Name: CECIRLY G.

PUIG

Course: PPTH 201

Lecture Report No. 6

EFFECTS OF DISEASE ON REPRODUCTION
I. Introduction
Pathogens that attack various organs and tissues of plants weaken and often kill these organs or
tissues, thereby weakening the plants.
A. Indirect Effect of Disease on Plant Reproduction:
1. Plants remain smaller in size, may produce fewer flowers, and may set fewer fruit and seeds;
2. The seeds may be of inferior vigor and vitality and, therefore, if planted, they may produce fewer and
weaker new plants.
B. Direct Effect of Disease on Plant Reproduction:
1. They attack and kill the flowers, fruit, or seed directly;
2. They interfere and inhibit their production, or the pathogens interfere directly or indirectly with the
propagation of their host plant.
C. Common Ways by Which Diseases Affect Plant Reproduction:
1. Infecting and killing the flowers of the host

Example 1: Brown rot of stone fruits caused by the fungus Monilinia sp. (Fig. 1)

Close-up of a flower (left photo) and macroscopic view of an apricot tree (right photo),
the flowers of which have been killed bythe brown rot fungus Monilinia fructicola.


Example 2. Bacterial canker and gummosis of stone fruit trees caused by Pseudomonas syringae.

Example 3. Fireblight disease of pears and apples caused by the bacterium Erwinia amylovora --the bacterium enter the host through the nectar cells of flowers and cause blossom blight
which reduces the yield of fruits. From the flower, the pathogen continues to colonize the
pedicel, the twig and the branches.

2. Premature dropping of fruits

Example 1: Post-bloom fruit drop of citrus --- the fruit, soon after set, drops prematurely as a
result of infection by the anthracnose fungus Colletotrichum acutatum.

Example 2. Plums drop prematurely from trees infected with the plum pox virus.
3. Killing the embryo

The pathogen interferes directly with the reproduction of the plant host by killing the embryo,
that would have produced the seed, and replacing the contents of the seed with its own fruiting
structure or its own spores.

Example 1: Ergot of grains (Fig. 2), caused by the fungus Claviceps purpurea;

A mixture of barley kernels (whitish-yellow) and ergot sclerotia (the larger black bodies) produced
by the ergot fungus Claviceps purpurea on the heads of grain crops in place of healthy kernels.


Example 2: Corn smut and the covered and loose smuts (Fig. 3) of the various cereals caused by
Tilletia and Ustilago sp.

Ear of corn having some of the corn kernels replaced by galls containing spores of the fungus Ustilago maydis (left photo).
A mixture of intact healthy wheat kernels and somewhat darker, broken wheat kernels filled with spores of the
common bunt (covered smut) fungus Tilletia sp. (right photo).

4. No flower production or sterile flowers

In some diseases caused by viruses, phytoplasmas, or phloem-limited bacteria, no flowers are
produced or those produced are sterile, and therefore few or no fruit and seed are produced.

Example 1: The phytoplasma that causes aster yellows causes phyllody --- the flower is
transformed into a green leafy structure.

Extremely leafy growth from flower of black-eyed Susan (Rudbeckia) caused by aster yellow (left photo); The normally beautiful flowers of this
sneezeweed (Helenium 'Helbro' MARDI GRAS) are discolored and distorted by aster yellows; note, the green leafy growth within
the flower petals (center photo); Leafy growth from flower of black-eyed Susan (Rudbeckia) caused by aster yellows (right).


Example 2: Smut fungi that colonize the floral parts, such as the anther smut pathogen, Ustilago
violacea --- replace the pollen with smut spores, teliospores.

Various pathogens remain dormant in the seed coat and as the seed germinates, invade the
young seedling. Such pathogen as Helminthosporium spp. and Fusarium spp. cause seedling blight,
damping-off and root rot.

II. Pathogens Associated to the Seed

As an introduction we will review some aspects of the morphology and anatomy of the seed, in
order to understand in a better way the effect pathogens have in the seed and later, the plant originated
from it.

A. The Seed: Brief Review on Morphology and Anatomy

1) Embryo
The embryo has a reproductive function, being capable of initiating cellular divisions and
growth. It is the most important part of the seed. It is an axis that originates growth in two directions,
with the objective of originating a root and a shoot. Usually, the embryo is very small, compared to
other parts of the seed. It is like a miniature plant. It is consists of a radicle, plumule, one or two
cotyledons, and hypocotyl or epicotyl, depending on the type of plant.
2) Storage tissues
Energy storage is localized in the cotyledons, in the endosperm or the perisperm. Cotyledons
originate from the zygote and are part of the embryo. In many species, storage substances are localized
in the cotyledons, and the embryo develops absorbing all the endosperm.

3) Seed coat
Episperm is the seed cover, consists of two layers, the testa and the endopleura. The outer layer
is the testa; it can be stony, leathery, membranous or fleshy. Over the testa we can recognize: the hilum,
scar or point of attachment of the seed to the funiculus, water penetrates easily through it; Micropyle,
the point upon the seed at which was the orifice of the ovule through which the pollen tube enters;
raphe, suture originated by the part of the funiculus that is fused along the side of the ovule. The
endopleura is the inner layer, it is thin and generally whitish. Teguments, testa or protective covers
delimit the seed. They are formed by one or more layers of cells originated from the ovule integuments
and sometimes from the pericarp made from the walls of the ovary (Quer et al.,1982; Hartman et
al.,1971 ).
B. Processes associated to seed-borne diseases:
a. Infection of the seed
b. Infection of the plant
c. Steps that can be taken to reduce damage caused by this relationship
Seed Pathology

The science that studies the relationship between pathogens and seeds;

Identifies the pathogen;

Studies the role of the seed as source of inoculum, the survival of the pathogen and the actions
taken to control the pathogens associated to it.

Uses the knowledge of General Plant Pathology, Microbiology and Seed Analysis
C. Classes of seed-borne microorganisms:
1. Pathogens for which the seed is the main source of inoculum

when seed infection is controlled, the disease is controlled;

Example: Lettuce Mosaic Virus - For these pathogens, the importance of seed-borne
inoculum has long been recognized, and control practices have been developed.
2. Pathogens in which the seed borne phase of the disease is of minor significance as a source of
inoculum

Examples are those in which the crop residues in the field were the major source of
inoculum.
3. Pathogens that have never been shown to cause disease as a result of their presence on seeds
4. Pathogens that can infect the seed either in the field or in storage and reduce yield and seed quality

Examples of field fungi are Diplodia, Fusarium, Cladosporium, etc. The storage fungi
Aspergillus and Penicillium can invade most types of seeds under high-moisture storage
conditions (McGee, 1981).
The process of seed infection is influenced by the conditions under which the crop grows.

the host and its genotype

the pathogen

the environmental factors

III. Processes of Seed Infection

A. Systemic Infection of the Seed
The establishment of a pathogen in any part of the seed is refereed as seed infection. It can be
Systemic, by the vascular system or plasmodesmata or directly by natural or artificial wounds. The same
pathogen can infect the seed using one or more of these mechanisms.

Example: Xanthomonas campestris pv. phaseoli can infect seed through the vascular system, by
natural openings (from the pod suture goes to the funiculus, then to the raphe and tegument, or
it can also happen through the micropyle).
1. Systemic infection through flowers, fruits or funiculus

Most of the systemic seed-borne bacteria and fungus reach and infect the embryo through the
flower or from the peduncule of the fruit, via funiculus.

Viruses go to the embryo from the systemically infected mother plant and the infected or
contaminated pollen. They rarely reach the embryo during the formation of the seed or the
embryo itself.

Examples of some infections that occur through the vascular system are: some forma speciales
of Fusarium oxysporum in pumpkin, pea and tomato; Plasmopara halstedii in sunflower;
Septoria glycines in soy; Verticilium dahliae in spinach and sugar beet; certain pathovars of
Xanthomonas campestris in bean, cabbage, rice and sweet pepper; and Pseudomonas syringae
pv. lachymans in cucumber.
2. Penetration through the stigma

During the infection, some pathogens follow the same path as the pollen grains do.

Spores of some fungus reach the stigma and germinate, producing a hypha that reaches the
ovary through the style, where they can stay as a dormant mycelium until seed germination.

Example: Ustilago nuda and U. tritici in barley and wheat, and Alternaria alternata in sweet
pepper.

Viruses can infect through infected pollen, the male gamete carries the virus, when joining
the ovule it generates an infected embryo. If both, the male and female gamete are infected
they can even produce an infected endosperm.
3. Penetration through the wall of the ovary or immature seed covers

Some fungi, like Ustilago nuda and U. tritici penetrate through the wall of the ovary as a
result of the germination of the Teliospores on the stigma or the wall of the ovary.

The pro-mycelium goes through the wall and other tissues until it reaches the embryo.

In some other cases, penetration occurs through breakages on the testa, establishing itself
in the endopleura or the endosperm.

In fleshy fruits, like cucumber, melon, eggplant, tomato, sweet pepper and others,
contamination can occur directly through the funiculus or in the tegument, during the
process of seed formation.

Examples: Colletotrichum lagenarium in watermelon and Rhizoctonia solani, when it invades
fleshy fruits, like the ones mentioned above, it is capable of infecting from the placenta and
penetrate to the developing ovule or seeds that are still in its formation process and have
not lignified its cover.

4. Penetration through wounds and natural openings

Natural openings like the hilum and the micropyle or wounds generated during the thresh
are spots where pathogens like Xanthomonas campestris pv. phaseolina in bean and
Pseudomonas syringae pv. lachrymans in cucumber.
B. Seed Contamination or Infestation
Contamination or infestation refers to the passive relationship of a pathogens and seeds. The
pathogen itself or parts of it can stick or can get mixed with the seeds during any of the processes during
seed recollection: harvesting, extraction, thresh, selection and packing.
1. Pathogens that stick to the surface of the seed

Pathogens that stick to seeds during harvest or postharvest do so by their spores
(Clamydospores, Oospores, Teliospores, Uredospores), bacterial cells and in some cases,
virions.

Spores of the following fungi can be carried on seed coat surfaces: Alternaria brassicae and
A. brassicicola in crucifers; A. longipes in tobacco; A. radicina in carrot; Ascochyta pinodella
in pea; Drechslera sorokiniana and D. oryzae in rice; D. avenae in oats; Fusarium oxysporum
f. sp. callistephi in China aster; Sclerotia of Rhizoctonia solani in eggplant, pepper, and
tomato; Tilletia caries, T. foetida, T. contraversa, and Urocystis agropyri in wheat.

A number of bacteria, such as the following, contaminate seed surfaces: Corynebacterium
flaccumfacjens pv. flaccumfacjens in bean, Pseudomonas syringae pv. phaseolicola in bean,
P. syringae pv. lachrymans in cucumber, P. syringae pv. tomato in tomato, C. rnichiganense
pv. michiganense in pepper, Xanthomonas campestris pv. campestris in cabbage.

Also some viruses as Tobacco mosaic virus, Tomato mosaic virus, Pepper Mosaic virus.
2. Accompanying contamination
This type of contamination refers to physical mixing of the seed with pathogen's propagation
organs like the sclerotia, nematode galls, contaminated plant parts or soil particles containing
pathogens.
a. Structures of the pathogens

Some fungi produce resistance structures named sclerotia, that are made of compacted
mycelium.

Under certain conditions of temperature and humidity it can germinate, it is common that
this occurs together with the seed, producing its infection, by direct penetration or by the
spores generated by the fructification organs (Apothecium or Perithecium).

These spores are carried by the wind and taken to susceptible tissues of the plant, generally,
some parts of the flower.

Sclerotia have many shapes and during thresh can be easily included with the rest of the
seed.

Examples of this are Sclerotinia sclerotiorum in horticultural, grain and flower crops,
Sclerotinia cepivorum in garlic.
b. Mix with infected plant parts

Infected plant parts and residues can carry fructifications or spores of fungi and bacteria.
This situation is particularly common in cereal, forage and oily crop's seeds.

Examples of this are Septoria nodorum in wheat, Puccinia malvacearum in hollyhock
(malvarrosa), Colletotrichum trifolii in clover, Erwinia carotovora pv. carotovora in tobacco,

Pseudomonas syringae pv. phaseolicola in bean and Sclerotinia sclerotiorum in sunflower,

soy and peanut.
c. Soil

Seeds can be mixed with contaminated soil and, for example, carry micro-sclerotiums of
Macrophomina phaseolina in dirty seeds of kidney bean, Verticillium oxysporum f.sp.
phaseoli in cotton seeds, Plasmodiophora brassicae in turnip and Fusarium oxysporum f. sp.
phaseoli in bean.

IV. Seed Transmission

We call seed-borne pathogens only those that can produce an infection.

Because they have to be distinguished from those that can associate to the seed but do not
produce an infection, these ones are called pathogens not transmitted by seed.

Example, the virus that causes curly top in sugar beet can be present in the perisperm but
does not cause an infection in the plant.

In general terms, infection can be classified into systemic and non systemic.

It is systemic when the pathogen introduces itself to the plant when the seed germinates,
and develops with it.

Non systemic infection occurs when there is a localized infection caused by the pathogen in
the seedling at the stage of pre or post emergence, in this situation there are no systemic
symptoms (Agrawal and Sinclair, 1987).
A. Systemic transmission

This type of infection can be produced by pathogens that are carried with the seed in
various parts, like the embryo, endosperm or episperm, or by contamination of the outer
portion of this one.
1. Infection of the embryo

When the seed germinates, if the embryo is infected, the pathogen initiates its growth
together with the plant.

Symptoms can show up during different stages of development. In the case of Ustilago
tritici, the mycelium grows together with the plant and expresses symptoms only at the
flowering stage, which are that all the tissues of the spike, except the rachis, are replaced by
spores.

Some pathovars of Xanthomonas campestris that infect cabbage, bean or sweet pepper
move between the cells of the host until they reach the vascular system and produce
symptoms in leaves or stems.

Most of seed-borne viruses persist inside the embryo. Its multiplication and movement
accompanies the plant during its development, and there can be symptoms at any stage,
from the formation of first leaves until flowering or fructification.

2. Non-embryo infection

Infection of the episperm (testa and endopleura) occasionally conducts to a systemic
infection.

Some bacteria, like Corynebacterium michiganense pv. michiganense in tomato and
Xanthomonas campestris pv. campestris in cabbage, penetrate through stomata of
cotyledons, and from there, reach the vascular system, initiating the systemic infection.
3. Episperm contamination

In some few cases this type of contamination conducts to a systemic infection.

Most of these exceptions are fungi that are highly specialized in their pathogenesis and
produce in cereals the so called smuts, rusts or mildews.

In these cases, generally, spores are carried outside the seed, they germinate, penetrate the
coleoptile, and start a systemic infection.

This can occur directly by a more complex system of haploid hypha fusion in genera like
Tilletia, Ustilago, Uromyces, Sclerospora, Pernospora and Puccinia.
B. Non-systemic transmission

Non systemic infection is very common, and in the same way as systemic infection, it can
come from an infection, outside contamination or by pathogens mixed with the seeds.
1. Infection of the embryo

This case is restricted to some pathogenic fungi that maintain itself in the embryo or the
episperm as hypha inside the seed.

Primary infection starts as injuries in the cotyledons or primary leaves, stems or petiole.
Fungi fructifications (Pycnidium, Acervulus) can develop on these organs, under certain
favorable conditions (temperature and humidity).

These fructifications produce spores that, with the action of water and wind, disperse the
disease to other parts of the plant and other plants.

This occurs in Ascochyta pisi in pea, Colletotrichum lindemuthianum in bean and C.
truncatum in soyabean.
2. Infection of the episperm

Generally, seeds in which the episperm is infected, do not geminate, or germinate and
contaminate the soil.

Rarely produce a systemic infection, but can infect the seedling from the outside.

Over the injuries, new inoculum is produced; this one infects other parts of the plant or
other plants.

Example, Septoria nodorum in wheat under high humidity conditions forms Picnidium in the
coleoptile, whose spores disseminate the disease to other plants.
3. Contamination of the episperm

Contamination outside the seed's testa can produce healthy seedlings, but the inoculum
infects the soil and from there it can cause infections at more developed stages of the plant.

Wheat and rice grains that are contaminated with Teliospores of Neovossia indica in wheat
and N. torrida in rice, produce ESPORIDISPORAS in the soil, that can be carried by the wind
and infect flowers, originating the smuts.

4. Accompanying contamination

The mixture of seeds with sclerotia of the fungi or contaminated soil particles produces
none Systemic infections, at any stage of the plant growth and development.

It is common for Sclerotinia sclerotiorum to produce mycelium from the sclerotia.

This mycelium can directly infect the seeds, plant or produce fructifications that produce
spores that can be carried by the wind and infect flowers of different species, like sunflower,
soy, peanut, etc.

V. Disease Cycle and Infection Course

A. Intraembryal infection followed by systemic infection

Embryo infection generally results in systemic infection.

The pathogen become active as the germination process begins.

Such pathogens follow the growing point of the plant and can express symptoms at different
stages of plant growth.

The mycelium of the smut fungus is present in all parts of the infected seed.

Including all parts of embryo (mostly as dormant mycelium in (scutellum) except the radicle.

As the seed germinates the hyphae grow intercellularly behind the growing point, upwards
through the stem into the leaves and primordial of the cars, as well as downwards in the
root system.

No symptoms produced on plant which can be apparent to human eye until the smutted
heads extrude earlier than the healthy heads and continue to appear throughout the
flowering period of the crop.

The teliospore are blown by wind to flowers where they germinate, conjugate and the
infective hyphae penetrates the young ovary wall, eventually themselves as dormant
mycelium in the embryo.

Mycelium invades all young spikelets where it becomes intracellular and replaces most
tissue of the spike except the rachis.

Mycelium in the infected seed is transformed into teliospores which are held together by
the delicate membrane of host tissue.

On maturity the membrane ruptures and the teliospores are released and carried to healthy
plants by air currents.

These teliospores fall on the flower of healthy plants and germinate through the formation
of basidium consisting of one to four cells (haploid hyphae).

The cells germinate and produce short uninucleate hyphae and sexually compatible haploid
hyphae fuses and then produce dikaryotic mycelium.

This dikaryotic mycelium penetrates the flower through the stigma or young ovary walls and
becomes established within the scutellum when seed mature; it then remains dormant until
seed germination.

Examples are: Ustilago tritici in wheat, Ustilago hordai in barley, Xanthomonas phaseoli in
mungbean, Colletotricum dematium in chilli, Bean common mosaic virus in beans.

Fig. 4. Life cycle of loose smut.

The loose smut fungus survives as a dormant fungal thread inside the embryo of wheat
seed.

The pathogen is activated when the infected seed germinates, and it extends toward the
growing point of the plant.

Evident from flowering onwards when the plant begins to form the head, the fungus invades
all of the young head tissue except for that of the rachis (backbone).

Production of plant growth hormones by the fungus results in infected plant heads reaching
flowering earlier than healthy heads.

The head produced by the infected plant contains black spore masses in place of the grain.

The spores are loosely held and are easily spread by wind onto neighboring healthy plants.

Because flowering of infected heads occurs earlier than healthy heads, production and
release of spores occurs when the rest of the crop is flowering.

Spores are blown by the wind into the flowers of the healthy plants.

The spores enter the ovaries and become part of the developing grain.

In this way, seed for the following year becomes infected.
B. Intraembryal infection followed by local infection

Embryo of the seed is infected by the pathogen which will produce conidia.

The conidia are spread from primary infection to leaves, petioles and stems.

They will germinate and the hyphae will penetrate the host and produce local lesions.

Examples: Aschocyta pisi, Colletotricum lindemuthianum in beans, Aschochyta rabiei in
chick pea.

Mycelium of the fungi is located on the seed coat and the cotyledons.

The fungus first appears on unfolding leaves and in stem near the point of attachment,
infection taking place as the seed germinates.

Lesions on the stems are slightly elongated.

Fungus is confined to epidermis and cortex.


Pycnidiospores ooze in the form of tendrils.

Spores are discharged and disseminated by free water in the form of rain, dew, wetting fog
etc.

Infection goes from one leaf to the other in a jumping way, involving ultimately all plant.

Pods evelope the same lesions as leaves and stems, even pycnidia are found on them.

Mycelium passes through pod wall and in the pod cavity, attacks the seed coat first and then
the cotyledons.

Seed infection can also be established in symptomless mother plant under unfavourable
condition.

In a seed certification scheme collection of seeds from healthy fields may not necessarily
mean that they are all disease free or better infection free.

Two out of 500 seeds have been found infected in such healthy plants.

Other examples include Colletotricum dematium in soyabean.

Fig. 5. Ascochyta blight symptoms develop underneath the plant canopy

Where it is humid.

Fig.6.Pea seed produced in ascochyta-infected pod.

The seed appears healthy but is small.

Fig. 7. Pea seedlings emerged from infected seed; from healthy (left)
to severe infection (right).


Ascochyta blight develops rapidly in cool (59 to 770 F) wet conditions.

High humidity and periods of morning dew also favor disease development and spread.

Hot, dry conditions can halt the development of disease, but spread can continue once
conditions become favorable again.

Ascochyta rabiei can overwinter in field stubble for several years, and the pathogen is also
seed-borne. In spring, sexual spores (ascospores) are produced on field stubble or seed and
dispersed by wind.

Ascospore dispersal can continue for several weeks and usually occurs before or at
flowering.

Spores can travel up to five miles, which allows disease to spread to new areas rapidly.

Ascospores that land on chickpea leaves and stems need at least two hours of surface
moisture (dew) to germinate, but the likelihood of infection increases if leaves and stems
are wet for more than six hours.

After infection, symptoms of disease may not appear for several days.

Once pycnidia are formed in lesions, they can produce asexual spores (conidia).

Conidia are dispersed by rain or other moisture on to surrounding plants, where they cause
new infections.

Repeated infection cycles can occur if conditions are favorable, allowing the disease to
spread quickly through a field.

Fig. 5. Generalised life cycle of ascochyta blight disease (Ascochyta fabae,Ascochyta rabiei and Ascochyta lentis) in pulse crops. A. The disease
causing fungus survives over summer in crop stubble and infected seed in a semi-dormant state. B. Ascospores produced by
pseudothecia on stubble are blown by wind and rain to infect the growing crop. C.Pycnidia form in lesions on leaves
and stems. D. As the crop grows,conidiospores from pycnidia spread the disease in the canopy by rain splash.
E. Disease infested stubble remains after harvest. Infected seed
is harvested with healthy seed.

C. Extraembryal infection in seed followed by systemic infection

The seed is infected outside the embryo i.e. endosperm, seed coat, pericarp.

The pathogen will grow into young plants during the germination of seeds and penetrates
further up during the growth of the plants.

Examples: Botrytis anthophila in red clover, Drechslera graminea in barley, cucumber
mosaic virus in cucumber.

Blossom blight of red clover or grey mould of red clover or anther mould mycelium of the
fungus located in seed coat.

No symptoms are seen on the plants. It is an organ specific disease where anthers are
replaced by conidia of Botrytis anthophila, i.e. male part is replaced by fungal fruiting
bodies.

About 40-70% of the pollen is found to be contaminated.

Dispersal of fungus is carried out by wind or bees. Infection of the seed coat from mother
plant takes place through funiculus and hilum and not through stigma and style.

In case of oat when infected by Ustilago avenae, the mycelium may persist in dormant stage
on the pericarp, or the seed may be passively contaminated by teliospores which are carried
beneath the lemma and palea.

The first case is parallel to earlier example, the infection following the same pattern.

The parasites invades the young seedling, the host is systemically penetrated by the
mycelium, mainly intercellularly in the coleoptiles and first internodes and generally
intercellularly in the first leaf and deeper tissues.

Mycelium grows along with the host height and finally enters the seed primordial where
teliospores are formed.

In its main feature this life cycle parallels the one of Botrytis anthophila in red clover with
the difference that in red clover the male reproductive organs are changed into the spores
masses.

Name: CECIRLY G. PUIG

Lecture-Report Topic Outline
Title: Effects of Disease on Reproduction
I. Introduction
A. Indirect Effect of Disease on Plant Reproduction
B. Direct Effect of Disease on Plant Reproduction
C. Common Ways that Diseases Affect Plant Reproduction
1. Infecting and killing the flowers
2. Premature dropping of fruits
3. Killing the embryo
4. No flower production or sterile flower production
II. Pathogens Associated to the Seed
A. The seed: brief review on morphology and anatomy
B. Process associated to seed-borne diseases
C. Classes of seed-borne diseases
III. Processes of Seed Infection
A. Systemic Infection of the Seed
a. Systemic infection through flowers, fruits or funiculus
b. Penetration through the stigma
c. Penetration through the wall of the ovary or immature seed covers
d. Penetration through wounds and natural openings
B. Seed Contamination or Infestation
a. Pathogens that stick to the surface of the seed
b. Accompanying contamination
IV. Seed Transmission
A. Systemic Transmission
a. Infection of the embryo
b. Non-embryo infection
c. Episperm contamination
B. Non-systemic Transmission
a. Infection of the embryo
b. Infection of the episperm
c. Contamination of the episperm
d. Accompanying contamination
V. Disease Cycle and Infection Course
A. Intraembryal Infection Followed by Systemic Infection
B. Intraembryal Infection Followed by Local Infection
C. Extraembryal Infection in Seed Followed by Systemic Infection

Course: PPTH 201