Module 7: Infectious Disease

NSWBiologySyllabus dot point

Inquiry Question 2: How does a plant or animal respond to infection?

Investigate the response of a named Australian plant to a named pathogen through the application of physical and chemical defences

A focused answer to the HSC Biology Module 7 dot point on plant defences. Covers the waxy cuticle, bark, stomatal closure, callose deposition, phytoalexins and the hypersensitive response, with a named Australian example (eucalypts and Phytophthora cinnamomi).

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What this dot point is asking

NESA wants you to describe how plants defend themselves against infection, distinguish between physical and chemical defences, and provide a named Australian plant and a named pathogen. Plant immunity is often examined in 3 to 6 mark short responses.

The answer

Plants lack mobile immune cells and circulating antibodies. Instead they rely on a combination of pre-existing structural defences and induced biochemical responses.

Physical defences (passive and structural)

Cuticle and bark. The outer surfaces of leaves and stems are covered by a waxy cuticle (cutin and waxes) that resists water loss and pathogen entry. Woody stems have lignified bark, a tough physical barrier that few pathogens can penetrate.

Cell walls. Each plant cell is enclosed in a rigid cellulose cell wall. Pathogens must produce wall-degrading enzymes (cellulases, pectinases) to enter.

Trichomes and thorns. Hair-like trichomes and physical spines deter macroparasites and reduce pathogen contact.

Stomatal closure. Stomata are the main entry point for airborne pathogens. Guard cells detect pathogen-associated molecular patterns (PAMPs) such as flagellin and close the stomatal pore.

Induced physical defences

Callose deposition. When a pathogen attempts to enter, the plant deposits callose (beta-1,3-glucan) into the cell wall at the site of attack, forming a localised plug.

Tylose formation. In xylem vessels, neighbouring cells extrude into the vessel lumen, forming tyloses that block fungal spread through the vascular system.

Chemical defences

Phytoalexins. Small antimicrobial molecules (often terpenes, alkaloids or phenolics) synthesised in response to infection. Examples include camalexin in Arabidopsis and the terpene-based oils in Eucalyptus species.

Reactive oxygen species (ROS). Plants produce hydrogen peroxide and superoxide at the infection site, damaging pathogen membranes and triggering further defence signalling.

Defensive enzymes. Plants produce chitinases (degrade fungal cell walls), glucanases and protease inhibitors that disable pathogen enzymes.

Pre-formed antimicrobials. Many plants store compounds in vacuoles or specialised cells that are released on wounding. Eucalyptus essential oils (cineole, pinene) and tea tree oil (terpinen-4-ol) are antimicrobial constituents of native Australian plants.

The hypersensitive response

The most dramatic plant defence. On detecting pathogen effector proteins, infected cells trigger programmed cell death, killing themselves and the pathogen at the infection site. The result is a small lesion of dead tissue that isolates the pathogen.

A linked response, systemic acquired resistance (SAR), primes the rest of the plant against future infection. Salicylic acid acts as the systemic signal.

Worked example: jarrah and Phytophthora cinnamomi

The jarrah tree (Eucalyptus marginata), a keystone species in Western Australia, is severely affected by jarrah dieback, caused by Phytophthora cinnamomi.

Pathogen. P. cinnamomi is an oomycete (water mould). It produces motile zoospores in moist soil that swim toward root exudates and infect fine roots.

Plant defences.

  1. Lignified bark and a waxy cuticle on stems and leaves prevent surface infection.
  2. Infected root cells deposit callose and lignin to seal off the infection.
  3. Eucalyptus species accumulate phytoalexins (terpenes and phenolic compounds) and produce reactive oxygen species at infection sites.
  4. Hypersensitive cell death isolates infected root tips.

Despite these defences, P. cinnamomi often overwhelms the plant in wet soils, and jarrah dieback has become one of Australia's most damaging plant diseases. Management focuses on hygiene and quarantine of soil and vehicles in affected areas.

Common traps

Forgetting to name an Australian plant. "A plant" earns no marks. Use jarrah, banksia, eucalyptus or wattle.

Confusing animal and plant immunity. Plants do not have antibodies, lymphocytes or mobile immune cells. Their defences are local and chemical.

Calling all defences "the immune response." Plants do not have classical immunity. Use terms like "physical defence," "chemical defence" and "hypersensitive response."

Missing the induced response. Many students list only pre-existing physical barriers. Markers expect induced responses (callose, phytoalexins, hypersensitive response) for full marks.

In one sentence

Plants resist infection through physical defences (cuticle, bark, cell walls, stomatal closure, callose deposition) and chemical defences (phytoalexins, reactive oxygen species, antimicrobial enzymes and the hypersensitive response), as seen in the response of jarrah (Eucalyptus marginata) to Phytophthora cinnamomi.

Past exam questions, worked

Real questions from past NESA papers on this dot point, with our answer explainer.

2022 HSC5 marksUsing a named Australian plant and a named pathogen, describe the physical and chemical defences the plant uses to resist infection.
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A 5-mark answer needs a named Australian plant, a named pathogen, at least two physical defences and two chemical defences.

Named plant and pathogen. The jarrah tree (Eucalyptus marginata), endemic to south-west Western Australia, is attacked by the water mould Phytophthora cinnamomi, causing jarrah dieback. Phytophthora spreads through soil water and infects roots.

Physical defences.

  1. Waxy cuticle and thick bark. The cuticle of leaves and the lignified bark of stems form a continuous physical barrier that pathogens must breach before reaching living tissue.
  2. Stomatal closure. Guard cells close stomata in response to pathogen-associated molecular patterns, denying entry through the leaf surface.
  3. Callose deposition. Where pathogens are detected, plants deposit callose (a beta-1,3-glucan polymer) into cell walls, physically blocking pathogen spread between cells.

Chemical defences.

  1. Phytoalexins. Eucalypts produce terpenes and phenolic compounds in response to infection. These small molecules damage Phytophthora cell membranes.
  2. Reactive oxygen species and the hypersensitive response. Infected cells generate hydrogen peroxide and undergo programmed cell death, isolating the pathogen in a ring of dead tissue.
  3. Tannins and essential oils. Eucalyptus leaves accumulate antimicrobial oils (1,8-cineole) that deter pathogens and herbivores.

Markers reward the named plant and pathogen, the use of correct terminology (callose, phytoalexins, hypersensitive response), and a clear distinction between physical and chemical categories.

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