Hi Tara. One honest piece of housekeeping before you start, because it should change how you spend your time. Cambridge numbers the whole of Topic 15 as a single section, 15.1. There is no official 15.2, 15.3 or 15.4 — that split is mine, for teaching and so the papers on this site can report your score in pieces. And this is the smallest topic on the 0610 syllabus: five objectives in total, four Core and one Supplement. You can learn every fact in it in an evening.
So budget accordingly. Do not give this topic the revision time you would give Topic 14. The recall is small, and once you have it, re-reading it a fifth time earns you nothing. What is worth your time is the other half: applying these five facts to data you have never seen, and to biology you already know — bacterial cell structure from Topic 2, diffusion from Topic 3, enzymes from Topic 5, and above all pathogens, transmission and body defences from Topic 10. That is where the questions actually live, and it is where this guide spends most of its words.
Here is the shape. 15.1 is the definition of a drug and what antibiotics do — including the idea that makes them possible at all, and how you measure whether one works. 15.2 is resistance and why antibiotics do nothing whatever to viruses; both of those are structural arguments, not vague ones. 15.3 is the Supplement objective: using antibiotics only when essential, and MRSA. 15.4 is the vocabulary that scores, the phrases that do not, and how to attack the data question.
The Definition, and It Is Worth Learning Word for Word
This is a one-mark answer that people write in four vague lines and still fail to score. Learn the sentence, not the idea.
A drug is any substance taken into the body that modifies or affects chemical reactions in the body.
Now look hard at what that sentence does not say. It does not say harmful. It does not say illegal. It does not say medicine. It does not say the substance has to be swallowed, or made in a factory, or prescribed by a doctor. Cambridge has written the widest definition it could, deliberately, and the exam question is usually testing whether you noticed.
So all of these are drugs, by that definition:
- Paracetamol, which changes the chemical reactions that produce the sensation of pain.
- An antibiotic, which affects chemical reactions — in the bacteria, which are inside the body.
- Insulin injected by a person with diabetes. It is a substance taken into the body and it changes how much glucose is taken out of the blood. That it is also a hormone the body normally makes itself does not stop it being a drug when it is injected.
The phrase that matters most is chemical reactions in the body, because that is the hook that ties this topic to the rest of biology. The chemical reactions of the body are controlled by enzymes — that is Topic 5 — so a drug typically works by changing the rate of a reaction: speeding one up, or blocking one by getting in the way of an active site. Whenever a question asks you to explain how a drug works, the word enzyme is usually the sentence you are reaching for.
“A substance that changes the chemical reactions in the body” scores. These do not: “a substance that makes you feel different” (no mention of chemical reactions), “a harmful substance you take” (the definition never says harmful), and “a medicine used to treat illness” (far too narrow — and it accidentally excludes half the things the definition covers).
What Antibiotics Are For — One Sentence, Then Three Things They Are Not
Cambridge’s wording is precise and short: antibiotics are used for the treatment of bacterial infections. They kill bacteria; some kinds instead stop the bacteria reproducing, which amounts to the same thing for your purposes, because a population that cannot reproduce stops growing and the body clears it.
Now three things an antibiotic is not, because these three misconceptions between them cause most of the lost marks in the whole topic.
| Students often write | What is actually true |
|---|---|
| “The antibiotic relieves the symptoms.” | An antibiotic is not a painkiller and does nothing directly to a sore throat or a fever. Symptoms improve because the number of bacteria falls, so less damage and less toxin are produced. The symptom relief is a consequence, two steps down the chain. |
| “The antibiotic boosts the immune system.” | It does no such thing. It reduces the bacterial population so that the body’s own defences can finish the job — the phagocytes that engulf and digest the pathogens, and the lymphocytes that produce antibodies, all of which you met in Topic 10. The antibiotic buys those cells time and reduces the workload; it does not make them stronger. |
| “The antibiotic cures the infection.” | “Cures” is not a mechanism and mark schemes tend not to credit it. Write kills the bacteria. That is the process; recovery is the outcome. |
The Idea That Makes Antibiotics Possible At All
Here is a question worth sitting with for a minute, because it is where the good marks are hiding. You are made of cells. Bacteria are cells. If a substance is poisonous enough to kill a bacterial cell, why does it not kill you as well?
The answer is that a useful antibiotic attacks something a bacterial cell has and a human cell does not. Nothing more clever than that. Go back to Topic 2.1 and put the two lists side by side.
| Structure | Bacterial cell | Animal cell |
|---|---|---|
| Cell wall | Yes | No — none at all |
| Cell membrane | Yes | Yes |
| Cytoplasm | Yes | Yes |
| Ribosomes | Yes, but not the same as ours | Yes |
| Nucleus | No — the DNA is a circular molecule loose in the cytoplasm | Yes |
| Plasmids | Yes — small rings of DNA | No |
| Mitochondria | No | Yes |
Every difference in that table is a possible target. Three of them are the ones worth knowing.
- The cell wall. Some antibiotics stop the bacterium building or repairing its cell wall. Since an animal cell has no cell wall at all, there is simply nothing in you for the drug to act on. This is the cleanest example of the idea and the one to quote if you are given a choice.
- The ribosomes. Ribosomes are where proteins are made (Topic 2.1). Bacterial ribosomes are not the same as human ribosomes, so a molecule can be shaped to bind to the bacterial one and not to yours. The bacterium then cannot make the proteins it needs — including its enzymes — and dies.
- An enzyme the bacterium uses and you do not. Straight Topic 5 reasoning: a molecule with a shape complementary to that enzyme’s active site occupies the site, the substrate cannot bind, and that reaction stops. You have no such enzyme, so no reaction of yours is affected.
“The antibiotic acts on a structure that a bacterial cell has and a human cell does not, so human cells are unaffected.” Then name the structure the question has given you. Almost every “suggest why” question about antibiotic safety is that sentence with one noun swapped.
Measuring Whether an Antibiotic Actually Works: the Plate
This is the single most examined practical in the topic, so learn it as a procedure and not as a picture. Bacteria of one species are spread evenly over agar to make a lawn. Small paper discs, each soaked in a different antibiotic, are placed on the lawn. The plate is incubated. Wherever the antibiotic has prevented growth, the agar stays clear.
Why is the clear zone circular, and why does it stop where it stops? Because of diffusion — Topic 3.1. The antibiotic is at high concentration in the disc and at zero concentration in the agar around it, so there is a concentration gradient in every direction, and the net movement of the antibiotic molecules is down that gradient, equally on all sides. That is why the zone is a circle centred on the disc. As you move outwards the antibiotic is spread through more and more agar, so its concentration falls with distance. Somewhere there is a distance at which the concentration is no longer high enough to prevent growth, and that circle is the edge of the clear zone.
A larger clear zone means the bacterium is more sensitive to that antibiotic. Sensitive, not weaker; and it says nothing about how dangerous the bacterium is.
No zone at all means the bacterium is resistant to that antibiotic. It has grown right up to the edge of the disc.
Measure the diameter, in millimetres, straight across the centre of the disc. Not the radius, not the gap from the edge of the disc to the edge of the zone, and never “the size of the white circle”.
“How much larger is C than A” divides by A, because A is the thing you are comparing to. Divide by 34 instead and you get 23.5 %, which is a real number answering a different question, and it earns nothing. Before you press a single key, write down what the denominator is. This is the commonest arithmetic error in the whole subject, and it costs two marks at a time.
Watching an Antibiotic Work in a Flask — and Why You Need the Second Flask
The plate tells you whether an antibiotic works. A liquid culture tells you what it does over time, and it is a favourite Paper 4 graph because it also tests whether you understand a control.
Read it carefully. Both flasks start at 10 thousand bacteria per cm³. For the first four hours the two curves are the same, which is what you expect, because until the antibiotic goes in nothing is different. At 4 hours the antibiotic is added to flask 2. Flask 1 carries on growing to 900 thousand per cm³ by 12 hours. Flask 2 peaks at about 62 thousand at 4 hours, is still 60 at 5 hours, and then falls away to 2 thousand by 12 hours.
Two details are worth more than the shape:
- Flask 1 is the control. Without it, if flask 2 stopped growing you could not say why. The broth might simply have run out of nutrients; the temperature might have drifted. Flask 1 is identical in every way except that no antibiotic was added, so it tells you what would have happened anyway. Any difference between the flasks after 4 hours must therefore be caused by the antibiotic.
- Flask 2 does not reach zero. Read the graph, not your expectations: 2 thousand per cm³ are still alive at 12 hours. That is a real and examinable observation, and later in this guide you will meet exactly what it implies.
Look at flask 2 straight after the antibiotic is added at 4 hours. The number stops rising and falls only slowly at first, from 62 thousand to 60 thousand per cm³ in the first hour. After that it falls quickly, to 2 thousand by 12 hours.
The early fall is slow because the antibiotic has to spread through the broth and reach the bacteria, and killing them takes time. A short delay between adding a substance and seeing its full effect is normal biology, and saying so, with the figures, is often a mark. Always describe what the graph actually shows, not what you expected it to show.
The Core Statement, and the Single Word That Decides the Mark
The Core objective is one sentence: some bacteria are resistant to antibiotics, which reduces the effectiveness of antibiotics. Notice how carefully that is worded. Not all bacteria. Not that antibiotics stop working altogether. Some bacteria, and the effect is a reduction in effectiveness.
And now the sentence that decides whether the rest of your answer scores:
The bacterium is resistant. The person never is.
Resistance is a property of the bacterial cell — something about that cell means the antibiotic cannot kill it. It is not something that happens to you, it does not build up in your body, and it is not passed from a bacterium to its host.
“My body has become resistant to antibiotics” is a sentence you will hear people say, and it is wrong in a way that destroys the whole answer. What is actually true is that the bacteria that person is carrying include resistant ones. Change the subject of the sentence from the person to the bacterium and everything else you write will point the right way.
Where Resistance Comes From: Variation, Then Selection
This is the piece of reasoning worth the most marks in the topic, and almost everyone gets the direction of causation backwards on the first attempt. Read the three stages slowly.
- There is variation. A bacterial population is not made of identical cells. In any large population there is variation, and a few bacteria are already resistant before the antibiotic is ever used. This is the step people skip, and it is the step the whole argument rests on. The feature is often carried on a plasmid — one of the small rings of DNA you met in the bacterial cell in Topic 2.1.
- The antibiotic selects. When the antibiotic is used, the non-resistant bacteria are killed. The resistant few are not.
- The survivors reproduce. Those survivors reproduce and pass the resistance on, and they do it with no competition for nutrients or space, because everything else has been removed. The proportion of the population that is resistant therefore rises.
The antibiotic does not create resistance. It selects for it.
If your answer contains “the bacteria became resistant because they were exposed to the antibiotic”, or “the bacteria got used to it”, or “the bacteria learned to survive”, you have described a bacterium changing itself in response to a threat. Nothing in biology works like that. The resistant ones were already there; the antibiotic simply removed everyone else.
Two consequences follow, and both turn up in data questions.
First, this happens fast. Bacteria divide very quickly — in favourable conditions a population can double in twenty minutes — so the make-up of a population can shift measurably over days, not years. That is why a graph of resistance against year can climb so steeply, and why an infection that responded to a drug last month may not this month.
Second, this is why the flask never reached zero. Go back to the growth curve in 15.1: flask 2 had fallen to 2 thousand bacteria per cm³ by 12 hours, the last reading, and it never reached zero. Those survivors are the least easily killed cells in the flask, and they now have the broth to themselves. If the antibiotic stopped working on them, or were used up, they could reproduce and the number would rise again. Hold on to that thought: it is the whole argument of 15.3.
Why Antibiotics Do Absolutely Nothing to a Virus
Cambridge states this as a fact: antibiotics kill bacteria but do not affect viruses. You will be asked to explain it, and the explanation is structural. It is not that antibiotics work “less well” on viruses, or that viruses are “tougher”. It is that there is nothing there to attack.
Go back to Topic 1.3, where the syllabus is unusually blunt: the features of viruses are limited to a protein coat and genetic material. That word limited is doing serious work. A virus is not a cell. It has:
- no cell wall — so an antibiotic that stops cell wall building has nothing to stop;
- no ribosomes of its own — so an antibiotic that binds bacterial ribosomes has nothing to bind to;
- no chemical reactions of its own, and therefore no enzymes of its own — so an antibiotic that blocks a bacterial enzyme has no enzyme to block.
A virus reproduces only inside a host cell, using that cell’s machinery. So the honest summary is: there is no target. And because the reason is a missing target rather than an insufficient dose, a bigger dose does not help. Doubling the amount of a key that does not fit the lock does not open the door.
The common cold. Influenza. Measles. HIV. All four are caused by viruses, so an antibiotic will do nothing for any of them. If a question names one of these and asks whether an antibiotic will help, the answer is no, and the reason is that a virus is not a cell and so has no structure for the antibiotic to act on.
Here is the sharper version of the point, and it is a Supplement-level idea worth having ready. Taking an antibiotic for a viral illness gives the patient no benefit at all — and it still selects for resistance among the harmless bacteria the patient is already carrying, on the skin and in the gut. So the pointless prescription is not neutral. It is a selection event with no upside, which is exactly why 15.3 exists.
This is the one Supplement objective in Topic 15: explain how using antibiotics only when essential can limit the development of resistant bacteria such as MRSA. It is worth noticing that the command word is explain. Cambridge is not asking you to list rules; it is asking you to say why the rules work. And the reason is a single sentence you already have.
Every use of an antibiotic is a selection event.
Each time an antibiotic is used, the non-resistant bacteria in that person are killed and the resistant ones survive and reproduce. So fewer uses means less selection, and the resistant minority stays a minority.
If you write that sentence and then apply it to whatever the question describes, you will score. Every measure below is the same sentence pointed at a different situation.
What “Only When Essential” Means in Practice
| Measure | Why it limits resistance |
|---|---|
| Prescribe antibiotics only for bacterial infections, never viral ones | An antibiotic given for a cold or influenza cannot possibly help the patient, but it still kills their non-resistant bacteria and lets the resistant ones reproduce. It is selection with no benefit at all — the easiest use to remove. |
| Complete the full course | Symptoms stop long before the bacteria do. The bacteria still alive when you feel better are the hardest to kill, so stopping early leaves exactly those alive to reproduce, with no competition. |
| Do not use antibiotics routinely in farm animals to make them grow faster | This is selection happening continuously, in enormous numbers of animals, with no infection being treated at all. Resistant bacteria selected there can reach people through food and the environment. |
| Keep some antibiotics in reserve | An antibiotic that is rarely used stays effective, because it is rarely selecting. Reserving it means there is still something left that works when an infection is resistant to everything else. |
| Hygiene — hand washing, and isolating infected patients | This one does not reduce selection; it reduces transmission. Straight from Topic 10: a resistant strain spreads by direct contact and from contaminated surfaces. Stopping it moving from patient to patient means fewer people need treating, which in turn means fewer selection events. |
Why Finishing the Course Matters — Read the Graph, Not the Slogan
“Finish the course” is something people are told and rarely understand. The graph makes the argument properly.
Both start with 1000 arbitrary units of bacteria. Both fall the same way: 700 on day 1, 420 on day 2, 210 on day 3. By day 3 the numbers are down by nearly 80 % and both patients feel well — and that is exactly the trap, because symptoms disappear long before the bacteria do.
The patient who finishes the ten days carries on down: 95, 40, 16, 6, 2, 1, and 0 by day 10. The patient who stops on day 3 leaves 210 bacteria alive, and they climb straight back — 240, 340, 520, 700, 860, 960 and 1000 again by day 10. The infection returns, and there is a second problem hidden inside the first.
Most candidates get the first half: stopping early means bacteria are left alive, so the infection can return. The second half is where the marks are. The bacteria still alive on day 3 are the least easily killed ones in the population — the more sensitive ones died first. So stopping early leaves behind precisely the bacteria you least wanted to keep, and hands them a body with no competition in it. That is why incomplete courses select for resistance particularly efficiently.
MRSA
MRSA stands for methicillin-resistant Staphylococcus aureus, and the first thing to fix is what kind of thing it is.
MRSA is a bacterium. Not a virus, not a disease you catch from dirt, and not a separate species — it is Staphylococcus aureus, a bacterium that many healthy people carry harmlessly on their skin and in their noses.
It is resistant to several antibiotics at once, which is why infections with it are hard to treat: the obvious choices simply do not work.
It matters most in hospitals. That is where people have broken skin from wounds, catheters and operations, where defences are already lowered by illness, and where antibiotics are used most, so selection pressure is highest.
Notice how neatly that last point ties Topic 15 to Topic 10. The skin is one of the body defences on the syllabus list, and a surgical wound is a hole in it. A bacterium living harmlessly on the skin is not a pathogen until it gets somewhere it should not be. That is why hand washing and isolation appear in an antibiotics question at all — they are working on direct contact and contaminated surfaces, the two transmission routes that matter most on a ward.
Reading a Resistance Trend — and Being Careful About What It Proves
P went from 4 % to 48 %. That is a rise of 44 percentage points. It is also a rise of (44 ÷ 4) × 100 = 1100 % of the original value. Both statements are true and they are answers to different questions. If the question says “calculate the percentage increase”, it wants the second one. If it says “how much did the percentage rise by”, it wants the first. Read which is being asked and say which you have given.
One more honest note about evidence, because a good evaluation sentence is often the last mark on a Paper 4 question. Countries and hospitals that have cut prescribing have seen resistance rates level off or fall. That is genuinely encouraging, and it is still correlation. An answer that says “this supports the idea that reducing use reduces selection, although other factors changed at the same time and were not controlled” is a stronger answer than one that says either “this proves it” or “this shows nothing”.
The recall in this topic is four sentences long. That means the marks are decided almost entirely by how you write, not by how much you know — which is unusual, and useful, because writing is something you can fix in an evening.
Reading the Command Word
State — one sentence, no reason wanted. “State what antibiotics are used to treat” wants bacterial infections. Adding a paragraph does not add a mark, and it costs you time you need later in the paper.
Describe — say what happens or what the data show. For a graph this means figures: start value, end value, and the shape between them.
Explain — say why. In this topic the explaining words are almost always variation, survive and reproduce, selected, not a cell or complementary. If an explain answer contains none of them, you have probably written a description.
Suggest — apply what you know to something unfamiliar. There is no hidden fact; the stem contains what you need. Find the thing the bacterium has and you do not, or find the transmission route.
Compare — every sentence must mention both things. “P rose more steeply than Q” is a comparison; “P rose steeply” on its own is not.
Calculate — show the working, give the unit, and state what you divided by. Two marks are usually available and one of them is for the method, so a wrong final number with correct working still scores.
The Quotable Definitions
A drug is any substance taken into the body that modifies or affects chemical reactions in the body.
Antibiotics are used for the treatment of bacterial infections.
Antibiotics kill bacteria but do not affect viruses.
Some bacteria are resistant to antibiotics, which reduces the effectiveness of antibiotics.
And one more that is not a definition but behaves like one, because it answers the Supplement objective on its own: every use of an antibiotic kills the non-resistant bacteria and allows the resistant ones to survive and reproduce, so using antibiotics only when essential means resistant bacteria are selected for less often.
The Phrases Mark Schemes Refuse
This table is the most valuable thing on the page. Every phrase in the right-hand column is one a real candidate wrote, and every one of them scored nothing.
| Write this | Never write this |
|---|---|
| antibiotics kill bacteria | antibiotics “kill germs” / “cure infections” / “fight illness” |
| antibiotics have no effect on viruses | antibiotics “work less well” on viruses |
| the bacterium is resistant | “the person becomes resistant” / “the body builds up resistance” |
| there is variation; a few bacteria are already resistant | bacteria “become resistant because they were exposed” / bacteria “learn” / “get used to it” |
| the antibiotic selects the resistant bacteria | the antibiotic “makes” or “causes” them to be resistant |
| they survive and reproduce, passing on the resistance | “the resistance spreads to the person” |
| MRSA is a bacterium | MRSA is a virus / a disease you catch from dirt |
| a larger clear zone means more sensitive | a larger zone means “more dangerous” / “stronger bacteria” |
| zone of inhibition or clear zone, diameter in mm | “the white circle” / “the gap” |
| resistance reduces the effectiveness of the antibiotic | “the antibiotic stops existing” / “the antibiotic goes off” |
| the body’s own defences finish the job | the antibiotic “boosts the immune system” |
Find every sentence in your answer that has a bacterium or a person as its subject, and check you have the right one. “She became resistant” and “the bacteria in her were resistant” look like the same claim and are not. That single check protects marks in more or less every question in this topic.
How to Describe a Graph So That It Scores
Data questions are half of Topic 15 in practice, and describing a graph is a skill with a fixed shape. Do it in the same order every time.
1. Read the axes and the units. Percentage of samples resistant is not the same as number of infections; bacteria per cm³ in thousands is not bacteria per cm³.
2. Say the overall direction in one short clause — rises, falls, rises then falls.
3. Quote the start and end figures with their units. “From 4 % in 2010 to 48 % in 2024.” This is very often a mark on its own, and it is the mark most often left on the table.
4. Say something about the shape. Steepest between which years? Is there a plateau? A curve that flattens is telling you something and the examiner knows it.
5. Stop. If the command word was describe, do not explain. You get no credit for the mechanism and you have spent time you needed elsewhere.
And the reverse trap: if the command word is explain, do not just re-describe the curve in words. “It went up quickly and then levelled off” is a description no matter how confidently it is written. The explanation is the selection sentence.
The Full Experimental Design Checklist — the Plate Investigation
If a question asks you to plan, describe or improve an investigation into which antibiotic is most effective, you are being marked against a list. Here it is. Work down it and you will not miss a mark.
| What to control or do | Why it matters |
|---|---|
| Use the same species of bacterium on every plate | Different species differ in sensitivity, so comparing across species compares nothing. |
| Spread an even lawn of the same concentration of bacteria | A patchy lawn gives a zone edge that depends on where the bacteria happened to be, not on the antibiotic. |
| Use identical discs with the same volume and same concentration of each antibiotic | This is the variable you are testing, so everything about the disc except which antibiotic it holds must be the same. A bigger drop of antibiotic gives a bigger zone whatever the drug. |
| Use the same agar in the same depth | Depth affects how far the antibiotic diffuses, and diffusion distance is what sets the zone size. |
| Incubate at the same temperature for the same time | Temperature affects both bacterial growth and the rate of diffusion (Topic 3.1); a longer incubation gives more growth. |
| Use aseptic technique — sterilised equipment, lid opened as little as possible | Other micro-organisms landing on the plate would produce zones or growth that have nothing to do with your antibiotics. |
| Include a control disc soaked in sterile water, or a disc with no antibiotic on it | This shows that the paper disc itself does not inhibit growth, so any zone round the other discs must be caused by the antibiotic and not by the disc. |
| Measure the diameter in mm across the centre of the disc | The standard measurement; the one every mark scheme uses. |
| Repeat and take a mean | Reduces the effect of random error and lets anomalies be identified. |
Everyone remembers “same temperature, same time”. Far fewer write the control disc soaked in sterile water, and it is often worth a mark on its own because it is the one that shows you understand why controls exist. Without it, a critic could say the paper disc, or the process of pressing it onto the agar, caused the clear area. With it, that objection is answered by your own data.
The Night-Before Checklist
The definition of a drug, word for word. Three things that count as drugs, and the three words the definition does not contain. What antibiotics treat. Why an antibiotic is not a painkiller and does not boost the immune system. The three targets that make an antibiotic safe — cell wall, ribosomes, a bacterial enzyme — and the reason all three work. What a bacterial cell has that an animal cell does not. How a disc diffusion plate works, why the zone is circular, and what a large zone, a small zone and no zone each mean. That the measurement is a diameter in mm. That the bacterium is resistant and the person never is. Variation, selection, survive and reproduce. That the antibiotic selects and does not create. Where resistance is often carried. Why viruses are untouchable: not a cell, protein coat and genetic material only, no wall, no ribosomes of its own, no reactions of its own, so no target at any dose. Four viral illnesses antibiotics cannot help. That every use is a selection event. The five measures, each with its reason. Why the survivors on day 3 are the worst ones to leave behind. That MRSA is a bacterium resistant to several antibiotics, and why hospitals. That trend data is correlation.
That list is the entire topic, recall and reasoning together. If you can say it out loud in five minutes, you are done — and you should go and spend the rest of the evening on Topic 14.