Biology- Communicable Diseases (4.1)

Microorganism that causes disease.
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Organism in which pathogens live in and creates good habitat for microorganisms.
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Reproduce rapidly, damage cells or release waste products/ toxins eg. tuberculosis.
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Invade cell, take over genetic machinery, cause cells to manufacture viruses eg. HIV.
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Hyphae (which form a mycelium) grow under skin surface. Can cause spores. eg. athlete's foot.
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Feed on contents of host cells.
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Bacterial Diseases
TB- kills cells and tissues (often in lungs). Bacterial meningitis- infection of membranes surrounding brain/ spinal cord causing swelling. Ring rot- ring of decay in vascular tissue of plants.
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Viral Diseases
HIV/AIDs- attacks immune system cells. Influenza- attacks respiratory system/ headaches. Tobacco mosaic virus- mottling/ discolouration of leaves.
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Fungal Diseases
Black sigatoka- leaf spots on banana plants, reducing yield. Ringworm- cattle, spore cases erupting through skin, causes rash. Athlete's foot- growth under skin.
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Protocistan Diseases
Blight- affects leaves/ potato tubers of tomatoes and potatoes. Malaria- parasite in blood, headaches/ fevers.
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Direct Transmission
Passing a pathogen from host to new host, with no intermediary.
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Physical contact
Touching infected person/ contaminated surface eg. HIV, ringworm.
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Faecal- Oral Transmission
Eating/ drinking contaminated food/ water. eg. cholera.
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Droplet Infection
Pathogen in water droplets in air eg. TB, influenza.
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Carried in air/ reside on surfaces/ soil. eg. anthrax, tetanus.
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Indirect Transmission
Passing a pathogen from host to new host, via a vector.
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Organism that carries a pathogen from one host to another.
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Primary Defence Against Disease
Prevents pathogens entering body.
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Outer layer consists of keratinocyte cells which migrate out of base to surface of skin. Dry out and cytoplasm replaced so dead when reach surface so act as effective barrier.
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Blood Clotting and Skin Repair
Clots make temporary seal to prevent infection/ repair skin. Involves calcium ions and at least 12 clotting factors which cause an enzyme cascade. Clot dries/ forms scab which draws cut together as dries. Skin repair- migration of stem cells.
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Mucous Membranes
Epithelial layer contains goblet cells. In airways, mucus lines passages and traps pathogens in air. Cilia waft mucus along, up to top of trachea, where enters oesophagus. It is swallowed and passes down digestive system. Pathogens killed by acidity.
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Presence of microorganisms detected by mast cells which release cell signalling substance, histamine. Causes increased production of tissue fluid, which causes swelling. Excess tissue fluid drained into lymphatic system, causes specific immune.
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Secondary Defences
Combat pathogens within body.
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Chemical markers on membrane of pathogen, identifies it as foreign matter/ known matter. Stimulate immune response. Usually proteins/ glycoproteins in plasma membrane.
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Type of antibody that attack antigens on surface of pathogen and enhance ability of phagocytic cells to bind/ engulf pathogen.
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Hormone like molecules used in cell signalling to stimulate immune response.
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Specialised cells in blood/ tissue fluid, engulf/ digest pathogens. Contain many mitochondria (ATP for exo and endocytosis and protein synthesis). Contain many ribosomes (protein synthesis of digestive enzymes). Lobed nucleus- squeeze through gaps.
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Type of phagocyte, multi lobed nucleus, engulfs/ digests pathogens. Lysosomes release lytic enzymes to digest pathogen.
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Engulf pathogens, but doesn't fully digest it. Antigen is saved and moved to special protein complex on surface of cell. Cell becomes antigen presenting cell that exposed antigen on surface.
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Macrophages travel in blood as monocytes.
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B Memory Cells
Remain in body for years (immunological memory).
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Plasma B Cells
Manufacture antibodies.
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T Helper Cells
Release cytokines that stimulate B cells to develop and stimulate phagocytosis.
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T Memory Cells
Long term immunity.
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T Regulator Cells
Shut down immune response after pathogen is removed (also involved in preventing autoimmunity).
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Cells communicate through release of cytokines. Complementary cell surface receptor. Macrophages release monokines (attract neutrophils and stimulate B cells.). T cells/ macrophages release interleukins (stimulate clonal expansion/ differentiation).
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Autoimmune Diseases
Immune system attacks own antigens/ part of body. Arthrits= inflammation of joints (antibodies attack joint membranes).
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Specific Immune Response
1. Infection. 2. Antigen Presentation- macrophages (engulfs, antigen presenting cell), infected cells or pathogen. 3. Clonal selection- complementary B/ T cells bind to phagocyte. 4. Clonal expansion- B/T cells divide by mitosis. 5. Differentiation.
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Immunoglobulins. Complex proteins produced by plasma cells. Specific/ complementary to particular antigen. Four polypeptide chains (2 light and 2 heavy). 2 binding sites for antigens. Variable region and constant region.Hinge region.Disulfide bridges
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Antibodies can act as opsonins- group of antibodies that bind to antigen on pathogen and act as binding sites for phagocytic cells, so can bind easier and destroy pathogen. Can be specific or non-specific.
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Antibodies can act as agglutinins- due to 2 identical binding sites, able to 'crosslink' pathogens by binding antigens on one pathogen to a no. binding sites. Large clump= non-infective and easily phagocytosised.
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Antibodies can act as anti-toxins- antibodies bind to toxins and render them harmless.
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Primary and Secondary Immune Response
Primary Immune Response- infecting agent first detected, immune system take few days to produce antibodies. Secondary Immune Response- antibodies don't stay in blood, B and T memory cells recognise specific antigens and produces antibodies faster.
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Deliberate exposure to antigenic material that has been rendered harmless, which activates the immune response.
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What can vaccines comprise of?
Whole, live microorganisms (not as harmful as real disease, but have similar antigens, so antibodies produced will be effective). Harmless/ attentuated (weakened) version. Dead pathogen. preparation of antigens from pathogen. Toxoid (harmless toxin).
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Herd Immunity
Vaccine provides immunity to all/almost all population at risk. Once enough people are immune, (80-85%), disease can't be spread.
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Ring Immunity
Vaccinating all people in immediate vicinity of new case(s).
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Active Immunity
Immune system is activated and manufactures own antibodies.
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Passive Immunity
Immunity achieved when antibodies passes to individual via breast-feeding or injection.
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Natural Immunity
Immunity achieved through normal life processes eg. infection or provided via placenta or breast milk.
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Artificial Immunity
Immunity achieved by medical intervention eg. vaccinations or by injection of antibodies by another individual.
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Rapid spread of disease through high proportion of the popul\tion.
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Worldwide epidemic.
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Chemical which prevents growth of fungi/ bacteria. Overuse= develops resistance.
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Accidental Discovery
Fleming discovered penicillin (releases compounds which kill bacteria) when noticed bacteria killed by naturally occurring penicillin mould.
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Traditional Remedies
Morphine's origin in use is in sap from unripe poppy seed heads- anesthetic which reduces nervous action in CNS- nerves can't carry impulse- pain isn't felt.
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Research into Disease-Causing Mechanisms
HIV virus binds to receptors on T-helper cells, so are trying to develop drug that mimics shape of receptor to bind to virus, blocking binding between pathogen and receptors.
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Personalised Medicine
Development of designer medicines for individuals. Sequencing technology and molecular modelling.
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Synthetic Biology
Re-engineering of biology. Either production of new molecules mimicking natural, or use of natural molecules to produce new biological systems.
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Passive Defences in Plants
Prevent entry/ spread of pathogens, present before infection.
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Physical Passive Defences in Plants
Cellulose cell wall (physical barrier). Lignin thickening (waterproof/ indigestible). Stomatal closure. Callose (polysaccharide deposited in sieve tubes and block flow in sieve tubes (can't travel). Tylose formation (swelling fills xylem vessel).
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Chemical Passive Defences in Plants
Anti-pathogenic properties. Some present before infection, but due to production requiring energy, many produced only when pathogen is detected.
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Active Defences in Plants
Induced when pathogen is detected. Specific chemicals (eg. proteins/ glycolipids) in pathogen cell wall detected by plant cells
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Physical Active Defences in Plants
Cell walls strengthened w/additional cellulose. Callose deposition between plant cell walls and plasma membrane impedes cellular perpetation.
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Chemical Active Defences in Plants
Terpenoids (antibacterial and antifungal). Necrosis (deliberate cell suicide- plant limits pathogen access to water/ nutrients- brought about by intracellular enzymes). Canker (causes death of cambium tissue in bark).
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