4.1.1 Communicable diseases, disease prevention and the immune system Flashcards
Communicable diseases, disease prevention, and the immune system - Topic 1.1
Communicable diseases, disease prevention, and the immune system - Topic 1.1
Definition
Disease
Impaired functions within the body
Defintion
Health
Good mental and physical wellbeing, plus an absence of disease
Defintion
Infectious disease
A communicable disease that can be transmitted from one organism to another via a pathogen
What is a communicable disease?
They are diseases that can be passed from one organism to another, of the same or different species.
What is a pathogen?
What are the 4 types?
Pathogen: a microorganism that causes disease
4 types:
- Bacteria
- Fungi
- Viruses
- Protocista
What are the components of a bacterial cell?
Bacteria diagram
Contains: (7)
- plasma membrane
- circular DNA
- peptidoglycan celll wall
- capsule
- ribosomes
- cytoplasm
- flagella
Pathogen 1
What are the shapes and function of bacteria?
Cocci (spherical) 🔘:
- has less surface area per volume than bacilli or spirilli so it can survive in denser environments
Vibrio (curved) 🦠:
- has greater S.A:V ratio and can take up nutrients from dilute solutions more efficiently
Bacilli (rod-shaped) ➖:
- has greater S.A:V ratop and can take up nutrients from dilute solutions more efficiently
Spirilli (spiral) 〰️:
- move with a corcscrew motion and therefore meet less resistance from surrouding water
Pathogen 1
Bacteria are characterised by their cell wall
The cell wall affects how bacteria respond to antibiotics.
- Gram Positive:
purple/blue under light micrsocope; stain with crystal violet; e.g. MRSA
- Gram Negative:
red under light microscope; stai with safranin; e.g. e-coli
Pathogen 1
How do bacteria reproduce?
How do bacteria cause disease?
They reproduce via binary fission. To calculate to 2^n. n= no. of divisions
They produce toxins and cause symptoms by cell damage. They damage cell membranes, enzymes, or genetic material.
Pathogen 2
What is the structure of viruses?
What is a bacteriophage?
Structure:
-some genetic material (DNA or RNA) surrounded by a protein shell
-non-living as they cannot replicate by themselves
Bacteriophage: a virus that infects bacterial cells
Pathogen 2
Explain the stages of viral reproduction.
- The virus attaches to a specific host cell
- The genetic material from the virus is injected into the host cell
- The viral genes causes the host cell to make the new viruses
- The host cell splits open releasing the new virus
- Process repeats to other cells producing lots of virus cell
What are the components of a fungus celll?
Fungi diagram
Contains: (7)
- cell wall
- plasma membrane
- cytoplasm
- ribosomes
- vacuole
- mitochondria
- nucleus
Pathogen 3
Fungi
How do fungi grow?
How do fungi cause disease?
- many fungi are sapotrophic and feed on dead and decaying matter
- parisitic fungi feed on living organisms; tese ones are pathogenic
Growth:
budding in yeast (unicellular)
in multicellular fungi, growth occurs at hyphal tips
- they digest living cells and destroy them
- some produce toxins which affect host cells
Pathogen 4
Protoctists
How are they transmitted?
How do they cause disease?
Eukaryotic cells
Protists which cause disease are parisitic
They need a vector to transfer them to their host. They may enter the body directly through water (amoebic dysentry)
They digest and use contents of host cell, then break them open when the new protists emerge. (They don’t take over genetic material)
How do pathogens cause disease?
- travel from host to host
- get into tissues
- reproduce
- cause damage
How are pathogens transmitted?
- vectors
- physical contact
- droplet infection
- non-direct contact
What is direct transmission?
When a pathogen is transmitted directly from one individual to another.
What is indirect transmission?
When a pathogen travels from one individual to another indirectly.
Why is it important to understand how pathogen are transmitted?
It allows us to work out ways to reduce/prevent diseases occuring.
What is a vector?
A living or non living factor that transmits a pathogen from one organism to another.
3 types
What types of direct transmission are there between animals?
1) Direct contact: Any contact with the body fluids of another person; Direct skin to skin contact; Micoroogranisms from faeces transmitted on hands
2) Inoculation: Through a break in the skin; From an animal bite; Through a puncture wound
3) Ingestion; Taking in contaminated food/drink; Transferring pathogens to the mouth from the hands
What types of indirect transmission are there between animals?
1) Fomites: Inanimate objects e.g. bedding socks can transfer pathogens between organsims
2) Droplet infection: Minute drops of saliva and mucus expelled and others breathe in the droplets
3) Vectors: Transmits communicable pathogens from one host to another- usually animals
4) Water: Can act as a vector of diseases
Animals
What are 3 key factors to reduce the spread of disease in humans?
1) regular hand washing
2) improvements in living & working conditions
3) disposal of both bodily & household waste effectively
Factors affecting tranmission in animals
- overcorwded living and wokring conditions
- poor nutrition
- compromised immune system
- poor disposal of waste
- climate change
- culture + infrastructure
- socioeconomic factors
Examples of transmission between humans and animals.
How can this be minimised?
e.g. bird flu strain; brucellosis
minimised by:
- minimising close contact with animals
- washing hands thoroughly folllwoing any contact
What is direct transmission between plants?
Involves direct contact of a healthy plant with any part of a diseased plant.
What types of indirect transmission are there between plants?
1) Vectors: e.g
-wind: bacteria, viruses,fungal,or oomycete spores may be carried on the wind
-water: spores swim in the surface film of water on leaves
-animals: insects and birds carry pathogen and spores from one plant to another as they feed
-humans: pathogens ans spores are transmitted by hands, clothing, fomites, farming practice etc.
2) Soil contamination: infected plants often leave pathogens or reproductive spores from protoctista or fungi in the soil. This can infect the next crop which will be planted on the same soil.
Wht are the 5 key factors to reduce the spread of disease in plants?
1) leave plenty of room between palnts to minimise the spread of pathogens
2) clear fiels as throughly as possible- remove a traces of plants from the soil at harvesting
3) rotate crops
4) follow strict hygiene practices
5) control insect vectors
Wha are the factors affecting transmission in plants?
- planting varieties of crops that are susceptible to disease
- over-crowding increases the likelihood of contact
- poor mineral nutrtion reduces the resistance of plants
- damp, warm conditions & survival & spread of pathogens
- climate change
What is an epidemic?
When a communicable disease spreads rapidly to a lot of people at a local/national level.
What is a pandemic?
When a communicable disease spreads rapidly to a lot of people across a number of countries.
List some bacterial diseases
1) Tubercolosis
2) Bacterial meningitis
3) Ring rot
Tubercolosis
casual agent: mycobacterium
symptoms: bloody cough, weight loss, ashy skin, chest pain
transmission: air-borne drplets
treatments: antibiotics, vaccines
economic impact: 1% of people every year infected, 10-15% get TB later on
Bacterial Meningitis
casual agent: Streptococcus preumoniae
symtpoms: vlotchy rash that doesnt dissapar, temperature, hearing loss, bulging fontanelle, irritability
transmission: nose, thorat, drect, repsiratory
treatments: vaccines, antibiotics
economic impact: 10% of infected die, 25% of infected and recovered have some permenant damage, mainly affects young children an teenagers 15-19
Ring rot
casual agent: Clavibacter michiganesis
symptoms: damages leaves, poattoes (udnergorund) and tomatoes
transmission: direct contact, direct handling of infected and non-infected plants, infected seed tubers
treatments: nothing- farmer has to leave field unsued for 2.5 years
economic impacts: big impact by farmer losing field and crops- redundant field and can’t earn anything from it
List some viral diseases
1) HIV/AIDS
2) Influenza
3) Tobacco mosaic virus
HIV/AIDS
casual agent: human immunodeficiency virus
symptoms: sore throat, tiredness, destroys T-helper cells (w/out this you don’t have an immune system)
transmission: sharing/exchange of bodily fluids, unprotected sex, shared needles, contaminated blood
treatments: anti-retro viral drugs ( because HIV is a retro virus- contains RNA) slow down the progress of the disease
economic impacts: ~39 million (around 70% of global total) have HIV. 800k people have died due to HIV
HIV: infected AIDS: when you get another illness due to HIV (weakened immune system)
What is opportunistic infection?
Infection which develops when immune system is weakened due to a primary infection/ immunodeficiency disorder
Influenza
casual agent: orthomyxoviridae spp.
symtpoms: headache, fever, muscular pain, coughing, runny/stuffy nose
transmission: dropleta, fomites
treatments: vaccines
economic impacts: poultry and swine can be affected by flu and call destroy all of the animals
Tobacco Mosaic virus
casual agent: tobacco mosaic virus
symtpoms: yellow leaves, affects plants leaves, flowers and fruit, stunts growth
transmission: direct contact between leaves, plants, or through farm worker
treatments: no treatment
economic impacts: big economic impacct- can lead to whole crop loss
List some protoctista diseases
1) Malaria
2) Potato/tomato late blight
Malaria
casual agent: Plasmodium species (impacts mosquitoes and humans)
symptoms: flu-like symptoms: high temp/fever, headaches, sweats, chills, vomiting
transmission: bites of infected female, pregnant anopheles mosquitoes (vector transmission)
treatments: anti-malarial tablets, no cure/vaccine; preventative measures: cover up arms and legs, insect repellant, mosquito nets, avoid stagnant water
economic impact: leading causes of death in developing countries, ~90% of death due to malaria occur in sub-sahran africa, half of world’s population are living in malaria affected countries
Potato/Tomato late blight
casual agent: Phytophthora infestans
symptoms: leaves destroyed; damaged fruit, tubers, and leaves due to hyphae
transmission: air-borne spores spread in the wind
treatments: no cure- resistant strains exist
economic impact: causes millions of pounds of damage of crop each year
List some fungal diseases
1) Black sigatoka
2) Ring worm
3) Athletes foot
Black sigatoka
casual agent: Mycosphaerella fijensis
symptoms: attacks and destroys leaves, turning them black and reduces their ability to photosynthesise
transmission: spreads through leaves of plant
treatments: good husbandry and fungicide treatment can control disease spread, no cure
economic impact: can cause 50% reduction in yield
Ring Worm
In cattle:
casual agent: Trichophyton verucosum
symptoms: grey-white, crusty infectious, circular areas of skin, may be itchy
transmission: direct contact with infected cattle
treatments: antifungal creams
Athletes foot
casual agent: Tinia pedia
symptoms: crackling and scaling skin; may become itchy and sore
transmission: direct skin to skin contact or indirectly with contact with an item of clothing
treatments: antifungal creams
How do plants deal with diseased tissue?
What are the 2 types of meristems?
- they seal it off and sacrifice it
- this is possible bevuase plants grow continuossly at the meristems so thye can replace damaged tissue
apical meristems: causes primary growth at shoots/roots
lateral meristems: causes secondary growth (produes bark on trees)
How do plants recognise an attack?
- reccognise pathogens by molecules that are produced
- this ability heps to prevent widespread infection as defence mechanism can be inititated quickly
- when a pathogen tries to enter a plant cell, receptors on the plasma membrane bind to either 1) molecules made by pathogens or 2) products of pathogenic enzymes that break down molecules in the cell wall
- the receptors are activated and cells will then release signalling molecules
- this switches on defensive genes in the nuclues
- this triggers cellular repsones such as producing chemicals, sending alarm singals and strengthening the cell wall
What physcial defences has a plant got?
- Cellulose cell wall: physcial barrier, lignin thiclens ell walll- waterproof and indigestable
- Waxy cuticle: prevents wtaer from collecting on the sruface (pathogens need water)
- Guard cellls: can close the stomata
- Callose: large polysaccharide that is deposited to seal of infected cells from neighbouring ones from the phloem
When is lignin added and what is its purpose?
- It is added once the nucleus has been alerted
- thickens cell wall
- water proof
- indigestable
What is callose?
What is its initial job and purpose for it?
What is the purpose of it in:
- plasmodesmata
- phloem vessels
- A polysaccharide containing beta 1-3 linkages and beta 1 -6 lonkages between the glucose monomers that is important in the plant repsone to infection
Callose is synthesised and depossited between the cell wall and cell membrane in cells next to infected cells.
Done to seal off the infected cells and this prevents pathogens from entering the plant cell around the site of infection
Plasmodesmata: string of cytoplasm through the cell walls
-barrier controlling the movement of molecules between plant cells
-helps in response to various developmental enviromental cues
Phloem vessels:
-blocks sieve plates sealing off infected part and preveting the spread of pathogens
What are non-specific defences?
Do not distinguish one infectious agent from another- respond in the same way
What are specific defences?
Recognise specific antigens
What are primary defences?
1) Barriers to prevent pathogen entry
2) Non-specific
3) Expulsive reflexes
What are some non-specific responses?
1) blood clotting
2) fever
3) inflammatory response
4) phagocytosis
4 barriers
What barriers have we got to prevent pathogen entry?
Skin:
- produces sebum which inhibits pathogen growth
- covers whole body and prvents entry of pathogens
- lots of healthy microogranisms on body which outocmpete pathogens for space on body surface
Mucuous membranes:
- body tracts lined by this
- secrete mucus which contains phagocytes which remove remaining pathogens
- traps microorganisms and contains lysozomes which destory bacterial and fungal cell walls
Lysozomes:
- in tears, urine, and stomach acid
- help to prevent a=pathogens getting into our bodies
Expulsive reflexes:
- coughs and sneezes eject pathogen-laden mucus from the gas exchange system
- vomiting and diarrhoea expel contents of gut alogn with any infective pathogens
What happens during blood clotting?
platelets trigger a chemical reaction cascade that results in the formation of fibrin, which forms a scab.
plateletes secrete:
1) Thromboplastin is an enzyme that catalyses a cascade of reactons resulting in the formation of a blood clot/ fibrin formation
2) Serotonin makes smooth muscle in the walls of the blood vessels contract (vasconstriction) so they narrow and reduce the supply of blood to the area
What is the procces of inflammation?/ What is the inflammatory response?
Local response to infection and tissue damage. It occurs via chemical signalling molecules which cause the migration of phagocytes into the tissue and increased blood flow:
1) Mast cells are activated in damaged tissue in repsone to pathogens/allergens/irritants and they release chemicals callled histamines and cytokines
2) Histamines make blood vessels dilate causing localsied heat and redness- raised temperature prevents pathogens reproducing. They also make blood vssel walls mroe leaky to let more phagocytes out to form more tissue fluid which leads to swelling
3) Cytokines attract white blood cells (phagocytes) to the site
4) Pathogens are disposed by phagocytosis
Why do cytokines encourage the hypothalamus to raise the temperature?
- Most pathogens reproduce best at 37 degrees celcius or lower => higher temperatures inhibit pathogen reproduction
- the specific immune system works better at higher temperatures
What are the different ype of leukocytes? (white blood cells)
Specifci defenses:
1) Lymphocyte: a) T lymphcyte b) B lymphocyte
Non-specifc defences
2) Phagocyte: a) Macrophage b) Neutrophil
What are phagocytes?
What are the 2 types?
Specialised white lood cells that build up at the site of infection
They engulf and destory pathogens
1) Neutrophils: smaller, 60% of all white blood cells, short-lived, multi-lobed nucleus, attracted by histamines
2) Macrophages: larger and involved in antigen presentation, more complex and slower process, round cnulues, cut up pathogen to produce an antigen presenting cell (APC)
What is an outline of phagocytosis?
What is an MHC?
What is an APC?
A pathogen is engulfed by a phagocyte. The pathogen is contained within a vauole called a phagosome and this combines with a lyosome to form a phagolysosome which digests and destroys the pathogen
MHC: major histocompatability complex (protein complex that can bind to a number of antigens
APC: antigen- preseting cell, these antigens now stimulate otther cells involced in the specific immune system response
What are the steps of phagocytosis?
In both neutrophils and macrophage
1) The phagocyte is attracted tot he pathogen by the chemicals it is producing
2) the pahgocyte can recognise th epathogen a being non-self
3) The pahgocyte is able to engulf the pathogen and froms a phagosome
4) A lysosome wil move towards a phagosome and fuse with it fomring a phagolyosome
5) A lysosome contains digestive enxymes
6) The digestive enxymes will then hyrdoluse the pathogen inside the phagolysosome
What is the step of phagocytosis if it continues in a neutrophil?
The whole process would take 10 minutes and waste materials are pushed out of the body
What is the step of phagocytosis if it continues in a macrophage?
1) Another process occurs after hyrdolysis of the pathogen
2) The antigens from the surface ofthe pathogen are comibined with the glycoproteins from the cytoplasm of the macrophage
3) The anitgens are combined with a group of glycoproteins known as MHC
4) The MHC complex moves the antigens towards the cell surface membrane of the macrophage
5) When the anitgens are on the cell surface membrane the macrophage becomes an atigen-presenting celll (APC)
6) The APCcan then stimulate the other cellls in the immune system to respond
What are cytokines?
Phagocytes produce cytokines
Act as self-signalling molecule, infroming other phagocytes that the body is under attack and simulating them to move tp the site of infection/inflammation
Can also increase the body temp and stimulate specific immune system
What are opsonins?
They bind to pathgoens and ‘tag’ them
This is sot hey can be mor easily recognised by phagocytes. phagocytes have receptrs on their cell membranes that bind to commmon opsonins and the pahgocyte then egulfs the pathogen
What are the 2 types of specific immune response?
1) cell mediated repsonse
2) humoral immunity
What is the process of cell mediated response?
1) Macrophages become APCs during non-spefici immune response
2) Receptors on same T-helper cells fit the antigens Clonal selection
3) 3) T-helper cells become activated, producing interleukins and dividing by mitosis Clonal expansion
4) Creates T-helper clones which have the corrrect receptor to bind to pathgoen
5) Cloned T-helper cells:
- develop into T-memory cells
- produce interleukins to stimulate phaocytosis
- produce interleukins to stimulate B cells
- develop into T killer cells that destroy infected cells
What is the process of Humoral immunity?
1) Millions of different B lymphocytes exist with different antibodies in their plasma membranes
2) when a pathogen enters the body, a B cell with the complementary antibody binds to the antigen on it, engulfs it, and processes the antigens to become B-APCs
3) Activated T-helper cells bind to the B-APC Clonal selection
4) Interleukins (from inside activated T-helper cells) activate the B APcell
5) B-APC divides by mitosis creating plasma cells Clonal expansion
6) Plasma cells produce antibodies
7) Some B cells develop into memory cells
What is difference between cell mediated and humoral immunity?
T-lymphocytes can only recognise APCs
B-lymphocytes can recognise free pathogens
Humoral immunity makes specific antibodies
7 of them ( 4 T, 3 B)
What type of lymphocytes are there in the specific immmune response?
1) T helper
2) T killer
3) T memory
4) T regulator
5) Plasma cell (B)
6) B effector
7) B memory
What is the role of a T-helper cell?
binds to the surface antigens on APC
increases antibody production and attracts and stimulates macrophages
makes interukins (type of cytokines) which stimulate B and T cells and macrophages
What is the role of a T-killer cell?
destory pathogen carrying antigen
makes perforin (creates holes in pathogen/infected cell membrane)
What is the role of a T-memory cell?
part pf immunological memory, if near antigen a second time, divide rapidly to form a huge no. of clones
What is the role of a T-regulator cell?
part of immune system acting to control and regulate it
stops immune repsonse once pathogen is eliminated
What is the role of a (B) Plasma cell?
releases anibodies into the bloodstream
produces ~2000 antibodies per second whilst alive
make antibodees for particular antigen
What is the role of a B-effector cell?
divide to from plasma cell clones
What is the role of a B memory cell?
provide immunological memory
programmed to remember a specific antigen and enable body to make rapid response to pathogen again by producing high conc of anitbodies in short period of time -> secondary response
What are antibodies?
produced by plasma cells
Y shaped glycoproteins called immunoglobulins
bind to specific antigens so have a specific, complementary shape
Diagram of antibody
Y
looks like a Y with double lines at top
- constant portion on bottom- allow antiobodies to bind to immune cells
- variable portion on top
- antigen binding site on the tp
- hinge region between straight and diagonal- creates flexibility when multiple antigens are bound
- ligh polpeptide chain and hevay polypeptide chain held together by disulfide bridge
What are the roles of antibodies?
What are agglutins
1) antibody is a part of antibody-antigen act as an opsonin (tags the antigen) sp that the pahgocyte can engulf it
2) prevent entry of pathgoens into host cells once bound to its antigen
3) act as agglutins which clump pathogens togther
4) act as antitoxins by binding to toxins and making them harmless
What is an autoimmune disease?
Why do they occur?
examples?
A condition in which the body’s immune system mistakes its own healthy tissues as foreign and attacks them.
- not yet fully understood
- tend to be genetic
- could be an abnormal response to a pathogen or normal body microorganisms
- could be T regulator cells not wokring properly
- immunosuppressants drug can be used to treat them bu they also supress the normal immune system
e.g.: rheumatoid arthiritis, lupus, odisaris syndrome, sjogren’s syndrome
What are the symtpoms and treatmnets of rheumatoid arthiritis?
symptoms:
- inflammation in joints
- painful deformity and immobility
Treatments:
- no cure
- only treated with immunosuppressants, steroids, anti-inflammtory drug
What are the symtpoms and treatmnets of lupus?
symptoms:
- headaches
- memroy loss
- scartchy rash
- fatigue
- swelling of legs
TreamtnetS:
- no cure
- treated with steroids, immunosuppresants, and anti-inflammatory drugs
What are the symtpoms and treatmnets of odisaris syndrome?
symtpoms:
- 70-90% caused by immune system
- weight loss
- hypotension
- vitiligo
Treamtnets:
- no cure
- must take hormones daily for lide e.g. caticosteroids to repalce cortsiol and adrenaline
- may need more salt in diet
What are the symtpoms and treatmnets of sjogren syndrome?
symtpoms:
- glands ifnlamed
- recues production of tear and saliva causing dry eyes and mouht
Treamtnets:
- no cure
- relive synmptoms with aritificla tears, moisture casuig glasses, chewing sugar free gm, punctal plugs (seal tear ducts)
How does autoimmunity happen?
Primary response to antigen A: - produces antibodies to antigen A
- slow first response
- ill during this time period
- t helper cells binds to anitgens on surface and increase antibody production
- B plasma cells release antiobides into bloodstream and T killer destroys the pathogen
Secondary response to antigen A: -
- T memory cells meet antigen second time and divide rapidlyto form clones
- B memory cells respond rapidly to pathogen so fells less ill or not ill at all
What are vaccines?
A way of artificially activating the immune system to produce antibodies
They can contain:
- whole live micoroogranisms e.g. small pox
- killed/inactive bacteria/viruses
- attentenuated versions
- harmless toxin
- antigens extracted from pathogn e.g. fl-changes shape
- geneticlaly engineered antigens e.g. hepititus
- genetically engineered RNA e.g. covid
Why are these vaccines effective?
- stable pathgoen - doesnt mutate
- live vaccine- more effective (c. 100%)
- easy to produce; cheap; hihg aailability
- esy storage; freeze dried; heat stable
- infected people easy to identify and coooperative
- easy to administer; no ooster needed (only 1 inncoulation)
- no otehr reservoir of infection- only human host
Problems with Vaccines
not all vaccination programmes are completely successful at eradicating diseases
examples:
- measles
- tuberculosis
- malaria
- cholera
-sickle cell anemia
What are two types of eradication programmes?
1) Herd vaccination - (vaccinate most/all people)- stops infection spreading iwthin a population
2) ring vaccination- vaccinate all people around victim - contains spred within ring and stops transmission; trace and isolte contacts; trvael restriciton; make disease notifiable
What are the different types of immunity?
1) Active immunity:
- natural (antibodies developed in resonse to an infection)
- artificial (antiboides developed in response to a vaccination
2) Passive immunity
- natural (antibodies recieved from mother, thorugh breast milk
- artificial (antiobides recieved from a medicine, from a gamma globulin infection or infusion)
Active Natural
Advantages:
- long term immunity
- make memory cells
Disadvantages:
- side ffects
- takes time for an immune response
- may suffer from severe symtpoms
Active Artificial
Advantages:
- lasts longer
- memory cell
- no severe symptoms
Disadvantages:
- side effects
- immune response takes time
- may need boosters
Passive Natural
Advantages:
- immediate protection
- lasts long enough until own made
- relevant to environment
Disadvantages:
- short term effection
- no memory cells produced
- immediate pr
Passive Artificial
Advantages:
- immediate protection- can be life saving
Disadvantages:
- side effects
- temporary
- no memory cells
Why do we need new medicines?
- pathogens become resistant to existing drugs e.g. antibiotics
- new diseases emerge
- new vaccines needed e.g. covid
- existing vaccines can be improved
How are new medicines discovered?
- by accident e.g. penicillin
- traditional medicine
- anaesthetics
- modern research: -analysing genomes of pathogens/ computer modelling of potential drugs
What are some common medicines from living organisms?
5 examples
- digoxin (foxgloves) - heart drug for atrial fibrillation + heart failure
- arnica (wolfsbane) - used to reduce brusing
- diamorphine (opium poppy) - painkillers including codeine + morphine
- Taxol (yewtree) - cancerdrug
- prialt (cone snail) - painkiller, 1000x more effective than morphine
What is pharmogenetics?
using information from the genome to personalise medicine that will worj with the individual’s genetics + disease
Pharmogenetics
What is personalised medicine?
combination of drugs that work with your individual combination of genetics + disease
Pharmogenetics
How has treatment for breast cancer improved as a result of it?
deaths reduced from HER 2 breast cancer by up to 50%
~30% of breast cancers have mutation in this gene
what is synthetic biology?
creating genetically modified organisms that produce drugs
synthetic biology
how can mammals be used to provde therapetic proteins?
g-m to produce much needed therapuetic proteins in milk
synthetic biology
what is nanotechnology?
nanoparticles used to deliver drugs to sites within a cell
Antibiotics
Why are they so widely used?
they were the first medicine to be effective against bacteria
Antibiotics
Why are they becoming less effective?
bactera are becoming more and more resitant to them
Antibiotics
Why do pop.’s of antibiotic-resitant bacteria grow very quickly?
bacteria reproduce very rapidly, so once a mutation occurs, it doesn’t take very long to grow a big population of antibiotic-resistant bacteria
Antibiotics
Where are antibiotics given routinely in animal feed and why illegal in uk?
USA
because evidence suggests over prescription of antibiotics is the prime cause of anitbiotic resistance
Antibiotics
What are 2 species of bacteria showing antibiotic resistance?
How can future antibiotic resistance be reduced?
- MRSA 2. C-difficile
- minimising the use of anitbiotics and ensuring course is complete
- good hygiene in hosptials and care homes
Why does overuse of antibiotics increase the risk of resistance?
overuse of antibiotics applies selection pressure
bacteria has to survive
natural selection becomes more resitant to antibiotics
