Zusammenfassung der Ressource
ocr biology a - communicable diseases
- organisms that cause disease
- transmission of pathogens
- indirect transmission
- plant defences against pathogens
- passive defences
- 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.
- 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
- active defences
- 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
- they also increase chemical production:
- terpenoids - antifungal + bacterial. can make a scent.
- phenols - antibiotic + fungal. to stop insect attack,
tannins bind to salivary proteins + digestive
enzymes and stop insects from growing so they
die - stops transmission
- 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
- defensins - anti-microbial activity - can inhibit transport channels in pathogens
plasma membranes
- hydrolytic enzymes - chitinases breaks down fungi walls,
glucanases hydrolyse glycosidic bonds, and lysozymes that
can break down bacteria walls.
- necrosis - cell suicide - pathogen has less access to water
and nutrients = stops spreading. happens by enzymes -
make brown spots on leaves
- canker - sunken necrotic lesion in woody tissue causes death of
cambium tissue in bark
- primary defences against disease
- secondary non-specific defences
- antigens and opsonins
- 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.
- phagocytes
- 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
- 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.
- 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.
- other cells in the immune system recognise the
antigen, and the special protein complex makes sure
the APC is not attacked by other phagocytes
- active immunity
- antigen presentation
- 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
- specific immune response
- 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
- cells produced in the immune response
- 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.
- B lymphocytes become: Plasma cells - make
and release antibodies. B memory cells - stay
in body for years = immunological memory
- cell signalling
- macrophages release monokines -
attract neutrophils by chemotaxis, or
stimulate B cells to differentiate and
release antibodies
- T cells + macrophages release
interleukins - stimulate clonal
expansion and differentiation of B and T
cells
- many cells - interferons -
stop virus replication and
stimulate T killer cells
- what haoppens
- pathogen in lymph is recognised, or from APC. T + B lymphocytes
recognise and have specific receptors - only 1 lymphocyte has
correct receptors
- specific B or T cell is activated - CLONAL SELECTION
- 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
- autoimmune diseases
- antibodies
- vaccination
- development and use of drugs