Cambridge International AS & A Level Biology 9700: Infectious diseases – Revision Notes

For full explanations and worked data examples, use the infectious diseases study guide. These notes condense topic 10 of the Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027: section 10.1 Infectious diseases (outcomes 1–4) and section 10.2 Antibiotics (outcomes 1–2). It is AS Level content, examined on Papers 1 and 2, and Paper 4 can draw on it too. Every outcome applies to all candidates.

Links: Cambridge AS & A Level Biology hub, printable checklist, practice questions for this topic, 9700 AS diagnostic and the next topic, immunity revision notes.

Key definitions

Term	What to write
Pathogen	An organism or virus that causes disease
Infectious disease	A disease caused by a pathogen that is transmissible from one host to another
Vector	An organism that carries a pathogen from one host to another (e.g. the female Anopheles mosquito)
Transmission	The way a pathogen passes from one host to the next
Antibiotic	A substance that kills bacteria or stops their growth, with little or no harm to human cells
Antibiotic resistance	The ability of a bacterium to survive and reproduce in the presence of an antibiotic
Selection pressure	An environmental factor (here, the antibiotic) that gives some variants a better chance of surviving and reproducing

10.1 The four diseases at a glance

Disease	Pathogen (exact names)	Type	Transmission
Cholera	Vibrio cholerae	Bacterium	Faecal–oral: water or food contaminated with faeces from an infected person
Malaria	Plasmodium falciparum, P. malariae, P. ovale, P. vivax	Protoctist	Vector: female Anopheles mosquito during a blood meal; also blood transfusion, shared needles, across the placenta
TB	Mycobacterium tuberculosis, Mycobacterium bovis	Bacteria	Airborne droplets from coughs and sneezes (M. tuberculosis); unpasteurised milk or undercooked meat from infected cattle (M. bovis)
HIV/AIDS	Human immunodeficiency virus (HIV)	Virus	Body fluids: unprotected sex, shared needles, unscreened blood; mother to child across placenta, at birth or in breast milk

Remember: no malarial life cycle is needed.

One-line mechanism for each disease

• Cholera: bacteria multiply in the small intestine and release a toxin; chloride ions and water leave the gut lining; severe watery diarrhoea and dehydration.
• Malaria: Plasmodium lives in liver cells and red blood cells, where it is hidden from much of the immune system.
• TB: bacteria infect the lungs; in many people the infection stays inactive until the immune system weakens.
• HIV: infects and destroys T-helper lymphocytes, so the immune system fails (AIDS) and opportunistic infections take hold.

10.1.4 Prevention and control

Method in steps: answering a “discuss” question

1. Name the control measure.
2. Say how it breaks the route of transmission.
3. Give a biological, social or economic factor that makes it work better or worse.
4. Repeat for a second measure. Aim for balance, not a long list.

Control measures and the factors that limit them

Disease	Main measures	Biological limit	Social limit	Economic limit
Cholera	Sewage treatment; chlorinated water; food hygiene; oral rehydration therapy	Symptomless carriers shed bacteria; vaccine protection is limited	Crowding in camps after disasters or war	Water and sewage systems are expensive
Malaria	Treated bed nets; indoor spraying; draining standing water; larva-eating fish; antimalarial drugs	Insecticide-resistant mosquitoes; drug-resistant Plasmodium; parasite hides in cells	Nets not used every night; clinics far away	Nets, sprays and drugs cost money
TB	BCG vaccine; contact tracing; long supervised multi-drug treatment; pasteurised milk; testing cattle	Drug-resistant strains; latent TB activates in people with HIV	Overcrowded, poorly ventilated housing; stopping treatment early	Long drug courses and supervision are costly
HIV	Condoms; testing; screening blood; needle exchange; ART	No vaccine; rapid mutation changes antigens; virus inside T-helper cells	Stigma reduces testing	ART is lifelong and expensive

10.2 Antibiotics

How penicillin works, in steps

1. The bacterial cell wall is peptidoglycan, held together by peptide cross-links.
2. A growing bacterium makes small breaks in its wall to insert new material.
3. Penicillin inhibits the enzymes (transpeptidases) that form new cross-links.
4. The wall becomes weaker.
5. Water enters by osmosis; the cell swells and bursts (osmotic lysis).

So penicillin affects only growing bacteria, and it does not harm human cells, which have no cell wall.

Why antibiotics do not affect viruses

• Viruses have no peptidoglycan cell wall, no ribosomes and no metabolism of their own.
• They replicate inside host cells using the host’s enzymes and ribosomes.
• So there is nothing for the antibiotic to target.

Resistance, in steps

1. A random mutation gives one bacterium a resistance allele (e.g. for an enzyme that breaks down penicillin).
2. The antibiotic kills susceptible bacteria: a selection pressure.
3. Resistant bacteria survive, face less competition and divide by binary fission.
4. The allele passes to offspring (vertical) and, on plasmids, to other bacteria (horizontal).
5. The proportion of resistant bacteria in the population rises.

Consequences and steps to reduce impact

Consequences	Steps to reduce the impact
Infections harder or impossible to treat	Prescribe only when needed; never for viral infections
More deaths from once-curable infections	Test the bacterium and use a narrow-spectrum drug
Longer hospital stays; higher costs	Take the full course as prescribed; do not share leftovers
Surgery and cancer treatment riskier	Rotate the antibiotics used
Multi-drug-resistant TB harder to control	Cut antibiotic use in farming
Newer drugs cost more	Better hospital hygiene; fund new antibiotics

Must-know distinctions

• Pathogen vs vector: Plasmodium is the pathogen; the mosquito is the vector.
• Bacterium vs protoctist vs virus: cholera and TB are bacterial; malaria is protoctist; HIV is viral. Only the bacterial diseases can be treated with antibiotics.
• M. tuberculosis vs M. bovis: airborne between humans vs from cattle in milk or meat.
• Mutation vs selection: the mutation is random and happens first; the antibiotic only selects.
• Vertical vs horizontal transmission of resistance: parent to offspring vs between bacteria on plasmids.
• HIV vs AIDS: HIV is the virus; AIDS is the condition that develops when T-helper cell numbers fall so low that opportunistic infections take hold.

Quick self-test

1. State what makes a disease infectious.
2. Name the type of pathogen that causes malaria, and name two species.
3. Give the two species of bacteria that cause TB.
4. Explain why cholera is common after a flood damages a town’s sewage pipes.
5. Give two ways, other than sexual intercourse, that HIV can be transmitted.
6. State the role of the female Anopheles mosquito in malaria.
7. Suggest one biological reason why malaria is difficult to control.
8. Explain why penicillin has no effect on a bacterium that has stopped growing.
9. Explain why penicillin does not damage human cells.
10. Explain why an antibiotic would not help a person with influenza.
11. Explain the role of plasmids in the spread of antibiotic resistance.
12. After a TB programme, cases in a district fell from 250 to 190 per 100 000 people. Calculate the percentage decrease.

Answers

1. It is caused by a pathogen and is transmissible: it can pass from one host to another.
2. A protoctist; any two of Plasmodium falciparum, P. malariae, P. ovale, P. vivax.
3. Mycobacterium tuberculosis and Mycobacterium bovis.
4. Faeces containing Vibrio cholerae enter the drinking water; people drink it and swallow the bacteria (faecal–oral transmission).
5. Any two: sharing needles; transfusion of unscreened blood; mother to fetus across the placenta; during birth; in breast milk.
6. It is the vector: it passes Plasmodium from an infected person to another person when it takes a blood meal.
7. Any one: mosquitoes have become resistant to insecticides; Plasmodium has become resistant to drugs; the parasite lives inside liver and red blood cells, hidden from the immune system; mosquitoes breed in any small area of standing water.
8. Penicillin inhibits the enzymes that form cross-links in new cell wall. A bacterium that is not growing is not making new wall, so its wall is not weakened and it does not burst.
9. Human cells have no cell wall (no peptidoglycan), so penicillin has no target in them.
10. Influenza is caused by a virus. Viruses have no cell wall, ribosomes or metabolism of their own, so there is nothing for the antibiotic to act on.
11. Resistance genes are often carried on plasmids, which can pass from one bacterium to another, even of a different species, so resistance spreads faster than by reproduction alone.
12. (250 − 190) ÷ 250 × 100 = 24.0% (24%).

Where marks are usually lost

• Calling Plasmodium a bacterium or a virus, or naming the mosquito as the pathogen.
• Misspelling “immunodeficiency”, Vibrio cholerae or Mycobacterium, or missing out the species name.
• Writing “HIV attacks white blood cells” instead of naming T-helper lymphocytes.
• Describing cholera transmission as “dirty water” without linking it to faeces from an infected person.
• Saying penicillin “makes holes in” or “digests” the wall rather than preventing cross-links forming.
• Leaving out osmosis when explaining why the bacterium bursts.
• Saying antibiotics cause mutations, or that bacteria “become immune” to them.
• On “discuss” questions, listing control measures without a biological, social or economic factor for each.
• Suggesting antibiotics as a treatment for HIV/AIDS itself: HIV is a virus.
• Spending time on the stages of the malarial life cycle, which the syllabus does not expect.

Official syllabus

Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027, Version 1 (published September 2022), Cambridge University Press & Assessment. Topic 10 Infectious diseases, sections 10.1 and 10.2.