This topic has very few facts in it and an unusually high number of ways to write them wrongly, because almost every wrong answer here is a sentence people say out loud every week. The thing that becomes resistant is the bacterium, never the person. The antibiotic does not make bacteria resistant, it selects the ones that already were. Antibiotics have no effect on viruses — not a weak effect, none — and no dose changes that, because a virus is not a cell and there is nothing to attack. A bigger clear zone on a plate means the bacterium is more sensitive, not more dangerous. And a drug is not the same word in biology as it is in a newspaper. Twelve traps, six walkthroughs, six lookalike pairs, a concept map and ten full practice questions below — over half of them built on data, because that is where the marks in this topic actually are.
Twelve traps that cost marks on Topic 15 challenge papers. Every one is an answer that sounds right and scores nothing.
Six challenge-level questions worked through in the order you should actually think about them. Four of the six are data or experiment questions, because that is where this topic is examined hardest. Try each part before revealing the next step.
One species of bacterium was spread as an even lawn over the agar. Four paper discs, each soaked in a different antibiotic, were placed on the plate and it was incubated for 24 hours. (a) Name the clear region around a disc and state how it should be measured. [2] (b) Place the four antibiotics in order, starting with the one this bacterium is most sensitive to, and state what disc D shows. [3] (c) Explain why each clear region is circular and why it stops where it does. [3] (d) Calculate how much larger the zone for C is than the zone for A, as a percentage. Give your answer to one decimal place. [2]
The clear region is the zone of inhibition, also accepted as the clear zone. “The white circle” and “the gap” score nothing. The measurement mark is for the diameter, in mm, measured across the centre of the disc — not the radius, and not the distance from the edge of the disc to the edge of the zone. Get into the habit of writing the unit; a bare number is often refused on a measurement mark.
C (34 mm), then A (26 mm), then B (14 mm), then D. A larger zone means the bacterium is more sensitive to that antibiotic. Disc D produced no zone at all: the bacteria grew right up to the disc, so this bacterium is resistant to antibiotic D. Do not write that C is the strongest antibiotic in general, and never write that any of this makes the bacterium more dangerous — the plate measures sensitivity and nothing else.
The antibiotic diffuses out of the disc into the agar. Diffusion is the net movement of particles down a concentration gradient as a result of random movement, and it happens equally in all directions, which is why the zone is a circle centred on the disc. The concentration therefore falls with distance from the disc, and the edge of the zone is the distance at which the concentration has dropped too low to stop the bacteria growing. Nothing pushes the antibiotic outwards and nothing draws a boundary; the boundary is simply where the concentration runs out.
The difference is 34 − 26 = 8 mm [1]. As a percentage of A, that is 8 ÷ 26 × 100 = 30.8% to one decimal place [1]. The commonest error is dividing by 34 instead of 26, which gives 23.5% — a perfectly tidy wrong answer. The phrase “larger than A” tells you A is the one on the bottom of the fraction.
| year | 2010 | 2012 | 2014 | 2016 | 2018 | 2020 | 2022 | 2024 |
|---|---|---|---|---|---|---|---|---|
| resistant to P / % | 4 | 7 | 12 | 20 | 30 | 38 | 44 | 48 |
| resistant to Q / % | 2 | 3 | 4 | 4 | 5 | 6 | 6 | 7 |
In any large population of bacteria there is variation, and a few bacteria are already resistant before an antibiotic is used. (a) Describe the results, using figures. [3] (b) Calculate the percentage increase in resistance to P between 2010 and 2024. [2] (c) Explain the difference between the two antibiotics. [4] (d) A newspaper says the data proves that prescribing antibiotics freely causes resistance. Comment on that claim. [2]
Resistance to P rose from 4% in 2010 to 48% in 2024, an increase of 44 percentage points [1]. The rise was steepest between 2014 and 2020, where it went from 12% to 38%, and it began to level off after 2022 [1]. Resistance to Q rose only slightly, from 2% to 7% over the same fourteen years [1]. Three marks, three figures-carrying statements — and not one word about bacteria yet, because the command word was describe.
The increase is 48 − 4 = 44 [1]. As a percentage increase that is 44 ÷ 4 × 100 = 1100% [1]. Both numbers are correct answers to different questions: 44 percentage points is the size of the change on the axis, 1100% is how much it grew relative to where it started. This question asked for percentage increase, so you must divide by the starting value. If you wrote 44%, you have quietly answered a third question that nobody asked.
(i) There is variation: a few bacteria were already resistant to P before it was used. (ii) P was used constantly, so the non-resistant bacteria were killed. (iii) The resistant ones survived and reproduced, passing the resistance on. (iv) So the proportion of resistant bacteria in the population rose, and the effectiveness of P was reduced. Q was hardly ever used, so there was far less selection and the resistant minority stayed a minority. Notice that the antibiotic never made anything resistant; every use of it was simply another selection event.
The data shows a correlation between heavy prescribing and rising resistance, and it is consistent with the explanation above — but it does not prove cause [1]. Only one hospital was studied, only one species was tested, and other things may have changed over fourteen years: hygiene practice, the number of patients, resistant strains arriving from elsewhere, or the way samples were collected [1]. To strengthen the claim you would want several hospitals, several species, and ideally a hospital that deliberately reduced its prescribing of P.
Keep two lists in your head. Describe: rose, fell, levelled off, from, to, steepest, percentage points, the actual numbers. Explain: variation, already resistant, killed, survived, reproduced, proportion, effectiveness reduced. If a word from the second list has appeared in your describe answer, you have started explaining early — and if a number has appeared in your explain answer, you are still describing.
| time / hours | 0 | 2 | 4 | 5 | 6 | 8 | 10 | 12 |
|---|---|---|---|---|---|---|---|---|
| flask 1, no antibiotic | 10 | 28 | 96 | 170 | 290 | 640 | 850 | 900 |
| flask 2, antibiotic at 4 h | 10 | 24 | 62 | 60 | 40 | 11 | 3 | 2 |
(a) Describe the results for flask 2 after 4 hours, using figures. [3] (b) Explain why flask 1 was needed. [2] (c) Two units of bacteria were still present at 12 hours. Suggest what this means and what could happen if the antibiotic were now removed. [3] (d) Explain why the two flasks had to be kept at the same temperature. [2]
Numbers peaked at 62 units at 4 hours, the moment the antibiotic was added [1]. They then fell, slowly at first — 60 at 5 hours — and then steeply, reaching 11 by 8 hours [1]. The fall then slowed and almost levelled off, 3 at 10 hours and 2 at 12 hours, so it did not reach zero [1]. Meanwhile flask 1 went on rising to 900. A very common loss here is writing that the bacteria “died immediately”; the data says the opposite, and the delay is the whole point of the next question in most papers.
Flask 1 is the control. Without it you could not tell whether the fall in flask 2 was caused by the antibiotic or by something that would have happened anyway — nutrients running out, waste building up, or the broth cooling [1]. Because flask 1 was treated identically apart from the antibiotic and its numbers rose to 900, the fall in flask 2 can be attributed to the antibiotic [1]. Always name the alternative explanation the control removes; “to compare” on its own is a weak mark.
The antibiotic did not kill every bacterium. The two units remaining are likely to be the least sensitive bacteria in the flask — in a large population there is variation, and a few were resistant from the start [1]. If the antibiotic were removed, those survivors would reproduce with no competition [1] and the population would grow back, with a higher proportion of resistant bacteria than it had at the start [1]. That is exactly the argument for finishing a course of tablets, in a flask instead of a patient.
Temperature must be kept the same so it is a controlled variable and only the antibiotic differs between the flasks [1]. Biologically, temperature affects the rate of the bacteria’s own enzyme-controlled reactions and therefore how fast they reproduce, so a warmer flask would grow faster whatever the antibiotic did [1]. A comparison is only worth making when one thing has been changed.
The only thing that should differ between the discs is which antibiotic is on them. So: the same species of bacterium, spread as an even lawn; identical discs, the same size and material, not hand-cut squares; the same volume and the same concentration of each antibiotic solution; the same agar; the same incubation temperature in an incubator, not a windowsill; and the same incubation time. Hand-cut squares are the sneaky one — a bigger piece of paper holds more antibiotic, so the discs themselves become a second variable.
Measure the diameter in mm across the centre of the disc, with the ruler against the plate rather than held above it, since holding it above introduces a parallax error. Then repeat the whole investigation and calculate a mean for each antibiotic. Repeats are worth a mark on their own in almost every practical question in this syllabus, and taking a mean is worth a second one. Add aseptic technique — sterilised equipment, lid replaced quickly, plate taped — so that no other organism grows on the plate and confuses the result.
She should have added a disc soaked in sterile water, or a disc with no antibiotic on it [1]. It shows that any clear zone is caused by the antibiotic and not by the paper disc itself, or by the liquid, or by the disc physically covering the agar [1]. If the water disc produces a zone, every other result on the plate is in doubt — which is precisely what a control is for.
9 mm is an anomalous result: it is far from the other two, which agree closely [1]. She should exclude it from the mean and repeat that measurement, and if possible look for a cause — that disc may have been dry, dropped in the wrong solution, or placed too near the edge of the plate [1]. The mean of 22 and 24 is 23 mm; including 9 would pull it down to about 18 mm and misrepresent every conclusion drawn from it.
Two patients had the same bacterial infection and were given the same antibiotic, prescribed for 10 days. Patient A took the full course. Patient B felt completely well on day 3 and stopped. Both curves start at 1000 units and are identical for the first three days: 1000, 700, 420, 210. After day 3, patient A continued to 95, 40, 16, 6, 2, 1 and 0 by day 10. Patient B rose again to 240, 340, 520, 700, 860, 960 and 1000 by day 10. (a) Compare the two patients after day 3, using figures. [3] (b) Explain why patient B felt completely well on day 3 even though 210 units of bacteria remained. [2] (c) Explain why the bacteria that regrew in patient B are a more serious problem than the original infection. [3]
In patient A the numbers went on falling, from 210 on day 3 to 0 by day 10 [1]. In patient B they rose again, from 210 on day 3 back to 1000 by day 10, the value they started at [1]. So the difference between them is a fall to zero against a complete recovery of the population, a difference of 1000 units by day 10 [1]. The word compare means the two must appear together; two separate paragraphs, one per patient, usually costs the third mark.
By day 3 the bacterial population had fallen from 1000 to 210, a drop of about 79% [1], and with far fewer bacteria there is far less damage and far less toxin, so the symptoms disappear — but 210 units of bacteria are still alive [1]. This is the sentence the whole objective hangs on: symptoms stop long before the bacteria do. There is no moment when your body tells you the last bacterium has gone.
The 210 units alive on day 3 are the ones the antibiotic found hardest to kill — there is variation in the population and the most sensitive bacteria died first [1]. Stopping the antibiotic lets those survive and reproduce with no competition [1], so the population that grows back has a higher proportion of resistant bacteria and the same antibiotic will work less well next time [1]. Patient B has not simply gone back to where he started; he has gone back to a worse version of it.
The Supplement objective is about limiting the development of resistant bacteria such as MRSA, and the single idea underneath it is that every use of an antibiotic is a selection event. A stopped course is the worst kind of use: enough antibiotic to kill off the sensitive bacteria and select the resistant ones, and not enough to finish them. If a question asks for ways to limit resistance, “complete the full course” belongs on the list next to “only prescribe for bacterial infections” and “keep some antibiotics in reserve”.
A patient with influenza, which is caused by a virus, asks her doctor for antibiotics. The doctor refuses. (a) Explain, in terms of structure, why an antibiotic would have no effect on the influenza virus. [4] (b) The patient says a higher dose would surely help. Explain why it would not. [1] (c) Explain why taking the antibiotic would not be harmless, even though the patient is not allergic to it. [3] (d) State what will actually clear the infection, and what could have prevented it. [2]
The features of a virus are limited to a protein coat and genetic material [1]. It has no cell wall, no cell membrane of its own, no cytoplasm and no ribosomes of its own [1], and it carries out no chemical reactions of its own, reproducing only inside a host cell [1]. So there is nothing for an antibiotic to attack [1]. Four marks, and every one of them comes from Topic 1.3 and Topic 2.1 rather than from Topic 15.
This is worth understanding even where it is not directly asked, because it makes part (a) obvious. An antibiotic can be swallowed safely only because it attacks something a bacterial cell has and a human cell does not: the cell wall, which an animal cell has none of at all; the ribosomes, which are not the same as human ribosomes, so a drug can bind to one and not the other; or an enzyme the bacterium uses and you do not, where a molecule shaped to fit the active site blocks the reaction in the bacterium only. A virus has none of those three things. Neither does it have anything else.
Increasing the dose increases the concentration of a substance that has nothing to act on, so the effect stays at zero [1]. Dose matters when there is a target and the question is whether enough of the drug reaches it — which is exactly the situation on an agar plate, where a bigger zone means the concentration stayed high enough further out. It is not the situation here.
The patient gains no benefit at all [1]. But she is carrying harmless bacteria in her gut and on her skin, and in any large population of those bacteria there is variation, with a few already resistant. The antibiotic kills the non-resistant ones and the resistant ones survive and reproduce [1], so the proportion of resistant bacteria she carries rises — and those bacteria can be passed to other people [1]. This is the whole Supplement objective in a single scenario: using antibiotics only when essential limits the development of resistant bacteria such as MRSA.
The infection will be cleared by the body’s own defences — phagocytes engulfing and digesting the pathogen, and lymphocytes producing antibodies with a shape complementary to the antigen [1]. It could have been prevented by vaccination, which works against viruses because it acts on her immune system rather than on the pathogen’s structure [1]. That contrast — vaccine acts on you, antibiotic acts on the bacterium — is the cleanest way to keep the two apart.
Six pairs that look almost identical and have different answers. The distinction is where the marks live.
Click each node. Three frameworks: what the words mean, where resistance comes from, and what to do about it. Almost every mark in this topic sits somewhere on one of these three chains.
Six real-sounding student answers. Find the fault before you reveal it. Three of the six contain a sentence you have almost certainly heard an adult say.
Ten Cambridge-style challenge questions. Write your answer first, then reveal the model answer and the examiner’s notes. Six of the ten need something from Topics 1, 2, 3, 5, 10 or 12 as well as Topic 15 — which is exactly how this topic is examined.