BIOLOGY YEAR 12

MODULE 7: INFECTIOUS DISEASE

Band 6 Crash Course Notes
Complete Definitions | All Dot Points | Exam Tips

IQ1 IQ2 IQ3 IQ4

Causes & Responses to Immunity Prevention & Control
Transmission Pathogens
IQ1: CAUSES & TRANSMISSION OF INFECTIOUS DISEASE
🔑 KEY DEFINITIONS
Pathogen An infectious agent capable of causing disease in a host organism.
Disease Any condition that disrupts the normal functioning of an organism.
Infectious Disease A disease caused by a pathogen that CAN be transmitted from one host to
another.
Non-Infectious A disease NOT caused by a pathogen and not transmissible between
Disease organisms (e.g. cancer, diabetes).
Host An organism that harbours and provides resources for a pathogen.
Epidemic An outbreak of disease that spreads rapidly to many people in a
population/region at the same time.
Pandemic An epidemic that has spread across multiple countries or continents, affecting
a very large number of people.
Vector An organism that transmits a pathogen from one host to another without
becoming infected itself, or while carrying the pathogen.
Biological Vector A vector inside which the pathogen develops or multiplies before transmission
(e.g. mosquito carrying malaria parasite).
Mechanical Vector A vector that passively carries a pathogen on its body without the pathogen
developing inside it (e.g. a fly carrying bacteria on its legs).
Koch's Postulates A set of four criteria used to establish a causal link between a specific
pathogen and a specific disease.

CLASSIFYING PATHOGENS
Pathogen Type Key Features Example Disease
Bacteria Single-celled prokaryotes; cell Tuberculosis, Cholera
wall present; reproduce by
binary fission; some produce
toxins
Viruses Non-cellular; protein coat Influenza, COVID-19, HIV
(capsid) around DNA/RNA;
obligate intracellular parasites
— must hijack host cell
machinery to replicate
Fungi Eukaryotic; cell wall of chitin; Tinea (ringworm), Candidiasis
reproduce via spores; many are
decomposers, some pathogenic
Protozoa (Protists) Single-celled eukaryotes; often Malaria (Plasmodium), Amoebic
motile; many are parasitic dysentery
Macroparasites (worms) Multicellular animals Tapeworm, Hookworm
(helminths); live in/on host,
absorbing nutrients
Prions Misfolded proteins (NOT Creutzfeldt-Jakob disease, Mad
 cellular, no DNA/RNA); cause Cow Disease
normal proteins to misfold;
extremely resistant to
destruction
★ EXAM TIP: Prions are the trickiest pathogen type — remember they contain NO genetic material at
all, just misfolded protein, which is why they resist normal sterilisation methods.

MODES OF TRANSMISSION
Mode Description Example
Direct Contact Pathogen passes directly Influenza (droplets), STIs (bodily
between hosts via touch, bodily fluid contact)
fluids, or droplets
(coughing/sneezing) over short
range
Indirect Contact Pathogen survives on a Touching a contaminated
contaminated surface or object doorknob then your face
(fomite) and is later picked up
by a new host
Vector Transmission Pathogen is carried from host to Malaria via Anopheles mosquito
host by a third organism (vector) (biological); Salmonella via flies
(mechanical)
Waterborne/Foodborne Pathogen ingested through Cholera (contaminated water),
contaminated food or water Salmonella food poisoning
Airborne Pathogen suspended in tiny Tuberculosis, Measles
aerosol particles, can travel
further than droplets and remain
suspended longer

KOCH'S POSTULATES & PASTEUR'S WORK

Koch's Postulates
● 1. The pathogen must be found in all organisms suffering from the disease, but not in healthy organisms
● 2. The pathogen must be isolated from the diseased host and grown in pure culture
● 3. The cultured pathogen should cause the same disease when introduced into a healthy host
● 4. The pathogen must be re-isolated from the experimentally infected host and shown to be identical to
the original
★ EXAM TIP: A common extended-response question asks you to EVALUATE Koch's postulates.
Limitation: they cannot be applied to all pathogens — e.g. some viruses cannot be cultured outside
living cells, and some pathogens (e.g. cholera) have asymptomatic carriers who test positive for the
pathogen but show no disease.

Pasteur's Experiments — Debunking Spontaneous Generation

● Pasteur boiled meat broth in swan-necked flasks to kill any existing microbes
● The curved neck trapped airborne dust/microbes, preventing them from reaching the broth, while still
allowing air in
● Broth remained sterile indefinitely — proving microbial growth came from contamination, NOT
spontaneous generation from non-living matter
● When the neck was broken (allowing dust to fall in), the broth quickly became contaminated and cloudy

CAUSES & EFFECTS OF DISEASE ON AGRICULTURAL PRODUCTION

Plant Diseases Animal Diseases
E.g. Panama disease (Fusarium fungus) E.g. Foot-and-mouth disease in cattle, Avian
devastates banana crops, wheat rust reduces influenza in poultry
global wheat yields
Spread via wind-blown spores, contaminated Spread via direct contact, contaminated
soil/water, insect vectors feed/water, vectors (e.g. ticks, mosquitoes)
Effects: reduced yield/quality, crop loss, trade Effects: mass culling required, reduced
restrictions on exports production, trade bans, major economic losses

PATHOGEN ADAPTATIONS FOR ENTRY & TRANSMISSION

● Enzymes that break down host cell walls/membranes to gain entry (e.g. hyaluronidase in some bacteria)
● Surface proteins that bind specifically to host cell receptors (e.g. viral spike proteins)
● High reproduction/mutation rates allowing rapid evolution to evade host immune defences (e.g.
influenza's antigenic drift)
● Production of large numbers of resistant spores/cysts that survive harsh environmental conditions
between hosts
● Toxins that disable host immune responses or damage tissue to aid spread
IQ2: RESPONSES TO PATHOGENS
🔑 KEY DEFINITIONS
Plant Defence The physical and chemical mechanisms a plant uses to prevent pathogen
Response entry or limit pathogen spread.
Hypersensitive A rapid plant defence where cells surrounding an infection site die
Response deliberately, starving the pathogen of nutrients and isolating it.
Phytoalexins Antimicrobial chemical compounds produced by plants in response to
pathogen attack.
Inflammation A non-specific (innate) immune response causing redness, heat, swelling and
pain at a site of infection/injury, increasing blood flow and immune cell
delivery.
Phagocytosis The process by which phagocytic white blood cells engulf and digest
pathogens/debris.

PLANT RESPONSES TO PATHOGENS

Physical/Structural Defences
● Waxy cuticle and bark act as a physical barrier preventing pathogen entry
● Cell walls (cellulose) provide a tough structural barrier against fungal/bacterial penetration
● Thorns and trichomes (hairs) deter feeding by herbivores/insect vectors

Chemical Defences
● Production of phytoalexins (antimicrobial compounds) at the site of infection
● Release of enzymes (e.g. chitinases) that break down fungal cell walls
● Hypersensitive response — cells around the infection deliberately die to wall off and starve the pathogen
★ EXAM TIP: Be ready to discuss a NAMED Australian plant-pathogen example, such as Myrtle Rust
(fungal pathogen) affecting native Myrtaceae species, or Citrus Canker (bacterial).

Named Australian Examples — Plants & Animals

Organism Pathogen / Disease Response
Eucalypts & Melaleuca Myrtle Rust (fungus, Some trees mount a
(Myrtaceae) Austropuccinia psidii) hypersensitive response,
sacrificing infected leaf tissue to
stop fungal spread;
susceptibility varies widely
between species/individuals
Banksia & Wollemi Pine Phytophthora dieback (water Root tissue dies back, restricting
mould, Phytophthora water/nutrient uptake; some
cinnamomi) plant populations show genetic
resistance via thickened root
tissue that resists pathogen
spread
Koala Chlamydia (bacterium, Inflammatory immune response
Chlamydia pecorum) in the urogenital/ocular tissue;
chronic infection often leads to
infertility and blindness despite
the immune response
Tasmanian Devil Devil Facial Tumour Disease Tumour cells evade the host
(transmissible cancer cells, immune system by suppressing
spread by biting) MHC molecule expression,
allowing the 'foreign' cancer
cells to avoid detection and
rejection

ANIMAL RESPONSES TO PATHOGENS — PHYSICAL & CHEMICAL CHANGES

Response Description
Inflammation Mast cells release histamine → blood vessels
dilate and become more permeable → increased
blood flow (redness, heat) and fluid/immune cell
leakage into tissue (swelling, pain)
Fever Hypothalamus raises body temperature in
response to pyrogens, inhibiting pathogen
reproduction and enhancing immune cell activity
Phagocytosis Neutrophils and macrophages engulf and digest
pathogens at the infection site
Complement system activation A cascade of blood proteins that can directly lyse
(burst) pathogen cells and enhance
phagocytosis/inflammation
IQ3: IMMUNITY
🔑 KEY DEFINITIONS
Innate Immunity The body's NON-SPECIFIC, immediate defence system present from birth;
responds the same way to all pathogens.
Adaptive (Acquired) The body's SPECIFIC immune response that targets particular pathogens and
Immunity improves with repeated exposure (immunological memory).
Antigen A molecule (usually a protein on a pathogen's surface) that triggers an
immune response and is recognised by antibodies/lymphocytes.
Antibody A Y-shaped protein produced by B cells that binds specifically to a particular
antigen, neutralising or marking the pathogen for destruction.
B Lymphocyte (B A type of white blood cell responsible for HUMORAL immunity — produces
cell) antibodies.
T Lymphocyte (T A type of white blood cell responsible for CELL-MEDIATED immunity —
cell) directly destroys infected cells or coordinates the immune response.
Memory Cell A long-lived B or T cell produced after first exposure to an antigen, enabling a
faster, stronger response on re-exposure.
Active Immunity Immunity gained when the body's OWN immune system produces antibodies,
either through natural infection or vaccination. Long-lasting due to memory
cells.
Passive Immunity Immunity gained from antibodies produced by ANOTHER organism (e.g.
maternal antibodies via placenta/breast milk, or antibody injections).
Temporary — no memory cells formed.

INNATE vs ADAPTIVE IMMUNITY

Innate Immunity Adaptive Immunity
Non-specific — responds the same way to ALL Specific — targets a particular pathogen/antigen
pathogens
Immediate response (minutes to hours) Slower first response (days), but FAST on re-
exposure
Includes: skin, mucous membranes, phagocytes, Includes: B cells (antibodies) and T cells
inflammation, fever, complement system
No memory — same response every time Immunological memory — stronger, faster
secondary response
Present from birth Develops/improves after exposure to specific
antigens

FIRST, SECOND & THIRD LINES OF DEFENCE

Line of Defence Components Type
First Line Skin, mucous membranes, Innate (non-specific) —
stomach acid, lysozymes in prevents pathogen ENTRY
tears/saliva
Second Line Phagocytes, inflammation, Innate (non-specific) — attacks
fever, complement proteins, pathogens that get past the first
natural killer cells line
Third Line B cells (antibodies), T cells, Adaptive (specific) — targets a
memory cells particular pathogen with
memory

HUMORAL vs CELL-MEDIATED IMMUNE RESPONSE

Humoral Response (B cells) Cell-Mediated Response (T cells)
B cells recognise a specific antigen and T cells recognise antigens presented on
differentiate into plasma cells infected/abnormal cell surfaces
Plasma cells secrete large quantities of specific Cytotoxic T cells directly destroy infected or
ANTIBODIES into the blood/lymph cancerous cells
Antibodies neutralise pathogens, mark them for Helper T cells coordinate and amplify both the
phagocytosis, or activate complement humoral and cell-mediated responses
Effective against extracellular pathogens (e.g. Effective against intracellular pathogens (e.g.
bacteria, toxins) viruses) and abnormal cells

PRIMARY vs SECONDARY IMMUNE RESPONSE

★ EXAM TIP: This is a classic exam graph question — be ready to sketch/interpret antibody
concentration vs time for both exposures: the secondary response is FASTER, STRONGER and
LONGER-LASTING due to memory cells.
Feature Primary Response Secondary Response
Trigger First exposure to an antigen Re-exposure to the SAME
antigen
Speed Slow (days) — naïve B/T cells Fast (hours) — memory cells
must be activated and already exist and activate
proliferate quickly
Antibody Level Lower magnitude Higher magnitude, produced
more rapidly
Outcome Pathogen may cause noticeable Pathogen is often cleared
illness before being cleared before symptoms develop

ACTIVE vs PASSIVE IMMUNITY

Active Immunity Passive Immunity
Body produces its OWN antibodies Antibodies are received from an external source
Long-lasting — memory cells formed Short-term — no memory cells formed
Slower onset of protection Immediate protection
E.g. natural infection, vaccination E.g. maternal antibodies (placenta/breast milk),
antivenom, immunoglobulin injections

THE LYMPHATIC SYSTEM

Lymphatic System A network of vessels, nodes and organs that drains excess tissue fluid (as
 lymph), transports immune cells, and is the site where antigen recognition by
lymphocytes occurs.
Lymph The fluid carried by the lymphatic system — formed when interstitial (tissue)
fluid drains into lymphatic vessels; contains lymphocytes and phagocytes.
Lymph Node A small bean-shaped structure (around 600 in the human body) that filters
lymph, trapping pathogens, cancer cells and debris for destruction by
phagocytes and lymphocytes.
Primary Lymphoid Sites where lymphocytes are PRODUCED and MATURE, e.g. bone marrow
Tissue (B cells) and the thymus (T cells).
Secondary Sites where mature lymphocytes encounter antigens and become activated,
Lymphoid Tissue e.g. lymph nodes, spleen, tonsils, adenoids, and Peyer's patches in the small
intestine.
● Returns fluid that leaks out of blood capillaries back to the circulatory system, maintaining blood volume
● Transports lymphocytes and antigen-presenting cells to lymph nodes, where they encounter antigens and
trigger the adaptive immune response — this is why lymph nodes swell during infection
● Provides the environment for lymphocyte maturation (thymus for T cells) and proliferation
● Also absorbs and transports fats/fatty acids from the digestive system
★ EXAM TIP: Don't confuse PRIMARY lymphoid tissue (where lymphocytes are made/mature — bone
marrow, thymus) with SECONDARY lymphoid tissue (where they are activated by antigens — lymph
nodes, spleen).
IQ4: PREVENTION, TREATMENT & CONTROL
🔑 KEY DEFINITIONS
Quarantine Isolating individuals/animals/plants suspected of carrying a disease to prevent
its spread to others.
Vaccination Introducing a weakened, killed, or partial form of a pathogen (or its antigens)
to stimulate active immunity WITHOUT causing the disease.
Herd Immunity When a sufficiently high proportion of a population is immune to a disease,
indirectly protecting non-immune individuals by limiting transmission.
Antibiotic A drug that kills or inhibits the growth of BACTERIA, typically by targeting
structures/processes unique to bacterial cells (e.g. cell wall synthesis).
Antiviral A drug that inhibits the replication of VIRUSES, e.g. by blocking viral entry or
enzymes needed for replication.
Antibiotic The evolved ability of bacteria to survive exposure to an antibiotic that
Resistance previously killed them, via natural selection of resistant mutants.
Epidemiology The study of the patterns, causes, and effects of disease in populations, used
to inform public health responses.

METHODS TO PREVENT THE SPREAD OF DISEASE

Method How It Works
Hygiene Practices Handwashing, food/water hygiene reduce
pathogen transfer via direct/indirect contact
Quarantine Physically isolating infected/exposed individuals
prevents contact-based transmission to the wider
population
Vaccination Stimulates active immunity (and herd immunity at
population level) without the risk of natural
infection
Public Health Campaigns Education on hygiene, safe sex, vaccination
raises awareness and changes population
behaviour
Pesticide Use Reduces vector populations (e.g. mosquito
control reduces malaria/dengue transmission)
Genetic Engineering E.g. genetically modified mosquitoes engineered
to be sterile or unable to carry pathogens,
reducing vector-borne disease transmission
★ EXAM TIP: Vaccination questions often ask you to explain herd immunity — remember it protects
people who CANNOT be vaccinated (e.g. immunocompromised, infants), not just the vaccinated
individual.

PHARMACEUTICAL TREATMENT STRATEGIES

Antibiotics Antivirals
Target bacteria-specific structures (e.g. cell wall Target virus-specific replication steps (e.g. entry,
 synthesis, ribosomes) enzyme activity)
INEFFECTIVE against viruses — a common Generally only effective against the specific virus
exam trap targeted
Overuse drives evolution of antibiotic-resistant Resistance can also evolve, though generally
bacteria via natural selection slower due to high viral mutation/short treatment
courses varying
E.g. penicillin disrupts bacterial cell wall formation E.g. oseltamivir (Tamiflu) blocks influenza viral
release from cells

EVALUATING ENVIRONMENTAL MANAGEMENT & QUARANTINE FOR

EPIDEMICS/PANDEMICS
● Border closures and travel restrictions can slow international spread but carry significant economic/social
costs
● Clean water supply and proper sewage treatment prevent waterborne disease transmission (e.g. cholera
control)
● Vector control programs (e.g. removing mosquito breeding sites) reduce vector-borne disease incidence
● Effectiveness depends on early detection, public compliance, and resourcing — poorer regions often
have less capacity to implement these measures effectively

INTERPRETING INCIDENCE & PREVALENCE DATA

Incidence The number of NEW cases of a disease occurring in a population within a
specific time period.
Prevalence The TOTAL number of cases (new + existing) of a disease in a population at a
given time.
● Mobility of individuals (e.g. travel, urbanisation) increases the speed and reach of disease spread
● The proportion of a population that is immune/immunised directly limits how far a disease can spread
(herd immunity threshold)
● Example: Malaria and Dengue Fever remain highly prevalent in South East Asia due to favourable vector
(mosquito) breeding conditions and high population density

ABORIGINAL AND TORRES STRAIT ISLANDER PEOPLES' PROTOCOLS IN

MEDICINE
● Aboriginal and Torres Strait Islander Peoples have practised traditional bush medicine for at least 65,000
years, with knowledge passed down through oral tradition, art and ceremony rather than written records
● Traditional healers — known by various community-specific terms such as ngangkari — diagnose and
treat both the physical and spiritual aspects of illness
● Recognition and protection of Indigenous Cultural and Intellectual Property (ICIP) is important when
biotechnology/pharmaceutical companies seek to commercialise traditional knowledge or native species
(avoiding 'biopiracy')
● Proper protocols require free, prior and informed consent from, and benefit-sharing with, Traditional
Custodians

Examples of Native Plants Used in Bush Medicine

Native Plant Traditional Use
Kangaroo apple Crushed and applied as a poultice for swollen
joints
Goat's foot Leaves heated and applied to skin to relieve pain
from marine stings
Lemongrass Boiled preparation used to treat fever, earache
and diarrhoea
Snake vine Crushed and applied as an anti-inflammatory for
headaches and arthritis
Kakadu plum / Davidson's plum Extremely high vitamin C and antioxidant content,
used traditionally and now studied for
antimicrobial properties
★ EXAM TIP: When discussing Indigenous medicine, focus on the SCIENCE (active compounds,
antimicrobial/anti-inflammatory effects) AND the ethical dimension (ICIP, consent, benefit-sharing) for
full marks.
⚡ QUICK REFERENCE — ESSENTIAL FACTS
Must-Know Facts
Pathogen with NO Prion (misfolded protein only)
genetic material
Pasteur's key Swan-necked flask
apparatus
Number of Koch's 4
Postulates
Cells that produce Plasma cells (differentiated B cells)
antibodies
Cells that directly Cytotoxic T cells
kill infected cells
Coordinates both Helper T cells
humoral & cell-
mediated responses
Antibiotics target Bacteria only — NEVER effective against viruses
Vector for malaria Anopheles mosquito (biological vector)
Immunity with NO Passive immunity
memory cells

Key Process Comparisons

Innate Immunity Adaptive Immunity
Non-specific, immediate Specific, develops over days but has memory
Skin, phagocytes, inflammation, fever B cells (antibodies), T cells
No memory formed Memory cells formed → faster secondary
response
Active Immunity Passive Immunity
Self-produced antibodies, long-lasting Received antibodies, short-term
Slow onset Immediate protection
E.g. vaccination, natural infection E.g. maternal antibodies, antivenom

🎯 TOP EXAM TIPS FOR MODULE 7

1. Prions contain NO DNA/RNA — don't classify them as living microorganisms
2. Always name BOTH a biological vector (e.g. mosquito) and a mechanical vector (e.g. fly) example
when asked to compare
3. Koch's postulates have known LIMITATIONS — name at least one (e.g. cannot culture some
viruses; asymptomatic carriers)
4. Innate = non-specific & immediate; Adaptive = specific & has memory — this distinction is tested
every year
5. Antibodies are made by B cells (plasma cells); infected cells are killed by cytotoxic T cells — don't
swap these
6. Vaccination triggers ACTIVE immunity via memory cell formation — it does NOT give instant
antibodies like passive immunity
7. Antibiotics ONLY work on bacteria — stating they treat viral infections is an automatic mark loss
8. Antibiotic resistance evolves through NATURAL SELECTION of resistant bacteria, not bacteria
'learning' resistance
9. For incidence vs prevalence: incidence = NEW cases in a time period; prevalence = TOTAL cases
at a point in time
10. Herd immunity protects those who CANNOT be vaccinated — always mention this when
explaining its importance