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6.3.1 Define Pathogen
An organism or virus that causes a disease
6.3.2 Explain why antibiotics are effective against bacteria but not viruses
- Antibiotic drugs may either
- • Kill microbes directly – bactericidal
- • Prevent them from growing and reproducing – bacteriostatic
- • There are many differences between bacterial, prokaryotic cells and human eukaryotic cells, and therefore useful antibiotics will block processes in bacterial cells while leaving eukaryotic cells unharmed
- • Viruses invade host cells, which may be eukaryotic and use the cellular organelles and process to carry out their own reproduction
- • Since antibiotics do no block the processes in eukaryotic cells they do not affect viruses, which are utilizing these processes, and so antibiotics are ineffective against viruses
Antiviral drugs do exist but are reserved for serious viral infections
6.3.3 Outline the role of skin and mucous membranes in defence against pathogens.
- The Skin
- • Physical barrier: outer layers of the skin are tough and difficult to penetrate
- • Natural populations of harmless microbes: through competition inhibit the growth of pathogenic microbes
- • Chemical secretions: sebaceous glands secrete lactic acid and fatty acids that make the skin surface acidic which prevents growth of bacteria
- • Tears and saliva: help to keep bacteria away
- Mucus Membranes
- • Found in the lining of the respiratory system, urinary, reproductive and gastrointestinal tracts
- • Mucus contains the enzyme lysosozyme which destroys many bacteria
- • In the respiratory tract pathogens get caught in the sticky mucous and cilla then push the mucous and bacteria up and out of the trachea, were they are swallowed and then digested.
6.3.4 Outline how phagocytic leucocytes ingest pathogens in the blood and body tissues.
- 1. Detection: Phogocyte detects microbes by the chemicals they give off (chemotaxis) and sticks the microbe to its surface
- 2. Ingestion: The microbe is engulfed by the phagocyte wrapping pseudopodia around it to form a vesicle
- 3. Vesicle Formation: A phagosome (phagocytic vesicle) is formed, which encloses the microbes in a membrane
- 4. Fusion with Lysosome: Phagosomes fuses with a lysosome (which contains powerful enzymes that can digest the microbe)
- 5. Digestion: The microbes are broken down by enzymes into their chemical constituents
- 6. Discharge: Indigestible material is discharged from the phagocyte cell
6.3.5 Distinguish between antigens and antibodies
- Antigens: foreign substance that stimulate the production of antibodies e.g. cell walls of bacteria or fungi, protein coats or viruses
- Antibodies : proteins that recognize and bind to specific antigens
11.1.2 Outline the principle of challenge and response, clonal selection and memory cells as the basis of immunity.
- Immunity to a disease is only developed if the immune system is challenged by the disease this is called challenge and responseDuring development, about1015 types of B cells are randomly generated
- Each cell is capable of producing antibodies to a different antigen
- Each B cell has 1 specific type of antigenic receptor in its PM that is identical to the antibody it can produce
- If a cell encounters an antigen to which its antigenic receptor binds, it will multiply to form a clones of many cells that will all secrete the antibody
- This is called clonal selection because the antigen selects the B cells that will proliferate
- Some B cells differentiate into long lived memory B cells which are retained in the lymph nodes and if a second infection occurs they will respond more rapidly and vigorously than in the first infection
6.1.2 and 11.1.4 Explain antibody production
- While antibody production is carried out by the B plasma cells their activation to do so is dependent on macrophages and helper T cells. Antibody production is divided into 5 stages:
- Stage 1: Antigen presentation
- • Macrophages take in antigens by endocytosis, process them and then attach them to membrane proteins called MHC proteins. The MHC proteins carrying the antigens are then moved to the plasma membrane by exocytosis and the antigens are displayed on the surface of the macrophage.
- Stage 2: Activation of Helper T cells
- • Helper T cells have antigen receptors in their plasma membrane that can bind to antigens presented by macrophages. Each helper T cell has receptors with the same antigen-binding site domain as an antibody. These receptors allow a helper T cell to recognize an antigen presented by a macrophage and bind to the macrophage. The macrophage passes a signal (Interleukin 1) to the helper T cell changing it from an inactive to an active state.
- Stage 3: Activation of B cells
- • Inactive B cells have antibodies in their plasma membrane. If these antibodies match an antigen, the antigen binds to the antibody. An activated helper T-cell with receptors for the same antigen can then bind to the B-cell. The activated helper T cell sends a signal (Interleukin 2) to the B cell, causing it to change from an inactive to an active state.
- Stage 4:Production of Plasma Cells
- • Activated B cells start to divide by mitosis to form a clone of cells. These cells become active, with a much greater volume of cytoplasm. They are known as plasma cells. They have a very extensive network of rough endoplasmic reticulum. This is used for synthesis of large amounts of antibody, which is then secreted by exocytosis.
- Stage 5: Production of Memory cells
- • Memory cells are B cells and T cells that are formed at the same time as activated helper T cells and B cells, when a disease challenges the immune system. After the activated cells and the antibodies produced to fight the disease have disappeared, the memory cells persist and allow a rapid response if the disease in encountered again. Memory cells give long term immunity to a disease.
6.3.7 Outline the effects of HIV on the immunes system.
- AIDS (acquired immunodeficiency syndrome) is considered a syndrome because it advents a group of symptoms that are found together produces by one underlying cause.
- Symptoms: low number of Helper T cells (Type of lymphocyte), weight loss, autoimmune disease, rare cancers, a variety of opportunistic infections caused by viruses, bacteria and protozoa.
- HIV causes a reduction in the number of active lymphocytes and a loss of the ability to produce antibodies.
6.3.8 Discuss the cause, transmission and social implications of AIDS.
- Causes of AIDS:
- • (HIV Human immunodeficiency virus)
- • A retrovirus (has RNA as its genetic material not DNA)
- • Infects helper T cells eventually destroying them and preventing the production of antibodies
- • Decline in the functioning of the immune system leaves the body vulnerable to pathogens that would normally be easily controlled
- • People die not from the HIV virus but from the diseases that result from a weakened immune system
- • HIV can’t survive long outside the body and can’t penetrate unbroken skin
- • Transmission via transfer of body fluids from an infected person to an uninfected person
- 1. Through small cuts of tears in the vagina, penis, mouth, or intestine during vaginal, oral and anal sex
- 2. Traces of blood on a hypodermic needle that is shared by intravenous drug abusers
- 3. Across the Placenta from a mother to a baby through cuts during childbirth or in milk during breast-feeding
- 4. In transfused blood or blood products such as Factor VIII used to treat hemophiliacs
- Social implications:
- • Grief of family and friends
- • Families become poorer due to a loss of wage earners and refusal of life insurance
- • Stigmatizing of individuals who may not find partners, friends, housing, employment
- • Decrease in sexual activity in the population due to a fear of contracting AIDS
11.1.1 Describe the process of blood clotting
- 1. The clotting process begins when the endothelium of a vessel is damaged and connective tissue in the vessel wall is exposed to blood. Platelets adhere to collagen fibres in the connective tissue and release a substance that makes nearby platelets sticky.
- 2. The platelets form a plug that provides emergency protection against blood loss.
- 3. This seal is reinforced by a clot of fibrin when vessel damage is more severe. Fibrin is formed via a multistep process. Clotting factors released from the clumped platelets of damaged cells mix with clotting factors in the plasma, forming an activation that converts a plasma protein called prothrombin to its active form thrombin. Thrombin itself is an enzyme that catalyzes the final step of the clotting process, the conversion of fibrinogen to fibrin. The threads of fibrin become interwoven into a patch.
11.1.3 Define active immunity and passive immunity
Active immunity: Immunity due to the production of antibodies by the organism itself after the body’s defences mechanisms have been stimulated by antigens.
Passive immunity: Immunity due to the acquisition of antibodies from another organism in which active immunity has been stimulated, including via placenta, colostrums, or by injection of antibodies.
11.1.5 (1) Describe the production of monoclonal antibodies
- 1. A mouse is injected with a foreign protein (antigen) that will stimulate the mouse to produce antibodies against it.
- 2. A few days later B-lymphocytes (that make the antibodies) are taken from the mouse’s spleen.
- 3. The mouse’s B-lymphocytes cells have developed an antibody to recognize the foreign protein (antigen).
- 4. Culture of tumour cells (mutant myeloma cells).
- 5. Pure tumour cells are harvested.
- 6. Some of the mouse cells fuse with tumour cells to make hybrid cells called hybridomas.
- 7. The mixture of cells is placed in a selective medium that allows only hybrid cells to grow.
- 8. Hybrid cells are screened for the production of the desired antibody. They are then cultured to produce large amounts of monoclonal antibodies.
11.1.5 (2) Describe the use of monoclonal antibodies
- 1. Diagnostic(ELISA test): A plate is coated with the monoclonal antibody and the sample being testes is left on the plate long enough for any antigen in the sample to bind to the antibodies – sample is rinsed off the plate. Any bound antigens are detected using more MC antibodies with enzymes attached that cause a colour change when they bind to the antigen.
- • Detection of HIV antibodies in the blood
- • Detection of cardiac isoenzyme from M.I
- .• Detection of HCG in the blood or wine during pregnancy
- • Detecting presence of pathogens such as malaria, Chlamydia Herpes virus I, II
- 2. Therapeutic
- • Treatment of anthrax, disease caused by a bacterium that produces toxins which can be lethal even after antibiotics – bacterium can produce spores that can be breathed in – MC antibodies can bind to and neutralize one of the toxins, sustaining patient until their own immune system produces antibodies.
- • MC antibodies in injection bind to rabies virus and control it until patients own immunity is high.
- • Prospect of using MC antibodies specifically targeted against cancer cells- attach a toxin to the antibody and it could deliver it directly to the cell leaving other cells alone.
11.1.6 Explain the principle of vaccination
- • A vaccine is a modified form of a disease-causing microorganism that stimulates the body to develop immunity to the disease, without fully developing the disease.
- • Could be weakened or killed forms of the microorganism, or chemicals produced by the microorganism that acts as antigens.
- • Vaccine can be injected or swallowed.
- • Vaccination is based on immunological memory (memory B and T cells).
- • Selective proliferation and differentiation of lymphocytes that occurs the first exposure to an antigen occurs is called the primary immune response.
- • In the primary immune response about 10-17 days is required to produce the maximum number of antibodies- during this time person may become ill but symptoms diminish as antibodies and T cells clear antigen form the body.
- • If a second exposure to the antigen occurs the production of antibodies is faster (only 2-7 days), of greater magnitude and more prolonged – this is called the secondary immune response.
- • Also antibodies produced in the secondary response tend to have greater affinity for the antigen than those produced in the primary immune response.
- • Secondary response is generated by immunological memory – initial exposure produced active B cells and activated T cells but also made long lived T and B memory cells.
- • These memory cells are poised to proliferate and differentiate rapidly when they contact the antigen the second time eliminating he pathogen before it can cause illness – thus resistance to infection is created (immunity).
11.1.7 Discuss the benefits and dangers of vaccination
- • Epidemics and pandemics are prevented and some disease can be eradicated (e.g. small pox)
- • Death due to disease can be prevented e.g. measles in children
- • Prevents disabilities due to disease e.g. deafness and blindness in babies who get rubella during pregnancy
- • Decrease health care costs
- • Serious adverse reactions (anaphylaxis) (rare)
- • Fever, pain, swelling and redness at the site of vaccination• Allergic reaction
- • Possible toxic effects of mercury in vaccines most now thimersol free
- • Possible overload causing damage to the immune system (Gulf war syndrome)