01/06/2026, 21:33 Module 7 — Infectious Disease

N S W B I O L O G Y S TA G E 6 · Y E A R 1 2 · M O D U L E 7

Infectious
Disease
Comprehensive notes including experiments, variables, validity, reliability & accuracy

CONTENTS

§1 — Causes of Infectious Disease Pathogens · Epidemics · Transmission

§2 — Experiment: Modes of Transmission UV Lotion Simulation

§3 — Experiment: Microbial Water Testing Agar Plate Culture

§4 — Koch & Pasteur Germ Theory · Postulates · Swan-Neck Flask

§5 — Agricultural Disease Plant & Animal Disease

§6 — Pathogen Adaptations Entry · Establishment · Evasion

§7 — Responses to Pathogens Plant Responses · Lines of Defence

§8 — Experiment: Innate Immune Model Sponge & Red Dye

§9 — Immunity Innate · Adaptive · B & T Cells

§10 — Prevention, Treatment & Control Vaccines · Antibiotics · Antivirals

§11 — Pathogen Adaptations vs Control Strategies Analysis Table

§12 — Aboriginal Protocols & Bush Medicine Indigenous IP

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1 7.1 · CAUSES OF INFECTIOUS DISEASE

Types of Pathogens

How are diseases transmitted?

Pathogen Structure Reproduction Treatment Example

Bacteria Prokaryote; cell wall; 3 Binary fission Antibiotics Tuberculosis —

shapes (coccus, bacillus, (asexual); (destroy cell Mycobacterium
spirillum); DNA in plasmid wall) tuberculosis survives
cytoplasm (no nucleus) replication inside macrophages

Fungi Eukaryote; cell wall; Asexual & sexual; Antifungals Athlete's foot —
unicellular or releases spores fungal species break
multicellular; nucleus down keratin in skin
present

Protists Single-celled eukaryote; Sexual → higher Antiprotozoals Malaria —

no cell wall; genetic variation Plasmodium causes
heterotrophic fever, muscle pain,
nausea

Virus Non-cellular; protein Uses host cell Antivirals & Influenza — damages
capsid + DNA or machinery to vaccines lung tissue; cytokine
RNA; capsids have replicate release causes most
unique surface symptoms
proteins; no ribosomes

Macroparasite Visible to naked eye; Sexual Antiparasitic Ticks, tapeworms,

multicellular; reproduction drugs fleas — suck blood;
eukaryotic; no cell wall; can cause secondary
specialised tissues infection

Epidemics

Term Def inition

Endemic level The background rate of a disease in a population at any given time

Outbreak Disease appears temporarily in an isolated area above endemic levels

Epidemic Increase in cases of a disease in a particular area above expected levels

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Term Def inition

Pandemic An epidemic that spreads across a continent or worldwide

Factors Contributing to Epidemics

PAT H O G E N - L E V E L FA C T O R S

Virulence — pathogen's ability to infect or damage a host; mutations can increase virulence,
allowing evasion of detection
Antibiotic resistance — resistant pathogens spread more easily and are harder to treat
Toxins — make hosts more susceptible; deter competing pathogens
Genetic shift — loss of genetic variation in host population lowers resistance
Herd immunity threshold — when insufficient population is immune, protection breaks down

H U M A N - L E V E L FA C T O R S

Migration — people act as vectors, carrying disease across geographic barriers to naïve (non-
immune) populations
Infrastructure — dense populations, lack of clean water, poor sewage, and limited healthcare
increase exposure
Healthcare access — without drugs and vaccines, disease spreads more rapidly

Case Study: Ebola Epidemic

Feature Details

Cause Ebola virus (Zaire ebolavirus species in the 2014–16 outbreak); severe and often fatal

Transmission Fruit bats → humans (zoonotic); then human-to-human via direct contact with bodily
fluids (blood, saliva, mucus, sweat, urine). Also droplet spread.

Transmission factors Population density, virulence of strain, population mobility, host susceptibility, cultural
practices (touching the dead), public health infrastructure

Host response Infects dendritic immune cells → prevents immune response → mass viral replication
in multiple organs → cytokine storm → blood vessel walls thin → haemorrhage →
shock → death (overactive immune system)

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Feature Details

Symptoms Incubation 2–21 days; initial: fever, fatigue, muscle pain, headache; severe: vomiting,
diarrhoea, rash, internal/external bleeding, organ failure

Control PPE, safe burials, contact tracing, quarantine, surveillance, social mobilisation; first
vaccine developed 2016

Modes of Transmission

Mode Mechanism Example

Direct contact Physical contact between infected and susceptible organisms; Ebola (bodily fluids),
person-to-person (handshaking, kissing, sexual intercourse, TB (droplets)
coughing/sneezing droplets), animal-to-person (bites,
scratches)

Indirect contact Via intermediates — air, water, food, contaminated objects Measles (air), Cholera
(fomites); pathogens survive outside a host on surfaces (water)

Vector transmission Living organism (usually insect) carries pathogen from host Malaria via female
to host; pathogen may replicate inside vector Anopheles mosquito;
Lyme disease via ticks

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2 E X P E R I M E N T · P R A C T I C A L I N V E S T I G AT I O N

Modes of Transmission Simulation

AIM

To model and compare the efficiency of direct contact, indirect contact, and vector transmission
in spreading a simulated infectious disease through a population.

I N D E P E N D E N T VA R I A B L E D E P E N D E N T VA R I A B L E C O N T R O L L E D VA R I A B L E S

Mode of transmission Number of "infected" students Controlled factors

Direct contact vs indirect contact vs Detected by UV torch after each trial Number of participants (30),
vector transmission (number of glowing hands/face) number of contacts per person (2
handshakes), duration of contact,
same UV lotion, same UV torch,
same room lighting

Materials

UV reactive lotion (invisible under normal light — simulates pathogen)

UV torch
Shared object (e.g. pen or ball)
30 students
Recording sheet and tally counter

Method

Part A — Direct Contact

1 Designate one student as Patient Zero; apply UV lotion invisibly to their hands.

2 All students shake hands with exactly two other people (standardised contact number).

3 Darken the room; use UV torch to identify "infected" students (glowing hands).

4 Record the number and pattern of infections. Repeat 3 times, rotating Patient Zero.

Part B — Indirect Contact

1 Apply UV lotion to a shared object (pen).

2 Each student handles the object for 5 seconds, then touches their own face once.

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3 Use UV torch to detect spread on hands and face. Record results.

Part C — Vector Transmission

1 Designate one student as the "vector" (mosquito); apply UV lotion to their fingertip.

2 The vector touches one other student's hand per round (5 rounds); not transmit — only the
bitten students do vector does.

3 Record infections; compare rate with Parts A and B.

What This Shows

Direct contact — rapid exponential spread (branching tree); each infected person infects 2+ others,
showing how quickly disease spreads through close-contact populations.
Indirect contact — spread depends on how many people touch the contaminated object; demonstrates
why surface cleaning and handwashing prevent indirect transmission.
Vector — spread is controlled by the vector's movement, not person-to-person contact; illustrates why
targeting vectors (mosquito nets, pesticides) can break the disease cycle.

VA L I D I T Y RELIABILITY ACCUR ACY

Directly tests transmission modes 3 repeats per transmission mode UV torch gives a clear visual
as required by the syllabus improve consistency indicator, reducing subjective
Controlled variables (handshake Standardised handshake number counting error
number, lotion type) isolate the (exactly 2) reduces variability Limitation: Real pathogens vary
IV Limitation: Human behaviour is in infectious dose and survival;
Threat: UV lotion does not unpredictable across cohorts lotion does not decay or replicate
replicate pathogen biology (no Limitation: Results may differ Limitation: Cannot account for
replication, immune evasion, or with different class sizes environmental factors (humidity,
infectious dose) temperature)
Threat: Students may deliberately
alter behaviour (Hawthorne
effect)

A D VA N TA G E S L I M I TAT I O N S

Safe — no real pathogens used UV lotion is not a biological pathogen — cannot

Visually striking; clearly demonstrates exponential model immune response or incubation
spread Small sample size (30) limits population
Directly compares all three modes in one experiment generalisability

Memorable and engaging for students Hawthorne effect — students may not behave
naturally
Does not model viral replication or pathogen decay
outside host

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3 E X P E R I M E N T · P R A C T I C A L I N V E S T I G AT I O N

Microbial Testing of Water Samples

AIM

To compare the bacterial load in different water sources (tap, purified, boiled, and dam water) by
culturing samples on nutrient agar and counting bacterial colonies.

HYPOTHESIS

Dam water will produce significantly more bacterial colonies than tap, boiled, or purified water,
as it lacks treatment. Boiling and purification tablets will substantially reduce colony counts
compared to untreated sources.

I N D E P E N D E N T VA R I A B L E D E P E N D E N T VA R I A B L E C O N T R O L L E D VA R I A B L E S

Water source / treatment Colony count per plate Controlled factors

Straight tap, purified tap, boiled tap, Number of distinct bacterial and Volume plated (0.1 mL), agar type,
straight dam, purified dam water fungal colonies observed after 48–72 incubation temperature (25°C —
h incubation avoids culturing human pathogens at
37°C), incubation duration, same
batch of agar plates

Materials

Water samples: straight dam water, purified dam water, straight tap water, purified tap water, boiled tap
water
Nutrient agar plates (sterile, pre-poured) — 3+ per water source
Water purification tablets
Bunsen burner; tongs; sterile spreaders; micropipette with sterile tips; labels; parafilm
Incubator set to 25°C; gloves, lab coat, safety glasses

Method

1 Clean work area with ethanol and paper towel.

2 Collect samples: dam water, tap water. Add purification tablet to separate samples of dam and tap water.
Boil a sample of tap water using a Bunsen burner; allow to cool.

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3 Label agar plates: water source, replicate number, date.

4 Using aseptic technique (near Bunsen flame), pipette 0.1 mL of each water source onto the centre of the
corresponding agar plate.

5 Use a sterile spreader to distribute evenly across the plate. Flame or replace spreader between plates.

6 Seal plates with parafilm. Invert plates (to prevent condensation dripping onto colonies).

7 Incubate at 25°C for 48–72 hours.

8 After incubation, photograph plates and count distinct Do not open Record data in results
colonies. plates. table.

9 Autoclave all plates before disposal.

Identifying Colony Types

Bacterial colonies — smooth, glossy, often coloured (white, cream, yellow, brown)
Fungal colonies — furry, large, thread-like; often white

Results Table (Class Observations)

Water Source Observations Coverage

Straight tap water Small brown speckles spread across plate ~90%

Purified tap water Small brown/yellow speckles (similar to tap) ~90%

Boiled tap water One small round shiny white colony; small brown ~93% (only 3% true
speckles colonies)

Straight dam water Large furry, thick, white mounds (fungal + bacterial) ~97%

Purified dam water Furry, thread-like, white colonies ~100% (TNTC)

Discussion

Dam water has the highest bacterial load — environmental contamination, no treatment.
Boiling significantly reduces viable bacteria — heat denatures proteins and disrupts membranes.
Purification tablets showed limited effectiveness against the high load in dam water — suggests tablets alone
insufficient for heavily contaminated sources.
Tap water has low but detectable colony counts — treated but not sterile; some bacteria survive chlorination.

VA L I D I T Y RELIABILITY ACCUR ACY

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IV: water source/treatment. DV: Improved by using 3+ replicates Micropipette more accurate than
colony count. Directly tests per source, same agar batch, droppers for volume measurement
microbial contamination as constant incubation conditions TNTC (Too Numerous To
required by syllabus Standardised volume (0.1 mL) Count) results for dam water —
Control: straight tap water reduces variability between plates serial dilutions should be
establishes a baseline Limitation: Environmental performed for accuracy
Threat: Not all microorganisms contamination during plating can Colony counting can be subjective
grow on nutrient agar at 25°C introduce error even with aseptic when colonies overlap
(fastidious organisms, anaerobes, technique
viruses may be missed)

A D VA N TA G E S L I M I TAT I O N S

Provides real, quantitative data on bacterial Only cultivable bacteria detected — viruses,
contamination protozoa, fungi not reliably counted
Demonstrates the effectiveness of water treatment in Cannot identify species without Gram staining or
reducing disease risk biochemical tests
Safe at 25°C — avoids culturing dangerous human Requires 48–72 hours — results not immediate
pathogens Aseptic technique failures can contaminate plates
Easily scalable to compare additional sources and skew results

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4 7.1.2 · HISTORICAL SCIENCE

Koch & Pasteur

Robert Koch — Germ Theory & Koch's Postulates

Koch was a German microbiologist who proved that specific microorganisms cause specific diseases. He
first demonstrated this with Bacillus anthracis (anthrax): isolated the bacterium from a deceased sheep,
cultured it, injected it into a healthy mouse, and observed the same disease develop. He also developed
staining techniques (methyl violet dye) and solid culture media (easier to handle than Pasteur's
liquids), enabling isolation of 21 disease-causing organisms in 21 years.

Koch's Four Postulates

1 The suspected pathogen must be present in every diseased individual and absent in healthy
individuals.

2 The suspected pathogen must be isolated from the diseased host and grown in pure culture.

3 A healthy host inoculated with the pure culture must develop the same disease as the original
host.

4 The pathogen must be re-isolated from the second host and shown to be identical to the original
culture.

L I M I TAT I O N S O F K O C H ' S P O S T U L AT E S

Viruses cannot be grown in pure culture outside a living host cell

Some diseases are polymicrobial (caused by combinations of pathogens)
Some carriers harbour the pathogen without developing disease (e.g. cholera)
Ethical constraints prevent deliberate human infection (Postulate 3)

Louis Pasteur — Germ Theory & Spontaneous Generation

Pasteur was a French microbiologist who discovered microbial fermentation, developed pasteurisation,
and disproved the theory of spontaneous generation.

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S WA N - N E C K E D F L A S K E X P E R I M E N T — M E T H O D

1 Prepare bone broth; divide equally into two glass flasks. One with a straight neck; one shaped
with a long, curved swan-neck.

2 Sterilise liquid in both flasks by heating to 60–100°C (kills all microorganisms).

3 Leave both undisturbed and observe over several weeks.

FINDINGS & SIGNIFICANCE

Straight-neck flask: broth became cloudy, developed scum and unpleasant odour — bacterial
contamination occurred as microorganisms from the air entered directly.
Swan-neck flask: broth remained clear — microorganisms in the air were trapped in the curved
neck before reaching the broth.
When the swan-neck was removed/tilted, bacteria grew — confirming that airborne particles were
the source of contamination, not spontaneous generation.
Conclusion: Living organisms arise only from pre-existing living organisms (germ theory).
Infectious diseases must originate from an external microbial source.
Led to pasteurisation (60–100°C kills most microbes in liquids) and development of vaccines for
rabies and anthrax.

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5 7 . 1 . 3 · A G R I C U LT U R A L I M PA C T

Causes & Effects of Disease in Agriculture

Structural Causes: Why Agriculture Promotes Disease

Artificial selection — selecting for desirable traits reduces genetic variation, making populations uniformly
susceptible to new pathogens
Intensification — high-density housing increases direct contact and transmission; overuse of antibiotics
promotes resistance
Movement of goods and people — transporting crops and animals between regions spreads pathogens to
naïve populations with no prior immunity; biosecurity measures (quarantine, airport monitoring) attempt
to limit this

Plant Diseases

Disease Pathogen Symptoms Management Agricultural Impact

Potato blight Fungus-like Small brown- Remove/destroy Drastically reduces

microorganism black spots infected plants; yield and quality;
(Phytophthora with pale halo; fungicides; reduced storability
infestans) watery rot of preventative sprays; and marketability;
leaves; rotting earth up potatoes to Irish Potato Famine
smell prevent spore (1845–49) caused ~1
penetration million deaths

Panama disease Soilborne fungus Yellowing of Manage soil, water, Persistent in soil for
(Fusarium lower/older plant material many years; rarely
oxysporum) leaves; brown movement; produces marketable
leaf edges; contain/destroy yield; threatens global
wilting and infected equipment; banana supply
death develop resistant
banana varieties

Animal Diseases

Agricultural
Disease Pathogen Symptoms Management
Impact

Anthrax Rod-shaped Fever, spasms, Burn infected Heavy livestock

bacteria trembling, carcasses; losses (cattle,
Bacillus unconsciousness, remove and sheep, goats);

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Agricultural
Disease Pathogen Symptoms Management
Impact

anthracis; difficulty breathing, incinerate top soil disturbance

spores persist in blood around orifices 20 cm of soil from spores
soil/grass of carcasses at carcass site increases
ongoing disease
risk; economic
losses to
farming
industry

Foot and mouth disease Virus; spreads Excessive nasal No specific Dramatic
between farms discharge/salivation; treatment; decrease in milk
via infected reluctance to move or antibiotics for and meat
animals, eat; drop in milk secondary production;
inhalation, production; blisters on infection; severe
consumption, feet, mouth, mammary vaccination constraint on
direct contact glands; depression programs international
(difficult due trade in
to many livestock and
strains) products

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6 7 . 1 . 4 · PAT H O G E N B I O L O G Y

Pathogen Adaptations

How Pathogens Establish Infection: The Four Stages

1. Entry

Pathogens enter via the respiratory tract, gastrointestinal tract, genitourinary tract, or skin.

2. Invasion & Spreading

Invasins — proteins that break down host defences and facilitate growth/spread
Spreading factors — enzymes disrupting the extracellular matrix between cells
Clotting factors — convert fibrinogen to fibrin, disguising the pathogen and protecting it from phagocytes
Active entry — pathogen disrupts cell membrane to force entry (releases proteins to induce uptake)
Passive entry — pathogen exploits natural cell mechanisms (e.g. endocytosis) without disrupting the
membrane

3. Establishment (Adhesion)

Structure Function

Pili & fimbriae Protein appendages that attach to glycolipids on the surface of host cells,
anchoring the pathogen

Capsules Polysaccharide layer surrounding bacteria; aids adhesion via

hydrophobic/hydrophilic interactions with host cell surface

Cell surface adhesion molecules Shapes that bind specifically to receptors on host tissue (molecular
recognition); used by many pathogens

Toxins Damage host tissues or disable immune response (e.g. cholera toxin binds
gut epithelial cells; botulinum blocks nerve cells)

4. Hiding (Immune Evasion)

Strategy Mechanism

Forming biofilms Clumps of cells producing a protective extracellular matrix that shelters the
pathogen from immune attack

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Strategy Mechanism

Changing surface antigens Pathogen displays host-like antigens to disguise itself as 'self', evading immune
recognition

Attacking immune cells Directly destroys antibodies, T cells, or B cells

Hiding Travels to areas immune system cannot reach (intestines, intracellular locations)

Capsule Polysaccharide layer prevents macrophages from engulfing the bacterium

Rapid mutation High mutation rates allow pathogens (especially viruses) to change surface
antigens, evading memory cells

Transmission Adaptations

Reservoirs — living/non-living sites where pathogens persist dormant; animals act as reservoirs for zoonotic
diseases
Use of vectors — replication inside vector (e.g. mosquito) increases efficiency and provides a living reservoir
between human infections
Viral envelopes — protein/lipid layer improves longevity outside host and may evade immune detection
Extremophile properties — ability to survive hostile conditions (pH extremes, variable oxygen levels)
inside or outside the host

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7 7.2 · HOST DEFENCE

Responses to Pathogens

How does a plant or animal respond to infection?

Plant Responses — Myrtle Rust Case Study

Myrtle rust (Puccinia psidii) is a fungal pathogen affecting the Myrtaceae family (eucalypts, bottlebrushes,
tea trees). First detected in Australia 2010; spreads via airborne spores.

Defence Layer Mechanism

Pre-formed physical Bark, thick cell walls (pectin + lignin), leaf cuticles (waxy cuticle made of
lignin and cutin), trichomes (bristles to repel insects), drooping leaves to
deter insect contact, leaf shape prevents water pooling

Pre-formed chemical Eucalyptus essential oils stored in sub-dermal cavities act as

antimicrobial agents; antimicrobial peptides; toxins target insects that
could carry viral pathogens

Basal resistance (innate) Closes stomata upon sensing pathogen (prevents entry); callose
deposition (polysaccharide) between cell wall and plasma membrane
blocks plasmodesmata, limiting disease spread between cells

Chemical immune response Saponins destroy pathogen membrane; phytoalexins impair pathogen
growth; defensins inhibit pre-existing ion channels or form pores
disrupting cellular ion balance

Gene-for-gene resistance Plant resistance gene matches pathogen's avirulence gene → plant
successfully resists infection. Pathogen must contain avirulence gene for
this to work.

Hypersensitive response Programmed cell death (apoptosis) at infection site restricts pathogen to
a localised area, preventing systemic spread

Systemic acquired resistance (SAR) After first exposure, plant mounts a faster and stronger response upon
subsequent exposure to the same pathogen

Animal Responses — First Line of Defence

Physical and chemical barriers that block pathogens from entering the body.

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Barrier Mechanism

Skin Tough, dry, closely packed keratin-filled cells form a physical barrier; keratin
strengthens skin; outermost layer constantly shed

Mucous membranes Line all body openings not covered by skin (respiratory, digestive, urinary,
reproductive tracts); secrete mucus that traps pathogens; contain lysosomes

Cilia Hair-like projections extending from respiratory epithelial cells; sweep mucus and
trapped pathogens toward the throat for coughing/swallowing

Chemical barriers Stomach acid (pH ~2), lysozymes in tears/saliva/mucus break down bacterial cell
walls; alkaline conditions in small intestine neutralise pathogens; acidic urine flushes
urinary tract

Microbiological barriers Normal flora (microflora) in mouth, skin, intestines compete for space and
nutrients, preventing pathogen establishment; produce antimicrobial chemicals;
skin microflora break down sebum to fatty acids, maintaining skin acidity

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8 EXPERIMENT · MODEL

Modelling the Innate Immune Response

AIM

To model the non-specific inflammatory response of the innate immune system using a sponge
(tissue), water, and red dye (blood/immune cells), demonstrating vasodilation and phagocytosis.

I N D E P E N D E N T VA R I A B L E D E P E N D E N T VA R I A B L E C O N T R O L L E D VA R I A B L E S

Presence of "pathogen" Distribution of red dye Controlled factors

Presence or absence of a small object Concentration and spread of red dye Same sponge size, same volume of
(e.g. marble) pressed into the sponge (simulated blood/immune cells) dye solution, same dye
to simulate infection around the wound site concentration, same "pathogen"
object size

Materials

Sponge (represents body tissue)

Red food dye solution (represents blood/immune cells)
Small objects to represent pathogens (e.g. marbles, pebbles)
Bowl or tray; measuring cylinder

Method

1 Set up sponge in tray — represents healthy, intact body tissue.

2 Press a small object (pathogen) into the sponge to simulate a wound or infection site.

3 Slowly pour a measured volume of red dye solution onto the sponge around the wound — simulates
vasodilation and increased blood flow to the site of infection (inflammation).

4 Observe: the dye concentrates around the wound site, modelling the inflammatory response (redness,
heat, swelling).

5 Gently squeeze the sponge around the "pathogen" — models phagocytosis (macrophages engulfing the
pathogen).

6 Record observations and draw a labelled diagram: wound site, inflammatory response, simulated immune
cell recruitment.

What This Shows

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Sponge absorbing dye near wound → increased vascular permeability (vasodilation) allows WBCs to migrate
into infected tissue
Concentration of dye at wound site → inflammation (redness, swelling, heat)
Squeezing pathogen out → phagocytosis (macrophages engulfing foreign material)
Links visible physical symptoms of inflammation to cellular-level immune processes

VA L I D I T Y RELIABILITY ACCUR ACY

Conceptually valid as an analogy Highly reproducible — same Results are qualitative only —
for vasodilation and immune cell physical result (dye concentrating cannot accurately measure
migration to infection site near wound) occurs every time immune cell numbers or cytokine
Threat: A sponge cannot replicate Standardised dye volume ensures concentrations
biological processes — no real consistent results across trials Model is a simplification and does
cells, cytokines, antibodies, or Limitation: Sponge porosity may not capture the molecular
enzymatic activity vary between trials if different complexity of inflammation (e.g.
Threat: Model does not sponge pieces are used cytokine signalling cascades, clonal
distinguish between different selection)
immune cell types

A D VA N TA G E S L I M I TAT I O N S

Safe, cheap, and easy to conduct in any classroom Cannot model specific immune response, antigen
Visually demonstrates increased blood flow to recognition, or antibody production
infection site Does not differentiate between cell types
Encourages understanding of the link between (macrophages, neutrophils, T and B cells)
physical symptoms (redness, swelling) and cellular Does not show the difference between innate and
mechanisms adaptive immunity
Provides no quantitative data

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9 7.3 · IMMUNITY

Innate & Adaptive Immune Systems

How does the human immune system respond to exposure to a pathogen?

Second Line of Defence — Innate Immune System

Phagocytosis

1 Phagocyte engulfs foreign material → forms a phagosome

2 Lysosome fuses with phagosome → forms a phagolysosome

3 Enzymes within the phagolysosome break down foreign material into smaller pieces

4 Waste fragments expelled from phagocyte by exocytosis

Cell Role

Neutrophils Quickly enter tissues; phagocytose pathogens in acute infection; release hydrogen peroxide
(disrupts bacterial/fungal membranes); release cytokines to recruit other immune cells and
promote inflammation

Macrophages Longer-lived; fight chronic infection; present antigens on their surface to activate T
lymphocytes; release cytokines

Natural killer cells Patrol the body; defend against virus-infected and cancerous cells; release cytotoxic
chemicals (e.g. perforin punches holes in target cell membrane) only when in close
proximity to target

Mast cells Respond to injury/infection by releasing histamines → vasodilation and increased

permeability of blood vessels

Inflammation

Accumulation of fluid, plasma proteins, and WBCs when tissue is damaged or infected.

Symptoms: Redness, heat, swelling, pain, loss of function in affected area.

Goal: (1) Confine pathogen to one area; (2) Destroy pathogens; (3) Remove pathogen, its products, and
damaged tissue.

1 Pathogen penetrates first line of defence or tissue is damaged

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2 Injured cells release chemokines → attract neutrophils (stop pathogen spreading) → act on mast cells →
release histamine → blood vessels dilate → extra fluid containing antimicrobial factors enters the area

3 Increased temperature slows pathogen replication and enhances WBC activity

Complement System

A set of 30+ proteins floating in blood. Activated when pathogen breaches barriers. Results in: (1)
punching holes in pathogen membrane; (2) promoting inflammation; (3) opsonisation (flagging antigen
for removal by phagocytes).

Third Line of Defence — Adaptive Immune System

B Lymphocytes (Antibody-Mediated Immunity)

Life cycle: Produced and mature in bone marrow → released into blood → accumulate in lymphoid
tissue → contact with specific antigen → activation → proliferate into millions of clones.

Cell Type Function

Plasma cells Produce specific antibodies released into bloodstream; antibody binds antigen (antibody-
antigen complex); strategies: neutralisation (blocks active site), precipitation (soluble
antigens form insoluble clumps), agglutination (antigens on cell surface form clumps),
complement activation (enhances phagocytosis and lysis)

Memory B cells Persist long-term; provide immunological memory; upon re-exposure, rapidly divide to
produce antibody-secreting plasma cells → faster, stronger, longer-lasting response

T Lymphocytes (Cell-Mediated Immunity)

Life cycle: Produced in bone marrow → mature in thymus → circulate in inactive state → contact with
specific antigen activates them.

T Cell Type Function

Cytotoxic (Killer) T cells Kill foreign, infected, and abnormal cells (virus-infected cells, cancer cells) by
secreting/injecting toxic chemicals (e.g. perforin)

Helper T cells Promote all other immune responses; secrete cytokines → increase phagocyte
activity, promote inflammation, stimulate cytotoxic T cell production, stimulate B
cells to form plasma and memory B cells

Suppressor T cells Turn off the immune response once the antigen has been successfully eliminated

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T Cell Type Function

Memory T cells Persist after infection; provide long-term defence; upon re-exposure, divide into
cytotoxic and helper T cells for a rapid secondary response

Types of Immunity

Memory
Type Duration Natural Example Artif icial Example
Cells?

Active Yes Many years (can Catching and Vaccination (attenuated/dead

be boosted) recovering from an antigens stimulate immune
infection response)

Passive No Weeks to Mother's antibodies via Injection of purified antibodies

months placenta or breast milk from immune individuals or
animals

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10 7.4 · CONTROL

Prevention, Treatment & Control

How can the spread of infectious diseases be controlled?

Methods of Prevention

Method Mechanism Example

Hygiene practices Remove pathogens from surfaces; prevent entry. Washing hands before
Hand washing (soap destroys germs, prevents eating
fomites); bathing; cooking meat (denatures
pathogens); boiling water; covering coughs; cleaning
wounds

Quarantine Restricts movement of diseased/potentially diseased COVID-19 isolation;

individuals, animals, or goods to prevent spread. Melbourne Cup horse
Types: border control (X-rays, detector dogs), quarantine; Panama
animal quarantine stations, human isolation, plant disease banana restrictions
quarantine

Vaccination (active) Attenuated/dead antigens introduced → stimulate HPV vaccine; MMR;

immune response → memory B and T cells formed COVID-19 vaccination
→ faster, stronger response on real exposure; creates
herd immunity when high proportion vaccinated

Public health campaigns Education and behaviour change; modify public Slip! Slop! Slap! (skin
behaviour to adopt safe practices; raise awareness of cancer); Grim Reaper
transmission AIDS campaign; 'Ending
HIV' by ACON

Pesticides Kill pathogenic organisms or eradicate vectors DDT against malaria

(mosquitoes, midges). Danger: biomagnification mosquitoes; insecticides
through food chains; resistance in pest populations on crops
through natural selection

Genetic engineering Modify organisms to be resistant to pests/disease or BT cotton (Bacillus

to disable vectors. CRISPR-Cas9 used to create thuringiensis gene kills
malaria-resistant mosquitoes (remove FREP1 gene); caterpillars); malaria-
gene drives spread the trait through wild resistant mosquitoes
populations

Antivirals
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Drugs that treat viral infections by reducing viral load — they inhibit viral development but do not
destroy viruses directly (viruses use host cell machinery, making specific targeting difficult).

Stage Targeted Mechanism Example

Before cell entry Block virus's ability to bind to host cell surface receptors; Entry inhibitors
inhibit viral particle mobility

During viral synthesis Inhibit reverse transcription (preventing viral DNA from Acyclovir (herpes);
being made); block transcription of viral genes; inhibit HIV antiretrovirals
protease activity needed for viral assembly

Release phase Block viral release from host cell, preventing spread to Zanamivir (influenza)
further cells

L I M I TAT I O N S O F A N T I V I R A L S

Viruses rapidly develop antiviral resistance, especially in immunocompromised hosts

Difficult to target viruses without also targeting host cell machinery
High cost — e.g. 12-week Hepatitis C treatment costs up to $113,400
Rapid viral evolution means drugs can become ineffective quickly

Antibiotics

Kill bacteria or inhibit bacterial growth by targeting biochemical pathways unique to bacteria (not found
in human cells). Originated as natural products from fungi/bacteria; now also synthesised artificially.

Target Mechanism Example

Cell wall synthesis Inhibit peptidoglycan synthesis → cell wall weakens Penicillin
→ water enters by osmosis → cell bursts and dies
Nucleic acid synthesis Inhibit folate production (required for DNA/RNA Sulfonamide drugs
synthesis) → bacteria cannot replicate

Protein synthesis Bind to bacterial ribosomes (30S or 50S subunits) to Tetracyclines,

prevent protein synthesis erythromycin

Cell membrane permeability Disrupt bacterial cell membrane integrity Polymyxins

A N T I B I O T I C R E S I S TA N C E — M E C H A N I S M S

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Arises through spontaneous mutation; resistant bacteria survive antibiotic treatment

Failure to complete antibiotic course allows resistant bacteria to survive and replicate
Bacteria pass resistance genes to each other via plasmids (horizontal gene transfer)
Resistance mechanisms: deactivating/degrading enzymes; efflux pumps that push antibiotics out of
the cell; entry blockers that prevent antibiotic uptake

Herd Immunity & Environmental Management

Herd immunity — when a sufficient proportion of the population is immune, susceptible individuals are
protected because transmission chains are broken; the more contagious the disease, the higher the
vaccination threshold (e.g. whooping cough requires 90–95%)
Environmental management — draining swamps (malaria vector control), improved sanitation, water
treatment, food safety regulations
Immunocompromised individuals (HIV patients, chemotherapy patients, very young/old) cannot be
vaccinated — rely on herd immunity for protection

Historical & Current Strategies to Predict & Control Disease

Era Strategy

Ancient Greece (460 BCE) Hippocrates — collected data on local conditions to predict disease occurrence;
knew recovered patients had 'acquired immunity'

1348 CE Venetian Republic — public health officials monitored ships; excluded those with
infected individuals (early quarantine)

1377 CE Marseille — detained travellers from plague-infected areas for 40 days (origin of
'quarantine' — quarantina, 40 days)

1849 CE Dr John Snow — mapped cholera cases to a public water pump; first
epidemiological study

1776 CE Daniel Bernoulli — modelled increased life expectancy if populations were

inoculated against smallpox

Current Surveillance (event-based, web-based); disease modelling (simulate spread, test

interventions); genomic tracking; vaccination programs; global reporting (WHO
24-hour notification)

Culturally Diverse Strategies

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Cultural and religious beliefs about health, disease, pharmaceuticals, and vaccination influence disease
spread. Example: during the 2013–16 Ebola epidemic in West Africa, cultural practices (hugging,
handshakes as greetings; traditional burial rites including touching the deceased) contributed significantly
to transmission. Many individuals avoided medical treatment due to fear of dying isolated from family
and community.

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11 ANALYSIS · EXAM SKILL

Pathogen Adaptations vs Control Strategies

For each pathogen adaptation, identify the specific control strategy that disrupts it and explain the
mechanism. This is the expected structure for extended-response exam answers.

How Control
How It Enables
Pathogen Adaptation Control Strategy Disrupts the
Infection
Adaptation

Toxin production Toxins damage Toxoid vaccination Antibodies

host tissue or produced pre-
disable immune emptively
response, helping neutralise the
pathogen invade toxin before it can
act on host cells

Bacterial capsule (prevents phagocytosis) Polysaccharide Opsonising Antibodies bind

capsule prevents antibodies (from to the capsule,
macrophages from vaccination) flagging the
engulfing the bacterium for
bacterium phagocytosis
regardless of the
capsule

Viral envelope Protein/lipid layer Antiviral drugs Drugs disrupt

evades immune targeting envelope viral envelope
detection and proteins integrity,
improves survival preventing the
outside cells virus from fusing
with host cell
membranes

Vector use (e.g. mosquitoes for malaria) Replication inside Pesticides, Removes or kills
mosquito vector mosquito nets, the vector;
maintains draining swamps physically breaks
continuous the transmission
transmission cycle chain between the
to human hosts reservoir and
human host

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How Control
How It Enables
Pathogen Adaptation Control Strategy Disrupts the
Infection
Adaptation

Animal reservoir (zoonotic disease) Pathogen persists Quarantine, Limits contact

in animal biosecurity, wildlife between reservoir
populations, monitoring species and
continually re- human
emerging to infect populations;
humans detects zoonotic
spillover early

Rapid mutation (antigenic drift) Virus changes Updated annual New vaccines
surface antigens, influenza vaccines target current
evading memory B dominant strain's
and T cells antigens, ensuring
produced from memory cells
prior infection or recognise the
vaccination circulating variant

Changing surface antigens (mimicry) Pathogen displays Targeted Monoclonal

host-like antigens immunotherapy; antibodies
to disguise itself as monoclonal engineered to
'self' and evade antibodies recognise
immune pathogen-specific
recognition epitopes
regardless of
surface mimicry

Adhesion molecules (colonisation) Pili, fimbriae, and Hygiene practices Physically

adhesins allow (handwashing, removes bacteria
bacteria to anchor wound cleaning) before they can
to mucosal adhere; prevents
surfaces and resist colonisation
flushing before infection is
established

Antibiotic resistance (plasmid transfer) Resistant bacteria Antibiotic Completing the

survive antibiotic stewardship; course kills all
treatment and pass completing full bacteria, leaving
resistance genes to course; developing none to pass on
other bacteria via new antibiotics resistance;
plasmids stewardship
reduces selection
pressure for
resistance

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How Control
How It Enables
Pathogen Adaptation Control Strategy Disrupts the
Infection
Adaptation

Biofilm formation Clumps of cells in Wound Physical removal

protective debridement; of biofilm
extracellular antiseptic irrigation disrupts
matrix shield protective matrix;
bacteria from antiseptics
immune cells and penetrate and kill
antibiotics bacteria before
biofilm can
reform

EXAM TIP — STRUCTURE YOUR ANSWER

Step 1: Identify the specific pathogen adaptation that enables transmission or infection
Step 2: Name the specific control method that targets that adaptation
Step 3: Explain the mechanism by which the control disrupts the adaptation

"Mosquitoes act as vectors for malaria by replicating Plasmodium in the salivary glands and delivering
sporozoites during biting. Mosquito nets physically prevent the vector from contacting the human host, thereby
interrupting the transmission cycle."

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12 7.4.7 · INDIGENOUS KNOWLEDGE

Aboriginal Protocols & Bush Medicine

Traditional Modern
Plant Properties
Use Application

Emu bush (Eremophila sp.) Properties equal Placed on hot Antibiotic

in strength to embers to applications;
established produce wound-healing
antibiotics and smoke for research
antibacterial sterilising
agents tools; cleansed
wounds;
gargled for
throat
ailments;
burnt for
inhalation to
treat colds,
headaches,
chest pains,
diarrhoea

Kakadu plum (Terminalia ferdinandiana) 50× more Sap and bark Nutritional
vitamin C than roasted/boiled; supplements,
oranges; strong applied to health foods,
antioxidants; treat skin pharmacological
antiseptic and conditions, products;
natural healing sores; bark tea freeze-dried
agent for colds and powder
flu

Tea tree oil (Melaleuca alternifolia) Antibacterial, Bundjalung Household

antifungal, Aboriginal cleaners; fungal
antioxidant; peoples (NSW infections (feet,
reduces coast): leaves nails); acne;
inflammation; crushed and burns; insect
enhances healing applied as bites; lice
paste to treatment
wounds;
brewed as tea
for sore throats

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Traditional Modern
Plant Properties
Use Application

Smoke bush (Conospermum sp.) — Western Australia Antiseptic, anti- Used by US National
inflammatory, Aboriginal Cancer Institute
antimicrobial, peoples of tested; found
antihemorrhagic; south-west conocurovone
wound healing WA for inhibits HIV in
and pain relief healing cuts low
and skin concentrations.
conditions; US/Australian
bark crushed patents filed
and boiled, ash 1993–94
made into without
paste compensation
to Aboriginal
Australians →
significant
ethical concern

T H E S M O K E B U S H P R O B L E M — I N T E L L E C T U A L P R O P E RT Y & E T H I C S

Inter-generational Indigenous knowledge identified smokebush as medicinal → led to its selection

for cancer/HIV screening
No royalties, compensation, or acknowledgement presented to Aboriginal Australians of Western
Australia
Demonstrates a fundamental flaw in patent law — inability to protect traditional knowledge
Risk: rights to entire species of flora could be sold to multinational companies, preventing
Aboriginal peoples from autonomously using their own cultural knowledge
Customary laws govern dissemination of Indigenous knowledge — some information is sacred and
restricted; these must be respected during commercialisation

P O S I T I V E D E V E L O P M E N T — T H E M U D J A L A P L A N T PAT E N T

Myardoo majala tree known to the Nyinkina Mangala community for healing and pain relief
Community elders approached Griffith University to create a research partnership
Result: Jarlmadangah Buru community and Griffith University became joint patent holders
Community continues to actively participate in harvesting and monitoring — ensures Aboriginal
communities benefit from commercialisation

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A model of ethical, collaborative bioprospecting

✦ ✦ ✦

NSW Biology Stage 6 Syllabus (2017) · Module 7 · Year 12

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