Communicable Diseases

The first sentence of any 4.3 answer should make the definition crystal clear:

Pathogen — a microorganism that causes an infectious (communicable) disease.

AQA recognises four families of pathogen. You will meet at least one named example from each in spec 4.3.1.2:

Pathogen group	Cell type	AQA example disease
Bacteria	Prokaryotic	Salmonella food poisoning, gonorrhoea
Viruses	Acellular (not a cell at all)	Measles, HIV, Tobacco mosaic virus (TMV)
Fungi	Eukaryotic	Rose black spot (plant)
Protists	Eukaryotic, single-celled	Malaria

A pathogen is communicable — it can pass from one organism to another. That makes 4.3 distinct from topic 4.2's non-communicable diseases such as coronary heart disease or many cancers.

Why bacteria and viruses cause symptoms so fast. Once they enter a body, both groups can reproduce extremely rapidly. A single bacterium can divide every 20 minutes under ideal conditions; viruses can produce hundreds of new particles inside each cell they hijack. That exponential growth is why symptoms appear within hours or days, not weeks.

Bacteria cause illness by reproducing inside the body and releasing chemicals called toxins. Toxins damage the tissues directly — for example, Salmonella toxins inflame the gut lining, producing diarrhoea and vomiting within 8–24 hours of swallowing contaminated food.

Viruses are not cells. To reproduce they must enter a living host cell, inject their genetic material and hijack the cell's machinery to copy themselves. New virus particles then burst out (a process called lysis), destroying the host cell. The dead-cell damage adds up to symptoms — e.g. measles destroys cells lining the airways, producing a cough and breathing difficulty.

Fungi typically grow on the body surface or inside tissues. They feed by secreting digestive enzymes that break down living cells (extracellular digestion). Some fungi also release toxins. In plants, fungi such as the rose black spot fungus penetrate leaves and reduce photosynthesis (4.3.1.2).

Protists are eukaryotic single-celled organisms. Most human protist diseases need a vector — an animal carrier such as the female Anopheles mosquito for malaria. Once injected into the bloodstream, malaria protists invade red blood cells and burst them open in synchronised waves, producing the cyclic fever and chills characteristic of the disease.

Why the numbers escalate so fast. A single bacterium dividing every 20 minutes becomes 1 → 2 → 4 → 8 → ... after 12 generations (4 hours) you have over 4,000 bacteria. After 24 hours, in theory, more than $10^{21}$. Real numbers are limited by nutrients and immune attack, but this exponential maths explains why a tiny initial dose can make you ill within a day.

AQA expects you to be able to describe the main routes by which a pathogen passes from one organism to another, and to suggest practical ways to interrupt each route. These appear on every Paper 1 exam under data-response questions about outbreaks.

Routes of spread:

Route	Example pathogen	How to reduce spread
Direct contact	Athlete's foot fungus	Don't share towels; cover lesions
Air (droplets)	Measles, influenza	Cover coughs/sneezes; ventilation; isolation
Water	Cholera bacteria	Sanitation; treat drinking water; hand washing
Food	Salmonella	Cook meat thoroughly; refrigerate; wash hands
Body fluids	HIV	Use barrier methods; sterile needles; screening
Vector	Malaria (mosquito)	Mosquito nets; insecticides; remove standing water

General prevention strategies that work across many routes:

• Hygiene — hand washing with soap, food preparation rules, surface disinfection. Cheap and effective.
• Isolation of infected individuals (e.g. measles patients should stay off school for at least four days after the rash starts).
• Vaccination — covered in detail in 4.3.1.4.
• Vector control — destroying mosquito breeding sites, insecticide-treated nets.
• Destroying infected plants or animals — culling, removing infected leaves, sterilising tools.

UK public-health context. Outbreaks of measles in the UK (e.g. London 2024) have been traced to falling MMR vaccination rates. Outbreaks of E. coli have come from contaminated salad leaves. Examiners often use these real-world scenarios in 6-mark extended-response questions.

Why understanding the route matters. A virus spread by airborne droplets (e.g. measles) needs different control (ventilation, masks) than one spread by body fluids (HIV — barrier methods, blood screening). Match the strategy to the route in your answers.

Three viruses appear by name in 4.3.1.2. Learn each one in the same format AQA marks against — cause, symptoms, spread, control.

Measles

• Cause: measles virus.
• Symptoms: high fever and a red skin rash.
• Spread: inhalation of droplets from sneezes and coughs of infected people.
• Control: the MMR vaccine (measles, mumps, rubella) given in childhood. Most young children in the UK are vaccinated.
• Risks: measles can be fatal — complications include pneumonia and encephalitis.

HIV (Human Immunodeficiency Virus)

• Cause: HIV.
• Symptoms: starts with mild flu-like symptoms; if untreated, HIV attacks the body's immune cells (T-helper lymphocytes), eventually causing AIDS (acquired immune deficiency syndrome) — the immune system becomes so weak the body can no longer fight even minor infections.
• Spread: sexual contact or exchange of body fluids such as sharing needles when injecting drugs. Not spread by casual contact, sharing cups or insect bites.
• Control: antiretroviral drugs stop the virus replicating, keeping levels low enough that the immune system can still function and onward transmission is reduced. Barrier methods (condoms) and screening blood donations reduce spread.

Tobacco mosaic virus (TMV)

• Cause: TMV — a plant virus that infects tobacco, tomatoes and many other species.
• Symptoms: a distinctive 'mosaic' pattern of discolouration (light/dark patches) on the leaves. Because chlorophyll is destroyed, photosynthesis is reduced, stunting growth and reducing crop yield.
• Spread: contact between plants, on gardeners' hands and tools, and by aphid feeding.
• Control: destroy infected plants; wash hands and tools; grow virus-resistant strains; control aphid vectors.

Salmonella food poisoning

• Cause: Salmonella bacteria — usually acquired from undercooked chicken or contaminated eggs.
• Symptoms: fever, abdominal cramps, vomiting and diarrhoea. Usually self-limiting in healthy adults within a week.
• Mechanism: the bacteria reproduce in the gut and release toxins that inflame the gut lining.
• Spread: eating food contaminated by bacteria or by an infected food handler's hands.
• Control in the UK: poultry are vaccinated against Salmonella to reduce contamination at source. Plus food-handling rules — cook to ≥70 °C, refrigerate, separate raw and cooked foods, wash hands.

Gonorrhoea

• Cause: the bacterium Neisseria gonorrhoeae.
• Symptoms: a yellow or green discharge from the penis or vagina, and pain on urination. Some infected people have no symptoms but can still transmit.
• Spread: a sexually transmitted disease (STD) — passed by unprotected sexual contact.
• Control: historically easily treated with the antibiotic penicillin, but many strains are now resistant — alternatives are used and the search for new antibiotics is urgent. Barrier contraception (condoms) reduces transmission.

AQA exam emphasis on resistance. Gonorrhoea is the AQA poster child for antibiotic resistance because it has gone from being a one-shot penicillin cure (1950s) to a stubbornly resistant STD in 70 years. You can quote this as evidence of why antibiotic stewardship matters (link to 4.3.1.5).

Rose black spot

• Cause: a fungus, Diplocarpon rosae, that infects rose leaves.
• Symptoms: purple or black spots appear on the leaves; the leaves often turn yellow and drop early. With less leaf area, photosynthesis is reduced, weakening the plant.
• Spread: by water (rain splash spreading spores) and by wind dispersing fungal spores.
• Control: chemical fungicides sprayed onto the plant; removing and destroying affected leaves so the spores can't spread to healthy tissue.

Why AQA picks plant diseases for exams. Plant pathogens are an easy way for examiners to test the 'photosynthesis link' — if leaves are damaged, photosynthesis falls, growth slows, yields drop. Make this link explicit in your answer: "the fungus destroys leaf tissue, which reduces the surface area for photosynthesis, so the plant grows poorly."

You will meet plant diseases in more detail in 4.3.3.1 (Biology-only). For 4.3.1.2 you only need rose black spot.

Malaria

• Cause: a protist (genus Plasmodium) — a single-celled eukaryote.
• Symptoms: recurrent episodes of fever with chills (often every 48 hours), headaches, sweats. Severe cases damage red blood cells and the brain. Can be fatal — globally one of the biggest infectious killers, especially of children under 5.
• Life cycle (don't need full detail at GCSE): The female Anopheles mosquito bites an infected person and takes in protists with the blood. The protists develop in the mosquito's gut. When the mosquito next bites a healthy person, protists are injected into the bloodstream. They invade red blood cells, multiply, then burst the cells — releasing more protists and producing the cyclic fever.
• Spread: the vector is the female Anopheles mosquito. Without the mosquito, malaria does not spread person-to-person.
• Control: mosquito nets (especially insecticide-treated bed nets); insecticide sprays; removing standing water where mosquitoes breed; antimalarial drugs for prevention (travellers) and treatment.

Before any pathogen gets close to your cells, your body throws up non-specific barriers — defences that don't target a particular microbe but block all of them. AQA names four:

Barrier	Where	How it works
Skin	Outer body surface	Tough layer of dead cells + sebum; physically prevents entry. Heals quickly if cut.
Hair + mucus in the nose	Nasal passages	Hair traps dust and microbes; mucus sticks them; you blow them out or swallow them.
Mucus + cilia in trachea and bronchi	Airways	Goblet cells secrete sticky mucus that traps inhaled microbes. Ciliated cells beat the mucus up to the throat where it's swallowed.
Stomach acid (HCl)	Stomach	Hydrochloric acid (pH ~2) kills most pathogens in food and swallowed mucus.

Why this matters. Only a tiny fraction of the millions of pathogens you encounter every day actually make it into your tissues — the rest are stopped or destroyed at these barriers. When they fail (e.g. a cut in the skin), the second line of defence (white blood cells) takes over.

When pathogens slip past the first line, white blood cells step in. There are two main types:

• Phagocytes — eat pathogens by engulfing them.
• Lymphocytes — produce antibodies and antitoxins (next section).

Phagocytosis has three stages you should be able to label on a diagram:

1. Recognition — the phagocyte detects the pathogen (it sticks to it).
2. Engulfment — the phagocyte flows its cell membrane around the pathogen, taking it inside a vesicle.
3. Digestion — enzymes inside the phagocyte (in a structure called a lysosome — you don't have to name it) break the pathogen down. The harmless products are released.

Phagocytes can engulf many pathogens in turn. The dead pathogens, broken-down debris and exhausted phagocytes form pus at infection sites.

Lymphocytes are the second main type of white blood cell. They have two AQA-named jobs: antibody production and antitoxin production.

Antigens and antibodies

Every pathogen has antigens — unique molecules (usually proteins) on its outer surface that act like an ID badge. Lymphocytes recognise these antigens as foreign (they don't match the body's own cells).

A lymphocyte then produces antibodies — Y-shaped proteins with a binding site shaped to fit one specific antigen, like a key for one lock. The antibody binds to the antigen, clumping pathogens together and marking them for destruction by phagocytes.

Specificity is key. Each antibody only fits ONE type of antigen. A measles antibody won't bind a flu virus. That's why you can catch many different infections — each needs its own antibody. After infection (or vaccination, 4.3.1.4), the body keeps memory lymphocytes that can make that specific antibody very quickly next time.

Antitoxins

Some bacteria release toxins as they reproduce (the cause of symptoms, 4.3.1.1). Lymphocytes also produce antitoxins — special antibodies that lock onto and neutralise toxin molecules, preventing them from damaging cells.

A vaccine contains a small amount of a dead or inactivated pathogen (or, in newer mRNA vaccines, the genetic instructions for a single harmless antigen). When the vaccine is injected, the body treats it like the real thing — but because the pathogen cannot reproduce, you don't get the disease.

The process inside the body has four stages you must be able to describe in order:

1. Antigen recognition. Lymphocytes recognise the antigens on the vaccine as foreign.
2. Antibody production. The matching lymphocytes divide and produce antibodies specific to that antigen.
3. Memory cells form. Some lymphocytes become long-lived memory cells that stay in the blood for years.
4. Secondary response. If the live pathogen enters the body later, memory cells recognise it immediately and produce large quantities of antibody very fast — destroying the pathogen before it can multiply enough to cause symptoms.

Why the secondary response is so much faster. The first time a pathogen appears (or a vaccine is given), the body has to find a lymphocyte with the right antibody shape, then make it divide. That takes days — long enough for symptoms to start. After vaccination, memory cells are already there and already 'pre-trained' — antibody levels rise within hours.

British examples (UK NHS schedule). The 6-in-1 vaccine (given at 8, 12 and 16 weeks) protects against diphtheria, tetanus, pertussis, polio, Hib and hepatitis B. The MMR vaccine (given at 1 and 3 years) protects against measles, mumps and rubella. The HPV vaccine is offered to all UK 12–13 year olds to prevent cervical and other cancers caused by HPV.

Herd immunity is a population-level effect. If a high enough proportion of a population is immune (through vaccination or recovery), the pathogen cannot find enough susceptible hosts to spread from. Outbreaks fizzle out before they reach vulnerable people.

This matters because some people cannot be vaccinated:

• Newborn babies (immune system not yet developed).
• People with weak immune systems (e.g. on chemotherapy for cancer).
• People with severe allergies to a vaccine ingredient.

These individuals rely on the rest of the population being immune. Herd immunity is essentially a community shield.

Threshold values. The proportion needed depends on how infectious the pathogen is:

Disease	Approximate herd immunity threshold
Measles	~95 % (extremely infectious)
Polio	~80 %
Mumps	~75 %
Diphtheria	~85 %

The UK saw a measles resurgence in 2023–2024 partly because MMR coverage in some areas dropped below the 95 % threshold (NHS England data). That's why MMR catch-up campaigns are run by GP surgeries.

Many exam questions ask you to evaluate vaccination — meaning give advantages AND disadvantages, then a conclusion.

Advantages:

• Prevents serious illness and death. UK life expectancy at birth jumped by years after the introduction of childhood vaccines in the 20th century.
• Eradication is possible. Smallpox was declared eradicated globally in 1980 thanks to vaccination. Polio is almost gone (only a handful of cases worldwide).
• Herd immunity protects vulnerable people (babies, cancer patients).
• Cheaper than treatment. It costs the NHS far less to vaccinate than to treat severe measles or whooping cough in hospital.

Disadvantages:

• Not 100 % effective. Some vaccinated people don't make a strong enough immune response — they can still catch the disease (though usually milder).
• Side-effects. Most are mild (sore arm, slight fever for a day or two). Serious reactions are rare but possible.
• Coverage required. Below the threshold, herd immunity fails — and so do public-health outcomes.
• Some people refuse on personal or religious grounds, which can lower coverage in their community.

Exam structure for an 'evaluate' answer:

1. Open with the main scientific principle (memory cells, fast secondary response).
2. Two clear advantages, with examples (UK MMR, smallpox eradication).
3. Two clear disadvantages.
4. Concluding sentence — AQA mark schemes specifically reward a justified conclusion. e.g. "On balance, the population benefits clearly outweigh the small risk of side-effects, which is why the NHS recommends the full schedule."

An antibiotic is a drug that kills bacteria inside the body. The first antibiotic, penicillin, was discovered by Alexander Fleming in 1928 at St Mary's Hospital in London and developed into a usable medicine by Florey and Chain in Oxford in the early 1940s. Antibiotics revolutionised UK medicine — wound infections, pneumonia and tuberculosis stopped being routine killers.

How they work (in outline). Different antibiotics interfere with different bacterial cell processes:

• Penicillin stops bacteria building new cell walls — when the bacterium tries to divide, it bursts.
• Other antibiotics block bacterial protein synthesis or DNA replication.

Crucially, body cells don't have bacterial cell walls or the same protein-making machinery, so a well-chosen antibiotic kills the bacteria without damaging human cells.

Specific antibiotic for specific bacteria. Different bacteria respond to different antibiotics. A GP will usually take a swab and culture the bacteria (4.1.1.6 culturing microorganisms) to identify the species, then prescribe the antibiotic most likely to work. Using the wrong antibiotic wastes time, gives the bacteria a chance to multiply, and contributes to resistance.

Why antibiotics don't kill viruses. Viruses are not cells. They reproduce inside the body's own cells, hijacking the cell's machinery. A drug that disrupted viral reproduction would usually have to enter and damage host cells too. There are some antiviral drugs (e.g. for HIV, herpes, COVID-19) but these are much harder to develop and less effective in general. For most viral infections (colds, flu, most sore throats), the immune system has to do the work and a doctor will only prescribe symptom relief.

Painkillers like paracetamol, ibuprofen and aspirin work on the body's pain pathways — they don't attack pathogens at all. They make you feel better while your immune system fights the infection.

Drug	What it relieves	British example
Paracetamol	Pain, fever	NHS first-choice for headache, flu symptoms
Ibuprofen	Pain, fever, inflammation	Used for muscular pain, sore throat
Aspirin	Pain, fever, inflammation	Adults only — not for under-16s (Reye's syndrome risk)
Decongestants	Blocked nose	Pseudoephedrine in cold remedies
Antihistamines	Itching, runny nose	Hayfever and allergic reactions

For a viral infection like the common cold, your GP will recommend rest, fluids and painkillers — there's no cure, just symptom management until the immune system clears the virus (usually within a week).

Why this distinction matters. Many UK GCSE answers mark down a student for saying "the painkiller cured my cold". It didn't — it just made you more comfortable. The cold cleared because your white blood cells (4.3.1.3) produced antibodies against the cold virus.

Antibiotic misuse. Patients sometimes pressure GPs to prescribe antibiotics for a sore throat or cold. If the infection is viral, the antibiotic does nothing — it just exposes the body's normal bacteria to selection pressure (next section). The NHS now runs public campaigns reminding patients that "antibiotics don't work on most coughs and colds".

Every time bacteria are exposed to an antibiotic, most are killed — but some carry random mutations that make them slightly resistant. Those bacteria survive, reproduce, and pass the resistance gene to their offspring. Over many generations, resistant strains dominate. This is natural selection in action (links to 4.6 inheritance, variation and evolution).

Why this is getting worse:

1. Overuse of antibiotics (e.g. prescribing for viral infections, or in farm animals as growth promoters — banned in EU/UK but common elsewhere) exposes bacteria to selection pressure more often.
2. Patients not finishing the full course leaves the strongest bacteria alive. These then multiply and spread.
3. Drug development is slow and expensive. Pharmaceutical companies have invested less in new antibiotics for decades because they're not as profitable as long-term medicines. The UK has stepped in with subscription-style payment models to encourage new development.

MRSA (methicillin-resistant Staphylococcus aureus) is the UK's headline example. It is resistant to most common antibiotics and causes hard-to-treat infections in NHS hospitals. Strict hygiene (hand-washing, isolation of infected patients) is the main control.

What students can do (and exam answers should mention):

• Only take antibiotics when prescribed by a GP.
• Always finish the full course, even if symptoms have gone — surviving bacteria are the most resistant ones.
• Don't share or save antibiotics.
• Use good hygiene to prevent the spread of any bacterial infection.

For thousands of years people noticed that certain plants relieved pain, slowed fevers or treated heart problems. Modern UK pharmacology grew out of this folk knowledge. AQA wants you to remember three named examples:

Drug	Source	Use
Digitalis	Foxglove plant (Digitalis purpurea)	Heart conditions (increases force of heartbeat)
Aspirin	Willow bark (used since antiquity; isolated in the 19th century)	Painkiller and reduces inflammation
Penicillin	Penicillium mould (Alexander Fleming, 1928)	Antibiotic — kills bacteria

These three appear repeatedly in AQA mark schemes. Learn the source AND the use — examiner reports flag candidates who write "from plants" instead of naming the actual plant.

Modern drug discovery. Most new drugs are now made by synthetic chemistry in pharmaceutical companies — but the original lead compound often comes from a plant, microorganism or animal. Once the chemists know the structure of the natural drug, they can:

• modify it slightly to make it more effective or less toxic;
• synthesise larger quantities than the natural source allows;
• design entirely new drugs based on knowledge of the disease.

Some examples of UK-developed drugs: digoxin (a purified form of digitalis still prescribed by the NHS), modified penicillins (amoxicillin), beta-blockers for heart disease (developed at ICI in the 1960s).

Before a new drug reaches NHS pharmacies, regulators (the UK MHRA — Medicines and Healthcare products Regulatory Agency) require evidence on three things. AQA mark schemes label these as the three test criteria:

1. Toxicity — is the drug safe? Does it harm cells, tissues or whole organisms? Many promising compounds fail at this stage.
2. Efficacy — does it actually work? Does it treat the target disease better than nothing (and ideally better than existing drugs)?
3. Dose — what amount is both safe and effective? Too little = no effect; too much = toxic. The right dose may differ between adults and children, or by body mass.

These three are tested in stages, starting in a laboratory (preclinical) and moving to live humans (clinical). Each stage adds cost, time and ethical constraints, so most drug candidates drop out along the way. Of about 10,000 compounds screened, fewer than 10 might make it to clinical trials and only 1–2 might be approved.

Why this matters. The Thalidomide scandal of the late 1950s — a sleep / morning-sickness drug that wasn't tested for effects on developing babies and caused thousands of severe birth defects in the UK and worldwide — drove the modern, much stricter testing system. UK drug regulation tightened dramatically after Thalidomide; modern preclinical testing on pregnant animals is one of the responses.

Preclinical testing — in the laboratory.

1. Cells and tissues. The drug is tested on cells grown in culture (e.g. cancer cells, liver cells) to check it has an effect and isn't toxic at the cellular level.
2. Live animals. If cells survive, the drug is tested on live animals (often mice or rats), to check effects on whole-body systems — circulation, kidneys, liver. UK law requires animal testing for new medicines unless an equally rigorous non-animal method exists.

Only drugs that pass both preclinical stages move forward.

Clinical trials — in humans. Run in three phases:

Phase	Who	Purpose	Number
Phase 1	Healthy volunteers, very low doses	Check for toxicity, side effects, dose tolerance	~20–80 people
Phase 2	Patients with the disease, optimum dose worked out	Check efficacy, refine dose	~100–300
Phase 3	Many patients, full dose	Confirm efficacy vs existing treatments, watch for rare side effects	~1,000–3,000

A drug only passes to the next phase if it does well in the previous one.

Placebo and double-blind trials. In Phase 2 and 3, patients are usually divided into two groups:

• Treatment group — gets the real drug.
• Control group — gets a placebo (a dummy treatment that looks identical to the real drug — same pill, same liquid — but contains no active ingredient).

Comparing the two groups shows whether the drug really helps or whether patients just feel better because they expect to (the placebo effect).

A blind trial = patients don't know which group they are in. A double-blind trial = neither the patient nor the doctor knows. This prevents the doctor unconsciously treating the two groups differently and prevents the patients reporting symptoms differently. Only an outside statistician knows the code, revealed when the data are analysed.

Approval (regulatory review). After successful Phase 3, the drug company submits all the data to the MHRA (UK) and equivalent agencies. They review the toxicity, efficacy and dose data and decide whether to license the drug for NHS use. After approval, Phase 4 (post-marketing surveillance) continues to monitor for rare or long-term side effects.

Placebo effect. Patients often report feeling better even when given a dummy treatment, simply because they expect to. This is real (well-documented in the British Medical Journal and elsewhere) and it could make a useless drug look effective unless we control for it.

How a placebo-controlled trial works:

1. Patients are randomly allocated to the treatment group or the control group.
2. The treatment group gets the real drug; the control group gets a placebo (identical-looking pill, injection or liquid with no active ingredient).
3. After a fixed time, the two groups' outcomes are compared. The drug is only judged effective if the treatment group does significantly better than the placebo group.

Levels of blinding:

• Open trial — both patient and doctor know which group the patient is in. Most prone to bias.
• Blind (single-blind) trial — patient doesn't know; doctor does. Reduces patient bias.
• Double-blind trial — neither patient nor doctor knows. The codes are held by a third party (e.g. a statistician) and only revealed at the end. This is the gold standard and is required for AQA full marks.

Ethics. Sometimes giving a placebo is unethical (e.g. for serious diseases with existing treatments). In that case, the control group gets the current best treatment rather than nothing, and the new drug is compared against the existing standard.