Chapter 12 Communicable Diseases Part 2 (defences) Flashcards
What are plant’s way of dealing with a pathogen, is it specific etc?
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
Plants have physical and chemical defences, what is the physical barrier defence
Physical includes waxy cuticle, cell wall bark ; a barrier against pathogen entry and stops water from staying too long which could be a vector
Describe the cascade of events when a pathogen meets and manages to break cell wall
What does the nucleus do (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.
Describe the entire mechanical route the nucleus takes :
- what is produced and deposited
- where (3) and why
- what is effect but why good
- 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
What about the chemical defence approach the nucleus takes?
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
What are main plant chemical defences
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
What is main difference between specific and non specific defence
Specific is to each pathogen, non is general but FASTER AND ALWAYS PRESENT
What are different non specific defences to KEEP PATHOGENS OUT (4)
+ how
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
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)
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 !
What does the inflammatory response look like
This is a localised response to pathogens at the damage site resulting in inflammation, which is shown by pain, heat and redness and swelling .
What happens in inflammatory response (what two released , how and what they do) !
Two for h
One for c
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
- How the non specific gets rid of pathogens
Two ways
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
Phagocytosis process again
What happens to neutrophils tho
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
How do phagocytes and what then become APC
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
What effect does phagocytes releasing cytokines do
How can they use opsonins
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 .
Where are t lymphocytes MATURE and where b
T in thymus
B in bone marrow
What is difference between cell mediated and humoral response
- what ways cause a cell mediated
What is humour
- what cause a humoral
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
-
Describe cell mediated all steps
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
Now describe humoral responses
How t helper cells involved
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
Primary vs secondary response
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
When do autoimmune response occur and why
Treatment but what bad
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
Types of autoimmune disease
Rheumatoid arthritis = joints
Type 1 diabetes = insulin producing cells
Vitiligo = melanocytes
Example for natural active immunity and natural passive
How do baby digestive system allow antibdoeis
Key difference between two?!!
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 )
Artificial passive ?
- what advantage but what disadvantage
#where do these even come from Why passive aswellm
- 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 )
Artificial active?
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
Why do boosters happen
This because immunity may only last like a year
So injected with booster so a response happens again
What is epidemic
How dealt with vaccines
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
Have vaccines been developed for everything ?
No - malaria and hiv , hard to deal with because they protect themselves using human antigens and disabled them too
Some medicine and where they come from examples
Penicikin = mould fungi = antibiotic Paclitaxekl = yew tree = breast cancer Aspirin = willow bark salicylic acid = painkiller Primal = come snail venimm& pain killer
Why biodiversity important relation to development medicines
Can potentially give us key to life saving drug, not just plants but everything (list sources). Aswell tropical areas have most bidodivereity
How we make drugs better for future (2 ) ways Gen synth (2 for this )
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
How do bacteria gain resistance to antibiotics ?
- 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
How have human activities accelerated this
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
What types of example of high antibiotic resistant strains of bacteria (2 and whwt problems )
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
How can antibiotic resistant strains be reduced (2 ways)
- 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
What is final problem if antibiotics vs resistance
At moment resistance being built faster than new antibiotics
Need to conserve more and more biodiversity and survive
What are physical barriers of plant
- epidermis and cell walls
- cuticle on top
- closing of stomata
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
No b t lmyphocytes
No memory cells
No antibodies produced
No ciruit worry system
When describing trends what to do
Describe why both increaeed or changed look at them separately
What is the structure of a virus and why is it considered not living
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.
What is opportunistic infection
This is when an infection only happens becsude of a weakened immune system , such a in HIV or malnutrition
How are HIV vs TB transmitted
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
Describe structure antibody
How does structure of antibodies help serve their function
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
What are 4 ways antibdoies help and explain
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
Specifically neutralisation and agglutination ?
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
Why can bacteria not be immune , what should this be
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
What is difference between primary and seoncdaryn( not specific snd nin soecific remembe)
Primary first time it meets memory etc NOT INVOLVED
Secondary is second so memory etc involved
