Principles Of Plant Disease & Nematode Management Notes PDF

Principles of Plant Disease and Nematode Management PAT 201 (1+1) UNIVERSITY OF AGRICULTURAL AND HORTICULTURAL SCIENCES, SHIVAMOGGA II B.Sc., Hons (Agri.) Course...

Principles of Plant Disease and Nematode Management PAT 201 (1+1) UNIVERSITY OF AGRICULTURAL AND HORTICULTURAL SCIENCES, SHIVAMOGGA II B.Sc., Hons (Agri.) Course Number: PAT 201 Credit hours (1+1) Synoptic Notes Principles of Plant Disease and Nematode Management Prepared by Dr.Narasimhamurthy H B Assistant Professor Department of Plant Pathology College of Agriculture, Shivamogga University of Agricultural and Horticultural Sciences, Shivamogga- 577204 2020 Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) COLLEGE OF AGRICULTURE, SHIVAMOGGA DEPARTMENT OF PLANT PATHOLOGY Course No. : PAT 201 Course Title: Principles of Plant disease and Nematode Management Credit hours: 2(1+1) Objectives : To import knowledge on plant pathogens that causes diseases in plants and their management COURSE OUTLINE Lecture No. TOPIC THEORY Defense mechanism in plants: structural, biochemical (pre and post-infection) and Lecture-1 host resistances Effect of plant pathogens on plant physiological process viz, photosynthesis, Lecture 2 respiration, translocation and transcription Epidemiology: Epidemics and factors affecting disease development, patterns of Lecture-3 epidemics and disease progress curves Lecture-4 Forecasting, Survey, surveillance and remote sensing of plant diseases Seed Pathology: Importance of seed health to man and animals, seed borne nature Lecture-5 of pathogens, Identification and detection of seed borne pathogens. Lecture-6 Assessment of disease severity and crop losses. Principles and methods of plant disease management: Avoidance of the pathogen, Lecture-7 Exclusion of inoculums, Eradication of pathogens, Biological methods of disease control, cross protection Chemical methods of plant disease management: Classification of fungicides, Lecture-8 bactericides and nematicides, mode of action, formulations and methods of applications. Lecture-9 Diagnosis of Plant diseases Lecture-10 Breeding for disease resistance Lecture-11 Biotechnological approaches of disease management and IPR related issues Nematodes: General morphology and reproduction, classification, symptoms and Lecture-12 nature of damage caused by Plant Parasitic Nematodes (PPNs) Integrated Disease management (IDM): Introduction, History, Importance & Lecture-13 concepts Lecture-14 Insect vector management PRACTICALS Practical-1 Methods and detection of different plant pathogens Practical-2 Methods for estimation of crop losses and disease severity Practical-3 Methods for detection and identification of seed borne pathogens Practical-4 Isolation of biocontrol agents Practical-5 Testing the efficacy of biocontrol agents by dual culture technique Practical-6 Mass multiplication of biocontrol agents Practical-7 Methods of application of biocontrol agents Practical-8 Study of fungicides, bactericides and nematicides and their formulations Practical-9 Preparation of Bordeaux mixture and calculation of fungicide concentration Practical-10 Bioassay of fungicides and antibiotics Practical-11 Methods of application of chemicals Practical-12 Study of pesticides compatibility and their safe use Practical-13 Study of plant protection equipments Practical-14 Methods of screening for disease resistances Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) DEFENSE MECHANISM IN PLANTS Plants represent a rich source of nutrients for many organisms including fungi, bacteria, virus, nematodes, insects, and vertebrates.Plant lacking an immune system comparable to animals.Plants have developed a stunning array of structural, chemical and protein-based defenses designed to detect invading organisms and stop them before they are able to cause extensive damage. In general plants defend themselves against pathogens by two ways: 1. Structural characteristics that act as physical barriers 2. Biochemical reactions that take place in cells and tissues that are either toxic to the pathogen or create conditions that inhibit the growth of the pathogen in the plant. The combinations of structural characteristics and biochemical reactions employed in the defense of plants are different in different host–pathogen systems. Flow chart of defence mechanism in plants 1. Structural defense mechanisms : These may be pre-existing, which exist in the planteven before the pathogen comes in contact with the plant or induced, i.e, even after the pathogen has penetrated the preformed defense structures, one or more type of structures are formed to protect the plant from further pathogen invasion.  First line of defense of defense mechansim  The surface of the plant or host is first line of defense against the pathogen.  The pathogen must adhere to the surface and penetrate, if it is to cause infection. Two type A) Pre-existing structural defense mechanism B) Post-infectional or induced structural defense A) Pre-existing structural defense structures These includes 1. Amount and quality of wax and cuticle 2. Thickness of cuticle 3. Structure of epidermal cell wall 4. Size, location and shapes of natural openings (stomata and lenticels) and 5. Presence of thick walled cells in the tissues of the plant that hinder the advance of the pathogen. 6. Sclerenchyma cells, trichomes 7. Lenticells i) Waxes:  Is the mixture of long chain of a polar lipid  It forming a protective coating on leaves and fruits  Synthesized by epidermis  Play defensive role by forming hydrophobic or water repellent surfacepreventing the germination of fungi and multiplication of bacteria. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) ii) Cuticle and epidermal cells:  A thick cuticle and tough outer wall of epidermal cellsmay increase resistance to infection in diseases in which the pathogen enters its host only through direct penetration. Example: 1. Disease resistance in Barbery species infected with Pucciniagraministriticihas been attributed to the tough outer epidermal cellswith athick cuticle. 2. In linseed, cuticle acts as a barrier against Melampsoralini. 3. The silicification and lignifications of epidermal cells offers protection againstPyriculariaoryzaeand Streptomyces scabies in paddy and potato, respectively. iii) Sclerenchyma cells:  The sclerenchyma cells in stems and leaf veins  It composed of thickened walls of lignin.  Brittle cells help in mechanical support of the plant.  Effectively blocks the spread of some fungal and bacterial pathogens that cause angular leaf spots. iv) Structure of natural openings: a) Stomata:  Most of the pathogens enter plants through natural openings.  Somepathogens like stem rust of wheat can enter its host only when the stomata are open.  The wheat varieties (Cultivar, Hope) in which stomata open late in the day are resistant as the germ tubes of the spores germinating in the night dew desiccate owing to evaporation of the dew before stomata begin to open. This can also be called as functional resistance.  The Structure of stomata provides resistance to penetration by certain plant pathogenic bacteria. Ex: The citrus variety, szinkum, is resistant to citrus canker because it posses a broad cuticular ridge projecting over the stomata and a narrow slit leading to the stomatal cavity thus preventing the entry of bacterial cells into the interior of the leaf. b) Lenticels:  Lenticels are opening in outer walls involved in gaseous exchange.  They are weak points in defense unless the cork cells within them are suberized. After suberizatoin and periderm formation, lenticels are more resistant to invasion by pathogens.  Lenticelsareopeningsonfruit, stem and tubers that are filled with loosely connected cells that allow the passage of air.  Shape and internal structure of lenticels can increase or decreasethe incidence of fruit diseases. Ex: Small and suberised lenticels will offer resistance to potato scab pathogen, Streptomyces scabies. B) Post-infectional structural defense mechanisms/Induced structural barriers:  Most pathogenmanage to penetrate theirhosts throughwounds and natural opening and to produce various degree of infection.  Pathogenpenetrationthroughthehostsurfaceinducedthestructural defense mechanism in the host cells. These may be regarded as 1. Histological defense barriers (cork layer, abscission layers,tyloses and and Gum deposition) and 2. Cellular defense structures (Swelling of cell wall of epidermal cells, Hyphal sheathing). Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) 1. Histological defense structures a) Cork layer:  Infection by fungi, bacteria, some viruses and nematodes induce plants toform several layers of cork cells beyond the point of infection and inhibits the further invasion by the pathogen beyond the initial lesion and also blocks the spread of toxin substances secreted by the pathogen.  Furthermore, cork layers stop the flow of nutrients and water from the healthy to the infected area and deprive the pathogen of nourishment. Ex:1. Potato tubers infected by Rhizoctonia; 2. Prunusdomestica leaves attacked byCoccomycespruniphorae. b) Abscission layers  An abscission layer consists of a gap formed between infected and healthy cells of a leaf surrounding the locus of infection due to the disintegration of the middle lamella of parenchymatous tissue.  Gradually, infected area shrivels, dies, and sloughs off, carrying with it the pathogen.  Abscissionlayersareformedonyoungactiveleavesofstone fruits infected by fungi, bacteria or viruses. Ex: Xanthomonaspruni,and Closterosporiumcarpophylumon peach leaves. c) Tyloses  Tyloses are the overgrowths of the protoplast of adjacent living parenchymatous cells, which protrude into xylem vessels through pits.  Tyloses have cellulosic walls and areformed quickly ahead of the pathogen and may clog the xylem vessels completely blocking the further advance of the pathogen in resistant varieties. In susceptible varieties, few or no tyloses are formed ahead of pathogen invasion. Ex:Tyloses form in xylem vessels of most plants under invasion by most of the vascularwilt pathogens. d) Gum deposition:  The gums and vascular gels quickly accumulate and fill the intercellular spaces or within the cell surroundings the infection thread and haustoria, which may starve or die.  Various types of gums are produced by many plants around lesions after infection by pathogen or injury.  Gums secretion is most common in stone fruit trees but occurs in most plants. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1)  Generally these gums are exudated by plant under stressed condition.  Gummosis is the process in which gum produced by the plants and trees. Ex: In plum: Silver leaf of plum (Stereumpurpureum) 2. Cellular defense structures: a) Hyphal sheathing:  The hyphae penetrating the cell wall and growing into the cell lumenare enveloped by a cellulosic sheath (callose) formed by extension of cell wall, which become infused with phenolic substances and prevents further spread of the pathogen. Ex:Hyphal sheathing is observed in flax infected with Fusariumoxysporumf.sp. lini. Different defense structures developed after infection; A) Gum deposition in cells; B) Abscission layer; C) Tyloses; Formation of sheath around developing hyphae; (E, F) Development of cork layer in tuber (E) and leaf (F) II) Biochemical defense mechanisms: These can be classified as pre-existing andinduced biochemical defenses. 1) Pre-existing chemical defenses:  Structural characteristics may provide a plant with various degree of defense against attacking pathogens.  It is clear that the resistance of a plant against pathogen attack depends not so much on its structural barriers as on the substances produced in its cell before or after infection.  Before infection or penetration of pathogens, host released some chemicals to defend themselves. Two types a) Inhibitors released by the plant in its environment:  Plants exude a variety of leaf and root exudates which contain aminoacids, sugars, glycosides, organic acids, enzymes, alkaloids, flavones, toxic materials, inorganic ions and also certain growth factors.  The inhibitory substances directly affect micro-organisms or encourage certain groups to dominate the environment which may act as antagonists to pathogen. Examples: 1. Tomato leaves secrete exudates which are inhibitory to Botrytis cinerea 2. Red scales of red onion contain the phenolic compounds, protocatechuic acid and catechol, which diffuse out to the surface and inhibits the conidial Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) germination of onion smudge fungus,Colletotrichumcircinans. However, these fungitoxic phenoliccompounds are missing in white scaled onions. 3. Resistant varieties of apple secrete waxes on the leaf surface which prevents the germination of Podosphaeraleucotricha (powdery mildew of apples). 4. In Cicerarietinum (chickpea), the Ascochyta blight resistant varieties have more glandular hairs which have maleic acid which inhibit spore germination. 5. Resistant varieties of linseed secrete HCN in roots which are inhibitory to linseed wilt pathogen, Fusariumoxysporumf.sp. lini. 6. Root exudates of marigold contain α-terthinyl which is inhibitory to nematodes. 7. Chlorogenic acid present in sweet potato, potato and carrot inhibits Ceratocystisfimbriata. Similarlycaffeic acidandphloretinare present in sweetpotato and apple, respectively. b) Inhibitors present in plant cells before infection:  It is becoming increasingly apparent that some plants are resistant to disease caused by certain pathogens of an inhibitory compound present in the cell before infection.  It stored in vacuoles of plant cells.  Antimicrobial substances pre-existing in plant cells include unsaturated lactones, cyanogenic glycosides, Sulphur containing compounds, phenols, phenolic glycosides and saponins  Several phenolic compounds, tannins, and some fatty acid like compounds such as dienes, which are present in high concentrations in cells of young fruits, leaves orseeds are responsible for the resistance of young tissues to Botrytis. These compounds are potent inhibitors of many hydrolytic enzymes.  Ex: Chlorogenic acid in potato inhibits common scab bacteria, Streptomyces scabies, and to wilt pathogen, Verticilliumalboatrum  Saponins have antifungal membranolytic activity which excludes fungal pathogensthat lack saponinases. Ex: Tomatine in tomato and Avenacin in oats  Similarly, lectins, which are proteins that bind specifically to certain sugars and occur in large concentrations in many types of seeds, cause lysis and growth inhibition of many fungi.  Plant surface cells also contain variable amounts of hydrolytic enzymes such as glucanases and chitinaseswhich may cause breakdown of pathogen cell wall. 2) Post inflectional or induced defense mechanisms: a) Phytoalexins (Phyton= plant; alexin= to ward off)  Muller and Borger (1940) first used the term phytoalexins for fungistatic compoundsproduced by plants in response to injury (mechanical or chemical) or infection.  Phytoalexins are toxic antimicrobial substances produced in appreciable amounts in plants only after stimulation by phytopathogenic micro- organisms or by chemical or mechanical injury.  Phytoalexins are not produced during compatable reaction.  Phytoalexins are not produced by uninfected healthy plants, but produced by healthy cells adjacent to localized damaged or necrotic cells in response to materials diffusing from the infected cells. These are not produced during compatible biotrophic infections.  Phytoalexins accumulate around both resistant and susceptible necrotic tissues. However, resistance occurs when one or more phytoalexins reach a concentration sufficient to restrict pathogen development. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Characteristics of phytoalexins 1. Fungitoxic and bacteriostatic at low concentrations. 2. Produced in host plants in response to stimulus (elicitors) and metabolic products. 3. Absent in healthy plants 4. Remain close to the site of infection. 5. Produced in quantities proportionate to the size of inoculum. 6. Produced in response to the weak or non-pathogens than pathogens 7. Produced within 12-14 hours reaching peak around 24 hours after inoculation. 8. Host specific rather than pathogen specific. Synthesis and accumulation of phytoalexins are shown in diversified families, viz., Leguminosae, Solanaceae, Malvaceae, Chenopodiaceae, Convolvulaceae, Compositae and Graminaceae. S.No. Phtoalexin Host Pathogen 1 Pisatin Pea Monilinia fructicola 2 Phaseolin Frenchbean Sclerotinia fructigena 3 Rishitin Potato Phytophthora infestans 4 Gossypol Cotton Verticillium alboatrum 5 Cicerin Bengalgram Ascochyta rabiei 6 Ipomeamarone Sweet potato Ceratocystis fimbriata 7 Capsidol Pepper Colletotrichum capsici b) Hypersensitive response (HR)  The term hypersensitivity was first used by Stakman (1915) in wheat infected by rust fungus, Puccinia graminis.  The hypersensitive response is a localized induced cell death in the host plant at the site of infection by a pathogen, thus limiting the growth of pathogen. In the infected plant part, HR is seen as water soaked large sectors which subsequently become necrotic and collapsed.  HR occurs only in incompatible host-pathogen combinations. HR may occur whenever virulent strains or races of pathogens are injected into non-host plants or into resistant varieties, and when avirulent strains or races of pathogens are injected into susceptible cultivars.  HR is initiated by the recognition of specific pathogen-produced signal molecules, known as elicitors. Recognition of the elicitors by the host results in altered cell functions leading to the production of defense related compounds. The most common new cell functions and compounds include:  A rapid burst of oxidative reactions + +  Increased ion movement, especially of K and H through cell membrane  Disruption of membranes and loss of cell compartmentalization  Cross-linking of phenolics with cell wall components and strengthening of plant cell wall  Production of antimicrobial substances such as phytoalexins and pathogenesis- related proteins (such as chitinases) Cellular responses during HR  In many host-pathogen combinations, as soon as the pathogen establishes contact with the cell, the nucleus moves toward the invading pathogen and soon disintegrates.  Brown resin like granules form in the cytoplasm, first around the point of penetration of pathogen and then throughout the cytoplasm  As the browning discolouration of the cytoplasm continues and death sets in, the invading hypha begins to degenerate and further invasion is stopped. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Pathogenesis-Related Proteins  Pathogenesis-related proteins, often called PR proteins, are a structurally diverse group of plant proteins that are toxic to invading fungal pathogens.  They are widely distributed in plants in trace amounts, but are produced in much greater concentration following pathogen attack or stress.  PR proteins exist in plant cells intracellularly and also in the intercellular spaces, particularly in the cell walls of different tissues.  They are either extremely acidic or extremely basic and therefore are highly soluble and reactive.  Seventeen families (Van Loon et al., 2006).  Inhibit the invading pathogens by their enzymatic activities  The signal compounds responsible for induction of PRPs include salicylic acid, ethylene, xylanase, the polypeptide systemin and jasmonic acid. The several groups of PR-proteins have been classified according to their function, serological relationship, amino acid sequence, molecular weight and certain other properties. Van Loun and Van Kammen (1970) worked on discovery of PR proteins -while working on HR of tobacco plants infected- TMV.Pathogenesis-related proteins are present in low levels. Production of PR proteins lead to the occurrence of systemic acquired resistance. 17 novel proteins have been identified till now. Pathogenesis-related proteins include β-glucanase, chitinase or lysozyme activity. Some are related to plant defensins while others are proteinase inhibitors that disrupt pathogen nutrition. Pathogenesis related proteins are sometimes present in low levels before infection and are induced following stress, wounding or flowering, indicating that they may have a wider function in plant growth and development than just disease resistance. Chitinase and glucanase accumulate in vacuoles, although some glucanase is secreted to the intercellular space. Characteristics of PR Proteins  Initially named “b” proteins (also known as stress proteins)  Present intercellularly or intracellularly  They are extreamly acidic or basic, therefore, well soluble and reactive  Different plant organs, e.g., leaves, seeds, and roots, may produce different sets of PR proteins.  There are several isoforms formed in different host plants  They are high molecular weight proteins that are constituively present, in order to inhibit spore germination and its release  There are 17 PR- proteins, typically  Size of different proteins, typically ranging from 5 to 75k Da.  Involved in Systemic Acquired Resistance (SAR) in plants Pathogenesis-Related Proteins Family Type /Member Properties Target pathogen site PR-1 Tobacco PR-1a Antifungal Active against Oomycetes PR-2 Tobacco PR-2 β-1,3-glucanase Cell wall glucan of fungi PR-3 Tobacco P,Q Chitinase type I,II,IV,V,VI,VII Cell wall chitin of fungi PR-4 Tobacco R Chitinase type I,II Cell wall chitin of fungi PR-5 Tobacco S Thaumatin like protein Active against Oomycetes PR-6 Tomato Inhibitor-I Protease inhibitor Active on nematodes and insects PR-7 Tomato P69 Endoproteinase Microbial cell wall dissolution Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Cell wall chitin of fungi, and PR-8 Cucumber chitinase Chitinase type III mucopeptide wall of bacteria Tobacco lignin forming PR-9 Peroxidase * peroxidase PR-10 Parsley PR-1 Ribosome inactivating protein Viral- RNA PR-11 Tobacco class V chitinase Chitinase type I Cell wall glucan of fungi PR-12 Radish R5 AFP-3 Defensins Antifungal and antibacterial activity PR-13 Arabidopsis TH.12-1 Thionins Antifungal and antibacterial activity PR-14 Barley LTP-4 Lipid transfer protein Antifungal and antibacterial activity Produces H2O2 that inhibits PR-15 Barley OxOa (germin) Oxalate oxidase microbes and also stimulates host defense Produces H2O2 that inhibits Oxalate oxidase-like with PR-16 Barley OxOLP microbes and also stimulates host superdismutase activity defense PR-17 Tobacco PRp27 Uncharacterized Unknown Occurrence & Molecular nature  The first PR- 1 protein was discovered in 1970. in tobacco TMV by Van Loon and Kammen, 1970)  identified in Arabidopsis, Barley, Tobacco, Rice, Pepper, Tomato, Wheat, Maize  These PR-1 having 14 to 17 kD molecular weight and mostly of basic nature.  PR-1 proteins have antifungal activity at the micromolar level against a number of plant pathogenic fungi, including Uromyces fabae, Phytophthora infestans, and Erysiphe graminis. Mode of action  Strengthening of host cell walls to prevent spread of the Pathogen  Inhibitory function on growth of the pathogen  In tomato leaves inhibit germination of zoospores and pathogenicity of Phytophthora infestance Plantibodies What are plantibodies??  A plantibody is a Antibody produce by genetically modified plant.  Antibody are part of Animal immune system, and produce in plant by transforming them with Antibody genes from Animals.  This was first done in 1989, with a mouse antibody made by Tobacco plant.  Mouse genes that produce antibodies against certain plant pathogens.  It shown in transgenic plant. Ex:- Artichoke mottled crinkle virus Full size monoclonal antibodies recently produced in transgenic plants Induced Resistance: Plants have evolved number of inducible defense mechanisms against pathogen attack. Induced Resistance (IR) is enhancement in the resistance of susceptible plant in response to an external pathogen without alteration in the genome.  Depending upon its mode of expression IR can be systemic or local.  Recognition of a pathogen triggers a localized resistance reaction as hypersensitive reaction, which is characterized by rapid cell death at site of infection.  Increased expression of natural defense mechanisms of plants against different pathogen provoked by external factors of various and manifested upon subsequent inoculation Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Systemic Aquired Resistance (SAR) can be triggered by exposing the plant to virulent, avirulent and non-pathogens and chemicals which is dependent on the accumulation of PR-proteins and salicylic acid (SA) throughout the plant. ISR is potentiated by plant growth promoting rhizobacteria (PGPR), dependent of the ethylene and jasmonate, but independent of SA and is not associated with the accumulation of PR proteins (Singh et al., 2002). Types of Induced Resistance 1. Systemic aquired resistance (SAR) , (Ross, 1961) 2. Induced systemic resistance (ISR) (Kuc et al.,1970) Difference between ISR and SAR ISR SAR No visible symptom Association with necrosis Does not required Salicylic acid Expression of SAR dependent on the accumulation of Salicylic acid It is without production of PR protein It is associated with the production of PR-protein It is dependent on the Jasmonic acid and SAR may not be involved JA and ET signaling. Ethylene signaling ISR usually induced by the non-pathogenic SAR generally induced by pathogen/chemical Mo‟s mediated resistance Host induction Pre challenge induction of defence As a result of resistance induction it is logical to assume that the genes involved in the enhanced state of resistance have been induced or expressed to a greater extent. In SAR PR-proteins have antifungual activity or they can degrade fungal cell wall in vitro. 1. Recently, Prats et al., 2002 they reported that resistance activator acibenzolar methyl (ASM) this induced resistance to prior treatment in case of Puccinia helianthi (Sunflower Rust) because ofCoumarin increased in leaf and germination of urediospores and appresorial formation rate is reduced. 2. Cucumber plants treated with silicon or giant knot weed extraction or PGPR - induced resistance to Powdery mildew and Pythium. Post challenge induction of defence Cucumber plants shows resistance against Colletotrichum arbicularia, Cladosporium cucumerium due to deposition of lignin which is more at the pint of site of infection. Phytoalexins production, cell wall alterations, hypersensitivity are also observed in induced plants after fungal infections. Examples commercially available induced resistance products; Product name Recommended as Disease Actigard/boost (Functional analogue Sclerotinia stem rot of of salicylic acid and acibenzolar Seed treatment and foliar spray Soybean methyl BABA-Beta amino butyric acid Foliar spray Downy mildew (Non protein amino acid) Akomin (Organic and inorganic Koleroga of arecanut, downy naturally occurring compound) Foliar sspray mildew of grape, betelvine Contains Phosphoric acid rots PGPR – Biological inducer Seed treatment and soil treatment Soil borne pathogens Diphenyl ester lactophen (Herbicide) It can able to block Seed treatment and foliar spray Sclerotinia stem rot Protoporphynogen oxidase because of accumulation of phytoalexins Benzoisothiazole/ probenazole Downey mildew (Induces accumulation of salicylic Foliar spray (Peranospora parasitica) acid and PR-Proteins) Application of Induced resistance:  It should be compatible with current agriculture practices.  It should be easy for application.  It should be reliable.  Product developed as a resistance activator but not as a microbial compound. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) EFFECT OF PLANT PATHOGENS ON PHYSIOLOGY OF PLANTS While necrotrophs have little effect on plant physiology, since they kill host cells before colonising them, biotrophic pathogens become incorporated into and subtly modify various aspects of host physiology, such as respiration, photosynthesis, translocation, transpiration and growth and development. What is Plant Physiology?  Plant physiology is the science which deals with the life processes of plants, or it deals with the functions of cells, tissues, organs or the plant as a whole.  Plant disease is an outcome of interaction between host and the pathogen.  Depending on the pathogen, plant organ and the tissue they infect interfere with the different physiological functions of the plant. The physiological function includes 1. Photosynthesis 2. Respiration 3. Transpiration 4. Transcription 5. Translation 6. Permeability of cell membrane 7. Translocation of water and nutrients Harmful effects caused by pathogens on physiology of plants  Disintegration of tissues.  Abnormal respiration.  Effect on growth due to hormonal imbalance.  Root pathogens affect translocation resulting in wilting and finally death of plants.  Foliar pathogens infect aerial parts thereby destroy chlorophyll formation, leading to reduced photosynthesis. 1. Effect on photosynthesis  In leaf spots, blights and foliar diseases- destruction of leaf tissues, thereby reducing photosynthesis.  Reduced amount of photosynthetic surface.  Chlorophyll degradation.  Stomata remain partially closed.  Produce toxins that inhibit enzymes. Ex: Ten toxin, tab toxin Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) 2. Effect on respiration  Affected tissue will take more reserve carbohydrate than healthy tissue (Increased respiration decrease in plant reserve).  Accumulation and oxidation of phenols also increases.  Respiration rate continuous to raise during multiplication and sporulation of the pathogen. Then, declines to normal or below the normal level.  Change in metabolism and protoplasmic streaming. Ex: Blast, Powdery mildews and Rusts. 3. Effect on transpiration  Disintegration of cuticle  Increased respiration  Disfunctioning in permeability of leaf cells.  Ex: Powdery mildew- epidermal cells invaded, Rust- rupture of epidermis Blight- number of active cells reduced 4. Effect on cell permeability  Cell membrane disruption leads to membrane disruption.  Enzymatic degradation and toxins production.  Membrane permeability- first detectable response to infection.  Membrane damage and leakage of electrolytes - secondary effect.  Ex: Fusicoccin produced by Fussicoccum amygdali activates membrane ATPase and disrtupts solute fluxes.  Sclerotium rolfsii- produces lipid degrading enzymes.  Rhizoctonia solani- degrades protein. 5. Effect on translocation of water and nutrients  Roots absorb less water and affects the function of root.  Flow of nutrients or water blocked.  Interfere with translocation functions of plant by causing excessive transpiration.  Ex: Root damage- Pythium and Rhizoctonia sp.  Xylem destruction- Canker/rot pathogens, gall formations  Xylem clogging(secretion of tyloses)- Fusarium, Verticillium Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) 6. Effect on Transcription  Disturbance in any transcription and translation process may effect the following: Expression of genes and cause a drastic unfavorable change in the structure and function of affected cells.  Some pathogens change composition, structure or function associated with chromatin.  Increase in activity of enzymes breaks down RNA. Ex: In biotrophic infections.  Higher energy needs- Increased activity in enzymes.  Increased production of phenols- used in defense reaction.  Resistant plants have increased protein synthesis in first few minutes of infection. PLANT DISEASE EPIDEMIOLOGY Edpidemiology or epiphytology is the study of the outbreak of disease, its course, intensity, cause and effects and the various factors governing it. Based on the occurrence and geographical distribution they are classified as follows: Endemic or Enphytotic When a disease is more or less constantly occurring year after year in a moderate to severe form in a country or locality then it is called as endemic disease. eg: wart disease of potato (Synchytrium endobioticum) is endemic in Darjeeling, citrus canker (Xanthomonas axonopodis pv citri)in Asia and sorghum rust (Puccinia purpurea). Epidemic or Epiphytotic It is a sudden outbreak of a disease periodically over a widespread area in a devastatingly severe form causing severe losses or complete destruction. This is constantly present in a locality but it assumes severe form only on occasions. This is because of the occurrence of favorable environment responsiblefor the rapid development of disease. eg: wheat stem rust (Puccinia graminis tritici) and powdery mildew (Erysiphe graminis vor tritici), late blight of potato (Phytophthora infestans), red rot of sugar cane (Colletotrichum falcatum), downy mildew of grapevine( Plasmophora viticola) and rice blast (Pyricularia oryzae). Certain disease are endemic in one area and become epidemic in another area. Eg: Citrus canker is endemic in Asia but epidemic in the introduced place, Florida (U.S.A).The downy mildew of corn is a endemic disease in India but became epidemic in the Philippines. Pandemic When an epidemic disease spreads over continents or subcontinents and involves mass mortality it is considered as pandemic. The outbreak of black stem rust of wheat in India during 1947 is best example for a pandemic disease. Sporadic Diseases which occur at irregular intervals over limited areas or locations are called sporadic. They occur relatively in few instances. Eg: Fusarium wilt of cotton (Fusarium oxysporum f sp. vasiinfectum) grain smut of sorghum (Sporisorium sorghi ) and loose smut of wheat (Ustilago nuda). An epidemic may cause widespread and mass destruction of crop in a short time or may persist for long periods depending upon the three following factors responsible for the disease: Epiphytology or Epidemiology- Appearance of a disease over large areas (on large no. individuals) in relatively short period of time  Epidemiology deals with outbreaks and spread of diseases in a population. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1)  It includes study of the rate of multiplication of a pathogen (which determines the capacity to spread a disease in plant population), characters of spread of disease and factors affecting outbreaks of epidemics; Environmental factors on disease prevalence, incidence, severity, survival and spread of plant pathogens.  Science of disease in populations (Vanderplank,1963). Sl. No. Compound interest disease/ polycyclic Simple interest disease/Monocyclic 1 Rate of increase of disease is Rate of increase of disease is mathematically analogous to compound mathematically analogous to simple interest in money (Interest is added interest in money (Interest is added periodically to the capital; interest gets only at the end; interest does not get interest) interest) 2 Pathogen produces spores at rapid rate Pathogen produces spores at very slow rate 3 Propagules disseminate by air Propagules disseminate by soil or seed 4 Incubation period and sporulation period Incubation period and sporulation is short period is long 5 There are several generations of the There is only one generation of the pathogen in the life of a crop pathogen in the life of a crop 6 Ex: Rusts of cereals Ex: Smuts of wheat, barley & sorghum Importance  of epidemiology:  Knowledge of epidemiology is useful in forecasting of a disease and also for the management of a disease To know how :  Plant disease epidemics occur in nature and how they can be monitored and analyzed.  Plant diseases cause crop losses, how these losses are quantified, and how losses are predicted.  Epidemiology is used to set the strategy of plant disease control.  To use some statistical procedures for quantifying and comparing and predicting epidemics.  Terms compound interest and simple interest diseases were given by Vanderplank (1963) in his book “Plant Disease Epidemics and control” Purpose of epidemiology  Model disease progress  Assess effectiveness of alternative control measures  Predicts disease spread  Predict yield loss  Disease forecasting Disease Triangle: The interactions of three components of disease, i.e., the host,pathogen and environment, can be visualized as a disease triangle. The length of each side is proportional to the sum total of the characteristics of each component that favour disease. The interaction of susceptible host plant, virulent pathogen and favourable environmental conditions leads to the development of the disease. Disease Pyramid: The disease triangle can be expanded to include two morecomponents, time and humans. The amount of each of the three components of disease and their interaction in the development of the disease are affected by fourth component, time. Thus addition of time component to the disease triangle results into a tetrahedron or disease pyramid. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) The effect of time on disease development becomes apparent when we consider the importance of time of year, the duration and frequency of favourable temperature and rain, the time of appearance of the vector, the duration of the cycle of a particular disease. If the four components of disease pyramid could be quantified, its volume would be proportional to the amount of disease on a plant or in plant population. Humans affect disease development in various ways. They affect the type of plants grown in an area, their level of resistance, time of planting, density of planting, etc. Essential components/conditions for an Epiphytotic or factors affecting development of epidemics: 1. Host factors 2. Pathogen factors 3. Environmental factors 1. Host factors i) Distance of susceptible plants from the source of primary inoculum: Longer thedistance from the source of survival of the pathogen, longer will be the time required for the buildup of an Epiphytotic in a susceptible crop. ii) Abundance and distribution of susceptible hosts: Continuous cultivation of asusceptible variety over a large contiguous area helps in the buildup of the inoculum and improves the chances of epiphytotics. iii) Disease proneness in the host due to environment: Susceptibility is geneticallycontrolled but the disease proneness in the plant to get infected can be induced by environment and other factors (Host nutrition, excessive application of nitrogenous fertilizers, etc). iv) Presence of suitable alternate or collateral hosts: These host plants help in thesurvival of inoculum of different pathogens in off season. Presence of Barbery which is an alternate host to Puccinia graminis tritici helps in the heterogenous infection chain. Presence of grass hosts helps in the survival of Pyricularia oryzae in the off-season. 2. Pathogen factors: i) Presence of virulent/aggressive isolate of a pathogen: For any epiphytotic, rapid cycleof infection is essential, and successful infection can be caused only by virulent isolates of the pathogen. ii) High birth rate: The fungi that assume epiphytotic form invariably have the capacityto produce enormous quantity of spores that are adapted to long distance dissemination in a short time. iii) Low death rate of the pathogen: Epiphytotics is attributed to low death rate of thepathogens in those in which the causal agent is systemic and protected by the plant tissues. iv) Easy and rapid dispersal of the pathogen: The ability of a pathogen to causeepiphytotics is much more dependent on its dispersal rate. The units of propagation need to be dispersed by external agencies, if epiphytotics are to develop. Ex: Fungal spores disseminated by wind, water, etc Viruses disseminated by insect vectors Bacteria dispersed through rain splashes and water v) Adaptability of the pathogen: Most of the pathogens causing epiphytotics adaptthemselves to various adverse conditions. 3. Environmental factors (Temperature, humidity, pH and light): Assuming that a particular fungus meets all the above requirementsfor causing an epidemic, the infection, invasion and development of epidemic may not occur if weather is not favourable for the germination of spores. Congenial environmental conditions, viz., optimum weather conditions for sporulation, dispersal, infection and survival of pathogen, are very important. Weather conditions such as, optimum temperature, moisture, light, etc., are very essential for the development of an epidemics. Science which deals with the relationship between weather and epiphytotics is called metereopathology. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Environmental Factors  Temperature  Relative humidity  Rainfall  Duration and intensity of light  These are actually the deciding factors and influence almost all the stages of disease cycle.  Favorable environmental conditions are needed for sporulation, liberation of spores, dissemination of pathogen, germination, infection and establishment of pathogen in the host. 4. Human activities: selection of site, propagative material, disease management practices, cultural practices, introduction of new pathogens. PATTERNS OF EPIDEMICS Interactions among the elements of epidemics, as influenced over time by factors of the environment and by human interference, are expressed in patterns and rates.  Disease–progress curve  Disease gradient curve Disease progress curve The progress of an epidemic measured in terms of the numbers of lesions/ the amount of diseased tissue, or the numbers of diseased plants plotted over time is called the disease progress curve. or This representation of plant disease over time is referred to as a “Disease Progress Curve” (A) Saturation type of curve: monocyclic diseases of different epidemic rates. (B) Sigmoidal curve: Polycyclic disease, such as late blight of potato. (C) Bimodal curve: polycyclic disease, such as apple scab, in which the blossoms and the fruit are infected at different, separate times. Saturation curve Sigmoidal curve Bimodal curve Three monocyclic diseases of Polycyclic disease Polycyclic disease different epidemic rates Eg: wilt, Blackleg of potato, Eg: Late blight of potato Eg: Apple scab in which the Verticillium wilt blossoms and the fruit are Cereal Cyst Nematode infected at different, separate times Saturation Curve Sigmoid curve Bimodal Curve Graphically, disease caused by monocyclic pathogens looks like a “saturation curve”. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Rate of increase of disease over time can be represented by a simple interest function. Disease gradient curve  The progress of an epidemic measured in terms of changes in the number of lesions/ the amount of diseased tissue, and the number of diseased plants as it spreads over distance, is called disease gradient curve (spatial pattern)  The percentage of disease and the scale for distance vary with the type of pathogen or its method of dispersal being small for soil borne pathogens or vectors and larger for airborne pathogens AUDPC: Area under disease progression curve  Area covered during the progress ofthe disease in field.  Area of graph under the time that depicts the progress of epidemic.  It is and integral model which relates the yield loss to sum of measurement of dises over a specific period of crop growth.  AUDPC is a useful to represent quantitative summary of disease intensity over time, for comparison across years, locations, or management tactics Extreme types of Epidemic Slow epidemic (Tardive epidemic)  Occurs in monocyclic diseases  On perennial long lived planrs such as fruit trees.  Infected pathogen survives for several years , epidemics take identical time to reach maximum potential  Pathogen multiplies due to lengthy sporulation period or incubation period  Having low death rate pathogens  E.g. citrus tristeza; Dutch elm disease Fast epidemic (Explosive epidemic)  In polycyclic diseases  Annual crops  Pathogen multiplies fast because of less incubation period  High birth rate resulting several generation with a short span of time  E.g. rice blast, potato blight Decline of epidemics: An epidemic of crop plant , after its full fledge development, and severity, commonly comes to a stage from where it starts declining. The reasons for epidemic to decline;  Saturation of pathogen  Decline proneness in the host plants  Unfavourable wheather condtions  Reduction pathogen agressivenss Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) DISEASE FORECASTING Forecasting involves all activities in ascertaining and notifying the farmers in a community that the conditions are sufficiently favourable for certain diseases, that the application of control measures will result in economic gains or that the disease expected is unlikely to be enough to justify the expenditure of time energy and money to be utilized for its control. Forecasting of plant diseases means predicting for the occurrence of plant disease in a specified area ahead of time, so that suitable control measures can be undertaken in advance to avoid losses. Disease forecasts are predictions of probable outbreaks or increase in intensity of disease. It involves well organized team work and expenditure of time, energy and money. It is used as an aid to the timely application of chemicals. Among the first spray warning services to be established for growers, were the grapevine downy mildew forecasting schemes in France, Germany and Italy in the 1920s. Disease forecasting methods are available for the following plant diseases Generally fore-casting systems are developed against  Those diseases which causes economic losses interms of quality and quantity of the produce e.g.. Apple scab  Those diseases whose occurrence, spread and destructiveness is variable and mostly depends on weather conditions e.g.. Potato late blight  Those diseases whose control measures are known and can be applied effectively and economically by the farmers  Those diseases whose epidemiology is fully known/studied Why Use Forecasting Models? Alternative to calendar spray programs  Enhance timing of fungicide sprays to disease development  Economic benefits (spray reduction)  Environmental benefits (spray reduction) Aims of disease forecasting:  To maxmise the economic returns of the crop  To provide useful tool to farmer for plant disease management  To identify and fillup the lacuna in epidemiological information of a disease Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Requirements for practical gain from forecasting:  The disease causes economically significant loss both in terms of quality & quantity of the produce in concerned area  Disease onset, spread, and epidemic level is highly dependent on weather variables  Farmers follow the advice of control measure when required  Information on weather disease relation ship is fully known.  The crop must be a cash crop (Economic value)  The disease must have potential to cause damage ( Yield losses)  The disease should not be a regular feature (Uncertainty)  Effective and economic control known (Option to the growers)  Reliable means of communication with farmers  Farmers should be adaptive and have purchase power  Control measures must be available at an economically acceptable cost. 3. The disease must vary each season in the timing of the first infections and its subsequent rate of progress. If it does not, there is no need for forecasting.  Growers must have sufficient man power and equipments to apply control measures when disease warning is given. Long-term warnings or predictions are more useful than short-term warning or predictions. Appraoches of Forecast system Short-term: prediction of the disease during the crop season or just before the crop season Long term :prediction of the disease made in year advance Types of Forecast system Positive Forecast: Employs need based chemical sprays, provides adequate protection to crop and reduce damage to environment. Negative Forecast: Avoids unnecessary chemical sprays, no risk to the crop health and no disruption of environment Forecasting system models  Empirical model  Fundamental model  Simulation models Empirical model: Based on experience of scientists, farmers or both Ex: Van Everdigen (1926): Dutch rules to forecasting of late blight of potato. The rulesenumerates the specific meteorological condition that must be fill before disease development takes place. Fundamental model: Involves research and experiment for establishing fruitful researches identifying critical factor and relative there to appearance of the disease amount of the disease and fundamental research is needed. This model is also called derived, inducive or logical system. Fundamental forecasting system is developed based on multiple regression analysis involving several independent biological and weather variables for the progress of an epidemic. Simulation models:  The use of mathematical models to quantitatively reproduce some aspects of the real world.  Use of model in specific conditions and attempt simulations in the aid of computer. It is dynamic and take into account of time factor and review the epidemic behaviour.  Wggoner & Horsfall (1969) Ist computer based simulation of plant disease epidemic is EPIDEM (early blight of tomato)  II nd model is EPIMEY by Wggoner et al., 1972 (southern leaf blight)  EPIPRE by Zodoks 1984: started with Puccinia striformis later its use extended to P.recondita, Erysiphe graminis, Septoria nodurum, S.tritici Simulation models: computer based forecast system  BLITECAST-Late blight of potato  EPIDEM-Early blight epidemics in tomato  EPIVEN-Apple scab  EPIBLAST- Blast of Paddy  MYCOS- Mycospherella leaf spot of chrysanthemum Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1)  PLASMO- Downy mildew of grapes  EPICORN- Maydis leaf blight  In India (UP) for late blight of potato – JHULCAST by Bhattacharya Criteria / Basis of forecasting 1. Forecasts based on assessment of amount of initial inoculum Ex: Stewart‟s wilt of corn, Blue mold of tobacco, Fire blight of apple, pea root rot 2. Forecasts based on weather conditions favoring development of secondary inoculum Ex: Late blight of potato, Tikka leaf spot of groundnut, leaf spots of cereals, pulses, oil seeds, downy mildew of grape, maize, sorghum, cucumber. 3. Forecasts based on amounts of initial and secondary inoculum Ex: Apple scab, leaf rust of wheat, powdery mildew of mango, ber, apple, downy mildew of grape, cercospora leaf spot of banana. Methods of disease forecastings: forecasting systems classified based on the primary and secondary inoculums as; 1. Forecasting based on primary / initial inoculums:  Presence of primary inoculum, its density and viability are determined in the air, soil or planting material.  Occurrence of viable spores or propagules in the air can be assessed by using different air trapping devices (spore traps).  In the case of soil-borne diseases the primary inoculum in the soil can be determined by monoculture method.  Presence of loose smut of wheat, ergot of pearlmillet and viral diseases of potato can be detected in the seed lots at random by different seed testing methods.  Seed testing methods can be used to determine potential disease incidence and enable decision to be made on the need for chemical seed treatment.  The extent of many virus diseases is dependent on the severity of the preceding winter which affects the size of vector population in the growing season. e.g., Sugarbeet yellows virus Ex: Tobacco blue mould, Stewart wilt of corn, Fire blight of apple, Vascularwilts, Pear root rot diseases Criteria / Basis of forecasting: 1. Forecasts based on assessment of amount of initial inoculum Ex: Stewart’s wilt of corn, Blue mold of tobacco, Fire blight of apple, pea root rot 2. Forecasts based on weather conditions favoring development of secondary inoculum Ex: Late blight of potato, Tikka leaf spot of groundnut, leaf spots of cereals, pulses, oil seeds, downy mildew of grape, maize, sorghum, cucumber. 3. Forecasts based on amounts of initial and secondary inoculum Ex: Apple scab, leaf rust of wheat, powdery mildew of mango, ber, apple, downy mildew of grape, cercospora leaf spot of banana. Forecasts based on assessment of amount of initial inoculum 1. Fire blight of apple and pear model: Erwinia amylovora  Occurs in high soil moisture and acidic soil condition. Disease appears before flowering and yield loss will be severe.  The pathogen multiplies much more slowly at temperatures below 15°C than at temperatures above 17°C.  Disease outbreak can be expected to occur in the orchard if the daily average temperatures exceed a “disease prediction line” obtained by drawing a line from 16.7°C on March 1 to 14.4°C on May 1.  Therefore, when such conditions occur, application of a bactericide during bloom is indicated to prevent an epidemic. 2. Stewart’s wilt of corn: Erwinia (Pantoea) stewartii  The pathogen survives the winter in the bodies of its vector, the corn flea beetle. Therefore, the amount of disease that will develop in growing season can be predicted if the number of vectors that survived the previous winter is known, as that allows an estimation of the amount of inoculums that also survived the previous winter. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1)  Corn flea beetles are killed by prolonged low winter temperatures. Therefore, when the sum of the mean temperatures for the three winter months December, January, and February at a given location is less than -1°C, most of the beetle vectors are killed and so there is little or no bacterial wilt during the following growth season. Warmer winters allow greater survival of beetle vectors and proportionately more severe wilt outbreaks the following season. 3. Downy mildew (Blue mold) of tobacco: Peronospora tabacina The disease in most years is primarily a threat to seedbeds in the tobacco- producing states. When January temperatures are above normal, blue mold can be expected to appear early in seedbeds in the following season and to cause severe losses. However, when January temperatures are below normal, blue mold can be expected to appear late in seedbeds and to cause little damage. If the disease is expected in seedbeds, control measures can be taken to prevent it from becoming established, and subsequent control in the field is made much easier. Since 1980, a supplementary blue mold warning system has been operated in North America by the Tobacco Disease Council and the Cooperative Extension Service. The warning system keeps the industry aware of locations and times of appearance and spread of blue mold and helps growers with the timing and intensity of controls. 4. Pea root rot: Pea root rot Caused by Aphanomyces euteiches and in other diseases caused by soil borne fungi and some nematodes, the severity of the disease in a field during a growing season can be predicted by winter tests in the greenhouse. In these tests, susceptible plants are planted in the greenhouse in soil taken from the field in question. If the greenhouse tests show that severe root rot develops in a particular soil, the field from which the soil was obtained is not planted with the susceptible crop. However, fields whose soil samples allow the development of little or no root rot can be planted and can be expected to produce a crop reasonably free of root rot. With some soil borne pathogens, such as fungi Sclerotium and Verticillium and the cyst nematodes Heterodera and Globodera, the initial inoculums can be assessed directly by isolating the fungal sclerotia and nematode cysts and then counting them per gram of soil. The greater the number of propagules, the more severe the disease produced. Forecasts based on weather conditions favoring development of secondary inoculum Forecasting Late blight of potato: Van Everdingen (1926) proposed Dutch Rules  Night temperature below dew point for atleast 4 hours  Minimum temperature of 100C or slightly above  Clouds on the next day  Rainfall during next 24 hours for atleast 0.1 mm (Van Everdingen, 1926) Late blight forecasting in India (West Bengal) Non-rainy years: 7 day moving graph  RH > 85% for > 50 hrs and temp. 7.2 - 26.60C for > 115 hrs.  (If above conditions prevail for 5 consecutive days blight would appear within 7-10 days) Rainy years: 7 day moving graph  Measurable rain (0.1-0.5 mm) for two consecutive days  Five-day moving RH > 85% > 50 hrs  Five days moving congenial temperature (7.2-26.6 0 C) for > 100 hrs.  (If above conditions prevail for five consecutive days blight would appear within 7-10 days) Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) BLITECAST-Late blight of potato BLITECAST is computerized forecast model being operated in the eastern USA. If the inoculum present in field, only weather is monitored for assessing severity. The farmer using BLITECAST inform the computer centre, the following weather parameters using recorded in his agro-metereological observatory installed in between potato rows.  Maximum and min. temp of the day  No. of hours with more than 90% RH  Max and Min temp when RH was 90%  Rainfall during the 24 hrs to 0.1 cm accracy Within 3 mins, the computer analyzes the data recommendations are issued to farmers when to begin spraying. 2. Leaf spots, Leaf spots caused by the fungi Cercospora on peanuts and celery and Exserohilum (Helminthosporium) turcicum on corn, can be predicted by taking into account the number of spores trapped daily, the temperature, and the duration of periods with relative humidity near 100%. An infection period is predicted if high (95–100%) relative humidity lasts for more than 10 hours, and growers are then urged to apply chemical sprays immediately. Forecasts based on amounts of initial and secondary inoculum 1. Apple scab model - Venturia inequalis The amount of initial inoculum (ascospores) and secondary inoculum is conidia. Forecast system based on the leaf wetness, which is require for spore germination and infection at different temperature. If the average day temperature is 28˚C, the leaves must be continuously wet for 14 hrs before infection which is favourable for disease. Apple scab forecast system can predict not only whether an infection period will occur, but also whether the infection periods will result in light, moderate, or severe disease EPIVEN computerized system to monitor environmental conditions and predict apple scab infection periods based on local conditions. Wheat Stem rust: Puccinia Path Puccinia path term was coined by Stalkman in 1934 Nagarajan and Joshi showed Puccinia path in India during 1980. Primary Foci of infection:  There are two foci for black stem rust and leaf rust (Brown rust)  Nilgiri and Palani hills  Himalayan mountain hills  Himalayan mountain hills is only one foci for Yellow rust (Stripe rust)  Movement of uredeospores from foci – can travel 1600 km with in two days there speed is 50-250 km/hr.  In Karnataka first will get leaf rust after 10 days stem rust appears  In North India will get all three types of rust  In South India will get stem rust and leaf rust  Secondary foci of infection for stem rust - Chikkamgalore and chitradurga During 1978, In Karnataka there was epidemic of stem rust in Bijiga yellow variety which having durable resistance. But this variety caused serious epidemic of stem because of 117 A-1 race of stem rust. But this race was not present in nilgiri and palani hills which main or primary foci for infection. Then the scientists/ researchers found secondary foci i.e Chikkamgalore and chitradurga areas where wheat is grown in kharif. Then scientists/ researchers collected the sample in the month of August this race (117 A- 1) was present in off season crop. This shows secondary foci plays important role in Karnataka to cause epidemic for rabi wheat. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) In India Uredeospspores of Puccinia graminis trictic moves from south to north and get deposited with rain drops. Based on this some synoptic maps have developed from October and Novemebr. It shows that when precipitation occurs over central India where washed down the uredeospores based on this 3 synoptic rules were developed called as Indian Stem Rules (ISR). Indian Stem Rules (ISR) given by Nagarajan and Singh.  ISR-1: Storm or depression formed in the Bay of Bengal or in Arbian sea anywhere in the region demarked by latitude 8 to 15º N should gradually move and dissipate over central India. Here the viable uredeospores are deposited all over central India where secondary foci appear. Since this ISR-1 invariably occurs only in November. This ISR situation brings stem rust inoculum causing epidemic.  ISR -2: There should exist a persistent high pressure cell over south central India. This results from precipitation over central India.  ISR -3: A deep trough extending into South India caused by onward movement of western disturbances and associated rainfall over central India known to occur. Because of this condition ISR-2 and 3 will occur after December month there after traces of infection appears. Because of weather condition set in ISR 2 and 3 never able to promote an epidemic. Based on this Nagarajan and Singh confirmed the occurrence of tropical uredeospores of some race moved to rabi wheat cause disease but it is not in nilgiri and palani hills. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) REMOTE SENSING Remote sensing is estimating an object/phenomenon without being in physical contact with it. Remote sensing is a science/art that permits us to obtain information about an object/a phenomenon through analysis of data obtained through sensory devices without being in physical contact with that object. Objectives of remote sensing in plant Pathology 1. Assessment of disease over a vast area 2. To know the relationship of diseases and environment 3. To know the origin and development of epidemics 4. Quantitative assessment of the disease Remote sensing techniques of importance to Plant Pathology 1. Aerial photography and 2. Satellite remote sensing 1. Aerial photography: Aerial photography can detect objects on land over a larger area. Colwell (1956) first used remote sensing technique for monitoring stem rust of wheat. Heshowed that panchromatic colour and especially infrared aerial photography could be used to detect rusts and viral diseases of small grains and certain diseases of citrus. Later, infrared photography was used in England for late blight of potato. The key to distinguish diseased and healthy parts of a crop is to use appropriate film or filter combinations. The main film types used are panchromatic, infrared, normal colour and colour infrared. The infrared films are preferred because of their superior sensitivity to visible light and to near infrared wavelengths of radiation (700-900 mµ). The colour infrared or Ektachrome Aero Infrared (Camouflage Detection Film) is superior as it can show the difference between diseased and healthy patches of plants in colour. The healthy foliage is highly reflective to the infrared wavelengths and appears red on this film whereas blighted or diseased foliage has low infrared reflectance and does not appear red in the photograph. 2. Satellite Imaging Weather satellites Often cyclones create heavy clouds with rains and an anti-cyclone creates a cloudless sky. All these can be effectively monitored by weather satellites. Sequential pictures show the movement of these systems before they arrive in an area. Therefore by monitoring epidemic favouring systems using a satellite, the disease occurrence on the field can be monitored. Ex: The spread and deposition of stem rust pathogen of wheat is influenced by definite synoptic weather conditions called Indian stem rust rules. Earth resources technology satellites (LANDSAT, 1972, USA) LANDSAT covers the entire globe every 18 days scanning the same area at a fixed time. The scanned data is compared for any major differences happened within 18 days. Nagarajan utilized LANDSAT infrared spectral bands 6 (0.7-0.8µm) and 7 (0.8-1.1µm) to differentiate healthy wheat crop of India and severe yellow rust affected crop of Pakistan. Examples: Coconut root rot and wilt, black stem rust of wheat, citrus canker Advantages of Remote sensing 1. Reveals pattern of disease incidence, intensity and development over large area 2. Data generated by remote sensing is amenable to multidisciplinary approach 3. Gives synoptic view of large areas 4. Data generated is on a permanent scale and is unbiased 5. Data acquisition is fast compared to traditional methods and data analyzed is effectively utilized 6. Satellite data (ERTS) obtains information of an area periodically so that the information can be updated. 7. It frequently poses questions for ground investigators which cannot be generated by ground parties Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) SEED PATHOLOGY Seed Pathology is the integral part of Seed Technology and Plant Pathology dealing with seed diseases, seed borne plant diseases, their detection and management etc. Paul Neergaard is considered the father of seed pathology Seed borne diseases  The pathogens are mainly perpetuates/survival and spread through different ways viz., seed, soil, air etc.,  The pathogen perpetuates through seed is called as seed borne pathogens & the diseases caused by these pathogens are called seed borne diseases  The seed borne diseases are mainly survive either internally or externally it is called as internally seed borne and externally seed borne Example: 1. Loose smut of wheat (Ustilago tritici)- internally seed borne 2. Grain smut of sorghum (Sphacelotheca sorghi)- Externally Fungal diseases 1. Anthracnose of bean (Colletotrichum lindemuthianum) 2. Head smut of maize (Ustilago maydis) 3. Grey leaf spot of maize (Cercospora zea maydis) 4. Stalk rot of maize (Fusarium graminearum) Bacterial disease: 1. Bacterial blight of Common bean (Xanthomonas oxonopodis phaseoli) 2. Bacterial blight (Xanthomonas compestris vignicola) Viral diseases: 1. Common bean mosaic virus  Seeds are attached by various fungi, bacteria virus and nematodes Seeds are attached by various stages, The establishment of a pathogen in, on and with the seed implies that the pathogen is seed borne. Seeds are attached by various fungi, bacteria and virus. Seeds are attached by various stages,  The mother plant get infected by the pathogen, it attack seed also.  During processing.  At the time of transportation.  During harvesting  During storage Significance of seed borne diseases 1. Reduction of Crop Yield: Seed borne pathogens are responsible for reduction of crop yield. Most important seed born disease is rice Blast (Magnaporthe grisea) was responsible for a famine in Japan during in 1930s. In Philippines, losses due to blast may be more than 50%. In 1942, the Bengal Famine in India was the failure of the rice crop because of brown spot (Bipolaris oryzae ). 2. Loss of Germination& vigor: Many seed borne pathogen active when seeds are sown, which may result is failure of seed germination, seed decay and / or pre- or post emergence damping-off and reduce seedling vigor. 3. Discoloration and shriveling: Discoloration can indicate undesirable physical qualities, some pathogen that cause discoloration in seeds affect seed coat color, damage tissues in the seed coat and embryo. 4. Biochemical change: Many seed borne fungi in the quantitative change in the physico-chemical properties of seeds, such as color, odor, oil content, iodine and saponification value and protein content. Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Mechanism of active seed infection 1. Direct Systemic infection via vascular system: Direct connection between embryonic & endospermic tissue becomes disconnected as seed develops Potential for transmission affected by degree of internal infection Many viruses: Pea Seed-borne Mosaic Virus (PSbMV), Lettuce mosaic virus (LMV), Alfalfa mosaic virus (AMV), Pea Early-Browning Virus (PEBV), Some fungi: Vascular wilts (Verticillium dahliae, F. oxysporum), some downy mildews few bacteria: Xanthomonas campestrispv. Campestris 2. Systemic infection via stigma to embryo Pathogen moved from infected plants to flowers may follow pollen pathway to embryo sac. Infected pollen may be less viable (poor fertilization) Examples: Pollen borne viruses – Lettuce mosaic virus (LMV), Cucumber mosaic virus (CMV), Nepoviruses (nematode transmitted polyhedral viruses) - Tobacco Ringspot Virus Fungus- Loose smut fungi (Ustilago tritici, Ustilagonuda) 3. Systemic infection through flowers, fruits or funiculus  Most of the systemic seed-borne bacteria and fungus reach and infect the embryo through the flower or from the peduncle of the fruit, via funiculus.  Viruses go to the embryo from the systemically infected mother plant and the infected or contaminated pollen.  Weak necrotrophs: Botrytis cinerea-infected petals remain attached to developing fruit  Aggressive necrotrophs: Attack floral parts directly, e.g., Ascochyta pisi, Alternaria brassicicola  Fleshy fruits (e.g., Solanaceae) – seed attached to central placenta - infect via calyx - placenta – funicle – embryo  Umbelliferae & Liliaceae – flowers exposed in umbels Importance of seed health to man and animals:  Healthy seed plays an important role in ensuring productivity and profitability of crops.  In India, maize, groundnut, rice, cotton seeds, and millets can be categorized as high-risk commodities  Contamination of seed with various toxins adversely impacts human and animal health.  Fungal species produce toxic metabolites called mycotoxins that contaminate staple foods and feeds.  Mycotoxin may be hepatotoxins, nephrotoxins, and neurotoxins. Majority of mycotoxins cause suppression of the immune system, and some are carcinogenic in nature and adversely affect human and animal health and reduce livestock production. Mycotoxins Many species of fungi produce secondary metabolites called mycotoxins. These toxins can be very detrimental to both humans and animals. The side-effects of ingesting these toxic substances are called mycotoxicosis, which can be a variety of medical conditions. The most common fungi that produce mycotoxins include Fusarium, Aspergillus, and Penicillium Turkey X disease This disease was the turning point for the use of the term mycotoxin. In the 1960s, about 100,000 turkey poults died near London, England due to peanut meal that was contaminated by Mycotoxins produced by Aspergillus flavus. Studies showed that the age group that was most affected was turkeys from two to twenty weeks old. Some of the first signs of Turkey X were neurological symptoms and coma, which would result in death Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) Negative Effects of Mycotoxins on Animals Negative Effects of Mycotoxins on Humans Humans are most commonly exposed to the effects of aflatoxin in three ways 1. Ingestion of food of vegetable origin (mainly corn and peanuts) contaminated with aflatoxin (AFB1). 2. Ingestion of contaminated milk and dairy products, including cheese and powdered milk (AFM1). 3. Ingestion of aflatoxin residues present in meat and meat products, as well as in eggs Bioterrorism 1. Mycotoxins can be used as chemical warfare agents Ex: In 1980s- Iraqi scientists developed aflatoxins. They cultured toxigenic strains of Aspergillus flavus and Aspergillus parasiticus and extracted aflatoxins to produce over 2300 liters of concentrated toxin. The choice of aflatoxins for chemical warfare seems curious because the induction of liver cancer is “hardly a knockout punch on the battlefield Methods for Detecting Seed Borne Fungi, Bacteria & Virus 1. Examination of dry seeds:  It is applied for detection of seed borne fungal pathogens which cause discoloration of the seed or change the shape and size of the seed.  Also applicable for detecting fungal structures present in, on or with seed. Examples: Karnal bunt of wheat Neovossia indic-Ergot of bajra claviceps fusiformis Dr. Narasimhamurthy H. B, Assistant Professor (Plant Pathology), CoA, UAHS, Shivamogga  Principles of Plant Disease and Nematode Management PAT 201 (1+1) 2. Microscopic examination of suspension obtained by Washing test:  This method is used particularly for smut and bunt fungi in gramineous hosts except loose smut of wheat and barley.  It can also be used for downy mildew (Peronospora manchuria) of soybean and tumor disease (Protomyces macrospores) of coriander. 1. NAOH seed soak method: Applied for Karnal bunt of wheat and bunt of rice. 3. Incubation tests 1. Blotter method: This method is widely used. All kinds of cereals, vegetables, crucifiers, legumes, ornamentals and forests seeds are tested by this method. 2. Seedling symptom test: This test is applicable for those fungi which are capable of producing symptoms on the root and shoot of the young seedlings. This test for certain pathogens, provide information pertaining to field performance of the seed lot. 3. Growing on test (for Bacteria): The „growing on‟ bioassay of a working seed sample involves the sowing of test seeds into seedlings under conditions optimal for the disease development in glass house or closed environmental chambers. „Growing on‟ test has been successfully used for a large number of Xanthomonads and Pseudomonad‟s. 4. Indicator test (for Virus): Viruses can be detected in seeds by assaying the extracts of different parts of seeds and seedlings raised from infected seeds on suitable indicator plants. This test has been used to detect BCMV in bean and LMV in lettuce, TMV in tomato and tobacco ring spot virus in soybean. Seed health testing Seed health testing is a procedure by which can be determined whether tile seed is healthy or diseased or it is a procedure by which the presence of absence of seed borne pathogen(s) in a seed lot can be determined. Meth