Communicable diseases Flashcards
Pathogen
A micro-organism that causes disease
Host
Organism in which a pathogen lives
How do pathogens live on a host
By taking nutrition from their host, which also causes damage in the process
Bacteria
-Prokaryote
-Reproduce rapidly - every 20 mins
-In the host they can multiply rapidly
-Presence causes disease by damaging cells/ releasing toxic waste products
Bacteria in plants
-Live in the vascular tissue
-Cause blackening and death
Examples of bacterial diseases in mammals
-Turberculosis
-Bacterial meningitus
TB
Mycobacterium tuberculosis
A disease that affects many parts of the body, killing the cells and tissues; lungs are most affected
Bacterial meningitis
Streptococcus pneumonia
-Infection of the meninges - membranes that surround the brain and spinal cord
-Membranes become swollen and may cause damage to the brain and nerves
Bacterial diseases in plants
Ring rot
Ring rot
Ring of decay in the vascular tissue of a potato tuber or tomato, accompanied by leaf wilting
How does a fungi infect mammals
Fungus lives in the skin of the animal
-Hyphae forms a mycelium under the skins surface
-Fungus can send out specialised reproductive hyphae, which grow to the surface of the skin to release spores
-Causes redness and irritation
How does a fungi infect plants
Lives in vascular tissue where it can gain nutrients
-Hyphae release extracellular enzymes i.e. cellulases
- Digest surrounding tissue which causes decay before dying
-Leaves will become mottled in colour, curl up, and shrivel before dying
-Fruit and storage organs (tubers- potatoes) will turn black and decay
Fungal diseases in mammals
Ringworm (cattle)
Athletes foot (humans)
Ringworm (cattle)
Growth of fungus in skin with spore cases erupting through skin to feel a rash
Athletes foot (humans)
Growth under skin of feet- particularly between toes
Viruses
Invade cells and take other the genetic machinery and over organelles of the cell
-Cause the cell to manufacture more copies of the virus
-Host cell bursts releasing many new viruses which will infect healthy cells
Viruses in mammals
HIV/AIDS
Influenza
HIV/AIDS
Human immunodeficiency disease
-Attacks cells in the immune system and compromises the immune response
Influenza
‘Flu’ Viruses
-Attacks the respiratory system and causes muscle pains and headaches
Plant viruses
Tobacco mosaic virus
Tobacco mosaic virus
Causes mottling and discoloration of leaves
Protoctista
Animal-like protocists
-Enter host cells and feed on contents as they grow
Malaria
Plasmodium falciparum
-Malarial parasite plasmodium has immature forms that feed on the haemoglobin in RBC
-Causes headache and fever and may progress to coma and death
What organism has been difficult to classify
Phytophthora (blight) was classified as a fungus but moved to protoctsita as it has many features that does not fit with other fungi
Pathogen life cycle
1) Transmission - travels from one host to another
2) entering the host’s tissues
3) Reproducing
4) Leaving the hosts tissues
Transmisson
Passing a pathogen from an infected individual to an uninfected individual
Direct Transmission
Passing a pathogen from host to new host with no intermediary
-Most common form of transmission
E.g of direct transmission
1)Direct physical contact i.e touching a person who is infected/ touching contaminated surfaces (including the soil) that harbor the pathogens.
2)Faecal - oral transmission, usually by eating food/drinking water contaminated by the pathogen
3) Droplet infection - pathogen carried in tiny water droplets in the air
4) Transmission by spores. resistant stage of the pathogen - carried in the air/surfaces/soil
Diseases transmitted through direct physical contact
HIV, Bacterial meningitis, ringworm, athlete’s foot
Factors that affect transmission by direct physical contact
Hygiene:
washing hands regularly - especially after using the toilet
Keeping surfaces clean - door handles
Cleaning and disinfecting cuts and abrasions
Sterilising surgical instruments
Using condoms during sex
Factors that affect transmission by Faecal -oral transmission
Using human sewage to fertilise crops is a common practice in some parts of the world:
-Treatment of waste products and treatment of drinking water are important ways to reduce risk
-Thorough washing of all fresh food (using treated water)
-Careful preparation and thorough cooking of all food
Factors that affect transmission by droplet infection
Catch it- Bin it - Kill it
Cover your mouth when coughing/sneezing
Use a tissue and ensure tissue is disposed of correctly
Factors that affect transmission by spores
Use of a mask
Washing skin after contact with soil
Social factors that affect transmission
-Overcrowding - many people living and sleeping together in a house
-Poorventiliation
-Poor health - particularly if a person has HIV/AIDS as thy ae more likely to contact other diseases
-Poor diet
-Homelessness
-Living/working with people who have migrated from areas where a disease is common
Transmission of TB
Not transmitted easily
-Takes close proximity to people with the disease for long periods of time
-BCG vaccination reduced in teenagers through Western Europe
-Increased migration/ economic migrants living in overcrowded poor ventilated areas causes cases in TB to rise
Indirect transmisson
Passing a pathogen from host to new host via a vector
Vector
An organism that carries a pathogen from one host to another
E.g of a vector
Plasmodium parasite that causes malaria enters the human host via a bite from the female Anopheles mosquito
Indirect transmission of Plasmodium
1) A person with malaria
2) Gametes of plasmodium in blood
3) Female Anopheles mosquito sucks blood
4) Plasmodium develops and migrates to a mosquito’s salivary glands
5) An uninfected person is bitten
6) Plasmodium migrates to the liver
7) Plasmodium migrates to the blood
8) Person has malaria
Direct transmission of plant pathogens
1) Pathogens present in soil will infect plants by entering the roots - especially if damaged as a result of replanting, burrowing animals, movement caused by a storm
2) Airborne transmission - fungi spores (prduced from sexual/asexual repro) carried in the wind
What happens when a pathogen is inside a plant
Infect vascular tissue
-Pathogens in leaves are distributed when leaves are shed and carry pathogen back to the soil where it can grow and infect another plant
Pathogens within fruit and seeds
Distributed in the seeds - so that offspring are infected
Indirect transmission in plants
Occurs as a result of insect attack
-Spores/bacteria become attached to a burrowing insect such as a beetle after it has attacked an infected plant
-When beetle attacks another plant pathogen transmitted
-Beetle -vector
Example of indirect transmission by plants
Fungus that causes Dutch elm disease is carried by the beetle Scolytus multistriatus
Disease and climate
Grow and reproduce more quickly in warm, moist conditions - more common in warmer climates cold climates - die
-A greater variety of diseases and animals/plants more likely to be infected
How are plants a rich source of nutrients
Manufacture sugars in photosynthesis and convert those sugars to a variety of compounds i.e. proteins and oils
Passive defenses
Defensespresent before infection and their role is to prevent entry and spread of the pathogen
-Physical barriers/chemicals
Physical defenses
-Cellulose cell wall
-Lignin thickening of cell walls
-Waxy cuticles
-Bark
-Stomatal closure
-Callose
-Tylose formation
How is the cellulose cell wall a physical defense
Physical barrier and contains variety of chemical defences that can be activated when pathogen is detected
How is the lignin thickening of the cell wall a physical defense
Lignin (phenolic compound) is waterproof and indigestible
How are the waxy cuticles a physical defense
Prevent water collecting on the cell surfaces
Pathogens collect in water and need water to survive, absence - defense
How is the stomatal closure a physical defense
Stomata possible points of pathogen entry
-Stomatal aperture controlled by the guard cells
-When pathogenic organisms are detected, guard cells will close stomata in that part of the plant
How is callose a physical defense
Callose is an large polysaccharide that is deposited in the sieve tubes at the end of the growing season
-Deposited around the sieve plates that block the flow in the sieve tube
-Prevents a pathogen from spreading around the plant
How is tylose formation a physical defense
A tylose is a baloon-like swelling/projection that fills the xylem vessel
-When tylose is formed plugs the vessel and so vessel can no longer carry water
-Blocking xylem prevents spread of pathogens through heartwood
-Tylose contains a high concentration of chemicals (terpenes) that are toxic to pathogens
Xylem - parenchyma cells
As wood ages, parenchyma cells become filled with terpenes
-Eventually will burst into dead cells through a pit connecting the two
-Parenchyma then dies
Chemical defenses
Chemicals have antipathogenic properties: terpenoids, phenols, alkaloids, hydrolytic enzymes
Passive: terpenes in tylose , tannins in bark
But because production requires energy many not formed until after infection
Active defenses
Pathogens attack specific chemicals in cell walls and can be detected by plant cells
Chemicals include specific proteins and glycolipids
-Plant responds by fortifying the defence already present
-Increasing physical defenses and producing defensive chemicals
Active defenses that increase the physical defense
1)Cell walls thickened and strengthened with additional cellulose
2)Deposition of callose between the plant cell wall and plasma membrane near invading pathogen
- Callose impedes cellular penetration at the site of infection
-Strengthens cell wall and blocks plasmodesmata
-Oxidative bursts produce highly reactive Oxygen molecules capable of damaging cells and invading organisms
-Increase in production of chemicals
Chemicals
-Terpenoids
-Phenols
-Alkaloids
-defensive proteins (defensins)
-Hydrolytic enzymes
Terpenoids
Range of essential oils that have antibacterial properties and antifungal properties
-Also create a scent i.e. menthols/ menthones produced by mint plants
Phenols - helps prevent spread of pathogens
Antibiotic/antifungal
Tannins:
-Found in bark inhibit insect attack
-Bind to salivary proteins and digestive enzymes such as trypsin and chymotrypsin, deactivating enzymes
-Insects that ingest high amounts of tannins do not grow and will die
Alkaloids
Nitrogen-containing compounds i.e. caffeine, nicotine, cocaine, morphine, solanine
-Bitter to inhibit herbivore feeding
-Act on a variety of metabolic reactions via inhibiting/ activating enzyme action
-Some alkaloids inhibit protein synthesis
-If plants can reduce grazing by large animals then suffer less damage
Defensive proteins (defensins)
Small cytsteine rich-proteins that have broad anti-microbial activity
-Appear to act upon molecules in the plasma membrane of pathogens possibly by inhibiting the action of ion transport channels
Hydrolytic enzymes
Found in spaces between cells
-Chitinases - break down chitin in fungal cell walls
-Glucanases - hydrolyse the glycosidic bond in glucans
-Lysozymes - degrade bacterial cell walls
Necrosis
Deliberate cell suicide
-Kills plant cells in infected areas and limits pathogens’ access to water and nutrients thus stopping it from spreading further around the plant
-Intracellular enzymes activated on injury
-Enzymes destroy damaged cells and produce brown spots on leaves/dieback
Canker
Sunken necrotic lesion in woody tissue ie. main stem/branch
-Causes death of the cambium tissue in bark
Primary defenses
Non- specific defenses that prevent pathogens entry into the body
What are the primary defenses
-Skin
-Blood clotting and skin repair
-Mucous membrane s
-Coughing/sneezing
-inflammation
The skin as a primary defense
Outer layer - epidermis and consists of layers of cells - Keratinocytes
-Produced by mitosis at the base of the epidermis
-Migrate out to the surface of the skin
-As migrate they dry out and cytoplasm is replaced with the protein keratin - Keratinisation
-30 days
-When cells reach the surface no longer alive
-Keratinsied layer of dead cells acts as an effective defense against pathogens
-Eventually dead cells slough off
What must happen when the skin is damaged
Abrasions/lacerations - the body must prevent excess blood loss by forming a clot, making a temporary seal to prevent infection, and repair the skin
Blood clotting
-Involves calcium ions and 12 factors (Clotting factors)
-many of the factors are released from platelets and from the damaged tissue (factors activate the enzyme cascade)
What must be prevented in blood clotting
Blood clots forming in the blood vessels
Once the clot has formed
Begins to dry out and form a scab
-Scab shrinks as it dries and draws the side of the cut together - temporary seal under which the skin is repaired
Stages of the skin repair
1) Deposition of the fibrous collagen under the scab
2) Stems cells in the epidermis divide by mitosis to form new cells
3) New cells migrate to the edges of curt and differentiate to form new skin
4) New blood vessels grow to supply O2 and nutrients to the new tissue
5) Tissues contract to draw edges of the cut together so repair can be completed
Formation of new skin
1) Deposition of fibrous collagen under the scab
2) Stem cells in the epidermis then divide by mitosis to form new cells
3) New cells migrate to the edges of the cut and differentiate to form new skin
4) New blood vessels grow to supply O2 to new tissues
5) Tissues contract to help draw edges of the cut together so that the repair can be completed
6) Scab released
Enzyme cascade
1) Damage to blood vessels releases clotting factors
2) Platelets bind to collagen to release clotting factors
3) Inactive thrombokinase in blood (factor X) to active thrombokinase (an enzyme)
4)Prothrombin in blood with calcium ions to active thrombin (an enzyme)
5) Solubefibrinoge in plasma to insolube fibrin
6) Fibres attach to platelets in the plug
7) Clot
Other ways in which a clot can be formed
1) Platelets bind to collagen and release clotting factors - temporary platelet plug formed - clot
2) RBC and platelets trapped - clot
Mucous membranes
Certain substances such as food and O2 enter the blood and may harbor microorganisms
-Exchange surfaces thinner and less protected
-Cilia/ goblet cells / extra mucous secreting gland under the epithelium - move down trachea where it can enter esophagus and killed by acidic conditions of the stomach
Where can mucous membranes be found?
Airways
-Gut
-genital areas
-Anus
-Ears
-Nose
Coughing/ Sneezing
The sudden expulsion of air will carry with it the microorganisms
What is inflammation detected by
Detected by mast cells which release histamine
Histamine effects
Vasodilation makes capillary walls more permeable to WBC and some proteins that enter tissue fluid
-Increased production of tissue fluid causes swelling (oedma)
-Excess TF drained into the lymphatic system where lymphocytes stored
Other primary defences
-Eyes are protected by antibodies and enzymes in the tear fluid
-Ear canal is lined by wax which traps pathogens
-Female reproductive system protected by a mucus plug in the cervix and by maintaining acidic conditions in the vagina
Secondary defences
Activated when the pathogen has entered the body
-Recognised as foreign by chemical markers on its outer membrane
Antigens
Membrane-bound chemical markers on the outer membrane used to recognise a pathogen
-proteins/glycoproteins intrinsic to the plasma membrane
-Specific to the organism
-Own cells have antigens but recognised as our own and so do not produce a response
What is an Opsonin
Protein that bind to the antigen on a pathogen and then allow phagocytes to bind
-type of antibody
-Some unspecific and can attach to a variety of pathogenic cells
Role of an opsonin
Role is to enhance the ability of phagocytic cells to bind and engulf a pathogen
Phagocytes
The first line of secondary defense is phagocytosis
-Specialised cells in the blood and tissue fluid engulf and digest the pathogens
Neutrophils
Most common type of phagocyte
A type of WBC that engulfs foreign matter and traps it in a large vacuole (phagosome) which fuses with lysosomes to digest foreign matter
Structure and role of neutrophil
-Multi-lobed nucleus
-Manufactured in the bone marrow
- Travel in blood and squeezed out into tissue fluid
-Short-lived but released in large numbers when infected
-Contain large number of lysosomes
-Engulf and digest pathogens and then die shortly after
Pus
Dead neutrophils that have collected in the area of infection
Phagocytosis
1) Neutrophil binds to opsonin attached to antigen of pathogen
2) Pathogen is engulfed by endocytosis forming a phagosome
3) Lysosome fuse to the phagosome and release lytic enzymes into it
4) After digestion the harmless products can be absorbed into the cell
Fungi plant diseases
Black sigatoka (Bananas)
Causes leaf spots which reduces yield
What do WBC differentiate into
Phagocytes (Neutrophils/macrophages)
Lymphocytes (B cells/ T cells)
What cells mature in bone marrow
-neutrophils
-B cells
Where do you T cells come from
Mature in the thymus gland
What is important to note about each antigen
A different antibody will be made for each
What are specialisations of Phagocytes
-Receptors on plasma Membrane that can bind to opsonin or a specific antigen
-Lobed nucleus
-well developed cytoskeleton
-Many lysosomes containing lysin
-many mitochondria
- ribosomes to synthesise enzymes involved
What does a well developed cytoskeleton for a phagocyte ensure
helps the cell to change shit to engulf pathogens and move lysosomes and vacuoles around inside the cell
Antigen presenting cell
A cell that isolates the antigen from a pathogen and places it on the plasma membrane so that it is recognised by the other cells of the immune system
E.g. of antigen-presenting cells
-Macrophage
-Infected cell
-Pathogens in bodily fluids
Macrophage
-Manufactured in the bone marrow and mature in the lymph nodes
-Travel in the blood as monocytes before settling into bodily tissues
-Large kidney shaped nucleus (largest WBC)
Dendritic cells
Type of macrophage
-Found in the peripheral tissues
Role of macrophages
When it engulfs a pathogen it does not fully digest
-Antigen is saved and moved to a special protein complex on the surface of the cell
-Antigen presenting
What does a lobed nucleus for a phagocyte ensure
that allows the cell to squeeze through narrow gaps
How is a macrophage an antigen presenting cell
It exposes the antigen on its surface so the immune system can recognise the antigen
-Special protein complex ensures antigen-presenting cell is not mistaken for being foreign
Outline the process of the specific immune response
1) Pathogen enters the cell lined with antigens
2) Antigens on pathogen are then presented on antigen presenting cells
3)Lymphocytes are made in the bone marrow (B cells mature here whilst T cells mature in thymus gland)
4)These then undergo clonal selection with the antigen presenting cell
5) clonal expansion (proliferation) occurs
6) Cells differentiate into specific functions
Clonal selection
Activation of the immune response
Selection of specific B/T cells that are specific shape so that it is complimentary to the specific shape of the antigen
How is clonal selection triggered
Contact between the antigen and lymphocytes can be achieved directly when pathogenic cells enter the lymph nodes or by the presentation of antigen-presenting cells
What is clonal expansion (proliferation)
-Once found the correct cells are many clones are made of the cell that has the specific complimentary receptors to the foreign antigen
Differntation
What are the different types of T cells
-T killer cells
-T memory cells
-T helper cells
-T regulator cells
T Killer
Cells that attack and destroy our own body cells that are infected by the pathogen
T memory
Remain in blood providing long-term immunity
T helper cells
Release cytokines that stimulate B cells to develop and stimulate phagocytosis by the phagocytes
T regulator cells
Shut down immune response after pathogen has successfully been removed
Also involved in preventing autoimmunity
What do the B cells differentiate into
B memory cells
Plasma cells which makes antibodies
B memory cells
Stay in the blood and hold the specific shape of the receptor which is complementary to the specific shape of the antigen of the pathogen to trigger when infected with the same pathogen again a faster response
Cells under microscope
Macrophage - Kidney shaped nucleus
Neutrophils - multi-lobed nucleus
B/T - smaller and nucleus fills cell
Cytokines
Hormone like molecules used in cell signalling to stimulate the immune response
How do cytokines work
Specific shape of receptor is complimentary to the specific shape of the cell surface receptor on the target cell
Eg of signalling molecules
-Macrophages release monokines
-T cells/ Macrophages release interleukins
-Many cells release interferon
The release of monokines
Some monokines attract neutrophils ( by chemotaxis- The movement of cells towards a particular chemical)
-Others stimulate B cells to differentiate and release antibodies
The release of interleukins
Stimulate clonal expansion and differentiation of B and T cells
The release of interferon
Inhibits virus replication and stimulates the activity of t killer cells
How does autoimmune disease occur
When antibodies attack own antigens as have receptors which have a specific shape complimentary to our own antigens
-Occurs possibly because antigens that are not normally exposed become exposed to attack
What usually prevents the probability of an autoimmune disease
B/T cells specific to our own antigens are destroyed during early development of the immune system
Causes of autoimmune disease
Not known
Environmental/genetics
e.g of auto immune disease
Arthritis / lupus
Arthiritis
Painful inflammation of a joint course is in certain that starts with antibodies attacking the membranes around the joint
Lupus
Can affect any part of the body causing swelling and pain
-May be associated with antibodies that attack certain proteins in the nucleus in cells and affected tissues
Antibodies
Have receptors with a specific shape that is complimentary to the specific shape of the antigen
-attach to pathogenic antigens neutralising them
-Own antigens recognised by the immune system so do not trigger a response
What type of protein is an antibody
Immunoglobulins (complex proteins produced by plasma cells in the immune system)
Antibody structure
-Y shape
-Two binding sites and and an end that can stimulate phagocytosis
- Variable /Constant region
-4X polypeptide chains 2x heavy 2x light
-disulphide bridges to hold polypeptides together
-Hinge region
Variable region
region with specific shape that is complementary to particular antigen
Constant region
Same in all antibodies may have a sight for easy binding of phagocytic cells
Hinge region of an antibody
to allow flexibility so molecule can grip more than one antigen
What must the immune system do for every antigen detected
-It must manufacture one type of antibody for every antigen that is detected
-it will then attach to the antigen and render it harmless
Why do B cells all carry a slightly different DNA code
So the antibodies it produces are slightly different from other B cells
-Plasma cell cloned from one antibody will all make identical antibodies
Role of opsonin as an antibody
Group of antibodies that bind to antigens on pathogen so phagocytes can recognise foreign cell
-then act as a binding site for phagocytic cells so these can easily find and destroy the pathogen
- Two types: non-specific/specific
Opsonins that are not specific
-Some are not very specific and stick to types of molecules that are not found in the host cell
-Peptidoglycan walls on bacteria
Opsonins that are specific
Produced as part of the specific immune response and bind to very specific antigens
-Neutralisation - Sometimes binds to pathogen before phagocyte comes along so it can’t invade other cells
-Assist in phagocytosis but also prevents pathogen entering a host cell before it can be attacked by phagocytes
Agglutinins
Each antibody has two identical binding sites so can cross-link pathogens
-binds to antigen on pathogen at one binding site and bind to another antigen on another pathogen at another other
Many antibodies clump (agglutinate) together
Advantages of agglutinins
agglutinated pathogens physically impeded from carrying out functions such as entering host cells - noninfective
-can be readily engulfed by phagocytes - particularly effective against viruses
Anti-toxins
-some antibodies bind to molecules that released by pathogenic cells (neutralisation)
- Molecules may be toxic and the action of anti-toxins render them harmless
What does the graph of a primary and secondary response look like
primary response:
-lower concentration of antibodies produced
-takes a few days before number of antibodies in the blood can rise to a level that can combat infection
Secondary response:
-more rapid
-produces a higher concentration of antibodies
Why is the secondary response more rapid
B memory cells produced in primary response stay in the blood and have the memory to create the right antibodies with complimentary receptors to the antigens
-this means it is much faster there is a greater production of antibodies
What happens in the primary response
differentiation occurs
-Takes a few days to happen but create memory cells that stay in the blood
Why don’t you have any symptoms from the pathogen in the secondary response
B memory cells in the blood recognise the antigens on the pathogen and B memory cells rapidly differentiate into B plasma cells that produces antibodies with the specific receptor complimentary to the specific shape of the pathogens antigen
- antibody is fast and occurs in high concentrations
Vaccination
A way of stimulating an immune response so immunity is received provides immunity to specific diseases
- created by deliberate exposure to antigenic material that has been rendered harmless
- antigenic material usually injected but some times can be taken orally
Why are vaccinations effective
immune system treats antigenic material as a real disease
-antibodies and memory cells produced
What are the different forms antigenic material can be used in vaccines
whole life microorganisms
-harmless or attenuated (weakened) version of pathogenic organism
-Dead pathogen
-preparation of antigens from a pathogen
- toxoid which is harmless version of a toxin
Use of whole life organisms for Vaccines
not as harmful as ones that cause real disease but must have similar antigens so antibodies produced will be effective against real pathogen
(e.g.smallpox vaccine which uses similar virus that causes cowpox)
e.g. of diseases where harmless or attenuated (weakened) version of pathogenic organism is used for vaccination
Measles and TB vaccines
e.g. of diseases where a dead pathogen is used for vaccination
Typhoid and Cholera
e.g. of a vaccine where preparation of antigens from a pathogen is used for vaccination
Hepatitis B vaccine
e.g. of a vaccine where a toxoid which is harmless version of a toxin is used for vaccination
tetanus vaccine
What is herd vaccination
using vaccines to provide immunity to all almost all of the population at risk
Once enough people are immune disease can no longer be spread through the population and you achieve ‘herd immunity’
-In order to be effective it is essential to vaccinate almost all population
How many people that need to be vaccinated to prevent the spread of measles
95%
How many people that need to be vaccinated to prevent the spread of smallpox
80-85%
What diseases are vaccinated to immunise young children in the UK
-Tetanus
-Meningitis
-Whooping cough
-Measles
What is ring vaccination
-used when a new case of disease is reported
- involves vaccinating all the people in immediate vicinity of new cases
-May mean vaccinating surrounding houses or even whole villages or towns
-Also used in many parts of the world to control the spread of livestock disease
What is a genetic mutation
Changes antigen so B memory cells may not recognise new antigens
-Pathogen may be transmitted and incidence of the disease increases
What is a deadly about genetic mutations
Replaces other versions of the virus
-affect important parts of the virus
-Increases viruses ability to infect cells
How do variants emerge
In patient with weakened immune system
- unable to beat the virus and instead the body becomes a breeding ground for virus to mutate
Do you vaccine still work against genetic mutations
Most vaccines train immue system to attack several different parts of the virus so eventhough mutated vaccine should still work
-However ‘vaccine escape’ - When virus changes so dodges full affect of vaccine and can continue to infect more people
What is some examples of different variants
Beta Variant S. Africa
Omnicrom
What is an epidemic
-Rapid spread of disease through a high proportion of the population
-when certain pathogens (influenza) Are unstable and regularly undergo changes in the antigens
Why do threats from epidemics need to be monitored
So new strains of the pathogen can be identified
-Enables health authorities to prepare by stockpiling suitable vaccines and vaccinating those who are at particular risk from the disease
What is a pandemic
Worldwide epidemic
Example of a disease that has caused a pandemic
Influenza
Those at particlular risk of influenza
65+
People with respiratory tract conditions
How another pandemic of influenza is prevented
-All people over 65 and at-risk immunized
-New versions of influenza vaccination administered via a nasal spray
-Worldwide research to determine the strain of flu
What is active natural immunity
immunity provided by antibodies made in the immune system as a result of infection
-person suffers from disease once and then is immune (chickenpox)
What is passive natural immunity
antibodies provided by the placenta or breast milk
-makes the baby immune to diseases to which the mother is immune
-useful in the first years of the babies life when it’s immune system is developing
What is active artificial immunity
-immunity provided by antibodies made in a new system as a result of vaccination
-Person is injected with a weakened dead or similar pathogen with antigens and this activates immune system
(TB and influenza)
-Giving antigenic material so you are making antibodies
What is passive artificial immunity
-immunity provided by injection of antibodies made by another individual (hepatitis A and B)
-If antibodies are given no memory cells are made = no immunity
-Stimulates a quick fast response
What are the reasons why we need to find new sources of medicine
-New diseases are emerging
-many diseases where treatment is ineffective
-Some antibiotic treatments are becoming less effective due to the pathogen gaining resistance
What do you use antibiotics against
The growth of fungi or bacteria
What are the two examples of bacteria that have become resistant to antibiotics
-C.diff
-MRSA
How has accidental discovery lead to new sources of medicine
Pencillin
- fungus Pencillium released compounds that kill bacteria
-Observed then scientists purified
How has traditional medicines contributed to sources of new medicines
many drugs have been used for centuries because people have noted that plants/extracts have a beneficial effect
E.g
-Poppies
-Willow bark
Poppies medicinal properties
- morphine and opium for anaesthetic - reduce nervous action in the central nervous system if the nerves cannot carry impulses then no pain is felt
Willow bark medicinal properties
- Relieves pain and fever after discovery of his active ingredient to reduce the side-effect of stomach leading by adding an aceytl group - ibuprofen and aspirin
How does observations of wildlife lead to a sources of new medicines
-Monkeys/bears etc rub citrus oils on the case as insecticides and antiseptics important to prevent insect bites/infection
-Birds line there nests with medicinal leaves in order to protect chicks from mites
What do chimpanzees do that humans have observed
Swallow leaves folded in a particular way to remove parasites from their digestive trac
How has research into disease-causing mechanisms contributed to new medicine
-use of receptors on plasma membrane
-Glycoprotein receptor molecules can be isolated in sequence
-once the amino acid sequence is known molecular modelling can be used to determine the shape of the receptor -Next step is to find a drug that mimics the shape of the receptor and can be used to bind to the virus itself which would block the virus from entering the t helper cells
- in a similar way drugs that inhibit the action of certain enzymes can also be developed
Plant research for medicinal drugs
Research into plants as traditional remedies:
Enables scientists to isolate the active ingredient
molecule can be analyzed and similair molecules can be manufactured
Plant research for medicinal drugs on tropical plants
Great diversity hopes that may contain molecules that form new medicinal drugs
Personalized medicine
The development of designer medicines for individuals
How his personalised medicine contributed to new medicines being found
Sequencing technology and molecular modelling has huge potential for future medicines:
-possible to screen for genomes of plants/microorganisms to identify potential medicine or compounds from DNA sequences
-hoped that this technology can be taken further once technology is fully developed
-may be possible to sequence change from individuals with particular conditions and develop specific drugs for condition
Synthetic biology
The re-engineering of biology
-Production of new molecules that mimic natural processes
-Use of new biological systems that do not exist in nature
How his synthetic biology contributed to new medicine
development of new molecules in particular enzymes that mimic biological systems is one form of synthetic biology
-Another way that synthetic biology is used is to design and construct new devices and systems that may be useful in research/healthcare/manufacturing
What are most antibiotics today derivatives from
Compound made by the genus Streptomyces
Leafcutter ants
Fam fungi which they feed to growing larvae
-In order to prevent infection in fungal gardens they carry symbiotic bacteria including Streptomyces which produce antibiotics
-Scientists are currently researching
