1 Disease

• Groups of pathogens that can cause communicable diseases

  • Bacteria
  • Fungi
  • Protoctista
  • Viruses
• How Mycobacterium tuberculosis causes disease

  1. Triggers inflammatory response by infecting phagocytes in lungs

  2. Infected phagocytes are sealed in waxy-coated tubercles so bacteria remain dormant. First infection has no symptoms

  3. If another factor weakens immune system, bacteria become active & destroy lung tissue
• How HIV results in the symptoms of AIDS

  1. Attachment proteins bind to complementary CD4 receptor on TH cells

  2. HIV particles replicate inside TH cells, killing or damaging them

  3. AIDS develops when there are too few TH cells for the immune system to function

  4. Individuals cannot destroy other pathogens & suffer from secondary diseases/ infections. May cause death
• How tobacco mosaic virus causes disease

  1. Affects plants. Mainly transmitted via infected sap

  2. Contains ssRNA, which is directly transcribed by host cell to assemble new virions

  3. Virions enter other cells via plasmodesmata then enter xylem & phloem

  4. Causes stunted growth & mottled leaves
• How influenza virus causes disease

  1. Transmitted via: droplet infection, contact with mucus containing virus, zoonotic infection, contact with fomites

  2. Injects viral RNA into ciliated epithelial cells of throat & lungs. Viral RNA hijacks cell biochemistry to produce new virions. Cell lysis releases virions

  3. 5-7 days of headache, coughing, sneezing, sore throat, vomiting, fever, muscular/joint pain
• Malaria is caused by female Anopheles mosquito acting as vector for Plasmodium spp. protoctista when it transfers saliva to another organism during feeding
• Potato/ tomato late blight is caused by the protoctista Phytophthora infestans, which behaves similarly to a fungus and is mainly transmitted via spores
• Ring rot of potatoes is caused by the Sepedonicus subspecies of the bacterium Clavibacter michiganensis, mainly transmitted by planting infected seeds/ contact with fomites. Plant-to-plant transmission is rare
• Bacterial meningitis is often caused by meningococcal bacteria A, B, C, W, X, Y, Z, as well as pneumococcal bacteria & Haemophilus influenzae type b (Hib) bacteria, which affect the meninges (protective membranes around the brain)
• 3 fungal infections


  • Black sigatoka in banana plants caused by the sac fungus Mycosphaerella fijiensislack
  • Ringworm caused by about 40 types of fungi, transmitted by contact with fomites, zoonotic infection, direct contact with infected individuals. Particularly affects cattle
  • Athlete's foot in humans (tinea pedis) caused by a range of fungi which can also affect hands or nails
• Direct transmission of communicable pathogens

  • Inhalation (droplet infection)
  • Skin-to-skin contact or exchange of fluids
  • Penetrate skin actively using enzymes or passively through wounds, hair follicles or sweat glands
• Indirect transmission of communicable pathogens

  • Consumption of contaminated food & drink
  • Via a vector e.g. mosquitoes transmit Plasmodium parasite
  • Spores
• Overcrowding increases direct transmission of communicable diseases. Climate determines which organisms can survive, e.g. malaria is more prevalent in tropical countries where mosquitoes (the vector) can breed. Social factors influence how quickly people are treated, which can increase/ decrease direct transmission
• Physical barriers to pathogen entry in plants

  • Cellulose cell walls
  • Lignified layer
  • Waxy upper cuticle
  • Old vascular tissue is blocked to prevent pathogens from spreading inside the plant
• Mechanical responses to infection in plants

  • Guard cells close stomata
  • The thick polysaccharide callose is produced & deposited between the cell wall & plasma membrane to increase entry distance/ limit spread
• Necrosis


  Injury activates intracellular enzymes in plants that kill cells near the site of infection to prevent pathogen from spreading. Necrosis of woody tissue is known as canker
• Chemical defences plants use against pathogens

  • Terpenoids (essential oils) e.g. menthols act as antibacterials
  • Phenols e.g. tannin inhibit insects from attacking by interfering with digestion
  • Alkaloids e.g. caffeine & morphins deter herbivores from feeding because they taste bitter
  • Defensins (cysteine-rich proteins) inhibit transport channels
  • Hydrolytic enzymes e.g. chitinases break down cell wall of invading organisms
• Barriers to infection in animals

  • Skin is tough keratin layer
  • Blood clotting prevents pathogens from entering through skin lesions
  • Hydrochloric acid in stomach kills bacteria
  • Harmless bacteria in gut & on skin surface increase interspecific competition with pathogens
  • Mucous membranes trap pathogens and may secrete antimicrobial enzymes
• Expulsive reflexes


  Body attempts to force foreign substances out: Irritation of mucous membranes in nostrils causes sneezing, Irritation of ciliated epithelium in respiratory tract causes coughing
• Ways the nonspecific immune system responds to infection

  • Inflammation
  • Phagocytosis
  • Digestive action of lysozymes
  • Production of interferon (antiviral agent)
• Inflammation


  1. Damaged vessels release histamines, causing vasodilation

  2. Blood flow & permeability of blood vessels increase

  3. White blood cells & plasma move into the infected tissue
• Blood clotting


  1. Blood platelets form plug & release chemicals that enhance clotting e.g. thromboplastin

  2. Prothrombin changes into thrombin, its active form

  3. Fibrinogen changes into insoluble fibrin which covers wound
• White blood cells involved in phagocytosis

  • Neutrophils
  • Macrophages (can become antigen-presenting cells)
• Phagocytosis


  1. Phagocyte moves towards pathogen which may have been marked by opsonins via chemotaxis

  2. Phagocyte engulfs pathogen via endocytosis to form a phagosome

  3. Phagosome fuses with lysosome (phagolysosome)

  4. Lysozymes digest pathogen

  5. Phagocyte absorbs the products from pathogen hydrolysis
• Antigen-presenting cells (APCs)


  • Macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis)
  • Enhances recognition by TH cells, which cannot directly interface with pathogens/ antigens in body fluid
  • Secrete cytokines that are involved in stimulating specific immune response
• How does phagocytosis destroy pathogens?

  1. Phagocyte moves towards pathogen which may have been marked by opsonins via chemotaxis.

  2. Phagocyte engulfs pathogen via endocytosis to form a phagosome.

  3. Phagosome fuses with lysosome (phagolysosome).

  4. Lysozymes digest pathogen.

  5. Phagocyte absorbs the products from pathogen hydrolysis.
• Antigen-presenting cells (APCs)


  Macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis). Enhances recognition by TH cells, which cannot directly interface with pathogens/ antigens in body fluid. Secrete cytokines that are involved in stimulating specific immune response.
• Lysozymes


  Digestive enzymes. Found in lysosomes as well as many secretions e.g. tears & mucus. Damage bacterial cell walls, causing osmotic lysis.
• How to prepare blood to be observed under a microscope

  1. Smear a drop of blood onto a slide using a spreader held at 45°.

  2. Add leishman stain then a buffer. Rinse.
• Types of specific immune response

  • cell-mediated
  • humoral
• Cell-mediated response


  1. Complementary TH lymphocytes bind to foreign antigen on APC.

  2. Cell signalling via secretion of interleukins stimulates:

  a. clonal expansion of complementary TH cells (rapid mitosis): become memory cells or trigger humoral response.

  b. clonal expansion of cytotoxic T cells (TC): secrete enzyme perforin to destroy infected cells.
• Humoral response


  1. Complementary TH lymphocytes bind to foreign antigen on antigen-presenting T cells.

  2. Release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes.

  3. B cells differentiate into plasma cells.

  4. Plasma cells secrete antibodies with complementary variable region to antigen.
• B and T lymphocytes

  Many specific receptors & immunoglobulins on surface.

  B cells differentiate into plasma cells to secrete antibodies.

  3 types of T cell: T helper (secrete cytokines), T killer (secrete perforin), T regulator (suppress other immune cells to prevent autoimmune disease).
• Antibody


  Proteins secreted by plasma cells.

  Quaternary structure: 2 'light chains' held by disulfide bridges, 2 longer 'heavy chains'.

  Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen.

  The rest of the molecule is known as the constant region.
• How antibodies lead to the destruction of a pathogen

  1. Agglutinins form antigen-antibody complexes to enhance phagocytosis.

  2. Activation of complement.

  3. Opsonins mark microbes for phagocytes.

  4. Antitoxins make toxins insoluble via precipitation/ neutralisation.
• Memory cells


  Specialised TH/ B cells produced from primary immune response. Remain in low levels in the blood. Can divide very rapidly by mitosis if organism encounters the same pathogen again.
• Passive and active immunity


  • Passive natural: antibodies in breast milk/ across placenta.

  Passive artificial: anti-venom, needle stick injections.

  Active natural: humoral response to infection.

  Active artificial: vaccination.
• Autoimmune disease


  Immune system produces antibodies against its own tissues.
• Autoimmune diseases


  • Rheumatoid arthritis: immune system targets synovium lined joints, causing inflammation.

  Lupus: results in inflammation throughout body.
• Principles of vaccination


  Vaccine contains dead/ inactive form of a pathogen or antigen.

  2. Triggers primary immune response.

  3. Memory cells are produced and remain in the bloodstream, so secondary response is rapid & produces higher concentration of antibodies.

  4. Pathogen is destroyed before it causes symptoms.