Plant Pathology: Diseases of Crops, Pathogenesis, Resistance, Defence Signalling and Plant-Microbe Interactions

This chapter answers Section XL2.8 of XL2 Botany, one of the five optional sections of the Life Sciences (XL) paper: “Plant Pathology”. The heading names the nature and classification of plant diseases; diseases of important crops caused by fungi, bacteria, nematodes and viruses and their chemical and biological control; the mechanisms of pathogenesis; resistance (basal, systemic and induced systemic resistance and the gene-for-gene concept); molecular detection of pathogens; plant-microbe interactions, both symbiotic (mycorrhiza) and pathogenic; the signalling pathways of plant defence; the roles of salicylic acid (SA) and jasmonic acid (JA) in plant-pathogen and plant-herbivore interactions and in necrosis; calcium signalling; and host-parasitic-plant interactions such as Cuscuta. For each disease the exam asks the standard causal organism, the crop and the control. The numericals are disease incidence, a disease severity index and control efficacy.

1. Nature and classification of plant diseases

A plant disease is a sustained disturbance of normal structure or function caused by a biotic or abiotic agent, expressed as symptoms (what the plant shows, such as wilt, chlorosis, necrosis, gall or rot) and recognised by signs (the pathogen itself, such as mycelium, spores, pustules or ooze). Diseases are grouped by cause: infectious (caused by living pathogens — fungi and oomycetes, bacteria, phytoplasmas, viruses and viroids, nematodes and parasitic plants, which spread) and non-infectious (abiotic — nutrient deficiency, drought, pollutants, temperature, which do not spread). A disease needs three things at once, the disease triangle: a susceptible host, a virulent pathogen and a favourable environment, over time.

Disease is measured in two ways that are often confused. Incidence is the proportion of plants (or plant units) that are diseased, however mild. Severity is how much of each plant is affected, scored on a rating scale and summarised as a severity index. A field can have high incidence but low severity (many plants, each lightly spotted) or the reverse.

2. Diseases caused by fungi and oomycetes

Important fungal and oomycete diseases with their standard causal organisms
Crop and diseaseCausal organismNote
Potato late blightPhytophthora infestansAn oomycete, not a true fungus; cause of the Irish famine
Wheat stem (black) rustPuccinia graminis f. sp. triticiMacrocyclic, heteroecious; alternate host barberry
Rice blastMagnaporthe oryzae (Pyricularia oryzae)Spindle-shaped leaf lesions; appressorium-driven penetration
Loose smut of wheatUstilago triticiInternally seed-borne; replaces grain with spore mass
Sugarcane red rotColletotrichum falcatumReddened internal stalk with white cross-bands
Pigeon pea / chickpea wiltFusarium oxysporum (formae speciales)Soil-borne vascular wilt
⚠️ Exam trap
Late blight is caused by an oomycete (Phytophthora), which has cellulosic walls and is more closely related to brown algae than to fungi; calling it a "fungal" disease loosely is a common slip the exam probes.

3. Diseases caused by bacteria, viruses and nematodes

Crop and diseaseCausal organismGroup / spread
Rice bacterial blightXanthomonas oryzae pv. oryzaeBacterium; enters via hydathodes and wounds
Citrus cankerXanthomonas citriBacterium; raised corky lesions
Crown gallAgrobacterium tumefaciensBacterium; T-DNA induces tumours
Tobacco mosaicTobacco mosaic virus (TMV)Virus; sap- and contact-transmitted
Banana bunchy topBanana bunchy top virus (BBTV)Virus; aphid-transmitted (Pentalonia)
Root-knot of many cropsMeloidogyne speciesNematode; root galls with giant cells
Molya disease of wheat/barleyHeterodera avenaeCyst nematode
ℹ️ Note
Many economically important viral diseases are spread by insect vectors: leaf curl diseases by whiteflies (begomoviruses), potato leaf roll and many mosaics by aphids, and rice tungro by leafhoppers. Controlling the vector is often the practical control of the virus.

4. Mechanisms of pathogenesis and disease control

Pathogenesis runs through a cycle: arrival (inoculation), attachment and entry (through natural openings such as stomata and hydathodes, through wounds, or by direct penetration using an appressorium), colonization, reproduction and survival (as resting spores, sclerotia or in debris and seed). To invade, pathogens secrete cell-wall-degrading enzymes (cutinases, cellulases, pectinases), toxins (host-specific toxins such as HC-toxin, or non-specific ones) and effectors that suppress host immunity; biotrophs keep the host cell alive and feed through haustoria, while necrotrophs kill tissue and feed on the remains, and hemibiotrophs do both in turn.

  • Chemical control: protectant fungicides applied before infection (copper compounds such as Bordeaux mixture, dithiocarbamates such as mancozeb) and systemic fungicides taken up and moved in the plant (such as the benzimidazoles and triazoles); antibiotics and copper for some bacteria; and seed treatment. Overuse selects for resistant strains.
  • Biological control: antagonists such as Trichoderma (mycoparasitism and antibiosis against soil fungi) and Pseudomonas fluorescens (siderophores, antibiotics and induced resistance); Bacillus strains; and hypovirulence. Often combined with resistant varieties, clean seed, crop rotation and sanitation in integrated disease management.

5. Plant resistance: basal immunity, the gene-for-gene concept, SAR and ISR

Plant immunity works in two layers. Basal resistance (PTI, PAMP-triggered immunity) begins when surface pattern-recognition receptors (PRRs) detect conserved microbial molecules (PAMPs/MAMPs) such as bacterial flagellin (the flg22 peptide) and fungal chitin, switching on a general defence. Adapted pathogens inject effectors that block PTI; the plant counters with intracellular R proteins (typically NB-LRR) that recognise specific effectors, giving the stronger, faster ETI (effector-triggered immunity), often ending in a hypersensitive response (HR): rapid, localised programmed cell death that walls the pathogen off and is most effective against biotrophs.

The gene-for-gene concept (Flor, from flax rust) states that for each resistance (R) gene in the host there is a matching avirulence (Avr) gene in the pathogen, and resistance (an incompatible interaction, with HR) appears only when the plant carries the functional R gene and the pathogen carries the matching Avr gene. If either is absent or non-functional, the interaction is compatible and disease follows. This is why single-R-gene resistance is readily overcome: a mutation that inactivates Avr makes the pathogen virulent.

FeatureSARISR
Full nameSystemic acquired resistanceInduced systemic resistance
TriggerA prior localized infection (often causing HR)Beneficial root-colonizing microbes (PGPR)
Main hormoneSalicylic acidJasmonic acid and ethylene
MarkerPR proteins accumulateLittle PR-protein accumulation; primed state
🎯 Why it matters
Both SAR and ISR are systemic, broad-spectrum and need the regulator NPR1, but SAR is salicylic-acid-dependent and marked by PR proteins, while ISR is jasmonate/ethylene-dependent and primes defence rather than switching on PR proteins.

6. Defence signalling, SA/JA, necrosis and molecular detection

Recognition at the cell surface or inside the cell triggers an early calcium influx: cytosolic Ca²⁺ rises within seconds and is read by sensors (calmodulin, calcium-dependent protein kinases) that turn on a MAP-kinase cascade, a burst of reactive oxygen species (the oxidative burst), callose deposition and defence-gene transcription. Two hormones then shape the response. Salicylic acid (SA) drives defence against biotrophic and hemibiotrophic pathogens and underlies SAR. Jasmonic acid (JA), with ethylene, drives defence against necrotrophic pathogens and against chewing herbivores (wound signalling). SA and JA pathways are largely mutually antagonistic (cross-talk), so a pathogen that pushes one can suppress the other.

Necrosis, the death of cells and tissue, is a symptom but also a weapon: the controlled cell death of the HR starves a biotroph, yet a necrotroph such as Botrytis actively induces host cell death because it feeds on dead tissue, so HR can even help a necrotroph. Molecular detection identifies pathogens fast and specifically, before or beyond symptoms: ELISA (antibody-based, much used for viruses), PCR and real-time qPCR, isothermal methods such as LAMP for field use, and sequence-based identification and DNA barcoding.

7. Plant-microbe interactions, mycorrhiza and parasitic plants

Not every plant-microbe interaction is harmful. Mycorrhizae are symbioses between roots and fungi: in arbuscular mycorrhiza (AM), Glomeromycota fungi grow inside cortical cells as tree-like arbuscules and greatly extend the root's reach for phosphate and water in exchange for plant sugars; ectomycorrhizae sheath the root of many trees. Nitrogen-fixing Rhizobium-legume nodules and plant-growth-promoting rhizobacteria are other beneficial interactions, and the same signalling that recognises a pathogen must also permit a symbiont, which is why symbionts dampen host defence locally.

Parasitic plants draw their nourishment directly from another plant through a specialised organ, the haustorium, which bridges to the host's vascular tissue. Cuscuta (dodder) is a stem holoparasite: a leafless, twining plant with almost no chlorophyll that coils around the host shoot, drives haustoria into its phloem and xylem, and depends on the host for water, minerals and carbon. (A hemiparasite such as Viscum, mistletoe, keeps chlorophyll and photosynthesises but taps the host for water and minerals.) Besides stealing resources, Cuscuta bridges can transmit viruses and even signalling molecules between host plants.

Key takeaways

  • Diseases are infectious (fungi/oomycetes, bacteria, viruses, nematodes, parasitic plants) or non-infectious (abiotic); disease needs a susceptible host, virulent pathogen and favourable environment (the disease triangle). Incidence is how many plants are diseased; severity is how much of each.
  • Standard causal organisms: potato late blight Phytophthora infestans (an oomycete), rice blast Magnaporthe oryzae, wheat stem rust Puccinia graminis, rice bacterial blight Xanthomonas oryzae pv. oryzae, crown gall Agrobacterium tumefaciens, root-knot Meloidogyne.
  • Pathogens enter via natural openings, wounds or appressoria and deploy enzymes, toxins and effectors; biotrophs feed through haustoria, necrotrophs kill tissue. Control is chemical (protectant and systemic), biological (Trichoderma, Pseudomonas) and integrated.
  • Immunity is layered: PTI (PRRs sense PAMPs) then ETI (R proteins sense effectors, often HR). Gene-for-gene: resistance needs both a functional R gene and a matching Avr gene. SAR is SA-dependent (PR proteins); ISR is JA/ethylene-dependent; both need NPR1.
  • An early calcium influx triggers MAP-kinase, an oxidative burst and defence genes. SA defends against biotrophs (SAR), JA/ethylene against necrotrophs and herbivores; the two pathways are antagonistic. Pathogens are detected by ELISA, PCR/qPCR and LAMP.
  • Not all plant-microbe interactions harm: arbuscular mycorrhizae aid phosphate uptake, and Rhizobium fixes nitrogen. Cuscuta is a stem holoparasite that taps host vasculature through haustoria; a hemiparasite like mistletoe keeps its chlorophyll.

Practice questions (15)

Attempt each one before opening the answer. Every explanation names the tempting wrong option as well as the right one, because that is where marks are lost.

  1. In plant pathology, what is the difference between a disease "symptom" and a "sign"?

    1. A symptom is the host's reaction; a sign is the pathogen itself, e.g. spores
    2. A symptom appears only on leaves, whereas a sign appears only on the roots and the stems
    3. A symptom is seen in bacterial disease, whereas a sign is seen only in fungal disease
    4. A symptom is a non-infectious disorder, whereas a sign is always an infectious disease
    Show answer

    Answer: A — A symptom is the host's reaction; a sign is the pathogen itself, e.g. spores

    A symptom is the plant's visible reaction to disease (wilt, chlorosis, necrosis, galls), while a sign is a visible part of the pathogen itself (mycelium, spores, pustules, bacterial ooze). Both can occur on any organ and in diseases caused by any pathogen group, and the distinction is not about infectious versus abiotic.

  2. Which of the following correctly matches a crop disease with its standard causal organism?

    1. Rice blast — Xanthomonas oryzae pv. oryzae
    2. Citrus canker — Puccinia graminis
    3. Root-knot disease — Fusarium oxysporum
    4. Potato late blight — Phytophthora infestans
    Show answer

    Answer: D — Potato late blight — Phytophthora infestans

    Potato late blight is caused by the oomycete Phytophthora infestans. Rice blast is caused by the fungus Magnaporthe oryzae, not by Xanthomonas (which causes rice bacterial blight); citrus canker is bacterial (Xanthomonas citri), not a Puccinia rust; and root-knot is caused by the nematode Meloidogyne, not by Fusarium (a wilt fungus).

  3. Which of the following statements about crop pathogens are correct?

    1. Potato late blight is caused by an oomycete, which has cellulosic walls and is not a true fungus
    2. Rice bacterial blight is caused by Xanthomonas oryzae pv. oryzae
    3. Tobacco mosaic is caused by a nematode transmitted through the soil
    4. Root-knot disease is caused by a virus carried by aphids
    Show answer

    Answer: A — Potato late blight is caused by an oomycete, which has cellulosic walls and is not a true fungus; B — Rice bacterial blight is caused by Xanthomonas oryzae pv. oryzae

    Late blight is an oomycete disease and rice bacterial blight is caused by Xanthomonas oryzae pv. oryzae, both correct. Tobacco mosaic is caused by a virus (TMV), not a nematode, and root-knot is caused by the nematode Meloidogyne, not an aphid-borne virus; the two wrong statements swap the pathogen groups.

  4. In a field of 150 tomato plants, 36 plants show symptoms of a wilt disease. Calculate the disease incidence as a percentage. Give the answer to one decimal place.

    Numerical answer — type the value.

    Show answer

    Answer: 24.0

    Disease incidence = (number of diseased plants ÷ total plants) × 100 = (36 ÷ 150) × 100 = 24.0%. Incidence counts how many plants are affected, regardless of how severely each is affected.

  5. Leaf disease severity is scored on a 0-to-4 scale (0 = healthy, 4 = most severe). Among 30 leaves the counts are: grade 0 on 4 leaves, grade 1 on 6, grade 2 on 10, grade 3 on 6 and grade 4 on 4. Using the McKinney index, severity (%) = [Σ(grade × number of leaves) ÷ (total leaves × maximum grade)] × 100. Compute the severity index to one decimal place.

    Numerical answer — type the value.

    Show answer

    Answer: 50.0

    Numerator Σ(grade × count) = 0×4 + 1×6 + 2×10 + 3×6 + 4×4 = 0 + 6 + 20 + 18 + 16 = 60. Denominator = total leaves × maximum grade = 30 × 4 = 120. Severity = 60 ÷ 120 × 100 = 50.0%. Dividing by total leaves alone (omitting the maximum grade of 4) is the usual error.

  6. A grower applies a copper-based protectant fungicide to healthy foliage before any infection is visible. On what principle does such a protectant fungicide act?

    1. It is absorbed and translocated through the plant to cure established internal infections
    2. It forms a toxic barrier on the plant surface that kills spores before they can penetrate
    3. It induces the plant to produce PR proteins throughout its tissues as in SAR
    4. It silences the pathogen's avirulence gene so that the host R gene recognises it
    Show answer

    Answer: B — It forms a toxic barrier on the plant surface that kills spores before they can penetrate

    A protectant (contact) fungicide stays on the plant surface and kills or inhibits spores before they penetrate, which is why it must be applied before infection; copper fungicides and dithiocarbamates act this way. Uptake and translocation to cure internal infection describes a systemic fungicide, not a protectant, and inducing PR proteins or silencing an Avr gene are not how a copper protectant works.

  7. Trichoderma species are widely used as biocontrol agents against soil-borne fungal pathogens. By which combination of mechanisms do they chiefly act?

    1. By fixing atmospheric nitrogen and raising soil pH to a level the pathogen cannot tolerate
    2. By acting as a systemic fungicide absorbed and translocated inside the crop plant
    3. By mycoparasitism, antibiosis and competition for space and nutrients against the pathogen
    4. By transmitting a virus that is lethal to the crop's insect pests but not to the crop
    Show answer

    Answer: C — By mycoparasitism, antibiosis and competition for space and nutrients against the pathogen

    Trichoderma suppresses soil pathogens by mycoparasitism (coiling around and digesting the pathogen's hyphae), antibiosis (secreting antifungal compounds) and competition for nutrients and space, and it can also induce host resistance. It is not a nitrogen fixer, not a systemic chemical fungicide, and does not work by transmitting an insect-killing virus.

  8. In a fungicide trial the untreated control plots have a mean disease severity of 60%, while the treated plots have a mean severity of 15%. Control efficacy (%) is defined as [(severity in control − severity in treated) ÷ severity in control] × 100. Compute the control efficacy to one decimal place.

    Numerical answer — type the value.

    Show answer

    Answer: 75.0

    Control efficacy = [(60 − 15) ÷ 60] × 100 = (45 ÷ 60) × 100 = 75.0%. This expresses the reduction in severity relative to the untreated control, not the absolute difference of 45 percentage points.

  9. According to the gene-for-gene concept, in which single combination will the host be resistant (an incompatible interaction with a hypersensitive response)?

    1. Host carries a functional R gene and the pathogen carries the matching functional Avr gene
    2. Host carries a functional R gene but the pathogen's matching Avr gene is mutated and non-functional
    3. Host lacks the R gene but the pathogen carries a functional Avr gene
    4. Host lacks the R gene and the pathogen also lacks the matching Avr gene
    Show answer

    Answer: A — Host carries a functional R gene and the pathogen carries the matching functional Avr gene

    Resistance in the gene-for-gene model appears only when both partners are present and functional: the host's R protein must recognise the product of the pathogen's Avr gene. If the Avr gene is lost or non-functional, or the host lacks the matching R gene, recognition fails and the interaction is compatible (disease). This is why a single mutation inactivating Avr makes the pathogen virulent.

  10. Which statement correctly distinguishes PAMP-triggered immunity (PTI) from effector-triggered immunity (ETI)?

    1. PTI is triggered by intracellular R proteins, whereas ETI is triggered by surface receptors
    2. PTI always produces a hypersensitive response, whereas ETI never involves cell death
    3. PTI begins when surface PRRs detect conserved PAMPs, whereas ETI begins when R proteins recognise specific effectors
    4. PTI works only against viruses, whereas ETI works only against nematodes
    Show answer

    Answer: C — PTI begins when surface PRRs detect conserved PAMPs, whereas ETI begins when R proteins recognise specific effectors

    PTI starts at the cell surface, where PRRs detect conserved PAMPs (flagellin, chitin); ETI starts inside the cell, where NB-LRR R proteins recognise specific effectors and mount a stronger response often ending in HR. The option placing R proteins at the surface and PRRs inside has the receptor locations reversed; HR is characteristic of ETI rather than PTI; and neither layer is restricted to one pathogen group.

  11. Which of the following statements about systemic acquired resistance (SAR) and induced systemic resistance (ISR) are correct?

    1. SAR is salicylic-acid-dependent and is marked by the accumulation of PR proteins
    2. ISR is typically triggered by beneficial root-colonizing rhizobacteria and depends on jasmonate and ethylene
    3. SAR acts only at the site of the first infection and gives no protection to distant tissues
    4. Both SAR and ISR provide broad-spectrum protection and require the regulatory protein NPR1
    Show answer

    Answer: A — SAR is salicylic-acid-dependent and is marked by the accumulation of PR proteins; B — ISR is typically triggered by beneficial root-colonizing rhizobacteria and depends on jasmonate and ethylene; D — Both SAR and ISR provide broad-spectrum protection and require the regulatory protein NPR1

    SAR is SA-dependent with PR-protein accumulation, ISR is rhizobacteria-induced and JA/ethylene-dependent, and both are broad-spectrum and need NPR1, all correct. The remaining statement is false because SAR is systemic by definition, protecting tissues far from the initial infection.

  12. A chewing caterpillar wounds a plant's leaves. Which hormone chiefly orchestrates the plant's defence against this herbivore?

    1. Salicylic acid, the same hormone that drives systemic acquired resistance to biotrophs
    2. Gibberellic acid, which is the main hormone of defence against all pests
    3. Abscisic acid, acting purely to close stomata and keep the insect out
    4. Jasmonic acid, together with ethylene, the wound- and herbivore-response pathway
    Show answer

    Answer: D — Jasmonic acid, together with ethylene, the wound- and herbivore-response pathway

    Wounding by a chewing herbivore activates the jasmonic acid (with ethylene) pathway, which induces defences such as protease inhibitors and volatiles. Salicylic acid chiefly defends against biotrophic pathogens (SAR), and the SA and JA pathways are antagonistic; gibberellic acid is a growth hormone, and abscisic acid's role in stomatal closure is not the main anti-herbivore defence.

  13. Within seconds of recognizing a pathogen, a plant cell shows a rapid rise in cytosolic calcium. Which sequence best represents the early defence signalling that follows?

    1. Calcium influx → calcium sensors and a MAP-kinase cascade → oxidative burst and defence genes
    2. Defence-gene expression → oxidative burst → only then any change in cytosolic calcium
    3. Oxidative burst → export of calcium out of the cytosol → shutdown of all kinase activity
    4. A fall in cytosolic calcium → inhibition of kinases → suppression of defence genes
    Show answer

    Answer: A — Calcium influx → calcium sensors and a MAP-kinase cascade → oxidative burst and defence genes

    The early cascade is: a rise in cytosolic Ca²⁺ is sensed by calcium sensors such as calcium-dependent protein kinases and calmodulin, which (with a MAP-kinase cascade) switch on the oxidative burst, callose deposition and defence-gene transcription. The other sequences put gene expression or the oxidative burst before the calcium signal, or have calcium falling and defence being suppressed, which reverses the actual order and direction.

  14. Cuscuta (dodder) is described as a stem holoparasite. Which set of features fits this description?

    1. A rootless soil saprophyte that absorbs decaying organic matter and makes its own food by photosynthesis
    2. A twining, almost chlorophyll-free plant that taps the host's vascular tissue through haustoria
    3. A green climber that keeps full chlorophyll and takes only water and minerals from the host
    4. A fungus that forms arbuscules inside root cortical cells and supplies the host with phosphate
    Show answer

    Answer: B — A twining, almost chlorophyll-free plant that taps the host's vascular tissue through haustoria

    Cuscuta is a twining stem parasite with almost no chlorophyll that drives haustoria into the host's phloem and xylem and depends on it for water, minerals and carbon, so it is a holoparasite. A green climber that keeps chlorophyll and takes only water and minerals is a hemiparasite (like mistletoe); a saprophyte feeds on dead matter, and the arbuscule description is arbuscular mycorrhiza, a mutualistic fungus.

  15. Which of the following statements about beneficial plant-microbe interactions are correct?

    1. Arbuscular mycorrhizal fungi improve the host's uptake of phosphate in exchange for plant sugars
    2. Rhizobium in legume root nodules fixes atmospheric nitrogen into a form the plant can use
    3. Arbuscular mycorrhizal fungi kill the host root cells they enter and feed on the dead tissue
    4. Some rhizobacteria prime the plant's defences and trigger induced systemic resistance
    Show answer

    Answer: A — Arbuscular mycorrhizal fungi improve the host's uptake of phosphate in exchange for plant sugars; B — Rhizobium in legume root nodules fixes atmospheric nitrogen into a form the plant can use; D — Some rhizobacteria prime the plant's defences and trigger induced systemic resistance

    Arbuscular mycorrhizae improve phosphate uptake for sugars, Rhizobium fixes nitrogen in legume nodules, and some rhizobacteria trigger ISR, all correct and all mutualistic. The false statement describes a necrotroph: AM fungi keep the colonized cortical cells alive, forming arbuscules across the living plasma membrane rather than killing the cells.