4.1.1

Question 1

bacterial pathogens summary

Answer 1

prokaryote
classified by shape/ cell wall
e.g. TB (respiratory) or ring rot (tubers)

Question 2

protist pathogens summary

Answer 2

unicellular eukaryote
e.g. potato blight (spotted leaves) or malaria

Question 3

viral pathogens summary

Answer 3

small & not cells which capture and hijack other cells
e.g. TMV or HIV (retrovirus, affects immune) or Influenza (3 types, flu-like)

Question 4

fungal pathogens summary

Answer 4

hyphae filament, multicell (vac & wall)
e.g. black sigatoka (banana) or athletes foot

Question 5

endemic definition

Answer 5

always present but low number e.g. flu

Question 6

epidemic definition

Answer 6

disease outbreak, still contained roughly

Question 7

pandemic definition

Answer 7

international disease outbreak

Question 8

factors affecting general disease transmission

Answer 8

pop. density
vector pop.
pathogen pop.
% susceptible or immune
general sanitation

Question 9

extra factors affecting plant disease transmission

Answer 9

soil health (& rotation)
control im/exports
climate
pop. (species & density)
pesticides

Question 10

plant physical barriers

Answer 10

waxy cuticle
cellulose walls
hairs
resin
bark
closed stomata
casparian strip

Question 11

plant physical defences

Answer 11

callose deposited between csm and wall, blocks sieve & plasmo
then lignin strengthen

Question 12

plant antifungal defences

Answer 12

chitinase (enzyme)
gossypol
caffeine
saponins

Question 13

plant insect defences and why

Answer 13

tannin (bitter & inhibitor)
citronella (repel)
caffeine & alkaloid (‘icide)
to lower vector numbers and hence spread of disease

Question 14

plant antibacterial and other defences

Answer 14

defensins
cyanide
glucanase
H2O2 and phenols (antiseptic)pockets between csm cell wall and callose

Question 15

callose is …

Answer 15

beta glucose, joined by 1,3 and maybe 1,6

Question 16

how do plants recognise and respond to an attack

Answer 16

foreign pathogen activates csm receptors and hydrolyses cellulose wall
signalling molecules sent to nucleus
genes turned on/off
more signals & defence is produced

Question 17

1st line/ primary of non-specific immune response

Answer 17

mucus + cilia
epiglottis + hairs
saliva
skin + sweat + sebum
urination
lachrymal apparatus

Question 18

2nd line/ secondary non-specific immune response

Answer 18

blood clots
inflammation
fever

Question 19

epiglottis

Answer 19

flap of cartilage protecting trachea

Question 20

sebum

Answer 20

natural oil on skin with unsaturated natural fatty acids, antimicrobial

Question 21

lachrymal apparatus

Answer 21

tear ducts to wash away/ dilute chemicals near eye

Question 22

blood clotting

Answer 22

activated platelets (by skin collagen) causes chemical cascade
thromboplastin trigger
fibrinogen to fibrin
rbc mesh and granulation

Question 23

inflammation

Answer 23

mast cells release histamine and cytokines to dilate b.v. (arteriole)
leaky capillaries swell area so wbc and cyto can reach

Question 24

fever

Answer 24

hypothalamus stimulates body temp >37
temp kills pathogens (denature)

Question 25

T specific immune response

Answer 25

cell mediated, attacks infected cells & intracellular pathogen

Question 26

T cell life

Answer 26

made in marrow, mature in thymus

Question 27

B specific immune response

Answer 27

humoral, attacks extracellular pathogen

Question 28

B cell life

Answer 28

made & mature in marrow

Question 29

how are T cells activated

Answer 29

marcophages (now APCs) are specific so clonal selection by TCRs then clonal expansion and differentiation

Question 30

types of T cells

Answer 30

memory regulatory killer helper

Question 31

phagocytosis

Answer 31

mass endocytosis, engulf pathogens/ other material

Question 32

how do phagocytes recognise pathogens

Answer 32

chemotaxis as attracted by cytokines (from mast) and chemicals released by pathogen & dying cells

Question 33

phagocytosis phases

Answer 33

chemotaxis endocytosis phagosome phagolysosome exocytosis of indigestible marcophages present

Question 34

pseudopodia

Answer 34

arm-like organelles, extend cytoskeleton to grab pathogens

Question 35

how do macrophages become APCs

Answer 35

phagocytosis antigen binds to MHC complex displayed on csm

Question 36

white blood cells other name

Answer 36

leukocyte

Question 37

regulatory T cell

Answer 37

suppresses immune response to avoid autoimmune response by interleukins

Question 38

killer T cell

Answer 38

contains perforin which makes holes in pathogen csm

Question 39

helper T cell

Answer 39

bind to APC by CD4 to produce interleukins to stimulate B and more T

Question 40

plasma cell

Answer 40

B cells which produce antibodies

Question 41

effector B cell

Answer 41

divide to form more plasma

Question 42

memory T cell

Answer 42

immunological memory rapidly divides for killer T if ill again

Question 43

memory B cell

Answer 43

immunological memory rapidly divides for plasma then antibody if ill again

Question 44

how are B cells activated

Answer 44

interact with helper T or with pathogen antigens

Question 45

antibody structure

Answer 45

2 heavy inside, 2 light outside joined by disulfide hinge variable regions for antigen binding site globular

Question 46

amino acid with sulfur in R group

Answer 46

Cystine

Question 47

antigen summary

Answer 47

molecule (typically protein) used for cell recognition/ ID as specific, on csm oe

Question 48

antibody summary

Answer 48

protein specific & complementary to antigen, part of humoral response, made by plasma

Question 49

three uses of antibodies

Answer 49

agglutination opsonisation neutralisation

Question 50

agglutination

Answer 50

agglutinins (antibodies) join multiple pathogens together for clumps then easier phagocytosis

Question 51

opsonisation

Answer 51

opsonins (antibodies) bind to pathogen, marking it so phagocytes can bind to constant then engluf

Question 52

neutralisation

Answer 52

antitoxins/ antibodies bind to toxins and viruses to block

Question 53

natural active immunity

Answer 53

natural infection, specific immune response

Question 54

natural passive immunity

Answer 54

mother to baby, placenta, breast milk/ colostrum

Question 55

artificial active immnunity

Answer 55

vaccines

Question 56

artificial passive immunity

Answer 56

medications e.g. antitoxins or antibodies when needed

Question 57

autoimmune disease

Answer 57

when antigen recognition fails, cant differentiate self &non-self

Question 58

autoimmune disease examples

Answer 58

HIV, MS, Rheumatoid arthritis

Question 59

Rheumatoid arthritis

Answer 59

autoimmune which targets skeleton, swelling and pain in joints

Question 60

vaccination

Answer 60

deliberate exposure to antigenic material to stimulate an immune response

Question 61

types of vaccination and example

Answer 61

whole live (smallpox) attenuated (TB) dead (typhoid) antigen (hep B) harmless toxin (tetanus)

Question 62

herd immunity

Answer 62

80-85% vaccinated so hard for pathogen to spread

Question 63

why doesnt herd immunity require 100% vaccination

Answer 63

may not be possible for some and some may have already had it and are hence immune

Question 64

ring immunity

Answer 64

vaccinate those in contact with infected to prevent spread

Question 65

primary vs secondary response

Answer 65

B memory already present so divide and plasma for antibodies and no need for T & B response faster longer lasting larger