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Biology > MODULE 4: BIODIVERSITY, EVOLUTION AND DISEASE - DISEASE AND THE IMMUNE SYSTEM > Flashcards

MODULE 4: BIODIVERSITY, EVOLUTION AND DISEASE - DISEASE AND THE IMMUNE SYSTEM Flashcards

1
Q

What is a communicable disease?

A

A disease that can spread between organisms

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2
Q

What is a disease?

A

A condition that impairs the normal functioning of an organism

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3
Q

What is a pathogen?

A

An organism that causes diseases (includes bacteria, viruses, fungi and Protocista)

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4
Q

Name three diseases that have the bacterium pathogen

A
  • Tuberculosis (animals, typically humans + cattle)
  • Bacterial meningitis (humans)
  • Ring rot (potatoes + tomatoes)
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5
Q

Name three diseases that have the virus pathogen

A
  • HIV/AIDS (humans)
  • Influenza (animals, including humans)
  • Tobacco Mosaic Virus (plants)
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6
Q

Name three diseases that have the fungus pathogen

A
  • Black Sigatoka (banana plants)
  • Ringworm (cattle)
  • Athlete’s foot (humans)
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7
Q

Name two diseases that have the protocist pathogen

A
  • Potato/tomato late blight(Potatoes/tomatoes)
  • Malaria (animals, including humans)
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8
Q

What is direct transmission?

A

When a disease is transmitted directly from one organism to another

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9
Q

What is indirect transmission?

A

When a disease is transmitted from one organism to another via an intermediate

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10
Q

How can a disease be transmitted directly?

A
  • Droplet infection (sneezing + coughing mucus or saliva droplets onto someone)
  • Sexual intercourse (e.g. HIV)
  • Touching an infected organism (e.g. Athlete’s foot)
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11
Q

How can a disease be transmitted indirectly?

A
  • Air (e.g. Potato/tomato late blight spores)
  • Water (e.g. Potato/tomato late blight spores)
  • Food
  • Vectors (e.g. Malaria w/ mosquitos)
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12
Q

List and explain factors affecting disease transmission

A
  • Overcrowding increases transmission (e.g. TB spread directly via droplets infection OR indirectly by lingering in the air)
  • Climate (e.g. with the changing climate and heat travelling North, mosquitoes can move to new areas and infect AND potato/tomato late blight in wet summers so spores can spread in water)
  • Social factors (HIV risk increased in places where there’s limited access to good healthcare and good health education)
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13
Q

How does skin help defend animals against infection by pathogens?

A
  • The skin is a physical barrier blocking pathogens from entering the body
  • Skin acts as a chemical barrier, producing chemicals that are antimicrobial and can lower pH, inhibiting the growth of pathogens
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14
Q

How do mucous membranes help defend animals against infection by pathogens?

A
  • They protect body openings that are exposed to the environment (e.g. mouth, nostrils, genitals and anus)
  • Some membranes secrete mucus (sticky substance that traps pathogens and contains antimicrobial enzymes)
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15
Q

How does blood clotting help defend animals against infection by pathogens?

A
  • A blood clot is a mesh of proteins (fibrin) fibres
  • Blood clots plug wounds to prevent pathogen entry and blood loss
  • Formed by a series of chemical reactions that take place when platelets (fragments of cells in the blood) are exposed to damaged blood vessels
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16
Q

How does inflammation help defend animals against infection by pathogens?

A
  • Signs of inflammation include swelling, pain, heat and redness
  • Triggered by tissue damage
    ^— damaged tissue releases molecules, increasing permeability of blood vessels so they leak into surrounding areas (causes swelling + isolates pathogens that may have entered damaged tissue)
  • Molecules also cause vasodilation (widening of blood vessels) which increases blood flow to affected area (makes area hot + brings white blood cells to fight of pathogens)
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17
Q

How does wound repair help defend animals against infection by pathogens?

A
  • The skin can repair itself after injury _ re-form a barrier against pathogen entry
  • Surface is repaired by outer layer of skin cells dividing and migrating to the edges of the wound
  • Tissue below the wound then contracts to bring the edges of the wound closer together
  • Repaired using collagen fibres - too. Many collagen fibres = scar
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18
Q

What are expulsive reflexes?

A

Coughs or sneezes initiated upon irritation of the respiratory tract

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19
Q

How do expulsive reflexes help defend animals against infection by pathogens?

A
  • A sneeze happens when mucous membranes in the nostrils are irritated by things such as dust or dirt
  • A cough stems from irritation in the respiratory tract
  • Both coughing and sneezing are an attempt to expel foreign objects, including pathogens, from the body

AUTOMATIC

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20
Q

How does the waxy cuticle help defend plants against infection by pathogens?

A
  • Waxy cuticle provides a physical barrier against pathogen entry
  • May also stop water collecting on the leaf, reducing risk of infection by pathogens that are transferred between plants in water
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21
Q

How does cell walls help defend plants against infection by pathogens?

A
  • Cell walls form a physical barrier against pathogens that make it against the waxy cuticle
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22
Q

How does callose help defend plants against infection by pathogens?

A
  • Plants produce a polysaccharide called callose
  • Callose gets deposited between plant cell walls and plasmas membranes during times of stress (e.g. pathogen invasion)
  • Callose deposition may make it harder for pathogen to enter cells
  • Callose deposition at the plasmodesmata (small channels in the cell walls) may limit the spread of viruses between cells
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23
Q

Give two examples of a plant chemical defence against pathogens.

A
  • Some plants produce saponins - thought to destroy the cell membranes of fungi and other pathogens
  • Plants produce phytoalexins - inhibit the growth of fungi and other pathogens
  • Other chemical secreted by plants are toxic to insects - reduces amount of insect-feeding on plants + reduces risk of infection by plant viruses carried by insect vectors
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24
Q

What are antigens?

A

Molecules (usually proteins or polysaccharides) found on the surface of cells

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25
Q

What do antigens do?

A

When a pathogen (e.g. bacterium) invades the body, the antigens on its cell surface are identified as foreign, whaich activates cells in the immune system
- The immune response involves specific and non-specific stages

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26
Q

What do antigens do?

A

When a pathogen (e.g. bacterium) invades the body, the antigens on its cell surface are identified as foreign, whaich activates cells in the immune system
- The immune response involves specific and non-specific stages

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27
Q

What is the non-specific immune response?

A

Happens the same way for all microorganisms - whatever foreign antigens they have

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28
Q

What is the specific immune response?

A
  • Antigen-specific
  • Aimed at specific pathogens, involving white blood cells called T and B lymphocytes
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29
Q

What are the four main stages of the immune response?

A
  • Phagocytes engulf pathogens
  • Phagocytes activate T lymphocytes
  • T lymphocytes activate B lymphocytes, which divide into plasma cells
  • Plasma cells make more antibodies to a specific antigen
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30
Q

Explain how phagocytes engulf pathogens

A
  • Phagocyte recognises the antigens on a pathogen
  • Cytoplasm of the phagocytes moves around the pathogen engulfing it | Made easier by opsonins (attach to foreign antigens to aid phagocytosis)
  • Pathogen is now contained in a phagosome (vesicle) in the cytoplasm
  • Lysosome fuses with the phagosome | enzymes break down the pathogen
  • Phagocyte then presents the pathogens antigens - sticks the antigens on its surface to activate other immune system cells | Antigenpresenting cell (APC)
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31
Q

Explain how phagocytes activate T lymphocytes

A
  • T lymphocyte surface is covered with receptors, which bind to antigens presented by APCs
  • Each T lymphocyte has 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 activate the T lymphocyte (process is called clonal selection)
  • T lymphocyte then undergoes clonal expansion - divides to produce clones of itself | different types of T lymphocytes carry out different functions
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32
Q

What do opsonins do?

A

Some hide the negative charges on the membrane of the pathogen, making it easier for the negatively-charged phagocyte to get closer to the pathogen

33
Q

What are the types of T lymphocytes?

A
  • T helper cells
  • T killer cells
  • T regulatory cells
  • T memory cells
34
Q

What are T helper cells?

A
  • They release substances (interleukins - type of cytokines) to activate B lymphocytes and T killer cells
  • Interleukins cause phagocyte activity to increase + activate B cells
35
Q

What are T killer cells?

A
  • Attach to and kill cells that are infected with a virus
  • Search for antigen presenting body cells
  • Attach to foreign antigens on the cell surface membranes of infected cells + secrete toxic substances that kill the infected body cells, along with the pathogen inside
  • Secrete perforins that punch holes in cell surface membrane of infected cells, allowing toxins to enter
36
Q

What are T regulatory cells?

A
  • Suppress the immune system from other white blood cells - helps to stop immune systems cells from mistakenly attacking the host’s body cells
  • Prevents T cells from attacking and killing uninfected host cells
  • Shuts down immune system once body is cleared of pathogen
37
Q

What are T memory cells?

A
  • Remain in the blood, so if same antigen is encountered again, the process of clonal selection will occur much more quickly
38
Q

What is clonal selection?

A
  • T cells with T cell receptors complementary to the specific pathogenic antigen bind to the APC
  • Binding to the complementary antigens causes the T cell to be activated
39
Q

What is clonal expansion?

A

Activated T cells divide by mitosis to produce clones

40
Q

What are the types of B lymphocytes?

A
  • Plasma (effector)
  • Memory
41
Q

What happens after T cells are activated?
Explain what happens when T lymphocytes activate B lymphocytes.

A
  • B lymphocytes are covered in antibodies (proteins)
  • 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 of a B lymphocyte meets a complementary shaped antigen, it binds to it - so each B lymphocyte will bind to a different antigen
  • This, together with substances released from T helper cells, activates the B lymphocyte (also clonal selection)
  • Activated B lymphocyte divides but mitosis, into plasma cells and memory cells (also clonal expansion)
42
Q

Explain what plasma cells do after clonal expansion

A
  • Plasma cells are clones of the B lymphocyte (identical)
  • Secrete loads of the antibody, specific to the antigen, into the blood
  • These antibodies will bind to the antigens on the surface of the pathogen to form a lot of antigen-antibody complexes
43
Q

Describe the structure of an antibody

A
  • Antibodies are glycoproteins made of 4 polypeptide chains - two heavy chains + two light chains (each has variable and constant region)
  • Variable region of the antibody form the antigen binding sites - this shape is complementary to a particular antigen | Variable regions differs between antibodies
  • Hinge region allows flexibility when the antibody binds to the antigen
  • Constant region allows binding to receptors on immune system cells (e.g. phagocytes) - constant region is the same in all antibodies (same amino acid sequence)
  • Disulfide bridges (type of bond) hols the polypeptide chains of the protein together
44
Q

How do antibodies help to clear an infection?

A
  • Agglutinating pathogens
  • Neutralising toxins
  • Preventing the pathogen binding to human cells
45
Q

Explain how antibodies agglutinate pathogens

A
  • Each antibody has two binding sites, so an antibody can bind to two pathogens at the same time - the pathogens become clumped together
  • Phagocytes then bind to the antibodies and phagocytose a lot of pathogens all at one - antibodies that act this way are called agglutinins
46
Q

Explain how antibodies neutralise toxins

A
  • Like antigens, 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 (inactivated)
  • Toxin-antibody complexes are also phagocytosed
47
Q

Explain how antibodies prevent the pathogen from binding to human cells

A
  • When antibodies bind to the antigens on pathogens, they may block the cell surface receptors that the pathogens need to bind to the host cells - means that the pathogen can’t attach or infect the host cells
48
Q

Describe the primary response

A
  • When a pathogen enters the body for the first time, the antigens on its surface activate the immune system
  • The primary response is slow because there aren’t any B lymphocytes that can make the antibody needed to bind to it
  • Eventually the body will produce enough of the right antibody to overcome the infection | meanwhile the infected person will show symptoms of the disease
  • After being exposed to an antigen, both T and B lymphocytes produce memory cells - these memory cells remain in the body for a long time
  • Memory T lymphocytes remember the specific antigen and will recognise it a sound time around | Memory B lymphocytes record the specific antibody needed to bind to the antigen
  • The person is now immune - their immune system has the ability to response quickly to a second infection
49
Q

Describe the secondary response

A
  • If the same pathogen enters the body again, the immune system will produce a quicker, stronger immune response - the secondary response
  • Clonal selection happens faster | Memory B lymphocytes are activate and divide into plasma cells that produce the right antibody to the antigen | Memory T lymphocytes are activated to kill the cell carrying the antigen
  • The secondary response often gets rid of the pathogen before you being to show any symptoms
50
Q

Describe the similarities and differences between the secondary and primary responses

A

Primary - Slow | B + T lymphocytes | Symptoms shown | Pathogen enters body for 1st time

Secondary - Fast | Memory cells | No symptoms | Pathogen enters body for 2nd time

51
Q

What structures are found on the surface of T lymphocytes?

A
52
Q

What are the four types of immunity?

A
  • Natural active
  • Artificial active
  • Natural passive
  • Artificial passive
53
Q

Describe natural active immunity

A

Immunity after catching a disease
E.g. having measles as a child, you shouldn’t be able to catch it again later in life

54
Q

Describe artificial active immunity

A

Immunity after being given a vaccination containing a harmless dose of an antigen

55
Q

Describe natural passive immunity

A

When a baby become immune due to antibodies it receives from its mother, through the placenta and in breast milk (colostrum)

56
Q

Describe artificial passive immunity

A

Immunity after being injected with antibodies from someone else
E.g. if you contract tetanus you can be injected with antibodies from the tetanus toxin, collected from blood donations

57
Q

Describe the similarities and differences between active immunity and passive immunity

A

Active - Requires exposure to antigen | Takes a while for protection to develop | Long-term protection| Memory cells are produced

Passive - No exposure to antigen | Immediate protection | Short-term protection | Memory cells aren’t produced

58
Q

Define active immunity

A

The type of immunity you get when your immune system makes its own antibodies after being stimulated by an antigen

59
Q

Define passive immunity

A

The type of immunity you get from being given antibodies made by a different organism- your immune system doesn’t produce any antibodies of its own

60
Q

What is an autoimmune disease?

A
  • Sometimes an organism’s immune system isn’t able to recognise self-antigens (antigens on the organism’s own cells)
  • When this happens, the immune system treats the self antigens as foreign antigens + launches an immune response against the organism’s own tissues
61
Q

Give two examples of an autoimmune system

A
  • Lupus
  • Rheumatoid arthritis
62
Q

Explain what lupus is

A
  • Caused by the immune system attacking cells in the connective tissues
  • This damages the tissues and causes painful inflammation
  • Lupus can affect the skin and joints, as well as organs such as the heart and lungs
63
Q

Explain what rheumatoid arthritis is

A
  • Caused by the immune system attacking cells in the joints
  • Causes pain and inflammation
64
Q

Explain how vaccines help prevent epidemics

A
  • While B lymphocytes are busy dividing to build up their numbers to deal with a pathogen, you suffer from the disease. Vaccination can help avoid this
  • Vaccines contain substances that cause your body to produce memory cells against a particular pathogen, without the pathogen causing disease - means you become immune without getting any symptoms
  • Epidemics can be prevented if a large percentage of the population is vaccinated - that way, even people who haven’t been vaccinated are unlikely to get the disease, because there’s no one to catch it from (herd immunity)
  • The substances in a vaccine may be antigens, which could be free or attached to a dead or attenuated (weakened) pathogen | The substances can also be other molecules, such as mRNA, designed to code for antigens found on a pathogen ? When the mRNA enters the body cells, it provides the instructions needed for cells to produce these antigens, which triggers memory cells to be made
  • Sometimes booster vaccines are given later (after several years) to make sure memory cells are produced
  • Vaccination is not the same as immunisation | Vaccination is the administration of a substance designed to stimulate the immune system | Immunisation of the process by which you develop immunity - vaccination causes immunisation
65
Q

What vaccines are given routinely (to everybody)?

A
  • MMR
  • Meningitis C vaccine
66
Q

What is the MMR?

A
  • Protects against measles, mumps and rubella
  • Usually given to children as an injection at around a year old + again before starting school
  • Contains attenuated measles, mumps and rubella viruses
67
Q

What is the Meningitis C vaccine?

A
  • Protects against the bacteria that cause Meningitis C
  • First given as an injection to babies at 3 months
  • Boosters are given to 1-year-old and teenagers
68
Q

How and why do vaccines change?

A
  • The influenza vaccine changes every year because the antigens on the surface of the influence virus change regularly - forms new strains of the virus
  • Memory cells produced from vaccination with one strain of the flu will not recognise other strains with different antigens - strains are immunologically distinct
  • Every year there are different stains of the influenza virus circulating in the population, so a different vaccine has to be made
  • Laboratories collect samples of these different strains, and organisations, such as the WHO (World Health Organisation) and CDC (Centre for Disease Control) test the effectiveness of different influenza vaccines against them
  • New vaccines are developed and one is chosen every year that is the most effective against the recently circulating influenza viruses
  • Governments and health authorities then implement a programme of vaccination using the most suitable vaccine | Sometimes people are given a vaccine that protects them from a strain causing an epidemic in another country - this helps to stop the strain spreading globally
69
Q

What is an epidemic?

A

When a communicable disease spreads rapidly to a lot of people at a local or national level

70
Q

What is a pandemic?

A

When a communicable disease spreads rapidly across a number of countries and continents

71
Q

What are antibiotics?

A
  • Chemicals that kill or inhibit the growth of bacteria
  • Used as drugs to treat bacterial infections - useful because they can usually target bacterial cells without damaging human body cells
  • Penicillin was the first antibiotic to be isolated (by Alexander Fleming in 1928)
  • Antibiotic use become widespread from the mid-twentieth century - partly thinks to the successful treatment of soldiers with penicillin in WW2
  • Past few decades, we’ve been able to deal with bacterial infections pretty easily using antibiotics - death rate from infectious bacterial disease has fallen dramatically
  • Despite their usefulness, there are risks to using antibiotics - e.g. they can cause side effects + severe allergic reactions
72
Q

Explain antibiotic resistance

A
  • There is genetic variation in a population of bacteria - genetic mutations make some bacteria natural resistant to an antibiotic
  • For the bacterium, this ability to resist an antibiotic is a big advantage - it’s better to be able to survive, even in a host who’s being treated with antibiotics to get rid of the infection, and so it lives for longer and reproduces many more times
  • This leads to the allele for antibiotic resistance being passed on to lots of offspring (example of natural selection) | How antibiotic resistance spreads and becomes more common in a population of bacteria over time
  • This is. A problem for people who become infected with these bacteria, because you can’t easily get rid of them with antibiotics
  • Increased use of antibiotics means that antibiotic resistance is increasing - ‘superbugs’ that are resistant to most known antibiotics are becoming more common | This means we are less able to treat some potentially life-threatening bacterial infections
73
Q

Name and explain two examples of antibiotic resistance

A
  • MRSA (meticillin-resistant Staphylococcus aureus) - causes severe wound infections and is resistant to several antibiotics, including meticillin (used to be called methicillin)
  • Clostridium difficile - infects the digestive system, usually causing problem in people who have already been treated with antibiotics | It is thought that the harmless bacteria that are normally present in the digestive system are killed by the antibiotics, which C. difficile is resistant to - this allows C. difficile to flourish | C. difficile produces a toxin, which causes severe diarrhoea, fever and cramps
74
Q

Give one way of reducing antibiotic resistant

A
  • Doctors are being encourages to reduce their use of antibiotics
    ^— e.g. not to prescribe them for minor infractions and not to prescribe them to prevent infections (e.g. the elderly or people with HIV)
  • Patients are advised to take all of the antibiotics they’re prescribed to make sure the infection is fully cleared and all the bacteria have been killed (which reduces likelihood of a population of antibiotic-resistant bacteria developing)
75
Q

What is cell-mediated immunity?

A

T lymphocytes respond to the cells of an organism that have been changed in some way (e.g. by infection, antigen processing or by mutation and to cells from transplanted tissue)

76
Q

What are the steps in cell-mediated immunity?

A
  • In the non specific defence system, macrophages engulf + digest pathogens in phagocytosis - they process the antigens from the surface of the pathogen to form APCs
  • The receptors on some of the T helper cells fit the antigens - these T helper cells become activated and produce interleukins, which stimulate more T cells to rapidly divide by mitosis | They form clones of identical activated T helper cells that all carry the right antigen to bind to a particular pathogen
  • The cloned T cells may: develop into T memory cells - give a rapid response if pathogen invades again, produce interleukins that stimulate phagocytosis, produce interleukins that stimulate B cells to divide, stimulate the development of a clone of T killer cells that are specific for the presented antigen and then destroy infected cells
77
Q

What is humoral immunity?

A
  • The body responds to antigens found outside the cells (e.g. bacteria and fungi, and to APCs)
  • Produces antibodies that are soluble in blood and tissue fluid and not attached to cells
78
Q

What are the steps in humoral immunity?

A
  • Activated T helper cells will bind to the B cell APC | This is clonal selection - the point at which the B cell with the correct antibody to overcome a particular antigen is selected for cloning
  • Interleukins produced by the activated T helper cells activate the B cells
  • The activated B cell divides by mitosis to give clones of plasma cells and B memory cells (clonal expansion)
  • Cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind to the antigens and disable them, or act as opsonins or agglutinins - PRIMARY IMMUNE RESPONSE (can take days or weeks to become effective | This is why we get ill (symptoms are the result of how our body react when the pathogens are dividing freely
  • Some cloned B cells develop into B memory cells | If the body is infected by the same pathogen again, the B memory cells divide rapidly to form plasma cell clones - these produce the right antibody + wipe out the pathogen quickly before it causes symptoms (SECONDARY IMMUNE RESPONSE)

Biology (26 decks)

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