AQA GCSE Biology (8461)

4.3.1 Communicable diseases

Communicable diseases is a huge GCSE topic — it covers the four types of pathogen, how they spread, the body's three lines of defence, vaccination, antibiotics, and drug development. This page works through each piece with the exact marking phrases AQA examiners want. By the end you'll be able to describe how a phagocyte engulfs a bacterium, explain why a vaccine gives long-term immunity, and write a 4-mark answer on why antibiotics don't work on viruses.

Why this matters

Throughout history, the biggest killers have been infectious diseases — plague, smallpox, cholera, tuberculosis, malaria. Today we control most of them in wealthy countries, but globally pathogens still kill millions every year (HIV, TB, malaria, plus emerging diseases like COVID-19). Understanding how pathogens infect, how the body fights back, and how vaccines and antibiotics work is some of the most important biology you learn at school. The four types of pathogen (bacteria, viruses, fungi, protists) all have different structures and life cycles, which is why the same drug can't treat all of them. The body's defences are layered — physical barriers (skin, mucus), chemical barriers (stomach acid), and the immune system itself (white blood cells). Vaccines train the immune system; antibiotics kill bacteria; the body does most of the rest.

How to learn this topic

Build on what you already know

GCSE 4.1.1: bacteria are prokaryotic; viruses are not cells; ribosomes / membranes / nucleus etc.
GCSE 4.2.2: blood contains white blood cells; the digestive system has hydrochloric acid.
KS3: germs spread between people; we get vaccinated against diseases.

Define pathogens and the four types — bacteria, viruses, fungi, protists.
Name one canonical disease example for each type.
How pathogens spread (air, water, direct contact, vectors).
Three lines of defence: physical barriers → chemical barriers → immune system.
How white blood cells work: phagocytosis + antibodies + antitoxins.
Vaccination: dead/inactive pathogen → triggers immune response → memory cells.
Antibiotics work on bacteria only (not viruses) — and antibiotic resistance is a growing problem.
Drug development pipeline: preclinical → clinical trials (3 phases) → approval.

Key terms

pathogen: A microorganism that causes an infectious (communicable) disease. Four types: bacteria, viruses, fungi, protists. (Examiners reward 'microorganism that causes disease'. Don't just say 'germ' or 'bug'.)
communicable disease: A disease that can be transmitted between organisms — caused by a pathogen.
antigen: A molecule on the surface of a pathogen that the immune system recognises as foreign. (Antigens are on the PATHOGEN. Antibodies are made by the BODY in response. Don't muddle them.)
antibody: A Y-shaped protein made by lymphocytes that binds specifically to one type of antigen and marks the pathogen for destruction. (Specific = one antibody binds one antigen. Antibodies do not 'eat' pathogens — they tag them. Phagocytes do the eating.)
phagocyte: A type of white blood cell that engulfs and digests pathogens (phagocytosis). A non-specific defence — works on any pathogen. (Phagocytes engulf. Lymphocytes produce antibodies. Different jobs.)
lymphocyte: A type of white blood cell that produces antibodies (specific to a particular antigen) and antitoxins, and forms memory cells after an infection. (Lymphocytes provide SPECIFIC immunity — they remember particular pathogens. Phagocytes are non-specific.)
antitoxin: A substance produced by lymphocytes that neutralises a toxin released by a bacterial pathogen. (Antitoxins target bacterial TOXINS — not the bacteria themselves.)
memory cell: A long-lived lymphocyte that remains in the body after an infection or vaccination. Responds rapidly to the same pathogen if it appears again. (Memory cells are the basis of long-term immunity AND of how vaccines work. Two marking-phrase contexts.)
vaccine: A preparation containing dead or inactive forms of a pathogen (or just its antigens). Introduced into the body to trigger an immune response and produce memory cells, without causing the disease. (Examiners want 'dead OR inactive' — vaccines do not contain live disease-causing pathogens.)
herd immunity: When a large enough proportion of the population is immune (through vaccination or recovery) that the pathogen cannot spread effectively. Protects unvaccinated individuals too. (Marking phrase: 'reduces the spread' or 'protects those who cannot be vaccinated'.)
antibiotic: A medicine, such as penicillin, that kills bacterial pathogens or stops them growing. Specific to bacteria — does NOT work against viruses. (AQA always tests 'antibiotics do not work against viruses' — memorise the reason: viruses live inside body cells, don't have bacterial machinery.)
antibiotic resistance: When bacteria evolve so antibiotics no longer kill them. Driven by overuse of antibiotics — random mutations that confer resistance are selected for. (Linking word: 'selection pressure'. Overuse selects for resistant strains.)

Notes

Pathogens — four types

A pathogen is a microorganism that causes a communicable disease. Four kinds you must know:

| Type | Structure | Example disease |

|---|---|---|

| Bacteria | prokaryotic cells (no nucleus, plasmids) | salmonella food poisoning; gonorrhoea (STI); tuberculosis |

| Viruses | not cells at all — just genetic material in a protein coat | measles, HIV, common cold, COVID-19 |

| Fungi | eukaryotic, often multicellular | rose black spot (plants); athlete's foot (humans) |

| Protists | eukaryotic, single-celled | malaria (caused by Plasmodium, spread by mosquitoes) |

How pathogens spread

Through the air — droplets from coughs/sneezes; inhaled by others (flu, measles, COVID).
Through water — drinking contaminated water (cholera).
Direct contact — touching infected skin or fluids (athlete's foot, STIs).
Vectors — animals that carry pathogens (mosquitoes spread malaria; ticks spread Lyme disease).
Food — eating contaminated food (salmonella from undercooked meat).

Reducing spread: hygiene (handwashing, food safety), isolating infected people, vaccination, destroying vectors, treating water supplies.

The body's three lines of defence

### 1. Physical barriers

Skin — tough, dry, mostly impenetrable to pathogens; produces antimicrobial secretions.
Nose — hairs and mucus trap pathogens before they reach the lungs.
Trachea + bronchi — lined with ciliated epithelial cells that beat in unison to sweep mucus (with trapped pathogens) up to the throat to be swallowed.

### 2. Chemical barriers

Stomach acid — hydrochloric acid (~pH 2) kills most pathogens swallowed in food or mucus.
Lysozyme in tears + saliva — enzyme that breaks down bacterial cell walls.

### 3. The immune system — white blood cells

If a pathogen breaches the physical and chemical barriers, white blood cells take over. Three things they do:

Phagocytosis — a phagocyte (a type of white blood cell) engulfs the pathogen and digests it using enzymes inside the cell. Non-specific — works on any pathogen.
Antibody production — lymphocytes detect the unique antigens on a pathogen's surface and produce specific antibodies that bind to those antigens. Antibodies clump the pathogens together (agglutination), marking them for destruction.
Antitoxin production — some lymphocytes produce antitoxins that neutralise the toxins released by bacterial pathogens.

After the infection clears, some lymphocytes become memory cells — they stay in the body and respond much faster (and produce many more antibodies) if the same pathogen ever returns. This is what gives long-term immunity.

Vaccination — training the immune system

A vaccine contains a dead or inactive form of the pathogen (or just its antigens). When you're vaccinated:

The dead/inactive pathogen carries the same antigens as the live pathogen — but can't make you ill.
Lymphocytes recognise the antigens and produce antibodies specific to that pathogen.
Memory cells are produced and remain in the body.
If the live pathogen ever infects you, the memory cells respond rapidly — producing antibodies fast enough to destroy the pathogen before symptoms develop.

This is active immunity — your own immune system has been triggered.

Herd immunity — if most of the population is vaccinated, the pathogen can't spread easily; even unvaccinated people are protected.

Antibiotics — only against bacteria

Antibiotics (e.g. penicillin) are medicines that kill bacterial pathogens inside the body. They work by interfering with bacterial cell processes (e.g. cell wall synthesis, protein synthesis on 70S ribosomes) — without harming our own cells (which lack a peptidoglycan cell wall and have 80S ribosomes).

Antibiotics do NOT work on viruses. Viruses live inside our own cells and don't have the bacterial machinery antibiotics target. Antivirals exist but are much harder to design.

Antibiotic resistance is a growing problem: bacteria with random mutations that make them survive an antibiotic course pass on those genes (especially via plasmids). Repeated antibiotic use selects for resistant strains. Slowing this requires: only using antibiotics when essential, finishing the full course, and developing new antibiotics. MRSA is a famous resistant strain.

Drug development pipeline

New drugs go through testing:

Preclinical testing — tested on cells, then on animals. Checks safety, efficacy, and dose.
Clinical trials phase 1 — healthy human volunteers, very low doses. Checks safety in humans.
Clinical trials phase 2 — small group of patients with the disease. Checks the drug works.
Clinical trials phase 3 — large group of patients, often double-blind placebo-controlled (neither doctor nor patient knows who's getting the real drug). Checks effectiveness vs control.
Approval + monitoring — drug licensed; long-term effects tracked after release.

The whole process typically takes 10+ years and costs hundreds of millions.

Plant diseases (briefly)

Plants get pathogens too:

Rose black spot — fungal disease; black/purple spots on leaves; reduces photosynthesis.
Tobacco mosaic virus (TMV) — viral disease; gives leaves a mottled appearance; reduces photosynthesis.

Plants defend themselves with: tough waxy cuticle, cellulose cell walls, antimicrobial chemicals (some make tannins, alkaloids, antifungal compounds), and physical responses (thorns, hairs that deter herbivores).

Exam tips

Always name the FOUR types of pathogen: bacteria, viruses, fungi, protists. Add one named disease example for each: salmonella, measles, rose black spot, malaria.
Antibodies are SPECIFIC — one antibody fits one antigen. State 'complementary shape' for the bind in extended answers.
Phagocytes ENGULF; lymphocytes PRODUCE ANTIBODIES. Don't muddle the jobs of the two white blood cell types.
Vaccines contain 'dead or inactive' pathogen — this is the exact marking phrase. Both halves needed.
On vaccination questions, name 'memory cells' explicitly — they're what give long-term immunity.
Antibiotics work on bacteria, NEVER on viruses. The marking-phrase reason: 'viruses live inside body cells / don't have bacterial cell walls or ribosomes'.
Antibiotic resistance = natural selection. Mutations are random; the antibiotic selects for the resistant bacteria. Don't say bacteria 'become' resistant — they ALREADY were, and the antibiotic killed the non-resistant ones.

Mark-scheme phrasing

Common misconceptions

Worked example

Question:

Answer:

Frequently asked questions

What are the four types of pathogen?

BACTERIA — prokaryotic cells (e.g. salmonella food poisoning, gonorrhoea, tuberculosis). VIRUSES — not cells; just genetic material in a protein coat (e.g. measles, HIV, COVID, common cold). FUNGI — usually eukaryotic and multicellular (e.g. athlete's foot, rose black spot in plants). PROTISTS — single-celled eukaryotes (e.g. malaria, caused by Plasmodium). Each type has different structure and life cycle, which is why different drugs are needed to treat each — antibiotics work on bacteria, antivirals (sort of) on viruses, antifungals on fungi.

How does the immune system fight pathogens?

If physical barriers (skin, mucus) and chemical barriers (stomach acid) fail to keep pathogens out, white blood cells take over. PHAGOCYTES engulf pathogens (phagocytosis) and digest them with internal enzymes — non-specific. LYMPHOCYTES recognise the unique antigens on each pathogen and produce ANTIBODIES specific to those antigens — antibodies bind to pathogens and clump them together (agglutination), making them easier for phagocytes to find. Lymphocytes also produce ANTITOXINS to neutralise bacterial toxins. After the infection is cleared, some lymphocytes become MEMORY CELLS that provide long-term immunity.

Why do antibiotics not work on viruses?

Because antibiotics target features specific to bacterial cells — like the bacterial cell wall (made of peptidoglycan) or the bacterial 70S ribosome. Viruses don't have those features. Viruses aren't really cells at all — they're packages of genetic material in a protein coat that hijack OUR body cells to reproduce. Designing a drug that kills viruses inside our cells without also harming the cells themselves is much harder than killing bacteria — which is why antivirals are rare and antibiotics are common.

How does a vaccine give long-term immunity?

A vaccine contains dead or inactive forms of a pathogen (or its antigens) — enough for the immune system to recognise but not enough to make you ill. When you're vaccinated: (1) lymphocytes detect the antigens; (2) they produce specific antibodies; (3) some become memory cells. The memory cells stay in your body for years — sometimes for life. If the real, live pathogen later infects you, the memory cells respond MUCH faster than they did the first time, producing antibodies before you even feel ill. That's why vaccinated people don't usually develop the disease.

What is antibiotic resistance and why is it a problem?

Antibiotic resistance is when bacteria evolve so antibiotics no longer kill them. It happens because: (1) random mutations in bacterial DNA sometimes confer resistance to a particular antibiotic; (2) when the antibiotic is used, the resistant bacteria survive while the non-resistant ones die — this is natural selection; (3) the resistant bacteria multiply and pass on the resistance genes (sometimes by plasmids, which can transfer between species). The problem is that as more bacteria become resistant, our antibiotics stop working — and developing new ones is slow and expensive. MRSA is a famous resistant strain.

What's the difference between an antigen and an antibody?

Easy to muddle. ANTIGEN: a molecule on the SURFACE of a pathogen (or any foreign cell) that the immune system recognises as foreign. ANTIBODY: a Y-shaped protein that the BODY makes (specifically, lymphocytes) in response to a particular antigen — antibodies bind to that antigen and mark the pathogen for destruction. Memory aid: anti-GEN = on the GERM; anti-BODY = made by the BODY.