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Yr 12 Biology A Level > Communicable diseases, disease prevention & the immune system > Flashcards

Communicable diseases, disease prevention & the immune system Flashcards

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1
Q

Define pathogen

A
  • Microorganism that causes disease
  • e.g. virus, bacteria
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2
Q

What are 4 types of pathogen?

A
  • Bacteria
  • Virus
  • Protista
  • Fungi
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3
Q

How do pathogens cause disease?

A

Damage host tissue directly
- e.g. viruses cause cell lysis as particles leave host cell
- e.g. some protists digest host cells as they reproduce
- e.g. fungi digest living cells and destroy them

Produce toxins
- e.g. bacteria produce toxins that damage host cells
- Break down membranes or inactivate enzymes
- e.g. some fungi also produce toxins

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4
Q

Define parasite

A
  • Lives in and gains nutrition from host
  • At the expense of host
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5
Q

Define vector

A
  • Something that carries pathogens from one organism to another
  • e.g. water, mosquitoes
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6
Q

Describe how ring rot is caused in plants

A
  • Bacterial disease
  • Damages leaves, tubers and fruit
  • No cure
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7
Q

What are the economic effects of ring rot?

A
  • Can destroy crops
  • Causes loss of income for farmer
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8
Q

Describe the effects of tobacco mosaic virus (TMV) on plants

A
  • Virus infects tobacco plants and other common fruits and flowers
  • Stunts growth, damages leaves
  • Can lead to almost total crop loss
  • No cure
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9
Q

Describe the effects of potato blight

A
  • Caused by protist
  • Penetrates host cells, destroying leaves, tubes and fruit
  • No cure
  • Resistant plant strains available
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10
Q

What are the effects of TB?

A
  • Destroys lung tissue
  • Suppresses immune system
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11
Q

Describe how the bacteria that causes TB is transmitted from one individual to another

A
  • Droplets containing pathogen released by coughing / sneezing
  • Inhaled by uninfected individual
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12
Q

Give the factors that increase the likelihood of contracting TB

A
  • Not vaccinated against TB
  • Weakened immune system (e.g. HIV)
  • Overcrowding
  • Consumption of milk or beef from infected cattle
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13
Q

How is TB treated?

A

Using antibiotics

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14
Q

How is the spread of TB prevented?

A
  • Improving living conditions
  • Vaccinations
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15
Q

What are the effects of bacterial meningitis?

A
  • Infects membrane on surface of brain
  • Can spread around body causing septicaemia
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16
Q

How is bacterial meningitis treated?

A
  • Antibiotics can cure disease
  • Vaccines can protect against disease
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17
Q

What does AIDS stand for?

A

Acquired Immunodeficiency Syndrome

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18
Q

Describe the structure of HIV

A
  • Retrovirus
  • Contains RNA and reverse transcriptase enzyme
  • Protein coat (capsid)
  • Surrounded by phospholipid bilayer formed from cell-surface membrane of host
  • Glycoproteins in bilayer allow virus to re-infect new host cells
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19
Q

Describe the action of HIV

A
  • Infects T-lymphocytes
  • Reverse transcriptase converts viral RNA to DNA in host nucleus
  • Viral DNA inserted into host DNA
  • Viral mRNA produced to code for viral proteins
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20
Q

How does HIV develop into AIDS?

A
  • HIV infects T lymphocytes
  • Causes reduction of active lymphocytes
  • Loss of ability to make antibodies (AIDS) results in lower immunity
  • Infections that would usually be destroyed by body no longer are and can be fatal
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21
Q

How can HIV be spread?

A
  • Blood on hypodermic needles shared by intravenous drug users
  • Across the placenta during pregnancy
  • Breast feeding
  • Infected blood transfusions
  • Small cuts in the penis, vagina, mouth, intestine during sex
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22
Q

What type of infective agency causes influenza (flu)?

A

Virus

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23
Q

Suggest why the influenza vaccine has to be changed each year

A
  • Flu virus mutates regularly
  • Different strains of the virus arise due to mutation
  • New strains have different antigens
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24
Q

Name the parasite that causes malaria

A

Plasmodium

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25
Q

Name the vector for the malarial parasite

A

Female Anopheles mosquito

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26
Q

Which human cells do malarial parasites reproduce in?

A
  • Hepatocytes (liver cells)
  • Erythrocytes
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27
Q

Describe how the female Anopheles mosquito transmits the malarial parasite to a humans

A
  • Mosquito is vector
  • Plasmodium present in mosquito saliva
  • Infected mosquito bites human
  • Plasmodium passes from saliva to blood
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28
Q

How is the spread of Plasmodium controlled?

A
  • Insecticides used to kill Anopheles mosquitoes
  • Removing breeding sites (standing water)
  • Use mosquito nets
  • Wear long-sleeved clothing
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29
Q

Identify the infective agent that causes ring worm

A

A fungus

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30
Q

Identify the infective agent that causes athlete’s foot

A
  • A fungus
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31
Q

How is ring worm and athlete’s foot treated?

A

Antifungal creams

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32
Q

Define direct transmission

A

Pathogen transferred from one individual to another - host to host

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33
Q

Give examples of direct transmission

A

Direct contact
- e.g. sexual intercourse, faecal-oral transmission, skin-to-skin contact
- e.g. direct contact of healthy plant with diseased plant

Inoculation
- Enters blood stream
- e.g. through break in skin, animal bite, sharing needles

Ingestion
- Consuming contaminated food or drink

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34
Q

Define indirect transmission

A

Pathogen travels from one individual to another via an intermediate

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35
Q

Give examples of indirect transmission

A

Fomites
- Objects such as clothing, bedding etc.
- e.g. athlete’s foot

Droplet infection
- Inhalation of droplets of saliva from sneezing/coughing
- e.g. TB, influenza

Vectors
- Transmit pathogens from one host to another
- e.g. female Anopheles mosquito transmits

Soil contamination (plants)
- Pathogens or spores left in soil by infected plants
- Can infect new crops
- e.g. black sigatoka, ring rot

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36
Q

Explain the difference between direct and indirect transmission

A

Direct
- Pathogen spread directly from one organism to another

Indirect
- Pathogen spread from one organism to another through another medium
- e.g. the air, water, a vector

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37
Q

Why is direct transmission more common in animals than plants?

A
  • Animals can move around
  • Means direct contact more likely
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38
Q

Give factors that increase the transmission of communicable diseases in humans

A
  • Weakened immune system (e.g. caused by HIV)
  • Poor diet / lack of protein
  • Homelessness / overcrowding increases likelihood of close contact
  • Poor ventilation in housing increases likelihood of indirect transmission
  • Climate change can introduce new vectors and diseases
  • Socioeconomic factors, e.g. lack of trained health workers
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39
Q

Give factors that increase the transmission of communicable diseases in plants

A
  • Planting varieties of crops that are susceptible to diseases
  • Over-crowding of plants increases likelihood of contact
  • Poor mineral nutrition reduces resistance of plants
  • Damp, warm conditions increase pathogen survival
  • Climate change
  • Increased rainfall and wind promote the spread of disease
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40
Q

Describe how a plant’s response to a pathogen is triggered

A
  • Receptors in plant respond to antigens from pathogens
  • Or to chemicals produced by plant cell wall when attacked
  • This stimulates release of signalling molecules
  • Switch on genes in the nucleus, triggering cellular response
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41
Q

What is callose?

A
  • Polysaccharide of β-glucose
  • 1,3 and 1,6 linkages
  • Produced by plants when attacked by pathogens
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42
Q

Describe the use of callose as a physical defence in plants

A
  • Callose barriers immediately synthesised upon infection
  • Deposited between cell walls and cell membranes in cells next to infection
  • Callose and lignin deposited in cell walls longer term
  • Callose blocks sieve plates to prevent spreading through the phloem
  • Callose deposited in plasmodesmata to prevent spread of pathogens from one cell to
    another
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43
Q

Describe the chemical defences that plants employ against pathogens

A
  • Insect repellents (e.g. pine resin, citronella)
  • Insecticides (e.g. caffeine is toxic to fungi and insects)
  • Antibacterial compounds (e.g. phenols act as antibiotics)
  • Antifungal compounds (e.g. chitinase enzymes break down chitin in fungal cell walls)
  • General toxins (e.g. cyanide is toxic to most living things)
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44
Q

Define non-specific defence

A

Able to break down or prevent entry from a range of different pathogens

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45
Q

What are non-specific defences used by animals?

A
  • Physical barriers
  • Production of enzymes and acids
  • Blood clotting at wounds
  • Inflammatory responses
  • Phagocytosis
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46
Q

Describe how entry of pathogens is prevented in animals

A
  • Tough skin acts as a physical barrier
  • Sebaceous glands secrete lactic acid and fatty acids preventing growth of pathogens
  • Mucous membranes (nose, trachea, vagina) trap pathogens
  • Lysozymes in tears and urine kill bacteria
  • Stomach acid destroys pathogens
  • Expulsive reflexes (e.g. sneezing) ejects pathogens from gas exchange system
47
Q

What is the role of cilia?

A
  • Waft mucus ladened with bacteria up to the mouth
  • Mucus swallowed
  • Bacteria destroyed by hydrochloric acid in the stomach
48
Q

Describe the role of platelets

A
  • Secrete clotting factors
  • Clot the blood at the site of a wound
49
Q

Explain how cuts in the skin are sealed by blood clotting

A
  • Thromboplastin and serotonin released from platelets
  • Thromboplastin triggers clotting process involving a cascade of reactions
  • Results in thrombin causing rapid conversion of fibrinogen into fibrin
  • Fibrin makes a mesh to seal the wound
  • Serotonin makes smooth muscle in blood vessels contract
  • Vessels narrow to reduce blood supple to area
50
Q

What is an inflammatory response?

A
  • Localised response to pathogens or damage
  • Results in inflammation at the site
51
Q

What is the role of mast cells in the inflammatory response?

A
  • Activated in damaged tissue
  • Secrete histamines and cytokines
52
Q

What are the physical signs of inflammation?

A
  • Pain
  • Heat
  • Redness
  • Swelling of tissue
53
Q

What is the role of histamine in the inflammatory response?

A

Makes blood vessels dilate
- Causes localised heat and redness
- Raised temperature helps prevent pathogen reproduction
Makes blood vessel walls ‘leaky’
- More blood plasma containing phagocytes forced out to become tissue fluid
- Causes swelling and pain

54
Q

Define allergy

A

Reactions by the immune system to usually harmless substances
- e.g. bee stings, pollen, nuts

55
Q

Describe what happens in an allergic reaction

A
  • Over-activation of mast cells
  • Over-secretion of histamine
  • Leads to inflammation of tissues, itching, sneezing, mucus secretion
  • Serious effect: anaphylaxis, swelling of throat and mouth, death
56
Q

What is the role of cytokines in the inflammatory response?

A

Attract phagocytes to site of infection/damage (cell signalling)

57
Q

What are the two types of phagocyte?

A
  • Neutrophils
  • Macrophages
58
Q

Describe the role of phagocytes

A
  • Destroy pathogens by ingesting them
  • Can squeeze out of the walls of capillaries
  • Engulf pathogens by endocytosis
  • Enzymes digest pathogens
  • Non-specific immune response
59
Q

Outline how phagocytes ingest pathogens

A
  • Phagocytes attracted to foreign pathogen (chemotaxis)
  • Foreign matter engulfed by phagocyte (phagocytosis)
  • Pathogen enclosed in phagosome
  • Phagosome fuses with lysosome to form phagolysosome
  • Lysosome contains lysozyme enzymes
  • Pathogen digested
  • Products absorbed into cytoplasm by diffusion
60
Q

What is the major histocompatibility complex (MHC)?

A
  • Glycoproteins found in cytoplasm of macrophage
  • Can combine with antigens from pathogen
61
Q

What happens once a macrophage digests a pathogen?

A
  • Antigens from pathogen combined with MHC in cytoplasm
  • MHC displayed on macrophage cell surface membrane
  • Macrophage become antigen presenting cell (APC)
62
Q

What are opsonins?

A

Chemicals that bind to pathogens
- Make pathogens easier to recognise by phagocytes
- e.g. IgG and IgM antibodies

63
Q

What are the two types of white blood cells?

A
  • Lymphocytes
  • Phagocytes
64
Q

What is the role of macrophages in the specific immune response?

A
  • Engulf and digest pathogens
  • Display antigens
  • Activate T lymphocytes
65
Q

Where do T lymphocytes mature?

A

Thymus gland

66
Q

Where do B lymphocytes mature?

A

Bone marrow

67
Q

What is the role of T killer cells?

A

Destroy pathogens by producing perforin

68
Q

What is the role of T memory cells?

A

Provide immunity - circulate in blood and recognise specific antigens

69
Q

What is the role of T regulator cells?

A

Control immune response once pathogen eliminated

70
Q

What is the role of plasma cells?

A

Produce and release antibodies specific to an antigen

71
Q

What is the role of B memory cells?

A

Provide immunity - circulate in blood and rapidly produce antibodies
upon reinfection

72
Q

Describe cell-mediated immunity

A

T lymphocytes respond to changes in an organism’s own cells
- e.g. viral infection, antigen processing (macrophage), cancer cells, transplanted
tissue

73
Q

Describe humoral immunity

A
  • Body responds to antigens found outside of cells
  • e.g. bacteria and fungi
  • B plasma cells produce antibodies
74
Q

Define clonal selection

A

Lymphocyte with correct antibody complementary to a specific antigen is selected for cloning

75
Q

Define clonal expansion

A

Activated lymphocyte divides by mitosis
- Produces clones

76
Q

Describe the cell-mediated immune response

A
  • Macrophages engulf and digest pathogen
  • Display antigen from pathogen (become APC)
  • T helper cells bind to specific antigens and are activated (clonal selection)
  • Activated T helper cells produce interleukins
  • Interleukins stimulate more T cells to divide rapidly by mitosis (clonal expansion)
  • Example of cell signalling
  • Cloned T cells all carry receptor for particular antigen
  • Cloned T cells can:
  • Develop into T memory cells
  • Provide rapid response to reinfection
  • Develop into T killer cells
  • Destroy infected cells
  • Produce interleukins
  • Stimulate phagocytes
  • Stimulate B cells to divide
77
Q

Describe the humoral immune response

A
  • B lymphocytes have IgM antibodies on cell-surface membrane
  • Antibody on B lymphocyte binds to one complementary antigen on pathogen
  • B lymphocyte engulfs pathogen, digests it and presents antigens to become APC
  • Activated T helper cell binds to B cell APC (clonal selection)
  • Interleukins produced by activated T helper cell activates specific B cells
  • Activated B cells divide by mitosis (clonal expansion)
  • Clones differentiate into plasma cells and B memory cells
  • Plasma cells produce antibodies specific for the antigen
  • B memory cells provide faster response to reinfection
78
Q

Describe how cytokine molecules (interleukins) can stimulate specific B lymphocytes to divide

A
  • Cytokine / interleukin receptor has specific shape
  • Cytokine / interleukin binds to receptor on cell surface membrane of B lymphocyte
  • Receptor and cytokine have complementary shapes
  • Activates clonal expansion of B cells
79
Q

Describe the structure of an antibody

A
  • Protein
  • Variable region - contains antigen binding sites
  • Constant region - aids recognition and binding to host phagocytes
80
Q

How do antibodies help fight infection?

A
  • Act as antitoxins - combine with and neutralise toxins produced by pathogens
  • Prevent viruses attaching to host cells (neutralisation)
  • Cause agglutination - stick pathogens together - more easily engulfed by phagocytes
  • Help lyse the pathogen
  • Act as opsonins - make pathogens easier for phagocytes to recognise
81
Q

Describe the processes of neutralisation

A
  • Antibodies block binding sites on pathogen
  • Bind to toxins
  • Prevent entry of pathogen to host cell
82
Q

Describe the processes of agglutination

A
  • Bind together many pathogens
  • Clumps too large to enter host cell
  • Increase likelihood of being consumed by phagocyte
83
Q

Describe how the structure of an antibody molecule is related to its function

A
  • Y-shaped molecule made from light and heavy chains
  • Disulfide bonds hold light and heavy chains together
  • Constant region
  • Binds to phagocytes
  • Variable region
  • Has complementary shape to antigen
  • Gives specificity
  • Hinge region
  • Allows flexibility
  • More than one variable region
  • Allows agglutination and blocking of pathogen’s binding sites
84
Q

Describe the role of memory cells when a pathogen re-enters the body

A
  • Recognise pathogen
  • Produce clones
  • B cell clones can form plasma cells to make antibodies
  • T cell clones can form T helper cells and T killer cells
  • Responsible for secondary response
85
Q

What is the difference between the primary and secondary immune response?

A
  • Primary response produces antibodies slower and at a lower level
  • Secondary response produces antibodies faster and in greater amounts
86
Q

Outline the principle of immunity

A
  • Immunity is the ability of an organism to resist infection
  • Due to presence of antibodies
  • Pathogen invades body
  • Leads to clonal selection of B memory cells
  • B-cells produce specific antibodies
  • If same pathogen enters body again, memory cells activated
  • Antibodies produced faster and in greater amounts
87
Q

Define passive immunity

A

Receiving antibodies from external sources
- e.g. across placenta, from breast milk, injection of antibodies

88
Q

Define active immunity

A

Body produces own antibodies
- e.g. from facing an infection directly or through vaccination

89
Q

Define natural immunity

A

Immunity occurs naturally in the body

90
Q

Define artificial immunity

A

Immunity provided by intentional exposure to small quantities of pathogen

91
Q

Explain the difference between the body’s response in active and passive immunity

A
  • Active immunity leads to creation of B and T memory cells
  • Leads to long lasting immunity
  • Passive immunity does not produce immune response
  • No memory cells made
  • Does not lead to faster secondary immune response
92
Q

Define autoimmune disease

A
  • Immune system stops recognising ‘self’ cells
  • Starts to attack healthy body tissue
  • e.g. type 1 diabetes, lupus, rheumatoid arthritis
93
Q

Discuss the problems that could arise from treating an autoimmune disease with
immunosuppressant drugs

A
  • Immunosuppressant drugs reduce activity of immune system
  • Prevent destruction of healthy tissue
  • But susceptibility to infection increases
  • Immune system less effective at recognising pathogens
94
Q

Explain how vaccinations work

A
  • Artificial active immunity
  • Inject dead, weakened or attenuated form of pathogen
  • Antigens stimulate specific immune response
  • T-cells activated
  • T-cells stimulate clonal expansion of B-cells
  • Memory cells are made
  • Specific antibodies produced by B-cells
  • Result is specific immunity
  • Vaccination causes slow production of antibodies and lower level of antibodies
  • Upon re-entry of pathogen, antibodies are produced sooner, faster, and in greater number
  • Second/booster shot may be given to stimulate memory cells
95
Q

Benefits of vaccines

A
  • Can eradicate diseases e.g. smallpox
  • Reduces deaths due to disease
96
Q

Risks of vaccines

A
  • Individual may react badly to vaccine
  • Immunity may not be life-long (booster required)
97
Q

Define epidemic

A

When a communicable disease spreads rapidly at a local/national level

98
Q

Define pandemic

A

When a communicable disease spreads rapidly on a global scale

99
Q

How can vaccination programmes help prevent epidemics?

A
  • Mass vaccination can prevent spread of pathogen into wider population
  • When a significant number of people have been vaccinated, it gives protection to those who do not have immunity (herd immunity)
100
Q

Why do vaccines have to be changed regularly?

A
  • Mutations in antigens on pathogens
  • Produces different strains with different antigens
  • New vaccine needed for most new strains
101
Q

State the biological reasons why it has not been possible to produce an effective vaccine for malaria

A
  • Different species of Plasmodium cause malaria
  • Different antigens due to mutation
  • More than one stage in the life cycle is within the human
  • Different stages have different antigens
  • Different vaccine for each stage required
  • Parasite hidden in cells
102
Q

State the biological reasons why it has not been possible to produce an effective vaccine for HIV

A
  • HIV hidden in cells
  • Infects and destroys immune system
103
Q

What are antibiotics?

A
  • Chemicals produced by microorganisms
  • Used to kill bacteria
104
Q

Explain how antibiotics work

A
  • Relies on differences between eukaryotes and prokaryotes
  • Only harmful to bacteria and not the host organism (usually humans)
  • Interrupts usual prokaryotic cell process, e.g.:
  • Prevents cross-linking of bacterial cell walls
  • Inhibition of protein synthesis
  • Inhibition of nucleic acid synthesis
105
Q

Explain why antibiotics cannot be used to treat viral diseases

A
  • Viruses are not living
  • Viruses lack metabolism
  • Antibiotics target cell wall production
106
Q

What is antibiotic resistance?

A
  • Some strains of bacteria have evolved genes that confer resistance to antibiotics
  • Some strains of bacteria have evolved resistance to multiple antibiotics
  • e.g. MRSA (methicillin-resistant Staphylococcus aureus)
  • e.g. Clostridium difficile
107
Q

What are the potential causes of antibiotic resistance?

A
  • Mutations leading to antibiotic-resistant strains
  • Prescription misuse of antibiotics for viral infections
  • Patient misuse by halting treatment too early
  • Overuse of antibiotics
  • Use of antibiotics in farming
108
Q

How can antibiotic-resistant infections be reduced?

A
  • Minimise use of antibiotics
  • Ensure every course of antibiotics is completed
  • Good hygiene in hospitals and care homes
109
Q

Why is antibiotic resistance a concern?

A
  • Bacterial infections harder to treat
  • Potential for large disease outbreak
  • Developing new antibiotics is long and expensive process
110
Q

How is penicillin used?

A
  • Extracted from mould growing on
    melons
  • Antibiotic - prevents cross-linking of
    bacterial cell walls
111
Q

How is aspirin used?

A
  • Extracted from compounds found in willow bark
  • Painkiller and anti-inflammatory
112
Q

Describe the different ways that medicines can be identified and developed

A
  • Compounds produced by fungi and other plants and animals isolated
  • Possible genes that may produce suitable drugs identified
  • Develop molecules that will fit into receptor proteins on membranes e.g. for hormones or
    neurotransmitters
  • Modification of existing drugs
  • Traditional plant remedies that offer potential medicines
113
Q

Define pharmacogenetics

A
  • Personalising medicines for the individual
  • Drug treatment based on individual’s genome
114
Q

Define synthetic biology

A
  • Using genetic engineering to produce drugs that are rare or expensive
  • Nanotechnology used to deliver drugs to specific targets

Yr 12 Biology A Level (15 decks)

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