light and electron microscopy
using stains such as Giemsa, thione, and toluidine blue.

Transmission of Mollicutes:
 • The mollicutes are transmitted by insect vectors, mainly by leafhoppers, also by
planthoppers and psyllids.

Diseases caused by Mollicutes:

• many of the “yellows” diseases not known to be caused by mollicutes were

previously attributed to viruses. It was in 1967 when Doi and c0-workers first
observed “mycoplasma-like organisms” to be associated with aster yellows,
mulberry dwarf and potato witches’ broom.

D. Protozoa as Plant Pathogens:

• Some microorganism that were previously classified with the fungi have been
placed under Kingdom Protozoa. These are the Myxomycetes or slime molds
which form naked, amorphorous plasmodia. The genera Fuligo, Mucilago and
Physarum from slime molds on plants lying close to the ground thereby
interfering with normal photosynthesis.

E. Fungal Plant Pathogens:

1. General Characteristics:

- Fungi are eukaryotic, non-chlorophyll-bearing, sporeforming microorganisms, with

a branched filamentous vegetative structure called mycelium. Fungi possess
true nuclei and cell walls. There are however exemptions to this general
descriptions of fungi. Some fungi are not filamentous such as the thallus
(fungus body) of Synchytrium spp. And of Saccharomyces spp. which are
unicellular.
- The mycelium may have cross walls or septa or may be continuous
(coenocytic). Septate mycelia may be uninucleate or binucleate or
multinucleate. Each branch of a mycelium is called hypha. Mycelial growth
occurs at the hyphal tips.
- Fungi reproduce mainly by spores. A spore is a specialized propagative body
which may be formed asexually by arising from modified mycelial portions or
sexually through the fusion of unlike celled (gametes). The spores function in
adverse conditions. Some fungi are hermaphroditic as they produce both male and
female gametes on the same mycelium. Homothallic fungi are those
wherein the male gametes can fertilize the female gametes on the same mycelium
whereas heterothallic fungi are those wherein the male gametes fertilize the
female gametes from a different mycelium.

• Classification of Plant Pathogenic Fungi

- Many changes have been made in the classification of fungi during the last
decade. The myxomycetes, Plasmodiophoromycetes amd the Oomycetes which
were traditionally classified with the fungi are now in different kingdoms or
 divisions as they are not considered related phylogenetically to what is now
known as the true fungi.
- The Myxomycetes and Plasmodiophoromycetes now belong to Kingdom
Protozoa.
- The Oomycetes (water molds, white rusts and downy mildews) are placed in
Kingdom Chromista. Many plant pathogens are in this group including Pythium
spp. which cause damping-off of seedlings, Phytophthora spp. which causes root
rots and fruit rots, Pseudoperonospora cubensis which cause downy mildew of
cucurbits and Peronosclerospora philippinensis, the cause of corn downy mildew.
- The true fungi, placed in the Kingdom Fungi, are those that do not have
chlorophyll, form thread-like mycelium with cell walls that contain chitin in
addition to glucans. They comprise a very large group of microorganisms
including the rust fungi, smut fungi, the powdery mildew fungi, the food-rotting
fungi and many other plant pathogens. Some fungi are beneficial such as the
edible mushrooms, the brewer’s yeasts and the antibiotic-producing penicillia.

F. Plant Pathogenic Pseudofungi

Class OOMYCETES
Order Saprolegniales
Order Peronosporales
Family Pythiaceae
Family Albuginaceae
Family Peronosporaceae

Isolation of Plant Pathogenic Fungi

• Isolation by planting of infected tissues
• Serial dilution method
• Trapping technique
Control of Fungal Diseases
• Use of resistant cultivars * Hot water treatment
 • Crop rotation * Use of antagonist
• Roguing * Control of vectors
• Proper Sanitation * Use of chemicals

G. Plant Parasitic Nematodes

General Characteristics:
• are thread-like unsegmented worms which are usually elongated and cylindrical
in shape. There is no internal separation of the organs.
• Nematodes may be saprophagous, predaceous, or plant parasitic
• Plant parasitic are mostly obligate parasites (needed a living host for survival)
• Most plant parasitic nematodes have stylet which is a hollow, needle-like spear.
• The nematode will undergo atleast 4 larval stages in its life cycle.

Groups of Plant parasitic Nematodes:

• Based on feeding position
• Ectoparasites – feeds from the outside and only the stylets enters the plant cells.
• Semi-endoparasites – feed by burying the front part of the body into the host
cells while the posterior portion is outside the host.
• Endoparasites – the entire nematode body enters the plant cells while it feeds.
• Based on movement while feeding
• Migratory - move from one part of the plant to another portion of the host or
move from the plant to the soil and back
• Sedentary – attached themselves to the roots or burrow into the roots; in each
case they remain sedentary.

Isolation of plant parasitic nematode:

• Isolation from soil – (a) by Baermann funnel (b) by Sieving
method
• Isolation from infected plant part
 Disease Complexes:
• is a physiological malfunctioning caused by two or more pathogens.
- Nematode + Bacteria
- Nematode + Fungi
- Nematode + Virus
- (Bacteria + Fungi)
- (Fungi + Viruses)
Control of Plant Parasitic Nematodes:
- Use of nematicide (last option)
- Use of Biological control (Paecilomyces lilacinus –
fungi)
- Crop rotation, solarization, use of trap crops, and use
of resistant varieties

NEMATODE

H. Parasitic Flowering Plants as Plant Diseases:

 There are over 2500 higher plant species that parasitize other plants in varying degrees of
dependence. However, only a few o them cause significant damage on crop plants or forest
trees. The phanerograms, or parsitic seed plants that are harmful to agriculture and forestry are
considered here:
• The Hemi-parasites – depends on their hosts for water and minerals but nor for
photosynthates because their leaves contain chlorophyll and can thus manufacture
food through photosynthesis. (i.e. witchweeds and true mistletoe)
• The True parasites – depends wholly on other plants and cause various diseases
such as “yellows”, wilting and stunting.

Amyema scandens (Loranthaceae) from New

Caledonia
-flowering from epicortical roots. - Photo:
Bernard Suprin.

VARIABILITY IN PLANT PATHOGENS:

Plant pathogenic microorganisms like other organisms, 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 genetic changes over a
period of time. Pathogens such as bacteria and fungi can grow and multiply rapidly.

Kingdom: Genus:
Phylum: Species:
Sub-phylum: forma speciales (f. sp.)
Class: Pathologic race:
Order: Pathovar (pv)
Family: Biotype:

Terminologies:

* Biotype – “population of life forms that are identical in all inheritable traits”.

* Pathovar – is a strain or group of strains at the infrasubspecies level, with identical or

similar characteristics based on pathogenicity, symptoms or signs and host range.

* Pathogenic race – another subdivision of the subspecies level which is made up of one or
more biotypes with morphologically identical members. Different pathogenic races differ
in the cultivar or host variety that each attacks. The development of pathogenic races is enhaced
by the absence of susceptible varieties, the presence of resistant varieties, sexual
reproduction of pathogen, obligate parasitism, and a narrow host range. These factors tend to
stimulate or even “force” an existing race to change in order to survive.

* Formae speciales (special form) – is based on the ability to attack different genera
of crop plants. Example is the Puccinia graminis with members that infect different cereal
crops with forma speciales tritici attacking wheat only and f.sp. avenae attacking oats only.

DISEASE CYCLES: (I.P.I.C.I.D.S.)

 Inoculation – this is the deposition of inoculum unto or into an infection court. Inoculum
is any part of the pathogen that can initiate disease. The infection court may be a natural
opening (stomata, lenticels, hydathodes, growth crack), a wound, or the intack host
surface.

 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.
o Passive penetration – if the pathogen plays no active part in entering the host
plant.
o Active penetration – the pathogen directly participates as when the fungal spore
germinates, form a germ tube, an appressorium for attachment, and penetrates
through the intact host surface by forming an infection hypha or penetration peg.
  Infection – the term infection has been used by plant pathologists to mean different
things. Infection occurs (after penetration) when the pathogen has become established in
the plant tissues and obtains nutrients from the host. Some consider infection to begin
with inoculation and end when the pathogen has started to obtain food from the host so
that penetration is part of the infection process. Others consider infection to mean the
activities of the pathogen between penetration and the time the pathogen starts to cause
the host to respond to the pathogen’s invasion.
 Colonization – the pathogen continues to grow and colonize the host. Colonization is the
growth or movement of the pathogen through the host tissues.
 Incubation – 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.
 Dissemination – after the symptoms has advanced, signs or pathogen structures are
usually 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, inoculum 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 secondary disease cycles.
Several secondary cycles occur within growing season of a plant.
 Survival - some pathogen structures may not land on a susceptible plant and certain
environmental factors may not favor their 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.

Infection Colonization

Active Phase

Penetration Incubation

Inoculation Dessimination

Survival Phase

Survival

INOCULUM, INOCULUM SURVIVAL AND INOCULATION

 • Inoculum is composed of pathogens structures capable of initiating disease
production. 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 serve as inoculum.
• Other inocula are cells of bacteria and mycoplasmas, rickettsia, virus particles,
viroids entities and seeds of parasitic flowering plants.

1. Sources of Inoculum
a) infected living plants
b) plant debris
c) infested soil
d) infected seeds and vegetative propagating materials
e) contaminated containers, storage areas and equipments
f) insects, nematodes and other living agents that carry inocula

2. Inoculum Dispersal

A. Wind dissemination – is the major means of spreading air-borne pathogens

such as fungal spores of leaf, stem and fruit pathogens. Before dissemination,
however, certain inocula have to be released in a passive or in an active (forcible)
manner. Dissemination by wind involves getting the inoculum into the air (take-
off), moving the inoculum from one place to another (flight), and the settling of
the inoculum from the atmosphere (deposition).

B. 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
inocula that they carry are deposited and are left on the injured portions where the
insects had just fed on.

C. Dissemination by seed and planting materials – viruses, viroids, mycoplasmas

and many bacteria are often carried internally in infected seed or vegetative
propagating materials.

D. Dissemination by rain – fungal spores and bacterial cells are carried to short
distances by rain splashes. As raindrops fall on bacterial exudates, the bacterial
cells 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. The first few drops of rain usually contain a large number of inocula
brought down from the atmosphere. The advantage of rain dissemination is that
when the inoculum lands on infection court, there is water available for
germination of fungal spores or for bacterial entry and multiplication, thus
infection is often assured.
 E. Dissemination by man – is the 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.

3. Survival of Inoculum

Pathogens must survive conditions of stress if they are to cause infection at a

future date. In temperate countries, the pathogen has to go through very cold
winters or overwinter some place, somehow. At times, it has to survive high
temperatures, moisture stress, or the absence of susceptible plants. The
Philippines, as well as other tropical areas like it, is “heaven” for plant pathogens
as there are practically no environmental extremes for the pathogens to tide over.
Pathogens may tide over adverse conditions by:
a. Surviving as saprophyte in dead plant debris in the soil,
b. Forming thick-walled resistant structures for survival
c. Surviving in weeds and other hosts
d. Surviving in vectors
e. Surviving in the seeds

A. Survival as saprophyte – many fungi and bacteria survive as saprophytes in

dead organic matter. Several soil-inhabiting fungi such as Pythium,
Phytophthora, Rhizoctonia, Sclerotium, Fusarium and Verticillium spend part of
their life histories in the soil and survive as saprophytes in the absence of their
respective living hosts.

B. Production of resistant structures – Fungi form a variety of specialized resting

structures that remain dormant and resist adverse environmental conditions.
Rhizoctonia and Sclerotium usually form sclerotial bodies (compact, hard
masses of parenchymatous tissues). Fusarium and Verticillium form
chlamydospores which are round, thick-walled bodies. Many sexual spores
are so structured to resist extreme environmental conditions such as for
overwintering.

C. Survival in weeds and other hosts – many pathogens have such a wide host
range that in the absence of one suscept they infect other hosts. The tobacco
mosaic virus (TMV) can go to tomato in the absence of tobacco.

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. Xanthomonas stewartii which causes Stewart’s
wilt of corn and Erwinia tracheiphila which causes wilt of cucurbits overwinter in
 the brassy flea beetle and in the cucumber beetle respectively. Other vectors may
be nematodes, fungi or mites.

4. 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 diseased to healthy plants.
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 especially as they can travel
relatively long distances and find their suscepts. As vectors of viruses, viroids,
fungi, bacteria and mycoplasmas, the insects are major inoculators. Nematodes
migrate through the soil looking for susceptible roots. Zoospores of
phycomycetous fungi are attracted by exudates from their hosts and they swim
until they find a suitable plant. Merril calls this phenomenon as inoculation by
“self locomotion”.

• In nature, inoculation by chance is also quite a common occurrence. Some of the

spores that are carried by wind and rain splashes may fall on a stomate or some
other infection court but the major proportion of these spores may be deposited in
way out places.

5. Inoculum Potential

• 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 symptoms that result from infection. The amount of tissues
invaded per infection may vary from a few cells as 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 infections that can occur.
6. Recognition Between Pathogen and Host
 a) The mechanism by which a pathogen recognizes its specific host plant or the
other way around – how a host recognizes a pathogen – has intrigued scientists for
many years.

b) It is believed that when a propagule of a would-be pathogen comes in contact with

a susceptible plant, an interaction occurs between the pathogen and the host. The
pathogen releases elicitor molecules for recognition by the host plant. These
substances may be polysaccharides, peptides or glycoproteins. Elicitors could be
enzymatic breakdown products of either the pathogen of the host surface.

• When the pathogen elicitors are recognized by the plant, the latter sends forth
alarm signals to its nucleus causing a variety of genes to be activated resulting in
the production of substances that are inhibitory to the pathogen. These
compounds are mobilized to the specific plant are under attack. This process is
called signal transduction.

• The initial recognition process may result in full-blown disease of the pathogen is
able to overcome the plant’s defense mechanism and thus continue to develop. If
the pathogen elicitor triggers an immediate and potent reaction such as the
formation of phytoalexins that inhibit the pathogen, then disease may not develop
or a sensitive reaction is obtained which is limited infection and does not spread.

PATHOGENS’ ENTRY INTO PLANTS

A. Pre-penetration

The inoculum deposited in or near the infection court may be affected 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 plant.
The leaf and other above-ground plant surfaces (called phylloplane or phytosphere)
support a normal or native microflora. Young seedlings harbor a few microflora composed
mostly of bacteria whereas older plant surfaces contain more microorganisms, predominantly
molds and yeasts. These native microflora compete among one another for the meager
supply of nutrients on the plant surface. Some may produce antibiotics which inhibit other
microorganisms including would-be plant pathogens. Small insects, such as aphids, may
also be present. Fungal pathogens may utilize the sugars in aphid “honeydew” which
provide the pathogen added vigor to penetrate the suscept.

The rhizosphere (layer of soil that directly affects the root) is highly populated with
diverse forms of minute flora and fauna which may affect inocula that are deposited on the
rhizoplane (root surface). The rhizoplane itself has the most active microbial activity as
metabolites which are secreted by the root are utilized by microorganisms.
 Many fungi can directly penetrate the intact host tissue but a series of events occur prior
to penetration. First, the spore that lands on an infection court germinates. Spore
germination is followed by the formation of an appresorium which attaches the pathogen
firmly to the host surface. The appresorium sends out a penetration peg which penetrates
through the cuticle and cell wall by direct pressure and/or enzymatic degradation. Some
fungi do away with the appresorium but form infection pegs.
Other fungi form knots or aggregates of hyphae on the host surface. This so-
called “infection cushion” functions as a multiple appresorium which sends out numerous
infection pegs effecting multiple penetration.

B. Portals of Entry

1. Natural Openings – Bacteria enter their host through natural openings and
through wounds. Bacterial leaf pathogens usually enter through stomatal openings.
Leaves that are water-soaked after a spell of rain facilitate the entry of bacteria as there is
a continuous column of water from the leaf surface to the stomatal cavity which allows
motile bacteria to swim through the stomata into the inside of the plant. Some bacteria
enters through lenticels and other enters through a hydathodes (pores often located at leaf
margins or tips that give off water). Trichomes (hair-like structures found on the surfaces
of leaves, some fruits, stems and petioles) are also avenues of entrance of some
pathogens. Nectary cells of flowers secrete drops of nectar that are frequented by insects
which may carry bacterial cells or other pathogens. The pathogens are deposited in the
remaining nectar wherein they multiply and later penetrate into ovary, flower pedicel and
the stem.

2. Intact host surface – even if the are no natural openings, such as hydathodes,
stomata and the like, pathogens can still enter its host through several processes such as
forming an appresorium and infection peg which passes through the cuticle and cell wall
and penetrating the host epidermis directly after spore germination, then forms a
haustorium with finger-like projections.

3. Through wounds – wounds are one of the portals in which the pathogens
can enter its host. Some pathogens are called weak parasites because they generally
enter through unsuberized wounds such as Penicillium spp. and Rhizopus spp. Viruses
as well needs wound to be able to enter their hosts.

COLONIZATION OF THE HOST

• after the pathogen has penetrated or gained entry into the host cells, it continues to
proliferate and is said to colonize the suscept/host. Colonization is the active or
passive movement of the pathogen through the host tissues. It is active when the
pathogen does something as when a fungal, for instance, grows as it passes from
cell to cell; and passive if the pathogen is merely carried though the
transpirational stream, as are some viruses. Colonization involves growth and
reproduction of the pathogen such as the formation of new spores, bacterial cells,
 virus particles, viroid entities, mollicute bodies, nematode larvae, or fungal
mycelia.

1. Colonization by Viruses, Viroids and Mollicutes

– Viruses, viroids and mollicutes are intracellular parasites. Viruses
colonize the epidermal cells, the palisade cells, the spongy mesophyll, and
the vascular system. Phytoplasmas have been found in phloem sieve tubes
and the phloem parenchyma. These pathogens are carried in the
transpirational stream through the host’s vascular system. Viruses have
been found to be moved from cell to cell through the plasmodesmata
(minute passageways between adjacent cells).

2. Colonization by Bacteria
• The bacteria that cause gall formation and vascular wilts are essentially found
intracellularly. The gall pathogens are believed to move from cell to cell
during mitosis for when an infected cell divides, some of the bacteria
associated with it are transferred to the daughter cells.
• The bacterial wilt pathogen multiplies in the vascular system and may actively
swim through the xylem vessels, or may be passively carried in the
transpiration stream.
• The soft-rotting bacteria produce pectinolytic enzymes which break down the
middle lamellae between cells. This allows the bacteria to proceed farther and
affect more cells. Affected cells release fluids which provide the liquid to
allow further spread of the pathogen.

3. 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)

A. Colonization on the host surface – The sooty mold fungi which are
saprophytic on the “honey dew” that aphids excrete are limited to
colonizing the leaf surfaces. A thick, black mycelial mat is formed on the
surface which reduces the amount of light available for normal
photosynthesis of the plant. This is a case of disease development (or
pathogenesis) without parasitism as the mycelium does not penetrate the
leaf.

B. External colonization with haustoria inside the host – the powdery

mildew fungi are limited to the outside host surface where they produce a
weft of hyphae. Penetration pegs are formed to push through the
epidermal cell walls and haustoria are formed intracellularly inside the
epidermal cells. These fungi are obligate parasites obtaining nutrients
from the host through the haustoria.
 C. External colonization without haustoria – many pathogens form
mycelia between the host cells and colonize intercellularly. The
pathogen penetrates the cuticle directly, then forms hyphae which
grow between the cells though the haustoria. The downy mildew
fungus (Peronosclerospora philippinensis), differs from most of the
downy mildew fungi in that it very rarely produces haustoria within
the host cells. It forms mycelia between the cells and therefore
essentially colonizes its host intercellularly.

D. Intercellular colonization with intracellular haustoria – many obligate

parasites and some facultative saprophytes produce mycelia between
the cells and send out haustoria into the cells for obtaining nutrients.

E. Intracellular colonization – the fungal pathogens (such as Fusarium,

Verticillium, Ceratocystis) that cause vascular wilts colonize the host
cells intracellularly as mycelia and spores fill and clog the xylem
vessels of infected roots, stems, etc. The pathogens may also produce
toxins which are carried to the leaves and other parts where symptoms
are expressed some distance from the colonize areas.

F. Intercellular and intracellular colonization – many fungi that cause

rotting of tissues colonize their hosts both inter- and intracellularly.
Pythium spp., for example, produce pectinolytic enzymes that
dissolve the middle lamellae of the host cells. This results in tissue
maceration and the pathogen further grows through the cells.

4. Colonization by Nematodes – on the case of nematode, mostly endoparasitic types are

involve on these process since there whole body will enter its hosts and colonize.
Either sedentary or migratory endoparasitic nematodes will colonize its host. But
some other types can also colonize through various ways.

5. Quiescent Infection – in certain diseases, colonization of the host is delayed due to

quiescent or latent infection. Verhoeff in 1974 defined latent infection as “a
quiescent parasitic relationship which can change into active one”, usually when the
infected fruit ripens. This phenomenon occurs in certain diseases as the anthracnose
of mango, citrus and banana. Quiescent 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 substance that
inhibit colonization or (3) the pathogen lacks enzymes needed to colonize the
immature fruit, (4) the ripe fruit has a decreased capacity for phytoalexin formation.
Phytoalexins are compounds formed in response to infection which are inhibitory to
the pathogen.

MECHANISMS OF PATHOGENICITY
- how do plant pathogens cause disease or bring about the “malfunctioning of the normal
physiology” of the affected suscept? This unit will show you how various activities of
the pathogen result in this malfunctioning and how this affect the plant’s physiological
functions.

A. Interference with the uptake of water and inorganic elements from the soil.
Root-rotting microorganisms invade and destroy the roots thereby reducing water-
absorbing capacity. Fungi and bacteria that colonize the xylem vessels interfere
with the translocation of water. So as well to the nematode (such as
Meloidogyne) in roots which enlarged cells that exert pressure on the xylem which
may crush or micplace the vessels such that water conduction is adversely affected.

B. 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 is impeded.

C. 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, little leaf and wilting. Some pathogens destroy the chloroplast
and reduce the chlorophyll needed for photosynthesis.

D. Increased transpiration
- Leaf pathogens (such as the 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.

E. 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 over-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.

G. Death of cells and tissues

- Necrotic diseases brought about by fungi, bacteria, viruses and other pathogens
cause disintegration of cell walls as well as of protoplasm.
 H. Direct utilization of Nutrients
- All obligate parasites and most facultative saprophytes use up host nutrients thereby
depriving the plant of needed food materials.

I. Blocking of Metabolic pathways

- Some pathogens block normal metabolic pathways of the plant causing accumulation
of compounds which may be toxic, diversion of metabolites and the formation of new
pathways that may lead to abnormalities.

MECHANISMS OF PLANT DEFENSE

Resistance to disease is quite common in the plant kingdom. The majority of plants are
not infected by a given pathogen. Plants that do not carry specific molecules called recognition
factors cannot be recognized by a given pathogenic microorganisms as its host. Similarly, if the
pathogen does not produce elicitor molecules that are recognized by the host, no host-pathogen
interaction and no infection occurs. Non-hosts and resistant plant cultivars are usually equipped
with pre-existing as well as inducible mechanisms for defending themselves against pathogenic
attack.

A. Defense mechanism to penetration

- Thick cuticles
- Waxy layers
- Thick and tough epidermis
- Semi-closed or closed stomata (w/ broad, projecting guard cells that
almost cover the opening)
- Formation of compounds (such as phenolic compounds) that are
inhibitory to some pathogens

B. Passive defense mechanisms to establishment of the pathogen

- Many microorganism 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
preformed defense mechanisms in the host. The pre-existing mechanisms of defense
include:

- (a) lack of a nutrient that is required by the microorganisms, (b) presence of toxic
substances,

- (c) inability of microorganisms 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.

C. Active defense mechanisms to pathogen establishment

- Active defense mechanisms 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.

- 1. Mechanical barriers – formation of protective barriers in response to the

pathogens activities such as the formation or corky layers, gums, resins and other
exudates.

- 2. Hypersensitivity – rapid localized death of host cells around the pathogen.

This results in the confinement or even death of the pathogen if it is an obligate
parasite, as it becomes surrounded by dead cells.

- 3. Plant immunization – an active immune system like that which is present

in animals is absent in plants as the latter do not produce antibodies. However,
through genetic engineering, mouse genes have been incorporated in the genome
of plants. These animal genes are expressed in the transgenic plants and produce
antibodies called plantibodies against certain pathogens in the transgenic plant.

- 4. Other post-infectional toxic substance – Aromatic copounds such as

phenolic glucosides, polyphenols, flavonoids, anthocyanins, aromatic amino acids
and coumarin derivatives are said to accumulate around infection sites where they
are believed to inhibit the pathogen. Polyphenol oxidases oxidize fungistatic
phenolics (of host or pathogen origin) to quinones which could be more toxic.

- 5. Detoxification – Some plants resist pathogenic invasion by inactivating

deleterious compounds produced during pathogenesis. Some hosts may
inactivate, inhibit or prevent enzyme synthesis by the pathogen thus reducing or
eliminating pathogenicity.

- 6. Induced resistance – induced or acquired resistance involves a change in

response to a stimulus which makes the plant more resistant to a given disease.
The resistance may be local or systemic and may be induced by living or non-
living agents or by natural or synthetic compounds. Induced resistance involves
an elicitor that triggers the defense reaction, and to which the plant has receptor(s)
for the elicitor.
EPIDEMIOLOGY OF PLANT DISEASES, DISEASE ASSESMENT AND
FORECASTING:

• Epidemiology is the study of disease development in plant populations. It takes

into account all the factors involved in disease production: (a) plant susceptibility,
(b) pathogen virulence, (c) the duration and intensity of the various environmental
factors, (d) time, (e) presence of vectors, and (f) intervention measures by man.
• The common definition of epidemic from a layman’s viewpoint is a widespread,
explosive disease outbreak. However, since the progress of an epidemic is
affected most by the interplay of factors during the early stages (or before it
becomes widespread and explosive), van der Plank in 1963 defined epidemics as
an increase in disease incidence within the plant population with time. It is in this
context that epidemiologist deal with an epidemic so as to better understand and
appreciate the factors that bring about a disease outbreak; in the early stages,
when something can still be done to prevent or at least delay an “explosive“
outbreak.
• Some purists use the term “epiphytotics” to refer to epidemics of plant diseases.
An endemic disease is one that is native or indigenous to a particular place in
contrasts to an exotic disease which had been introduced from some other area.
Both endemic and exotic diseases can develop into explosive epidemics. A
pandemic disease is one of worldwide or widespread occurrence throughout a
continent or a region. Sporadic diseases are those that occur at irregular intervals.

Factors affecting the development of epidemics

• the occurrence of an epidemic requires that susceptible plants at a susceptible

stage be exposed to abundant viable inoculum of a virulent pathogen during
favorable environmental conditions for pathogen multiplication, infection and
dissemination.
• 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.
• All factors in the environment must favor the pathogen throughout the disease
cycle – from inoculation, to spore germination, to penetration, to colonization,
sporulation, spore liberation, and subsequent dissemination. The environment
should also favor the multiplication and spread of vectors, if there are any.

Analysis of epidemics

• the increase in the amount of disease at any one time is dependent on the following: (a)
the initial amount of disease or initial inoculum, (b) the rate of disease increase, (c) the
 duration of disease increase or the period of time involved. As van der Plank stated, this
is similar to the increase in money invested at different interest rates wherein the amount
of money one has at any one time depends on the initial amount, the interest rate, and the
duration of investment. Just as the money invested at compound interest or at simple
interest so does he group diseases as “compound interest” diseases and “simple interest”
diseases. “Compound interest” diseases are those wherein the pathogens are readily
spread from plant to plant during the disease cycle (as the rust and powdery mildews).
Repeating cycles occur with several generations of the pathogen. “Simple interest”
diseases are those where no plant to plant spread occurs during the primary cycle (or only
one generation occurs during the growing season as in root knot diseases and vascular
wilts caused by soil-borne pathogens).

• 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 until the
remaining uninfected plant population decreases, thereby limiting disease increase. If
disease incidence is therefore plotted against time, one gets a sigmoid epidemic curve.
• The epidemic starts at that point where the sigmoid curve begins to leave the horizontal
line and to approach the vertical line. For some time, soon after the onset of the
epidemic, disease incidence becomes logarithmic until the amount of susceptible plant
tissues decrease. The epidemics 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.
• Zadoks and Schein (1979) divide an epidemic into 3 phases: (a) exponential or
logarithmic phase, (b) logistic phase and (c) terminal phase.
• During the early part of the epidemics when there is a logarithmic increase of disease,
the basic compound interest formula can be used to determine the amount of disease at
any one time:
X = Xoert
 X – amount of disease
 Xo – initial amount of disease or initial inoculum
 e – base of natural logarithms (2.718)
 r – rate of infection or disease increase
 t – time

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.
• 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.
 • Control practices that reduce the amount of initial inoculum or initial plant disease
cause delay of the specific point of time at which a given disease level is reached but
they do not change the rate of disease increase. Roguing diseased plants, chemical
eradication, hot water treatment, destroying infested plant debris, soil fumigation, and
using varieties with vertical resistance reduce the initial effective inoculum. The crop
may still be completely devastated but at a later date.
• Control measures such as modification of the environment, cultural practices that
hinder the growth and reproduction of the pathogen, and planting varieties with
horizontal resistance reduce r or the rate of disease increase such that maturity may be
reached and one may harvest before any significant damage to the crop occurs.
• As a measure of the rate of disease increase in the population, r reflects the integral
effects of all the factors that contribute to disease development. The state of plant
susceptibility, degree of pathogen virulence and the relative effects of the various
environmental factors are all reflected in r. Thus the rates of spore germination,
appresorium formation, penetration, colonization, sporulation, spore discharges as
well as the number of viable spores all contribute to r. Diseases with secondary
repeating cycles are characterized by a high r whereas diseases with only primary
infection have low r value.

Assessment of Disease Incidence and Crop Loss:

• A perennial question that growers face is whether or not the amount of losses (in
monetary terms) due to disease is worth the application of control measures. Would it
pay to apply costly chemicals as well as other measures? The answer lies in accurate
assessment (based on symptomatology) of diseazse severity and incidence and expressing
this in terms of yield and money. An underestimate of losses may find the farmer with
such reduced yield that can cause enormous losses which are passed on to the consumers.
An overestimate can mean a waste of scarce resources (for unnecessary measures) which
should otherwise have been chanelled to more profitable areas. Accurate disease
assessments are difficult to make and in most cases educated guesses will have to suffice.
The ideal assessment scheme requires research with sufficiently replicated trials run for
several years.
• The purpose 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.

Methods of Measuring plant disease:

• Methods used for measuring plant disease should be objective, simple, reasonably rapid
to use, and must yield comparable results when used by different people at different
times. Before an accurate method of disease appraisal can be evolved, one should have a
thorough knowledge of the host-pathogen interaction at various stages of host
development. Disease severity in individual plants and prevalence (percentage diseased
plants) are often considered.

- Determining the percentage of diseased plants, organs or tissues.

- Diseases that exhibit systemic symptoms or kill the host rapidly such as wilt,
damping-off, root rots and those caused by viruses can be assessed by
determining the percentage of diseased plants. Diseases that damage entire
organs such as fruit rots, leaf blights and inflorescences smuts may be measured
by recording the percentage of infected organs.
- Certain diseases show varying amounts of infection in different plants and/or in
different parts of the plant. This makes disease assessment a more difficult task
as in leaf-spot diseases where some leaves have only a few lesions while others
have numerous spots and differences are also observed from plant to plant. In
such cases more reliable estimates may be obtained by determining not only the
percentage infected plants but also the percentage of affected leaves and the
percentage of infected leaf tissues. This is rather a laborious procedure.
- 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%.

- Use of desciptive disease ratings on a numerical scale.

- Scales 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 IRRI 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
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 wok, 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 or 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 – 1to5%; 3 – 6to10%; 4 – 11to20%;
5 – 21to30%; 6 – 31to40%; 7 – 41to60%; 8 – 61to80%; 9 – 81to100%. 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.
- Methods of measuring crop losses:
- 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.
- Experimental methods – should be properly designed for sound statistical
analysis. Adequate replicates carried over several different seasons in various
places should be provided.
- Plant 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
physiologic races, (b) detect and monitor newly introduced pathogens and (c’)
determine the distribution of alternative and alternate hosts. All these will aid in
the evaluation of the relative importance of diseases and assist in the development
of a cooperative control program.
- Forecasting of Plant Diseases – The incidence and severity of plant diseases vary
with the season and from year to year due to differences in the weather and other
environmental conditions, amount of inoculum, vector activity and other factors
that affect pathogenesis and pathogen dissemination. There is a need to predict
when a particular disease will occur and how severe it will be so that farmers will
be properly guided in making decisions on disease control.

- Methods Used in Forecasting:

1. Empirical Forecasting – Empirical forecasting of disease occurrence has been

done for several years based on field observations and practical experience. More
recent empirical methods have been devised based on pathogen development and
its life cycle as affected by various environmental conditions. The weather
conditions during the cropping season and intercropping months, prevailing
moisture-temperature relations at critical periods during the growing season,
sources of inoculum, vector activities and other factors that affect disease
development are taken into account.

2. Forecasting by “van der Plant” analyses – the progress of epidemic (or the
increase in disease incidence in the host population) can be predicted from data on
X (initial amount of disease) and r (rate of disease increase) as discussed in the
previous topics. Merril applied this in the analysis of the Dutch elm disease.
Knowing the proportion of infected trees and the rate of increase of the disease
incidence, Merril found that in some places the epidemic was delayed for 30 years
whereas in other places the delay was only 7 years. On this basis the concerned
areas then decided whether or not to proceed with expensive control programs.

3. Computer simulation – Simulation involves the systems concept where

every stage in the life cycle of the pathogen is modeled, taking into consideration
the effects of factors in the environment. The steps are then integrated using the
computer. This method utilizes quantitative data regarding the effects of
temperature, rainfall, light, wind, and humidity, on: pathogen growth,
multiplication, penetration, colonization, dissemination, production of primary
and secondary inocula, vector activities, competitors, antagonists, as well as
genetic variation in the pathogen and the host. These data, together with the
existing environmental information on the amount of rainfall, amount and
duration of dew, intensity and duration of light, speed and direction of wind,
ambient temperature and relative humidity are fed into a computer. The simulator
then predicts the actual amount of disease in the field at that particular time. A
simulator, to be effective, requires a diet of sufficient and accurate data. A lot of
the required information for most of the major disease has still to be gathered by
researchers.
CONTROL OF PLANT DISEASES:

Principles of Plant Disease Control

The raison d’ etre of the science of plant pathology is the control of plant diseases. In
fact, practically all studies conducted in the name of phytopathology are ultimately aimed at
finding effective control measures. Studies on the causal organism, host-pathogen interaction,
diagnosis, epidemiology, disease forecasting and so on, lead directly or indirectly to disease
control.
One prime requisite of a control measure is that it must be economical or that the amount
of money spent on control should be more than compensated for by the increased quantity and
quality of the produce as a direct result of applying the control measure. Most control measures
are preventive in nature although the use of systemic chemicals has provided control for certain
deep-seated infections.
Farmers can often tolerate a certain level of disease in their crop. Control measures are
therefore aimed at “preventing an intolerable build-up of disease within a plant population”, not
for total absence of disease. This is true for field crops, vegetable crops, plantation crops, etc.,
with the exception of high-priced individual plants such as prize orchids. The purpose of plant
disease control are to: (a) prevent disease development, (b) maintain a tolerable disease incidence
and (c) minimize yield losses.
There are four general principles of plant disease control, name exclusion, protection,
eradication and immunization. Each of the available control measures is based on one of these
principles.

1. Exclusion – is the prevention of a “new pathogen” from being introduced into a

locality where it is currently unknown. This necessarily involves legal methods
of control. Some plant materials may be allowed to enter if they pass an initial
inspection by quarantine officials. Some diseases, however, cannot be detected
by immediate visual inspection. An example is potato late blight which may pass
undetected in the tubers unless the tuber is planted and the plant grown to a
certain age. Quarantine officials therefore hold such materials under post-entry
quarantine. Plants are grown in nurseries or greenhouses and observed for
symptoms of disease before they are released if found to be free of disease.
Effective quarantine laws are “worth their weight in gold” as evidenced from past
epidemics that occurred due to the introduction of a pathogen to new areas. The
reason that exotic pathogens may be disastrous is that the plants in the new
locality had no chance to evolve resistance against the pathogen.
A. 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, by animals and by people on
their bodies, through contaminated luggage, containers, ships, planes,
and even by air currents.
2. 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 must be treated at once, the uninfected 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.

3. Eradication – eradicative measure are intended to eliminate, inhibit or

kill the pathogens that have become established within the plant or in an area.
• Eradication by disinfection 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.
Benomyl, thiabendazole, carboxin, and the oxathins are systemic
fungicides. Streptomycin, penicillin and some other antibiotics
against bacteria are systemic.

• Disinfection by hot water treatment is an eradicative measure against

established infections in fruits, bulbs and seeds. It has been found
effective in controlling mango anthracnose caused by Colletotrichum
gloeosporioides and loose smut of cereals there the mycelium inside the
seed could not be reached by superficial chemicals.
• Heat treatment has been therapeutic against diseases caused by viruses,
viroids, mycoplamas and rickettsia present in dormant planting materials
and growing plants. Hot water (35 -53 C) is usually used for dormant
plant parts and hot air (35 – 40 C) for growing plants. The temperature
use for heat treatment is critical because it should be high enough to kill
the pathogen but low enough not to injure the host.
• Soil maybe disinfested by chemical treatment or by heat to kill pathogens.
Soil fumigation will eliminate nematodes and other organisms. Soil
treatment is aimed at controlling soil-borne pathogens that cause damping-
off, root and crown diseases, seedling blights, etc.
• The use of irradiation to control posthatvest infections has been tried.
Gamma rays were found effective in killing pathogens found on tomato,
strawberry and mango fruits. However, the effective dosage for control
was usually injurious to the host tissues causing off-flavors, changes in
textures and other undesirable characteristics.
• 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 plats is economically feasible. Diseased plant parts may also be
removed.
• The eradication of alternate hosts, wild hosts, and weeds that may harbor
the pathogens will do a lot towards eradicating the pathogen.
• Crop rotation is quite effective in reducing the inoculums level although it
may not totally eradicate the pathogens. The success of a crop rotation
program depends on the length of time the host is not available, how long
 the pathogen could remain dormant in the soil, and the absence of
alternative hosts. Crop rotation is normally effective against soil-borne
pathogens. Eradication of infested plant debris where pathogens tide over
adverse conditions or remain in the absence of the host, may successfully
eliminate the pathogen.

4. 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. Resistance may range from very low level to a very high level.
 Susceptibility is the opposite of resistance; the more resistant a plant is, the
less opposite it is.
 Tolerance is the ability of a suscept to undergo severe infection without a
serious reduction in yield.
 Klendusity is the lack of infection in a susceptible variety due to the
suscept’s effect on something other than the pathogen such as on the vector.
The suscept may remain healthy because the insect vector of the virus does
not feed on the plant that is susceptible to the virus.
 Escape occurs when a susceptible plant does not become infected due to
certain circumstance such as unfavorable environmental conditions, lack of
inoculums and the like.
 Virulence is the measure of the degree of pathogenicity.
 Aggressiveness is a measure of the rate at which virulence is expressed.

Induced resistance (systemic or local) has been exhibited by various

plants. Certain microorganisms and chemicals were shown to induce
resistance.
Two recognized types of resistance:
 vertical resistance (also called major gene resistance,
oligogenic resistance, specific resistance)
 horizontal resistance (minor gene resistance, polygenic
resistance, non-specific resistance, generalized resistance,
field resistance).
 Vertical resistance is controlled by one to a few genes and is
effective only against one or a few specific races of the pathogen.
It is therefore easily overcome by other races of the pathogen or
new races that may develop and build-up. When this happens host
resistance is said to “break down”.

 Horizontal resistance is believed to be controlled by several genes

and is theoretically effective against all races or strains of the
pathogen. Unlike vertical resistance, horizontal resistance is
difficult to breed into a cultivar because of the number of genes
involved. This resistance should be more lasting because it would
 be difficult for a pathogen to come up with a new strain or race
with the necessary virulence genes against the various resistance
genes in the suscept.
The use of resistant variety is often the most effective and most
economical method of plant disease control.

Methods of Plant Disease Control:

1. Sanitation
a) Destroying plant refuse or debris (which harbor the pathogens) by burning or
burying them
b) Cleaning and disinfecting implements used for pruning or trimming
c) Cleaning, disinfesting, fumigating warehouse before and during storage of
produce
2. Cultural Methods
a) Eradication of diseased plants (or rouging) in greenhouses, nurseries, or in the
field to reduce or eliminate inoculums sources
b) Crop rotation or planting non-hosts of the pathogen for a number of years
c) Practices that improve the growing conditions of plants such as proper
drainage, tillage, fertilization, irrigation.
d) 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
e) 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 spp.
3. Physical Methods
a) Heat treatment of plants, plant parts, soil, containers, etc. using hot water, moist
heat, dry air or the sun.
b) Low temperature storage
c) Controlled atmosphere storage
d) Irradiation
4. Chemical Methods
a) Seed treatment with chemicals
b) Fumigation of soil, warehouses
c) Chemical control of insect vectors of pathogens
d) Use of chemical protectants and chemotherapeutants which include copper
compounds, inorganic and organic sulfur compounds, benzene compounds,
quinones, heterocyclic compounds, the systemic biocides, antibiotics, growth
regulators, and other organic fungicides.
5. Biological Methods – employ the use of microorganisms that compete with,
parasitize, or are antagonistic to the pathogen
a) 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
which causes more severe symptoms.
 b.) Interference – Roots 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 interference. 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.

c.) Use of Bacteriophages – Lab experiments have indicated control of bacterial

pathogens by mixing bacterial inoculums with the phage. Its widespread use as
control measure has, however, not been successful.

d.) Use of parasites or other antagonists of the pathogen – several

mycoparasites has been observed on many pathogenic fungi. Fusarium root rot of
corn can be controlled by treating the seeds or dipping in solutions
containing the antagonistic microorganisms. Soil amendments that favor the
growth of antagonist may be added to the soil, thus reducing the numbers of
the pathogenic population. Hyperparasitic fungi that attacks fungal pathogen
such as rusts, downy mildews, root rotting fungi, etc., have been reported, but so
far have found no widespread application. Nematodes are parasitized by bacteria,
fungi, viruses, protozoa, and other soil organisms. Their use to control the
nematode populations is promising but field application has not been too
successful.

6.) Use of resistant varieties

i. 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.
ii. 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 inoculums 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.

iii. Multiline Varieties – is a mixture of several lines with similar

agronomic characteristics but each with a different gene resistance.
A pathogen race would tend to invade only one or two of the
varieties in the multiline.
 THE CONTROL DECISION

The decision whether or not to control a certain disease, when to control, and
what to control to apply depends on the characteristics of the causal agent, disease
severity or crop loss estimate, use and value of the crop, and cost of control.
A cost/benefit analysis is prepared on the assessed crop loss, crop value and use,
and on the cost osf applying certain control measure(s). The cost of the control should be
much less than the value of the expected harvest.
Usually a threshold level of disease or of pathogen population is determined,
beyond which it is no longer economically feasible to control the malady. Very few
growers practice a control program with a sound basis. The threshold level has not been
established for the majority of diseases.

SELF CHECK

Select the best answer:

1. population of life forms that are identical in all inheritable traits

a) Pathovar
b) Biotype
c) Cultivar
d) Forma specials
2. On the principles of plant disease control, there are intended to eliminate, inhibit
or kill the pathogens that have become established within the plant or in an area.
a) Eradication
b) Exclusion
c) Protection
d) Immunization

3. In the disease cycle, it is the growth or movement of the pathogen through the
host tissues?
a) Inoculation
b) Penetration
c) Colonization
d) Dissemination
4. ______ is the deposition of inoculum onto or in the infection court, can be carried
out in several ways
a) Inoculation
b) Isolation
c) Protection
d) Association
5. Which of the following is not a source of inoculums?
a) Infected living plant
b) Sterilized utensil
c) Infested soil
 d) Plant debris
6. Are obligate parasites that are ultramicroscopic, composed of a nucleic acid core
at surrounded by a protein coat?
a. Bacteria
b. Virus
c. Nematode
d. Fungi
7. Technical term to refer to a round shaped bacteria.
a. Cocci
b. Bacilli
c. Spirilla
d. Circli
8. Are thread-like unsegmented worms which are usually elongated and cylindrical
in shape.
a) Nematode
b) Virus
c) Worm
d) Bacteria
9. Which among the choices below does not belong to the common symptom a
bacteria can cause?
a. Blight
b. Soft rot
c. Die-back
d. Wilting
10. Below are physical properties of viruses except:
a. Thermal inactivation point
b. Dilution End point
c. Longevity of Viruses in Vitro
d. Dilution inactivation in vitro