ocr biology a - communicable diseases

organisms that cause disease
transmission of pathogens
1. indirect transmission
plant defences against pathogens
1. passive defences
  1. PHYSICAL: cellulose cell wall = physical barrier + has chemical defences. lignification of walls = almost undigestible. waxy cuticles = water doesn't collect on cell surfaces, that pathogens need to survive. bark = chemical defences. somatal closure = guard cells close stomata when pathogens detected. callose = polysaccharide in sieve tubes - blocks tube so stops pathogen travelling this way. tylose formation = balloon projection plugs xylem - pathogens cant get through, also has chemicals toxic to pathogens.
  2. CHEMICAL: plants have lots of chemicals toxic to pathogens; terpenoids, phenols, alkaloids and hydrolytic enzymes. they are there before infection but not a lot because they take a lot of energy to produce
2. active defences
  1. chemicals can detect when a pathogen is invading - a plant will fortify its already present defences. they will: thicken and strengthen cell walls with cellulose, put callose between wall and membrane (blocks plasmodesmata), oxidative bursts to damage cells of invading organisms
    1. they also increase chemical production:
      1. terpenoids - antifungal + bacterial. can make a scent.
      2. phenols - antibiotic + fungal. to stop insect attack, tannins bind to salivary proteins + digestive enzymes and stop insects from growing so they die - stops transmission
      3. alkaloids - have nitrogen, e.g. caffeine, bitter tasting to stop being eaten, can also inhibit enzymes. some inhibit protein synthesis. not being eaten = no damage = harder for pathogens to get it
      4. defensins - anti-microbial activity - can inhibit transport channels in pathogens plasma membranes
      5. hydrolytic enzymes - chitinases breaks down fungi walls, glucanases hydrolyse glycosidic bonds, and lysozymes that can break down bacteria walls.
  2. necrosis - cell suicide - pathogen has less access to water and nutrients = stops spreading. happens by enzymes - make brown spots on leaves
    1. canker - sunken necrotic lesion in woody tissue causes death of cambium tissue in bark
primary defences against disease
secondary non-specific defences
1. antigens and opsonins
  1. opsonins - a type of antibody that attach to a pathogens antigens - making it easier for phagocytes to bind and engulf it. Can be specific and non-specific.
2. phagocytes
  1. neutrophils - made in bone marrow and travel in blood and tissue fluid. they have lots of lysosomes, and engulf and digest pathogens. dead neutrophils collect in infected area = pus
    1. neutrophil binds to opsonin on pathogens antigens, and engulfs it - forms phagosome. lysosomes fuse to phagosome (phagolysosome) - releasing lytic enzymes into it. after its digested - harmless products are absorbed by cell.
  2. macrophages - made in bone marrow and travel in blood as monocytes. important in initiating specific responses to pathogens. when it engulfs a pathogen - it doesn't fully digest - the pathogen's antigens are saved and moved to a protein complex on the cell surface - it becomes and ANTIGEN PRESENTING CELL.
    1. other cells in the immune system recognise the antigen, and the special protein complex makes sure the APC is not attacked by other phagocytes
3. active immunity
  1. antigen presentation
    1. the APC comes into contact with the specific B or T lymphocyte that can activate the full immune response - there may be ony one T and B cell with the specific recognition site for the antigen. the APC increases the chances of the antigens and correct lymphocyte coming into contact
  2. specific immune response
    1. activation of specific B and T cells = clonal selection. this starts the whole response, and the events are stimulated by chemical messangers called cytokines - they stimulate differentiation and activity in macrophages and B and T cells.
the specific immune response
1. cells produced in the immune response
  1. T helper cells - release cytokines to stimulate B cells to develop, and stimulate phagocytosis by phagocytes. T killer cells - attack and kill host cells with foreign antigens. T memory cells - long term immunity.
  2. B lymphocytes become: Plasma cells - make and release antibodies. B memory cells - stay in body for years = immunological memory
2. cell signalling
  1. macrophages release monokines - attract neutrophils by chemotaxis, or stimulate B cells to differentiate and release antibodies
  2. T cells + macrophages release interleukins - stimulate clonal expansion and differentiation of B and T cells
  3. many cells - interferons - stop virus replication and stimulate T killer cells
3. what haoppens
  1. pathogen in lymph is recognised, or from APC. T + B lymphocytes recognise and have specific receptors - only 1 lymphocyte has correct receptors
    1. specific B or T cell is activated - CLONAL SELECTION
      1. then correct lymphocytes are stimulated by T helper cells releasing interleukins to undergo mitosis - CLONAL EXPANSION
        the lymphocyte clones differentiate to Tk, Th, Tm, B memory + plasma cells - DIFFERENTIATION
4. autoimmune diseases
antibodies
vaccination
development and use of drugs

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ocr biology a - communicable diseases

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	Creado por Saoirse Fletcher hace más de 6 años