Module 4.1 Flashcards
name of disease 1
tuberculosis
type of pathogen of disease 1
bacteria
transmission of disease 1
droplets / airborne (sneezing )
symptoms of disease 1
tiredness , night sweats , lack of appetite
organisms affected by disease 1
humans
Prevention / treatment of disease 1
vaccination - prevention
treatment - antibiotics
name of disease 2
athlete’s foot / tinea pedis
type of pathogen in disease 2
bacteria
transmission of disease 2
contaminated towels / clothes and surfaces
symptoms of disease 2
itchy red rash between toes
organisms affected by disease 2
humans .
prevention/ treatment of disease 2
antifungal medication
name of disease 3
bacterial meningitis
type of pathogen of disease 3
bacteria or virus
transmission of disease 3
droplets from coughing sneezing etc
symptoms of disease 3
babies - high fever , drowsiness
older children - seizures , muscle pain
organisms affected by disease 3
humans
prevention / treatment of disease 3
intravenous anitbitoics
name of disease 4
potato / tomato blight
type of pathogen in disease 4
proctoctist (protist)
transmission of disease 3
direct contact with watery rot on the surface .
symptoms of disease 4
tomato - leaves and stems , brown patches may appear on stem .
-fruit may decay more rapidly . Same for potatoes .
organisms affected by disease 4
tomatoes and potato
prevention / treatment of disease 4
growing more tomato’s and potato’s in a greenhouse .
name of disease 5
HIV
type of pathogen in disease 5
virus
transmission of disease 5
unprotected sex , sharing blood
symptoms of disease 5
fever , rash , muscle and joint pain
organism affected by disease 5
humans
prevention / treatment of disease 5
treatment is antiretroviral drugs
prevention is to use condoms
name of disease 6
black sigatoka
type of pathogen in disease 6
fungus
transmission of disease 6
rain splash , wind during wet conditions .
symptoms of disease 6
mottling , yellowing of tissues , poor yield
organisms affected by disease 6
plants
prevention / treatment of disease 6
destruction of infected individual
name of disease 7
ring rot
TYPE OF PAthogen in disease 7
bacterium
transmission of disease 7
direct contact with infected tubers
symptoms of disease 7
skin of the potato may crack and ooze can emerge from the heel end and soil
organisms affected by disease 7
potato
prevention / treatment of disease 7
prevention is use seeds that are pathogen free .
-there is no treatment
name of disease 8
malaria
type of pathogen in disease 8
parasite -
Plasmodium falciparum
transmission of disease 8
mosquito
symptoms of disease 8
vomiting , diarrhoea , sweats and chills
organisms affected by disease 8
humans
prevention / treatment of disease 8
wearing bug repellent spray and sleeping inside a mosquito net /
name of disease 9
tobacco mosaic virus
type of pathogen disease 9
virus
transmission of disease 9
infected leaves rub against healthy plant
symptoms of disease 9
defective fruit
organisms affected by disease 9
plants
prevention / treatment of disease 9
application of fungicide , removal of affect leaves .
name of disease 10
ring worm
type of pathogen of disease 10
fungus
transmission of disease 10
human- human contact
human- animal contact
-human - object contact
(rare ) = human - soil contact
symptoms of disease 10
silvery , red ring- like rash on skin
organisms affected by disease 10
humans
prevention / treatment of disease 10
antifungal drugs
-keep area dry
name of disease 11
influenza
type of pathogen disease 11
virus
transmission of disease 11
airborne (coughs and sneezes )
Symptoms of disease 11
high temperature , 38 above , tiredness , weakness and headaches .
organisms affected by disease 11
huamans
prevention / treatment of disease 11
bed rest
One way of transmission
direct contact
-direct physical contact , such as touching a person who is infected or touching contaminated surfaces (including soil ) that harbour the pathogens . (HIV , bacterial meningits ring worm and athlete’s foot . )
ways to prevent direct contact transmission
hygiene ; washing hands regularly - especially after using the restroom .
keeping surfaces clean - especially door handles.
-cleaning and disinfecting cuts and abrasions .
-sterilising surgical instruments .
-using condoms during sexual intercourse .
faecal-oral
usually by eating food or drinking water contaminated by the pathogen .
-for example ; cholera , food poisoning .
ways to prevent faecal oral transmission
using human sewage to fertilise crops is a common practice in some parts of the world .
-treatment of waste water and treatment of drinking water are important ways to reduce the risk .
-thorough washing of all fresh food (using treated water ) .
-careful preparation and thorough cooking of all food .
third way of transmission
droplets
-droplets infection , in which the pathogen is carried in tiny water droplets in the air
for example tuberculosis , influenzas and covid
ways to prevent droplet transmission
catch it , bin it and kill it .
-cover your mouth when coughing or sneezing . Use a tissue and ensure the tissue is disposed correctly .
-face masks .
fourth way of transmission
spores
transmission by spores which are resistant stage of the pathogens , these can be carried in the air or reside on surfaces or in the soil .
(example anthrax and tetanus )
ways to prevent spores transmission
use of a mask
washing the skin after contact with the soil
indirect - malaria
a vector is another organism that maybe used by the pathogen to gain entry to the primary host .
(e.g malaria caused by plasmodium parasite enters the human host via a bite by the female mosquito )
transmission of plant pathogens
–pathogens prevent in the soil can enter the plants via roots .
-fungi produce spores that can be airborne .
-infected leaves shed and carry pathogens back into the soil .
-pathogens can enter fruit and seeds , infecting offspring .
-infects can indirectly plants and vectors .
the effect of climate
many proctitis bacteria and fungi can grow and reproduce rapidly in warm and moist conditions .
-Therefore ,they , tend to be more common in warmer climates
in cooler climates
-these pathogens maybe damaged or even killed by cold winter weather 0 such weather will certainly reduce the ability to grow and reproduce .
-as a result there is a greater variety of diseases to be found in warmer climates , and animas or plants living in these regions are more likely to become infected .
Communicable diseases
can be spread between organisms either of the same sspecies , or sometimes between different species .
-communicabe diseases spread by pathogens ,
-pathogens are micorgansims that cause disease .
host –> organisms are what pathogens infects .
bacteria (2)bacteria (2)
also , bacteria do not have other membrane bound organelels like motochondira .
-bactceira are also surroudned by a cell wall containing the chemical petidogylcen .
how bacteria enter the cell
-once they ener the body , pathogenic bacteri can release toxins .
-Toxins are chemcials which damage the host cells and tissues leding to be symp whattt
-another way bacteria can enter host cells
-some bacteria can enter host cells and prevent them from functioning normally - e.g bacteira that cause tuberuclosis are much smaller than baceria .
-difference between bacteira and virus
-unlike bacteria , virusses are non-living no cells trucutre at all .
-viruses consits of genetic mterials can be dna / rna .
-the genetic material is wrapped around a protein strucutre called a capsid .
viruses also attach what ?
viruses also have attachment proteins , which allow the virus to attach virus to attach to hsot cell .
-some viruses also contain a lipid envelop e.
Key feature ; virsues ,,c annot reporduce outside of a hsot cell –? to reproduce a virus attaches to the host cell and hen passes thorugh the cell meembrna
how do viruses work with the hos cel .
virus then copies itsel using the enzyme of the host cel .
-the virus particles now leave the host cell and gd go on infect new host cells and continue reporducing .
-virus prevents the hsot cells from functioning normally . In many cases , virus can lead to the death of the host cell .
Fungi
-are eukryotic organismd .
-they can be unicellular or multiceullar .
FUNGI : obtain their bnutrients by releaasing enzymes and digresting the matrrial around htem .
the products of digestion are then absorbed BACK INTO THE fungal cell .
-Tjis process of digestion can cause damage to hot cells and tissues .
-when they reproduce , fungi release a large amount of spores .
-so fungal diseses can spread very wideluy .
-Many species of fungi are found on the remiansresad very widey .
-Many species of fungi are found on the remains of dead organsisms , where hey ake part in the decay proces .
However , pahogenic fungi are found on lviing organssms where hehy cuse disease .
-e.g in humans fungi causes thrush and athlete’s foot .
-fungi can cuase a range of disease in plans . incluing some which re very destructive .
-by dmging the leaves , fungi can reduce the rate of photosynthesis . severyly reducign the yield of plant crops .
protoctista (protista) –> eukaryotic organsimss .
-these protoctista act as pathogenic parasites in humans .
-ciarda cises doarrpea ad si transmited when humans dink water coaining infexrws water .
-plasmodium is the pthogen that causes malria in huans and is transmitted between uhmans by mosquitoes .
human body has a number of ways to protect itself from infection bbyoathgoens .
-number one specific immune sytem –? respone of he specific immune system is tailored to each pathogen .
-w-when the specific immune sytem fights off aprticular pathogen , it then becomes more effective at fighting off a second infection , by the same pathogen .
–body has w hole rnge of non-specific diefences precent pthogens from gainign acess to the body .
-unlie tthe specific , the no-speciifc defence is the same for all pathogens .
1.line of defence is the skin
Which provides a protective layer for the majority of body surfaces .
SKIN —> has many layers of cdlls , including a layer of desd cells. This makes the skin difficult for pathogens to penetrate .
What is the surface of the skin covered with
It is covered with an oily denim produces by sebaceous glands .
-this forms a slightly acidic layer , which can prevent thee growth of harmful bacteria .
-healthy skin is also
Covered worj harness
Micrograjosms which reduces fhe growth of pathogens by competing for resources .
However , pathogens CAN enter the body via openings e.g breathing and digestive system .
These are lined with a protective layer called mucus membrane .
-SHEIN for the trachea in the breathing Sheen .
-l
What do mucus membranes do
Mucus membranes , secrete mucus which trap
Microorganisms .
-these microorganisms can be destroyed by white blood cells got phagocyte.
-mucus also contains the enzyme
Lysosome which destroys bacteria by digesting the bacteria cell wall .
Where else is lysozyme also found in?
Lysozyme is also found in tears .
Helps to prevent pathogens from entering via the eye .
In the stomach , mucus contains hydrochloric acid .
-hcl helps to kill any pathogens in food :water .
Sometimes , pathogens can made the body through openings such as the mouth or nose .
-in this case , the body tries to expel the pathogen .
-These are Ken as expulsion refluxes .
-these include sneezing , coughing , vomiting and diarrhoea .
-Anotjer way pathogens can enter , is the skin is damaged e.g a cut
-in this case , the body responds by trying to seal the damaged area .
Before , a large number of pathogens can enter aka blood
WHWRE
Blood clotting invovles platelets which are found in the blood stream
Platelets - tiny - short lived fragments of cells with no nucleus .
-platelets are formed y continuing in the bomearrow before being released into
The blood .
The scab protects , the underlying tissue from
Pathogens while wound healing takes place .
Skin cues , under the scab divide and repair the samamage ,
Eventually , scab falls off and freshly repaired skin continues its
Job from
Protecting the body from
Pathogen entry .
Tissue damages can also result in inflammation .
-this is when the tissue is damaged and activates most cells .
-when most cells are activated , they release a chemicals
Called jsofkme
.
-histamine has multiple effects .
Histamine effect in je
Histamine causes something blood vessels go dilate or widen .
-scientists cal fhis vasodilation .
-this increase the supply of blood to the effected area /
-causes the area to feel
Appear red
-increased temperature reduce pathogenic ability to reproduce .
Second effect of histamine
-blood vessels walla , are more
Permeable .
-histamine allows
More blood
Plasmas tk
Leave and fork tissue fluid .
The effect of this is to cause nearby tissues to swell and feel
Painful .
Scientist cal tjis sweeping oedma.
As well as histamine , most cells also release chemicals called cytokines
Cytokines wee a whole range of chemicals produced by the body .
-ok fhe respond to an intense
Cytokines attract phagocytosis’s to the damaged area in order to caddy out phagocytosis of any pathogen and prevent it from.
Some cytokines can reveal to the hypothalamus in the brown where they trigger an increase in body temperature
This increase in body temperature reduced the pathogens ability to reduce .
Picture shown of small arteriole
Walls of the blood besssl have a layer of cells called the endothelium .
Just outside the endothelium there are smootj
Muscle
Cells and proteins such as collagen
-of the endothelium
Is
Damaged sxmplas the skin is cut ,
What would happen .
Then the platelets are
Exposed to the
Proteins outside the endothelium
.
This activates the plates which now trigger blood
Clotting .
-blood clotting is complexed
So only
Noeed
Do know
Somploef beesion.
-when activated , platelets form a plug over the damaged area .
-the platelets also release cjemcoals called clogging factors including
Thromboplastin
Thromboplastim , together with calcium
Ions on the blood , now act in a blood protein called prothrombin .
-this concerts the prothrombin into an active enzyme called thrombin .
Thrombin now acts in a soluble blood
Protein called fibrinogen .
Catalysing the formation
Of ineoldune for mom
.
The insoluble fibrin forms
W
Mesh , with traps res blood cells forming a blood clot
Or thrombus .
-as well as triggering a blood clot , the actives platelets Wlso
Release a chemical called serotonin.
Seretomim causes the smooth muscle cells in the blood vessel walls to contact .
This narrows the blood besses reducing the blood
Flow
To
The damaged area .
-body can now start to repair the damaged blood vessels .
Blood clot also
Prevents energy of pajtiehjs , overtime clot dries to form a scab on the surface of the skin
…
Key ; as well as red blood cells , the blood aso has white blood cells .
-there are two categroies of white blood cells what is the first one ?
-first , catgeort is phagocytes .
-however , macrophagesges also play a role in the specific immune sytem .
we also have neutrophills .
The secondary category is lymphocytes
There are two types of lymphocytes
B lymphocytes and t Limpopo it’s
Lymphocytes form the specific immune syfem
Shown a bacterial cell
KEY: surface of pathogens —> bacteria are covered with chemiCals fhag are not found in humans .
-usuallg , in the case do bacteria fhe chemicals are often part of the bacterial cell wall .
What does the bloood contain fhags super sick
Blood contains special molecules which can recognise these foreign chemicals and Stirck to them .
-scientists call these molecules opsonis
By sticking to the pathogens what do opsonins do ?
They tag the pathogen as foreign aka not part of the human body .
-opsonins include antibodies as well as other molecules which are called complements.
What is the purpose of opsonins ?
-to attach to foreign molecules and tag them as foreign
Showing phagocyte (neutrophil in this case )
-bacteria tagged w opsus
Jus look at the image
Phagocytes such as neutrophils are attracted to molecules produced by pathogens
Receptors on the phagocytes membrane now attach to the opsonins and the phagocytes engulfs with the pathogens .
The pathogens are now in a special vacuole called a phagosome
Now , lysosomes move towards the ohagosome and fuse with it , forming a phagolysososme .
-lysosomes enzymes now break down the pathogen and destroy it .
Summarise neturophils stats
Neutrophils can rapidly engulf and destroy pathogens at the site of the infection .
Macrophages , can also destroy pathogens by phagocytosis . BUT they also have an additional function , what is this ?
This is called ANTIGEN PRESENTATION
-Macrophage about to gestroy bacteria .
-this bacteria has foreign chem jams on its surface .
-in this case , we are going to refer to these foreign chemicals as antigen .
-just like before , the pathogen js engulfed into a phagosome and lysosome joking to form a what ?
Phagolysososme .
-as before , the lysosomes enzyme digest the pathogen .
HOWEVER , at this stage GLYCOPROTEINS from the cytoplasm
Love to the phagolysososme .
Bind to the antigens molecules .
These glycoproteins are called the MAJOR histocompataboloty complex kf
Mhm.
When the mhc binds go antigen , it forms an MHC antigen complex
MHC antigen complex , now moves
To the cell surface membrane .
-the antigens are presented to the exterior of the cell . AT RHIS PLINF , we say macrophage is functioning as an antigen presenting cell or APC
Antigen presenting cells , plays a critical role in specific immune system .
By presenting the antigens tk lymphocytes .
-when a phagocyte engulf a pathogen .
-the phagocytes released chemicals called cytokines
What do cytokines do ?
Cytokines signal phagocytes and other immune cells to (move to the site of infection )
Cytokines also trigger inflammation and fever
The specific immune system includes antibodies as well as lymphocytes as b lymphocytes and t lymphocytes .
-the specific immune system , responds to each pathogen in an individual way .
-once fhe specific immune shygen has defended against a pathogen .
It will
Produce a more EFFECTIVE RESPONDE , if it encounters the same pathogen again .
KEY : specific immune systems can recognise individual pathogens
…
The surface of all cells are covered with molecules such as proteins and polysaccharides
-these molecules , carry out normal cellular functions .
-acis it’s refer to these molecules as antigens .
What can the immune system detect ?
Immune systems can detect antigens on the surface of the pathogens .
-the immune syfem , can see those antigens as foreign or “non self” leading to an immune response .
What do antibodies do during an immune response !
Antibodies will be produced specifically bind tk the antigen .
KEY WHY DONT ANTIGENS ON THE SURGACE OF THE BODY CELL MOT TRIGGER IMMJNE SUSTEMS
As the immune systems recognise these antigens as “self” (normal
Part of the body )
General structures of an antibidy molecule
-name the parts
Fhere are also referred to as immunoglobulins .
There are several different classss of protein .
THE ONE SHOSN IS IMMUNGLOBULIN G of IgG
Need to know this
Antibodies are glycoproteins consisting of 4 polypeptide chains
-we have 2 long heavy chains which are identical to eachother .
-2 shorter lihjt chains also identical toegyehr .
What are the chains held together by ?
-disulfide bridges shown as black lines
How many antigen bonding sites were there ?
There are two antigen binding sites , which are shown .
-Meaninf one antibody molecule bonds to two identical antigen molecules .
What do we cal the antigen binding complex
The antigen antibody complex
What is important about the the tertiary structure of the antigen binding site
It is complementary to the structure of the antigen .
(Antigens fits perfectly into the antigen binding site )
-meaning antibodies are highly specific for the antigen they bind to .
The bing refion is flexible so what does this allow
Allowing the distance between the two antigen binding sites dk vary .
What are antibodies produced by
B lymphocytes
-the role of antibodies in our immune system is known as humeral immunity .
Showing antibodies from
Two different b lymphocytes
As you can see , both a kf bodies have a region which is the same .
Aka the constant region shown in rlhanhe red
What is important about the constant region
The constant region has the same structure for every antibody no matter what b lymphocyte is produced .
HOWEVER : the ends of the antibody molecules are different , Abt are they called ?
These are called variable regions (110 amino acids log. On each chain )
What do variable regions do
The variables regions form the antigen sides .(£3 stone of bair bale regions are different from the anti lefties produced by different b lymphocytes if will bind to different antigens
The human body has millions of different b lymphocytes sometimes of angiogenesis .
WhTtt
First function of antibodies
Opsonins tagging foreign bodies by phagocytosis
Second function of antibodies
Antibodies can stick pathogens togeyher , preventing them from
Spreading around the body ,scientists . call that agglutination
Third function of lymphocytes
By sticking to pathogens aka viruses
Antibodies prevent them from invading host cells .
Fourth function of antibodies
Lastly, antibodies is constructive bacterial toxins, preventing toxins from harming body cells. These antibodies are called antitoxins.
thousands
Thosudanss of different medicines are commonly used to treat humans a -e.g antibiotic , so what’s are they ?
Antibiotics are chemicals used to treat disease caused by bacteria .
-although antibiotics are toxic to bacteria they are relatively harmless for hismnc ells .
Thosudanss of different medicines are commonly used to treat humans a -e.g antibiotic , so what’s are they ?
Antibiotics are chemicals used to treat disease caused by bacteria .
-although antibiotics are toxic to bacteria they are relatively harmless for hismnc ells .
What is a commonly used antibiotic
-penicillin
Which came into use in the 1940:z
Summary of the penicillin discovery (-)
Penicillin was discovered by scientists Alexander’s Fleming .
Fleming was culturing bacteria . Then one day he found that one of his bacterial plates was contaminated with a fungus .
Summary of the penicillin discovery part 2
Fleming noticed that the bacteria near the fungus had been killed
-fhis was produced because the fungus produced a chemical . Which was toxic to bacteria . Sceitntks cl this chemical Lenin .
Overtime penicillin was then used in large quantities , what else have they done to penicillin .
Scientists have chemically modified penicillin to improve its effectiveness.
Soo now we have a c while range of anti bodies vaxes’ k on of no ill in .
Amoxicillin
Doxycycline first one
How was aspirin discovered
Painkiller aspirin was discovered in b willow trees
Where the heart medication digoxin was b discovered in foxgloves .
Soo plants and microorganisms are b an improtant source of
Medicine
The habitats for many of these b organism are being destroyed.
For example , the tropical rainforest
This could lead to the loss of many undiscovered potential medicines.
Soo we need to make sure b we preserve biodiversity .
What is personalised media
Every person responds slightly differently b to different medicinal drugs .
Why is there this difference in drug b reactions?
This can be often due to C the b persons b genetic.
-scientists call this study pharmogenom is
For example some people have alleles which cause their body to break b down drugs more rapidly than other people .
Soo quart can B these alleles do too bb optimum dosage
Can affect optimum dosage how much b is needed to treat the patient
What could be n possible in the b future
A patients genome will be analysed before they are treated .
That way allele variations can be C determined and the best drug treatments can be b decided
How is the way we are producing drugs changing ?
For example , bacteria b and other organism can be genetically engineered to synthesise large quantities of drug molecules .
-scientist s call this synthetic biology:
What may we be b slr b to do in the future n in terms of drug deciding ?
We will be able to design drugs yo precisely fit into target molecules . For C example the enzymes or receptors b proteins found in cancer cells.
Antibodies paly a crucial role in the specific immune system .
Humoral immunity .
-A key part of this process involves a type of cell called T helper cells .
Imagine a pathogen has entered the human body (1)
-Like all the pathogens this is covered with antigen molecules .
Pathogen is engulfed by a macrophage . during phagocytosis .
Imagine a pathogen has entered the human body (2)
The macrophage digests the pathogen and processes the antigen molecules .
Imagine a pathogen has entered the human body (3)
The macrophage now displays the antigens on its surface ,attached to the MHC molecules .
Imagine a pathogen has entered the human body (4)
In this way , the macrophage is acting as an antigen-presenting cell (saw in phagocytosis)
Imagine a pathogen has entered the human body (5)
At this stage , macrophage interacts with the t helper cell .
-like all t lymphocytes , t helper cells are formed int he BONE MARROW and mature in the thymus gland .
Imagine a pathogen has entered the human body (6)
Each t helper cell has a unique t cell receptor on its surface .
-the t cell receptors on each t helper cell are specific for an individual antignen .
Imagine a pathogen has entered the human body (7)
after some time , macrophage will encounter a t helper cell with a receptor that matches the antigen displayed on he macrophages surface .
Imagine a pathogen has entered the human body (8)
The t helper cell now binds its receptor for the antigen .
Imagine a pathogen has entered the human body (9)
the t helper cells also has a surface molecule called CDU which lock onto the MHC molecule on the macrophage .
Imagine a pathogen has entered the human body (10)
Once the t cell receptors is bound to the correct antigen , the t helper cells are attracted .
Imagine a pathogen has entered the human body (11)
activated t helper cells produce chemicals called interleukins which are a type of cytokine .
Imagine a pathogen has entered the human body (12)
the interleukins trigger the activated t helper cells to undergo mitosis , forming identical clones of activated t helper cells .
Imagine a pathogen has entered the human body (13)
interleukins also structurally include macrophages to carry out phagocytosis . the end
where a b lymphocytes formed ?
b lymphocytes are formed int he bone marrow ,w here they also make before being relleased into the blood .
similarities between b and t lymphocytes .
-just like t lymphocytes , b lymphocytes have antigen receptors attached to their surface membrane .
-HOWEVER , in the case of b lymphocytes , the antigen receptors are membrane bound antibodi3es .
-these antibiosis are lgm which are simialr to lgc .
what is important about all the antibodies ono ne b lymphocyte ?
they will bind to the same antigen .
-however , the antibodies’ on a different b lymphocyte will bind to a different antigen .
-as there are millions of b lymphocytes , there will be one that binds for every possible antigen .
If a pathogen has infected the body ,a t some point it will encounter a b lymphocyte , with the correct antibody to bind to the antigen on the pathogens surface .
now the b lymphocyte attaches to the pathogen and the pathogen is engulfe .
pathogen encountering a b lymphocyte (3)
the pathogen is digested and antigens are presented on the surface of the b lymphocytes attach tot he mhc moelclule .
pathogen encountering b lymphocyte (4)
as you can see , b lymphocytes are now acting as an antigen presenting cell .
pathogen encountering b lymphocyte (5)
now the activated t helper cells that we saw earlier use t cell receptors to attaché to the antigen n the b lymphocytes surface .
pathogen encountering b lymphocyte (6)
because the correct b lymphocyte has now selected by the t helper cell , scientists call this clonal selection .
pathogen encountering b lymphocyte(7)
now , the t helper cells produce interleukins which activate the b lymphocyte .
pathogen encountering b lymphocyte (8)
at this stage , the activated b lymphocyte undergoes mitosis forming clones of two types of cells called plasma cells and b memory cells .
-scientist call this clonal expansion .
pathogen encountering b lymphocyte (9)
clonal plasma cells now release identical antibodies which bind to the antigens on the pathogen surface .
-this disables the pathogen and marks it for phagocytosis or triggers agglutination
- what is process of antibody production called ?pathogen encountering b lymphocyte(10)
primary immune response
-this can take days / weeks to develop , during this time , pathogens can reproduce causing the infected person to show symptoms .
do b memory cells remain in the blood ?
pathogen encountering b lymphocyte(11)
yes ready for a second infection with he same pathogen .
-if a second infections happens , the b memory ells rapidly turn into plasm cells and release antibodies.
-this second production of antibodies is called the secondary immune response .
check the graph
as yyouc an see ,s econdary immune response , produces a muc higher level of antiboides .
-this is reposne can effectivelu destoryt he pathogens before anys symptoms ar shown ..
active immunity
t lymphocytes and b les are activated .
-antbioies were porduced and memeorycells were formed .
in humans , active immunity can heppen in two ways .
-wha is the first way ?
-Infected with a pathogen .
-as the pathogen infection is a naurally occuring process . Scienitsts call this natural active immunity .
second way in which active imunity can be achieved .
YoHumans can be vaccionted agaisnt a pthogen .
-vaccines contain dead or weakened pathoegnes or antignens whcih are extracted from pathogens .
What is the role that vaccines do
vaccines stimult immune sytem activaing b and t lymphocytes .
-triggering production of antibodie and the formationof ememoryc ells so vccination is an active immunity .
what is a vaccine known as
because vaccintion is a medical procedurehwe than a natrual process .
-scientisits refer artifical active immunity .
What is passive immnit
IN passive immunity immune isnt a ctive . there is two ways this happnes
passive immunity way one
babbies
-new b0orn babies and not they dont make antiibdoies effectively .
-as their immune system is not fully devloped . however , s fetus , the aby recieves antiviodies from the mother though the placent .
-
how babies get their ntibioies
the first few days aftae r a baby is born ,t heeas milk is rich in ntiboidies .
-the reast milk is called colostrum .
Wha is the role of antibiodies in our immune system referred to s
humoral immunity .
-antiboidies bind to moelcules on the surfac of pathogens –> like bacteira .
-these molecules inludes protiens and polyccharides , scienits call thes emoelcules ANTIGENS .
how does the immune system recognise an anitgen on the pathogens surface
as non self .
-this tirggers an mmune system to poduce antiboddies agaisnt them . t them .
key ; our body cells , do not triggger an immune response .
-what would u describe an immune sytem as ?
the immune styem reconises the body self \9not a freign )
Key : our body cells do not trigger an immune response as it recognise body scales as self
Where are t lymphocytes produced
T lymphocytes are produced in the bone marrow , but then migrate to the thymus gland in your chest .
What do y lymphocytes do , once they are in the thymus gland
The t lymphocytes Mature before being released into the bloodstream.
What to do t is there on the surfce of the membrane
nd what is their jobs .
we find t cell receptors
-as there are millions of unique lymphocytes which can atatch to every posisble antigen .
Key: t lymphocytes only recognise antigens ,w hich are on the surfce of our cells .
one situation where antigens are r
cell is infected with a viurs
-during a viral infecntion , ntigens from the virus attcth to the mhc moelcule . and presented on the surface of the infected cells .
second situation where antigens are recognised
when a mutation ,t akes place , in a norml bodyc ell , turning into cancer cells .
-cancer cells often produce porteins which re not porduced by healthyc ells .
-again , these brnoaml porteins can be attached to mhc and presented on cell surface
third situation where antigens are recognised
cells / tisues have been transplaned from one person into naother .
-int his cse , antingens oplanted into cells will not be ideniical to the antigens on host cells .
-to the host immune system will idnietify these antignens as non-self or foreign .
fourth situaiton where antigens re recognied .
lastly , when a amcrophage enuls a pathogen , the pathogens ont he antignens are dipslayed on the macropahges surfaces .
what is the common thing about all of thes efour situations where antigens are presented .
…..
how are the antiboidies are manfuactured
by onjecting with nactivated tetnus toix .
-these have make antibiodies tot he tenus toixn nd thes entbidoeis are extracted from the horse’s from the blood
what is
What is the common thing about all four of these situations where antigens are displayed on the macrophages surface
-in all of thee cases , cell is acting as an antigen presenting cell .
- in all of theee fweee , the displayed antigen can be recognised as a tlympjocyte , provided that the tlimpjofyte has the correct T cell receptor for that specific antigen .
What is the common thing about all four of these situations where antigens are displayed on the macrophages surface
-in all of thee cases , cell is acting as an antigen presenting cell .
- in all of theee fweee , the displayed antigen can be recognised as a tlympjocyte , provided that the tlimpjofyte has the correct T cell receptor for that specific antigen .
There are several types of t lymphocytes
First one and function
- helper cells - imagine a macrophage has engulfed by any and presented on the cell surface example antigens from a cancer cell
T- helper cells - with the Correct T cell receptor now attached to the surface antigen .
Part two - t helper cell
T helper cell is now activated and undergoes mitosis producing identical clones .
Part three t helper cell
The activated f helper cell also produces molecules interleukins which are a type of cytokines
Part four t helper cell
These interleukins also trigger somehting to increase the rate of phagocytosis .
-the interleukins can also stimulate b lymphocytes to divide by
Logpsod (previously
Learnt )
What is another thing that interleukins do
T helper cells also abridge cytotoxic T cells or t killer cells
What do girl I. Or t killer cells do
-identify abrnomally virally infected. Rlly .
attach to something
-odfcfom somdfhing hu forming holes in the cell membrane .
T helper cells also form t memory cells , explain
T memory cells long lived and can rapidly differentiator into cutocic T cells if ur body is infected with the same pathogen again .
What is the final group of t lymphocytes ?
- t regulator cells
- they regulate the immune system once the pathogen has been destroyed .
-they also have to ensure the body Dosent attack self antigens .
-by doing this , t regulator cells reduce e the chance is auntioimmune disorders like rhenufiidarthritis
Make sure to do b lymphocytes firsttt black sheet before blue sheet
…
Back to the active and passive immunity
- what does the colostrum
The antibodies in the colostrum pass from the baby’/ digestive strum into the baby’s blood steam .
Back to the active and passive immunity
- what does the colostrum
The antibodies in the colostrum pass from the baby’/ digestive strum into the baby’s blood steam .
What type of immunity is the baby going through ?
-As the baby has received antibodies from its motet the baby has SOME IMMUNITY to the pathogens .
HOWEEVER —> as the antibodies were not
Made by the baby’s own immune system —> is a naturally occurring process that takes places in all mammals . NATURAL PASSIVE IMMUNITY
Imagine a patient with tetanus . How is it caused and what effect does this .
Tetanus covered by bacterium found in the soil .
-This bacterium can pass into wounds of the skin .
Tetanus (1)
-in the body , the bacteria produce a toxin , —> causes males to undergo spasms , making them unable to break .
What can tetanus do ?
Tetanus can lead to death , the immune system can produce antibodies against the .
-so patients give an injection of antibodies against the tetanus toxins .
How are the antibodies extracted
And these antibodies are extracted from the horses blood .
- when these antibodies are injected into a patient with tetanus —> fhe antibodies attach to tetanus to prevent it fr harming patient .
What type of immunity is tetanus
-As there another product by sltirnyimminity is a passive immunity . -as this is a medical produces and does not take place naturally ARTIFICAL PSSSIVE IMMUNITY .
Why is both types of passive immunity are temporarily .
-as the antibodies which has been given or gradually broken down .
What are vaccines used for ?
- vaccines can be used to for epidemic and pandemics .
What is an epidemic ?
- is when an infectious disease spreads rapidly in a population , either a specific location such as a city or across a whole country .
What is a pandemic ?
- An infectious disease spreads rapidly across several countries.
-a continent or across the whole world .
/e.g COVID they use of vaccines is a powerful tool in our fight against epidemics and pandemics .
How are vaccines usually given ?
-usuallg giben via mouth , or injection , bloodstream .
What do vaccines contain ?
Vaccines contains antigens from the pathogen , vaccines contains antigens from the pathogen , that we want to protect the body of against it .
What can some vaccines also contain
Attached or weakened strain of a (bacterium or virus )
/in this case. , the bacterium or virus can infect the petting .
-but js js essily fought of the immune system .
Other : vaccines contain cafe risk cells which have been killed
Or what ?
Virus particles which have been inactivated
In these cases , the pathogen cannot cause an infect ?
-but the antigens can trigger an immune response , other vaccines only contain the antigen molecules .
- these antigens may be extracted from the pathogen or they can be manufactured using genetic engineering .
Finally , some vaccines provide protection against a bacterial toxin , heo ?
-Im this case , the vaccines contain toxin molecules which have been modified .
-Thea modifications make the Rodin harmless but still allow it to act as an antigen .
Star one on vaccine groip
-once the vaccines enters the human body , this stimulated a primary immune system .
Star two on vaccine group
This leads to the production of antibodies and b memory cell
Star three vaccine group
T lymphocytes are also activated
Star four on the graph
If the person later comes into contact with the pathogen - then the secondary immune response is triggered .
-In the seoncdary immune response , a large amount antibodies js produced rapidly .
/ in this case , the prjohej is destroyed before many ehmptome kf the disease develop .
What does vaccine allow lerosn to develop ? And what is this called ?
Remember , this is an example of artifical actihr immunity
How are vaccines the concept of herd immunity .
-in any population. , some pope m will not have been vaccination (young children ) or people with a weakened immune suree for them vaccinations may not work effectively.
Herd immunity part two
Bevause , vaccinated people do not catch the disease .
-they cannot pass the pathogen on to the unvaccinated person .
-this means that the unvaccinated person is unlikely to catch the infectious disease .
What happens if enough dk the population has been vaccinated ?
Some protection , to people who have not been vaccinated herd immunity .
How does herd immunity work ?
-only Sofia for a high percentage of people have been vaccinated .
-this can happen for example —> for example , if a large number of people chose not to be vaccinated .
For example flu vaccine
-the effectiveness of vaccines depends on the disease .
-influenza mutates registry and changed the surface antignens .
Scientists call this antigenic variably so people get revax
The cold virus
-types of cold virus / which is why fhere isn’t one set vaccine for cold .
What are bacteria used for and give an example ?
Antibiotics are used to treat bacterial infections .
-peniclllin interefferes sofj the cross-linking of the molecule leriod fly en - which is found in the bacterial cell wall .
What happens when bacteria interfere with the cell wall ? For peniccikkkn
-as the bacteria are now unable to form their cell walls properly . SO when , water enters the bacteria cell walls by by osmosis, the cell bursts .
Penicillin was widespread when ?
-949 , different antibiotics have diffeeent effects on bacteria cells .
-e.g antibiotics are toxic to bacteria they do not human cells
Why don’t antibiroics interfere with viruses ?
As viruses use their host cell to manufacture proteins and reproduce .
- so viruses do not contain why target lodicules to antibiotics to act upon :
So can’t be used for horses
What is the problem with using bacteria ?
-large number of bacterial species have become resistant to antibiotics .
- so they do work and FHESE is cause by overuse antibiotics examole when ur prescribed when it does not be needed or not effective .
How antibiotics resistance develops part one
Random mutations are continually taking blade within bacteria
How antibiotics resistance develops part one part two
Sometimes a bacterium developed a mutation for antibiotic resistance
How antibiotics resistance develops part three
In the acc ende of antibiotics , bacterium has no advantages of the Jon present bacteria so both bacteria have the same chance of surviving and reproducing
How antibiotics resistance develops part four
Antonio is applied and kill the Jon resistant bacteria but resistant bacterium survived
How antibiotics resistance develops part five
As reactant bacteria sr eork diced a large population have a large amount of resistance .
Mess methicill was tewadbsle no teisitsnf
Examole geo c diff the large intestine produce toxins which can lead to diarrhoea and FIFA. The problem is when a patient takes antibiotics for another infection as Cedus is resistant to the antibiotics it will survive and reproduce and then it could take over your whole digestive system.
What can you do to prevent antibiotic resistance?
They use antibiotics, essential and practice hygiene in places where things can spread, but just the hospital
what does hiv mean
human immunodeciencey virus
vir
hiv is an rna virus
containing 2 rna trands k .
-the rna strands are foundithin a protein capitsid .
-iside the capsid m we aksi we also find anzymes inlcuding revrse raspitse .
Jub is an tan vidus contains two rna strands
-the dna strands are found within a protein capsid Janice RHE capsid we also find enzymes is Chong reverse trasncfpats
-on the kfjsids kf hub looks envelop on the reserve we find attached proteins .
The attachment proteins allow hoc to attach to tjis Jake cell .
-inside looks wnvellpe we find the matrix which help to makankfans structure kf virus .
How jog replicates one
Once a person is infected , hives particles circulate the blood steam .
- an infected person is said to be huh psofibe
How jog replicates one
Once a person is infected , hives particles circulate the blood steam .
- an infected person is said to be huh psofibe
What is the main target for T cells
Main one is t helper cells which we saw in a previous video
Huh one
The attachment protein in a hiv attached fona molecule , on the surface of helper T cells are called cd4.
Hub stage two
Once the hiv attaches to the cd4 , the hub lipid envelope fuses with cel memmbrans .
Stage thre jub
Now the capsid and ifs contends pass into the cell .
- af fhis stage , the reverse transcriptase senzhmd converts the viral rna into double stranded dna
HIV state three
At this stage , the reverse transit private now moves into the fellnjicelis and inter heated with the host dna .
Stage four of hiv
-at this stage the bridal dna can remain dormant for several years .
However at some point the hib dna becomes active and produces rna
Stage five of hiv
This includes messenger rna encoding the hiv viral proteins . And the hub rna genome
Stage six of hives
As they leave each virus is surrounded by cell membrane forming thenlopidnengelope kownwnkeyvwtwge of replication of hiv involves the conversion of the rna into dna by reverse transcriptase bevause of this process hiv is an example of a retrovirus .
Stage 8 of hiv
- once hiv becomes active and replicated this leads to the death of the helper T cells
What happens as the number of helper T cells decreed
The patients immune system can no longer function effectively
-without enough helper T cells both antibody production by lymphocytes and the cell mediated immune response becomes less effective .
Stage 9 of hiv
At this point. (£3 patient is described as having acquired immunodeficiency syndrome or aids
-without an effective immune system , the patient is much more vulnerable . To infections such as tuberculosis .
-acis it’s refer to these as opportunistic infections. .
What is a patients with aids also at higher risk of developing
Cancer
8! Fact these diseases are the cause of death in patients with aids .
Key - antibiroics can’t be used to treat viral infections .
-antibiroics kill bacteria by targeting the bacterial cell structures or by targeting the metabolic processes sighing bacterial cells .
Brodie’s do not have any cellular structure so what ?
Rather than having their own metabolism , viruses take advantage of if the metabolic process kf their host cell
For these reasons brisuses cannot be treated using antibiroics .
Sooo how are viral disease reated
Using antiviral drugs for example the antiviral drugs against hives inhibit key enzymes in the hiv replica room cycle such as reverse transcripitatse
