Pathogens and Disease Transmission

A pathogen is a microorganism that causes disease. This lesson covers the different types of pathogens, how diseases are transmitted, and the mechanisms by which pathogens cause disease. These are essential topics for the Edexcel A-Level Biology (9BI0) specification.

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What is a Pathogen?

A pathogen is an organism or agent that causes disease in its host. Pathogens include:

Type	Examples
Bacteria	Mycobacterium tuberculosis (TB), Vibrio cholerae (cholera), Salmonella typhi (typhoid)
Viruses	HIV, influenza, SARS-CoV-2
Fungi	Candida albicans (thrush), Aspergillus (aspergillosis)
Protoctista	Plasmodium (malaria), Trypanosoma (sleeping sickness)

Communicable vs Non-Communicable Diseases

Type	Definition	Examples
Communicable (infectious)	Caused by pathogens; can spread from one organism to another	TB, cholera, malaria, influenza, HIV/AIDS
Non-communicable	Not caused by pathogens; cannot spread between organisms	Cancer, coronary heart disease, diabetes, asthma

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Modes of Disease Transmission

Pathogens can be transmitted between hosts by several routes:

1. Direct Contact

Mode	Description	Example
Person to person	Physical contact (skin, body fluids)	HIV (via blood, sexual contact), athlete's foot
Vertical transmission	Mother to offspring (across placenta, during birth, or via breast milk)	HIV, rubella

2. Indirect Contact

Mode	Description	Example
Airborne (droplet)	Pathogen carried in respiratory droplets or aerosols	TB, influenza, COVID-19
Waterborne	Pathogen transmitted via contaminated water	Cholera (Vibrio cholerae), dysentery
Foodborne	Pathogen transmitted via contaminated food	Salmonella, E. coli O157
Fomites	Transmission via contaminated objects (door handles, bedding)	Norovirus, MRSA

3. Vector-Borne Transmission

A vector is an organism that transmits a pathogen from one host to another without being affected itself.

Vector	Pathogen transmitted	Disease
Female Anopheles mosquito	Plasmodium	Malaria
Aedes aegypti mosquito	Dengue virus, Zika virus	Dengue fever, Zika
Tsetse fly	Trypanosoma	Sleeping sickness
Rat flea	Yersinia pestis	Plague

Exam Tip: A vector does not cause the disease — it merely transports the pathogen. The mosquito is the vector for malaria; Plasmodium is the pathogen. Be precise with terminology in your exam answers.

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How Pathogens Cause Disease

Pathogens cause disease through two main mechanisms:

1. Damage to Host Cells and Tissues

Mechanism	Detail	Example
Cell lysis	Viruses replicate inside host cells and burst them upon release	Influenza virus destroys respiratory epithelial cells
Nutrient competition	Pathogens consume host nutrients	TB bacteria consume host resources in the lungs
Tissue destruction	Bacteria destroy tissues directly	Mycobacterium tuberculosis destroys lung tissue (cavitation)
Blockage of vessels	Parasites block blood vessels or lymphatic channels	Plasmodium-infected red blood cells block capillaries

2. Production of Toxins

Toxin type	Description	Example
Exotoxins	Proteins secreted by living bacteria into the surrounding environment	Vibrio cholerae produces cholera toxin, which causes intestinal cells to secrete Cl⁻ and water → severe diarrhoea
Endotoxins	Lipopolysaccharides (LPS) in the outer membrane of Gram-negative bacteria; released upon cell death/lysis	Salmonella; causes fever, inflammation, and septic shock

Cholera: A Case Study

Vibrio cholerae causes cholera through the following mechanism:

1. The bacterium is ingested through contaminated water.
2. It colonises the epithelial cells of the small intestine.
3. It produces cholera toxin, which binds to receptors on intestinal epithelial cells.
4. The toxin causes chloride ion (Cl⁻) channels to open permanently.
5. Cl⁻ ions flood into the intestinal lumen.
6. The increased ion concentration lowers the water potential of the lumen.
7. Water moves into the lumen by osmosis from the blood and tissues.
8. This causes severe watery diarrhoea (up to 20 litres per day), leading to rapid dehydration and potentially death if untreated.

Treatment of Cholera

The primary treatment is oral rehydration therapy (ORT) — a solution of water, salts (NaCl, KCl) and glucose.

• Glucose is included because it enhances the absorption of sodium ions (Na⁺) via a sodium-glucose cotransporter on the intestinal epithelium.
• Water follows Na⁺ by osmosis, rehydrating the patient.

Exam Tip: ORT does not kill the bacterium — it treats the symptoms (dehydration). The body's immune system eventually clears the infection. Antibiotics may also be given to reduce the duration of the disease.

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Tuberculosis (TB): A Case Study

Mycobacterium tuberculosis causes TB, primarily affecting the lungs (pulmonary TB).

Transmission

• Spread by airborne droplets (coughing, sneezing, talking).
• Requires prolonged close contact for transmission (unlike highly infectious diseases such as measles).

Pathogenesis

1. Inhaled bacteria are engulfed by macrophages in the alveoli.
2. M. tuberculosis can survive and replicate inside macrophages (it prevents phagosome-lysosome fusion).
3. The immune system walls off the bacteria in structures called granulomas (tubercles).
4. In latent TB, the bacteria remain dormant within granulomas — the person is asymptomatic and not infectious.
5. In active TB (if the immune system weakens), the bacteria multiply, destroying lung tissue (cavitation), and the person becomes symptomatic and infectious.

Symptoms

Symptom	Cause
Persistent cough (often with blood)	Lung tissue destruction
Weight loss and fatigue	Chronic infection; diversion of nutrients
Night sweats and fever	Immune response to infection

Treatment

• A course of multiple antibiotics for 6–9 months (e.g. isoniazid, rifampicin, ethambutol, pyrazinamide).
• Multiple drugs are used to reduce the risk of antibiotic resistance developing.
• BCG vaccine provides partial protection against TB.

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HIV/AIDS: A Case Study

HIV (Human Immunodeficiency Virus) attacks the immune system, specifically CD4⁺ T helper cells.

Transmission

• Via body fluids: blood, semen, vaginal fluids, breast milk.
• Routes include: unprotected sexual contact, sharing needles, mother-to-child transmission.

Pathogenesis

1. HIV attaches to CD4 receptors on T helper cells using its glycoprotein gp120.
2. The viral RNA is reverse-transcribed to DNA by reverse transcriptase.
3. The viral DNA is integrated into the host cell's genome by integrase.
4. The host cell produces new viral particles, which bud from the cell (eventually killing it).
5. Over years, the number of T helper cells declines.
6. When the T helper cell count drops below 200 cells per mm³, the patient is diagnosed with AIDS (Acquired Immunodeficiency Syndrome).
7. The patient becomes susceptible to opportunistic infections (e.g. pneumonia, TB, Kaposi's sarcoma).

Treatment

• Antiretroviral therapy (ART) using combinations of drugs that target different stages of the viral replication cycle (reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors).
• ART suppresses viral replication but does not cure HIV.

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Key Terms

Term	Definition
Pathogen	A microorganism that causes disease in its host
Vector	An organism that transmits a pathogen between hosts without being affected
Exotoxin	A toxin protein secreted by living bacteria
Endotoxin	A toxin (lipopolysaccharide) in the outer membrane of Gram-negative bacteria, released on cell lysis
Communicable disease	A disease caused by a pathogen that can be transmitted between organisms
Oral rehydration therapy	A treatment for dehydration using a solution of water, salts and glucose

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Summary

• Pathogens include bacteria, viruses, fungi, and protoctista.
• Transmission occurs by direct contact, airborne droplets, water, food, fomites, or vectors.
• Pathogens cause disease by cell damage, tissue destruction, or toxin production.
• Cholera toxin opens Cl⁻ channels, causing osmotic water loss and severe diarrhoea.
• TB bacteria survive inside macrophages and are walled off in granulomas.
• HIV destroys T helper cells, leading to immunodeficiency (AIDS).

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A-Level Deep Dive: Pathogens and Disease Transmission

Spec mapping

The Edexcel 9BI0 specification places pathogens and disease transmission within Topic 6: Immunity, Infection and Forensics, where it bridges microbial biology and clinical/epidemiological reasoning. Where lesson 1 introduced the four pathogen classes (bacteria, viruses, fungi and protoctista) and lesson 2 quantified how bacteria proliferate inside a host (the lag–log–stationary–death curve applied to in vivo growth), this lesson asks the more public-health question: given a pathogen, how does it move from host to host, and how does that movement explain the shape of an outbreak? Synoptic links run forward to lessons 6 and 7 (innate then adaptive immune responses to invading pathogens), to Topic 7: Run for Your Life (vector-borne diseases interact with the circulatory system — Plasmodium-infected erythrocytes alter capillary haemodynamics; cardiovascular tropism of Trypanosoma cruzi; sepsis-driven septic shock), and to Topic 8: Genetics, Populations, Evolution and Ecosystems, where whole-genome sequencing of outbreak isolates (genomic epidemiology) traces transmission chains by identifying SNPs accumulated between linked cases. Relevant statements concern: distinguishing types of pathogens; describing modes of transmission (direct, indirect — including airborne droplet, food, water, fomite, vertical and vector-borne); explaining how pathogens cause disease by cellular damage and by toxin production (exotoxins versus endotoxins); and applying these ideas to the case studies of cholera, tuberculosis, HIV/AIDS and malaria (refer to the official Pearson Edexcel 9BI0 specification document for exact wording).

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Worked example with full mark scheme

Question (8 marks):

The malaria parasite Plasmodium falciparum is transmitted between human hosts only by the bite of an infected female Anopheles mosquito. Patients with untreated P. falciparum infection typically develop a cyclic fever pattern with peaks every 48 hours.

(a) Outline the stages of the malaria life cycle from mosquito bite to release of further infective forms into the blood, identifying where the parasite reproduces asexually and where sexual reproduction occurs. (5)

(b) Explain why the human-stage fever pattern is cyclic with a period of approximately 48 hours rather than continuous. (3)

Solution with mark scheme:

(a) Stage 1 — inoculation. The female Anopheles mosquito injects sporozoites into the human bloodstream during a blood meal; salivary-gland sporozoites enter the dermal capillary network within minutes.

M1 (AO1.1) — sporozoites injected by Anopheles mosquito. Common error: writing "mosquito injects malaria" without naming the infective stage.

Stage 2 — liver phase. Sporozoites travel via the bloodstream to hepatocytes in the liver, where they undergo asexual replication (schizogony) over 7–10 days, generating thousands of merozoites per infected hepatocyte.

M1 (AO1.2) — sporozoites enter hepatocytes; asexual replication produces merozoites.

Stage 3 — erythrocytic phase. Merozoites are released into the blood and invade erythrocytes (red blood cells), where each undergoes a further round of asexual replication (every 48 hours for P. falciparum); erythrocyte rupture releases new merozoites that invade further erythrocytes.

M1 (AO1.2) — invasion of erythrocytes; cyclic asexual replication every 48 hours.

Stage 4 — sexual stages. A subset of intra-erythrocytic parasites differentiates into gametocytes (male and female), which circulate without further replication and are taken up by a feeding mosquito.

M1 (AO1.1) — gametocytes form within erythrocytes and are taken up by the mosquito vector.

Stage 5 — mosquito phase. In the mosquito midgut, gametocytes fuse to form zygotes, which develop into ookinetes and then oocysts in the gut wall; oocysts release sporozoites that migrate to the salivary glands, ready for transmission at the next bite.

A1 (AO3.1a) — sexual reproduction occurs only in the mosquito; the human host supports two asexual rounds (liver and blood). The mosquito is therefore the definitive host; humans are intermediate hosts.

(b) M1 (AO2.1) — fever is triggered by rupture of infected erythrocytes, which releases pyrogenic parasite molecules (e.g. GPI-anchored membrane components) and triggers macrophage release of interleukin-1 and tumour necrosis factor.

M1 (AO2.1) — P. falciparum asexual replication in erythrocytes is synchronised to a 48-hour cycle, so erythrocytes burst in a coordinated wave rather than continuously.

A1 (AO3.1a) — synchronised waves of cytokine release explain the cyclic spike-and-trough fever pattern; loss of synchrony in severe infection blurs this pattern, which is itself a clinical warning sign.

Total: 8 marks.

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Specimen question modelled on the Edexcel 9BI0 paper format

Question (6 marks): Compare the modes of transmission of tuberculosis, HIV and malaria, and explain why the contact-tracing strategy used by public-health authorities is different for each disease.

Mark scheme decomposition by AO:

Marking point	AO	Credit-worthy content
1	AO1.1	States that TB is transmitted by respiratory droplets (close-contact airborne) so contact tracing focuses on prolonged household, classroom or workplace contacts (typically those sharing indoor air for $>$>8 hours cumulatively).
2	AO1.2	States that HIV is transmitted by blood and sexual contact (and vertically mother-to-child) so contact tracing focuses on sexual partners, needle-sharing partners and infants of HIV-positive mothers.
3	AO2.1	States that malaria is transmitted by vector (Anopheles mosquito) with no direct human-to-human transmission, so traditional person-to-person contact tracing is not applicable; surveillance instead targets the vector population (insecticide-treated bed nets, indoor residual spraying, larval source management) and treats the human reservoir to interrupt transmission.
4	AO2.1	States that the R$_0$0​ (basic reproduction number) and the window of infectivity differ markedly: TB is moderately infectious over weeks-to-months in active disease, HIV is infectious for years (lifetime without treatment), malaria infectivity depends on gametocyte density and mosquito biting rates.
5	AO3.1a	Explains that genomic epidemiology — whole-genome sequencing of pathogen isolates — distinguishes recent transmission from independent acquisition by counting SNPs accumulated since the most recent common ancestor; this is now standard for TB outbreak investigation in many UK regions.
6	AO3.2a	Concludes that the optimal control strategy reflects the transmission route: droplet $\to$→ ventilation, masking, treatment of active cases; bloodborne/sexual $\to$→ behavioural prevention, pre-exposure prophylaxis, needle exchange, antiretroviral treatment-as-prevention; vector-borne $\to$→ vector control plus chemoprophylaxis and case management.

Total: 6 marks split AO1 = 2, AO2 = 2, AO3 = 2. Edexcel rewards candidates who connect mechanism to public-health response (AO2/AO3 — why droplet transmission demands ventilation, why vector-borne disease demands vector control) rather than merely listing modes of transmission (AO1).

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Synoptic links

1. Topic 6 — Immunity, Infection and Forensics, lesson 1 introduced the four pathogen classes; this lesson layers transmission mode on top of taxonomy. Different classes favour different routes: enveloped viruses (HIV, influenza) tend to require body-fluid or droplet contact because the lipid envelope desiccates rapidly on fomites; non-enveloped viruses (norovirus, rotavirus) survive on surfaces for days and dominate fomite-driven outbreaks; spore-forming bacteria (Clostridium difficile, Bacillus anthracis) persist in dust and soil for years.
2. Topic 6 — Immunity, Infection and Forensics, lesson 2 provided the lag–log–stationary–death curve. In vivo, bacterial growth in host tissues follows the same kinetics, but the host immune response (lessons 6–7) modifies the curve: macrophage phagocytosis suppresses log-phase growth, and antibody opsonisation accelerates clearance. The cholera-toxin pathology described here depends on bacterial population density crossing a quorum-sensing threshold in the small intestine.
3. Topic 7 — Run for Your Life intersects through cardiovascular involvement of vector-borne and bloodborne pathogens. Plasmodium-infected erythrocytes adhere to capillary endothelium (cytoadherence via PfEMP1), causing microvascular obstruction in cerebral malaria. Trypanosoma cruzi infects cardiac myocytes, causing chronic cardiomyopathy decades after the initial bite. Sepsis driven by Gram-negative endotoxin causes the cardiovascular collapse of septic shock — vasodilation, capillary leak, and DIC — bridging this lesson to circulatory pharmacology.
4. Topic 8 — Genetics, Populations, Evolution and Ecosystems brings whole-genome sequencing to outbreak investigation. Genomic epidemiology sequences pathogen isolates from linked cases and counts SNPs accumulated since the most recent common ancestor; isolates differing by very few SNPs imply recent transmission, while many SNPs imply independent acquisition. This approach, now standard in UK TB and E. coli O157 outbreak response, depends on the molecular-clock concepts taught in Topic 8.
5. Lessons 6 and 7 of this course describe the host immune response to invading pathogens. The transmission mode determines the route of immune encounter — droplet pathogens meet mucosal IgA in the respiratory tract, food/water pathogens meet gut-associated lymphoid tissue, vector-borne pathogens bypass the skin barrier and meet circulating innate immunity directly. This shapes vaccine design (lesson 9): mucosal vaccines for respiratory pathogens, intramuscular vaccines for bloodborne and vector-borne pathogens.

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Mark-scheme literacy

AO	Typical share on this topic	Earned by
AO1 (knowledge)	35–45%	Defining pathogen, vector, reservoir; naming exotoxin and endotoxin examples; reciting transmission routes (direct contact, droplet, food, water, fomite, vector, vertical); recalling case-study mechanisms (cholera-toxin opens Cl$^-$− channels; HIV targets CD4$^+$+ T helper cells)
AO2 (application)	35–45%	Applying transmission knowledge to outbreak scenarios; predicting which control measure suits which route; calculating R$_0$0​ from secondary-case data; matching exotoxin or endotoxin to disease presentation
AO3 (analysis / evaluation)	15–25%	Evaluating why R$_0 > 1$0​>1 implies an epidemic and R$_0 < 1$0​<1 implies decline; comparing transmission strategies across pathogen classes; critiquing data on outbreak source attribution; reasoning about why some pathogens persist as endemic disease while others appear in episodic outbreaks