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Communicable Disease
A Level Biology
| Question | Answer |
|---|---|
| State the kingdom of organism that causes each of the following diseases: tuberculosis, Black Sigatoka, Athlete's foot, malaria | Bacteria, fungi, fungi, protoctists |
| State the kingdom of organism that causes each of the following diseases: blight, ringworm, ring rot, bacterial meningitis | Protoctists, fungi, bacteria, bacteria |
| Give one plant disease caused by each of the following: viruses, bacteria and fungi | Tobacco mosaic virus, ring rot, black sigatoka |
| State three factors that would affect the speed of disease transmission in plants | Overcrowding; poor mineral nutrition; damp, warm, humid conditions; climate change |
| State how the influenza virus is most likely to be transmitted between different humans | Respiratory droplets (inhalation) |
| State four different types of vector that can be used to transmit a communicable disease | Water (e.g. diarrhoeal diseases); animals (e.g. mosquito transmits Plasmodium); wind (carries spores); humans (hands, clothing etc.) |
| State three passive physical defences that prevent plants being infected by a pathogen | Bark, waxy cuticle, thorns, spines, lignified cell walls, cellulose etc. |
| State three active physical defences a plant would employ against an invading pathogen | Callose synthesised and deposited between plasma membrane and cell wall; callose blocks sieve plates in phloem; callose deposited in plasmodesmata between infected cells and their neighbours; lignin added to cell walls; tyloses block xylem vessels |
| State three chemical defences a plant would employ against an invading pathogen | Antibacterial compounds like phenols, alkaloids; terpenes; hydrolytic enzymes like glucanases and chitinases; caffeine; tannins etc. |
| Describe the role of the skin as a primary non-specific defence | Dead outer layer of keratin prevents pathogen entry; skin flora outcompete pathogens for space; oil secretions inhibit pathogenic growth |
| Describe the role of mucous membranes as a primary non-specific defence | Mucus traps pathogens and contains lysozymes; phagocytes engulf and digest pathogens in mucus |
| Which enzyme catalyses the conversion of prothrombin to thrombin | Thromboplastin (thrombokinase) |
| Describe the role of thrombin in the clotting process | Causes the conversion of soluble fibrinogen into insoluble fibrin fibres |
| Describe the process of inflammation as a secondary non-specific response | Mast cells release histamines; histamines increase permeability of capillaries meaning plasma leaks into tissue fluid (pain and swelling); vasodilation of arterioles so more blood reaches infected area (heat and redness); neutrophils attracted to area for |
| Describe the process of phagocytosis | Phagocyte engulfs pathogen into a phagosome; lysosomes fuse with phagosome to form a phagolysosome; enzymes, hydrogen peroxide and nitric acid break down the pathogen |
| Describe how macrophages process antigens for presentation on their cell surface membrane | Antigen fragments combined with MHC (special glycoproteins in cytoplasm) |
| What name is given to small protein molecules that act as cell-signalling compounds? | Cytokines |
| Describe how neutrophils are specialised for their role | Plasma membrane contains receptors for opsonins, well developed cytoskeleton for phagocytosis, many mitochondria for respiration, many ribosomes to make enzymes, many lysosomes. |
| Opsonins are non-specific. Explain why | Opsonins can attach to many types of pathogen and help the process of phagocytosis, by giving the phagocyte something to bind to. They must be non-specific, so they can attach to many different pathogens. |
| Where do B lymphocytes and T lymphocytes mature? | Bone marrow and thymus respectively |
| What is meant by the term 'autoimmunity' and give two examples of autoimmune diseases | Destruction of self-tissue; rheumatoid arthritis, lupus, type I diabetes |
| What is the role of T regulatory cells? | Dampen down the immune response; prevents destruction of self tissue (autoimmunity) |
| Describe how an antigen presenting cell leads to large numbers of T helper cells | APC binds specifically to a Th cell (clonal selection). This selected Th cell then proliferates by mitosis (clonal expansion) |
| Describe how B lymphocytes are activated and the role of activated B lymphocytes | Th cell binds specifically to B lymphocyte; B lymphocyte differentiates into a plasma cell. Plasma cells release antibodies specific to the particular antigen |
| Describe how T killer cells destroy a virally infected cell | Release perforins which punch holes in the membrane of the cell; Tk cell inserts channels through which it floods hydrogen peroxide/nitric acid/hydrolytic enzymes |
| Dinstinguish clearly between an antigen and an antibody | An antigen is a cell-surface molecule that is specific to the cell (and a particular antibody); an antibody is an immunoglobulin manufactured by the plasma cells (which binds specifically to an antigen). |
| Antibodies are made by plasma cells. Explain how plasma cells are specialised for their role | Plasma cells have a lot of ribosomes, rough endoplasmic reticulum, Golgi apparatus and mitochondria. |
| Describe how opsonins function | Opsonins bind specifically to an antigen on a pathogen (via the variable region), clearly marking the pathogen for destruction by a neutrophil. A neutrophil will bind to the constant region of the opsonin and destroy the pathogen by phagocytosis |
| Describe how agglutinins function | Agglutinins cross link pathogens by binding specifically via their variable regions. Pathogens are clumped together (agglutinated), meaning they cannot enter host cells and are easier to phagocytose |
| Describe how antitoxins function | Neutralise toxin molecules released by a pathogen through direct binding |
| Describe how the structure of an antibody enables it to perform its function | The variable region is specific to the antigen – it has a shape that is complementary to the shape of the antigen; the disulfide bridges hold the four polypeptide chains together; the hinge region allows some flexibility so that the molecule can bind to m |
| Explain why it may take several days for the primary immune response to become effective | After infection, the pathogen must be detected and attacked by macrophages; antigen presentation occurs to select the correct B and T cells (clonal selection); these cells must reproduce in clonal expansion; then they must differentiate to form plasma cel |
| Explain why a secondary immune response is so much faster than a primary immune response | B memory and T memory cells are circulating in the blood. On second encounter with a pathogen, the correct B/T memory cell is clonally selected and can very quickly differentiate into correct specific Th/Tk/plasma cell. Plasma cells can produce antibodies |
| Give an example of both natural active immunity and natural passive immunity | Natural active - antibodies made by immune system in response to infection; natural passive - antibodies provided via placenta/breast milk (useful in developing immune system) |
| Explain why passive immunity only provides short-term immunity | Passive immunity is provided by an external supply of antibodies – these are proteins and will not last long in the body. They may even act as antigens and be attacked by antibodies from our immune system. |
| Give an example of artificial active immunity | Immunity provided by antibodies made in response to vaccination (dead/inactive pathogens injected) |
| Define the term epidemic | A rapid spread of disease through a high proportion of a population (usually within a country) |
| Describe the difference between herd vaccination and ring vaccination | Herd vaccination is where everyone, or almost everyone, is vaccinated. Ring vaccination is vaccinating people around the site of the outbreak, so that the pathogen will not be transmitted across that ring to the whole population. |
| Describe how a microorganism can become resistant to an antibiotic | Bacteria that survive a treatment will be slightly resistant to the antibiotic and the antibiotic acts as a selective force which selects the resistant individuals. When they reproduce, some of their offspring may be more resistant, thus resistance evolve |
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Davenant Foundation School
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