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GRIP Disease Management Ontology
The master ontology for the GRIP Disease Management suite developed at Kansas State University. This umbrella ontology imports three domain modules — pathogen, disease, and management — and defines the shared root concept (Disease Management) that connects them. It also bridges to the GRIP Nutrient Management ontology for shared concepts (Environment, Cultivar, Crop Species, Management Practices).
The overarching discipline of preventing, diagnosing, and controlling plant diseases to protect crop yield and quality. Disease management integrates knowledge of the pathogen (biology, survival, dispersal), the disease (symptoms, assessment, yield impact), and the available management strategies (chemical, cultural, genetic) within the constraints of the environment and the host genotype. This root concept connects all three modules of the disease management ontology and bridges to the nutrient management ontology for shared environmental and crop concepts.
Links Disease Management to the Disease(s) it targets.
A plant disease caused by a bacterial pathogen. Generally less common than fungal diseases in wheat but important in broader crop systems. No curative chemical treatments comparable to fungicides; managed primarily through copper applications, resistant cultivars, and cultural practices.
Caused by Xanthomonas translucens. Produces water-soaked, translucent streaks on leaves that become necrotic. Favoured by warm, humid conditions with wind-driven rain. No effective chemical control; managed by resistant cultivars and clean seed.
Caused by Barley Yellow Dwarf Virus, transmitted by cereal aphids. Causes yellowing or purpling of flag leaves and reduced grain fill. Managed by insecticidal seed treatment to control aphid vectors and by tolerant cultivars.
Also called stinking smut. Caused by Tilletia spp. Infected kernels are replaced by masses of dark, foul-smelling teliospores (bunt balls). Seedborne and soilborne; infection occurs at germination when cool, moist soil conditions prevail. Almost completely controlled by modern fungicidal seed treatments.
A pathological condition of a plant characterised by a set of symptoms that result from the interaction between a susceptible host, a virulent pathogen, and a favourable environment (the disease triangle). A disease is distinct from the pathogen that causes it: Leaf Rust is a disease; Puccinia triticina is the pathogen. This distinction allows the same pathogen to cause different diseases under different conditions, and the same disease symptoms to sometimes result from different pathogens.
The quantitative or qualitative evaluation of disease presence and severity on a crop. Disease assessment provides the data needed to make treatment decisions, evaluate cultivar resistance, and estimate yield loss. The two standard metrics are incidence and severity.
The proportion of plant units (plants, tillers, leaves, or heads) that show any disease symptoms, expressed as a percentage (0–100%). Incidence measures the spatial spread of disease within a field or plot but does not indicate how severely individual plants are affected.
An ordinal classification of overall disease reaction, typically on a 0–9 or 1–9 scale, used in disease nurseries and variety trials to summarise combined incidence and severity into a single score for cultivar comparison.
An evaluation of a specific cultivar's genetic resistance to a specific disease, expressed on a standardised ordinal scale. This entity connects three things: the cultivar (who), the disease (which disease), and the resistance level (how resistant). A single cultivar may have different ratings for different diseases.
The proportion of plant tissue area that is visibly affected by disease symptoms, expressed as a percentage (0–100%). Severity is typically estimated using standard area diagrams or visual rating scales. It is the more informative metric for predicting yield loss because it reflects the actual amount of photosynthetic tissue destroyed.
The foundational conceptual model of plant pathology: disease occurs when and only when three conditions are simultaneously met — (1) a susceptible Host is present, (2) a virulent Pathogen is present with sufficient inoculum, and (3) the Environment is favourable for infection and disease development. If any one vertex is absent or unfavourable, disease does not occur. Each management strategy (host resistance, chemical control, cultural practice) works by disrupting one or more vertices of the triangle.
A plant disease caused by a fungal pathogen. The largest category of crop diseases; includes rusts, smuts, blights, rots, and leaf spots. Fungal diseases are the primary targets of chemical control (fungicides) and host resistance breeding.
A soilborne disease caused by Fusarium spp. that attacks the crown and lower stem of wheat. Causes browning of the stem base, stunting, and premature death of tillers. Favoured by wet, cool soil conditions. Managed by seed treatment, crop rotation, and avoiding compacted soils.
Also called scab. Caused by Fusarium graminearum. Infects spikelets at flowering, causing premature bleaching of the head. Produces the mycotoxin deoxynivalenol (DON/vomitoxin) that causes grain quality rejection. Favoured by warm, humid conditions during anthesis. Managed by moderately resistant cultivars, fungicide at flowering, and crop rotation.
Moderate disease development; the cultivar is neither clearly resistant nor clearly susceptible. May show variable response across environments. Typical severity 20–40%.
The most common rust disease of wheat worldwide. Caused by Puccinia triticina. Produces small, circular, orange-brown pustules (uredinia) primarily on the upper leaf surface. Favoured by moderate temperatures (15–22 degrees C) and high humidity. Yield losses of 10–30% are typical in susceptible cultivars during epidemic years. Managed by resistant cultivars and foliar fungicides applied at flag leaf.
A complex of diseases caused by Zymoseptoria tritici (Septoria tritici blotch) and Parastagonospora nodorum (Stagonospora nodorum blotch). Produces tan to brown necrotic lesions with dark fruiting bodies (pycnidia). Residue-borne; rain-splash moves spores upward through the canopy. Favoured by cool, wet conditions.
Caused by Ustilago tritici. The entire head is replaced by a mass of dark spores that are dispersed by wind. Unique infection cycle: the pathogen infects the developing embryo at flowering and remains dormant inside the seed until the next season. Only controlled by systemic seed treatments that penetrate the embryo.
Low disease development; symptoms present but limited in extent. Partial resistance slows epidemic progress. Typical severity 5–20%.
Substantial disease development; symptoms widespread but yield loss is partially limited by residual resistance. Typical severity 40–60%. Fungicide application is often economically justified.
An ordinal category on the standard 5-point resistance scale used in wheat disease nurseries and variety performance trials. Ranges from Resistant (minimal symptom development) to Susceptible (severe symptom development and yield loss).
Little or no disease development under favourable conditions for infection. The cultivar carries effective major genes or strong quantitative resistance. Typical severity <5%.
Caused by Rhizoctonia cerealis. Produces sharp-bordered, eye-shaped lesions on the stem base. Soilborne; favoured by cool, wet conditions and conservation tillage that retains surface residue. Managed by seed treatment and crop rotation.
Caused by Puccinia graminis f. sp. tritici. Produces large, elongated, dark reddish-brown pustules on stems, leaves, and heads. Favoured by warm temperatures (25–30 degrees C). Historically the most destructive wheat disease; the Ug99 race group threatens global wheat production. Yield losses can exceed 50% in susceptible cultivars.
Caused by Puccinia striiformis f. sp. tritici. Produces yellow to orange pustules arranged in stripes along the leaf veins. Favoured by cool temperatures (10–15 degrees C) and high humidity. Increasingly important in the southern Great Plains due to adaptation of new races to warmer climates.
Severe disease development with extensive symptom coverage and significant yield loss. No effective genetic resistance; chemical or cultural control is essential. Typical severity >60%.
Caused by Gaeumannomyces graminis var. tritici. A soilborne root and crown rot that blackens the root system and causes whiteheads (premature ripening of individual heads). No effective fungicides; managed by crop rotation (2+ years away from wheat/barley) and maintaining soil pH below 6.5.
A plant disease caused by a viral pathogen. Characterised by mosaic patterns, stunting, and chlorosis. No curative treatments exist; management relies entirely on prevention: resistant cultivars, vector control (insecticide seed treatments), elimination of the green bridge, and certified virus-free seed.
A fungal disease that affects wheat (Triticum aestivum). This subclass groups the ten major fungal diseases of wheat modeled in this ontology. While the ontology is wheat-primary, the parent class (Fungal_Disease) is crop-agnostic and extensible.
Caused by Wheat Streak Mosaic Virus, transmitted by the wheat curl mite. Produces yellow-green mosaic patterns and leaf streaking. Managed by eliminating volunteer wheat (the green bridge), delayed planting, and resistant cultivars.
The reduction in crop yield attributable to disease, expressed as a percentage of the disease-free yield potential or as an absolute quantity (kg/ha). Yield loss is the economic consequence of disease that drives management decisions: treatment is justified when the cost of yield loss exceeds the cost of control.
Links a Disease to the Cultivar (host) it infects. Represents the host vertex of the disease triangle.
Links a Disease to the Pathogen (causal organism) that produces it. Every disease has exactly one primary causal agent, though disease complexes may involve multiple species.
Links a Disease to the Yield Loss it produces when left unmanaged in a susceptible cultivar.
Links a Disease to the Environment that determines whether conditions are favourable for infection. Represents the environment vertex of the disease triangle.
Links a Disease Resistance Rating to the specific cultivar being evaluated.
Links a Disease Resistance Rating to the specific disease against which resistance is being rated.
Links a Disease to its quantitative assessment (incidence, severity, or rating score) observed in a specific trial.
Links the Disease Triangle to its environment vertex — the weather and soil conditions that determine infection favourability.
Links the Disease Triangle to its host vertex — the cultivar whose susceptibility is being evaluated.
The measured disease incidence as a percentage (0–100).
Links the Disease Triangle to its pathogen vertex — the organism whose virulence and inoculum pressure are assessed.
The disease rating on a standardised ordinal scale (e.g., 0–9).
Links a Disease Resistance Rating to its ordinal category on the standard resistance scale.
The measured disease severity as a percentage of tissue area affected (0–100).
The estimated yield reduction caused by disease, expressed as a percentage of disease-free yield potential.
Links Disease Management to the strategies (chemical, cultural, genetic) deployed to control disease.
Links Disease Management to the Cultivar being protected. Bridges to the nutrient module for shared cultivar concepts.
Links Disease Management to the Pathogen(s) causing the diseases being managed.
The specific chemical compound within a fungicide product that is responsible for its biological activity against the target pathogen. A single commercial product may contain one or more active ingredients, often from different FRAC groups to broaden the spectrum and delay resistance development.
The crop growth stage at which a fungicide is applied. Timing relative to infection is critical for efficacy: preventive applications must occur before spore germination; curative applications must occur within 24–72 hours after infection. Growth stages reuse concepts from the nutrient management ontology where applicable.
Fungicidal seed treatment applied before or during planting. Targets seedborne pathogens (bunt, smut) and soilborne seedling diseases (Fusarium, Pythium, Rhizoctonia) during germination and emergence.
Disease management through the application of synthetic or biological chemical compounds (fungicides) that kill or inhibit pathogen growth. Chemical control disrupts the pathogen vertex of the disease triangle by directly reducing pathogen viability or preventing infection. Effective but must be integrated with other strategies to manage fungicide resistance.
Growing non-host crops in alternating seasons to break the disease cycle by depriving soilborne and residue-borne pathogens of their host. Particularly effective for take-all (requires 2+ years of non-cereal crops) and Fusarium foot rot. Less effective for wind-dispersed pathogens (rusts) whose inoculum arrives from distant sources.
Disease management through agronomic practices that reduce pathogen inoculum, break disease cycles, or create conditions unfavourable for infection — without applying chemical products. Cultural control disrupts the environment and/or pathogen vertices of the disease triangle. Often the most sustainable and cost-effective approach, especially for soilborne diseases where chemical options are limited.
An intervention that prevents, reduces, or eliminates plant disease by disrupting one or more vertices of the disease triangle. Integrated disease management (IDM) combines multiple strategies — chemical, cultural, and genetic — to achieve durable control while minimising fungicide resistance risk and environmental impact.
The disease severity or incidence level at which the cost of yield loss from the disease exceeds the cost of applying a fungicide treatment. Below the threshold, the disease is present but treatment is not economically justified. The threshold depends on fungicide cost, application cost, expected yield, grain price, and the efficacy of the fungicide against the specific disease.
Quinone outside Inhibitors, commonly called strobilurins. Block mitochondrial respiration at Complex III. Broad-spectrum with strong preventive activity. Examples: azoxystrobin, pyraclostrobin, trifloxystrobin. High resistance risk; widespread resistance in Septoria and powdery mildew populations in some regions.
A pre-mixed fungicide product combining FRAC 3 (DMI) and FRAC 11 (QoI) active ingredients. Provides broad-spectrum control with both systemic curative and preventive modes. Resistance monitoring is important for the QoI component.
A pre-mixed fungicide product containing active ingredients from both FRAC 3 (DMI) and FRAC 7 (SDHI) groups. Combines the curative activity of triazoles with the preventive activity of SDHIs. The current standard for cereal disease management in many regions.
Demethylation Inhibitors (DMIs), also called triazoles or sterol biosynthesis inhibitors (SBIs). Inhibit ergosterol biosynthesis in fungal cell membranes. The most widely used fungicide class in cereals. Examples: propiconazole, tebuconazole, prothioconazole. Moderate resistance risk.
Succinate Dehydrogenase Inhibitors. Block mitochondrial respiration at Complex II. Relatively new class with expanding use in wheat. Examples: fluxapyroxad, bixafen, pydiflumetofen. Medium to high resistance risk; should be mixed with other modes of action.
A classification category defined by the Fungicide Resistance Action Committee (FRAC) that groups fungicide active ingredients by their biochemical mode of action. Products within the same FRAC group share the same resistance risk: repeated use of a single group selects for resistant pathogen populations. Alternating or mixing FRAC groups is a core resistance management strategy.
Fungicides that act on multiple biochemical sites simultaneously, making resistance development extremely unlikely. Examples: chlorothalonil (M5), mancozeb (M3). Protectant-only (no curative activity); must be applied before infection. Low resistance risk.
Fungicide application at or just after flag leaf emergence (Feekes 8–9). The most common timing for foliar fungicides in wheat: protects the flag leaf, which contributes 60–80% of grain fill photosynthesis.
Fungicide application at anthesis (Feekes 10.5.1). The critical timing for Fusarium head blight (scab) control: the infection window coincides with open florets during pollen shed.
A fungicide applied to the crop canopy as a spray to control foliar and head diseases (rusts, leaf spots, head blight). Applied at specific growth stages (flag leaf, flowering) using ground or aerial equipment. Subject to pre-harvest intervals that restrict the minimum time between application and harvest.
A chemical product applied to control fungal diseases. Each fungicide contains one or more active ingredients, belongs to a FRAC mode-of-action group, and is applied at a specified rate and growth stage. Fungicides may be preventive (protectant), curative, or eradicant depending on their mode of action and timing relative to infection.
The minimum number of days (pre-harvest interval, PHI) that must elapse between the last fungicide application and crop harvest. Required by regulatory agencies to ensure pesticide residues decline to safe levels before grain enters the food or feed supply. PHI values are product-specific and stated on the fungicide label.
Also called quantitative, race-nonspecific, or partial resistance. Conferred by multiple minor-effect genes that reduce disease severity without complete immunity. Effective against all races of a pathogen; provides durable, long-lasting protection. Slower epidemic development rather than outright prevention.
Disease management through the deployment of genetically resistant crop cultivars. Host resistance disrupts the host vertex of the disease triangle by reducing the plant's susceptibility to pathogen infection or colonisation. The most cost-effective and environmentally sound management strategy; requires no additional inputs once the resistant cultivar is selected.
Shifting the planting date to avoid environmental conditions that favour infection. Delayed planting in winter wheat reduces fall infection by the wheat curl mite (Wheat Streak Mosaic Virus) and by early-season Septoria. Early planting increases fall tillering and biomass but can elevate disease risk.
Fungicide application before flag leaf emergence (Feekes 7–8). Targets early-season foliar diseases (Septoria, early rust) to protect the upper canopy as it develops.
Tillage or other practices that bury, remove, or accelerate decomposition of infected crop residue. Reduces surface inoculum for residue-borne pathogens (Septoria/Stagonospora, Fusarium head blight). Conservation tillage increases residue-borne disease pressure but benefits soil health — a trade-off that must be managed.
The genetic and mechanistic category of host resistance. The two fundamental types — vertical and horizontal — differ in their genetic basis, specificity, durability, and breeding implications.
A fungicide applied directly to seed before planting to protect against seedborne and soilborne pathogens during germination and early seedling growth. Includes contact treatments (surface protection) and systemic treatments (absorbed and translocated within the seedling). Essential for bunt, smut, and seedling blight control.
Modifying the plant population density to affect canopy microclimate. Higher seeding rates produce denser canopies with greater humidity and leaf wetness duration, promoting foliar diseases. Lower seeding rates improve air circulation but may reduce yield potential.
Also called qualitative, race-specific, or major-gene resistance. Conferred by single major R-genes that interact in a gene-for-gene manner with pathogen avirulence genes. Provides complete or near-complete protection against specific pathogen races but can be overcome when new virulent races evolve. Often not durable over many years.
Destroying volunteer wheat plants that emerge between crop seasons. Volunteer wheat serves as the 'green bridge' that maintains obligate biotrophs (rusts) and virus-vectoring mites between crops. A critical cultural practice for Wheat Streak Mosaic Virus management.
Links Chemical Control to the Fungicide product applied.
Links a Disease Management Strategy to the vertex or vertices of the Disease Triangle it acts upon. Chemical control disrupts the pathogen vertex; cultural control disrupts the environment and/or pathogen vertices; host resistance disrupts the host vertex.
Links Host Resistance to the Cultivar in which it has been evaluated and characterised.
Links a Fungicide product to its Active Ingredient(s).
Links a Fungicide application to the growth stage at which it is applied.
A qualitative or semi-quantitative rating of the fungicide's effectiveness against a specific disease, typically expressed as Excellent, Good, Fair, Poor, or Not Effective.
Links a Fungicide or Active Ingredient to its FRAC mode-of-action classification.
Links a Fungicide to its Harvest Restriction (pre-harvest interval).
The pre-harvest interval in days for a specific fungicide product.
The commercial trade name of a fungicide product as registered with the EPA.
The maximum labelled application rate in fluid ounces per acre.
The minimum labelled application rate in fluid ounces per acre.
Links Host Resistance to its genetic category (vertical or horizontal).
The disease severity percentage at which treatment becomes economically justified.
Links a Disease Management Strategy to the Disease it aims to control.
Links Disease Management to the Environment that constrains disease development and management decisions. Bridges to the nutrient management environment module.
A prokaryotic microorganism that causes disease in plants. Bacterial pathogens typically enter through natural openings (stomata, lenticels) or wounds, and often require free water on plant surfaces for infection. Managed primarily through copper-based bactericides, resistant cultivars, and cultural practices. Less common than fungal diseases in wheat but important in other crop systems.
A Luteovirus transmitted by cereal aphids (Rhopalosiphum padi, Sitobion avenae). Causes yellowing or reddening of flag leaves and reduced grain fill. Managed by insecticidal seed treatments to control aphid vectors and by resistant cultivars.
Above- and below-ground plant debris from previous crops. The primary inoculum reservoir for residue-borne pathogens (Septoria/Stagonospora, Fusarium graminearum). Tillage buries residue and accelerates decomposition, reducing surface inoculum.
A physical or biological process by which pathogen inoculum (spores, cells, viral particles) is transported from its reservoir to a new host. Dispersal determines the spatial scale of disease spread: wind can move rust spores hundreds of kilometres, while rain-splash moves Septoria spores only a few metres vertically within the canopy.
A eukaryotic, heterotrophic organism belonging to the kingdom Fungi that causes disease in plants. Fungal pathogens are the most important group of crop pathogens worldwide, responsible for roughly 70–80% of plant diseases with known causal agents. They reproduce via spores and may be obligate biotrophs (rusts, smuts) or necrotrophs (Fusarium, Rhizoctonia).
The principal causal agent of Fusarium head blight (scab) in wheat. A necrotrophic fungus that survives on crop residue and produces the mycotoxin deoxynivalenol (DON/vomitoxin). Infection occurs at flowering when warm, humid conditions coincide with anthesis.
A complex of Fusarium species that cause foot rot, crown rot, and seedling blight in wheat. Soilborne; survives in soil and on crop debris. Favoured by wet, cool soil conditions at planting and by compacted or poorly drained soils.
The causal agent of take-all disease in wheat. A soilborne necrotrophic fungus that attacks roots and the stem base, causing blackening of the root system and 'whiteheads.' No effective fungicides; managed primarily by crop rotation and soil pH management.
An environmental factor that promotes or suppresses pathogen development and host infection. Infection conditions represent the environment vertex of the disease triangle as it affects the pathogen: temperature optima for spore germination, humidity thresholds for infection, and rainfall duration for leaf wetness. These are the same physical variables defined in the environment module of the nutrient management ontology but viewed through the lens of disease epidemiology.
A substrate or environment in which a pathogen survives between crop seasons (the 'off-season'). The reservoir is the source of primary inoculum that initiates disease in the next crop. Understanding the reservoir is essential for cultural control strategies: if the pathogen survives in residue, residue management breaks the cycle; if it survives in seed, seed treatment is the intervention point.
An arthropod that acquires a pathogen from an infected plant and transmits it to a healthy plant. Primarily relevant for viral pathogens: the wheat curl mite vectors Wheat Streak Mosaic Virus; cereal aphids vector Barley Yellow Dwarf Virus. The vector itself serves as a mobile reservoir.
Living plant tissue that maintains the pathogen between crop seasons. Obligate biotrophs (rust fungi) cannot survive without a living host; volunteer wheat, alternative hosts, and the 'green bridge' serve as reservoirs. Destroying volunteer wheat before planting is a key cultural control.
The mechanical movement of pathogen-infested soil or residue by tillage implements, harvesters, or transport equipment. Relevant for soilborne pathogens (Fusarium, Rhizoctonia, Gaeumannomyces) that can be dragged between fields.
A biological agent capable of causing disease in a living host organism. In the context of this ontology, pathogens are microorganisms (fungi, bacteria, viruses) that infect crop plants and cause economically significant yield or quality losses. Pathogen is one vertex of the disease triangle.
The causal agent of wheat stem rust (black rust). An obligate biotroph with an alternate host (Berberis spp.). Historically the most destructive wheat disease; the Ug99 lineage remains a global threat to susceptible cultivars.
The causal agent of wheat stripe rust (yellow rust). An obligate biotroph favoured by cool temperatures (10–15 degrees C) and high humidity. Aggressively adapted to a wide range of wheat cultivars through rapid evolution of new races.
The causal agent of wheat leaf rust (brown rust). An obligate biotroph that requires a living host to survive. Produces urediniospores for secondary spread by wind over long distances. The most common rust disease of wheat worldwide.
The short-distance dispersal of spores by raindrop impact. The dominant mechanism for Septoria/Stagonospora leaf spot complex: rain splashes pycnidiospores from infected lower leaves upward through the canopy.
The causal agent of sharp eyespot in wheat. A soilborne necrotrophic fungus that infects the stem base, producing characteristic sharp-bordered, eye-shaped lesions. Favoured by high soil moisture and cool temperatures.
Infected seed as a carrier of seedborne pathogens. Tilletia spp. (bunt) contaminate the seed surface with teliospores; Ustilago tritici (loose smut) harbours dormant mycelium inside the embryo. Fungicidal seed treatment is the primary intervention.
The spread of pathogens via contaminated or infected seed. Relevant for bunt (surface-contaminated teliospores), loose smut (internal embryo infection), and some bacterial diseases. Clean, certified seed and seed treatment break this pathway.
A complex of fungal species including Zymoseptoria tritici (Septoria tritici blotch) and Parastagonospora nodorum (Stagonospora nodorum blotch) that cause the leaf spot complex in wheat. Survive on crop residue; rain-splash is the primary dispersal mechanism.
The soil matrix as a survival site for soilborne pathogens. Organisms like Gaeumannomyces, Rhizoctonia, and Fusarium spp. persist as mycelium or resting structures (chlamydospores, sclerotia) in the soil for months to years.
The causal agents of common bunt (stinking smut) of wheat, primarily T. tritici and T. laevis. Soilborne and seedborne; teliospores contaminate seed and infect at germination. Effectively managed by fungicidal seed treatment.
The causal agent of loose smut of wheat. Infects the developing embryo within the grain during flowering; the mycelium remains dormant in the seed until the next season. Managed exclusively by systemic seed treatments that penetrate the embryo.
The biological transmission of a pathogen by an arthropod vector. The vector acquires the pathogen during feeding on an infected plant and transmits it to a healthy plant during subsequent feeding. Primary pathway for viral diseases.
An obligate intracellular parasite consisting of nucleic acid enclosed in a protein coat that causes disease in plants. Viral pathogens require a living host cell to replicate and are typically transmitted by insect vectors (aphids, leafhoppers), infected seed, or mechanical contact. No curative chemical treatments exist; management relies on resistant cultivars, vector control, and certified seed.
A Tritimovirus transmitted by the wheat curl mite (Aceria tosichella). Causes mosaic patterns, leaf streaking, and stunting. Managed by controlling volunteer wheat (the 'green bridge'), resistant cultivars, and delayed planting to avoid mite populations.
The transport of airborne spores by wind currents. The primary dispersal mechanism for rust fungi (Puccinia spp.) and loose smut (Ustilago tritici). Wind enables long-distance, inter-regional spread of inoculum.
The causal agent of bacterial leaf streak and black chaff in wheat. Enters through stomata; favoured by warm, humid conditions with wind-driven rain. No effective chemical control; managed by resistant cultivars and certified seed.
Links a Pathogen to the Dispersal Mechanism that transports its inoculum from the reservoir to a new host. Determines the spatial scale and timing of epidemic development.
Links a Pathogen to the environmental conditions (temperature, humidity, rainfall) that promote its development and infection success. Represents the pathogen-environment edge of the disease triangle.
Links a Pathogen to the Inoculum Reservoir in which it persists between crop seasons. Understanding survival sites is the basis for cultural control strategies.
Stub — defined in environment module (nutrient management). The environmental context including weather, soil, and location.
Stub — defined in environment module. Rainfall; provides leaf wetness for infection and rain-splash dispersal of spores.
Stub — defined in environment module. Relative humidity; high values promote spore germination and foliar infection.
Stub — defined in environment module. Soil moisture; influences soilborne pathogen mobility and root disease severity.
Stub — defined in environment module. Soil temperature; governs soilborne pathogen activity and seed rot/seedling blight risk.
Stub — defined in environment module. Air temperature; a key driver of pathogen development rate and infection success.
Stub — defined in environment module. Wind speed; primary mechanism for long-distance dispersal of airborne spores.
Stub — defined in fertilization module. An agronomic action that modifies crop production conditions. Cultural disease control practices overlap with nutrient management practices.
Stub — defined in nutrient module. The botanical species of the crop being grown.
Stub — defined in nutrient module. A named crop variety; the host component of the disease triangle.
Stub — defined in nutrient module. A named crop variety; the subject of host resistance evaluation.
Stub — defined in nutrient module. Crop yield measurements that may be reduced by disease.