discuss the biological, social and economic factors that need to be considered in the prevention and control of cholera, malaria, TB and HIV (details of the life cycle of the malarial parasite are not expected)
Infectious Diseases – Prevention and Control (Cambridge International AS & A Level Biology 9700 – Topic 10)
This note is organised to match the syllabus requirements. For each disease a learning‑outcome checklist is given first, followed by a systematic discussion of the biological, social and economic factors that influence prevention and control, and finally the key control strategies. The antibiotic sub‑topic is included at the end as required by 10.2.
Why integrate biological, social and economic factors?
Biological factors – characteristics of the pathogen (type, mode of transmission, survival outside the host, drug‑ or insecticide‑resistance) that determine how the disease spreads and how it can be treated.
Social factors – human behaviours, cultural practices, living conditions and health‑seeking attitudes that affect exposure, diagnosis and compliance with control measures.
Economic factors – resources needed for prevention, diagnosis and treatment, and the wider impact of disease on productivity, education and national development.
Examiners expect an integrated discussion that links the three groups for each infection.
1. Cholera
Learning‑outcome checklist
State the pathogen and its type.
Describe the mode of transmission and the key steps in pathogenesis.
Identify at least three biological, three social and three economic factors that affect control.
List the main preventive and control measures (including vaccination).
Transmission: Faecal‑oral route via contaminated water or food.
Pathogenesis: Cholera toxin activates adenylate cyclase → massive Cl⁻ and water secretion into the intestinal lumen → profuse watery diarrhoea and rapid dehydration.
Environmental survival: Thrives in warm, brackish water; can persist in biofilms on aquatic plants, shellfish and in stagnant water.
Drug resistance: Rare, but severe cases may require antibiotics (e.g., doxycycline, azithromycin) in addition to rehydration.
Social Factors
Poor sanitation and lack of safe drinking‑water supplies.
Population displacement (refugee camps, post‑disaster settlements) that forces reliance on unsafe water sources.
Low public awareness of hand‑washing, safe food handling and the importance of oral rehydration.
Cultural practices involving communal water use, shared meals or open defecation.
Stigma in some communities that delays seeking treatment.
Economic Factors
High capital cost for water‑treatment plants, sewage networks and latrine construction.
Cost of oral rehydration salts (ORS) and, for severe cases, intravenous fluids and antibiotics.
Loss of labour productivity, school attendance and tourism revenue during outbreaks.
Funding required for mass vaccination campaigns where oral cholera vaccine (OCV) is used.
Prevention & Control Strategies
Provision of safe drinking water (chlorination, filtration, protected wells, point‑of‑use treatment).
Improvement of sanitation (construction of latrines, sewage treatment, safe waste disposal).
Health education on hand‑washing, safe food preparation, and the correct use of ORS.
Rapid case detection and rehydration therapy (ORS ± IV fluids); antibiotics for severe disease.
Targeted oral cholera vaccination (killed‑cell or recombinant OCV) in high‑risk or outbreak settings.
2. Malaria
Learning‑outcome checklist
Identify the causative agents and the vector.
Explain how the vector transmits the parasite and note any resistance issues.
List three biological, three social and three economic factors influencing control.
State the principal preventive measures (vector control, treatment, surveillance).
Biological Factors
Pathogen:Plasmodium spp. – protozoan parasites; P. falciparum and P. vivax cause most severe disease.
Vector: Female Anopheles mosquitoes; bite between dusk and dawn.
Transmission: Inhalation of aerosolised droplets from individuals with active pulmonary TB.
Latent infection: Up to one‑third of the world’s population harbour dormant bacilli; reactivation occurs when immunity declines.
Drug resistance: Multidrug‑resistant (MDR) and extensively drug‑resistant (XDR) strains limit treatment options.
Co‑infection: HIV markedly increases susceptibility and accelerates disease progression.
Social Factors
Overcrowded housing, prisons, refugee camps and poorly ventilated workplaces.
Stigma that discourages people from seeking diagnosis, adhering to treatment, or disclosing disease status.
Limited public knowledge of cough etiquette, infection‑control practices and the importance of completing therapy.
Migration and urbanisation that facilitate rapid spread.
Co‑infection with HIV, especially in high‑prevalence settings.
Economic Factors
Long‑duration therapy (minimum 6 months) and the cost of first‑line (isoniazid, rifampicin, ethambutol, pyrazinamide) and second‑line drugs.
Loss of income while patients attend clinics for directly observed therapy (DOT) and during periods of ill‑health.
Resource constraints for laboratory diagnostics (smear microscopy, GeneXpert MTB/RIF, culture).
Funding needed for contact tracing, community outreach and BCG vaccination programmes.
Prevention & Control Strategies
Active case finding and contact tracing, especially in high‑risk environments.
Directly observed therapy (DOT) to ensure adherence to the full drug regimen.
BCG vaccination of newborns in countries with high TB prevalence (protects against severe childhood TB).
Improving ventilation in homes, schools, workplaces and health‑care facilities.
Integration of TB and HIV services for co‑infected patients (screening, joint treatment).
Public education on cough etiquette, early symptom recognition and the importance of completing treatment.
4. Human Immunodeficiency Virus (HIV)
Learning‑outcome checklist
Identify the pathogen and its classification.
State the main routes of transmission.
Explain why the virus rapidly develops drug resistance.
Identify three biological, three social and three economic factors influencing control.
List the principal prevention and treatment measures.
Biological Factors
Pathogen: Human immunodeficiency virus – RNA retrovirus that integrates into host DNA.
Target cells: CD4⁺ T‑lymphocytes, macrophages and dendritic cells.
Transmission: Unprotected sexual contact, contaminated blood (transfusion, needle sharing), perinatal (mother‑to‑child) and occupational exposure.
High mutation rate: Reverse transcriptase lacks proofreading → rapid generation of diverse sub‑types and drug‑resistant mutants.
No cure: Lifelong antiretroviral therapy (ART) required to maintain immune function and suppress viral load.
Social Factors
Stigma and discrimination that impede testing, disclosure, and adherence to ART.
Gender inequality limiting women’s ability to negotiate condom use or access services.
Legal and social barriers for key populations (sex workers, men who have sex with men, people who inject drugs).
Insufficient comprehensive sexuality education in schools and communities.
Migration and mobile workforces that increase exposure and complicate continuity of care.
Economic Factors
Cost of lifelong ART, routine viral‑load monitoring, and management of opportunistic infections.
Reduced workforce participation and increased health‑care expenditure at national level.
Funding gaps in low‑ and middle‑income countries for prevention, testing, treatment and community outreach.
Economic impact of orphanhood and loss of skilled labour in heavily affected regions.
Prevention & Control Strategies
Universal access to confidential HIV testing and post‑test counselling.
Provision of ART to all diagnosed individuals (treatment‑as‑prevention) with adherence support.
Pre‑exposure prophylaxis (PrEP) for high‑risk groups and post‑exposure prophylaxis (PEP) after occupational or sexual exposure.
Promotion of consistent condom use, safe‑injection practices, and male circumcision where culturally acceptable.
Community‑based education campaigns to reduce stigma, encourage testing and support treatment adherence.
Integration of HIV services with reproductive health, TB, and sexual‑health programmes.
5. Antibiotics (Cambridge Syllabus 10.2)
How penicillin works
Penicillin is a β‑lactam antibiotic. The β‑lactam ring binds irreversibly to penicillin‑binding proteins (PBPs) that catalyse the final cross‑linking step of peptidoglycan synthesis.
Inhibition of PBPs weakens the bacterial cell wall, causing osmotic lysis of actively dividing Gram‑positive bacteria – a bactericidal effect.
Why antibiotics do not affect viruses
Viruses lack a peptidoglycan cell wall and do not perform the enzymatic reactions targeted by β‑lactams.
Viral replication relies on host‑cell machinery; therefore drugs that target bacterial‑specific structures have no viral target.
Consequences of antibiotic resistance
Production of β‑lactamases (e.g., penicillinases, extended‑spectrum β‑lactamases) that hydrolyse the β‑lactam ring.
Alteration of PBPs (e.g., MRSA – altered PBP2a) reduces drug binding.
Efflux pumps and reduced membrane permeability limit intracellular antibiotic concentrations.
Suggested diagram: Flowchart showing how biological, social and economic factors interact to shape prevention and control strategies for cholera, malaria, TB and HIV.
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