Plant Pathology (Phytopathology): An Introductory Guide microbiologystudy

Plant Pathology or Phytopathology is the study of plant diseases, their cause, symptoms, effects, and management approaches of plant diseases.

Objectives of Plant Pathology

• Study of disease or disorders caused by biotic and abiotic agents (Etiology).
• Study of the mechanism of disease development by the pathogens (Pathogenesis).
• Study of interaction between plant and pathogen in relation to the environment (Epidemiology).
• To develop suitable management strategies for managing the diseases and losses caused by them (control/management).

History of Plant Pathology

The history of plant pathology is divided into five different eras-

1. Ancient Era: Antiquity to 5th Century (476 A.D.)

The primal study of plant diseases goes back to ancient civilizations, where early observations and remedies were recorded. The ancient Hebrews, Greeks, Romans, Chinese, and Indians recognized plant diseases like rusts, smuts, and mildews.

In India, it finds a reference in an ancient text on plant health entitled “Vrikshayurveda”.

Theophrastus is often described as the “Father of Botany” and by about 300 B.C. this Greek philosopher made some of the first recorded systematic observations about plant diseases and their occurrence and some of the simple control methods.

2. Dark Era: 5th Century to the 16th Century (476 A.D. to 1600)

In the so-called “Dark Era” scientific progress in general was severely retarded in Europe and indeed for the most part in the world as far as plant pathology is concerned.

However, the Islamic civilization preserved and extended knowledge in what would later be written about different plant diseases and their control by scholars such as Ibn al-Awwam. 

The invention of the printing press in Europe, in about 1440, once more kindled an interest in learning and science hence creating the base for further development. 

Although the rate of advancement was not rapid, this period provided a background for the re-awakening of scientific interest in the succeeding centuries.

3. Pre-modern Era: 17th Century to 1853 (1600-1853)

The pre-modern era is considered a watershed in plant disease studies, which was propelled by unprecedented technological advancement in the invention of the microscope.

The work of Robert Hooke in 1665 developed the cell theory, while Anton van Leeuwenhoek’s discovery of microorganisms in 1676 opened a whole new world of biological understanding.

The study of fungi did not become more organized until P.A. Micheli described fungi in 1729, and Carl Linnaeus developed the system of binomial nomenclature in 1753.

The Irish Potato Famine of the 1840s, caused by the late blight pathogen Phytophthora infestans, emphasized the importance of plant diseases to humankind and is considered the end of this era.

4. Modern Era: 1853 to 1906

With that, modern pathology veers to the pathogen as a causal agent in plant disease.

The work of Anton de Bary, done in 1853, confirming that the Irish Potato Blight was caused by the fungus Phytophthora infestans provided a scientific foundation for plant pathology. Major contributions by T.J. Burrill regarding the bacterial nature of fire blight in apples and pears and the establishment of Koch’s postulates by Robert Koch to prove the causal relationship between a microbe and a disease were also made during this era.

Other important breakthroughs during this period pertained to the preparation of Bordeaux mixture by P.A. Millardet against grape downy mildew and the description of the Tobacco Mosaic Virus in 1886 by Adolf Mayer.

5. Present Era: 1906 Onwards

Beginning from the early 20th century has been an era of immense discoveries concerning plant pathology. With the advancement in molecular biology, genetics, and biotechnology, science has entirely been transformed. The concept of solar heat treatment of wheat smut by J.C. Luthra in 1931.

Other examples of such milestones include the crystallization of the Tobacco Mosaic Virus by Wendell Stanley in 1935 and the discovery of a gene-for-gene relationship by G.H. Flor in 1955. The identification of Mycoplasma-like organisms in the 1960s by Doi and Asuyama and current studies on the interaction of plants with viruses have also kept the pace going. 

Definition of Disease

Any deviation from the healthy condition which interferes with the normal structure and performance of vital functions of a plant is called a disease.

The British Mycological Society (1950) defines disease as a harmful, deviation from the normal functioning of the physiological processes of a plant.

Classification of Plant Disease

Based on the nature of the causal agent, the plant disease is classified into

• Non-parasitic or abiotic diseases– These are induced by unfavorable environmental conditions such as mineral deficiencies or excess, low or high temperatures, improper water, oxygen, and light relations. Examples are the black heart of potatoes, heat canker of flax, scald of apples, etc.
• Parasitic diseases– These are caused by the attack of some living agents called the causal agents which may be a plant, an animal, or a virus. In this case, the diseased plant is called a host and the causal organism is called a pathogen. Most plant diseases are caused by fungi, bacteria, algae, angiosperms, nematodes, and viruses.

According to occurrence, they are divided into three categories

• Endemic diseases– A disease that is regularly present in a certain region or a country in a moderate to severe form is called endemic disease. Example-Wart disease in potato.
• Pandemic diseases diseases occur over very large regions, sometimes globally, affecting multiple crops and plants. Example- Chestnut blight.
• Epiphytotic disease (epidemic) – It is the kind of infectious disease that spreads widely but occurs periodically. The causal agent may be regularly present in the environment but its rapid development may only occur periodically and thus this type of disease is responsive to environmental variations. Example- rust, blight, mildews.
• Sporadic disease– These are the plant diseases that occur at irregular intervals or occasionally. Example leaf blight, wilt etc.

Based on perpetuation and primary infections, plant diseases are classified as

• Soil-borne diseases– There are several pathogens whose infectious agents are present in soil and primary infection takes place through soil. They infect through roots. Examples of pathogens are- Phytophthora, Fusarium, etc. Examples of diseases are- Root rot, wilt, and seedling blight.
• Seed-borne diseases– In this type of disease, the pathogens survive as dormant mycelium in the seeds or other propagating materials of host plants. Example of pathogen- Ustilago
• Examples of disease- damping off, smut, etc.
• Airborne diseases– In this type, the pathogens infect the host plant through air and bring primary as well as secondary infection. The spores of such pathogens are disseminated by wind. Examples of pathogens- are Puccinia, Rhizopus, etc. Examples of diseases are blight, rust, and powdery mildew, etc.
• Vector-borne disease– In this type, the diseases are transmitted by vectors such as insects that carry pathogens from one plant to another.

Based on the extent of infection it is of two types

• Localized– In this type, only a particular part of the plant is affected. Example root rot, leaf spot etc.
• Systemic– In this type, the pathogen spreads throughout the plant body. Example Downey mildew.

Based on pathogen generations

• Monocyclic disease/ simple interest disease– In this type of disease the pathogens have only one generation in one cropping season. Example- Loose smut of wheat.
• Polycyclic disease/ compound interest disease– In this type of disease the pathogen has more than one generation in one cropping season. Example- Late blight of potato.
• Polyetic disease– These are polycyclic diseases but complete their disease cycle in more than one year or above. Example- Cedar apple rust.

Based on symptoms, they are of mainly three types

1. Necrosis- Death or killing of the host tissues due to the pathogen is called necrosis. The types of necrotic symptoms are-

• Spots- Spots are localized brown or black-colored areas surrounded by purple color margins. Spores may occur as fungal leaf spots or bacterial leaf spots.
• Blights- These are rapid discoloration of infected parts like leaves, stems, or twigs in response to the pathogen infection and followed by death of these parts.
• Blasts- These are the sudden death of the unopened buds or inflorescences.
• Scorch- Scorches are blight-like but occur in irregular patterns usually along the leaf margins.
• Cankers- These are localized necrotic areas with open wounds often sunken in the woody tissues like stems surrounded by living tissues. Canker is a dead lesion.
• Scabs- A scab is an epidermal infection which are mostly rough, and crust-like.
• Rots- Rots are infections of various soft tissues of the host and may involve various parts of the plant. Rots represent the dead and decomposed tissues due to disintegration by the enzymes secreted by the pathogen.
• Anthracnose- This destroys the collenchyma and cambium layers and is difficult to distinguish from the cankers. In this case, the lesions are sunken in the center with raised margins.
• Wilts- Wilts are secondary symptoms in which the leaves and shoots lose their turgidity and droop.
• Damping off- It is the rapid death and collapse of the seedlings at the soil line.
• Mildews- These are chlorotic or necrotic areas covered with pathogens due to their vigorous growth. There are two types of mildews- powdery and downy mildews. Powdery mildews appear as white or brown dust on the leaves and stems of the host. Downy mildews are deeply affected by narcotic and chlorotic lesions on the leaves and stems.
• Streak and stripe- These are elongated necrotic areas along the stem and leaf veins.
• Ring spots- These are symptoms of viral infections found on leaves and stems which may be present in single or in groups.
• Rusts- These are small, local pustules of various colors on stems or leaves giving a rusty appearance.
• Smuts- These are shooty or charcoal-like powdery masses appearing on different parts.
• Scald- Scald is the blenching of epidermal and adjacent tissues of fruits and leaves.
• Dieback- Dieback results from severe necrosis of fruits and branches beginning from the tip region that advances downwards. Dieback is seen in old plants.

2. Hyperplasia and hypertrophy- Hyperplasia is the abnormal increase in the cell number due to rapid division. The rapid growth in cell divisions is called hyperplasia.

Different hypertrophic and hyperplasic symptoms seen in plants are-

• Galls/tumors- These are irregular growth or elongations of parts due to fungal or bacterial infections.
• Leaf curls- These are thickened, swollen, distorted, and curled down leaves due to hypertrophy on the upper surface.
• Warts- These are small protuberances developed on galls/tumors giving a discolored or warty appearance.
• Witches broom- It is a special type of overdevelopment where a large number of special branches arise from a single localized area.
• Enations- These are small outgrowths occurring on veins and midribs on the lower side of leaves.

3. Hypotrophy and hypoplasia- Hypotrophy is the reduction in growth and hypoplasia is a reduction in a number of cell divisions. Different hypoplasic symptoms are as follows-

• Chlorosis and yellowing- It is the distortion of green color due to lack or reduction of chlorophyll synthesis, the leaves and the entire plant look pale green and yellow.
• Mosaic- It is the irregular color development where a mixing of green with other colors is found giving a mosaic appearance.
• Dwarfing and stunting- This symptom is manifested by proportionate reductions in the growth of all parts as a result the plant becomes dwarf-stunted or underdeveloped.
• Leaf curling- This is the upward curling of leaf lamina due to reduced growth of veins in comparison to lamina growth.
• Pallor- This is due to the destruction of chlorophyll in the leaves. It occurs due to the presence of parasites in this pale area or around it.
• Little leaf- This represents the reduced growth of the lamina due to virus infection.
• Rosette- The length of the internode is shortened due to reduced growth.

Based on duration and severity

• Acute diseases– These diseases develop rapidly and cause severe damage over a short period. Example- Fire blight.
• Chronic diseases– These diseases progress slowly, causing long-term damage and a decline in plant health. Example- Oak wilts.

Based on the part affected

• Foliar disease– These diseases primarily affect the leaves. Example- leaf spots.
• Stem diseases– These diseases primarily affect the stems. Example- stem rust.
• Root diseases– These diseases impact the root system. Example nematode infestations.
• Fruit and seed diseases– These diseases affect the reproductive part of the plant leading to issues like poor fruit development and seed viability. Example Seed smut.

Some important Phytopathology terms and definitions

Disease– A malfunctioning of host cells and tissues that results from continuous irritation by a pathogenic agent or environmental factor and leads to the development of symptoms. (G.N. Agrios, 1997).

Disorder– Non-infectious plant diseases due to abiotic causes are called disorders.

Pathogen– An entity; usually a micro-organism that can incite disease. A pathogen is any agent that causes disease. 

Parasite– It is a living organism that derives the nutrition for its growth from another living organism. A parasite may not always cause a disease.

Pathogenicity– It is the ability of a pathogen to cause a disease.

Pathogenesis– It is a chain of events that leads to the development of disease in the host or a sequence of progress in disease development from the initial contact between the pathogen and its host to the completion of the syndrome.

Sign- It is the pathogen or its parts or products seen on a host plant.

Symptoms– It is the external or internal reactions shown by the plant as a result of a disease.

Syndrome– A set of varying symptoms characterizing a disease are collectively called a syndrome.

Biotroph– An organism that can live and multiply on another living organism by obtaining its food from living tissues on which it completes its life cycle.

Hemibiotroph– The parasite that attacks living tissue as a biotroph but continues its life cycle even after the death of the host tissue is called hemibiotroph or facultative saprophytes.

Alternate host– It is a host that helps in the completion of the life cycle of the pathogen and its survival and belongs to a different group.

Perthotrophs (Necrotrophs) – A parasite is a necrotroph when it kills the host tissues in advance of penetration and lives saprophytically.

Inoculum- It is part of the pathogen in different forms; such as spores, dormant mycelium, etc. which on contact with a susceptible host plant causes infection and is called inoculum.

Incubation period- The period between penetration of a host by a pathogen and the first appearance of symptoms on the host is called the incubation period.

Penetration- The invasion of the host tissue by the pathogen is called penetration.

Hypersensitivity– Excessive sensitivity of a plant to pathogens is called hypersensitivity.

Infection- It is the establishment of the pathogen within the tissue of the host plant after penetration is called infection.

Disease cycle– A series of events between infection and the complete development of a given disease is called a disease cycle.

Epidemiology– It is the study of the rate of multiplication of pathogens and the spread of a disease caused by it in a plant population.

Disease triangle and disease pyramid

The interactions of three components of disease i.e. the host, the pathogen, and the environment is called the disease triangle.

The disease triangle can be expanded to include two or more components, time and humans. The amount of each of the three components of disease and their interaction in the development of disease is affected by the fourth component i.e. time. Thus addition of the time component to the disease triangle forms a digit pyramid or tetrahedron.

If the four components can be quantified, their volume would be proportional to the amount of disease in a plant population.

Agarios (2006) added that humans are the fifth factor at the peak of the disease triangle.

Test of pathogenicity and Koch’s postulates- pathological diseases in plants as well as animals are caused due to infection by particular pathogens which may be bacteria, viruses, fungi, etc. Pathogenicity is a test conducted to confirm whether a pathogen is the real cause of the disease or not.

Robert Koch (1882) laid down the conditions to identify the real causal agent of a disease. These are called Koch postulates which are as follows-

1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
2. The organism must be isolated from the diseased organism and can be grown in pure culture.
3. The cultured organism should cause disease when introduced into a healthy organism and exhibit similar symptoms.
4. The microorganism must be re-isolated from the inoculated, diseased experimental host, and should show similar features with and identical to the original specific causative agent isolated from the diseased organism.

What is Pathogenesis?

The process of infection or the ability of the pathogen to cause disease is called pathogenesis. Entry and colonization of pathogen in the host tissues is known as establishment and the infective propagules coming in contact with the host are called inoculum.

Inoculum potential– It is the inoculum required for successful infection. 

The process of infection depends upon various factors

• Disease proneness– It depends upon external factors such as host nutrition i.e. more potash application makes the host less susceptible and more nitrogen application makes the host more susceptible.
• Environmental factors such as humidity, temperature, etc. also affect infection.
• Multiplication rate of pathogen– A high multiplication rate increases the chances of infection.
• Proper inoculum potential– In the case of specialized pathogens, a very few amount of inoculum can cause infection successfully. In the case of non-specialized pathogens, a high density of inoculum is required.
• Susceptibility of host– It is controlled by DNA and can be inherited by offspring.
• Virulence of the pathogen– It is determined by the genetic material of the pathogen.

Stages of Infection in Plant Pathology

The process of infection has three stages-

1. Pre-penetration phase

The pre-penetration phase includes the germination of the pathogen before penetrating the host and also includes the interaction of the pathogen host and the environment. It is divided into the following sub-stages-

• Recognition and attachment- The pathogen must recognize a suitable host and this involves chemical signals or surface molecules that indicate the presence of a host. The pathogen then adheres to the plant surface which is often mediated by fungal spores, bacterial pili, and viral particles that bind to specific molecules on the host surface.
• Spore germination- This process takes place for fungal pathogens. The spore forms a germ tube which either develops a hyphae or an appressorium for penetrating the host surface.
• Production of extracellular enzymes- Pathogens may secrete different enzymes to degrade the plant’s cell wall and cuticle layers which helps in destroying the protective barriers such as the epidermis.
• Chemical signaling and evasion of plant defenses- Pathogens may release effector molecules to suppress the plant’s immune responses. Some pathogens can modify or mask their surface molecules to avoid detection by a plant’s immune system.
• Preparation for penetration- Some pathogens apply mechanical pressure or certain pathogens induce localized cell death to facilitate entry.

2. Penetration phase

Pathogens penetrate plant surfaces by direct penetration or indirectly through natural openings.

Direct penetration

Most fungi, nematodes, and parasitic higher plants are capable of penetrating the host surface directly. However, the plants are provided with different mechanisms of defense which include structural features of the host, chemical coverings on the cell wall, and anti-infection, biochemical nature of the protoplasm.

• Breakdown of physical barriers– Viruses have no mechanical force or enzyme system to overcome chemical barriers and therefore come in contact with host protoplasm only through wounds. Fungi and nematodes can employ force for direct penetration. 
• Breakdown of chemical barriers– The host is provided with a defense mechanism against invasions which includes the presence of a cuticular layer, lack of suitable nutrients for the pathogen, presence of inhibitory or toxic substances in the host cells, exudation of substances toxic to a pathogen or stimulatory to antagonists of the pathogen.
• Fungal spores germinate to form appressoria that penetrate the plant cuticle by specialized hypha called the infection peg. The infection peg enters the epidermis and then establishes infection within the plant tissues either intracellularly or intercellularly. In other parasitic plants, the penetration is accomplished by haustoria formation.

Penetration through natural openings

• Stomata– The majority of bacteria and fungi enter through stomata. Bacteria often enter through stomata, where the entry is facilitated by moisture or other conditions that promote stomatal opening. In Puccinia graminis tritici the germ tube of uredospore grows over the leaf and approaches stoma. There is an accumulation of germ tube protoplasm at its tip which swells to form an appressorium in the stomatal aperture. A blade-like wedge grows from the appressorium through the stomatal slits and it swells to form a sub-stomatal vesicle. The contents of the appressorium pass in the vesicle. One or more penetration hyphae grow from this vesicle and they form infer or intracellular mycelium and are cut off by the formation of the cross wall. And haustorium is soon produced in the host cell.
• Lenticels– These are the pores on tubers and are filled with cells that are loosely arranged. These are often considered secondary entrances for a pathogen.
• Hydathodes– These are the pores on the tip of a leaf and are responsible for guttation. Some bacteria use these pores as an entrance into the host.
• Some other pathogens may enter through trichomes and nectaries.

Penetration through wounds

Pathogens like nematodes, and fungus often enter through physical damage which provides direct access to the plant’s internal tissues, allowing the pathogen to colonize and grow rapidly. Mostly nematodes use a needle-like structure to pierce plant cells and inject digestive enzymes creating entry points for pathogens or directly feeding the plant’s contents.

Through non-cutinized and cutinized surfaces

Some pathogens penetrate through seedlings, root hairs, buds, flowers, nectaries, stalks, and cuticles.

3. Post penetration

Once the pathogen successfully penetrates the plant surface, it begins to invade and colonize the host tissues.

• Invasion and Colonization: After penetration, the pathogen spreads within the plant, establishing either a local or systemic infection. The incubation period—the time between initial infection and symptom appearance—varies depending on the pathogen and environmental conditions.
• Fungal Pathogens: Fungal pathogens typically invade by extending hyphae through the plant tissues, forming intracellular or intercellular networks. Some fungi also produce haustoria, specialized feeding structures that extract nutrients from the host cells.
• Bacterial and Viral Pathogens: Bacteria and viruses do not increase in size but multiply within the host. Bacteria proliferate in intercellular spaces, often producing extracellular polysaccharides that aid in colonization. Viruses move from cell to cell through plasmodesmata, eventually reaching the vascular system for systemic spread.
• Local vs. Systemic Colonization: Pathogens may cause localized infections, affecting specific tissues or organs, or they may spread systemically, infecting the entire plant. Systemic infections are often more damaging as they disrupt the plant’s overall physiology.
• Tissue Specificity: Some pathogens are highly specific to certain tissues, such as root, leaf, or vascular tissue, while others can infect a wide range of tissues. This tissue specificity often determines the symptoms and severity of the disease.

Defense Mechanism in Plants

Plants generally defend against pathogens in two ways- Structural characteristics which act as physical barriers and chemical reactions or chemical barriers.

Structural Defense Mechanism

These may be pre-existing i.e. which exist before the pathogen comes in contact with the plant or can be induced.

a. Pre-existing structural defense mechanism

Various types of pre-existing structural defenses are as follows:

1. Cuticle Layer– 

Cuticle: The cuticle is a hydrophobic layer made of cutin, a waxy substance that covers the epidermis of leaves, stems, and fruits. It acts as a primary barrier against water loss and pathogen entry. The thickness and composition of the cuticle can vary depending on environmental conditions and the plant species, offering a strong defense against fungal spores and bacteria that try to adhere to the plant surface.

2. Epidermal Cell Walls– 

The outer layer of the plant, composed of epidermal cells, is fortified with a robust cell wall made of cellulose, hemicellulose, and pectin. This wall serves as a rigid barrier against pathogen entry. In some cases, the cell walls are further reinforced with lignin, suberin, or other phenolic compounds, making them even more resistant to penetration by pathogens.

3. Stomata and lenticels–

Stomatal: Stomata are small pores on the leaf surface that facilitate gas exchange. However, they can also be entry points for pathogens, particularly bacteria and fungi. Plants can close their stomata in response to Pathogen-Associated Molecular Patterns (PAMPs), reducing the chances of pathogen entry. This rapid closure is part of the plant’s innate immune response to environmental cues signaling a potential infection.

Lenticels: Lenticels primarily function in gaseous exchange but pathogens can easily enter through it so for the prevention, small and suberized lenticels are produced to offer resistance to the pathogen.

4. Trichomes (Plant Hairs)- 

Trichomes are hair-like outgrowths from the epidermis that can serve multiple defensive functions. They can physically deter herbivores by making the plant surface less palatable or difficult to navigate. Some trichomes are glandular and can secrete toxic or sticky substances that trap and kill small insects or deter feeding by larger herbivores.

5. Structural Adaptations in Seeds and Fruits

Seed Coats: The hard, impermeable seed coat protects the embryo from pathogens and physical damage. The composition of the seed coat can vary, with some being particularly thick and lignified, making them more resistant to invasion.

Fruit Skins: The outer skin of fruits, like the peel of citrus or the skin of grapes, provides a protective barrier against microbial invasions.

b. Induced structural defenses

1. Bark and Cork Layers–

Some pathogens induce plants to form several layers of cork cells beyond the point of infection inhibit the invasion and also block the spread of toxin substances secreted by the pathogen. The cork layer also stops the flow of nutrients from healthy to infected areas.

2. Tyloses and gum deposition-

Tyloses: These are balloon-like outgrowths from parenchyma cells into xylem vessels. They block the vessels and prevent the spread of pathogens, particularly in the case of vascular wilt diseases.

Gum Deposition: Some plants produce gums or resins in response to injury or infection. These substances can seal off wounds or infected areas, preventing the spread of pathogens and limiting their ability to colonize the plant tissues.

3. Suberin and Callose Deposition–

Suberin: Found in the cell walls of cork cells and certain roots, suberin acts as a waterproof barrier that protects against pathogen entry.

Callose: Callose is a polysaccharide deposited in the cell walls of plants in response to biotic and abiotic stress. It accumulates at sites of infection, such as at the plasmodesmata to limit pathogen spread.

4. Abscission layer– It consists of a gap between infected and healthy cells of a leaf surrounding the locus of infection due to the disintegration of the middle lamella of the parenchymatous tissue.
5. Cellular defense- These are the biochemical mechanisms that develop at the cellular level. It includes thickening of cell walls to ensheath the hyphae of the pathogen. It is the last line of structural defense.

Biochemical defense mechanisms

These can be classified as pre-existing and induced biochemical mechanisms-

a. Pre-existing biochemical defenses

1. Inhibitors released by the plant in the environment– Plants exude a variety of molecules such as amino acids, glycosides, flavones, alkaloids, and also certain growth factors. These molecules directly affect the pathogen and may act antagonistically. Example- Scales of red onion contain the phenolic compound, protocatechuic acid, and catechol, which diffuse out and inhibit the germination of onion smudge fungus.
2. Inhibitors present in plant cells– Antimicrobial substances such as unsaturated lactones, cyanogenic glycosides, phenols, fatty acids, various enzymes, etc. are present in the cells which may also act as antagonists to pathogens. Example- Chlorogenic acid in potatoes inhibits some bacteria like Streptomyces scabies.

b. Post-infectional or induced biochemical defenses

1. Phytoalexins- These are toxic antimicrobial substances produced in certain amounts only after stimulation by pathogens or by mechanical or chemical injury. Phytoalexins are not produced in healthy plants but are produced by cells adjacent to damaged cells. These are not produced during compatible biotrophic infections. Phytoalexins are fungi toxic and bacteriostatic at low concentrations and synthesis can be seen in families like Malvaceae, Solanaceae, Chenopodiaceae, Compositae, Graminae, and Leguminosae.
2. Hypersensitive response (HR) – Hypersensitive response is localized induced cell death in the host plant at the site of infection, thus limiting the growth of the pathogen. HR occurs only in incompatible host-pathogen interactions. It is initiated by recognition of specific molecules produced by the pathogen which are known as elicitors. During HR, as soon as the pathogen establishes contact with the host cell, the nucleus moves towards the pathogen and soon disintegrates. Brown-coloured granules are formed in the cytoplasm and the brown discoloration continues to spread around the invading pathogen till the invasion is stopped.
3. Systemic Acquired Resistance (SAR): SAR is a resistance produced in the whole plant that involves the upregulation of PR proteins and other defense mechanisms throughout the plant body, providing long-lasting protection against a broad spectrum of pathogens.
4. Plantibodies- Some genetically modified plants have certain genes incorporated in their genome which can produce antibodies that are encoded by animals but produced in the plant against pathogens. 
5. Oxidative burst and generation of NO: The plant generates reactive oxygen intermediaries ROI which include O₂-, H₂O₂, and OH–. They directly combine with NO causing a hypersensitive response.

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