Chapter 12 Communicable Diseases Part 2 (defences)

Question 1

What are plant’s way of dealing with a pathogen, is it specific etc?

Answer 1

Not specific but is a rapid response. The idea is to block and kill infected cell before it can spread to other areas, and then regrow later

Question 2

Plants have physical and chemical defences, what is the physical barrier defence

Answer 2

Physical includes waxy cuticle, cell wall bark ; a barrier against pathogen entry and stops water from staying too long which could be a vector

Question 3

Describe the cascade of events when a pathogen meets and manages to break cell wall
What does the nucleus do (3)

Answer 3

This is when a pathogen comes in

1) some of the molecules of pathogen may already be detected BUT a pathogenic enzyme breaks down the cell wall of the plant. The BROKEN products of cell wall are then recognised by receptors and start to signal nucleus to attack .
2) NUCLEUS then will respond in 3 ways to deal with situation
- they produce defensive molecules to directly attack pathogen
- produce defensive chemicals to alert other cells to get ready before attacked
- produce LIGNIN AND CALOSE to strengthen and section cells.

Question 4

Describe the entire mechanical route the nucleus takes :

• what is produced and deposited
• where (3) and why
• what is effect but why good

Answer 4

• nucleus rapidly produces high amount of callose. This is a chemical that strengthens the cell wall and makes it difficult for pathogen to enter
• the callose is deposited at the cell membrane and walls bordering cells next to them - to completely block off infected cell with other
• at the same time lignin is added making the mechanical barrier STRONGER
• callose also deposited between PLASMODESMATA : so pathogens can’t escape through connected cytoplasm to other cells
• callose also deposited in between siege plated in phloem, so that if pathogen here it can’t travel and absolutely kill rest of plant

= effects is cell die, but worth

Question 5

What about the chemical defence approach the nucleus takes?

Answer 5

Produce powerful chemicals to kill insects, bacteria , fungi, oomcytets general etc

• antibacterial impounds like antibiotics like phenols , lysosomes (enzymes that attack) defending that kill
• anti fungal compounds like phenols , saponins, CHITINASES (enzymes that break chitin cell wall of fungus )
• anti oomcyetes, like GLUCANASE (enzymes that break down glucans which polymers in oomcytes )
• general toxins such as CYANIDE

insect repellants fro, citronella
- insecticides too like caffeine

Question 6

What are main plant chemical defences

Answer 6

Produce anti fungal chitinases
Produce anti oomcytets glucanses
Produce general toxins like cyanide toxic to most things
Insecticides = caffeine , insect replannts like citronella
Antimicrobial phenols and antibiotics

2) less insects = promoted less spread through vector like something carry fungal spores

Question 7

What is main difference between specific and non specific defence

Answer 7

Specific is to each pathogen, non is general but FASTER AND ALWAYS PRESENT

Question 8

What are different non specific defences to KEEP PATHOGENS OUT (4)
+ how

Answer 8

1) barrier = skin
- prevents entry, has biome of microorganisms that outcompete bacteria to live on skin, sebum that oil prevents pathogen from living and can lose pH

2) mucous membranes in airways and openings of body
- in moth nostrils ears, genitals anus have these which secrete sticky mucus to trap them, then after that lysozyme phagocyte destroy

3) lysozyme in tears, urine , acid : kill
4) expulsion reflexes : coughing sneezing for gas exchange system expel, vomiting and diarrhoea in digestive

Question 9

What about non specific respond of wound repair to prevent them coming in?
How does body seal a wound from one broken (what two main things end up being released)

Answer 9

1) first skin / blood vessel wall breaks, and this releases broken collagen. When this comes into contact with platelets , they become activated and release many substances:
2) one is thromboplastin , an enzyme triggers cascade reaction to make clot, including making fibrinogen into fibrin to make network of fibres to trap blood cells and make a clot
3) but also SEROTONIN , which makes smooth muscle in blood vessels contract, narrowing blood supply to area to stop blood leaking out !

Question 10

What does the inflammatory response look like

Answer 10

This is a localised response to pathogens at the damage site resulting in inflammation, which is shown by pain, heat and redness and swelling .

Question 11

What happens in inflammatory response (what two released , how and what they do) !
Two for h
One for c

Answer 11

Mast cells are activated in the damaged tissue and release HISTAMINES AND CYTOKINES

1) histamines
- histamines make the blood vessles near VASODILATE, causing more blood to the area and thus redness shown, but this increases temperature here which stops pathogens from REPRODUCING
- histamines make blood vessel walls more Leaky so blood plasma is forced out, and tissue fluid causes swelling and pain but essentially diluted the pathogen rendering it harmless (ya solution pollution dilution )

2) cytokines
- these attract white blood cells phagocytes to the site and they dispose of pathogens by PHAGOCYTOSIS

Question 12

4. How the non specific gets rid of pathogens

Two ways

Answer 12

1) fevers
- cytokines stimulates hypothalamus in brain to increase bidy temo from 37° to stop pathogens reproducing
- make immune system work faster as they do at higher temp

2) phagocytosis
- phagocyte like neutrophil macrophage dendrite recognise non self
- engulfs pathogen and invaginate making phagosome
- combines with lysosome to make phagolysome
- enzymes digest and it dies

Question 13

Phagocytosis process again

What happens to neutrophils tho

Answer 13

phagocytosis

• phagocyte like neutrophil macrophage dendrite recognise non self
• engulfs pathogen and invaginate making phagosome
• combines with lysosome to make phagolysome
• enzymes digest and it dies

Neutrophils die too once digest by doing apoptosis

Question 14

How do phagocytes and what then become APC

Answer 14

only macrophage dendeite because neutrophil dies

1) . After digest, process products of digestion
2) combines antigen found here with major histocompatibility complex
3) moved this using cytoskeleton to the csm

Now oresents antigen to start the specfic response

Question 15

What effect does phagocytes releasing cytokines do

How can they use opsonins

Answer 15

Finally phagocytes release cutokines to alert other phagocytes under attack and come

They have couple common receptors to common opsonins which are antibodies and attach to the constant region which essentially Tage them for them and tells them to attack .

Question 16

Where are t lymphocytes MATURE and where b

Answer 16

T in thymus

B in bone marrow

Question 17

What is difference between cell mediated and humoral response
- what ways cause a cell mediated

What is humour
- what cause a humoral

Answer 17

1) Cell mediated is response to bodies OWN cells thst have been changed , for example
- by a virus
- antigen processing
- mutation like cancer
- transplanted tissue cells

Cell mediated is vital for cancer and viruses

However humoral is defence against Antigens found on cells OUTSIDE the body cells
- so bscteria, fungi
APCs
These are found in thr humour = body fluid
-

Question 18

Describe cell mediated all steps

Answer 18

1) An APC releases cytokines in order to attract and find the correct complimentary receptor T helper celll, this is clonal selection and can take a decent amount of time
2) once found the correct receptor complimentary t helper cells binds to the APC and then released interleukins. These Signal to other t helper cells to divide by mitosis and differentiate into other t helper cells - this is clonal expansion .
This becomes
- cytotoxic t killer cells (these kill, they release perforins and gransozymes which create pores and breakdown )
- normal t helper cells
( needs more to repeats profess faster rate)
- t memory cells
(These keep note of the receptor in order to mass produce in case same pathogen appears again)
- t regulatory cells
( this is to regulate and stop an auto immune response after (as some antigens looks the same ))

Regulated and stored in memory . Now t helper cell can cause a humoral response too

Question 19

Now describe humoral responses

How t helper cells involved

Answer 19

1) instead of macrophage dendrite, now B cell engulf snd processed antigens snd becomes APC
2) they release cytokines that activate t helper cells. They do this and once a t helper cell that is complementary to antigen binds, this is clonal selection and takes time
3) once binded now T cells activwted produced interleukins that stimulate b helper cells to divide by Mitleid and differentiate = clonal expansion
This becomes
- b plasma cells
- b memory cells

4’ b plasma cells receptors are still comolemtary to the pathogen , but can detach - these sre now antibodies l they are soluble and can deal with pathogens on their own . This is the primary response !

B memory cells re,Eber receptors to madd produce on second infection , secondary reponse

Question 20

Primary vs secondary response

Answer 20

Primary response involves the time it takes to Clonal select and expand firdt time around , for cell mediated time to make cytotoxic t killer and also intimate humoral and humoral Time it twkes to make plasma cells. This can take weeks and this is why we feel symptoms, because that is effect of pathogens before body deals wothnit

Seojcdwry response insane quick because selection is very quick due to memory cells. As a result pathogen dealt with even before symptoms have chance to show

Question 21

When do autoimmune response occur and why

Treatment but what bad

Answer 21

Don’t know, but maybe because some antigens are very similar to human one so mismatch
Also happens because t regulatory cells don’t work effectively

• bad is immunosuppressive can be used but thst stops bidy from natural defence for other basic disesdes

Question 22

Types of autoimmune disease

Answer 22

Rheumatoid arthritis = joints
Type 1 diabetes = insulin producing cells
Vitiligo = melanocytes

Question 23

Example for natural active immunity and natural passive

How do baby digestive system allow antibdoeis

Key difference between two?!!

Answer 23

1) active = the immunity you make yourself from specific immune response humoral and cell mediated. This aquifer immunity’s active because your own body made antibodies and memory

2) natural but passive
- baby immune system not work at birth
- but they passively acquire immunity through transfer of antibodies from placenta while in uterus + antibodies from breast fed milk l
- baby digestive system don’t digest So they just go to blood stream

As a result baby has same immunity as mother BUT ONLY TEMPORARILY (key difference )

Question 24

Artificial passive ?
- what advantage but what disadvantage

#where do these even come from 
Why passive aswellm

Answer 24

• body cannot sometimes produce own antibodies fast enough before pathogen kill you
• so you are transferred antibodies already produced to counter
• this gives you TEMPORARY but lifesaving immunity they won’t be long term

2) antibodies come from like an animal thst was injected with snd produced their own antibodies disease and then transferred to you by drop = artificial but passive
(passive because you didn’t contribute at any stage yourself )

Question 25

Artificial active?

Answer 25

This is vaccines. Active because you do contribute to immunity at some point

1) pathogen injected is not live version thst causes fatal but still has ANTIGENS TO STIMULATE RESPONSE
- here they are weakened strains, killed inactive, ATTENUATED ! Generically enginered, isolated antigens some thst were altered
2) injecte into bloody, primary response happens and memory cells hold info like normalem
- now if come into contact again secondary respond trigger snd minor

Question 26

Why do boosters happen

Answer 26

This because immunity may only last like a year

So injected with booster so a response happens again

Question 27

What is epidemic

How dealt with vaccines

Answer 27

Communicable disease spreads rapidly to a lot of people but national level

• everyone vaccinated as much as can , and these may have to change to match changing strains
• eventually do many vsccijsted it offers protection to those who aren’t = herd immunity

Question 28

Have vaccines been developed for everything ?

Answer 28

No - malaria and hiv , hard to deal with because they protect themselves using human antigens and disabled them too

Question 29

Some medicine and where they come from examples

Answer 29

Penicikin = mould fungi = antibiotic 
Paclitaxekl = yew tree = breast cancer 
Aspirin = willow bark salicylic acid = painkiller 
Primal = come snail venimm& pain killer

Question 30

Why biodiversity important relation to development medicines

Answer 30

Can potentially give us key to life saving drug, not just plants but everything (list sources). Aswell tropical areas have most bidodivereity

Question 31

How we make drugs better for future  (2 ) ways 
Gen synth (2 for this )

Answer 31

1) personalised drugs based on genome
- analyse and make. For example in Brest cancer 30% have mutation and medicine made to counter this
2) synthetic biology
- this is using bacteria / mammals to mass produce medicine by genetic engineering , which is good as it woulda be too rare expensive etc.
- also using nanotechnology to deliver medicine to minute place like sites in cells

Question 32

How do bacteria gain resistance to antibiotics ?

Answer 32

• antibiotics only work because 1) bacteria have binding site to drug and 2) drug stops a key metabolic pathway
• however if a Random mutation occurred such that bacteria is not affected by antibiotic anymore then this is advantageous and survives whilst other dies
• bacteria will pass this on to others due to giving it by plasmids and dividing so within no time big population made

Question 33

How have human activities accelerated this

Answer 33

If you constantly introduce selection pressure , the antibiotic , this forces only the resistant one to survive by natural and causes it to pass down the gene and creating entire succeufk population

However if selection pressure not therenss much, immune system would destroy anyways / thst resistant one would not have reason to pass down l to entier population

More a selection pressure introduced, higher chance of mutation
- here we do this by giving animals antibtoifs when we shouldn’t snd using them when we don’t have to and not finishing course

Question 34

What types of example of high antibiotic resistant strains of bacteria (2 and whwt problems )

Answer 34

MRSA, which was treated effectively , but then an even more effective strain came

C, difficile here treated by antibotics but if survive it reproduced quickly and mutated

Question 35

How can antibiotic resistant strains be reduced (2 ways)

Answer 35

• minimsiing use of antibiotics for no reason, and if they are used then they have ti be completed so that all bacteria are wiped out and don’t have chance to mutate due to selection prestue
• good hygiene in hospitals care hokes etc , as this is where antibiotic strains were mostly spread

Question 36

What is final problem if antibiotics vs resistance

Answer 36

At moment resistance being built faster than new antibiotics

Need to conserve more and more biodiversity and survive

Question 37

What are physical barriers of plant

Answer 37

• epidermis and cell walls
• cuticle on top
• closing of stomata

Question 38

Plants do not have a specific immune response in which they specifically target a pathogen at hand, they only have a general response that involves cutting the infected region off fro, the rest of the plant and using chemical defences to dewl with them broadly. As plant cells do not have any sort of memory cells either , they can’t aquifer immunity

WRONG what is answer

Answer 38

No b t lmyphocytes
No memory cells
No antibodies produced
No ciruit worry system

Question 39

When describing trends what to do

Answer 39

Describe why both increaeed or changed look at them separately

Question 40

What is the structure of a virus and why is it considered not living

Answer 40

A virus is a strain of RNA incased around some proteins with enzymes

• it is not living because it can’t carry out the 7 life process by itself
• only after it takes over other genetic material can it take over and use other resources to reproduce, it does nor reproduce itself
• as a result it can only survive with a host cell, living a borrowed life

A cell is the smallest unit of living.

Question 41

What is opportunistic infection

Answer 41

This is when an infection only happens becsude of a weakened immune system , such a in HIV or malnutrition

Question 42

How are HIV vs TB transmitted

Answer 42

hIv = through sexual contact , bodily fluids transmissions , needles , contaminated blood etc

TB= through droplets after coughing sneezing, poor ventilation but also HIV bodily fluids etc

Question 43

Describe structure antibody

How does structure of antibodies help serve their function

Answer 43

Structure includes 2 heavy 2 light chains,
a constant region (for all same type of immunoglobulin ),
variable region ( different base don antigen )
and a hinge region, with disulfide bridges holding chains together .
Includes epitope at variabel region

Constant region
- region where phagocytes bind to when they act as opsonins
Variabel region
- This is different based on antigen complimentary , allows to bind to them in a lock and key hypothesis type of way and either neutralise toxins
- or just stop the pathogen fro, entering a host cell by binding .
- also act as agglutins and stick multiple together , making it easier for phagocytes to kill + prevents easy spread

• hinge region allows movement of antibody to reach antigen

THE FACT THAT THERE ARE TWO VARIWBLE REGIONS MEANS THEY CAN ACT AS AGGLUTINS AND BIND TI MORE THAN ONE

Question 44

What are 4 ways antibdoies help and explain

Answer 44

1) neutralises toxins produced by bacteria by producing a complementary antibody that binds to it and render it harmless
2) antigen antibody complexes made can stop the pathogen from invading the host cell as their antigens are blocked
3) act as opsonins, binding to the antigens which flag them up for phagocytes which will then bind to their constant region and phagocytosis
4) the fact has two variable regions means it can act as an agglutins and bind to ore than one, essentially collecting togetehr make easier for phagocytes to digest and stops spread

Question 45

Specifically neutralisation and agglutination ?

Answer 45

1) neut
- binging to toxins rendering harmless
- binding to many antigens such that they can’t bind to host cells anymore

2) agglutins
- can clump to more than one making easier and preventing spread for phagocytes
- by clumping it also is too big to enter

Question 46

Why can bacteria not be immune , what should this be

Answer 46

Resistant - immune is collecting memory cells and specific response now, resistant is when antibiotic just doesn’t work in them anymore

ONLY MULTICELLULAR CELLS CAN HAVE AN IMMUNE RESPONSE, NOT ONE CELL

Question 47

What is difference between primary and seoncdaryn( not specific snd nin soecific remembe)

Answer 47

Primary first time it meets memory etc NOT INVOLVED

Secondary is second so memory etc involved