Communicable Diseases, Disease Prevention and the Immune System Flashcards
(170 cards)
1
Q
Different types of pathogen
A
Bacteria, virus, protoctista, fungi
2
Q
Diseases caused by bacteria
A
Tuberculosis, bacterial meningitis, ring rot
3
Q
Diseases caused by viruses
A
HIV/AIDS, influenza, tobacco mosaic virus
4
Q
Diseases caused by protoctista
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Malaria, potato/tomato late blight
5
Q
Diseases caused by fungi
A
Black sigatoka, ring worm, athlete’s foot
6
Q
Organisms affected by ring rot
A
Potatoes, tomatoes
7
Q
Organisms affected by black sigatoka
A
Bananas
8
Q
Organisms affected by ring worm
A
Cattle
9
Q
Types of transmission of communicable pathogens
A
Direct, indirect
10
Q
Direct transmission
A
The transfer of a pathogen directly from one individual to another
11
Q
Methods of direct transmission in humans
A
Direct contact, inoculation, ingestion
12
Q
Types of direct contact
A
Kissing, contact with bodily fluids, direct skin-to-skin, microorganisms from faeces
13
Q
Things kissing and contact with bodily fluids can pass on
A
Bacterial meningitis, STDs
14
Q
Things direct skin-to-skin contact can pass on
A
Ring worm, athlete’s foot
15
Q
Things microorganisms from faeces can pass on
A
Diarrhoeal diseases
16
Q
Types of inoculation
A
Break in the skin, animal bite, puncture wound, sharing needles
17
Q
Things breaks in the skin can pass on
A
HIV/AIDS
18
Q
Things animal bites can pass on
A
Rabies
19
Q
Things puncture wound/sharing needles can pass on
A
Septicaemia
20
Q
Things ingestion can pass on
A
Amoebic dysentery, diarrhoea diseases
21
Q
Methods of indirect transmission in animals
A
Fomites, droplet infection, vectors
22
Q
Examples of fomites
A
Bedding, socks, cosmetics
23
Q
Things fomites can pass on
A
Athlete’s foot, gas gangrene, Staphylococcus infections
24
Q
Examples of droplet infection
A
Expulsion of saliva and mucus
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Things droplet infections can pass on
Influenza, tuberculosis
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What do vectors do?
Transmit communicable pathogens from one host to another
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Things vectors can pass on
Malaria, bubonic plague, rabies
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Examples of vectors
Mosquitoes, rat fleas, dogs, foxes, bats, water
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Factors affecting the transmission of communicable diseases in animals
Overcrowding living and working conditions, poor nutrition, compromised immune system, poor disposal of waste, climate change, culture, infrastructure, socioeconomic factors
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How can climate change affect transmission of communicable diseases?
Introduce new vectors and new diseases
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Example of direct transmission in plants
Direct contact of a healthy plant with any part of a diseased plant
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Things that direct contact in plants can pass on
Ring rot, tobacco mosaic virus, tomato/potato blight, black sigatoka
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Examples of indirect transmission in plants
Soil contamination, vectors
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Things that soil contamination can pass on
Black sigatoka spores, ring rot bacteria, spores of P. infestans and TMV
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Examples of vectors for plants
Wind, water, animals, humans
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Things that wind as a vector in plants can pass on
Black sigatoka, P. infestans sporangia
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Things that water as a vector in plants can pass on
Potato blight
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Examples of animal vectors in plants
Insects, birds, aphids
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Examples of things humans do as vectors for plants
Hands, clothing, fomites, farming practices, transporting plants and crops around the world
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Things humans as vectors can pass on for plants
TMV, ring rot
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Factors affecting the transmission of communicable diseases in plants
Varieties of crops that are susceptible to disease, over crowding, poor mineral nutrition which reduces the resistance of plants, damp and warm conditions, climate change
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How does climate change affect the transmission of communicable diseases in plants?
Increased rainfall and wind promote the spread of diseases, animal vectors can spread to new areas, drier conditions reduce the spread of the disease
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General pattern of defence in plants
Receptors in cells respond to molecules from the pathogen or chemicals produced when the cell wall is attacked, signalling molecules released which switch on genes in the nucleus, triggers cellular responses such as producing defensive chemicals and sending alarm signal to unaffected cells to trigger their defences
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Structure of callose
Beta 1,3 and 1,6 linkages
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Roles of callose in plant defences
Deposited between cell walls to act as barriers to prevent pathogens entering cell walls around the site of infection, lignin can be added to the callose deposits, blocks sieve tubes in the phloem to sell off the infected part, blocks plasmodesmata between infected cells
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Why can plants react by sealing off and sacrificing?
They are continually growing at the meristems so can replace damaged parts
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Examples of chemicals produced by plants in defence
Insect repellents, insecticides, antibacterial compounds, anti fungal compounds, anti-oomycetes, toxins
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Examples of insect repellents produced by plants
Pine resin and citronella from lemon grass
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Examples of insecticides produced by plants
Pyrethrins from chrysanthemums, caffeine
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Examples of antibacterial compounds produced by plants
Phenols, gossypol from cotton, defensins, lysosomes
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Examples of anti fungal compounds produced by plants
Phenols, gossypol from cotton, caffeine, saponins, chitinases
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Examples of anti-oomycetes
Glucanases
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Glucanases
Enzymes made by some plants that break down glucans
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Glucans
Polymers found in cell walls of oomycetes
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Non-specific animal defences against disease
Skin, blood clotting, wound repair, inflammation, expulsive refluxes, mucous membranes
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How does the skin defend against disease?
Prevents entry, healthy microorganisms that outcompete pathogens, production of sebum that inhibits the growth of pathogens
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How do mucuous membranes defend against disease?
Secrete mucus that traps microorganisms and contains lysozymes and phagocytes
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Blood clotting cascade
The tissue is damaged, platelets are activated by damaged tissues, thromboplastin is released which catalyses the production of thrombin, Ca2+ and prothrombin will affect the production of thrombin, thrombin catalyses the production of fibrin, fibrinogen will affect the production of the fibrin, fibrin forms the clot
59
What does serotonin do in blood clotting and wound repair?
Makes the smooth muscle in the walls of the blood vessel contract so they narrow and reduce the supply of blood to the area
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What happens after clotting in wound repair?
Clot dries out, scab formed to keep pathogens out, epidermal cells below the scab start to grow which leads to permanent sealing and damaged blood vessels regrow, collagen fibres are deposited, new epidermis reaches normal thickness, scab sloughs off
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Inflammatory Response
The localised response to pathogens, resulting in inflammation at the site of a wound
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Characteristics of the inflammatory response
Pain, heat, rednesss, swelling of tissue
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What happens in the inflammatory response?
Mast cells are activated in damaged tissue to release histamines and cytokines
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What do histamines do?
Makes the blood vessels dilate to cause localised heat and redness, raised temperature prevents pathogens reproducing, make blood vessel walls more leaky so blood plasma is forced out in the form of tissue fluid which causes swelling and pain
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Oedema
Swelling
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What do cytokines do in the inflammatory response?
Attract white blood cells
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Phagocytes
Specialised white blood cells that engulf and destroy pathogens
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Types of phagocytes
Neutrophils, macrophages
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What is in pus?
Dead neutrophils and pathogens
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Stages of phagocytosis
Phagocytes recognise non-human proteins on the pathogen, phagocyte engulfs the pathogen, puts it in a phagosome, phagosome fuses with lysosome to form a phagolysosome, lysins from the lysosome digest and destroy the pathogen by hydrolysis, parts of the pathogen absorbed into the cytoplasm
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How do macrophages work? (This is the antigen presenting cell stuff)
Macrophage digests a pathogen, combines antigens from the pathogen surface membrane with glycoproteins in the cytoplasm called the major histocompatibility complex, MHC complex moves the pathogen antigens to the macrophage's own surface membrane to become an antigen presenting cell
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General use of cytokines
Act as cell-signalling molecules to inform phagocytes that they need to move to the site of infection or inflammation, increase body temperature
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General use of opsonins
Chemicals that bind to pathogens and tag them so they can be recognised by phagocytes. Phagocytes have receptors in cell membranes that bid to opsonins so the phagocyte then engulfs the pathogen
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Role of plasma cells
Produce antibodies for a particular antigen and release them into circulation
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Role of T helper cells
CD4 receptors on the cell surface membrane will bind to surface antigens on antigen presenting cells, producing interleukins. Interleukins then stimulate the activity of B cells, increase antibody and T cell production and stimulate macrophages to ingest pathogens
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Role of T killer cells
To destroy the pathogen containing the antigen by producing perforin which kills the pathogen by making holes in the cell membrane
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Role of T regulator cells
To suppress the immune system and regulate it, to stop the immune response once the pathogen has been eliminated, to make sure the body recognises self antigens and does not set up autoimmune response
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When are interleukins particularly important?
In preventing the set up of autoimmune responses
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Role of T memory cells
To provide immunological memory, to rapidly divide to form a large number of clones of T killer cells during the second exposure to the pathogen
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Role of B memory cells
To provide immunological memory, to remember specific antigens and to enable the body to make a rapid response when a pathogen is encountered again
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Process of cell mediated immunity
Macrophages engulf and digest pathogens in phagocytosis, process the antigens from the surface of the pathogen to make APCs, receptors on T helper cells fit some of the antigens in clonal selection, T helper cells become activated and produce interleukins to stimulate more T cell to divide by mitosis in clonal expansion
82
What can the cloned T cells do in the cell mediated response?
Develop into T memory cells, produce interleukins to stimulate phagocytosis or the division of B cells, stimulate the development of a clone of T killer cells that are specific for the antigen
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Process of humoral immunity
Activated T helper cells bind to the B cell APC in clonal selection, interleukins are produced by the activated T helper cells, activate the B cells, activated B cells divide by mitosis to give clones in clonal expansion, cloned plasma cells produce antibodies that act as opsonins or agglutinins in the primary immune response, cloned B cells develop into B memory cells which will divide rapidly to form plasma cell clones if infected again in the secondary immune response
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Humoral immunity
When the body responds to antigens found outside the cells and APCs.
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What does the humoral immune system do?
To produce antibodies that are soluble in blood and tissue fluid but aren't attached to cells
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General structure of antibodies
Made of two polypeptide chains called the heavy chains and two other chains called light chains, chains held together by disulfide bridges, the binding site is an area on both the heavy and light chains called the variable region, the variable region is a different shape on each antibody
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How antibodies defend the body
Antibodies in the antigen-antibody complex can act as an opsonin so the complex is more easily engulfed, act as agglutinins to clump antigen-antibody complexes together, antitoxins
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How do agglutinins help?
They cause antigen-antibody complexes to clump together so they don't spread through the body which makes it easier for the phagocytes to engulf a number of pathogens at the same time
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How do anti-toxins help?
They bind to the toxins produced by pathogens which makes them harmless
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How do opsonins help?
They bind to pathogens and tag them so they can be recognised by phagocytes as phagocytes have receptors on their cell membranes that bind to opsonins so they can engulf stuff
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Important opsonins
Immunoglobulin G, immunoglobulin M
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Natural active immunity
The body has acted to produce its own antibodies and memory cells, making it active, and exposure to the antigen occurred in a not medical intervention way
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How does natural active immunity develop?
Meet a pathogen for the first time, activation of the immune system, antibodies are formed, T and B memory cells produced, meets pathogen for a second time, immune system recognises the antigen, destroys it before causing any symptoms
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Active immunity
Body has acted to produce new antibodies and memory cells
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Example of natural passive immunity
Breastfeeding, placenta
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How does natural passive immunity develop?
First milk a mother makes is called colostrum which is high in antibodies, glycoproteins pass into the baby's bloodstream
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When does natural passive immunity last until?
Until the baby starts to make its own antibodies
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How does artificial passive immunity develop (In the broadest sense of the word)?
Injecting antibodies into the bloodstream
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Examples of diseases that need artificial passive immunity to fight
Tetanus, rabies
100
How does artificial active immunity develop?
Immune system of the body stimulated to make its own antibodies by a safe form of the antigen
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Stages of a vaccination
Pathogen made safe, small amount of safe antigen injected into the blood, primary immune response triggered by foreign antigens and body produces antibodies and memory cells, secondary immune response will be triggered if you come into contact with the pathogen again
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How can a pathogen be made safe?
Killed, inactivated, attenuated strains, altered toxin molecules, isolated antigens from the pathogen, genetically engineered antigens
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Example of pathogen made safe by killing or inactivation
Whooping cough
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Example of pathogen made safe by attenuated strain
Rubella, polio
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Example of pathogen made safe by altered toxins
Diphtheria, tetanus
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Example of a pathogen made safe by isolated pathogens
Influenza
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Example of a pathogen made safe by genetically engineered pathogens
Influenza
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Example of artificial active immunity
Routine vaccinations
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Autoimmune disease
When the immune system stops recognising self cells and starts to attack healthy body tissue
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Examples of autoimmune diseases
Type 1 diabetes, Rheumatoid arthritis, lupus
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Body part affected by type 1 diabetes
Pancreas
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Treatments for type 1 diabetes
Insulin injections, pancreas transplants, immunosuppressant drugs
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Body part affected by Rheumatoid Arthritis
Joints
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Treatment for rheumatoid arthritis
No cure, anti-inflammatory drugs, steroids, immunosuppressants, pain relief
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Body part affected by lupus
Skin, joints, causes fatigue, any organ
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Treatment for lupus
No cure, anti-inflammatory drugs, steroids, immunosuppressants
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Reasons for changes to vaccines
Different strains of a pathogen may have mutated so the antigens are different shapes, if the pathogen spends time inside body cells so is protected by self antigens, if the pathogen spends time inside the immune system itself
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Epidemic
When a communicable disease spreads rapidly to a lot of people at a local or national level
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Pandemic
When a disease spreads rapidly across a number of countries or continents
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Vaccines in epidemics/pandemics
Mass vaccination can prevent the spread of the pathogen into the wider population
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Herd immunity
When a significant number of people in the population have been vaccinated
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Why does herd immunity work?
There is minimal opportunity for an outbreak to occur
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Examples of drugs derived from bioactive compounds
Penicillin, docetaxel, aspirin
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Source of penicillin
Mould growing on melons
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Function of penicillin
Antibiotic
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Source of docetaxel
Yew trees
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Function of docetaxel
Treatment of breast cancer
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Source of aspirin
Compounds from sallow bark
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Function of aspirin
Painkiller, anticoagulant, antipyretic, anti-inflammatory
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Personalised medicine
Combination of drugs that work with your individual combination of genetics and disease
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How is personalised medicine done?
Human genome is analysed
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Pharmacogenomics
Interweaving knowledge of drug actions with personal genetic material
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Example of pharmacogenomics
Breast cancer with mutation of HER2 gene can be shut down by trastuzumab and lapatinib
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Synthetic biology
Developing populations of bacteria or mammals that produce much needed drugs that would be too rare, expensive or not available otherwise
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Nanotechnology
When tiny non-natural particles are used to deliver drugs to a very specific site within cells
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How penicillin was made an economically viable antibiotic
Grown from a mould by Alexander Fleming, not enough could be extracted, Florey and Chain developed industrial process
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How scientists design drugs
Build up 3 dimensional models of key molecules in the body, models of drug molecules built up which are specific for the pathogen, computers search through libraries of chemicals
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Examples of habitats being destroyed
Rainforests, coral reefs
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Need for maintenance of biodiversity
To make sure that we don't destroy an organism that could be used in a life-saving drug
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Example of antibiotics being used to benefit society
At the beginning of the 20th century, 36% of all deaths were from communicable diseases. This had fallen to 7% by the beginning of the 21st century
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Benefits of antibiotics
Selectively toxic, effective against bacteria
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Selective toxicity
Interfering with the metabolism of bacteria without affecting the metabolism of human cells
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Disadvantage of antibiotics
Development of antibiotic resistance
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Causes of antibiotic resistance
Use in agriculture, overprescription, not carrying a course to full
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Where is antibiotic resistance a particular problem?
Hospitals, old people's homes
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Examples of antibiotic resistant bacteria
MRSA, C. difficile
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What is MRSA?
Bacterium carried by 30% of population on skin or in the nose, can cause boils and septicaemia
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Antibiotic used to treat MRSA
Methicillin
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What is C. difficile?
Bacterium in the guts of 5% of the population, produces toxins that damage the lining of the intestines, causes diarrhoea and bleeding and death
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How is overuse of antibiotics causing problems with C. difficile?
Commonly used antibiotics will kill off gut bacteria so C. difficile can survive and reproduce and take hold
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How does antibiotic resistance develop?
Chance mutation in one bacterium makes it antibiotic resistant, antibiotic provides a selection pressure, strong natural selection for antibiotic resistant bacteria, continued selection pressure means almost all bacteria in population are resistant
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How to reduce antibiotic resistant infections
Minimise use of antibiotics, make sure everyone completes courses of antibiotics, good hygiene
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Implications of antibiotic resistant bacteria
Death
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Site of production of B cells
Bone marrow
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Site of maturation of B cells
Bone marrow
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Site of production of T cells
Bone marrow
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Site of maturation of T cells
Thymus gland
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Structure of neutrophils
Multi-lobed nucleus, membrane channels in the plasma membrane, complex cytoskeleton, contain a large amount of glycogen, specialised lysosomes
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Structure of antigen-presenting cells
Antigens released from a pathogen in phagocytosis are on the cell surface membrane bound to the MHC
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Major histocompatibility complex
Set of cell surface proteins used in recognising foreign molecules
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Role of the hinge region
To allow the antigen to bind to more than one antigen
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Role of the constant region
To bind to the phagocyte
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Role of disulfide bridges
To hold the heavy and light chains together
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Neutralisation
Antibody blocks binding sites to prevent the entry of the pathogen into a host cell
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Why does the secondary immune response take less time than the primary immune response?
Time for antigen presentation and clonal selection not required, memory cells divide rapidly and develop into plasma cells
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Why is there a gap in time between infection and appearance of antibodies?
Time for antigen presentation, clonal selection, clonal expansion and the production of antibodies by protein synthesis
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Parasite
An organism that lives in a host and causes it detriment
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Name of bacteria that causes tuberculosis
Mycobacterium
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Immune response
Response to antigens that involves lymphocytes
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How to identify a lymphocyte down a light microscope
Large nucleus, very little cytoplasm, non-granular cytoplasm
