AS 10 Infectious diseases | A Level Biology 9700

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🎯What you need to be able to do

State that infectious diseases are caused by pathogens and are transmissible.
Name the pathogen and type of pathogen for cholera, malaria, tuberculosis and HIV/AIDS.
Explain how each of these four diseases is transmitted.
Discuss the biological, social and economic factors involved in preventing and controlling them.
Outline how penicillin acts on bacteria and why antibiotics do not affect viruses.
Discuss the consequences of antibiotic resistance and the steps that reduce its impact.

📚The biology

The four diseases

An infectious disease is caused by a pathogen and is transmissible from one host to another. Learn the pathogen names precisely — they carry marks on their own, and the binomials must be written correctly, genus capitalised and species lower case, italicised or underlined.

Cholera — the bacterium Vibrio cholerae.
Malaria — the protoctists Plasmodium falciparum, P. malariae, P. ovale and P. vivax. Four species, and the syllabus names all four.
Tuberculosis (TB) — the bacteria Mycobacterium tuberculosis and Mycobacterium bovis. Two species; M. bovis comes from cattle.
HIV/AIDS — the human immunodeficiency virus (HIV).

Transmission

Cholera — water-borne and food-borne. The bacterium is ingested in water or food contaminated with faeces from an infected person; it survives the stomach if acid is dilute, reaches the small intestine and releases a toxin causing severe watery diarrhoea, which contaminates water supplies again. It spreads where sanitation and clean water are lacking.
Malaria — by a vector, the female Anopheles mosquito, which takes a blood meal and injects Plasmodium with its saliva. It can also pass across the placenta or in transfused blood. You do not need the details of the parasite's life cycle.
TB — airborne droplets from coughing, sneezing, talking or laughing by an infected person, inhaled by another. Transmission is favoured by overcrowding and poor ventilation. M. bovis can also be transmitted in meat or unpasteurised milk from infected cattle.
HIV — in body fluids: unprotected sexual intercourse, sharing contaminated needles, infected blood or blood products, and mother to child across the placenta, during birth or in breast milk.

Controlling them

Questions here ask you to discuss, which means bringing together biological, social and economic factors rather than listing treatments.

Cholera — biologically straightforward: provide clean piped water, treat sewage, chlorinate supplies, and treat cases with oral rehydration therapy, which is cheap and highly effective. The barriers are economic (infrastructure is expensive) and social (displacement, refugee camps and natural disasters destroy sanitation exactly when crowding is worst).
Malaria — attack the vector: insecticide-treated bed nets, draining or spraying standing water where larvae develop, and larvivorous fish; protect people with prophylactic drugs; treat cases promptly. Difficulties: mosquitoes evolve insecticide resistance and Plasmodium evolves drug resistance; there is no long-lasting fully protective vaccine in wide use; and control programmes are expensive to sustain over the many years required.
TB — contact tracing, BCG vaccination, improved housing and nutrition, and long courses of several antibiotics together. The central difficulty is that treatment lasts six months or more; patients feel better and stop early, which selects for resistant strains. Directly observed therapy, where a health worker watches each dose taken, exists precisely to prevent this. HIV co-infection greatly increases susceptibility.
HIV — no vaccine and no cure; control depends on preventing transmission: education, condoms, screening blood products, needle exchange, and antiretroviral drugs, which suppress viral load and so also reduce transmission. Social factors dominate — stigma discourages testing, and the long asymptomatic period means people transmit the virus without knowing they carry it.

How penicillin works

Penicillin inhibits the enzymes that cross-link the peptidoglycan of the bacterial cell wall. It only affects bacteria that are actively growing and making new wall. With the wall weakened, water enters by osmosis and the cell bursts (lyses), since without an intact wall there is nothing to resist the pressure.

Antibiotics do not affect viruses. Viruses are non-cellular: they have no cell wall, no ribosomes and no metabolic pathways of their own, so there is nothing for an antibiotic to target. They replicate inside host cells using the host’s machinery, so a drug that damaged that machinery would damage the host too. This is why antibiotics are useless for colds, influenza and HIV, and why prescribing them for viral infections is one of the drivers of resistance.

Antibiotic resistance

Resistance arises by random mutation in a bacterium — it is not caused by the antibiotic. What the antibiotic does is select: in its presence, non-resistant bacteria die while the resistant ones survive, reproduce and pass on the allele, so the resistant proportion of the population rises. This is natural selection (Topic 17) observable within days. Resistance genes are often carried on plasmids, which can be passed between bacteria of different species, so resistance spreads faster than inheritance alone would allow.

Consequences: infections that were routine become difficult or impossible to treat, hospital stays lengthen, routine surgery and chemotherapy become dangerous because they depend on antibiotic cover, and multi-drug-resistant strains such as MRSA and MDR-TB emerge.

Steps to reduce it:

prescribe antibiotics only when necessary, and never for viral infections;
use the narrowest-spectrum antibiotic that will work;
complete the full course, so partially resistant survivors are not left behind;
avoid routine use in agriculture as growth promoters;
rotate antibiotics and use combinations, so a strain resistant to one is killed by another;
strict hygiene and isolation in hospitals to limit spread;
continued development of new antibiotics, though this is slow and expensive.

Bacteria do not “become resistant because of the antibiotic”. The mutation is random and pre-existing; the antibiotic changes which individuals survive. Nor do people become resistant — the bacterium does. Both are standard mark-losing phrases, and both are easy to avoid once you have noticed them.

✏️Worked example

In a hospital, the proportion of Staphylococcus aureus isolates resistant to a particular antibiotic rose from 4% to 61% over eleven years, during which the antibiotic was used routinely for all suspected infections. (a) Explain, in terms of natural selection, how this increase occurred. (b) A doctor suggests that “the antibiotic caused the bacteria to mutate”. Explain what is wrong with this. (c) Suggest three measures the hospital could take, and explain how each would help.

(a) Within the bacterial population there was already variation, arising by random mutation: a small minority — about 4% — carried an allele conferring resistance, for example one coding for an enzyme that breaks the antibiotic down. Routine use of the antibiotic created a selection pressure: non-resistant bacteria were killed, while the resistant ones survived.

The survivors reproduced, and because bacteria divide rapidly by binary fission, they passed the resistance allele to their offspring. Over many generations the frequency of the resistance allele in the population rose, to 61%. Resistance genes carried on plasmids can also be transferred directly between bacteria, including between species, which accelerates the spread further.

(b) The antibiotic did not cause the mutation. Mutations are random and occur regardless of whether the antibiotic is present — resistant individuals existed before the antibiotic was introduced, which is why 4% were already resistant at the start. What the antibiotic did was select between individuals that already differed, by killing the susceptible ones. Saying the antibiotic caused the mutation is a Lamarckian error: it implies the environment directs a useful change, when in fact it only determines which pre-existing variants survive.

(c) Any three, each with its mechanism:

Prescribe antibiotics only when a bacterial infection is confirmed, ideally after culturing the organism. This reduces the selection pressure, so resistant strains gain no advantage most of the time and their frequency stops rising.
Ensure patients complete the full course. Stopping early leaves the least susceptible survivors alive to reproduce, which selects for increasing resistance in exactly the wrong direction.
Rotate antibiotics, or use two together. A bacterium resistant to one drug is killed by the other, and the chance of a single cell carrying mutations conferring resistance to both is very small.
Isolate infected patients and enforce hand hygiene. This does not slow the evolution of resistance but limits the spread of strains that have already evolved.

Check it. Test your explanation against the numbers. Natural selection requires pre-existing variation, and the data supply it: 4% were resistant before the selection pressure was sustained. If your answer implies the resistant strain appeared from nothing during the eleven years, it contradicts the starting figure. Also check that you have written about a change in the proportion of a population, not about individual bacteria changing — that distinction is the whole of natural selection.

Writing that bacteria ‘adapt’, ‘learn’ or ‘want to survive’. Individual bacteria do not change; the composition of the population changes because some individuals die and others do not. Similarly, avoid “the patient became resistant to the antibiotic”: it is the bacterium that is resistant, not the person. Examiner reports flag this phrasing every single session, and it converts an otherwise correct answer into a lost mark.

📝Practise

Work through these, then reveal the answer. Each question targets a different objective from the list above.

1. Name the pathogen and the type of pathogen causing cholera, malaria, TB and HIV/AIDS.

Cholera — the bacterium Vibrio cholerae. Malaria — the protoctists Plasmodium falciparum, Plasmodium malariae, Plasmodium ovale and Plasmodium vivax. Tuberculosis — the bacteria Mycobacterium tuberculosis and Mycobacterium bovis. HIV/AIDS — the human immunodeficiency virus, a virus. Write binomials with the genus capitalised and the species in lower case, italicised or underlined; after the first mention the genus may be abbreviated, as in P. vivax. Note that malaria and TB each have more than one named pathogen, and questions often award a mark for completeness.

2. Explain why cholera spreads rapidly in refugee camps but rarely in cities with treated water supplies.

Cholera is transmitted by the faecal–oral route: Vibrio cholerae is ingested in water or food contaminated with faeces from an infected person. Infected people produce large volumes of watery diarrhoea containing enormous numbers of bacteria. In a refugee camp there is typically no sewage treatment, no piped clean water, and high population density, so faecal material readily contaminates the water people drink and one case rapidly produces many. Malnutrition and lack of medical care worsen outcomes. In a city with treated water, sewage is separated from the drinking supply and the supply is chlorinated, killing the bacterium, so the transmission route is broken. The disease is therefore an engineering and economic problem as much as a biological one: the biology of prevention is simple and well understood, and the barrier is the cost of infrastructure.

3. Outline how penicillin kills bacteria and explain two reasons why it has no effect on HIV.

Penicillin inhibits the enzymes that cross-link peptidoglycan in the bacterial cell wall, so a growing bacterium cannot build a complete wall. Water then enters the cell by osmosis and, with no intact wall to resist the pressure, the cell bursts (lyses). Penicillin therefore only kills bacteria that are actively growing and synthesising new wall. It has no effect on HIV because: (i) HIV is a virus and has no cell wall — there is no peptidoglycan and so no target for the drug; (ii) more generally, viruses have no ribosomes, no enzymes and no metabolic pathways of their own, so none of the processes antibiotics disrupt is present, and they replicate using the host cell’s machinery, which cannot be attacked without harming the host.

4. Discuss why tuberculosis remains difficult to control despite effective antibiotics being available.

Biological: treatment requires several antibiotics taken together for six months or more, because Mycobacterium grows slowly and has a waxy cell wall that is hard for drugs to penetrate. Multi-drug-resistant strains have evolved, particularly where courses were not completed. HIV co-infection destroys the T-lymphocytes needed to contain the bacterium, so latent infections reactivate. Social: transmission is by airborne droplets and is favoured by overcrowded, poorly ventilated housing and by homelessness; patients feel better within weeks and stop taking the drugs, which selects for resistance; stigma discourages testing and contact tracing. Economic: long courses and case-finding are expensive; directly observed therapy, where a health worker watches every dose, works but is labour-intensive; poverty and malnutrition raise susceptibility and are not solved by medicine. The point to make is that the limiting factors are social and economic rather than pharmacological.

5. A patient with a sore throat is prescribed antibiotics and feels better after three days, so stops taking them. Explain the two problems this creates.

First, if the sore throat is viral, as most are, the antibiotic was never going to help — viruses have no cell wall, ribosomes or metabolism of their own for the drug to target — so the patient has been exposed to a selection pressure for no benefit, and any bacteria harmlessly present in the body have had resistant variants selected for. Second, if the infection was bacterial, stopping early means the least susceptible bacteria survive: the most susceptible die first, so the population remaining after three days is enriched for those hardest to kill. These reproduce, the infection may return in a more resistant form, and resistance alleles — often on plasmids that can be passed to other bacteria, even of other species — spread. Completing the course is intended to kill the whole population, leaving no survivors to select from.

6. Explain why malaria control programmes that rely on a single insecticide tend to lose effectiveness over time.

Within any mosquito population there is genetic variation arising by random mutation, and a few individuals will by chance carry an allele conferring resistance to the insecticide — for example one coding for an enzyme that breaks it down. Applying the insecticide creates a strong selection pressure: susceptible mosquitoes die, resistant ones survive and reproduce, passing the allele to their offspring. Mosquitoes have short generation times and produce large numbers of offspring, so the frequency of the resistance allele rises quickly through the population and the insecticide becomes ineffective within a few years. The same argument applies to Plasmodium and antimalarial drugs. Control programmes therefore rotate insecticides, use combinations, and combine chemical control with non-chemical measures such as bed nets and draining breeding sites, so that no single selection pressure is applied consistently.

🔗Go deeper — other people’s work

These are external resources, not mine. If one stops working, tell me and everything above it on this page still stands.

World Health Organization fact sheets on cholera, malaria, tuberculosis and HIV — current figures and control strategies, ideal for the ‘discuss’ questions
WHO and CDC material on antimicrobial resistance — the scale of the problem stated in a way that makes the topic feel less abstract
Any documented case study of an MRSA or MDR-TB outbreak — a concrete example makes the natural selection argument much easier to write under exam conditions