Antibiotics
Revise Antibiotics for Biology 4 (IAL) WBI14 (A2 Level) — revision notes and instant AI marking. Free to start.
Summary — What This Chapter Covers
- What antibiotics are, and the difference between bactericidal (kill) and bacteriostatic (inhibit growth) antibiotics
- The four main ways antibiotics attack bacteria: cell wall enzymes, ribosomes, cell membranes, and DNA coiling
- Why antibiotics harm bacteria but not human cells (and don't touch viruses at all)
- Core Practical 14 — testing antibiotic effectiveness using aseptic technique and the disc diffusion method
- How to interpret "clear zones" on an agar plate
- Hospital-acquired infections (HAIs) and how poor hygiene spreads them
- How antibiotic resistance evolves by natural selection, using MRSA as the case study
- Hospital strategies to slow resistance: narrow-spectrum antibiotics, no unnecessary prescriptions, rotating antibiotics
1. What Are Antibiotics?
When you get a bacterial infection, your doctor might prescribe an antibiotic — a chemical substance that damages bacterial cells while leaving your own (human) cells largely unharmed. The most famous one, penicillin, was discovered by Sir Alexander Fleming in 1928, almost by accident, when he noticed mould killing off bacteria in a petri dish he'd forgotten about.
Think of an antibiotic like a key that only fits bacterial locks. Bacterial cells (prokaryotic) are built differently from your cells (eukaryotic) — they have cell walls, different ribosomes, and different enzymes. Antibiotics are designed to exploit exactly those differences, which is why they can be so selective.
Bactericidal vs Bacteriostatic
Antibiotics fall into two broad categories based on what they actually do to bacteria:
| Type | What it does | Key detail |
|---|---|---|
| Bactericidal | Actively kills bacterial cells | Bacteria die directly from the antibiotic's action |
| Bacteriostatic | Inhibits bacterial growth processes (doesn't necessarily kill) | At a high enough dose, bacteriostatic antibiotics will also cause bacterial death |
"-cidal" = kills (like "suicide", "homicide"). "-static" = stays still/stops growing (think "static" = not moving). Bacteriostatic antibiotics essentially press pause on bacterial reproduction, giving your immune system time to mop up the infection — but push the dose high enough, and even these become lethal to the bacteria.
A student says "bacteriostatic antibiotics never kill bacteria." Explain why this statement is not entirely accurate.
2. How Antibiotics Attack Bacteria
Antibiotics work by interfering with bacterial growth or metabolism. There isn't just one mechanism — different antibiotics target different structures. Edexcel wants you to know four main routes of attack:
① Inhibiting cell wall enzymes (e.g. Penicillin)
Bacterial cell walls are built using specific enzymes that form bonds between wall components. Penicillin blocks these enzymes, so the cell can't properly build or repair its wall. As the bacterium tries to grow, water keeps entering the cell by osmosis (because the cytoplasm is more concentrated than the surroundings), and without a strong wall to resist that pressure, the cell literally bursts (lyses).
② Binding to ribosomes → blocking protein synthesis
Some antibiotics bind directly to bacterial ribosomes, preventing them from making proteins. Since enzymes are proteins, this stops the bacterium producing the enzymes it needs to run its metabolism — everything from respiration to reproduction grinds to a halt.
③ Damaging the cell membrane
Other antibiotics punch holes in or otherwise damage the bacterial cell membrane. This causes two problems at once: useful metabolites (sugars, ions, amino acids) leak out, and water floods in uncontrollably — both of which disrupt the cell's internal environment fatally.
④ Preventing DNA from coiling into rings
Bacterial DNA is normally supercoiled into a compact circular shape so it fits inside the cell. Some antibiotics interfere with the enzymes responsible for this coiling. If the DNA can't coil properly, it becomes too large and disorganised to fit inside the bacterial cell, disrupting replication and cell division.
Four antibiotic attack routes: (1) cell wall enzymes → osmotic lysis, (2) ribosomes → no protein synthesis, (3) cell membrane → leakage/flooding, (4) DNA coiling → DNA doesn't fit in the cell.
Explain, in terms of osmosis, why a bacterial cell treated with penicillin eventually bursts.
3. Why Human Cells & Viruses Aren't Affected
This is a classic exam favourite: "Explain why antibiotics do not affect human cells / viruses." You need specific, structural reasons — not just "because they're different."
Human (mammalian) cells are safe because...
- Human cells are eukaryotic, not prokaryotic
- They do not have cell walls — so cell-wall-targeting antibiotics like penicillin have nothing to bind to
- They have different enzymes from bacteria
- They have different (larger) ribosomes than bacterial ribosomes, so ribosome-targeting antibiotics don't bind to human ribosomes
Viruses are unaffected because...
Viruses aren't cells at all — they don't have the structures antibiotics are designed to target. No enzymes, no ribosomes, no cell walls means nothing for the antibiotic to attack. This is exactly why doctors won't prescribe antibiotics for a cold or flu (both viral) — it would do nothing, and it contributes to antibiotic resistance (more on that later).
A patient with a viral cold asks their doctor for antibiotics. Explain, using biological reasoning, why the doctor should refuse.
4. Core Practical 14 — Testing the Effects of Different Antibiotics
This is a required practical, meaning you could be asked to describe the method, explain a step's purpose, or interpret results from it. The technique used is called the disc diffusion method, and it relies heavily on aseptic technique.
Aseptic technique — the golden rule
"Aseptic" simply means free from unwanted microorganisms. Every step of this practical is about preventing contamination — either bacteria from the air landing on your plate, or your cultured bacteria escaping and contaminating you/the room. Aseptic technique includes:
- Sterilising equipment (high heat or antibacterial chemicals)
- Wiping work surfaces with disinfectant
- Working near a Bunsen burner flame, which creates an updraft — hot air rises, carrying airborne microorganisms away from your work area instead of letting them settle onto it
Method — step by step
| Step | What you do | Why |
|---|---|---|
| 1 | Set up sterile area; light Bunsen burner | Creates updraft, prevents contamination |
| 2 | Spread bacterial culture evenly onto an agar plate | Creates an even "lawn" for testing |
| 3 | Soak paper discs in different antibiotics (or use pre-soaked discs) | Tests multiple antibiotics — or concentrations — at once |
| 4 | Add a disc soaked in distilled water only (negative control) | Shows any effect is due to the antibiotic, not another factor |
| 5 | Place discs on agar using sterile forceps, spaced apart | Prevents cross-contamination and overlapping zones |
| 6 | Lightly tape lid, invert dish, incubate at 25°C for 24–48 hrs | See note below |
Lightly tape, don't seal → allows oxygen in for the bacteria to respire.
Invert the dish → stops condensation dripping onto the agar and contaminating/smearing results.
Incubate at 25°C (not 37°C) → this is around room temperature, which limits the growth of pathogens that thrive at human body temperature — keeping the experiment safer in a school lab. (Research labs may use warmer temperatures for faster results, since they have better safety controls.)
Reading the results — clear zones
Bacteria grow into a "lawn" that covers the agar surface. Where an antibiotic has worked, no bacteria can grow around that disc — this gap is called the clear zone (or zone of inhibition).
Bigger clear zone → more effective antibiotic (it diffused out and stopped/killed bacteria over a wider area).
No clear zone at all → bacteria is resistant to that antibiotic.
In this practical, why is a disc soaked only in distilled water included on the agar plate, and what result would you expect around it?
Explain why the petri dish is inverted (turned upside down) during incubation.
5. Hospital-Acquired Infections (HAIs)
A hospital-acquired infection (HAI) is one a patient picks up while they're in hospital — not the illness they came in with. Hospitals are actually a dangerous environment for infection spread because you've got lots of vulnerable people with weakened immune systems in close proximity, alongside lots of bacteria (some of it resistant — see next section).
How HAIs spread
- Staff/visitors not washing hands regularly
- Uncontained coughing and sneezing
- Failing to disinfect equipment and surfaces between uses
How hospitals reduce HAI spread
- Mandatory regular hand-washing for staff and visitors
- Moving infected patients to an isolation ward
- Disinfecting surfaces and equipment after every single use
6. Antibiotic Resistance & Natural Selection
This is where biology, evolution, and public health collide — and it's one of the most commonly examined ideas in this chapter. You need to be able to explain how resistance evolves, not just state that it happens.
MRSA — the classic example
MRSA stands for Methicillin-Resistant Staphylococcus aureus. It's a strain of the bacterium S. aureus that has evolved resistance to the antibiotic methicillin, making infections much harder to treat and a serious risk in hospitals.
The step-by-step evolution of resistance
This is a textbook natural selection argument — practise writing it out in full sentences, because "state the process of antibiotic resistance" questions are marked on getting every link in the chain:
Selection pressure = a factor in the environment that drives natural selection by affecting survival/reproduction (here: the presence of an antibiotic). Horizontal gene transfer = bacteria exchanging genes directly with each other (not through reproduction) — this is how resistance can jump between different species/strains of bacteria.
Reducing the risk of resistant HAIs — hospital strategies
| Strategy | Why it works |
|---|---|
| No antibiotics for minor/viral infections | Reduces unnecessary exposure → less selection pressure |
| No antibiotics as a preventative measure | Same reasoning — only use when actually needed |
| Prescribe narrow-spectrum antibiotics where possible | Targets a narrow range of bacteria, so even if resistance genes transfer to other species, they cause less widespread harm (since other bacteria are treated differently) |
| Rotate different antibiotics | Reduces the chance of bacteria developing resistance to any single antibiotic, since the selection pressure keeps changing |
Narrow-spectrum = effective against a small/specific range of bacteria. Broad-spectrum = effective against many different types of bacteria. Broad-spectrum sounds "better" but is actually more likely to drive widespread resistance because it puts selection pressure on many bacterial species at once.
Using your knowledge of natural selection, explain how a hospital population of bacteria could become resistant to an antibiotic that was previously effective against it.
Suggest why prescribing a narrow-spectrum antibiotic, rather than a broad-spectrum one, can help reduce the overall problem of antibiotic resistance.
What to Memorise
Concepts Checklist
Exam Tips
- 3. Why Human Cells & Viruses Aren't Affected
- 6. Antibiotic Resistance & Natural Selection
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