HookThe number that decides whether a disease dies out
Measles is the most contagious human disease we know of. Drop one infected person into a room of people with no immunity and they will, on average, infect 15 others — a figure epidemiologists call \(R_0\). Chickenpox sits around 10, seasonal flu closer to 1.3. That one number explains why measles needs a vaccination rate above 90 per cent to stop spreading, why the UK lost its 'measles eliminated' status in 2019 when uptake slipped, and why a disease that kills one or two in every thousand people it infects keeps returning the moment a community's defences drop.
B3 is the biology behind that arithmetic. It asks what a pathogen is and how it spreads, how your body fights one off with white blood cells before you even feel ill, how a vaccine trains that response in advance, and where the drugs that finish the job came from and how they are tested. It is, in short, the story of the arms race between us and the microbes that live off us.
ModelPathogens and how disease spreads
A communicable disease is one that can be passed on, and it is caused by a pathogen — a microorganism that infects a host. There are four kinds: bacteria, viruses, protists and fungi. Bacteria and viruses make you ill in different ways. Many bacteria reproduce rapidly inside the body and release toxins that damage tissues and produce the symptoms. Viruses are much smaller; they take over the host's own cells, reproducing inside them until the cell bursts, which damages tissues directly.
Pathogens spread by three main routes: through the air (droplets released when you cough or sneeze, as with measles and flu), through water (drinking or bathing in contaminated water), and by direct contact (touch, or in some cases sexual contact). Because the routes are limited, so are the defences: better hygiene such as handwashing, destroying the vectors that carry pathogens, isolating infected individuals, and vaccination. Every 'suggest how to reduce spread' question is answered by matching a control to the route the pathogen actually uses.
CaseFour kinds of pathogen, four sets of named diseases
AQA names specific diseases and expects the detail, following the same pattern each time: the pathogen, the symptoms, how it spreads and how spread is prevented. Viral — measles spreads in droplets and causes fever and a rash, and is dangerous enough that children are vaccinated; HIV spreads in body fluids and, untreated, attacks white blood cells until the immune system can no longer cope, the stage called AIDS, and is now controlled with antiretroviral drugs; tobacco mosaic virus gives plants a mosaic of discoloured leaf that reduces photosynthesis.
Bacterial — Salmonella causes food poisoning, with fever, cramps, vomiting and diarrhoea from the toxins it releases, and in the UK poultry are vaccinated against it; gonorrhoea is a sexually transmitted disease with a thick yellow-green discharge and pain on urinating, once cured easily with penicillin but now often antibiotic-resistant, so barrier contraception matters.
Fungal — rose black spot marks leaves with purple-black patches, cutting photosynthesis and growth, spreads in water and wind, and is treated with fungicides or by removing affected leaves. Protist — malaria is caused by a protist carried by mosquitoes acting as vectors, causes recurrent bouts of fever, and is controlled by killing mosquitoes and stopping bites with nets.
MechanismYour body's defences
Before any specific response, the body keeps most pathogens out with non-specific barriers. The skin is a physical barrier and secretes antimicrobial substances. The nose has hairs and mucus that trap particles. The trachea and bronchi are lined with mucus and cilia that waft trapped pathogens back up to be swallowed. The stomach produces hydrochloric acid that kills most pathogens in swallowed mucus and food.
If a pathogen gets past these, white blood cells attack in three ways. Phagocytosis — a white blood cell engulfs and digests the pathogen. Antibody production — white blood cells release proteins with a shape specific to that pathogen's antigens, locking onto that one pathogen and marking it for destruction. Antitoxin production — other proteins neutralise the toxins that bacteria release. The specificity is the whole point: an antibody made against measles will not touch the flu, which is precisely why being immune to one disease gives you no protection against another.
MechanismVaccination and herd immunity
A vaccine contains small quantities of a dead or inactive form of a pathogen. Introduced into the body, it carries the pathogen's antigens, so white blood cells respond by producing the matching antibodies — all without you becoming ill. If the real pathogen later invades, the white blood cells 'remember' it and produce the correct antibodies rapidly and in large numbers, destroying it before it can make you sick.
Vaccinate enough of a population and the pathogen can no longer find enough susceptible hosts to spread, so even people who cannot be vaccinated are protected. This is herd immunity, and how high the threshold sits depends on how contagious the disease is — which is exactly the arithmetic behind the measles story in the introduction.
The fraction of a population that must be immune for herd immunity can be estimated from \[\text{threshold} = 1 - \dfrac{1}{R_0},\] where \(R_0\) is the number of people one case would infect in an unprotected population. For measles, \(R_0 \approx 15\), so the threshold is \(1 - \dfrac{1}{15} = 1 - 0.067 = 0.933\) — about 93 per cent of people must be immune. For a less contagious disease with \(R_0 = 4\), it is \(1 - \dfrac{1}{4} = 0.75\), just 75 per cent. This is why measles needs one of the highest vaccine coverage rates of any disease: its \(R_0\) is so high that even a small drop in uptake pushes the immune fraction below the threshold and lets the disease spread again.
MechanismAntibiotics, painkillers and the resistance problem
Antibiotics, such as penicillin, kill bacteria inside the body, and their introduction dramatically cut the number of deaths from bacterial disease. Two limits are tested constantly. First, specific bacteria need specific antibiotics, so the right one must be chosen. Second — and this is the classic trap — antibiotics cannot kill viruses, because a virus reproduces inside the body's own cells, where a drug cannot reach it without also damaging the cell. A sore throat caused by a virus will not respond to antibiotics at all.
Painkillers and similar medicines treat the symptoms of a disease but do not kill the pathogen — paracetamol lowers a fever without touching the microbe causing it. Meanwhile the overuse of antibiotics has driven antibiotic resistance: bacteria such as MRSA that happen to survive treatment go on to reproduce, so the resistant strain becomes more common. That is natural selection playing out in a hospital ward, and it is why doctors now avoid prescribing antibiotics for mild or viral infections.
CaseWhere drugs come from and how they are tested
Many drugs began in plants and microorganisms. Digitalis, a heart drug, comes from foxgloves; the painkiller aspirin originates in willow bark; and penicillin was discovered by Alexander Fleming in 1928, when a mould of the genus Penicillium killed the bacteria on a culture plate he had left out. Most new drugs today are synthesised by chemists, but the starting point is still often a natural compound.
A new drug is then tested in stages for toxicity (is it safe?), efficacy (does it work?) and dose (how much is needed?). Preclinical testing uses cells, tissues and then live animals. Clinical trials use human volunteers: very low doses are given first to healthy people to check safety, then patients receive it to find the optimum dose. To remove bias, trials are often double-blind — neither the patient nor the doctor knows who is receiving the drug and who is receiving a placebo — and the results are peer-reviewed before publication so that false claims are caught. That sequence, from foxglove to peer review, is a favourite 'describe how a new drug is developed' answer.
VocabularyKey terms the mark scheme pays for
TrapsMisconceptions that cost marks
ExamWhat examiners want
B3 rewards precision with categories. If a question gives you a disease, state the type of pathogen — bacterium, virus, protist or fungus — because the mark scheme keys the symptoms and controls to it. The single most-tested trap is that antibiotics do not kill viruses, so expect it and explain why: viruses reproduce inside the body's own cells. Across the paper about 40 per cent of marks are AO1 recall and 40 per cent AO2 application, and B3's applied marks usually come from an unfamiliar disease or a set of vaccination-uptake data, so read graphs carefully and quote the figures.
Command words matter here too. 'Describe how the body defends itself' wants the ordered sequence — barriers first, then phagocytosis, antibodies and antitoxins — not a jumble. 'Explain how a vaccine works' must reach the second exposure: the rapid production of antibodies on re-infection is the marking point students most often forget. On the 6-mark extended responses examiners use levels of response, so answer drug development or immune defence as one logical chain. Where a question includes data — resistance rates, coverage percentages, contagiousness — an AO3 evaluation that quotes the numbers and states a limitation will always outscore a purely verbal answer.