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A Level Biology > Chapter 12: Communicable Diseases > Flashcards

Chapter 12: Communicable Diseases Flashcards

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1
Q

Define communicable disease.

A
  • Disease that can be passed from one organism to another, of the same or different species.
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2
Q

Define vector.

A
  • A living or non-living factor that transmits a pathogen from one organism to another.
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3
Q

How do viruses take over host cell + reproduce?

A
  1. Virus attached to host cell.
  2. Viral DNA inserted into host DNA.
  3. Viral DNA replicates.
  4. Synthesis of viral protein.
  5. Assembly of viral protein.
  6. Lysis of host cell.
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4
Q

Define parasite.

A
  • Lives off host.

- Feeds off /gain nutrition from host at the expense of the host.

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5
Q

Example of plant diseases.

A
  • Black Sigatoka (fungal).
  • Tobacco Mosaic Virus (viral).
  • Ring rot (bacterial)
  • Potato blight (fungal).
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6
Q

How does reverse transcriptase in HIV lead to AIDS?

A
  1. RT in host nucleus.
  2. Viral DNA inserted into host DNA.
  3. Viral mRNA/RNA transcribed/produced.
  4. Codes for/translates viral proteins.
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7
Q

How does the Anopheles mosquito cause malaria?

A
  1. Mosquito –> vector.
  2. Plasmodium present in mosquito saliva/salivary gland.
  3. Infected mosquito feeds on human/bites skin –> creates a break in the skin.
  4. Plasmodium passes from saliva into blood.
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8
Q

Methods of direct transmission.

A
  • Direct contact.
  • Inoculation.
  • Ingestion.
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9
Q

Methods of indirect transmission.

A
  • Fomites.
  • Vectors.
  • Droplet infections.
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10
Q

Factors affecting transmission of communicable diseases in humans.

A
  • Overcrowded living + working conditions.
  • Poor nutrition.
  • Compromised immune system.
  • Poor disposal of waste.
  • Culture + infrastructure –> traditional medicines.
  • Socioeconomic factors –> lack of trained workers + warning when there is disease outbreak.
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11
Q

Methods of indirect transmission in plants?

A
  • Soil contamination.

- Vectors –> wind, animals, humans and water.

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12
Q

Factors affecting spread of communicable diseases in plants.

A
  • Plant varieties of crop that are susceptible to disease.
  • Overcrowding –> increases chance of contact.
  • Poor mineral nutrition –> reduces resistance.
  • Damp, warm conditions –> increase spread of spores + survival of pathogen.
  • Climate change.
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13
Q

How to prevent/reduce spread of disease in plants.

A
  • Leave room between plants –> minimise pathogen spread.
  • Rotate crops.
  • Clear fields.
  • Strict hygiene practices.
  • Control insect vectors.
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14
Q

How does callose prevent spread of infection in plants?

A
  • Callose papillae act as barriers.
  • Prevent pathogens entering site around infection.
  • Contain deposits of lignin –> makes barrier thicker + stronger.
  • Callose blocks sieve plates –> prevents spread of pathogen + sealing off infected parts.
  • Callose deposited in plasmodesmata between infected + healthy cells –> seal of infected + prevent spread.
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15
Q

Describe process of blood clotting.

A
  1. Blod clots rapidly to seal wound.
  2. Platelets in contact with collagen in skin or wall of damaged blood vessel –> adhere + secrete thromboplastin + seretonin.
  3. Thromboplastin –> enzyme that sets of a cascade of reactions that leads to the formation of a blood clot.
  4. Seretonin –> makes SM in vessel walls contract, constricting vessel –> reduce blood supply to damaged area.
  5. Clot dries out –> forming hard tough scab that keeps pathogen out.
  6. Epidermal cells below scab start to grow + seal wound permanently and damaged blood vessels regrow.
  7. Collagen –> deposited to give new tissue strength.
  8. Once epidermis reaches normal thickness –> scab sloughs off + wound healed.
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16
Q

List + explain features of the primary non-specific defence system.

A
  • Skin = physical barrier to entry of pathogen.
  • Mucous membrane/goblet cells = produce mucus to trap pathogen.
  • Nasal hairs/cavity = trap pathogen.
  • Ciliated epithelium = waft mucus.
  • Sebum = inhibits growth of pathogens.
  • Lysozyme/urine/tears = kills bacteria using antibacterial agent.
  • Expulsive reflexes = coughing/sneezing expels pathogen from gas exchange system + vomiting/diarrhoea expels pathogen from digestive system.
  • Stomach acid/gastric juices = kill pathogen –> low pH denatures enzymes + alters tertiary structure of active site.
17
Q

Explain the stages of phagocytosis.

A
  1. Pathogen produce chemicals that attract phagocytes –> phagocyte receptors bind to antigens on pathogen.
  2. Phagocytes recognise non-human proteins on the pathogen –> response not to a specific type of pathogen but to a cell/organism that is no-self.
  3. Phagocyte engulfs pathogen + encloses it in a vacuole known as a phagosome.
  4. Lysosomes move towards + fuse with phagosome forming a phagolysosome.
  5. Enzymes from lysosomes digest + destroy pathogens into amino acids + glucose.
  6. Break down products absorbed into cytoplasm by diffusion/active transport.
  7. Cytoskeleton provides tracks for movement of vesicles.
18
Q

What happens when macrophage has digested pathogen?

A
  1. Combines antigens from pathogen’s cell surface membrane with special glycoproteins in cytoplasm called the major histocompatibility complex.
  2. MHC moves pathogen antigens to macrophage’s surface membrane to form antigen presenting cell (APC).
  3. APC can now stimulate other cells involved in specific immune response.
19
Q

How do cytokines perform their function of cell signalling?

A
  1. Cytokine/interleukin has specific shape.
  2. Cytokine/interleukin binds to receptors in cell surface membrane of B lymphocyte.
  3. Cytokine/interleukin + receptors are complementary.
  4. Activates clonal expansion/mitosis.
20
Q

Structure of antibody.

A
  • 2 heavy + 2 light chains held by disulfide bridges.
  • Hinge region –> allows flexibility.
  • Constant region –> allows binding to phagocyte.
  • Variable region –> allows binding to more than one of the antigen + allows specificity to different antigens.
21
Q

Describe agglutination.

A
  1. Clump together many pathogens containing antigen-antibody complex.
  2. Clump too large to enter host cell membrane.
  3. More pathogens consumed by phagocytes at once.
22
Q

Describe neutralisation.

A
  1. Antibody blocks binding site on pathogen.
  2. Binds to toxin.
  3. Preventing entry to host cell.
23
Q

Role of T helper cells?

A
  • Produce interleukins + bind to B cell APC.
24
Q

Role of T killer cells?

A
  • Destroy pathogen carrying the antigen.

- Perforin –> kill pathogen by making holes in cell surface membrane –> freely permeable.

25
Q

Role of T regulator cells?

A
  • Stop immune response when pathogen eliminated.

- Prevent autoimmune response.

26
Q

Role of plasma cells (type of B cell)?

A
  • Produce antibodies to a particular antigen.
27
Q

Role of T memory cell?

A
  • Part of immunological memory.

- If pathogen met a second time –> divide rapidly to form T killer cell clones.

28
Q

Role of B effector cells?

A
  • Divide to form plasma cell clones.
29
Q

Role of B memory cells?

A
  • Provide immunological memory.

- Antigen encountered again –> form plasma cell closes –> produce antibodies –> wipe out pathogen.

30
Q

Outline the steps of cell mediated immunity (response to antigens inside cell).

A
  1. In the non-specific defence system –> macrophages digest + engulf pathogens in phagocytes and process pathogen antigen’s to form APCs.
  2. Some receptors on T helper cells are complementary + can bind to the antigens.
  3. These T cells become activated + produce interleukins that:
    - Stimulate more T cells to divide by mitosis.
    - Produce more clones of identical T helper cells that contain the complementary antigen for a pathogen.
  4. T cell clones may:
    - Develop into memory cells –> provide rapid response if pathogen encountered again.
    - Produce interleukins that stimulate phagocytosis + B cells to divide.
    - Produce T killer cell clones –> specific for presented antigen + destroy infected cells.
31
Q

Outline steps of humoral immunity (response to antigen outside cell).

A

Primary Response:

  1. B cell carries antibody on its surface.
  2. Antibody specific to one antigen.
  3. Clonal selection = activated T helper cell binds to B cell APC.
  4. Interleukins produced by activated T helper cells activate B cells.
  5. Clonal expansion = activated B cells divide by mitosis to differentiate into plasma cell clones + B memory cells.
  6. Cloned plasma cells produce antibodies –> specific to antigen.

Secondary Response:

  1. Memory cells remain in circulation –> form immunological memory.
  2. Recognise pathogen –> B memory cells divide rapidly to form plasma cell clones.
  3. Plasma cell clones –> produce specific antibodies to antigen + wipe out pathogen before symptoms of disease.
32
Q

Role B memory cells when pathogen in body.

A
  • Recognise pathogen/virus.
  • Produce clone.
  • Divide to form plasma cell clones.
  • Make antibodies.
  • Responsible for secondary immune response.
  • Can change to form T killer cells.
33
Q

Describe the actions of B lymphocytes.

A

Humoral response:

  • B cell carries antibody on its surface
  • Complementary to one antigen.

Clonal selection:

  • Interleukins produced by activated T helper cells activate B cells.

Clonal expansion:

  • Activated B cells divide by mitosis to form plasma cell clones + B memory cells.
  • Plasma cell clones –> produce antibodies –> complementary to antigen.
  • B memory cells –> immunological memory –> secondary response.
34
Q

Why cannot plants obtain immunity?

A
  • No circulatory system.
  • No B or T lymphocytes.
  • No antibodies.
  • No memory cells.

A Level Biology (21 decks)

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