The following points highlight the three main stages of host pathogen relationship. The stages are: 1. Pre-Penetration Stage 2. Penetration Stage 3. Post-Penetration Stage.
1. Pre-Penetration Stage:
During pre-penetration stage the pathogen (inoculum) on arrival on the host surface interacts sharply with the surrounding environment and host itself. The environment which is an aggregate of all external conditions including temperature, moisture (relative humidity), light and the competing microorganisms; affects the life and form of the pathogen of the inoculum.
The optimum environmental condition for ideal growth of a pathogen again varies on the nature of the pathogen and the host surface. For example, the development and abstraction of conidia are favored by high air temperature and humidity in downy mildew.
Whereas in powdery mildew both the number of spores and their germination are greater in bright sunlight. In cereal rusts uredospore’s germinate at low temperature, but the infection process is delayed at this temperature. Again soil pH plays a very vital role in the growth of bacterial plant pathogen in the rhizosphere (area of soil immediately surrounding the roots).
Whether a pathogen will survive and grow on the host surface also depends on its behavior with the exudates of, the host surface and the microbial population present on it. The exudates of the host surface may encourage or inhibit the growth of the pathogen. The root exudates mainly sugars and amino acids are nutrients for the growth of fungi and bacteria.
But root exudates like hydrocyanic acid, various organic acids and antibiotics are antifungal and antibacterial. For example, spores of Rhizopus arrhizus germinate only in presence of proline (amino acid) present in the rhizosphere region; whereas exudates of root of onion varieties inhibit spore germination of Colletotrichum circinaus.
Leaves also exude substances which may go in favor or against the growth of the pathogen. The glands of leaf hairs of gram contain malic acid which is antifungal and arrests the growth of Uromyces ciceris arietini.
Protocatechuic acid, an exudate of onion skin is also antifungal. The pathogen has to neutralize these exudates or has to be resistant to them for survival. Besides these, the rhizosphere region contains microbial population which is antagonistic to the growth of the pathogen. As such, the pathogen has to overcome the above barriers during pre-penetration stage before it can survive for host penetration.
Once a favorable relationship is established with the host surface, multiplication or growth of the pathogen begins. Rapid proliferation of cells of bacterial pathogen results in a relatively short time. The bacterial cells so formed being delicate structures may be easily killed by unfavorable conditions.
Hence they survive under layers of slime. Again development of fungal phytopathogen usually includes spore germination by germ tube which grows producing infection hypha as a result of hyphal tip growth or may give rise to an aspersorium which anchors the fungus to the host surface.
Penetration peg is produced from the aspersorium with which the pathogen causes host penetration. But multiplication of viruses takes place only in the living host cells.
2. Penetration Stage:
The success of host penetration leading to disease development is a very complicated process which is a combined effect of various factors like:
(i) The nature and behavior of the pathogen including its multiplication capacity,
(ii) Favorable physical conditions, and
(iii) Host susceptibility.
Of all these factors, the factor nature and behavior of the pathogen is the most important one which controls the overall disease development. The nature and behavior of pathogen encompass the inoculum potential of the pathogen. The inoculum potential is again a measure of the biological energy available for the colonization of a host.
It is a function of:
(i) Inoculums density which refers to the number of viable propagules per unit area of leaf or stem or per unit volume of soil;
(ii) The nutrients available to the infectious units that allow them to germinate or grow;
(iii) The environment (temperature range of 15 to 25°C, moisture content 70 per cent, and relative humidity 90 to 95 per cent);
(iv) The virulence (aggressiveness) or genetic capacity of the pathogen to cause disease; and
(v) The susceptibility of the host.
Besides these, the physiological state of the host may have an effect on the ability of the pathogen to attack it or on the extent to which a pathogen may harm it. The concept that encompasses this phenomenon is termed predisposition.
Factors involved in predisposition are:
(i) Age of the host;
(ii) Environmental conditions to which the pathogen has been exposed, i.e., light, humidity, soil environment, and temperature;
(iii) Infection by other pathogens; and
(iv) Presence of chemicals, i.e., pesticides, herbicides.
Generally adverse conditions predispose a plant to greater susceptibility to attack by a pathogen. Temperature predisposition phenomenon in nature is extremely variable depending on the nature of host and pathogen. In most bacterial and fungal diseases, free moisture is necessary for pathogen development.
Most known cases of predisposition usually result in increased susceptibility of plants that were genetically resistant. A few cases are known in which a predisposing treatment has greatly increased resistance of plants that were genetically susceptible.
Certain fungal pathogens exhibit specificity in the part of host tissue infection. For example, some of them may remain restricted in the cortical tissue only throughout the entire period of attack and cause damage to it. Again others remain restricted in the vascular tissue only. Whereas, still others do not attack plant unless its heart wood is developed and the pathogen remains confined there causing damage.
With favorable inoculum potential associated with aggressiveness under favorable predisposition, the pathogen will now enter the host tissue which is designated as host penetration. The entry of pathogen in the host tissue is essential for success of infection.
The host penetration and establishment of host-pathogen relationship and the subsequent development of disease symptoms involve a chemical interaction between host and pathogen.
The pathogen employs offensive chemical weapons to breach host barriers. Parasitism and host resistance run parallel and are inseparable.
A kind of biochemical warfare continues between the host and the pathogen in which one tries to outwit the other. Enzymes, toxins, growth regulators, polysaccharides, antibiotics are the important biochemical offensive weapons secreted by the pathogens (fungi and bacteria). Fungi produce great variety of enzymes, no doubt related to the nature of the materials colonized.
Those normally produced have been called constitutive enzymes as distinct from adaptive or inductive enzymes whose formation is stimulated by the presence of the appropriate substrate. Enzymes catalyse many of the biochemical processes of living organisms and thus play a fundamental role in the host-pathogen interaction.
They are concerned not only in the initial entry of the pathogen and its spread within the host but also the degradation of host tissue into metabolites which the pathogen can utilize. Enzymes break down cells walls and connective cell layers.
They also seriously affect the respiratory processes, growth, ionic exchange of the host cell causing interference with the cell permeability and other normal functions. Viruses, however, on account of their basic nature cannot produce any of these substances. They multiply by directing the host cell to manufacture viral nucleic acid and viral protein.
Host penetration takes place:
(i) Through natural openings,
(ii) Through wounds,
(iii) By direct penetration of surface cells causing tissue disintegration, and
(iv) Through specific parts or organs.
Both bacteria and viruses enter the host tissue mainly through wounds. Whereas, the fungal pathogens gain entrance in the host through natural openings, wounds and by direct penetration through cuticle and outer wall of the surface cells, or root hairs, or through specific parts or organs of the host.
The direct penetration process is more complicated than the entry through natural openings and wounds. It is performed by breaking the host structural barriers through wide range of chemical actions.
(i) Entry through natural openings:
Both bacteria and fungi gain entrance into the host through natural openings such as: stomata, lenticels, hydathodes, nectaries, leaf scars, stigma, etc. This is a process in which the pathogens have an easy access to the host, except in cases where sub-stomatal hairs may cause resistance against the host entry.
(ii) Entry through wounds:
Wounds caused due to natural calamities (storm, fire, etc.); during field operations; by insects, by accidental breaking of parts or otherwise; offer easy passages of pathogens in the host. But so far as viruses are concerned, the host entry is only through wounds.
(iii) Entry by direct penetration of surface cells:
The entry of pathogen by direct penetration of the outer wall of the host surface cells is rather a difficult process for which the pathogen usually requires high moisture or free water supply. It is even more difficult in leaves with waxy covering on their surface which allows water to rim off freely.
Fungal pathogens penetrate into host either by boring through the outer wall of the surface cell or penetration is effected by pressure and sometimes due to chemical softening or solubilizing of the barrier caused by the solvent action of enzymes secreted by the infecting organ.
After the hypha made contact with a suitable host surface, some growth in close contact with it takes place. This is followed by the development of an aspersorium or increase in diameter of hypha serving as adherent area from which develops penetration tube.
The penetration tube penetrates through the cuticle at a point softened by enzymatic action and followed by mechanical pressure. In some cases germ lube produced by spore germination passes down between the racial wall of the adjoining cells without actually entering the cells.
Other fungi send only haustona in the epidermal cell through the outer cutinized wall In certain others, the penetration hypha penetrating the cuticle induces the formation of a local interna swelling of the underlying cellulose wall, so that a small papilla projects from the underside of the wall into the cell.
This papilla is penetrated by the penetration hypha which enters the host cell and ultimately develops into a haustorium.
Bacteria are mostly weak parasites which cannot employ force to effect penetration. Their penetration is effected by chemical action. The plant parasitic nematodes pierce the host surface with spears or stylet.
The entire process of Direct Penetration, however, depends on:
(a) The nature of cell wall layers,
(b) The potentialities of the enzyme system of the pathogen, and
(c) The potential force the pathogen can exert.
The main components of the host ‘cell wall are pectin, cellulose, hemicellulose, lignin and small quantity of protein. The three main softening or solubilizing enzymes found in fungi are: pectolytic, cellulolytic, and lignolytic. The outer layer of host plant cell may have a layer of wax which is followed by cuticle impregnated with wax.
The cutin gradually decreases with the depth of the epidermis and is replaced by pectin which occurs as a homogeneous layer in some host plant. Subsequently in the secondary wall of the cell pectin is replaced by cellulose. Cellulose layers contain appreciable amounts of protein.
No pathogen secretes enzymes that would degrade wax. Only mechanical entry can enable a pathogen to breach this layer. Cutin layer is penetrated either by pressure (mechanically exerting force) or by the action of degrading enzymes: cutinase, cutin esterase, and carboxyl cutin esterase. Cutinase breaks cutin into fatty acid and hydroxyfatty acid.
Pectic substances which form basic material of middle lamella, primary and secondary walls are degraded by pectinolytic enzymes.
The pectinolytic enzymes act against pectin and pectic substances in many steps:
(a) The enzymes pectin methyl esterases (PME) hydrolyse the pectic substances into methanol and pectic acid;
(b) The enzymes pectin glycosidases, polygalacturonases (PG) and polymethyl galacturo- nases (PMG) degrade the pectic acid and methylated chains of pectin. Besides these, wall modifying enzyme (WME) modifies the pectic material for subsequent degradation.
The degradation of pectic substances provides nutrients for many fungal pathogens and due to weakening of the cell wall facilitates inter- and intra-cellular invasion by hyphae. Pectic enzymes are produced both constitutively and adaptively. High C/N ratio of the substrate favors increased mycelial growth and low enzyme synthesis whereas lower ratios give poorer growth but increased enzyme synthesis.
Pectic enzymes have no effect on protoplast and thus cannot do much Killing of host cells. They may be secreted by some of the pathogens involved in spotting and blotching of leaves, although the macerating effect may be masked by necrosis caused by toxins.
Cellulose forms the structural framework of cell walls. Cellulolytic enzymes act upon the cellulose and break it to simple compounds and make the way for the easy penetration of the pathogen into the host cell. There are two theories to explain the mechanism of cellulose degradation and maceration by cellulolytic enzymes which are adaptive enzymes: the unienzyme theory and the multienzyme theory.
According to unienzyme theory, complete degradation of cllulose into glucose units is by a single enzyme: Cellulose Cellulose Cellobiose Cellobiase Glucose. Whereas, the multienzyme theory explains cellulose degradation in a series of steps through two groups of enzymes.
One group of enzymes loosens the cellulose fibrils of the crystalline area by hydrolytic mechanism. The other group of enzymes penetrates the cellulose lattice and causes hydrolytic cleavage of hydrogen bondage.
In the spaces between the cellulose microfibrils of the cell wall, hemicelluloses are present which are degraded by hydrolytic cleavage by enzymes hemicellulases.
The degradation of hemicelluloses by the enzymes hemicellulases produces simpler sugars. In vascular wilt diseases the molecules released by cellulose degradation can cause plugging of the vessels.
The most complex chemical compound in the plant cell wall is lignin which occurs chiefly in the matrix surrounding the cellulose fibrils. It is one of the most structurally complex biopolymers whose degradation is caused by polyphenol oxidases produced by wood-rotting fungi. But fungi cannot utilize the degradation products.
The attack of nematodes is both internal as well as external. Both endophytic and ectophytic nematodes use force as well as enzymes to dissolve or break the cell wall to come in contact with cell protoplasm through their stylet. But endophytic nematodes enter bodily in the host cell, whereas the ectophytic ones remain outside the host.
(iv) Entry through specific parts or organs:
In such cases the pathogens exhibit specificity of host parts or organs (stem, leaf, root hairs, floral parts, coleoptile, buds, etc.) during their entry in the host.
Some examples are:
Synchytrium endobiuticwn infects and remains confined in the epidermal cells of potato tuber, Erysiphe graminis infects the epidermal cells of leaves of cereals and grasses, Ustilago nuda causes infection only in the flowers of wheat, Claviceps purpurea infects the ovaries of rye flower, certain wood rotting fungi are – Merulius lacrimans and Fomes annosus; soil inhabiting pathogens inter through root hairs – Plasmodiophora brassicae.
Besides these, there are highly specialized insect parasitizing fungi — members of the order Entomophthorales and Laboul beniales.
3. Post-Penetration Stage:
Usually with the success of the penetration process, post-penetration is successful. But the entry of the pathogen in the host tissue may not always ensure immediate infection leading to disease development. The process may be delayed or there may be failure for various reasons.
The delay may be in cases where the pathogen has incubation period and infection is established only after the expiry of the incubation period. The success of post-penetration process depends largely upon competition of pathogen for nutrition, and production of enzymes and toxic substances and their effects on host metabolic activities.
Again due to toxic effect of host cytoplasm, the pathogen may fail to establish biological relationship with the host. Host-pathogen interaction may also result hypersensitivity of the host tissue, whereby rapid death of the affected cells prevents the further spreading of the pathogen due to shortage of nutrition.
But in most of the plant diseases, host infection is followed by invasion, a condition when a pathogen grows rapidly in the host tissue. For example, bacteria invade host tissues intracellular and destroy them. Whereas, fugal mycelia invade inter- or intracellular but may or may not cause destruction immediately after invasion. Viruses always invade host tissues intracellular.
They multiply in the living host cells by directing them to manufacture viral nucleic acid and viral protein, their movement from cell to cell is through plasmodesmata. Again fungal hyphae and spores, and bacterial cells may move through vascular tissues once they gain entrance in them. Successful host invasion of the pathogen is invariably associated with disease syndromes of various types of varying degrees.
After penetrating the host cell walls, the pathogen comes in contact with the host cytoplasm from which it gets its required nutrition. In response to the activities of the pathogen, the host metabolic processes (osmoregulation, respiration, photosynthesis, etc.) get upset.
Depending on the nature of host and virulence of pathogen and their relationship, the host interacts in the following manner:
(i) Increase respiratory rate:
Level of many enzymes associated with respiration increases resulting in accumulation and oxidation of phenols. Break down of ATP is accelerated causing an increase in respiratory rate. A host-pathogen relationship is known as incompatible relationship when increase in respiratory rate takes place in the early stage of infection.
Again it is designated as compatible relationship where the pathogen is an obligate parasite and there is little change in respiratory rate of the infected tissue.
(ii) Dis-balance of photosynthetic process:
The photosynthetic process is impaired by the breakdown of chlorophyll through the enzyme chlorophyllase causing chlorosis. There may also be increase in the amount of chlorophyll exhibited by green islands on the affected leaf surface.
(iii) Dislocation of normal growth:
The normal synthesis of growth promoting substances (auxins, gibberellins, and- cytokinins) is dis-balanced resulting in overgrowth, subnormal growth and correlated symptoms. There may be rapid development of growth inhibitors (dormin and other substances) leading to premature ripening of fruits and causing formation of abscission layers resulting in premature fall of leaves, flowers, and fruits.
(iv) Influence on reproductive structures:
There may be halting of development of reproductive structures (abortion) or due to localized or systemic infection there may be destruction of ovaries.
(v) Effect on transporting organs:
The transporting organs are affected in various ways:
(a) Plugging and rupturing of xylem vessels due to growth of pathogen in their lumen;
(b) Presence of pathogen in the vascular tissue causes formation of toxins and development of tyloses in the xylem vessels from the adjacent parenchyma causing obstruction to the passage of water;
(c) Vascular infection produces pectic enzymes in the xylem vessels whose middle lamella is degraded releasing pectic acid and other substances which form gels and gums to plug the lumen of xylem vessels;
(d) Polysaccharides secreted by vascular pathogens have more often been regarded as “wilt toxins”, dissolved or suspended in the xylem sap exert their action at a distance from the cells of the pathogen.
Bacterial and fungal wilts are often associated with the movement of the pathogen in, and colonization of, vascular elements of the host. Again phloem necrosis caused by viruses obstructs the movement of carbohydrates synthesized in the leaves causing many deformities of the leaf surface.
(vi) Dislocation of tissues:
Secretion of lytic enzymes causes loss of coherence of the tissues, breakdown of cell walls, and death of protoplasts. Death of aerial parts may result from the transport of toxic substances from the diseased tissues or from ionic imbalance caused by the failure of selective absorption.
(vii) Result abnormal growth:
Increase or decrease in host cell number and size are attributed to the metabolism imbalance regardless of whether growth disturbances are caused by fungal, bacterial, viral or nematode infection.’ Metabolism imbalance disturbs normal hormonal balance. The hormone kinetin works together with indoleacetic acid (IAA) for cell expansion and cell division causing tissue proliferation.
(viii) Cause tissue destruction:
As the pathogen grows in the host tissue, cell wall degrading enzymes, like cellulases, hemicellulases, pectinases, etc., induce maceration processes. Tissue-disintegration of the host continues further accompanied by the activity of several oxidative enzymes such as peroxidase, polyphenol oxidase and ascorbic acid oxidase.
Perhaps the most refined type of pathogenesis may be observed with the viruses. With the aid of their nucleic acids they give the host cells incorrect information which carry out damage. As the pathogen grows, it also interferes with protein metabolism of the host tissue causing reduction in the protein and nitrogen level in the affected tissue.
During post-penetration stage offensive biochemical weapons—enzymes, toxins, growth regulators, polysaccharides, and antibiotics are employed simultaneously by the pathogen for degrading and macerating of host cell wall and ultimately killing and/or interacting with the host cells.
This behavior of the pathogen, besides causing dis-balance of the host metabolic processes, also triggers several metabolic systems in the host cells resulting in formation of defense chemicals phenolic substances with which the host tries to repel the attack of the pathogen. These two processes continue simultaneously. These aspects are treated separately under separate headings.
That cell wall destruction and maceration are done by various enzymes. These processes are closely followed by the action of toxins and other offensive biochemical weapons.
Toxins are biochemical substances produced by pathogens during host infection. They are responsible for disease symptoms in the host plant. That toxins are responsible for the death of host cells was first pointed by DeBary (1886). The term toxin can have different meaning for different workers. Owens defined toxins as non-enzymatic substances which injure plant cells or disrupt their metabolism.
Toxins also inactivate the enzymatic reactions of host tissue.
They are produced by microorganisms (fungi and bacteria) in a variety of environments and are injurious or lathal in low concentration to macro-organisms. Hence it is the suspect, a macro- organism, instead of a microorganism that distinguishes toxins from antibiotics.
Again substances that are toxic in excessive doses, although they are excreted by microorganisms are not considered as toxins. Toxin may thus be defined as a chemical substance produced by microorganisms during their interaction with host. It affects the host metabolism in a subtle manner.
Toxin also acts directly on living host protoplasm to influence either the course of disease development or symptom expression. A toxin has a low molecular weight, extremely mobile and easily reaches the subcellular levels of the hosts. Toxins are different from enzymes due to the fact that they do not attack the structural integrity of the hose tissue but-affect the metabolic activities of the host cells.
They can be antimetabolites in action and can reduce the amount of specific growth factor. They also disturb the osmotic relations of host cells and most of them affect respiration directly or indirectly.
In contrast with the enzymes, the effect of toxins is direct on the protoplast. Scheffer and Briggs (1981) defined toxin (for plant pathological purposes) as a microbial product other than enzyme, which causes obvious damage to plant tissues, and which is known with reasonable confidence to be involved in disease development. Most toxins are not specific in their action.
They harm many species belonging to different unrelated genera or family. A few toxins are species-specific. They only affect plants susceptible to the pathogen; resistant plants are not damaged. Host specific toxins are also designated by some workers as pathotoxins.
These toxins are able to produce in susceptible host plants all characteristic disease symptoms, but have little or no effect on resistant species, unless used in massive concentrations. The pathogen and pathotoxins exhibit similar host specificity. The virulence of the pathogenic strain varies directly with their ability to produce toxin. Host-specific toxins are complex chemicals.
It is relatively difficult to isolate any of these toxins in pure form and still retain the property of specific toxicity. Some of them are low molecular weight peptides. They rapidly act upon both cell and plasma membrane causing changes in permeability and respiration of diseased tissues.
Some toxins affect various kinds of plant tissue whereas others damage a single type of tissue. They may induce a particular syndrome when applied to plant in suitable concentrations.
Wilting, for example, is a common effect of many toxins which cause loss of cell turgor and leaf flaccidity, and eventually a general wilting of the whole shoot. Such toxins are known as marasmins or wilting toxins. Lycomarasmin and fusaric acid are also of this category of toxins. Again toxins causing necrosis are the necrotoxins and are produced by species of Altemaria, Phytophthora and Pseudomonas.
Toxin concentration may not be correlated with virulence. A single toxin may induce all symptoms. The ability of a microorganism to produce a toxin or an enzyme is, of course, fixed genetically, but certain chemicals may be able to repress activation of genetic information or to prevent it from functioning the cell metabolism.
Toxins are classified in three categories:
(i) Animal toxins or zootoxins, produced by animals;
(ii) Plant toxins or phytotoxins, produced by fungi or higher plants; and
(iii) Microbial toxins, produced by microorganisms.
Phytotoxins may be (a) pathotoxins which are capable of producing all of the disease symptoms, and (b) vivotoxins produce portion of disease symptom in vivo.
According to Diamond and Waggoner (1963) vivotoxin is a substance produced in the infected host tissue by the pathogen and/or its host, which functions in the production of disease, but it is not itself the initial inciting agent of disease.
The phytotoxins have the properties like:
(a) Can induce the same plant response but may have different mechanisms, of action;
(b) Different pathogens can synthesize the same phytotoxin;
(c) Most phytotoxins are composed of simple carbohydrate and/or amino acid residues;
(d) The pathogen and the toxin may not exhibit the same host range;
(e) Toxin concentration may not be correlated with virulence;
(f) Toxigenicity is not always a requisite for pathogenicity;
(g) The rates of synthesis and degradation may vary depending upon the nature of microorganism, environment and host;
(h) May not act alone but in concert with other pathogen- and host-produced substances in a dynamic, interrelated system;
(i) Have low molecular weight and are mobile in plant tissues;
(j) Maybe intrinsically unstable;
(k) May be irreversibly reacting with cell constituents; and
(l) may act in combination with other components found in diseased tissue.
Other types of toxins are: endotoxins, intracellular toxins formed in bacterial cells and are not liberated until the latter die; and exotoxins, extracellular toxins which diffuse from the living bacterial cell.
Most of the toxins produced by plant pathogens seem to be pleiotropic, that is, they have multiple effects on the host cells, but the ‘wildfire’ toxin produced by Pseudomonas tabaci is monotropic, as are many of the toxins produced by bacteria which attack animals. This is an unstable toxin.
The varied mechanisms by which microbial toxins damage a host are not clearly understood. However, toxins must eventually influence adversely the membrane system, whether these be the limiting cytoplasmic membranes, the internal membranous cytoskeleton or the diverse membranes of organelles, including vacuoles. Toxins damage permeability of plant membranes.
Bacterial phytotoxins respond to plants in only a few days, mainly by the development of chlorosis, growth abnormalities, necrosis, water soaking or wilting. The response will depend upon phytotoxin concentration, environmental conditions and/ or physiological state of the host.
These responses by the plant are not only limited in kind but are non-specific in that different agents acting in different ways can induce the same response.
A number of storage fungi as well as some other fungi are known to produce substances which have toxic effects on animals and humans. These toxic substances are known as mycotoxins and the diseases they cause in animals are the mycotoxicoses.
Interest in mycotoxins resulted from the discovery of aflatoxin, a metabolite of Aspergillus flavus Link ex Fries produced in kernels of groundnut, reported for the first time by K. Sargeant and others (1961). “Aflaroot” disease induced by A. flavus which is a seed and soil borne disease of groundnut causes post-harvest aflatoxin problem in groundnut by developing in poorly dried pod shells and kernels.
Aflatoxins are thus produced in kernels of groundnut particularly in improperly dried pods. Natural occurrence of aflatoxins has been reported in a wide range of commodities, particularly in improperly dried pods and seeds both in field and storage conditions.
In course of time aflatoxin contamination of food and feedstuff has posed a storage problem as because aflatoxin contaminated food consumed produces deleterious effects. Among the various derivatives, aflatoxin B1 is the most toxic and generally produced in higher amounts. Mycotoxins in general, and aflatoxins in particular, in food and feedstuff have carcinogenic and toxinogenic properties.
Some of the mycotoxins produced by storage fungi are: sterigmatocystin, ochratoxin, citiinin, and patulin.
There are similarities between bacterial and fungal infections and the resulting symptoms. In general, virus infection reduces the capacity of the host for starch synthesis accompanied by reduced degeneration of starch, resulting in accumulation of starch in the foliage and other plant parts. Virus infection also enhances respiratory activity and alters auxin levels in the host cells.
The host-pathogen interaction ultimately may produce symptoms like:
(c) Hypertrophic, and
The pathogen may also establish a relationship or association with the host in such a manner that none of the above conditions are produced. Either after some of its growth or at least when it reaches a particular organ of the host or both, then only the pathogen produces symptoms that will be visible from outside.
In infected green tissues chlorophyll may be reduced or destroyed turning brown. Or in certain areas due to preservative action of certain parasites on the chlorophyll apparatus of leaf tissues there is marked formation of green islands of tissues after the rest of the green tissue withers, this is known as green island effect.
There is evidence that not only is the chlorophyll preserved but also the chloroplasts are stimulated to increased activity by the pathogen. There may be a development of red or purple pigment due to the formation of anthocyanin resulting from infection.
There are a group of cellulose dissolving fungi which are responsible for rots of wood. This is a large group comprising both parasites and saprophytes. Though their activities are more or less restricted to cellulose and substances similar to cellulose of the wood they also attack all the major components of the cell walls of the wood.
There is no uniformity of sequence or proportion of their destruction. Some attack the chief components of the wood simultaneously, whereas others cause delignification before the cellulose is depleted, others again show a delayed delignification. The variations are due to differences in the nature and time of enzyme becoming active and its course of action.
Wood Decay by Fungi:
Wood which is a rich organic substrate provides a suitable food base for fungi. Fungi draw their nourishment from the cell wall material, which they breakdown by enzymatic activity.
The hyphae exude various enzymes into their substrate. These enzymes convert the chemically complex wall material into simpler water-soluble products, which are further acted upon by endoenzymes in course of fungus metabolism. The enzymes are selective in action. The ability of fungi to attack various components of wood is determined by the nature of enzymes they secrete.
There are various stages of decay as wood is changed from sound to completely decayed. In the early or incipient stage, also known as incipient decay, the wood appears like normal, except in few cases by a change in color. This stage can be easily overlooked and as such incipient decay is dangerous.
From this stage the wood becomes noticeably affected until it finally changed completely in structure and appearance. This is the advanced stage of decay.
Change in color of wood is not always a criterion for decay, since it may be due to other causes, either parasitic, e.g., fungi causing sap stain in wood or due to chemical action. Some decays are associated with formation of dark-brown to black zone lines, and also possess mush-roomy odour. In incipient decay the wood may not always weaken.
But is advanced stage of decay all mechanical properties of wood are seriously affected and such wood is useless for any college botany purpose where strength is required.
Decay results in decrease of specific gravity of wood, so that the amount of wood substance per unit volume becomes less. Decayed wood, based on volume, has thus less calorific value and yields low grade fuel. The microscopic characters of decay include presence of hyphae in the cells.
The hyphae pass from cell to cell consuming food materials during decay; the penetration occurring probably by chemical action, resulting in bore holes in the wall.
In utilizing the cell wall material as food, the hyphae cause corrosion marks, uneven thickness of secondary walls leading to their disintegration, enlargement of pits and dissolution of bordered pits. The damage in the cell wall mainly accounts for reduced strength of decayed wood.
Besides enzymes, for causing decay, fungi require an optimum concentration of air (oxygen) and moisture for their growth. Insufficient air may act as a limiting factor and if air is removed by saturation of the wood with water, the fungi die. Fungi cannot grow in the wood if the moisture is below 20 per cent, based on oven-dry weight of wood.
If, however, the infected wood is air-dried, the fungus does not die but its active growth ceases and may remain dormant for several years in this condition. If such wood is moistened, the fungus may revive and continue its growth in the wood.
With respect to temperature, wood-decaying fungi make optimum development over a range of 60°F. to 90°F. temperature. Rainfall also greatly influences the occurrence of decay fungi. A certain amount of moisture in the substrate and in the atmosphere is necessary for the fungi to develop sporophore.
In dry localities, therefore, as in deserts, decay fungi are few. In tropical conditions with high temperature and rainfall, decay fungi are diverse and also large in number. They remain active for greater part of the year. In temperate regions, fungi are fewer. They remain active for a shorter period, i.e., during summer.
Some wood decaying fungi which can tolerate wide range of temperature are:
Fomes lividus, Polyporus gilvus, P. hirsutus. Others, like F. badius, F. pachyphloeus, Gano- derma lucidum, Polyporus palustris, P. tulipiferae, thrive at high temperatures. Fungi which thrive at low temperatures are: Fomes annosus, F. robustus, F. roseus, F. pini, Lenzites sepiaria, Merulius lacrymans, Polyporus abietinus, P. pargamems, P. versicolor, Poria monticola, P. xantha.
For practical purpose two kinds of wood decay are generally recognized:
White rot and brown rot. Both kinds of decay are caused by large number of Ascomycetes and Basidiomycetes. In both these kinds of wood decay, hyphae penetrate deep into the tissues of the wood and inhabit the lumen of vessels of host cells.
They pass cell to cell through bore holes. The white rot causing fungi breakdown lignin with oxidising exoenzymes. They also remove a small amount of the structural carbohydrates leading to a lightening of the wood. But the brown rot inducing fungi remove the structural carbohydrates like cellulose and hemicelluloses, leaving the lignin relatively unchanged.
Hence the wood, after decay, appears more brown than normal wood. In both the cases the decay in wood is generally associated with a change of colour. In case of white rot the colour is bleached and in case of brown rot the color turns dark. The initial darkening caused by the white rot fungi may be due to oxidation of phenols. The decayed wood shrinks. This is more in case of brown rot than in white rot.
In case of decay caused by brown rot fungi, at the initial stage there is no thinning of the cell wall. The white rot can be fibrous or spongy (white fibrous or spongy rot) or pockets may be developed in the wood in which the tissues are white and fibrous and such pockets are delimited by thin brown areas, less decayed (white pocket rot).
The decayed wood also cracks in all directions into cuboidal blocks, which easily become powdery under pressure. When such decay occurs in structural timbers, as in buildings it is termed dry rot. The term dry rot is a misnomer, since such rot’ as well as others occur only under damp condition. There is another form of decay in timber, termed soft rot, which is recognized by its brittle fracture when broken across the grain.
The fungi attack mainly cellulose and the hyphae are mostly confined to secondary wall in which dissolution occurs in the form of pits or cavities. The fungi causing soft rot belong to the Ascomycetes and Deuteromycetes. Soft-rot fungi are nearly restricted to the surface of the secondary wall and there they thrive producing large cavities by enzymes which lie in parallel to the microfibrils.
The diagnosis of decay can be done when the decay is in the advanced stage, by gross characters. Incipient decay can be determined by microscopic characters of decayed wood and by isolation of the fungus in culture.
Fungi may attack sapwood or heartwood in trees or timbers. The decay of heartwood is—heart rot. Fungi attacking trees may or may not decay timber after conversion. When such rot occurs in converted wood, the term ‘inactive rot’ may be applied to it.
Sap stain fungi form another group causing defect in trees and timber.
They do not attack the cell wall but live on cell contents stored in the sapwood only; thus the heartwood where no such food material is present remains un-effected. Since cell wall is not attacked, most of the properties of wood, except thoughtless, remain un-effected. However, stain depreciates value of wood due to unsightly appearance. Sap. stain is caused by some members of the Ascomycetes and Deuteromycetes.
Cell to cell colonization of mesophyll cells may cause leaf spot symptoms, wilting may develop if vascular cells are invaded, or a soft rot may be caused by breakdown of the living parenchymatous cells of cortex or pith.
Changes in Vascular System:
The vascular system of a disease-free plant serves as a pathway for the movement of water carrying nutrients.
But in some diseased plants the vascular system may serve as a pathway for the movement of the pathogens. Again the pathway of water and nutrients may be clogged by metabolites produced by the pathogen, by the pathogen itself by its growth, or by the debries of the host tissue produced by infection and pathogen. This will ultimately result wilting of plant.
The wilt diseases have a multiplicity of causes rather than a single cause; but are largely due to deficiency of water supply. Water becomes deficient in wilt- diseased plants as a result of a number of events.
(i) Vessels become completely plugged by tyloses and gums.
(ii) Resistance to flow of water through vessels increases as a result of development of vascular gels, the presence of mycelium, and the lodging of propagules in the lumen of vessels.
(iii) Resistance to transfer of water from vessel to vessel and to redistribution of water in the plant also increases in diseased plants as a result of the plugging of pit membranes by compounds of high molecular weight like polysaccharides excreted by the pathogen, the resinous melanoid pigments associated with vascular browning, and the partially hydrolysed cleavage products of cells walls by hydrolytic enzymes of the pathogen.
(iv) Flow of water and nutrients may be impaired in cases where vascular tissues are crushed locally due to growth of the pathogen.
(v) Wilt disease may be induced by wilt toxin produced in the xylem vessels.
In addition to above factors, glycopeptides produced by some pathogens accumulate at termini of the vascular system in leaf margins, where they accumulate in the membranes of parenchyma cells and damage differential permeability.
The non- symptomatic leaves on infected plants may have transpiration loss about one-third of those of healthy plants receiving a normal supply of water. Stomata remain closed. Tissues are subjected to an ever-increasing shortage of water.
Infected plants may have a lower photosynthetic rate than healthy plants. Depressed rates of photosynthesis and transpiration are attributed to limited supply of water. Both terminal and cambial growth are reduced in infected plants. Again the cells in which the parasite penetrates get killed prior to which there may be change of pigmentation of cells and destruction of protoplasm.
In others, the parasite may produce certain substances which produce streaking or staining of certain parts of the host tissue.
Some woody tissues react to parasitic attack by the secretion of gum and by the development of tyloses in the vessels of the wood. In this respect the conifers are important because several fungi and bacteria cause an outflow of resin from them. Again there are certain fruit trees from which gum is exuded due to both parasitic and nonparasitic causes which is known as gummosis.
When the exudate is resin it is known as resinosis. Again there may be slime flux when the exudation product is a slimy substance.