Communicable diseases, disease prevention and the immune system

Bacterial pathogens

Prokaryotic, single-celled organisms (no nucleus or membrane-bound organelles).

Reproduce by binary fission.

Cause disease by:

• Producing toxins.

• Damaging host cells/tissues.

Examples:

• Tuberculosis (TB) – infects the lungs in humans.

• Ring rot – infects potatoes, causing rotting and reduced crop yield.

Viral pathogens

Acellular (not made of cells).

Consist of DNA or RNA enclosed in a protein coat (capsid).

Obligate intracellular parasites – can only reproduce inside living host cells.

Cause disease by replicating inside cells, often destroying them.

Examples:

• HIV/AIDS – attacks helper T cells of the immune system.

• Influenza – infects the respiratory tract of animals.

• Tobacco Mosaic Virus (TMV) – damages chloroplasts, causing leaf mosaic patterns and reduced photosynthesis.

Protoctistan pathogens

Eukaryotic, mostly single-celled organisms.

Have a nucleus and membrane-bound organelles.

Often have complex life cycles, sometimes involving vectors.

Examples:

• Malaria – caused by Plasmodium, transmitted by female Anopheles mosquitoes; infects liver and red blood cells.

• Potato/Tomato late blight – caused by Phytophthora infestans; destroys leaves and tubers, reducing crop yield.

Fungal pathogens

Eukaryotic organisms with chitin cell walls.

Grow as hyphae, forming a mycelium.

Reproduce by spores.

Cause disease by invading tissues and digesting them externally.

Examples:

• Black sigatoka – infects banana leaves, reducing photosynthesis and yield.

• Athlete's foot – fungal infection of the skin, causing itching, redness, and peeling.

Transmission of communicable pathogens in animals

Direct contact – touching infected individuals.

Droplet infection – coughing or sneezing spreads pathogens.

Contaminated food or water – ingestion of pathogens.

Vectors – organisms that transmit pathogens between hosts (e.g. mosquitoes transmit malaria).

Body fluids – blood, sexual contact, shared needles (e.g. HIV).

Living conditions affect transmission:

• High population density/overcrowding ↑ spread.

• Poor sanitation and hygiene ↑ spread.

• Limited healthcare/vaccination ↑ spread.

Plant communicable pathogen transmission

Direct contact between infected and healthy plants.

Wind – carries spores and pathogens.

Water – rain splash, irrigation, flooding.

Vectors – insects transfer pathogens while feeding (e.g. aphids transmit viruses).

Spores – fungal spores disperse by wind or water and germinate on plants.

Contaminated soil, tools, or seeds can spread disease.

Climate affects transmission:

• Warm, humid conditions favour many pathogens.

• Wind increases spore dispersal.

• Wet conditions promote infection and spread.

Plant Chemical Defences Against Pathogens

• Plants produce antimicrobial chemicals to kill or inhibit pathogens.

• Defensins → antimicrobial peptides that disrupt fungal cell membranes.

• Alkaloids → nitrogen-containing compounds that interfere with pathogen enzymes and metabolism.

• Terpenoids → found in essential oils and resins; have antifungal and antibacterial properties.

• Phenols → damage microbial proteins and cell membranes.

Plant Responses That Limit Pathogen Spread

Plants can produce callose (a polysaccharide) to block plasmodesmata.

• Prevents pathogen movement between cells.

Plants may form physical barriers:

• Strengthen cell walls with lignin.

• Seal damaged areas to stop pathogen entry.

Infected cells may undergo cell death:

• Creates a barrier around the infection site.

• Limits pathogen spread to healthy tissues.

Skin (Primary Non-specific Defence) in animals

• Acts as a physical barrier preventing pathogen entry.

• Outer layer contains dead, keratinised cells that are difficult for pathogens to penetrate.

• Produces antimicrobial chemicals that inhibit microbial growth.

Inflammation (Primary Non-specific Defence)

• Damaged cells release histamine by mast cells (which also release cytokines).

• Histamine causes:

  • Vasodilation → blood vessels widen → increased blood flow.

    • Causes redness and heat.

    • Brings more immune cells to the area.

  • Increased capillary permeability → plasma leaks out.

    • Forms tissue fluid containing immune cells.

• Phagocytes leave blood and enter infected tissue attracted via cytokines.

• Tissue fluid drains into the lymphatic system (lymph nodes contain lymphocytes to destroy pathogens) and returns to the blood.

• Increased temperature:

  • Speeds up enzyme-controlled immune reactions.

  • Increases activity of phagocytes.

  • Reduces pathogen reproduction (many pathogens have optimum temperatures lower than body temperature).

Wound Repair (Primary Non-specific Defence)

• Clot prevents further pathogen entry.

• New cells divide by mitosis to replace damaged cells.

• Tissue is repaired, restoring the protective barrier.

Expulsive Reflexes (Primary Non-specific Defence)

Rapidly remove pathogens from the body.

Examples:

• Coughing removes pathogens from airways.

• Sneezing removes pathogens from nasal passages.

• Vomiting removes harmful substances from the digestive system.

Mucous Membranes (Primary Non-specific Defence)

• Line areas exposed to the outside environment (e.g. respiratory tract).

• Produce mucus via goblet cells that traps pathogens.

• Cilia (on cilliated epithial cells) move mucus towards the throat where it can be swallowed (hydrochloric acid in the stomach destroys pathogens) or expelled.

• Prevents pathogens reaching body tissues.

Blood clotting (Primary Non-specific Defence)

Damage to blood vessels activates platelets.

Platelets release substances that trigger a cascade of reactions.

The cascade results in:

• Prothrombin → thrombin (requires Ca²⁺ ions as a cofactor).

• Fibrinogen → fibrin (catalysed by thrombin).

Fibrin forms a mesh network that:

• Traps platelets and blood cells.

• Forms a blood clot.

• Seals the wound to prevent pathogen entry.

The clot provides time for wound repair and restoration of the barrier.

Phagocytes

Phagocytes are non-specific immune cells that engulf and destroy pathogens by phagocytosis.

Neutrophils:

• Most abundant phagocyte in blood.

• Have a multi-lobed nucleus.

• Rapidly move to sites of infection by chemotaxis.

Antigen-presenting cells (APCs) (e.g. macrophages):

• Have a large irregular nucleus and abundant cytoplasm.

• Display pathogen antigens on their surface after phagocytosis to activate T cells.

Mode of action of phagocytosis

• Pathogen is recognised and attached to the phagocyte.

• Pathogen is engulfed, forming a phagosome.

• Lysosomes fuse with the phagosome and forms a phagolysosome and release digestive enzymes (hydrolytic such as lysozyme which breaks down).

• Pathogen is broken down and destroyed.

Macrophages only:

• APCs present antigens to lymphocytes to trigger a specific immune response.

Blood smear identification phagocytes

Neutrophil:

• Small white blood cell.

• Multi-lobed nucleus (3–5 lobes).

• Fine granules in cytoplasm.

• Most common leukocyte.

Antigen-presenting cell (macrophage):

• Larger cell.

• Large, single irregular nucleus.

  • More cytoplasm.

Roles of opsonins and cytokines in immune response

Opsonins:

• Molecules that bind to pathogens and mark them for destruction.

• Make pathogens easier for phagocytes to recognise and engulf.

• Increase efficiency of phagocytosis.

Cytokines:

• Signalling proteins released by immune cells.

• Coordinate immune responses by:

  • Attracting phagocytes to infection sites (chemotaxis).

  • Activating other immune cells.

  • Increasing inflammation.

Active immunity

Active immunity:

• Body produces its own antibodies after exposure to an antigen.

• Involves activation of B cells and memory cells.

• Slow response initially but provides long-lasting protection.

Examples:

• Infection with a pathogen (natural active).

• Vaccination (artificial active).

Passive immunity

Passive immunity:

• Body receives ready-made antibodies from another source.

• No memory cells are produced.

• Immediate protection but short-lived.

Examples:

• Antibodies passed from mother to baby through placenta/breast milk (natural passive).

• Injection of antibodies (e.g. antivenom or monoclonal antibodies) (artificial passive).

Natural Immunity

Natural immunity:

• Immunity gained through normal biological processes.

Examples:

• Natural active: becoming immune after recovering from an infection.

• Natural passive: antibodies transferred from mother to baby.

Artificial immunity

• Immunity gained through medical intervention.

Examples:

• Artificial active: vaccination introduces antigens → immune system produces antibodies and memory cells.

• Artificial passive: injection of antibodies provides immediate protection

Principles of vaccination

• Vaccines contain antigens from a pathogen (e.g. weakened/inactivated pathogen or antigen fragments).

• Antigens stimulate specific immune responses without causing the disease.

• B cells are activated and produce specific antibodies.

• Memory cells are produced, allowing a faster and stronger secondary response if the pathogen is encountered again.

• This provides long-term immunity.

Role of vaccination in prevention of epidemics

• Large-scale vaccination increases the proportion of immune individuals in a population.

• This reduces the number of people available for a pathogen to infect.

• Reduces transmission between individuals.

• Provides herd immunity, protecting vulnerable people who cannot be vaccinated.

• Prevents pathogens spreading widely and causing epidemics.

Routine vaccinations

Routine vaccinations are vaccines given regularly to populations, often during childhood.

They protect against common or serious infectious diseases.

Examples:

• MMR vaccine → measles, mumps, rubella.

• Polio vaccine → poliovirus.

• HPV vaccine → human papillomavirus.

Programmes ensure high vaccination rates to maintain herd immunity and prevent outbreaks.

Changes to vaccines and vaccination programs

New scientific evidence → improved vaccine design or understanding of immunity.

Pathogen evolution → mutations may change antigens, reducing vaccine effectiveness.

Improved technology → safer or more effective vaccines developed.

Disease prevalence changes → vaccines may be added, removed or targeted differently.

Safety monitoring → programmes are adjusted if side effects or risks are identified.

Global issues:

• Different diseases are common in different regions.

• Limited resources, cost, storage and transport challenges affect vaccine availability.

• International programmes aim to increase vaccination coverage and control global outbreaks.