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Chapter X
EFFECT OF INFECTION ON PHYSIOLOGY OF THE HOST.
In preceding chapters a brief account of the process of infection, its establishment, and the
potential activities of the pathogen was given. After establishment of infection, when the
infections causal agent of a disease starts parasitic or pathogenic action, host tissues show
different types of responses to these activities. In the initial stages of penetration there
may be a striking increase in protoplasmic strands and the nucleus of the cell may move
to the site of penetration. Cytoplasmic particles, in rapid Brownian movement, appear
fallowed by granulation of the cytoplasm and appearance of many more particles in
Brownian movement.Later the cellcontents become yellow and finaly dark brown when
Brownian movement ceases and the cell is dead.
Normal physiological activities of the host cells are disturbed and anatomical and
morphological changes (morbid anatomy ) Appear as visible changes. In pathogenesis the
first stage after infection is the manifestation of these responses of the host cells which
appear in the following forms:
1.- Structural changes: In diseased plants usually adnormal structures are seen. Examples
are overgrowth (Hyoertrophy), sterile flowers, phyllody, hairy roots, witch´s broom,
bunchy top, crown gall, root knots, etc.. These abnormalities are discussed in the present
and the following chapters. However, the apperance of abnormal structures on the sick
plants is not due to physical but to chemical reactions occurring within the plant body
and are therefore, expression of physiological malfunctioning of the host cells.
2.- Physiological changes: Harmful effects of infection on host physiology are yhe main
causes of symptom expression and loss.
In this chapter, brief account of following harmful effects is given.
- Desintegration of tissues by the action of enzymes of the pathogen.
- Effect of pathogenesis on growth of the host plant due to growth regulators produced
by the pathogen or by the host under the influence of the pathogen.
- Effect on reproductionof the host.
- Effect on uptake and translocation of nutrients and water.
- Abnormal respiration of the host tissues due to disturbed enzyme system associated
with respiration.
- Reduction in photosynthesis due to destruction of leaves or loss of chlorophyll.
- The role of toxins in disturbing the phisiology of the host has been discussed in the
following chapter.
Tissue desintegration
Among diverse symptoms of plant diseases the most common are those caused by
didintegration of tissues. There are very few diseases that do not show tissue disintegration
and death of cells at some stage after infection by the pathogen. These symptoms are so
prominent that they had attracted the attentoin of man in ancient times. Usually the word
“rot” is used for such symptoms. The word is derived from “ret” connected with “retting”,
the process of soaking fibre-bearing tissues in water and macerating the tissues by
biological action to separate the fibre. Thus, in tissue disintregration the cells and tissues of
the host plant are separated from each other resulting in condition known as rot. This
condition is present even in many necrotic spots. The material binding the cells to form
tissues is destroyed by the pathogen to enable it reach the host protoplasm. Such pathogens
are mostly facultativa parasites or saprophytes. However, obligate parasites or pathogens
and even non-parasitic causes of disease can induce tissue disintegration through indirect
effects. As a result of tissue disintegration or rot the symptoms known as blight, canker,
anthracnose, etc. Appear on the plant.
Fungi, bacteria and nematodes bring about tissue disintegration through the action of
enzymes secreted by them. These enzymes are of different types for action on different
tissues and chemical constituents of the cell wall.
(i)
(ii)
(iii)
Cuticular enzymes: The epidermis of plant is covered by cuticle and propagules of
the pathogen first contact the host on this surface. The major chemical substance in
cuticle is a cutin framework with waxes embedded in it and extruded from its
surface to give a waterproof surface (the cuticular wax). The central region of the
cuticle consists of cutin, a polyester of hidroxylated monocarboxylic acids each
containing 16 to 18 carbon atoms and 2 to 3 hydroxyl groups. On hydrolysis the
polyesters yield fatty and hydroxy-fatty acids. The wax portin consists of complex
mixtures of long chain paraffins, alcohols, ketones, esters and acids. Paraffins and
esters predominate on the outer surface. Small quantities of other substances such
as proteins, carbohydrates, pigments and occluded pectin and cellulose may also by
present. The thickness of cuticle varies with plant species. The amount of wax also
similarly varies with plant type.
The role of fungal enzymes in degradation of complex chemical structure of
cuticle is not well understood . It is presumed that the cuticular enzymes
mainly help in penetration of infection thread by pressure. Various enzymes
suggested to be envolved in dissolution of cuticle are: (1) cutinase which
catalyses the breakdown of cutin, hydrolysing it into cutin acids ( fatty and
hydroxy- fatty acids), (2) those enzymes which help in the breakdown of fatty
acids, and (3) enzymes which degrade other cuticular substances such as
proteins, cellulose, pectin, pigments, etc. Germinating spores of Colletotrichum
gloesporioides are reported to degrade the cuticle of orange leaves (Chaudhuri,
1935). Similar reports exist for Sphaerotheca pannosa ( powdery mildew of rose),
Venturia inaequalis(bittler rot of apple), and Helminthosporium victoriae (Blight
of oats).
Pectic enzymes: After cuticle has been penetrated the pathogen comes in contact
with cell wall protecting the protoplasm. The main components of cell wall are
pectin or pectic substances, cellulose, hemicellulose, lignin and a small quantity
of protein. Fungi, bacteria and nematodes which feed on the protoplasm have to
degrade these substances to dissolve the middle lamella and cell walls so that
protoplasm may be reached.
Pectin or pectic substanses are major chemical components of middle lamella
which binds the cells together.The pathogens like fungi, bacteria and nematodes are
knowm to contain pecticor pectinolytic enzymes and use these enzymes against
this group of materials. Extensive literature exists on the significance of pectic
enzymes in plant diseases.
Pectic substances are polymers consisting primarily of - 1,4 linked galacturonic
acid units. The carboxyl group on carbón 6 may be unesterified an is
polygalacturonic acids which . if colloidal, are known as pectic acids which, if
colloidal, are known as pectic acids..The esterified carboxyl group of pectic acids
on esterification with methyl alcohol. Pectina are pectinic acids of hihg methoxy
content or more of the methylated carboxyl groups.
The degradation of pectyic substances is brought about by two groups of
pectinolytic enzymes: The pectinesterases and polygalacturonases. Pectinesterases
are widely distributed in plants and microorganisms. Those in fungi have a lower
optimun pH for their activity. The pectinesterases or pectinmethilesterases (PME)
catalyse hydrolysis of the methil ester groups of pectinic acids to methyl alcohol and
pectinic acids of reduced methoxy content. Eventually pectic acid is formed. This is
attacked by polygalacturonase group of enzymes which includes glycosidases
and lyases (eliminative mechanism) . These enzymes break the links between
adjacent galacturonic acid units. Polygalacturonase (PG) attacks pectic acid and
polymathilgalacturonase (PMG) attacks pectin.
The presence and amount of pectinolytic enzymes differ in different fungi and
is governed by many factors such as pH. The fact that the same fungi will produce
the same enzymes in the host also and the enzymes will play some role in
pathogenesis. Under certain conditions the pectinolytic enzymes are inactivated or
rendered ineffective. Phenolic compounds or their oxidation products common in
darkened tissues at sites of injury inavtivate pectic and other enzymes. Indole acetic
acid also inhibits certain pectic enzymes..
The degradation of pectic substances provides nutrients for many fungal
pathogens and due to weakening of the cell wall facilitates inter- and intracellular
invasión by hyphae. There is no evidence so far to show that pectic enzymes
affect the protoplasm of host cell. These enzymes are apparently of primary
importance in soft rot diseases such as those caused by Erwinia dissolvens, E.
Carotovora, E aroideae, Pseudomonas spp. Botrytis cinerea, Sclerotinia
sclerotiorum, Scleritium rolfsii, Rhizoctonia solani, species of Pythium ,
Phytophthora and Rhizopus. However, more specialised pathogens such as
Puccinia graminis tritici also produce pectic enzymes duryn spore germination.
This facilitates the movement of hyphae in between the cells. The activity of pectic
enzymes may be aggravated by synergostic action of other enzymes and
metabolites. In the invasion of Sclerotium rolfsii oxalic acid produced by the
pathogen plays a similar role.
( iii).Cellulolytic enzymes: Cellulose is the major component and bassic unit of
structural framework of plant cell wall . Comparatively little is known about the
significance of celullolytic enzymes and enzymated degradation of cellulose in plant
diseases. Howeber, since in most diseases where tissue desintegration is a common feature,
degradation of cellulose does occur to ennable the pathogen dissolve the cell wall.
Celllulolyted enzymes (celluloses) are fourd in fungi , bacteria, many nematodes and
phanerogamic plant parasites . Some workers believe that a single enzyme converts
cellulose into glucose by random cleavage of the molicule.. Others have suggested that
native cellulose is converted to the disaccharide cellobiose by one enzyme and thence to
glucose by a second one. Still others suggest that a series of steps are involved in the
conversion of cellulose into glucose. The native cellulose molecules are released or
loosened from the chains by the action of C1 enzymes. These loosened molecules then take
up water and are hydrolysed by Cx enzymes to soluble low molecular cellosaccharides and
finally to cellobiose and glucose. These are then attacked by -Glucosidases to form
glucose.
The degradation of pectic substances and cellulose not only helps the pathogens in
invasion of tissues and their desintegration, it causes other effects also.. The degraded
products are used by fungi as food. Large molecules released by degradation often cause
plugging of vessels thus partly contributing to development of synptoms of wilt in many
plants.
(iv).- Hemicelluloses: In addition to cellulose and pectin, the plant cell walls contain the
complex water –insoluble polysaccharides known as hemicelluloses which are attached
with cellulose and lignin. The Hemicellulose are important constituents of mature and
thickened cell walls. They contain complex mixtures of such pentosans as xylans ,
mannans, galactans and arabans. The process of degradation of hemicelluloses is not much
known. Many parasitic and saprophytic
microorganisms produce the enzymes
hemicelluloses for hydrolysis of these polysaccharides and produce simpler sugars. Certain
components of hemicelluloses are degraded by cellulolytic enzymes also. The degradation
of hemicelluloses exposes the cellulose and lignin of the cell wall for action of enzymes of
the fungi.
Reports implicating hemicelluloses in plant diseases are few . Xylanase and arabinase
has been found in hypocotyl of sunflower attacked by Sclerotinis sclerotiorum, Sclerotinia
fructigena produces arabinofuranosidase in cultures . Scleritium rolfsii produces,
exogalactonase endomannnse, galactosidase, and endoxylanase in culture.
(v).- Lycnolitic enzymes: The most complex chemical compound in plant cell walls is
lignin the mechanism of degradation of which is least known . Pectic materials and
cellulose are the major constituents of of herbaceous agricultural crops which contain lignin
mostly in walls of their xylem vessels and in fibrous tissues. Howeber, woody perennial
plants contain relatively much larger amounts of lignin . In woody cells lignin constitutes
almost all of the middle lamella and forms its own framework in the walls so that the latter
are strengthened and remain intact even after cellulose and hemicellulose are removed.
Deposition of lignin is usually followed by death of the cells and the fungi which attack
lignified tissues are usually perthotrophos.
Lignin is a three dimensional, branched polymer formed by the oxidative polymerisation
of three substituted cinnamaryl alcohols: -coumaryl alcohol, coniferyl alcohol and sinapyl
alcohol. The amount of these alcohols in lignin differs with plant species.
Most of the knowledge about degradation of lignin has been accumulated from studies
of the action of wood rotting fungi ( Basidiomycetes, chieffy white rot type) although the
foot rot of cereals in which fairly high amounts of lignin are present indicates that
lignolytic enzymes might be involved. It is believed that these fungi produce polyphenol
oxidases and through their action assimilate and metabolise lignin . Many wood rotting
fungi degrade lignin but cannot utilise it. Among other fungi reported to cause partial
degradation of lignin are Alternaria, Cephalosporium, Chaetomium, Xylaria, Pestalozzia,
Fusarium and Penicillium. Among phytopathogenic bacteria the species of Pseudomonas
and Xanthomonas can cause degradation of lignin.
(vi).- Ither enzymes involved in degradation of cell wall and cell contents: After
decomposing the cell walls the fungal hyphae come in contact with the host protoplasm.
They get the required food from this sourse. The protosplasm contains mainly proteins,
starch and lipids. In addition, phosphorus, potash, sulphur and iron are also present .
Nucleic acids and protein are constituents of the nucleus.
There is little information as to whether protein breakdown plays any part in the
degradation of cell walls. Mechanism of protein breakdown by plant pathogens is the same
as found in plants and animals . The enzymes peptidase attack and break down the
polypeptides into lower peptides and amino acids which are utilised by the pathogens,
Starch is hydrolysed by enzymes amylase to produce glucose used by the pathogens as
nutrients. Lipids are degraded by enzyme lipase.
The nucleic acids (ribonucleic acid or RNA and deoxyribonucleic acid or DNA) are
present in the cell and may be degraded by the action of plant pathogens.DNA is mainly
present in the nucleus and in very small quantities in the chloroplasts and mitochondria.
RNA is present throughout the cell. These acids contain linear chains of alternating
molecules of phosphate and a sugar (ribose in RNA and deoxyribose in DNA). Hydrolisis
of these acids by enzymes ribonuclease and deoxyribonuclease results in formation of
mononucleotides. Nonspecific phosphatases hydrolyse nucleotides . Further action by
deaminases separates de amino groups from the nucleosides and makes them available to
the parasite. From the above description it is obvious that tissue desintegration is a
function of enzymes secreted by the pathogenic organisms. The destruction of cell walls
leads probably to plasmolysis of protoplasts and death of the cell and utilisation of cell
contens by the parasite. These degrading processes result in rots, blights and cankers, etc.
The tissues thus broken are only those present at the site where the parasite is active.
Sometimes desintegration of tissues occurs at a distance from this site . It is due to
traslocated toxins produced by the pathogen. Necrosis caused by many obligate parasites
and pathogens including viruses is not due to enzymic acxtion of their own but due to
indirect effect. This may include hypersensitive reaction of the host, toxins, starvation of
the cells and nonavailability of materials required for synthesis of cell walls. In deficiency
diseases the necrosis representing tissue desintegration is due to shortage of elements
required for cell wall synthesis and inhibition of other cellular activities.
Effect on Growth of the Host
The growth of plants is controlled by naturally present growth regulators in the plant
body, In some diseases this control is disturbed and various structural abnormalities
appear on the host. The regulatory substances are of two types: growth promoting which
include specific hormones and growth inhibitory substances. Auxins, gibberellins and
cytokinins are the known growth promoting substances . In a broad sense, gibberellins
and cytoquinins are also auxins but in strict sense only indole acetic acid ( IAA) is
known as auxin. Dormin, ethylene, etc are growth inhibitors or induce such reactions in the
plant that lead to premature ripening of fruits and untimely formation of abscission layers
leading to fall of leaves, fruits and flowers. The growth inhibitors can inhibit the action of
growth promotors or the farmer can be rendered ineffective by the latter. This depends on
the condition of the plant and its response to infection by a pathogen. The pathogens (
fungi, bacteria, nematodes) also producegrowth regulators . When such substances are
produced during the period of infection the host cells are induced to show
growthresponses. These responses at wrong time produce adverse effect on normal growth
of the plant. Pathogens also produce substances as metabolites that are not hormones but
effect the regulatory mechanisms in the plant thereby causing unrestricted production of
growth regulators by the plant. Production of growth promoting substances in excess of
normal requirements of the plant causes overgrowth of cells and tissues. In addition to
their own effect the growth inhibitors produced by the pathogen can render the growth
promoting substeances of the plant ineffective or inhibit their production thus causing
growth retardation or stunting of organs or the entire plant. The imbalance in growth
promoting and growth inhibiting substances causes appearance of symptoms known as
hypertrophy and atrophy. Hypertrophy may appear as tumours, galls, knots, abnormal
increase in organss size ¨, witch¨s broom, etc.
Auxins:The naturally occurring auxin in the plants is indole acetic acid (IAA). Many
plants pathogens produce small quantities of IAA or induce the plant to produce more of
this substance . Although tryptophan is most important precursor of this auxin, it appears
that differentorganisms have envolved different pathways of IAA synthesis involving
precursors other than tryptophan. It is also possiblethat some auxin, other than IAA or
gibberelins, may be involved in pathogenesis. IAA regulates cell
growth and
differentiation. It also effects cell wall permeability . Due to effect of IAA on oxidative
enzyme system of the plant there may be abnormal increase in respiration of the tissues. It
has also been suggested that this auxin even effects the genetics of the plant.
The increase in the amount of indole (indolyl) acetic acid has been noticed in many
diseased conditions of plants. These diseases can be due to any type of infections causes
such as bacteria, fungi, nematodes and virus. The fungi causing late blight of potato
(Phytopthora infestans), smut of matize (Ustilago maydis), Panama disease of banana (
Fusarium oxysporium f. Sp cubense), downy mildews of maize and bajira ( Sclerospora
sacchari, S. philippinensis, S graminicola) and the nematode causing root knot
(Meloidogyne spp) not only induce the plant to synthesise more IAA but also themselves
produce this auxin. The conversion of tryptophan into IAA takes place in following steps:
Tryptophan
Tryptophan
Indole pyruvic
Or
Tryptamine
Indole acetaldechyde
IAA
Indole acetaldechyde
IAA
It is not clearly understood whether the excess of IAA detected in diseased plants is due to
the plant or the pathogen or due to interaction of both. It could be due to excessive
production of IAA by the diseased plant or due to production of this compound by the
pathogen in the plant tissues or it could be due to its reduced destruction in the diseased
tissues. Plants contain enzymes (IAA oxidase) that can degrade indole acetic acid . These
enzymes keep the amount of IAA in the plant under check to permit its normal growth. It is
possible that the pathogen inactivates these IAA oxidising enzymes by its metabolites and
thus the level of IAA in the plant continues to rise. This condition has been proved in maize
smut ( Ustilago maydis ) and wheat rust (Puccinia graminis) Hyperauxinity (excess of IAA)
has been detected in many other diseases such as rust of Euphorbia Cyparissias caused
by Uromyces pisi , powdery mildew (Erisiphe graminis) on wheat and white blister of
Brassica napus (Albugo candida).
The production and activities of auxins have been studied in some detail in bacterial plant
diseases. Two such examples are given here. In bacterial wilt and brown rot of potato
caused by Pseudomonas solanacearum the bacterium grows in vascular bundles of the
tuber and stem and causes vascular browning, rot and wilt. Biochemical analysis has
shown that diseased plants contain 100 times more IAA than the Healthy plants. At the
same time phenolic compounds (scopoletin) also increase 10 times. Phenols are known
to suppres the activities of IAA oxidase. Thus, one of the explanations for increased amount
of IAA in diseased potato plants can be that the rise in phenols in diseased tissues
suppresses the IAA oxidising enzyme that regulates the production and accumulatiun of
the auxin . However, the level of this auxin rises in the beginning of pathogenesis also
suggesting that the plant also syntheses it to some extent. After the death of the plant rise in
level of the cause continues. This suggests that the bacterium also synthesizes the auxin in
dead tissues. Thus,all the three possbilities of the cause of hyperauxinity exist in this
disease. The hifh level of IAA in the plant increases plasticity and permeability of cell
walls. This makes the pectin , cellulose and proteins easily available to the pathogen.
Although phenols help in lignin synthesis which makes tissues resistant this does not
happen in the diseased plant because IAA interferes with lignification of tissues. Thus, the
bacterium gets more time for tissue desintegration. Increased respiration and transpiration
are other effects produced by IAA through altered cell wall permeability.
The second example is that of Agrobacterium Tumafaciens . This bacterium attacks more
than 100 plant species and produces galls on root crown, stems and petioles. Crown gall
caused by this bacterium has served as the classic model for investigations of the role of
auxins, indoleacetic acid and related indole compounds in plant pathogenesis . The
extensive research on this disease , was spurred by its similarity to carcinigenesis in
animals . The bacterium is not present in galled tissues.
The gall or tumour is initiated in two phases. The first is conditioning phase in which a
fresh wound is required without the presence of the bacterium. Then the bacterium enters
the host and second phase stars. The conditioned cells are transformed into tumour cells by
an agent, termed the tumour – inducing principle (TIP) produced by the bacterial
pathogen. This phase occurs only at temperatures below 29 0C . Afterwards, there is no
function of the host or the bacterium in the development of the tumour. The tumour cells
multiply and develop the galls. The process cannot be checked by killing the bacterium.
The tumour cells multiply and develop the galls. The process cannot be checked by
killing the bacterium.
The tumour cwlls contain more than normal quantity of IAA. In addition, they contain
cytokinins.Althouth the bacterium is capable of porducing indole acetic acid the tumour
cells free from bacteria also contain higher level of IAA suggesting that the cells
themselves are capable of synthesising this auxin. Since the enzymes capable of oxidising
IAA are in identical amounts in normal and tumour cells it is evident that the excess auxin
in tumour cellsin due to its synthesis rather than due to lackof its degradation. However,
the auxin alone has no capacity to convert the normal cells into tumour cells.
Conclusive evidence of the identity of the transforming agebt (TIP) is lacking. At
various times TIP has been suggested to be bacterium itself a virus associated with the
bacterium , a metabolic product of the bacterium, a coverted host component, or most
recently, bacterial DNA which is taken up, incorporated and translocated in the tissue.
There are indications that several metabolic systems are gradually, but permanently,
activated during the transition from a normal cell to fully altered tumour cell.
Viral infections also disturb the balance of auxin in plant. An excess of auxin results in
overgrowth or its deficiency causes atrophy or growth retardation in viral diseases .
Howeer, the mechanism by which the virus alters the balance is not known.
In some viral diseases there is no correlation between synthoms and the amount of auxin
detected in the diseased organ.
Gibberellins. The role of Gibberellins in pathogenesis, although well recognised,has been
studied in relatively few diseases . The Gibberellins were discovered by Japanese workers
investigating the bakanae or foolish scedling disease of rice caused by Gibberella fujikuroi,
as ascomycetous fungus with its imperfect stage in Fusarium moniliforme. The disease is
characterised by abnormal elongation of stem due to excessive elongation of internodes.
Rellins, a group of chemically related growth regulators, were insolated from these
seedlings. So far 38 of these compounds have been reported. They are different from each
other in their structure and /or biological activity. The best known gibberellin is gibberellic
acid (GA3).
Gibberellins are considered as normal constituents of green plants and are also found in
microorganisms. They perform numerous functions. Oue of the important functions is their
role as chemical signals which activate cell extension, dormancy breaking and flowering
etc. These chemical signals activate various enzymes in the plant body. Thus, during seed
germination the embryo secretes the hormone which activates the cells of aleurone layer to
secrete hydrolytic enzymes for liquefying the reserve starch. It also promotes enzymes
that aid in digestion of endosperm cells and softening of seed coat. Other enzymes are also
helped by Gibberellins. The proteinase enzymes synthesised under the signal from
Gibberellins cause degradation of protein releasing various amino acids. Among these
acids tryptophan, the precursor of IAA may be one. Thus, there is a close relationship
between Gibberellins and IAA. Tissues treated with Gibberellins (Gibberellic acid) may
develop higher concentration of IAA. The latter often helps the functions of Gibberellins
and both substances seen to work synergistically for maximun stem elongation. It is
possible that Gibberellic acid neutralizes some growth inhibiting system in the plant, such
as IAA oxidase.
Gibberellins have strong ggrowth promoting qualities. These include elongation of root
and shoot, excessive flowering, fruiting, etc. Synthoms of growth inhibition can be
reversed by appication of Gibberellic acid. These compounds are suspected to be operating
in many other host- pathogen systems such as downy mildew of sugarcane (Sclerospora
sacchari), rust caused by Uromyces Pisi on Euphorbia cyparassias, smut of Bromus caused
by Ustilago hypodytes, etc.
The site of activity of Gibberellins in the cell is close to the nucleic acid system. It
activates inactive genes and in this process synthesises new messenger RNA which directs
the synthesis of various enzymes for different functions.
Cytokinins (kinins): The best known Cytokinin, is kinetin (6- furfuryl-amino- purine).
These growth regulating substances are derivatives of adenine, a constituent of DNA and
RNA. As such they are essential for growth and differentiation of cells and tissues. The
type of tissues and plant organs is deternined by amount of Cytokinin in the primordial
tissue. Low Cytokinin activity causes root formation while high levels of these
substances. Induce bud formation. In presence of auxin these compounds induce rapid cell
division. They prevent degardation of protein and nucleic acid thereby delay senescense.
Amino acids and other chemicals flow towards points where Cytokinin activity is higjh.
The mode of action of cytokinins is similar to that of gibberellins and they also often
function synergistically with auxins.
The significance of kinins in pathogenesis is uncertain. However , role of kinins in many
host- pathogen interactions has been suspected. These include bean rust, root knot,
Victoria blight and some bacterial disease. Increase in the level of kinin- like substances in
leaves of bean (Phaseolus vulgaris) attacked by Uromyces phaceoli and leaves of Vicia
faba attacked by Uromyces fabae is reported to induce formation of “green islans” around
the infection centres. Nutriens accumulate in the green tissue. The tissues with low
cytokinins thus become senescent.
Growth and differentiation inhibitors. Many chemically different substances work as
growth inhibitors in the plant and are synthesised by them. Excess of these substances
causes such effects as inhibition of cell division, induction of dormancy, formation of
abscission layer, epinasty, etc. The growth inhibitors may interact with growth promoting
substances in the plant and render them ineffective. Thus, normal growth of the plant
organs is arrested. Two such chemicals have been studied in some detail. They are dormin
and ethylene
Dormin or abscission II induces dormancy by converting developing leaf primordia of a
bud into dud scales. The inhibitory effects of dormin are counteracted by presence or
application of gibberellins. On the other hand, dormin can function as antagonist of
gibberellins in the plant. Dormin can also mask the effect of IAA which cannot be
reversed by application of additional IAA although gibberelins can offset this effect of
dormin on IAA activity. The role of dormin in pathogenesis is not known.
Ethylene (C2H4) is a highly active growth regulator best qualified for a primary role in
pathogenesis . It is produced by plants independently or under the influence of
pathogenesis.It is the earliest known growth regulator and is biologically active in even as
low concentration as 0.1 part per million. Some promitent effects of ethylene are epinasty,
tissue proliferation, marked increase in rate of respiration, premature senescence and
shedding of leaves , and stimulation of root formation . It is highly mobile in plants, and
does not accumulate in tissues. However, whent the pathway for its movement is blocked
suchas when vascular occlusions and stomatal closure occur in bacterial and fungal wilts,
ethylene may accumulate and synptoms of epinasty become apparent.
A number of bacterial and fungal pathogens produce ethylene and in case of fusarium wilt
of tomato (Fusarium oxysporium f. Sp. lycopersici), ethylene production by the pathogen is
sufficient to account for the epinastic synptoms of the disease . However, in most cases, the
production of ethylene is by the damaged tissues. In a number of viral diseases , leaves
with necrotic local lesions produce more ethylene tham those from systematically
infected plants without necrotic lesions. Necrosis induced by toxic chemicals also results in
increased ethylene evolution. This suggests that in such cases ethylene is a product rather
than cause of tissue damage.Banana plants attacked by Pseudomonas solanacearum
(bacterial wilt) show premature ripening and yellowing of fruits which is linked with high
level of ethylene in the yellowed fruits. Other species of Pseudomonas , some species of
Xanthomonmas and Erwinia also produce such effects.
From the above account of the effect of pathogenesis on growth of the plant in can be
concluded that changes in growth pattern are caused by imbalance in production,
accumulation and translocation of growth regulators in the plant. The normal plant
synthesises growth promoting substances in quentities just enough for its normal growth.
The plant also produces growth inhibitors to rergulate the activity of growth promoters and
other chemical substances. In pathogenesis this regulatory mechanisms is disturbed or
destroyed and as a consequence there is unregulated synthesis of growth hormones and
other substances and therefore the changes in growth habit are seen.
Effect on Reproduction of the Host
From practical viewpoint the loss from disease is due to reproduction in reproductivity of
the plant. Reproduction in plant is determined by its agen nutrition, enviroments ( light,
moisture, temperature) and normal physiological activity . Disturbance in one physiological
activity initiates a chain reaction that affects other activities thus influencing growth and
reproduction. Inanimate causes or unfavourable environment mainly reduce the
reproduction of plants. There are also many infectious diseases which reduce or completely
suppress reproduction of the host.
EXAMPLES OF PLANT DISEASES IN WHICH SYMPTOMS SUGGEST
OVERACTIVITY OF GROWTH REGULATORS.
Disease and
Symptoms
Crown gall
Smut
Wart
Host
I.- Galls caused by cellular proliferation.
Many
Maize
Potato
Parasite.
Agrobacterium tumefaciens
Ustilago maydis.
Synchytrium endobioticum.
II.-Increase in the lengthof stem.
Downy mildew
Bakanae disease
Rust
Rust
Sugarcane
Rice
Euphorbia
Wheat
Sclerospora sacchari
Giberella fujikuroi
Uromyces pisi
Puccinia graminis.
III.- Suppression of abscission layer.
Leaf blight
Cherry
Gnomonia erythrostroma.
IV.-Stimulation of abscission layer.
Leaf blight
Coffee
V.-Excessive abnormal branching
Omphalia flavida
Witches broom
Witches broom
Downy mildew
Various trees
Sweet pea
Maize
Many fungi.
Corynebacterium fasciens
Sclerospora sacchari
As has been discussed in the preceding section the abscission layers aren formed by the
action of growth regulators. Under normal conditions this layer develops when the fruit has
ripened and contains viable seeds and when the leaf has reached senescence. However
pathogenesis induces formationof these layers, through the activity of growth regulators
formed by the pathogen or by the host, untimely. When abscission layer develops in
immature fruits there is loss in reproduction.
The infectious diseases, localised or systemic, affect physiological activities of the plant.
When pathogenesis reaches a particular stage reproductive process of the plant is also
aaffected. These effects can be direct as well as indirect. The direct effects usually lead to
partial or complete destruction of fruits,seeds , etc. While indirect effects are the result of
weakening of the plant or loss of the crop resulting from seeds produced by diseased
plants. The processby which pathogens reduce reproduction in plants is mediated by the
physical and chemical means given in the preceding sections. Some examples of direct and
indirect effects on reproduction are given below.
In many plant diseases the host produces normal fruits and viable seeds. However, the
inoculum gets mixed with the seed and reaches the next crop where it harms the young
plants or detroys the reproductive organs. In wilt disease of tomato (Fusarium oxysporium
f. Sp. lycopersici) the fungos is often associated with the viable seeds and harms the young
plants developing from these seeds. In seed rot and stalk rot of maize (Fusarium
moniliforme, Cephalosporium acremonium, C. Maydis) the fungi are present in and on the
seed. When the seed is planted these pathogens, depending on environments, many cause
rottingof seedsand seelings. F. Moniliforme causes direct loss ol seeds also when it attacks
the cobs and rot . In loose smut of wheat (Ustilago nuda tritici) the seed itself is not
damaged by infection but the plant developing from it in the next season produces ears
completely devoid of grains and full of smut spores. The green ear disease of bajra
(Sclerospora graminicola ) is carried by seed and soil and the infection becomes systemic in
the plant developing from contaminated seedor on contaminated soil. The plants turn
yellow, remain stunted and may never reach the flowering stage . If ears develop they bear
leafy structures in place of grains. Since the infection is systemic in such diseases there is
complete loss of productivity in them. Downy mildews of maize caused by Sclerospora
sacchari and Sclerophthora macrospora also often cause complete loss of seed formation.
The direct infection and loss of floral organs and seed occurs in such localised diseases as
smut of bajra. The grains are partielly or completely damaged although majority of grains
remain unaffected.
The loss of germinability of seeds is another factor in causing losses in yields. Many
viral diseases of potato reduce the sprouting capacity of the tubers. In addition almost all
diseases of potato caused by viruses cause reduction in number and size of tubers.The
same is true for late blight of potato.
The above examples are only of those diseases where the loss in reproductive parts or the
pproduce is conspicuous and forms part of symptoms. But, loss of reproduction occurs in
all diseases because of interference in physiological systems resulting in general weakness
of the plant . The powdery mildews do not show serious effect on reproductive organs or
seeds but the seeds are weak or pod development may by significantly reduced due to
disturbed physiology of the host including serious loss of photosyntesis. The increased
transpiration in plants affected by rusts also results in shrivelled grains of low viavility.
Thus, the effects on reproductivity of the diseased plants, as stated earlier, are the result of
direct consumption of floral or reproductive parts by the pathogen or due to altered
physiology such as low uptake of water and nutrients (root diseases), low rate of
translocation of water and nutrients, tissue desintegration before flowering, lack of normal
photosynthesis ( powdery mildews) or photosyntetic area (leaf spot diseases).
Effect on Uptake and Translocation of Water and Nutrients.
Living cells of plants need sufficient water and nutrients (organic and minaral) for their
normal activity. If there is interferebce with the availability of these requirements the cells
fail to perform their physiological functions. Minerals and water are absorbed by roots and
translocated by xylem vassels upwards towards leaves. A part of absorbed and
translocated water and the entire, amount of mineral nutrition is used up for various
activities of the cells. However, a major portion of water reaches the intercellular spaces
and is diffused into the atmosphere through stomata and lenticels in the process of
transpiration . The organic nutrition of the plant is mostly Synthesised by photosynthesis
in the leaves and translocated through phloem vessels downwards up to the roots. The
excess of organic nutrients, in various forms (amino acids, sugars, organic acids, etc) is
exuded out into the soil in the root exudates. It is, thus, obvious that if due to effects of
pathogenesis uptakeand and translocation of minerals and water is checked the plant
tissue will starve and when due to starvation the physiological activities of these tissues
are affected thrre will be deficiency of substances produced by these tissues for the entire
plant. In this way the entire plant will be sick. For an example, if water is not absorbed by
roots or there is obstruction in its translocation the leaves will cease to be active and
photosynthetic activities will cease or decrease. The organic nutrition will not be
available to roots. Thus, not only the leaves but roots also will be adversely affected. The
effect of pathogens on photosynthesis is discussed elsewhere. Here only the uptake and
translocation of minerals and water is being considered .
Effect on absorption of water by roots.The water uptake capacity of roots can be affected
inthree ways, viz, roots are injured, permeability of root, cell walls is altered and
development of roots is checked.The fungi causing damping off and root rot and most of
the phytopathogenic nematodes and some viruses cause sfficient injury to the roots before
visible symptoms appear on the aerial parts. Such injuries or wounds reduce the number
of active roots and water uptake is decreased in the same proportion.Some vascular
parasites reduce the number of root hairs thus decreasing active surface area and
therefore reduced uptake of water.
Roots absorb water and mineral solutions through the process of osmosis. If the
pathogen or its growth regulators, toxins and enzymes alter cell wall permeability of roots
the osmosis is also affected. The role of enzymes and growth regulators on cell wall
permeadility has already been discussed. Effect of toxins is given in a later chapter. The
reduced osmotic activitycauses decrease in water uptake.If the root cells are killed, plant or
pathogen generated toxins can enter the roots and affect physiological activities of the
plant.
Effect on translocation of water by xylem vassels: The fungi and bacteria causing damping
off, stalk rots and canker can enter the xylem vessels. If the plant is young these vessels
can be desintegrated . In affected vessels organs of the pathogen or biochemical substances
produced by the pathogen or the diseaseed plant may also be present and cause
obstructions. Desintegration as well as obstructions both reduce de water carrying capacity
of the root system. The crown gall bacterium, Agrobacterium tumefaciens, club root fugus,
Plasmodiophora brassicae, and the root knot nematodes ( Meloydogyne spp) develop galls
on roots and stem due to overgrowth of cells. The xylem vessels abjacent to these
proliferating tissues are crushed or dislocated and thus lose their normal water
conducting capacity. A common example of malfuntioning of xylem is the group of wilt
disease in which the pathogens invade the xylems vessels.. Although these pathogens
(species of fusarium, Verticillium, Pseudomonas, Erwinia) can obstruct water transport by
their physical presence sometimes the obstruction by fungal hyphae or bacterial cells is
not much but symptoms of wilt appear. Obviously, some additonal factors apart from
presence of pathogen organs operate in causation of obstruction intransport of water. In
this way, it is apparent that translocation of water is reduced or obstructed by any of the
following mechanisms in addition to desintegration of the xylem vessels:
1.- Presence of fungus mycelium , spores and slimy bacterial mass in the xylems:
Plugging of xylem vessels has at least partly been atributed to presence of these forms
of the pathogens causing vascular wilt diseases.
2.- Enzymes: The production of pectic enzymes in vascular infections by wilt causing
pathogens has been noted . These enzyme degrade the middle lamella and release pectic
acid and other substances which form gels and gums. These pathogens also produce
cellulolytic enzymes. When middle lamella of xylem vessels are desintegrated by these
enzymes the pectic substances form plugs which obstruct the passage. Browning of
vessels is a common feature in vascular wilts. This is due to a pigment called melanin. The
pigment is formed by the action of enzymes. The pectinolytic enzymes of the pathogen
desintegrate the host cells and star oxidation of phenolic compounds. The oxidised
products form moolecules of the pigment. Since the action of enzymes and growth
regulators alters cell wall permeability these pigments easily enter the xylem vessels.
3.- Pathogenic polysaccharides. Bacteria and gungi are capable of producing
polysaccharides that can induce wilt sumptoms in vitro. In many wilt diseases the
symptoms have been atributed to these complex substances. These polysaccharides are
different from those produced by the plant. The pathogenic polysaccharides are
macromolecular substances that cannot pass through openings in cells walls. Their
entrapping in the cell wall openings causes abstruction in the flow of water from one
vessel to another and laterally to other cells. Increase is viscosity and thereby decrease in
rate of flow of tracheal fluid is also attributed to polysaccharides and partly accounts for
wilt symptoms. In bacrterial brown rot and wilt of potato (Pseudomonas solanacearum)
the amount of polysaccharide produced by the pathogen is proportional to the severity of
the symptoms.
4.- Hiperplasia: The tomato mosaic virus causes necrosis in the stem . Cells adjacent to
necrotic area show hyperplasia and the vessels that come in the path of this overgrowth
are rendered nonfuntional due to pressure. Adnormal development of xylem vessels . even
in areas of the plant not yet invaded by the pathogen, often occurs in vascular wilts. The
walls of the new vessels are thinner than normal and they are usually flattened instead of
circular and appear collapsed. These changes in the xylem reduce water transport in the
plant.
5.-Tyloses: The production of gels and gums as a result of enzymic action of the pathogen
and formation of plugs was mentioned above.In many fungal, bacterial and viral vascular
disease the presence of the pathogen , its toxins, and permanent deficiency of water
causes development of tyloses in the xylem vessels . Tyloses are outgrowth of parenchyma
adjacent to the xylem and appear as peg- like structure. They obstruct passage of water
inthe same manner as the gels and gums.
Effect on transpiration: In the above account only the uptake of water from soil has been
mantioned. Pathogens also affect transpiration in addition to uptake and translocation of
water , Increased transpiration has been noticed in most of the leaf diseases (rusts,
powdery mildews, etc). The main cause of this increase in transpiration or loss of water
from plant body is desintegration of the cuticle.Increased cell wall permeability and
malfunctioning of stomata are also contributory factors. In rust diseases a major portion of
leaf surface is exposed due to rupture of the epidermis by the pustules. This causes
unrestricted loss of water. If there is no translocation of water from roots in proportion to
water lost in transpiration symptoms of wilt may appear. The increased suction tension
caused by increase in transpiration may result in collapse of vessels or formation of tyloses.
In some diseases, such as blights, death of leaf cells reduces the number of healthy and
active cells. This decreases the suction tension .Therefore the transport of water to leaves
by the xylem vessels is also reduced. Reduced permeability of cell walls also produces
similar effects. On the other hand in some wilt diseases the related toxinas (fuisaric acid,
lycomarasmin, etc) enhance cell wall permeability. In this situation also the loss of water is
increased.
Physiological and pathological wilting: Wilt symptoms usually indicate water deficiency in
the plant. This deficiency may occur in plant without infection due to non-availability of
water. No pathogen is involved in these cases . The wilting thus caused is known as
physiological wilting in contrast to pathological wilting in which non-availability of water
in directly or indirectly associated with some pathogen. Soil moisture has no relationship
with pathological wilting..
Effect on translocation of nutrients and their deficiency in plants: The materials from soil
enter the roots as solutions in water and are translocated through the xylem. Therefore, the
abnormalities thet obstruc water uptake and translocation affect the uptake and movement
of mineral nutrients also.
The organic nutrients synthesised in leaf cells enter the phloem vessels through
plasmodesmata . Due to difference in osmotic pressure they move down the sieve tubes
and during this downward movementthey continue passing again into the adjacent
nonphosynthetic cells through plasmodesmata . These cells them use the nutrients for their
vatious activities or store
Smut