Antibiotics, Painkillers and Drug Development

An antibiotic is a medicine that cures bacterial disease by killing the infective bacteria inside the body. Penicillin is the classic example. Because antibiotics kill the pathogen itself, they tackle the cause of the illness, not just how it makes you feel.

A key point in the specification is about matching: specific bacteria should be treated by specific antibiotics. There is no single drug that deals with every bacterial infection. A doctor identifies which bacterium is causing the disease, then chooses an antibiotic known to kill that type. Using the wrong antibiotic may have little effect on the infection.

Antibiotic: a medicine (such as penicillin) that kills infective bacteria inside the body, curing the bacterial disease.

The arrival of antibiotics changed medicine dramatically. Before them, infections we now treat easily could be fatal.

Claim about antibiotics	True or false?
They kill bacteria inside the body	True
One antibiotic treats every bacterial infection	False
They kill viruses	False
They have greatly reduced deaths from bacterial disease	True

The use of antibiotics has greatly reduced deaths from infectious bacterial diseases — a major reason average life expectancy rose through the twentieth century.

Antibiotics work on bacteria only. They have no effect on viral pathogens — so they cannot cure a cold, flu, or any other viral illness. This is one of the most heavily tested ideas in the topic, and the reason follows from what a virus is.

A virus is not a living cell. It reproduces inside the body's own cells, hijacking them to make copies of itself. Antibiotics target structures and processes that bacterial cells have; a virus has none of these, and it hides inside your cells. That is why it is difficult to develop drugs that kill viruses without also damaging the body's tissues — a drug reaching the virus would have to act inside your own cells and risk harming them too.

Feature	Bacteria	Viruses
Living cell?	Yes	No
Where it reproduces	Inside the body, on its own	Inside the body's own cells
Killed by antibiotics?	Yes	No
Easy to target with a drug?	Yes	Hard — would risk harming body cells

Exam tip: antibiotics kill bacteria, not viruses. Viruses reproduce inside body cells, so a drug that destroys them tends to damage those cells as well.

Worked walk-through 1 — why the doctor won't prescribe antibiotics for a cold. A patient asks for antibiotics for a heavy cold. A cold is caused by a virus. Antibiotics kill bacteria, not viruses, so they would do nothing for the cold. The doctor declines because the medicine cannot treat the cause — and needless use drives antibiotic resistance (next slide). They advise rest and a painkiller for the symptoms instead.

This slide draws the single most important distinction in the whole topic: some medicines kill the pathogen, and others only relieve how you feel.

Painkillers and other medicines treat the symptoms of disease but do not kill pathogens. A painkiller such as paracetamol can ease a headache or lower a fever, making you more comfortable while your immune system fights the infection — but it does nothing to the bacterium or virus causing the illness. Antibiotics are different: they attack the bacterial pathogen directly.

Type of medicine	What it acts on	Does it kill the pathogen?	Example use
Antibiotic	Bacteria	Yes (bacteria only)	Curing a bacterial chest infection
Painkiller	Symptoms (e.g. pain, fever)	No	Easing aches during flu

Key idea: painkillers relieve symptoms; they do not kill the pathogen. Only antibiotics kill the pathogen — and only when that pathogen is a bacterium.

So during a viral illness like flu, a painkiller is genuinely useful — it makes the symptoms bearable — even though no medicine on the shelf will kill the virus for you. Your own immune system does that work.

Antibiotics have saved countless lives, but their success is now under threat. The emergence of strains of bacteria resistant to antibiotics is of great concern, and the problem is increasing.

Resistant bacteria are strains that the antibiotic can no longer kill. When a population of bacteria is treated, a few may by chance carry a mutation that lets them survive the drug. The antibiotic kills the non-resistant majority, but the resistant survivors reproduce and pass on their resistance. Over time the resistant strain spreads. The more often antibiotics are used — especially when they are not needed — the faster this happens.

Of great concern: if resistant strains spread faster than new antibiotics are developed, common infections could once again become difficult to treat.

This is exactly why the doctor in Slide 2 refused antibiotics for a viral cold: every unnecessary course of antibiotics gives bacteria another chance to evolve resistance. Doctors now prescribe antibiotics only when they are genuinely needed, and patients are told to finish the full course.

(Extra context — not required by AQA 8461.) The detail of how resistance evolves by natural selection, and named examples such as MRSA, belong to the evolution and inheritance topics. Here you only need that resistant strains are emerging and that this is a serious concern.

Before chemists could build medicines, drugs were extracted from plants and microorganisms. AQA names three you must know.

Drug	Original natural source	What it does
Digitalis	Foxgloves (a plant)	A heart drug
Aspirin	Willow (a plant)	A painkiller
Penicillin	Penicillium mould (a microorganism)	The first antibiotic

Penicillin has a famous discovery story: it was discovered by Alexander Fleming from the Penicillium mould. Fleming noticed that a mould contaminating one of his bacterial culture plates had killed the bacteria around it — the mould was producing a substance that destroyed them. That substance was penicillin, the first antibiotic.

Remember the three sources: digitalis from foxgloves, aspirin from willow, penicillin from Penicillium mould (Fleming).

Today, most new drugs are synthesised by chemists in the pharmaceutical industry. However, the starting point may still be a chemical extracted from a plant — nature gives chemists a useful molecule, which they then refine, copy, or improve in the laboratory.

A promising new substance is not a medicine yet. New drugs must be tested and trialled before use to check that they are safe and effective. Every new drug is extensively tested for three things:

• Toxicity — is it harmful? Does it have dangerous side effects?
• Efficacy — does it actually work? Does it treat the disease?
• Dose — how much should be given? What is the right amount to be both safe and effective?

Testing happens in a fixed order, moving from the lab to people only once earlier stages look safe. The pipeline below is the sequence the specification asks you to know.

Three things every drug is tested for: toxicity (is it safe?), efficacy (does it work?) and dose (how much to give?).

This ordering matters: testing on cells and animals first means a dangerous drug is caught before it is ever given to a person.

Here is the pipeline in detail, with the reason each stage exists — exactly the kind of "explain why" answer examiners reward.

Stage	Tested on	Why this stage is needed
Preclinical testing	Cells, tissues, then live animals	Checks toxicity and efficacy safely, before any human is exposed
Clinical trial — start	Healthy volunteers, very low doses	Checks the drug is safe in people before testing higher amounts
Clinical trial — later	Patients with the disease	Checks it works on the illness, and finds the optimum dose

Preclinical testing is done in a laboratory using cells, tissues and live animals. Clinical trials then use people: first healthy volunteers given very low doses, and — if the drug is found to be safe — further trials on patients to find the optimum dose (the dose that is most effective with the fewest side effects).

To judge whether a drug truly works, trials use a placebo — a dummy treatment with no active drug. Some patients receive the real drug, others the placebo; comparing the groups shows whether improvements are due to the drug itself. In a double-blind trial, neither the doctor nor the patient knows who has the real drug and who has the placebo until the trial ends. This stops expectations from either side biasing the results.

Double-blind: neither the patient nor the doctor knows who received the placebo. This removes bias from both directions.

Finally, results are published only after peer review — other independent scientists scrutinise the work before it is accepted. Peer review helps detect false claims and errors, so doctors can trust the published findings.

Worked walk-through 2 — putting the stages in order and justifying each. A new bacterial-infection drug is ready to test.

1. Cells and tissues in the lab — cheap and safe; catches obvious toxicity before any living thing is harmed.
2. Live animals — checks effects on a whole body before any human is exposed.
3. Healthy volunteers, very low dose — confirms the drug is safe in people without risking a large dose.
4. Patients, building to the optimum dose, with a double-blind placebo comparison — proves it actually treats the disease and finds the best amount.
5. Peer review, then publish — independent scientists check the results before anyone relies on them.

Each step gates the next: people are not moved to higher doses, or to patients, until the earlier, safer stage has passed.

1. Saying antibiotics kill viruses

Antibiotics kill bacteria only. They have no effect on viruses, because viruses are not cells and reproduce inside the body's own cells. A cold or flu cannot be cured with antibiotics.

2. Confusing painkillers with antibiotics

Painkillers treat symptoms (pain, fever) and do not kill the pathogen. Only antibiotics kill the pathogen — and only when it is a bacterium. Writing "a painkiller cures the infection" is wrong and is unlikely to gain credit.

3. Forgetting that specific bacteria need specific antibiotics

There is no universal antibiotic. The right drug must be matched to the bacterium causing the disease; the wrong one may not work.

4. Mixing up the natural sources of drugs

Keep them straight: digitalis → foxgloves, aspirin → willow, penicillin → Penicillium mould (Fleming). Swapping these around is a common slip.

5. Getting the testing order wrong

The sequence is cells and tissues → live animals → healthy volunteers (very low dose) → patients (optimum dose) → peer review and publish. Testing on patients before preclinical work, or skipping the low-dose start, is incorrect.

6. Misdefining a double-blind trial

In a double-blind trial neither the doctor nor the patient knows who has the placebo — not just the patient. Saying "only the patient doesn't know" describes a single-blind trial, which is unlikely to gain credit if the question asks about a double-blind trial.