Describe the causes and means of transmission of malaria, HIV/AIDS and TB.

1. Describe the causes and means of transmission of malaria, HIV/AIDS and TB.

2. Malaria • Caused by 4 different Plasmodium species, these are parasitic protozoa,(eukaryotic) • Each spends part of its life cycle in female Anopheles mosquitoes. These act as vectors they transfer the Plasmodium to and from the human host. • Female mosquitoes need a blood meal to help their eggs develop, male mosquitoes only feed on plant sap

3. More than 40% of global population are at risk of Malaria

4. Plasmodium life cycle Plasmodium reproduces, bursts out of RBCs and infects more RBCs Mosquitoes breed in stagnant water Bites usually occur in the evening on exposed skin Gametes fuse in the mosquito’s intestine and produce more plasmodium

5. Malaria Control Measures • Destroy mosquito breeding sites, clear stagnant water • Prevent mosquito bites, use nets for sleeping, wear cover-up clothing, use insecticide spray on skin • Introduce predators of mosquito larvae • Use insecticide to control populations of mosquitoes • Use anti-malarial drugs to prevent people being infected by the parasite. Most work by inhibiting enzymes in the parasite and preventing normal metabolism and reproduction

6. Problems with control • Insecticides kill useful pollinating insects too • Mosquitoes become resistant to insecticides • Plasmodium mutate and become resistant to anti-malarial drugs egchloroquine, • New anti-malarials have unpleasant side – effects, so they are not always taken • No effective vaccine- Plasmodium (protoctist) surface antigens change due to mutation, many different antigens on cell surface • Plasmodium only exposed in blood stream for a short time, spends most of time in human in liver cells or RBCs • Mosquito larvae predators get out of control and become pests • Global warming may extend Anopheles mosquito territories • Political unrest in many malarial areas prevents adoption of effective control measures

7. Tuberculosis (TB) • Contagious, pandemic disease caused by the bacteria Mycobacterium tuberculosis or Mycobacterium bovis • In 1993 WHO declared the situation with TB a global emergency • By 1998 WHO estimated that about 1/3 of the world’s population were infected • Between 2002 and 2020 approx 1000 million people will be newly infected, over 150 million will become ill, 36 million will die

8. Global TB deaths 1990-1999

10. Tuberculosis • Spread by droplets from an infected person, produced when they cough, sneeze, talk or spit. • Most easily spread when people live and sleep in over-crowded conditions • M. bovis spreads in meat and milk from infected cattle

11. Control measures • BCG vaccine reduces chance of developing disease • Multi antibiotic treatment, ie DOTS (direct observation therapy, short course) for 6 – 12 months • TB testing of cattle, destruction if infected • Pasteurising milk to kill the bacteria • Isolate people while they are still infectious • Contact tracing to find others likely to be infected

12. Problems with control • Many people with TB live in LEDCs so medical facilities are inadequate to ensure vaccination and /or DOTS takes place • Contact tracing expensive and time-consuming, unlikely where funding for medical treatment and control is limited • Many people stop treatment when they feel better, bacteria are still present in lungs and will reproduce and spread to other tissues and be passed on to others • Repeated use of a range of anti-biotics is leading to development of resistant strains • Inadequate housing and overcrowding means infection is passed on within these populations • Poor populations reluctant to kill infected cattle

13. HIV/ AIDS Pandemic • Caused by Human Immunodeficiency Virus • Passed on by sexual intercourse, infected blood and blood products, sharing or re-using hypodermic needles used by an infected person, across HIV particles passing across placenta from mother to foetus • Global spread, highest prevalence in Africa and South-east Asia

14. Prevalence of HIV/AIDS

15. HIV /AIDS • Initial HIV infection may cause swollen lymph glands or a short-lived viral illness • Initial level of HIV in blood spikes and then falls again • Over time HIV causes number of T helper cells (important components of the immune system that activate other cells) to fall dramatically • Eventually the immune system starts to fail and AIDS (aquiredimmuno deficiency syndrome) develops • AIDS is recognised by the range of opportunistic infections and unusual cancers that occur in patients, these are usually kept in check by a healthy immune system

16. Control measures • Using condoms during sexual intercourse • Health education about “Safe Sex” • Contact tracing to find sexual partners and people likely to be infected • Blood donations screened for HIV • Blood and blood products heat treated to prevent virus infecting • Drug treatment to prevent HIV replicating in cells and slow AIDS development

17. Problems with control • Limited success changing sexual practices and increasing condom use by education programs • Limited success with preventing drug users sharing needles • Long latent period when HIV+ person can continue to pass on virus to others • No successful vaccine yet, HIV mutates quickly, hides inside body cells • Drugs to delay onset of AIDS are expensive • Lack of funds in LEDCs for education programs and drug treatment • Reluctance to know if HIV+ due to discrimination

18. Learning Outcomes Describe the primary lines of defence against pathogens and parasites (including skin and mucous membranes) and outline their importance (no details of skin structure are required). Describe the structure and mode of action of phagocytes. Define the term immune response

19. Describe the primary lines of defence against pathogens and parasites and outline their importance • Carry out the card sort activity and then complete the fill in the blanks sheet. (10 minutes total)

20. Different types of blood cells • Phagocytes eg: Neutrophils , monocytes and macrophages • Lymphocyteseg: B cells, plasma cells, B memory cells T cells, T killer, T helper and T memory cells

21. Work in groups to make a table about the structure and roles of the following cells (10 mins) Be prepared to feedback to class • Phagocytes • Neutrophils • Monocytes • Macrophages • B plasma cells • T killer cells • T helper cells • T and B memory cells

22. Functions of White Blood Cells

23. Phagocytosis

24. Describe in detail and illustrate the 4 stages of phagocytosis (use AS vocabulary and knowledge of cell ultrastructure) • Recognition • Engulfing • Digesting • Release of waste products • Describe and illustrate what happens at the end of phagocytosis if the phagocyte becomes an APC (Antigen Presenting Cell)

25. Immune response • The specific response to a pathogen which involves the action of the lymphocytes and the production of antibodies.

26. Learning Objectives • Define the terms antigen and antibody. • Describe, with the aid of diagrams, the structure of antibodies. • Outline the mode of action of antibodies, with reference to the neutralisation and agglutination of pathogens. • Compare and contrast the primary and secondary immune responses.

27. Definitions • ANTIGEN Any molecule that can stimulate an immune response. Usually proteins, carbohydrates or glycoproteins of cell membranes or virus coats • ANTIBODY Molecules made of protein, produced by plasma cells in response to antigens found on pathogens. Each has a binding site with a complementary shape to its specific antigen. Plasma cells can produce thousands of antibody molecules per second. What difference is there between an undifferentiated B lymphocyte and a plasma cell?

28. Describe with the aid of diagrams, the structure of antibodies. • 4 polypeptide chains (2 light+ 2 heavy) held together by di-sulphide bonds • Constant region that helps the antibody be recognised by and attach to phagocytes • Variable region that is specific and complementary to each antigen. Millions of different ones are possible due to the huge variability of protein structures • Hinge region that allows flexibility and attachment to more than one antigen molecule A polypeptide is a long chain of amino acids joined by peptide bonds (ref to other module of AS spec)

29. Antibody structures

30. Antibody action • Antibody molecules can: • Bind to antigens preventing pathogens entering cells (neutralisation) • Immobilise bacteria by sticking them together in clumps (agglutination) • Immobilise bacteria by binding to flagella • Bind to pathogens “flagging them up” to phagocytes • Bind to toxins preventing them having an effect on cells

31. Outline the mode of action of antibodies, with reference to the neutralisation and agglutination of pathogens. • Antibodies bind to the antigens on the outside of pathogens. These antigens may usually be used to bind to the host cells. The pathogen is “neutralised” and cannot infect the host cells • Large antibodies with many antigen binding sites can bind to many pathogens at the same time. The pathogens clump together “agglutination”

32. Compare and contrast primary ad secondary immune response

33. Compare and contrast primary ad secondary immune response • PRIMARY RESPONSE • Few cells with specific receptors for antigen • Slow growth of specific lymphocyte population • Slow production of required antibody • Slow elimination of pathogen • Symptoms of infectiondevelop • SECONDARY RESPONSE • Many cells with specific receptors for antigen (memory cells from previous infection) • Fast production of antibody • Fast elimination of pathogen • Symptoms of infection rarely develop

34. Complete the cloze exercises on cell mediated and humoral responses • Humoral • Disease, mitosis, plasma, pathogen, vesicles, selection, expansion, antigen-presenting cells, interleukins, RER, phagocytosis, plasma membrane, decrease, antigen, • Cell mediated • Short, antigen, symptoms, antibodies, replicating, selection, proteins, plasma, enzymes, expansion