Communicable diseases

• Bacteria:

  Ring rot (plants)

  • caused by gam positive bacteria
  • damages leaves and fruits
  • destroys crops
  • no cure
  • field cannot be used to grow potatoes on for another 2 years
• Bacteria:

  TB: (animals)

  • damages and destroys lung tissue, suppresses immune system so body is less able to gift off other diseases
  • curable with antibiotics, preventable with vaccines and better living standards
• Bacterial meningitis:


  Bacterial injection of the meninges of the brain

  • can spread to the rest of the body and cause blood poisoning and rapid death
  • mostly affects very young kids and teens
  • blotchy red rash
  • antibiotics cure if delivered early, Vaccines an protect against the disease
• Viruses:

  Non living

  • structure: some genetic material surrounded by protein
  • invade living cells, genetic material if the virus takes over the biochemistry of the host cell to make more virus
  • Virus reproduces rapidly and evolves to the host
  • Versus burst out of cell, speeding to infect other cells
  • Bacteriophage - viruses which attack bacteria
• Virus:

  TMV:

  • damages leaves, flowers and fruit
  • stunts growth and reduces yields
  • Can cause total cop loss
  • can get resistant crop strains but no cure
• Viruses:

  HIV:

  • targets t-helper cells, gradually destroys immune system so affected people are more at risk to other diseases
  • HIV is retrovirus: Hase reverse transciptase so can make DNA from RNA
  • passed via bodily fluids
  • no vaccines and no cure
• Viruses:

  Influenza:

  • viral infection of the ciliated epithelial cells in the gas exchange system
  • Kills the ciliated epithelial cells so the airways are left to secondary infection
  • High temp, aches and fatigue
• Protista:

  Potato blight:

  • caused by fungus
  • transmitted through spores
  • small dark brown marks on leaves which quickly increase in size and numebr
  • penetrate host cells, destroys leaves
  • no cure resistant strains, careful management and chemical treatment to reduce infection risk
• Protista:

  Malaria:

  • parasite spead by mosiquitos
  • fever chills, fatigue
  • reproduce inside the pregnant mosiwuoto which then feeds to get proteins before she lays her eggs. When feeding, the parasite is passed on to people
  • invades red blood cells, liver and brain
  • no vaccines limited cures
  • preventative measures: mosquito nets
• Fungi:

  Black Sigatoka:

  • affects banannas
  • attacks and destroys leaves
  • penetrate and digest the cells, turing the leaves black
• Fungi:

  Ring worm:

  • grey- white crusty infectious circular area of skin
  • not damaging, looses unsightly and is itchy
  • anti fungal cream - cure
• Fungi

  Athelets foot:

  • affects humans
  • form of ringworm that grows and digs the warm, moist skin between toes
  • causes cracking itchy and sore
  • antifungal creams- cure
• Plant defences:

  Recognising an attack:

  • receptors in the plant cells respond to molecules from the pathogens or to the chemicals produces when the cell wall is attacked
  • stimulates the release of signalling molecules which switch genes on and off
  • triggers response defences
• Plant defences:

  Physical defences- callous

  • callous is made and deposited between cell walls and cell membrane in the cells next to the infected cells
  • acts as a barrier, prevents pathogen entering surrounding cells
  • more callous is deposited and lignin is added to make the barrier thicker and stronger
  • callous blocks the sieve plates to prevent the spread
  • callous blocks plasmodesmata between infected and healthy cells so sealing off and preventing spread
• Plant defences:

  Chemical defences:

  • insect repellent ie pine resin
  • insecticides ie caffeine toxic to insects and fungi
  • antibacterial compounds such as phenol and lysomomes which contain hydrolysis enzymes and break down bacterial cell walls
  • Anti-fungal compounds ie phenols
• Primary non-specific defenced in animals:

  skin:

  • physical barrier
  • produces sebum- oily inhibits growth of pathogens

  Mucous membrane:

  • secure mucus to trap pathogens
  • contains lysosomes which destroy bacterial and fungal cell walls
• Primary non-specific defenced in animals:

  Blood clotting and wound repair:

  1. Platelets are activated by damaged tissue. Platelets adhere and release thromboplastin- triggers the reaction causing blood clot. Serotonin causes blood vessels to contract reduce blood supply to area
  2. Fibrin (catalysed by thrombin) forms clot. Clot dries and scab forms. Epidermal cells below scab start to grow and damage vessels regrow. Collagen fibres are deposited to give the new tissue strength. Scab falls off
• Primary non-specific defenced in animals:

  Inflammatory response:

  1. Mast cells activated in damage tissues, releasing histamines and cytokines. Histamines dilate blood vesicles, increasing the temperature leading to less bacteria reproducing due to high temp. Makes blood vessels more leaky forcing out blood plasma to make tissue fluid causing pain and swelling. Cytokines attract phagocytes to the site of incision to engulf potential pathogens.
• Stages of phagocytosis:

  .

  1. Pathogens produce chemicals which attract phagocytes
  2. Phagocytes recognise non-self antigens on pathogens and bind to the pathogen
  3. Phagocyte engulfs pathogen and encloses it in a vesicle (phagosome)
  4. Phagosome combines with lysosomes to form phagolysosome
  5. Hydrolytic enzymes from lysosomes digest destroy pathogen

  IF the phagocyte is a macrophage then

  6. Antigens on the pathogen are combined with the major histocompatablity complex (MHC) which are glycoproteins in cytoplasm

  7. MHC complex moves to macrophages surface membrane and forms APC stimulates other cells
• Opsonins:


  binds to pathogens and tags them so they are recognised easier by phagocytes

  Receptors on the phagocytes bind to the tags and engulf pathogen
• Cell mediated immunity:

  response to change in cell

  1. During non-specific defence system phagocytosis occurs from a macrophage and makes an APC
  2. T helper cell has receptors to the antigen on the APC, binding to the antigen on the APC
  3. Activates the T helper cell therefore produces interleukins which stimulates the production of T cell clones
  4. The cloned T cells then:

  • develop into T memory giving a rapid response is the pathogen invades again
  • produce interleukins to stimulate phagocytosis by attracting macrophage
  • interleukins stimulate B cells to divide
  • turn into T killer cells
• Humoral immunity:

  1. Antigen on pathogen enters the body and the B lymphocyte with the complementary antibody on its surface binds to the antigens, engulfs it and presents the antigens on surface
  2. Activated T helper cells binds to APC - clonal selection the B cell with the antibody complementary to antigen is selected for cloning
  3. T helper cell produces interleukins activates B cell
  4. B cell divides by mitosis to make clones of plasma cells produces antibodies complementary to antigen and B memory cells clonal expansion
• Humoral immunity:


  5. Antibodies bind to the antigens and act as opsonins or agglutinin 1st immune response

  6. B memory cells stay in blood to form plasma cells if infected again 2nd immune response
• How antibodies defend the body:

  1. Act as opsonins- tag pathogens so it is easier for phagocytes to locate2. binds to antigens to form antigen-antibody complexes so it can no longer effectively invade3. act as agglutinins- cause the pathogens carrying the anitigen-antibody complexes to clump together so more can be engulfed at once to prevent the spread4. act as antitoxins- bind to toxins and neutralise them
• Autoimmune disease

  immune system doesn't recognise self antigens and starts to attack healthy body tissues

  1. Lupus:

  • affects the skin and joints
  • can attack any organ in the body ie brain
  • treatment: No cure, immunosuppressants
• Natural passive immunity:


  antibodies cross from placenta from mother to baby in uterus to give some immunity at birth

  • During breastfeeding colostrum which is high in antigens is passed to the baby
• Natural active immunity:

  body contracts pathogens and forms antibodies.

  • T and B memory cells are made so the response in quick for second infection
  • active because the body produces the antibodies and memory cells itself
• Artificial ative immunity:


  Vaccination:

  • immune system is stimulated to make own antibodies after infection of safe form of the antigen

  1. Pathogen is made safe as its inactive
  2. Antigen injected into the blood triggering the primary immune response
  3. If infected again, second immune system is triggers and no symptoms show
• Possible sources of medicine


  Penicillin:

  • mould on melon
  • antibiotic

  Aspirin:

  • willow bark
  • painkiller

  need to protect biodiversity as we must not destroy a plant which could go on to produce a life saving drug. Plants and fungus are source of many existing medicine so very likely that some plant produces an undiscovered drug with socioeconomic benefits
• Pharmacogenetics

  • drugs which work with the disease and the patients genetics. Doctors look at the patients genome before they treat them so treatment is personalised for them
• Synthetic biology

  • re-engineering biological systems for new purposes in medicine
  • Nanotechnology using non-natural particles for biological purposes (drug delivery)