Parts of the Immune System 1. Blood - White Blood Cells in particular. 2. Lymph nodes 3. Thymus Gland – Produces T Lymphocytes 4. Bone Marrow – Produces B Lymphocytes 6.3.1 Define Pathogen Organism or virus that causes a disease in any other organisms. Pathogens = disease causing micro-organisms bacteria virus fungi, protozoa, parasite, worms prion Foreign Invaders Called Pathogens Viruses, bacteria or other living thing that causes disease/immune response. Antigens Toxins that pathogens produce that cause harm to an organism. The Big three diseases Disease Cause Pathogen Tuberculosis Bacterial infection Mycobacterium tuberculosis AIDS Vidal infection Human inmunodeficiency virus (HIV) Malaria Protozoan Plasmodium sp. infection Critical considerations These diseases are classified as the “neglected tropical diseases” and share the following criteria. - They have burdened humanity for centuries - They are poverty- promoting conditions - They are associated with social stigma. - They are most common in low- income countries. - Effective, low cost treatment are available. Protozoan infections Disease Pathogen African typanosomiasis Trypanosoma gabiense, T. rhodiense Kala- azar (viceral leishamiasis) Leishmania donovani Helmit (worm) infections Soil transmitted infections: Pathogen: Ascaris Ascaris lumbricoides Trichuriasis Trichuris trichiura Hookworm infection Nectar americanus Schistosomiasis: Pathogen Urinary schistosomiasis Schistosoma haematobium Hematobiliary schistomiasis Schistosoma mansoni Lymphatic filariasis Wuchereria ancrofti Onchocerciases Onchocerca volvulus Dracunculiasis Dracunculus medinensis Bacterial Infections Pathogen Trachoma Chlamydia trachomitis Leprosy Mycobacterium leprae Buruli ulcer Mycobacterium ulcerans 1- Suggest factors that might lead these diseases to be neglected 2- Suggest reasons why these diseases do not occur in high- income countries. 3- To what extent does using terms such as “Big three diseases” and “neglect diseases” limit or affect our thinking? 4- Discuss how “social stigma” might be a barrier to eradication programmes and suggest how it might be overcome. 6.3.2 Explain why antibiotics are effective against bacteria but not against viruses Antibiotics, such as the aminoglycosides, chloramphenicol, erythromycin, and clindamycin, block protein synthesis in bacteria but not in eukaryotic cells. Bacteria and animal cells synthesise proteins in a similar manner, though the proteins involved are not the same. Those antibiotics that are useful as antibacterial agents use these differences to bind to or inhibit the function of the bacterial proteins. In this way, they prevent the synthesis of new proteins and new bacterial cells without damaging the ‘patient’. Most bacteria have a cell wall. Antibiotics may disrupt this cell wall which will interfere with the life cycle of the bacteria. Eukaryotic animal cells do not have cell walls so are not affected by the antibiotic. Viruses do not have a cell wall so are also not affected by antibiotics. Viruses invade a cell and get this host cell to produce the protein and DNA that the virus needs to reproduce. As the virus uses it host’s processes, antibiotics do not hurt them. If they did, the antibiotic would also disrupt the process of protein synthesis in the host (which would be a serious problem). Many anti-viral drugs focus on disrupting the protein coat of a virus and will therefore not usually cause harm to the host. 6.3.3 Outline the role of skin and mucous membranes in defence against pathogens. The skin plays a major role in this. When unbroken, it is almost impossible for any microorganism to penetrate the skin. Baby and fungi pH of skin 8 7 6 5 4 neonates 3 adults 2 1 0 Soles back abdomen pamls forearm forehad 1- Compare the skin pH of neonates and adults. 2- Suggest how the adult skin pH might be established 3- Suggest why the use of soap (which are basic) might have more irritating effect on the skin of a neonate. 4- Deduce how basic soaps might undermine the skin’s defensive function. First lines of defence saliva tears antibacterial antibacterial enzymes enzymes mucus linings skin traps dirt and prevents microbes entry stomach acid “good” gut low pH kills bacteria out harmful compete bad microbes Second lines of defence Involves white blood cells Non-specific response invading pathogens are targeted by macrophages Specific response lymphocytes produce chemicals called antibodies that target specific pathogens Phagocytes Phagocytes Monocytes and macrophages (sangre y tejido) Provide a non-specific response to infection http://www.microbelibrary.org/images/ tterry/anim/phago053.html Phagocytosis Stages in phagocytosis 1. Phagocyte detects chemicals released by a foreign intruder (e.g. bacteria) 2. Phagocyte moves up the concentration gradient towards the intruder 3. The phagocyte adheres to the foreign cell and engulfs it in a vacuole by an infolding of the cell membrane. 4. Lysosomes (organelles which are rich in digestive enzymes & found in the phagocytes cytoplasm) fuse with the vacuole & release their contents into it. Phagocytosis 5. The bacterium is digested by the enzymes, and the breakdown products are absorbed by the phagocyte. During infection, hundreds of phagocytes are needed. Pus is dead bacteria and phagocytes! link to phagocytosis Pus An accumulation of : - dead phagocytes destroyed bacteria dead cells Lymphocyte Lymphocytes Provide a specific immune response to infectious diseases. There are 2 types: - T-cells - B-cells = They produce antibodies. Antigens all cells have surface markers called antigens. body can recognise these as self or non- self (foreign) Specific response Lymphocytes detect presence of foreign antigens Stimulated to produce specific proteins called antibodies. antibodies combine with their specific antigen (like a lock and key) this renders the pathogen harmless. = primary response Immunity = the bodies ability to resist infection can be natural or acquired Immunological memory after an infection is fought off some lymphocytes become memory cells. if same pathogen returns memory cells stimulate the produce the specific antibody very rapidly. the infection is fought off before symptoms appear = secondary response vaccines can stimulate same response Immune system Can you Outline the stages in phagocytosis. Describe how antibodies work and how they are specific. Blood Cells Phagocytes Lynphocytes Macrophages Cells of the Immune System White Blood Cells Phagocytes - Neutrophils - Macrophages Lymphocytes Phagocytes Produced throughout life by the bone marrow. Scavengers – remove dead cells and microorganisms. Macrophages – Phagocytosis Lymphocytes Produce antibodies B-cells mature in bone marrow then concentrate in lymph nodes and spleen T-cells mature in thymus B and T cells mature then circulate in the blood and lymph Circulation ensures they come into contact with pathogens and each other B -Lymphocytes There are c.10 million different B-lymphocytes, each of which make a different antibody. The huge variety is caused by genes coding for abs changing slightly during development. There are a small group of clones of each type of B- lymphocyte B -Lymphocytes At the clone stage antibodies do not leave the B- cells. The abs are embedded in the plasma membrane of the cell and are called antibody receptors. When the receptors in the membrane recognise and antigen on the surface of the pathogen the B- cell divides rapidly. The antigens are presented to the B-cells by macrophages B -Lymphocytes B -Lymphocytes Some activated B cells PLASMA CELLS these produce lots of antibodies, < 1000/sec The antibodies travel to the blood, lymph, lining of gut and lungs. The number of plasma cells goes down after a few weeks Antibodies stay in the blood longer but eventually their numbers go down too. B -Lymphocytes Some activated B cells MEMORY CELLS. Memory cells divide rapidly as soon as the antigen is reintroduced. There are many more memory cells than there were clone cells. When the pathogen/infection infects again it is destroyed before any symptoms show. Antibodies Also known as immunoglobulins Globular glycoproteins The heavy and light chains are polypeptides The chains are held together by disulphide bridges Each ab has 2 identical ag binding sites – variable regions. The order of amino acids in the variable region determines the shape of the binding site How Abs work Some act as labels to identify antigens for phagocytes Some work as antitoxins i.e. they block toxins for e.g. those causing diphtheria and tetanus Some attach to bacterial flagella making them less active and easier for phagocytes to engulf Some cause agglutination (clumping together) of bacteria making them less likely to spread Different Immunoglobulins Type Number of Site of action Functions ag binding sites IgG 2 •Blood •Increase •Tissue fluid macrophage activity •CAN CROSS •Antitoxins PLACENTA •Agglutination IgM 10 •Blood Agglutination •Tissue fluid IgA 2 or 4 •Secretions (saliva, •Stop bacteria tears, small intestine, adhering to host vaginal, prostate, cells nasal, breast milk) •Prevents bacteria forming colonies on mucous membranes IgE 2 Tissues •Activate mast cells HISTAMINE •Worm response T-Lymphocytes Mature T-cells have T cell receptors which have a very similar structure to antibodies and are specific to 1 antigen. They are activated when the receptor comes into contact with the Ag with another host cell (e.g. on a macrophage membrane or an invaded body cell) T-Lymphocytes After activation the cell divides to form: T-helper cells – secrete CYTOKINES help B cells divide stimulate macrophages Cytotoxic T cells (killer T cells) Kill body cells displaying antigen Memory T cells remain in body Active and Passive Immunity Active immunity Lymphocytes are activated by antigens on the surface of pathogens Natural active immunity - acquired due to infection Artificial active immunity – vaccination Takes time for enough B and T cells to be produced to mount an effective response. Active and Passive Immunity Passive immunity B and T cells are not activated and plasma cells have not produced antibodies. The antigen doesn’t have to be encountered for the body to make the antibodies. Antibodies appear immediately in blood but protection is only temporary. Active and Passive Immunity Artificial passive immunity Used when a very rapid immune response is needed e.g. after infection with tetanus. Human antibodies are injected. In the case of tetanus these are antitoxin antibodies. Antibodies come from blood donors who have recently had the tetanus vaccination. Only provides short term protection as abs destroyed by phagocytes in spleen and liver. Active and Passive Immunity Natural passive immunity A mother’s antibodies pass across the placenta to the foetus and remain for several months. Colostrum (the first breast milk) contains lots of IgA which remain on surface of the baby’s gut wall and pass into blood This is a specific response to a specific pathogen/antigen. The response involves the creation of Antibodies. - Dead cells (tissue) - Red Blood cells dispersed - Bacteria or possible infections. Deactivation of a bacterium by an antibody. How an antibody operates/works? The Pathway of Specific Immune Response Step 1 Pathogens eaten by Macrophage Step 2 Displays portion of Pathogen on surface Step 3 Pathogens Helper-T cell recognizes Pathogen Activates Cytotoxic Activates B- Cell T- Cell Memory B-Cell Memory T-Cell Antibodies Kills Infected Cells Immune Response Summary Displays copy of antigen on surface of cell Antigen Macrophage Helper T - Cell Antibody Immunity Cellular Immunity Active Cytotoxic T-Cell Active B - Cell Kills Infected Cells Memory T- Cell Plasma Cell Memory B-Cell Antibodies Deactivates Antigens Primary .vs. Secondary Immune Response Primary Immune Response This is a response to an invader the First time the invader infects the body. No measurable immune response for first few days. Next 10 – 15 days antibody production grows steadily Secondary Immune Response A more rapid response to an invader the 2nd time it invades the body. Antibody production increases dramatically and in a much shorter time period.. Primary .vs. Secondary Immune Response 11.1.7 Discuss the benefits and dangers of vaccination. Benefits of vaccination 1- Eradication of some diseases (e.g. smallpox). 2- Fewer people get certain diseases For example, measles, polio and diphtheria because when they come into contact with the pathogen, they will have a secondary response rather than a primary response 3- Prevents disability For example, polio can cause paralysis and when pregnant women get rubella, the baby's vision may be affected. Christina, the youngest sister of Queen Beatrix of the Netherlands, has eye problems due to her mother (Juliana) contracting rubella during pregnancy. 4- Herd immunity If many people in a population are vaccinated, the disease will not spread and even the individuals not vaccinated will be protected because they probably will not come into contact with the disease. Dangers of vaccination 1- Overloading the immune system with an antigen will reduce the ability to handle other infections (Gulf War syndrome?). 2- Other pathogens could grow in the solution with the vaccine. 3- The vaccine could contain other harmful substances e.g. although no evidence has been found of harmful effects of mercury in vaccinations, as a precaution, it is now used less and less. 4- In tests, vaccines are studied when administered individually, but usually the effect of a mixture of antigens (as in MMR vaccination) is not considered. 5- Artificial immunity is less effective; childhood diseases avoided as a child may cause a more serious disease as an adult (e.g. measles). Side effects of vaccination: 1- In 1998 Dr. Wakefield et al suggested a possible link between MMR vaccination and an increased chance of autism; studies carried out since have failed to confirm this link and most of Dr. Wakefield’s coauthors have retracted the interpretation of the results. 2- Vaccination against whooping cough, using a whole cell vaccine, may increase the chances of brain damage; again, further studies have not shown a link. 3- Malnourished individuals may not be able to make the antibodies (which are proteins) because they do not have enough amino acids. Vaccination A preparation containing antigenic material: Whole live microorganism Dead microorganism Attenuated (harmless) microorganism Toxoid (harmless form of toxin) Preparation of harmless ags Vaccination Injection into vein or muscle Oral Vaccination Why aren’t they always effective? Natural infections persist within the body for a long time so the immune system has time to develop an effective response, vaccinations from dead m-os do not do this. Less effective vaccines need booster injections to stimulate secondary responses Vaccination Why aren’t they always effective? Some people don’t respond well/at all to vaccinations Defective immune systems Malnutrition particularly protein Vaccination Why aren’t they always effective? Antigenic variation caused by mutation Antigenic drift – small changes (still recognised by memory cells) Antigenic shift – large changes (no longer recognised) Vaccination Why aren’t they always effective? No vaccines against protoctists (malaria and sleeping sickness) Many stages to Plamodium life cycle with many antigens so vaccinations would have to be effective against all stages (or be effective just against infective stage but given in very small time period). Vaccination Why aren’t they always effective? Sleeping sickness – Trypanosoma has a thousand different ags and changes them every 4-5 days Vaccination Why aren’t they always effective? Antigenic concealment parasites live inside body cells Plasmodium – liver and blood cells Parasitic worms – cover themselves in host proteins HIV – live inside T-helper cells Smallpox Symptoms Red spots containing transparent fluid all over body. Spots fill with pus Eyelids swell and become glued together Smallpox Mortality 12-30% died Survivors often left blind and disfigured with scabs. Smallpox Eradication programme Started by WHO in 1956 Aimed to rid world of smallpox by 1977 Involved vaccination and surveillance Over 80% of populations at risk of the disease were vaccinated After any reported case everyone in the household and 30 surrounding households vaccinated – RING VACCINATION Smallpox Eradication programme Last case of smallpox reported in Somalia in 1977 World declared free of smallpox in 1980 Smallpox Eradication programme – why was it successful? Variola virus stable -> cheap as everyone used same vaccine Vaccine made from harmless strain of similar virus (vaccinia) Vaccine could be used at high temperatures Easy to identify infected people Smallpox doesn’t lie dormant in body Smallpox Eradication programme – why don’t all work? Political instability Poor infrastructure Unstable m-os Measles Caused by an airborne virus 9th leading cause of death worldwide Causes rash and fever Can have fatal complications Passive immunity from mothers in infants under 8 months Now quite a rare disease in developed countries due to vaccination Measles Transmitted easily in overcrowded, insanitary conditions Mainly affects malnourished infants with vitamin A deficiencies Responsible for many cases of childhood blindness and can cause severe brain damage Herd immunity of 93-95% needed to prevent transmission within a population. Blood from a cut will react with air and substances from damaged cells and platelets. Damaged cells will release the enzyme thrombokinase (or thromboplastin) which, together with factor X and factor VII and Ca2+ ions, will change prothrombin into thrombin. Thrombin will hydrolyse soluble fibrinogen into smaller insoluble fibrin molecules. These will form a network which captures erythrocytes and becomes a clot. HIV H – Human: virus can only infect humans I – Immuno-deficiency: the effect of the virus is to create a deficiency, a failure to work properly with the body’s immune system. V – Virus: one of its characteristics is that it is incapable reproducing by itself. It reproduces by taking over the machinery of the human cell How is HIV spread Bodily Fluids Blood Semen Vaginal secretions Breast milk Sexual Contact Sexual intercourse Oral sex Anal sex Blood to Blood Contact Sharing needles or syringes Tattooing - Piercing Accidental needle stick in a medical setting Incidental Cases Mother to baby during pregnancy and delivery Mother’s milk to baby During Dental Procedures The following body fluids are NOT infectious Saliva Tears Sweat Feces Urine Signs and symptoms HIV There are no true signs of having HIV. One may experience flu – like symptoms of chills, fever, night sweats, rashes, etc. Some will have no signs or symptoms. How HIV Works HIV gets into the bloodstream HIV targets white blood cells (T4 cells) Virus slowly destroys T4 cells Forces T4 cells to make copies of HIV Eventually the cell dies Moves on to other T4 cells Can be up to 10 years before person shows signs Phases of HIV infection Infection with no signs or symptoms HIV – does not mean AIDS Signs and symptoms AIDS – T4 cells are less than 200 cells per microliter of blood or serious conditions from long-term, damage to immune system Opportunistic Infections Testing ELISA – blood test that identifies whether a person has antibodies for HIV Western Blot Test – done to confirm the results of the Elisa test. Incubation Window – it can take 6 wks to 6 mths for anti. to form after exposure to HIV. This test should be done at least 6 wks after a person is or thinks they are infected. AIDS A – Acquired: a condition one must acquire or get infected with. I – Immune: it affects the body’s immune system, the part of the body which usually works to fight off germs such as bacteria and viruses. D – Deficiency: makes it not work properly S – Syndrome: a group of symptoms Signs and symptoms of AIDS There are no common signs or symptoms for AIDS People may experience opportunistic infections – when the immune system is weakened and can attack the body. EX.- pneumonia. AIDS is not spread by: Casual contact – dry mouth kissing, hugging, being sneezed on or coughed on. Mosquito bites How to Protect yourself Abstinence - 100% Have Safe Sex - Practice Monogamy – (when two people have intercourse with only each other for their entire lives). Don’t use dirty needles Get tested Some statistical information shows the extent of the problem. In 2006, nearly 40 million people were estimated to be living with HIV/AIDS, of whom 4.3 million had been newly infected. More than 60% of the people infected with HIV/AIDS were living in Sub- Saharan Africa. Nearly 3 million people died in 2006 of AIDS-related diseases and 2 million of these lived in Sub-Saharan Africa. In North America and Western Europe, the number of new infections has remained the same. In many other countries, the decrease in the number of new infections has slowed or in other countries the number of new infections has increased. It is believed that this is caused by a reduction in HIV prevention programmes. The social implications of AIDS are many and can be found on any of numerous websites. Some of these implications are listed below: 1- People with HIV/AIDS can suffer from stigma and discrimination. 2- Women are more likely to contract HIV from sex with an infected partner than men. This further increases the inequality between men and women in some countries. 3- People who die as a result of HIV/AIDS are often at an age where they are the most productive members of society. In countries were AIDS causes many deaths, a relatively large proportion of the work force may be removed, delaying economic growth. 4- If both parents die because of AIDS, the country will need to spend resources on caring for the orphans. 5- If one adult in a household suffers from HIV/AIDS, s/he may face unemployment and not be able to earn an income. This may push the entire household into poverty, further reducing the chances of obtaining anti-viral drugs. 6- Poverty in itself increases the chances of contracting HIV/AIDS due to a lack of information (no school) and/or being forced to have sex in exchange for food/money. Also the incidence of rape may increase, which is also a factor in spreading HIV/AIDS. 7- It is expensive to treat people with HIV/AIDS so obtaining insurance might be a problem. 8- Use of condoms increases.
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