Infectious Disease

Module 7 averages about 25 marks a year (2020–2025). Prevention, treatment and control is the most examined inquiry question here (about 10 marks a year), followed by causes of infectious disease (about 8) and immunity (about 5). Responses to pathogens is examined less often but still turns up.

The syllabus has four inquiry questions:

• Causes of infectious disease: types of pathogens and how they are transmitted; microbial testing of food or water; the work of Koch and Pasteur; pathogen adaptations; effects of disease on agriculture.
• Responses to pathogens: how a named Australian plant responds to a named pathogen; physical and chemical changes in an infected animal.
• Immunity: the innate and adaptive immune systems, and how immunity is acquired.
• Prevention, treatment and control: incidence and prevalence; hygiene, quarantine, vaccination, pesticides and genetic engineering; antibiotics and antivirals; managing epidemics and pandemics; Aboriginal and Torres Strait Islander knowledge of bush medicines and the protocols for researching it.

An infectious disease is caused by a pathogen and can be passed between hosts. A pathogen is any agent that causes disease.

Viruses are not cells: they can only reproduce inside a host cell, using its ribosomes and enzymes. Prions cause normal proteins to misfold too, which is why they are so hard to destroy. Macroparasites can live inside the host (endoparasites such as worms) or on it (ectoparasites such as ticks and lice).

Transmission

• Direct contact: touching, body fluids, sexual contact (eg HIV).
• Indirect contact: contaminated objects called fomites, such as door handles.
• Droplets and aerosols: coughing and sneezing (influenza, COVID-19).
• Contaminated food or water: cholera spreads through water polluted with faeces; Salmonella through undercooked food.
• Vectors: an organism that carries the pathogen between hosts. Anopheles mosquitoes carry malaria; Aedes mosquitoes carry dengue.

Koch and Pasteur

Louis Pasteur used swan-neck flasks of boiled broth. The curved neck let air in but trapped dust and microbes, so the broth stayed clear; when the neck was broken, it went cloudy. This disproved spontaneous generation and supported the germ theory: microorganisms come from other microorganisms and cause decay and disease. He also developed pasteurisation and early vaccines (anthrax, rabies).

Robert Koch identified the bacteria causing anthrax, tuberculosis and cholera. His postulates set the standard for proving a microbe causes a disease:

1. The microbe is found in every case of the disease and not in healthy hosts.
2. It can be isolated and grown in pure culture.
3. The cultured microbe causes the same disease when put into a healthy host.
4. The same microbe can be isolated again from the newly infected host.

The postulates have limits: viruses and prions cannot be grown on agar, some people carry a pathogen without symptoms, and it is unethical to deliberately infect humans.

Microbial testing of water or food

In the depth-study style investigation, samples are spread on nutrient agar using aseptic technique (sterilised loops and equipment, flaming the bottle neck, working near a flame, sealing plates without fully taping them shut) and incubated at about 25–30 °C, not body temperature, to avoid growing human pathogens. Plates are never opened after incubation. A control plate (sterile water) checks that the technique did not introduce contamination.

To count bacteria, the sample is serially diluted so a plate has a countable number of colonies (roughly 30–300). Each colony is assumed to come from one cell, a colony-forming unit (CFU).

Worked example: counting bacteria

A creek water sample is diluted to $10^{-4}$ of its original concentration. Spreading 0.1 mL of the dilution gives 46 colonies.

To improve reliability, plate each dilution in triplicate and average the counts. The count underestimates the true number if some colonies grew from clumps of cells.

Pathogen adaptations

Pathogens are adapted to enter a host, avoid its defences and spread.

• Entry and attachment: pili and surface proteins to stick to host cells; enzymes that break down tissue.
• Avoiding defences: capsules that resist phagocytosis; changing surface antigens (influenza's antigenic drift and shift) so memory cells no longer recognise them; hiding inside host cells (HIV, malaria parasites in liver and red blood cells).
• Spreading: toxins that cause diarrhoea or coughing; fast reproduction; using vectors or resistant spores to survive between hosts.

Disease in agriculture

Plant and animal diseases reduce yields, kill stock and close export markets. Examples include Panama disease (Fusarium wilt) in Queensland bananas, myrtle rust in native and commercial Myrtaceae, and the risk of foot-and-mouth disease, which Australia's strict biosecurity aims to keep out. Responses include quarantine, culling infected stock, disease-resistant cultivars and movement controls on equipment and soil.

An Australian plant

You need one named Australian plant and named pathogen. A good choice is Phytophthora cinnamomi (a fungus-like water mould, or oomycete; many texts call it a fungus; it rots roots) infecting Banksia or jarrah; another is myrtle rust (Austropuccinia psidii) on paperbarks and eucalypts. Plants have no immune cells, so their responses are local and chemical.

• Physical: thick waxy cuticle and bark block entry; cell walls are thickened with lignin and callose to wall off the infection; stomata close; infected leaves are dropped.
• Chemical: antimicrobial compounds and phytoalexins are made at the infection site; enzymes break down pathogen cell walls; the hypersensitive response kills cells around the infection so the pathogen is starved and trapped; signals such as salicylic acid trigger systemic acquired resistance in the rest of the plant.

Animals

When a pathogen enters an animal, cells and tissues change: damaged cells release chemicals that trigger inflammation; blood vessels dilate; white blood cells move in and engulf pathogens; infected cells may die; lymph nodes swell as lymphocytes multiply; fever may raise body temperature. These responses lead into the immune system below.

Innate immunity (non-specific)

First line stops pathogens getting in:

• Physical barriers: intact skin, mucous membranes, cilia that sweep mucus out of the airways.
• Chemical barriers: stomach acid, lysozyme in tears and saliva, acidic sweat and sebum.
• Normal flora: harmless bacteria that outcompete pathogens.

Second line responds the same way to any pathogen that gets through:

• Phagocytes (neutrophils and macrophages) engulf and digest pathogens.
• Inflammation: mast cells release histamine, so blood vessels widen and leak. More blood flow and fluid bring phagocytes and proteins to the site, causing redness, heat, swelling and pain.
• Fever slows pathogen reproduction and speeds up immune reactions.
• Natural killer cells destroy virus-infected cells; interferons warn nearby cells; complement proteins burst pathogens and mark them for phagocytosis.

Adaptive immunity (specific)

The third line is specific to each antigen and has memory. An antigen is a molecule (usually a protein on the pathogen surface) that the immune system recognises as foreign.

1. A macrophage or dendritic cell engulfs the pathogen and displays its antigen on MHC markers. It is now an antigen-presenting cell.
2. A helper T cell with a matching receptor binds and is activated. It releases cytokines that activate the matching B and cytotoxic T cells. Only the lymphocytes that match the antigen multiply: clonal selection.
3. Humoral response: activated B cells divide into plasma cells, which secrete antibodies, and memory B cells.
4. Cell-mediated response: cytotoxic T cells bind to and kill body cells displaying the antigen, such as virus-infected cells. Memory T cells also form.
5. After the infection, regulatory (suppressor) T cells shut the response down.

Antibodies are Y-shaped proteins with variable tips that bind a specific antigen. They neutralise toxins and viruses, clump pathogens together (agglutination) and mark them for phagocytes.

Memory and vaccination

In a primary response, antibody levels rise slowly over one to two weeks, and the person may get sick. Memory cells last for years, so in a secondary response antibodies rise faster, higher and for longer, usually before symptoms appear.

Active immunity makes memory cells and lasts; passive immunity is immediate but fades in weeks because no memory cells form. Vaccines contain dead or weakened pathogens, inactivated toxins, purified antigens or mRNA that instructs cells to make an antigen.

Measuring spread

Incidence is the number of new cases in a period; prevalence is the total number of people with the disease at one time. An endemic disease is always present in a region; an epidemic is a rapid rise above normal levels; a pandemic is an epidemic across many countries (COVID-19 was declared one in March 2020). Population mobility (travel, migration, crowding) speeds up spread.

The basic reproduction number $R_0$ is the average number of people one case infects in a fully susceptible population. If enough people are immune, each case infects fewer than one other and the disease dies out: herd immunity. This formula is not in the syllabus, but questions sometimes give it: the fraction that must be immune is

Worked example: herd immunity for measles

Measles is extremely contagious, with $R_0$ commonly estimated at 12–18. Using $R_0=15$:

So about 93% of people must be immune. Two doses of measles vaccine are about 97% effective, so the vaccination coverage needed is

or about 96%. This is why even a small drop in vaccination rates lets measles outbreaks return.

Strategies

• Hygiene: handwashing, safe food handling, clean water and sewage treatment break transmission routes.
• Quarantine and isolation: separating sick or exposed people (or animals, plants and goods at the border) stops contact with susceptible hosts.
• Vaccination: protects individuals and, through herd immunity, people who cannot be vaccinated.
• Pesticides and vector control: killing mosquitoes or removing standing water reduces malaria and dengue.
• Genetic engineering: crops and livestock engineered to resist disease.
• Biological control: releasing mosquitoes carrying Wolbachia bacteria (not genetically modified), which reduce dengue transmission, has been followed by almost no locally acquired dengue in Cairns and Townsville.

Treatment

• Antibiotics kill bacteria or stop them growing by targeting structures that human cells lack, such as cell walls and bacterial ribosomes. They do not work on viruses. Overuse selects for antibiotic-resistant bacteria, so they should only be used when needed and the full course taken.
• Antivirals interfere with a stage of the viral life cycle. For example, oseltamivir blocks the influenza enzyme neuraminidase so new viruses cannot leave the infected cell. Viruses mutate quickly, so resistance is also a problem.

When asked to evaluate a strategy for a localised outbreak, an epidemic or a pandemic, consider how well it breaks transmission, cost, how quickly it can be applied, public compliance and side effects.

Aboriginal and Torres Strait Islander knowledge

Aboriginal and Torres Strait Islander peoples have long used plants as medicine. Bundjalung people are reported to have used crushed tea tree (Melaleuca alternifolia) leaves on wounds and for coughs, and tea tree oil is now known to be antimicrobial. Smokebush (Conospermum), a plant with traditional Aboriginal medicinal uses in Western Australia, was collected for drug screening, and in the 1990s a compound from it was licensed for development as an anti-HIV drug, raising questions about who benefits from traditional knowledge.

Research must follow protocols: get free, prior and informed consent from the community, recognise the knowledge as Indigenous cultural and intellectual property, share benefits (including any profits or patents) fairly, respect secret or sacred knowledge and keep the community involved throughout.

• Calling viruses living cells or saying antibiotics can treat viral infections.
• Saying antibodies kill pathogens directly or that T cells make antibodies.
• Writing that a pathogen "becomes immune" to antibiotics. Bacteria with a resistance allele survive and reproduce: natural selection.
• Mixing up incidence (new cases) and prevalence (all current cases).
• Listing Koch's postulates without explaining how they prove cause.
• Describing aseptic technique without saying why each step matters.
• Choosing a plant pathogen without naming both the plant and the pathogen.

• Explain how vaccination works: antigen → activation of specific B and T cells → memory cells → faster, stronger secondary response. Mention herd immunity if the question is about populations.
• Describe the immune response: use the correct cell names in order (antigen-presenting cell, helper T, B cell, plasma cell, antibody, memory cell).
• Evaluate a control strategy: give strengths and limitations with evidence (data, a named disease), then a judgement.
• Data questions: epidemic curves often ask for the peak, the trend and a reason for it (eg a quarantine introduced in week 4). Quote values and units, and calculate rates where asked.
• Investigation questions: for microbial testing, link each step to safety, validity or reliability.

• Module 5: antibodies, cytokines and MHC markers are proteins made by polypeptide synthesis; IgG crossing the placenta is passive immunity.
• Module 6: antibiotic resistance and antigenic drift arise from mutation and selection; recombinant DNA makes vaccines; GM crops can carry disease resistance.
• Module 8: incidence, prevalence and epidemiological study designs are used for non-infectious disease too; fever is a homeostatic set point being raised.