The shape of the lesson
By the end of the lesson, learners can
- How penicillin bursts a bacterium: Leave the target on growing bacterium and press Add penicillin.
- Why antibiotics do not touch viruses: With the virus selected, the penicillin molecules drift around the particle and never bind to anything.
- Selecting for resistance: Press Run 20 years with every box unticked: 1% of the 200 bacteria on the dish start resistant (orange).
- Penicillin: inhibits transpeptidase, so no new peptidoglycan cross-links in growing bacteria.
- Lysis: weak wall, water enters by osmosis, cell bursts; human cells have no wall.
- Viruses: no wall, no ribosomes, no metabolism of their own: nothing to target.
- Resistance: random mutation, selection by the antibiotic, spread on plasmids.
One picture every idea returns to
An antibiotic is a chemical that kills or stops the growth of bacteria without harming human cells. Penicillin acts on growing bacteria: it inhibits the transpeptidase enzymes that form cross-links between the peptidoglycan chains of new cell wall. The wall becomes weak, water enters the cell by osmosis, and the cell swells and bursts (osmotic lysis). Human cells have no cell wall or peptidoglycan, so they are not affected. Antibiotics do not affect viruses: viruses have no cell wall, no peptidoglycan, no ribosomes and no metabolism of their own, and they replicate inside host cells using the host's enzymes. Antibiotic resistance arises by chance mutation; each use of an antibiotic selects resistant bacteria, which multiply and pass on the resistance gene. The consequences are infections such as MRSA and MDR-TB that are hard or impossible to treat. The impact is reduced by prescribing antibiotics only when needed, finishing the course, hospital hygiene, less use in farming, changing the antibiotic used and developing new ones.
Forty-five minutes, phase by phase
| Time | Phase | What happens in the room | Grouping |
|---|---|---|---|
| 0 to 5 min | Hook: predict | Open with the question in the title, Burst the wall, then outrun the mutants.. Penicillin stops growing bacteria from cross-linking their cell walls, so they burst. Put the figure on the board: it is the one picture every idea in the lesson returns to. | Whole class, then pairs |
| 5 to 13 min | Teach and check: How penicillin bursts a bacterium | Leave the target on growing bacterium and press Add penicillin. Project tab 4 of the lab (Infectious diseases lab, how penicillin works) and let a student drive it while the class predicts. | Whole class, then pairs |
| 13 to 21 min | Teach and check: Why antibiotics do not touch viruses | With the virus selected, the penicillin molecules drift around the particle and never bind to anything. | Pairs |
| 21 to 30 min | Teach and check: Selecting for resistance | Press Run 20 years with every box unticked: 1% of the 200 bacteria on the dish start resistant (orange). Project tab 5 of the lab (Infectious diseases lab, antibiotic resistance) and let a student drive it while the class predicts. | Frayer Model |
| 30 to 36 min | Check | The four Stage 1 questions from the student lesson, answered on mini whiteboards or by show of fingers. Re-teach the one most get wrong. | Individual, then whole class |
| 36 to 43 min | Plenary | The exam-style questions from Stage 2, one at a time: thirty seconds alone, then a random call. The feedback lines in the key give the examiner's wording. | Individual, random call |
| 43 to 45 min | Exit and homework | Set the worksheet below (6 questions, 21 marks). Learners self-assess against the objectives before they leave. | Individual |
Protect the parts that carry the learning
The sequence carries about fifty minutes of material, so the lab is driven by one student while the class predicts rather than explored freely. Times are a guide.
Protected: the check at 30 minutes. It is the only individual read on whether the key idea landed, and it is not cut.
Cut first if the build overruns: the last check in Selecting for resistance, never the check or the plenary.
In a 60 minute block: run worksheet questions 1 to 3 in class as a Rally Coach set and model both the hardest worked example and its check live.
Frayer Model
Pairs fill a four-box grid for the key term: definition, characteristics, examples and non-examples. The non-examples box is where the misconceptions surface, so give it the most time.
The full structure, with its variations and the other twelve, is on the cooperative-learning page.
What to head off, and how
| Trap learners fall into | Teaching move that pre-empts it |
|---|---|
| Penicillin does not dissolve or digest the wall that is already there. | It stops new cross-links forming, so it works only on bacteria that are growing. The cell is killed by water entering by osmosis, not by penicillin entering the cytoplasm. |
| Bacteria do not become resistant because they "get used to" an antibiotic, and people do not become resistant: bacteria carry resistance genes that arose by chance mutation, and the antibiotic selects them. | Return to Selecting for resistance: ask a pair to state the correct version and show it on the lab before moving on. |
Antibiotics: penicillin and resistance: worksheet
6 questions, 21 marks. Written in the style of the papers; no past paper question is reproduced.
Outline how penicillin acts on bacteria.
Explain why antibiotics are not effective in treating diseases caused by viruses, such as HIV/AIDS.
Suggest why penicillin does not harm the cells of the person taking it.
Explain how a population of bacteria that is resistant to an antibiotic can develop in a patient who is being treated with that antibiotic.
Discuss the consequences of antibiotic resistance for health care.
In the lab's resistance model, 1% of bacteria are resistant at the start. After 20 years of antibiotic use with no steps taken, almost 100% are resistant. With all five steps taken, only about 4% are resistant. Describe and explain how two of the steps reduce the rise in resistance.
Answer key and marking notes
- Penicillin acts on bacteria that are growing (making new cell wall).
- It inhibits transpeptidase enzymes that form cross-links between peptidoglycan chains.
- The new cell wall is weak.
- Water enters the cell by osmosis; the wall cannot resist the pressure, so the cell bursts (osmotic lysis).
- Viruses have no cell wall or peptidoglycan for penicillin to act on.
- Viruses have no ribosomes or metabolic enzymes of their own, which other antibiotics target.
- Viruses replicate inside host cells using the host's machinery, so there is nothing for the antibiotic to inhibit.
- Human (animal) cells do not have a cell wall.
- They contain no peptidoglycan and no transpeptidase that makes it, so there is no target for penicillin.
- A random mutation produces a gene giving resistance (for example coding for an enzyme that breaks down the antibiotic).
- The antibiotic kills the susceptible bacteria but resistant bacteria survive.
- The resistant bacteria reproduce by binary fission with less competition, passing the resistance gene to their offspring.
- The gene may also be passed to other bacteria on plasmids by conjugation, so the proportion of resistant bacteria increases.
- Infections such as MRSA or MDR-TB become hard or impossible to treat, so more patients die.
- Patients stay in hospital longer, and second-line drugs are more expensive and may have more side effects.
- Operations, cancer chemotherapy and transplants become riskier because infections cannot be controlled.
- New antibiotics are needed, but developing them is slow and costly.
- Prescribing antibiotics only when needed (not for viral infections): the antibiotic is used less often, so there is less selection pressure favouring resistant bacteria.
- Finishing the course: all the bacteria, including less susceptible ones, are killed, so fewer survive to reproduce.
- Hospital hygiene: resistant bacteria are not passed from patient to patient, so they spread less.
- (Also: less use in farming reduces selection in animals; rotating antibiotics means no single antibiotic selects continuously.) Any two, each with an explanation.
8 multiple-choice questions on this lesson
From the topic question bank. Assign them in the app for a marked score in your gradebook, or run the topic as a class game.
Penicillin inhibits an enzyme in bacteria. What does this enzyme normally do?
- Aforms cross-links between peptidoglycan chains in new cell wall
- Bbreaks down existing peptidoglycan so the bacterium can divide
- Cjoins amino acids together on the ribosomes of the bacterium
- Dcopies the DNA of the bacterial chromosome before binary fission
A patient with influenza asks for penicillin. The doctor refuses. Which is the best biological reason?
- Ainfluenza is caused by a virus, which has no cell wall for penicillin to act on
- Binfluenza viruses are already resistant to penicillin because of plasmids
- Cpenicillin would kill the patient's own cells, which have peptidoglycan walls
- Dpenicillin only works on viruses that have a lipid envelope from the host
Penicillin is added to two cultures of the same growing bacterium. Culture 1 is in a dilute nutrient solution; culture 2 is in a nutrient solution containing a high concentration of sucrose. The bacteria in culture 1 burst, but those in culture 2 do not. Why?
- Ain culture 2 the water potential outside is low, so little water enters the cells
- Bin culture 2 the sucrose breaks down the penicillin before it reaches the wall
- Cin culture 2 the bacteria use the sucrose to repair the cross-links
- Din culture 2 the bacteria stop growing, so they make no new cell wall at all
Which is a consequence of antibiotic resistance for health care?
- Ainfections after routine operations can become difficult or impossible to treat
- Bviral infections such as HIV become resistant to antiretroviral drugs
- Cvaccines against bacterial diseases stop working in the whole population
- Dpatients become resistant to antibiotics and must stop taking them
Which practice is most likely to increase the spread of antibiotic resistance?
- Aadding antibiotics to animal feed to make healthy livestock grow faster
- Bwashing hands with alcohol gel between seeing hospital patients
- Cisolating patients in hospital who carry resistant bacteria
- Dtaking every dose of an antibiotic until the course is finished
The graph shows the growth of two identical cultures of a penicillin-sensitive bacterium. Penicillin was added to culture X at 3 h and to culture Y at 8 h. Which explains why penicillin had little effect on culture Y?
- Aat 8 h the bacteria had stopped growing, so they were not making new cell wall
- Bat 8 h the bacteria had become resistant after mutations caused by penicillin
- Cat 8 h the bacteria had used up all the water, so no water could enter them
- Dat 8 h the bacteria had lost their cell walls, so penicillin had no target
A hospital laboratory tested samples of Staphylococcus aureus from patients. In 2015, 90 of 600 samples were resistant to methicillin. In 2023, 270 of 600 samples were resistant. What was the percentage increase in the proportion of samples that were resistant?
- A200%
- B30%
- C67%
- D300%
A patient's gut contains a harmless strain of Escherichia coli that is resistant to ampicillin. The patient then catches Salmonella food poisoning; tests show this Salmonella strain is killed by ampicillin. After a few days of ampicillin treatment, ampicillin-resistant Salmonella is found in the patient. Which is the most likely explanation?
- Aa plasmid with the resistance gene passed from E. coli to Salmonella by conjugation, and ampicillin selected it
- Bampicillin caused a mutation in Salmonella that made it resistant, and the mutation spread
- Cthe E. coli cells changed into Salmonella cells after being exposed to ampicillin
- Dthe patient's immune system became resistant to ampicillin and protected the Salmonella
Quiz key
Penicillin inhibits transpeptidases, the enzymes that form the peptide cross-links between peptidoglycan chains as new wall is built. Enzymes that break down peptidoglycan to make room for growth (autolysins) keep working, which is why the wall weakens; penicillin does not inhibit them. Protein synthesis on ribosomes is the target of some other antibiotics, not penicillin. DNA replication is not affected by penicillin.
Influenza is caused by a virus. Viruses have no cell wall or peptidoglycan, no ribosomes and no metabolism of their own, so penicillin has nothing to act on, and using it only adds selection pressure for resistant bacteria. Viruses do not have plasmids and are not resistant; they are simply not targets. Human cells have no cell wall and no peptidoglycan, which is why penicillin is safe for us. Penicillin does not act on any virus, enveloped or not.
Cells with weakened walls burst only when water enters by osmosis. A concentrated sucrose solution has a low water potential, close to or below that of the cytoplasm, so little or no water enters and the weakened cells do not swell and burst. Sucrose does not break down penicillin. Penicillin still blocks the transpeptidase, so the bacteria cannot make cross-links whatever sugar is present. The question states the bacteria are growing in both cultures.
Surgery relies on antibiotics to prevent and treat bacterial infection; if the bacteria (such as MRSA) are resistant, the infection may not respond, patients stay in hospital longer and some die. Resistance of HIV to antiretrovirals is a separate problem of antiviral drugs, not a consequence of antibiotic resistance. Antibiotic resistance does not change how vaccines work. It is the bacteria, not the patients, that become resistant.
Routine antibiotics in animal feed expose huge numbers of bacteria in the animals' guts to the drug, selecting resistant strains, and resistance genes can pass to bacteria that infect humans. Hand hygiene and isolating carriers stop resistant bacteria spreading between patients, so they reduce the problem. Finishing the course kills more of the infecting bacteria, so fewer survive to reproduce.
By 8 h culture Y was in the stationary phase: numbers were no longer rising, so few cells were growing or dividing and little new wall was being cross-linked, which is what penicillin interferes with. Culture X was in the exponential phase at 3 h, so its cells were building new wall and burst. Penicillin does not cause mutations, and resistance would not appear in a few minutes. The bacteria are still surrounded by the nutrient solution, so water is not used up. Stationary-phase bacteria still have their cell walls.
2015: 90 ÷ 600 = 15% resistant. 2023: 270 ÷ 600 = 45% resistant. Percentage increase = (45 − 15) ÷ 15 × 100 = 200%. 30 is the rise in percentage points, not a percentage increase. 67% divides the rise by the 2023 value instead of the 2015 value. 300% is the 2023 value as a percentage of the 2015 value (3 times as many), not the increase.
Resistance genes are often on plasmids, which can be passed between bacteria of different species by conjugation (horizontal transmission). Ampicillin then killed the sensitive Salmonella, selecting the ones that had gained the plasmid. Antibiotics do not cause the mutations that give resistance; mutations are random. One species of bacterium does not turn into another. Resistance is a property of bacteria, not of the patient's immune system.
What to project
The student lesson embeds these tabs. Open them full screen on the projector; every slider has a drag handle on the stage.
Slides for this lesson
A projectable deck for every pack is on the way. Until then, present the student lesson full screen: its sections, figure and lab tabs follow the same order as the plan above.