4.1.1 Disease and the Immune System Flashcards
1
Q
What is a disease?
A
- a condition that impairs the normal functioning of an organism
2
Q
What is a pathogen?
A
- a disease-causing organism
- can be bacteria, fungi, viruses and protoctista
3
Q
What is a communicable disease
A
- a disease that can be spread between organisms
- aka infection disease
4
Q
What causes tuberculosis and what does it affect?
A
- bacterium
- animals, typically animals and cattle
5
Q
What causes bacterial meningitis and what does it affect?
A
- bacterium
- humans
6
Q
What causes ring rot and what does it affect?
A
- bacterium
- potatoes, tomatoes
7
Q
What causes HIV/AIDS and what does it affect?
A
- virus
- humans
8
Q
What causes influenza and what does it affect?
A
- virus
- animals
9
Q
What causes tobacco mosaic virus and what does it affect?
A
- virus
- plants
10
Q
What causes black sigatoka and what does it affect?
A
- fungus
- banana plants
11
Q
What causes ringworm and what does it affect?
A
- fungus
- cattle
12
Q
What causes athlete’s foot and what does it affect?
A
- fungus
- humans
13
Q
What causes potato/tomato late blight and what does it affect?
A
- protoctist
- potatoes and tomatoes
14
Q
What causes malaria and what does it affect?
A
- protoctist
- animals
15
Q
What is direct transmission?
A
- when a disease is transmitted directly from one organism to another
16
Q
give examples of direct transmission
A
- direct physical contact
- droplet infection
- sexual intercourse
- transmission by spores
- faecal
17
Q
What is indirect transmission?
A
- when a disease is transmitted from one organism to another via an intermediate
18
Q
Give examples of indirect transmission
A
- intermediates such as
- air
- water
- food
- vector (another organism)
19
Q
What three factors affect disease transmission?
A
- overcrowding: living condition increase transmission of many communicable diseases
e. g. TB is spread directly via droplet infection - climate:
e. g. potato/tomato late blight is common during wet summers because spores need water to spread
e. g. malaria because ideal for mosquito - humans, social factors:
e. g. healthcare and education - poor ventilation
- homelessness
20
Q
Give examples of the primary non-specific defences to prevent pathogens entering an organism
A
- skin
- mucous membranes
- blood clotting
- inflammation
- wound repair
- expulsive reflexes
21
Q
Explain how skin acts as a primary, non-specific defence
A
- physical barrier, blocking pathogens from entering the body
- acts as a chemical barrier by producing chemicals that are antimicrobial and can lower pH, inhibiting growth of pathogens
22
Q
Explain how mucous membranes acts as a primary, non-specific defence
A
- these protect body openings that are exposed to environment such as mouth, nostrils, ears, anus etc
- goblet cells secrete mucous
- mucus lines the passages and traps any pathogens
- epithelium also has militated cells
- they move the mucus to the top of the trachea, where it enter the oesophagus
- it is swallowed and passes down the digestive system
- this is killed by stomach and pathogen’s enzyme denatured
23
Q
Explain how blood clotting acts as a primary, non-specific defence
A
- a blood clot is a mesh of fibrin fibres
- blood clots plug wounds to prevent pathogen entry and blood loss
- they’re formed by a series of chemical reactions that take place when platelets are exposed to damaged blood vessels
24
Q
Explain how inflammation acts as a primary, non-specific defence
A
- include swelling, pain, heat and redness
- can be triggered by tissue damage, as it releases molecules, increasing permeability of blood vessels, leaking fluid and causing swelling
- molecules also cause vasodilation, which increases blood flow
- makes area hot and brings white blood cells to the area to fight off any pathogens
25
Q
Explain how wound repair acts as a primary, non-specific defence
A
- surface is repaired outer layer of skin dividing and migrating to the edges of the wound
- tissues below the wound then contract to being edges of the wound closer together
- repaired using collagen fibres
- scar formed when too many collagen fibres
26
Q
Explain how expulsive reflexes acts as a primary, non-specific defence
A
- e.g. coughing and sneezing
- attempts to expel foreign objects, including pathogens
- occurs automatically
27
Q
Describe physical defences plants have
A
- leaves and stems have a waxy cuticle, which provides a physical barrier against pathogen entry
- may also stop water collecting on the lead, reduces risk of infection that are transferred between plants in water
- plants are surrounded by cell wall
- forms a physical barrier against pathogens that makes it past the waxy cuticle
- plants produce a polysaccharide called callose
- callose gets deposited between plant cell walls and plasma membranes during times of stress
- callose deposition may make it harder for pathogens to enter cells
- callose deposiition at the plasmodesmata may limit the spread of viruses between cells
28
Q
Describe chemical defences plants have
A
- antimicrobial chemicals that kill pathogens or inhibit their growth
e. g. saponins: destroy cell membranes of fungi and other pathogens
e. g. phytoalexins: inhibit growth of fungi - other chemicals are toxic to insects: reduces the amount of insect-feeding on plants,
reduces infection by plant viruses carried by insect vectors
29
Q
What are antigens?
A
- antigens are molecules, usually proteins or polysaccharides, found on the surface of cells
30
Q
What is the difference between non-specific and specific immune responses?
A
- non specific happens the same way for all microorganism
- specific is antigen specific, involving t and B lymphocytes
31
Q
What are the four main stages in the immune response?
A
- phagocytes engulf pathogens
- phagocytes activate T lymphocytes
- T lymphocytes activates B lymphocytes, which divide into plasma cells
- Plasma cells make more antibodies to a specific antigen
32
Q
Describe the first stage in the immune response
A
- a phagocyte recognises the antigens on a pathogen
- the cytoplasm of the phagocyte moves round the pathogen, engulfing it
- this may be made easier by the presence of opsonins, molecules that attach to foreign antigens to aid phagocytosis
- the pathogen is now contained in a phagosome, a type of vesicle in the cytoplasm of the phagocyte
- a lysosome fuses with the phagosome, and the enzymes break down the pathogen
- the phagosome then presents the pathogen’s antigens
- it sticks the antigens on its surface to active other immune system cells
- this is known as an antigen-presenting cell (APC)
33
Q
What is a phagocyte?
A
- a phagocyte is a type of white blood cell that carries out phagocytosis (engulfment of pathogens)
- found in blood and in tissues and carry out a non-specific immune response
34
Q
What are neutrophils?
A
- a type of phagocyte
- first white blood cells to respond to a pathogen inside the body
- neutrophils move towards a wound in response to signals from cytokines, which are released by cells at the site of the wound
35
Q
Describe stage two of the immune response
A
- a T lymphocyte is another type of white blood cell
- surface is covered with receptors
- receptors bind to antigens presented by APCs
- each T lymphocyte has a a different receptor on its surface
- when the receptor on the surface of a T lymphocyte meets a complementary antigen, it binds to it, so each T lymphocyte will bind to a different antigen
- this activates the T lymphocyte, called clonal selection
- then the T lymphocyte undergoes clonal expansion
36
Q
What are the different types of activated T lymphocytes (stage 2)?
A
- T helper cells: release substances to activate B lymphocytes and T killer cells
- T killer cells: attach to and kill cells that are infected with a virus
- T regulatory cells: suppress the immune response from other white blood cells
- some become memory cells
37
Q
Describe the third stage of the immune response
A
- B lymphocytes are another type of blood cell
- they’re covered with proteins called antibodies
- antibodies bind to antigens to form an antigen-antibody complex
- each B lymphocyte has a different shaped antibody on its surface
- when the antibody on the surface meets a complementary shaped antigen, it binds to
- together with substances from T helper cells activates the B lymphocyte
- this is another example of clonal selection
- the activated B lymphocytes divides, by mitosis into plasma cells and memory cells
- this is called clonal expansion
38
Q
What is cell signalling (stage 3)?
A
- how cells communicate
- a cell may release a substance that binds to the receptors on another cell
- really important in the immune response because it helps to activate all the different types of white blood cells needed
- e.g. t helper cells release interleukins (a type of cytokine_ that bind to receptors of B lymphocytes
- activates B lymphocytes
39
Q
Describe stage four of the immune response
A
- plasma cells are clones of the B lymphocyte
- they secrete loads of antibody’s specific to the antigen into the blood
- this will from a lot of antigen-antibody complexes
40
Q
Describe the structure of an antibody
A
- variable region: form the antigen binding sites
- the shape of the variable region is complementary to a particular antigen. differs between antibodies
-hinge region: allows flexibility when the antibody binds to the antigen
- constant regions: allow binding to the receptors on immune system cells. constant region is the same (same sequence of amino acids) in all antibody s
- disulphide bridges hold the polypeptide chains of the protein together
41
Q
How do antibodies help clear infections
A
- agglutinating pathogens: each antibody has two binding sites, so an antibody can bind to two pathogens at the same time, making the clumped together
- phagocytes called agglutinins then bind to the antibodies and phagocytose a lot of pathogens all at once
- neutralising toxins: toxins have different shapes. antibodies called anti-toxins can bind to the toxins produced by pathogens. this prevents the toxins from affecting human cells, so the toxins are neutralised. the toxin-antibody complexes are also phagocytose
- preventing the pathogen binding to human cells: antibodies may block the cell surface receptors that the pathogens need to bind to the host cells. meaning the pathogen can’t attach to or infect host cells
42
Q
Describe why the primary response is slow
A
- when a pathogen enters the body for the first time, the antigens on its surface activate the immune system. this is the primary response
- the primary response is slow because there aren’t many B lymphocytes that can make the antibody needed to bind to it
- eventually the body will produce enough to overcome the infection, but showing symptoms of disease
- after exposure, both B and T lymphocytes produce memory cells, which remain in the body for a long time
- Memory T lymphocytes remember the specific antigen and will recognise it
- Memory B lymphocytes remember the specific antibodies needed to bind to the antigen
- the person is now immune
43
Q
Describe the secondary response
A
- if the same pathogen enters again, immune system will produce a quicker, stronger immune response
- known as secondary response
- clonal selection happens faster
- memory B lymphocytes are activated and divide into plasma cells that produce the right antibody to the antigen
- memory T lymphocytes are activated and divide into the correct type of T lymphocytes to kill the cell carrying antigen
- secondary response often begins before any symptoms are shown
44
Q
What is active immunity?
A
- when your immune system makes its own antibodies after being stimulated by an antigen
45
Q
What are the two different types of active immunity?
A
- natural: when you become immune after catching a disease
- artificial; when you become immune after vaccination
46
Q
What is passive immunity?
A
- the type of immunity from being given antibodies made by a different organism
- immune system doesn’t produce antibodies of its own
47
Q
What are the two types of passive immunity?
A
- natural: when a baby becomes immune due to the antibodies received from mother through placenta and breast milk
- artificial: when you become immune after being injected with antibodies from someone else
48
Q
which type of immunity require exposure to antigen?
A
- active
49
Q
which type of immunity takes a while to develop?
A
- active
50
Q
which type of immunity has long-term protection?
A
- active
51
Q
Which type of immunity produces memory cells?
A
- active
52
Q
What is an autoimmune disease?
A
- when an organism’s immune system isn’t able to recognise self-antigens
- immune system treats the self-antigens as foreign antigens and launches an immune response on its own tissues
53
Q
give examples of autoimmune diseases
A
- lupus: immune system attacking cells in the connective tissues. damages tissues and causes painful inflammation. affects skin, joints, organs
- rheumatoid arthritisL caused by the immune system attacking joints.
54
Q
How do vaccines control disease and prevent epidemics?-
A
- vaccines avoid you suffering symptoms from the disease as the B lymphocytes usually have to divide to deal with pathogen
- vaccines contain antigens that cause your body to produce memory cells against a particular pathogen, without cause disease. you become immune without symptoms
- disease becomes rare if most people in a community are vaccinated. herd immunity. prevents epidemics
- vaccines always contain antigens that may be free, or attached to a dead or attenuated pathogen
- booster vaccines may be given later on to make sure memory cells are produced
55
Q
Is vaccination the same as immunisation?
A
- no
- vaccination is the administration of antigens into the body
- immunisation is the process by which you develop immunity
- vaccination causes immunisation
56
Q
Give examples of routine vaccines
A
- MMR
- meningitis C
57
Q
Why do vaccination programmes change?
A
- flu vaccine changes every year because antigens on the influenza virus change regularly, forming new strains
- memory cells produced from vaccination with one strain will not recognise other strain with different antigens
- the are immunologically distinct
- a different vaccine has to be made every year
- labs such as WHO and CDC collect samples of different strains to test for effectiveness
- new vaccines developed and choose most effective
- governments choose
58
Q
what are antibiotics and why are they useful?
A
- antibiotics are chemicals that kill or inhibit the growth of bacteria
- used by humans to treat bacterial infections
- useful because they can target bacterial cells without damaging human body cells
59
Q
Describe antibiotic resistance and why it is a problem
A
- there is genetic mutation in a population of bacteria
- genetic mutations make some bacteria naturally resistant to an antibiotic
- the bacterium is more adapted for survival and so it lives longer and reproduces
- this leads to the allele for antibiotic resistance being passed onto offspring
- antibiotic resistance spreads and becomes more common over time
- a problem because you can’t get rid of them with antibiotics
- increased use of antibiotics means antibiotic resistance is increasing
- superbugs are becoming more common meaning we are less able to treat potentially life threatening bacteria infection
60
Q
Give examples of antibiotic-resistant bacteria
A
- MRSA (meticillin resistant staphylococcus aureus): causes serious wound infections and is resistant to several antibiotics, including meticillin
- clostridium difficile: infects digestive system. c. difficile produces a toxin, causes fever diarrhoea and cramps
61
Q
Descrive sources of medicine
A
- natural compounds: plants, animals and microorganisms
- only a small population of organism have been investigated so far, so perhaps many more antibiotics
- we need to protect sources of drugs by maintaining biodiversity, or it could die before studied
- using new technique to look at already studied organisms
62
Q
What is the future of medicine?
A
- personalised medicine:
- genes determine how body responds to drugs. different people respond different, making it more effective for some than others.
- personalised medicine is tailored to an individual’s DNA. doctors may be able to predict how you will respond to different drugs and prescribe most effective
- hope more effective drugs
synthetic biology:
- using technology to design and make artificial proteins, cells and microorganisms
- e.g. engineering bacteria to destroy cancer cells
