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AS Level Biology - 10/11) Infectious Diseases and Immunity

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Finally, to end the AS level syllabus - learn about the diseases that pose threats not only to ourselves but to the community as a whole for being contagious. Also learn about how our body organizes a military section to protect us - discover how the army can be come turncoat and how espionage and information collection can be helpful in secondary responses.

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AS Level Biology - 10/11) Infectious Diseases and Immunity

  1. 1. Infectious Diseases And Antibiotics
  2. 2. Infectious Diseases  Diseases caused by pathogens  Some disease affect us for short periods of time – common cold measles, influenza  Others are more chronic – TB, AIDs  Infectious diseases are not like COPD or coronary heart diseases which are degenerative and are not caused by pathogens
  3. 3. Infectious Diseases  Some diseases may even be transmitted without the person contracting it – such person is called carrier  Pathogens pass from one host to another in a transmission cycle  The 5 major diseases required in this syllabus include: Cholera, Malaria, HIV-AIDs, Measles, TB
  4. 4. More definitions  Endemic: Describing a disease that is always present in a population  Incidence: The number of people diagnosed with a disease over a period of time  Prevalence: The number of people with the disease at any one time  Pandemic: An increase in number of cases throughout a continent or across the world
  5. 5. Cholera
  6. 6. Cholera  Caused by Vibrio cholerae  Food-borne, Water-borne  Distribution: Asia, Africa, Latin America  Incubation period: 2 hours – 5 days  Site of action: Small intestine  Diagnosis: Microscopic examination of feces
  7. 7. Cholera Causes  Vibrio Cholerae inhibits the cell in the small intestine – release choleragen  Disrupting the osmotic balance, causing the cell to release large quantity of water due to lost of salt  Transmitted in water – uncontaminated food, feces, in cooking utensils, vegetable irrigated with infected water  Hence the disease is endemic in areas with poor sanitation
  8. 8. Cholera Symptoms  Loss of fluid  Loss of salt  Dehydration  Weakness  Severe diarrhea (rice water)
  9. 9. Treatment/ Prevention  Rehydration – could be through Oral Rehydration Therapy (ORT)  Uses glucose is effective – it is taken right into the blood  Prevention include development of sewage system  Provision of clean water  No inadequate cooking  Always tracing cholera epidemic  Vaccines are short term and not very effective
  10. 10. Different Strains  O1 – original strains  EL TOR – transmitted by ship sewage and into sea food  1992: new strain O139 – replaces El Tor very quickly – may be more virulent
  11. 11. Malaria
  12. 12. Malaria  Caused by protoctist – Plasmodium  Insect vector – female anopheles mosquitoes  Distribution: The tropics  Site of action: Liver, Red Blood Cells, Brain  Incubation: A week to a year  Diagnosis: Microscopial examination of blood. Dip stick test
  13. 13. Malaria transmissions  Anopheles feeds on human blood that is infected  Pathogen gametes taken up – fuses in the mosquito’s gut – enters the salivary gland  When it bites another person, it is released with the anticoagulant the mosquito uses to prevent blood clot  Malaria can be transmitted through placenta  Also, by blood transfusion  Plasmodium multiplies in both human and mosquito  People can become immune from malaria – nut only as long as they are constantly in contact with the disease
  14. 14. Treatment  Anti-malarial/ prophylactic (preventive) drug: Quinine, Mefloquine  Chloroguine (inhibits protein synthesis)  Proguanil (inhibits sexual reproduction)  Strains of drug resistant plasmodium have developed (one resisting mefloquine appear in Thailand-Laos border)  Some doctors can misdiagnose initial malaria symptom as influenza  Some people do not realize they lose immunity when they re- enter their home country after years of being away
  15. 15. Prevention  Reduce number of mosquitoes - Destroy its habitat, release males with no gamete, use of insecticides  Avoid being bitten - nets, insect repellants  Drugs - Chloroquine
  16. 16. AIDs Acquired Immuno Deficiency Virus
  17. 17. AIDs  A syndrome caused by a retrovirus  Retrovirus: Those with RNA  Human immunodeficiency virus
  18. 18. HIV  Infects and destroy T-helper cells of the immune system  Immune systems therefore do not respond effectively  The body is made vulnerable to other diseases – common cold and TB  AIDs – is a conglomeration of opportunistic diseases
  19. 19. HIV Transmission  HIV is transmitted by sexual intercourses – bodily fluid exchange  Transmitted in blood transfusion  Across placenta from mother to child  Needle sharing  If someone is discovered to have HIV – they are asked to contact sexual partner immediately
  20. 20. HIV Transmission  Pregnant woman are advised not to breastfeed their children  Viral particles can be found in breast milk  HIV positive woman use antiretroviral drug before delivery
  21. 21. Treatment  Cannot be cured  Spreads of AIDs can be slowed down  Using variety of drugs – problems here are side effects and cost  Zidovudine – binds to/ block action of reverse transcriptase – stopping replication  Increasing life expectancy
  22. 22. Prevention  Controls of HIV include contact tracing  Programs to exchange used needles for better ones  More care/ control into working on blood transfusion  Ante-natal care
  23. 23. TB Tuberculosis
  24. 24. Tuberculosis  Pathogens: Mycobacterium Tuberculosis, Mycobacterium Bovis  Transmissions: Airborne droplets, undercooked meat, unpasteurized milk  Distribution: Worldwide  Incubation: Weeks – years  Site of action: primary infection in lungs, secondary in lymph nodes, bones, guts  Diagnosis: microscopic examination of sputum, chest X-ray
  25. 25. Tuberculosis Symptoms  Coughing blood  Coughs  Chest pain  Shortness of breath  Fever  Sweating  Weight Loss
  26. 26. Transmission  Airborne disease – in aerosol droplets  Infect the malnutritioned  Those living in overcrowded conditions – at risk  Opportunistic infection of AIDs  TB transmission can come from cattle milk/ meat  1940s: introduction of Streptomycin  1950s: Introduction of Vaccines  The disease was thought to have been eradicated, now it’s on the rise
  27. 27. Treatment Tuberculosis  When diagnosed – the patient should be isolated  Treatment: Uses several drugs to ensure death to the bacteria  6 – 9 months long  The bacteria – slow growing and not sensitive to drugs  The patient MUST complete the whole course of drug or risk the bacteria becoming resistant
  28. 28. Drug Resistance  Some bacteria survive the treatment, mutate and become drug resistance  DOTS (Direct Observational Treatment Program) used to ensure complete process in the course of treatment  Isoniazid/ Rifampicin used
  29. 29. Drug Resistance  MDR-TB (Multiple-Drug-Resistant) are on the rise  They are now resistant to Isoniazid and Rifampicin
  30. 30. Tuberculosis prevention  BCG Vaccine  Protects 70-80% of people receiving it  Effectiveness of vaccine reduces with age unless exposed to TB  TB can still be transmitted between cattle and human – cattle are tested on routines, milk is always pasteurized  Contact tracing is very important
  31. 31. Measles
  32. 32. Measles Cause  Virus enters the body and infects respiratory tract  Rash appears, runny nose, cough, watery eyes, white spots inside the cheek  Pneumonia  Sinus infection  Brain damage  Are all symptoms
  33. 33. Measles transmission  One of the most contagious disease  Sneezing/ Coughin can release droplets with millions of viruses  Initial immunity provided for infant from antibodies  May infect those deficient of vitamin A
  34. 34. Antibiotics
  35. 35. Antibiotic  Selective toxins  Kill or disable pathogen without harming the host  Only work on bacteria and some on virus  They are derived from living organisms  Bacteriostatic: Stop/ prevent bacterial growth  Bactericidal: Kills Bacteria
  36. 36. Penicillin  When bacteria grow – they punch holes into their walls with enzyme autolysin – then they use peptidoglycan to form crosslinks within those holes to strengthen the cell wall  Penicillin prevents Peptidoglycan from forming – hence the cell wall of the bacteria continues to find new holes until they take up too much water and burst
  37. 37. Antibiotic Resistance  Tuberculosis has impermeable wall and has an enzyme that can break down penicillin  Bacterial membranes can sometimes pump out antibiotics  Eg. Enzyme beta-lactamase can be found in soil bacteria which grow in unfavorable condition – this enzyme can break down penicillin – it is transmitted via horizontal and vertical transmission to other bacteria
  38. 38. Antibiotic Resistance  Pathogens can develop resistance to antibiotics  Developing enzymes for destroying penicillin  Can develop if people misuse antibiotic  There are two ways by which resistance can be transmitted – vertical and horizontal
  39. 39. Effectively Using Antibiotic  Widespread use of antibiotic can lead to bacteria developing multiple resistance (one plasmid carrying resistance for many antibiotics)  Should be used sparingly  Only use against bacteria and not virus
  40. 40. Immunity And Vaccines/ Monoclonal Antibodies
  41. 41. External Defences  Defenses that act as the first line of defense for our body  The external defenses of our body include:  Our skin  Our respiratory tract’s goblet cells and nasal hair  Our stomach acid
  42. 42. Internal Defences
  43. 43. Phagocytes
  44. 44. Phagocytes  White blood cells produced in bone marrows  When pathogens attack a cell – the cell releases histamine  In the process of chemotaxis – the cell uses histamine, in combination with bacterial chemical to call for phagocytes  The phagocytes connect with the antigen – engulfing them in phagocytosis and destroying them
  45. 45. Neutrophils  Produced in the bone marrow  Travel throughout the body  Usually conduct phagocytosis on antigens  Short lived cells  Patrol tissues
  46. 46. Macrophages  Larger  More like bodyguard – found in specific parts of the body – spleen, kidney etc.  Travels in blood as monocyte until reaching the place of guardian  They cut up pathogens to be displayed to T-Cells
  47. 47. Lymphocytes
  48. 48. Lymphocytes  Smaller than phagocytes  Have large nucleus that fill most of the cell  B-Lymphocytes  T-Lymphocytes  Only mature lymphocytes can carry out immune responses  Each lymphocyte specialized to respond to specific antigens
  49. 49. T-Cells  Have specific receptors – specific to one antigen  Activated when antigen is in contact with cells or presented to them by macrophages  Release cytokines – stimulate B-cells to divide – stimulates Cytotoxic T-cells to differentiate
  50. 50. B-Cells  B-cells produce antibodies  They can only produce for one type of pathogen  When received messages from T-cells the B-cells begin the process of clonal selection
  51. 51. Clonal Selection  B-cells specific to the antigen begins to divide  Some differentiate into memory cells  Others into plasma cells
  52. 52. Clonal Expansion  Plasma cells divide and release antibodies  Memory cells divide and remain in the body  If the pathogen returns, they respond pretty much immediately
  53. 53. Primary Responses  Macrophage will attack  B-cells will go through clonal selection and expansion  It will take more time for antibodies to be produced and invaders to be suppresses
  54. 54. Secondary Responses  The memory cells recognize the pathogens  Immediate attacking  The invaders are immediately suppresses  Memories are over a lifetime  Except for common cold and influenza that mutate all the time
  55. 55. Antibodies  Globular glycoproteins  Used to identify and neutralize foreign objects  They can protect the cells by neutralizing toxins, kill the bacteria by causing bursting, top the pathogen by sticking to it, attaching to its flagella
  56. 56. Antibodies
  57. 57. Immunity Active, passive, Artificial, Natural
  58. 58. Active Immunity  Immunity that are derived from real infections  Can be artificial: In the form of vaccination  Can be natural: in the form of actual infection
  59. 59. Passive Immunity  Immunity that is given and is usually temporary  Artificial: Usually by injections of anti toxins  Natural: Antibodies passed on the children in breast milk (in colostrum – has IgA)
  60. 60. Vaccines
  61. 61. Vaccines as an Artificial immunity  A prepared antigen used to stimulate an immune response artificially  May use dead pathogens  Or those that attenuated
  62. 62. Problem: Poor Responses  Sometimes there is poor response  The person may have a lack lusting immune system  May be malnutritioned – cannot produce antibodies  May require buffer
  63. 63. Problem: Live Virus/ Herd immunity  Sometimes virus can continue to infect other people  Herd immunity is required to protect the entire community  This means the entire or most of the population are vaccinated sot he virus cannot survive
  64. 64. Problem: Antigenic Variation  Virus may mutate into many forms and strains  For example, Cholera has mutated several times over the past decades  Tuberculosis mutated to resist drug treatments in the forms of MDR-TB (Multiple-Drug Resistant Tuberculosis)
  65. 65. Problem: Antigenic Concealment  Virus may hide itself  For example, Cholera can conceal itself in the small intestine
  66. 66. Autoimmune Disease
  67. 67. Autoimmune Disease  Usually when T-cells are produced that are somehow meant to attack self-antigen they are destroyed in early stages  But in rare circumstances, they escaped detection  These T-cells proceed to order the attack of the human it was create to protect
  68. 68. Myasthenia Gravis  This is caused by a complex process where certain inhibition by antibodies caused by the deformed T-Cells stop transmission of electrical impulse between nerve cells and muscle cells  This causes muscle weakness
  69. 69. Multiple Sclerosis  Destruction of the myelin sheath on the nerve cells  Nerve impulses not transmittedLost of work in the CNS (Central Nervous System)  MRI scan can detect the plaque/ degenerative area  Symptoms: Muscle weakness, loss of sensory input, poor vision, mental problems
  70. 70. Rheumatoid Arthritis  Attack the joints and spread to the rest of the body  Start in fingers, hands then spread to the rest of the body  Tendons inflames, muscle spasm and pain
  71. 71. Type 1 Diabetes  Inhibition of the islets of Langerhans  Stop the production of insulin  Hence leads to high blood sugar content
  72. 72. Monoclonal Antibodies
  73. 73. Monoclonal Antibodies  Antibodies that are produced by human over and over again for uses that we want  Important because it can be use for diagnosis and treatment  Normal antibodies are hard to replicate because B- cells that divide do not produce antibodies and plasma cells that produce antibodies, do not divide.
  74. 74. Making such Antibodies  Inject an animal with an antigen that would induce an immune response that would produce the kind of plasma cell we want  Extract the plasma cell from the spleen of the animal  Fuses the plasma cell with cancer cell  The cell will begin to divide
  75. 75. Diagnosis with Mabs  Mabs are marked by radioactive markers  They are sent into the blood (sometimes to detect blood clot)  When they reach the ‘destination’ – the doctors can detect the clot
  76. 76. Treatment with Mabs  Can pose problems because they have to be administered more than once  Because the Mabs are from animals – they are still non-self, so our immune response will soon detect that too  We can still modify the sugar chains of the antibodies to make them look like ours  Or change the gene that code for those chains… same result
  77. 77. Trastuzumab  Treat breast cancer  Binds to cells that multiply in abnormal quantity  Marks for destruction for immune response
  78. 78. Ipilumab  Treat for Melanoma – a skin cancer  Blocks the actions of the proteins that stop the production of T-cells  Hence sustain the immune response
  79. 79. Infliximab  Treat Rheumatoid Arthritis  Binds to the proteins secreted by T-cells that damage the joints  Usually takes up to 2 months to treat  Important that these antibodies are humanized
  80. 80. Rituximab  Binds to the surface membrane of B-cells  Cause the death of the cell eventually  Used to treat diseases where there are over production of B-cells – leukemia (cancer of the bone marrow – causing deformed cells to be created)  May be used against Rheumatoid arthritis, Multiple Sclerosis and Myasthenia Gravis