10. Infectious Diseases
- Syllabus
- 9700–2028–2029
- Section
- 10
- Level
- AS
Exam analysis
Most tested topics
10.1 Infectious Diseases
- Syllabus
- 9700–2028–2029
- Topic
- 10.1
- Level
- AS
Infectious diseases are caused by transmissible pathogens
An infectious disease is caused by a pathogen and can be transmitted from one host to another. A pathogen is the disease-causing infectious agent; the disease is the harmful condition that results in the host.
Transmissible means that the pathogen can reach a new host by a suitable route, either directly or indirectly. The route may involve contaminated material, droplets, body fluids or a vector, but the vector or medium is not itself automatically the pathogen.
Not every disease is infectious: inherited and deficiency diseases are not caused by transmissible pathogens. A mosquito that carries a pathogen is a vector, not the disease-causing organism.
Four diseases are identified by exact pathogen names and types
| Disease | Pathogen name | Pathogen type |
|---|---|---|
| Cholera | Vibrio cholerae | bacterium |
| Malaria | Plasmodium falciparum, P. malariae, P. ovale, P. vivax | protoctists |
| Tuberculosis (TB) | Mycobacterium tuberculosis, M. bovis | bacteria |
| HIV/AIDS | human immunodeficiency virus (HIV) | virus |
Malaria is the disease; its pathogen is one of the named Plasmodium species, while a female Anopheles mosquito is only the vector. HIV is the virus; AIDS is the disease state that may develop after HIV damages immune function.
Scientific names identify the pathogen and must not be replaced by the disease name. Mycobacterium and Vibrio are bacteria; Plasmodium is eukaryotic and is classified here as a protoctist; HIV is not a cell.
Each infectious disease follows a specific transmission chain
| Disease | Transmission chain |
|---|---|
| Cholera | V. cholerae leaves an infected person in faeces → contaminates water or food → is ingested by a new host |
| Malaria | A female Anopheles mosquito feeds on an infected person and acquires Plasmodium → later injects the pathogen while feeding on another person |
| TB | M. tuberculosis in droplets/aerosols released by an infectious person is inhaled; M. bovis may be acquired from infected cattle through unpasteurised milk or contaminated animal products |
| HIV | Infected blood, semen, vaginal fluids or breast milk reaches another person through sexual contact, contaminated needles/blood, or mother-to-child transfer during pregnancy, birth or breastfeeding |
A complete explanation names the source, the compatible route or vector, and entry to the new host. The pathogen must survive that route; merely being near an infected person does not establish every form of transmission.
The female Anopheles mosquito is a vector, not the malaria pathogen. HIV is not spread by ordinary casual contact. Detailed stages of the malarial parasite life cycle are outside this syllabus outcome.
Disease control must be biologically effective and socially feasible
Prevention and control must match the pathogen and transmission route, but success also depends on social acceptance, infrastructure, access and cost. A discussion therefore links each measure to both its biological effect and its practical limitation.
| Disease | Biological factors and route-matched measures | Social and economic factors that affect success |
|---|---|---|
| Cholera | Safe water, sewage treatment, hygiene and vaccination interrupt faecal–oral transmission; rapid detection and rehydration reduce harm during outbreaks | Water and sanitation infrastructure are expensive; disasters, overcrowding, education, reporting and vaccine access affect coverage |
| Malaria | Insecticide-treated nets, indoor spraying and breeding-site reduction target the Anopheles vector; preventive drugs, diagnosis, treatment and vaccination can reduce infection or transmission | Mosquito/drug resistance and many breeding sites limit biology; climate, housing, correct net use, healthcare access and continuing programme cost affect control |
| TB | Ventilation, reduced crowding, case detection, contact tracing, effective multidrug treatment and BCG vaccination reduce transmission or susceptibility; cattle testing and milk pasteurisation limit M. bovis | Long treatment encourages incomplete courses and resistance; stigma, delayed diagnosis, crowded housing, clinics, drug supply and programme funding affect control |
| HIV | Condoms, sterile needles, screened blood, testing and antiretroviral therapy reduce body-fluid transmission or viral load; treatment in pregnancy reduces mother-to-child transmission | Long asymptomatic infection delays diagnosis; stigma, consent, education, sexual behaviour, unequal access and lifelong treatment cost affect uptake and continuity |
Evaluation rule: identify where a measure breaks the transmission chain; state the biological limitation; then explain one social or economic condition that changes coverage, adherence or sustainability. Layered control is usually stronger because no single measure removes every route or constraint.
Treatment and prevention are not interchangeable, and the same measure does not fit every disease. Do not list controls without explaining why they work and why implementation may still fail. Detailed malaria parasite life-cycle stages are not required.
10.2 Antibiotics
- Syllabus
- 9700–2028–2029
- Topic
- 10.2
- Level
- AS
Penicillin weakens growing bacterial cell walls by stopping peptidoglycan cross-links
Penicillin stops new peptidoglycan molecules from forming the cross-links that strengthen a growing bacterial cell wall.
- A growing bacterium makes small holes in its wall so the wall can stretch; enzymes called autolysins continue to create these holes.
- Normally, new peptidoglycan is added and cross-linked to reinforce the wall. Penicillin prevents the cross-linking step.
- The holes therefore accumulate while reinforcement is reduced, so the wall becomes progressively weaker.
- Bacteria take up water by osmosis. A weakened wall cannot withstand the pressure from inside indefinitely, so a growing susceptible bacterium can burst.
The effect depends on growth: once bacterial growth is complete, autolysins no longer create new holes and no further cross-links form, so this penicillin mechanism is most effective while the bacterium is growing.
Penicillin weakens a bacterial wall by interrupting its reinforcement; it does not dissolve every bacterium immediately. This card stops at the cell-wall mechanism: the distinction between bacterial and viral targets and the development of antibiotic resistance belong to the neighbouring cards.
Antibiotics cannot treat viruses because viruses lack bacterial targets
Antibiotics work against bacterial structures or processes, but a virus is not a bacterial cell. A virus therefore does not provide the bacterial targets that an antibiotic such as penicillin is designed to affect.
- Bacterial target exists: an antibiotic can interfere with a bacterial cell-wall process, membrane protein, enzyme, DNA process or protein-synthesis process. Penicillin, for example, acts on strengthening a growing bacterial cell wall.
- Viral target is absent: viruses have no bacterial-style cell wall and do not carry out growth and reproduction as independent bacterial cells. During replication they use the host cell’s transcription and translation machinery.
- Treatment consequence: blocking a bacterial target cannot stop the virus from using host-cell machinery, so an antibiotic does not treat the viral infection.
This is a target-matching rule, not a diagnosis from symptoms alone. Cholera and TB are bacterial diseases for which antibiotics may be relevant, whereas HIV is viral and is not treated by antibiotics.
“Antibiotics do not affect viruses” means that antibacterial targets are absent from viruses; it does not mean that no medicine can ever act against a virus. Resistance and other reasons for treatment failure are separate topics, not part of this target distinction.
Antibiotic resistance spreads by selection and makes bacterial infections harder to control
Antibiotic resistance is a population change: a chance mutation can produce a resistance allele, and antibiotic treatment selects bacteria that survive, allowing resistance to become more common.
- Variation first: random mutation creates genetic variation; the antibiotic does not direct a bacterium to mutate.
- Selection: treatment kills susceptible bacteria, while a bacterium with a resistance allele survives with less competition.
- Frequency increases: the resistant survivor reproduces, so its allele is passed to more offspring and becomes more frequent in the population. Short generation times, clonal offspring and horizontal gene transfer can speed spread.
- Clinical consequence: commonly used antibiotics can become less effective; multidrug-resistant strains can make infections difficult to treat and require complicated, expensive treatments that may not be available to everyone.
- Reduce selection: prescribe antibiotics only when needed, do not use them for viral infections, avoid unnecessary wide-spectrum use, complete the prescribed course and tighten control of antibiotic use in agriculture.
- Limit spread: maintain good hygiene, especially handwashing or sanitiser use in clinical settings, and isolate infected patients when resistant strains could spread.
- Maintain options: develop new antibiotics and alternatives, recognising that this is expensive and time-consuming.
Antibiotics select pre-existing resistant variants; they do not train every bacterium or create a targeted mutation. Resistance is a change in allele frequency in a bacterial population, not immunity of the patient. The penicillin wall mechanism and the virus target boundary are covered by the neighbouring cards.