Presentation on theme: "Malaria Caused by 4 different Plasmodium species, these are parasitic protozoa,(eukaryotic) Each spends part of its life cycle in female Anopheles mosquitoes."— Presentation transcript:
1 Describe the causes and means of transmission of malaria, HIV/AIDS and TB.
2 MalariaCaused 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 cyclePlasmodium reproduces, bursts out of RBCs and infects more RBCsMosquitoes breed in stagnant waterBites usually occur in the evening on exposed skinGametes fuse in the mosquito’s intestine and produce more plasmodium
5 Malaria Control Measures Destroy mosquito breeding sites, clear stagnant waterPrevent mosquito bites, use nets for sleeping, wear cover-up clothing, use insecticide spray on skinIntroduce predators of mosquito larvaeUse insecticide to control populations of mosquitoesUse 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 insecticidesPlasmodium mutate and become resistant to anti-malarial drugs eg chloroquine,New anti-malarials have unpleasant side – effects, so they are not always takenNo effective vaccine- Plasmodium (protoctist) surface antigens change due to mutation, many different antigens on cell surfacePlasmodium only exposed in blood stream for a short time, spends most of time in human in liver cells or RBCsMosquito larvae predators get out of control and become pestsGlobal warming may extend Anopheles mosquito territoriesPolitical 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 bovisIn 1993 WHO declared the situation with TB a global emergencyBy 1998 WHO estimated that about 1/3 of the world’s population were infectedBetween 2002 and 2020 approx 1000 million people will be newly infected, over 150 million will become ill, 36 million will die
10 TuberculosisSpread 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 conditionsM. 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 monthsTB testing of cattle, destruction if infectedPasteurising milk to kill the bacteriaIsolate people while they are still infectiousContact tracing to find others likely to be infected
12 Problems with controlMany people with TB live in LEDCs so medical facilities are inadequate to ensure vaccination and /or DOTS takes placeContact tracing expensive and time-consuming, unlikely where funding for medical treatment and control is limitedMany 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 othersRepeated use of a range of anti-biotics is leading to development of resistant strainsInadequate housing and overcrowding means infection is passed on within these populationsPoor 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 foetusGlobal spread, highest prevalence in Africa and South-east Asia
15 HIV /AIDSInitial HIV infection may cause swollen lymph glands or a short-lived viral illnessInitial level of HIV in blood spikes and then falls againOver time HIV causes number of T helper cells (important components of the immune system that activate other cells) to fall dramaticallyEventually the immune system starts to fail and AIDS (aquired immuno deficiency syndrome) developsAIDS 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 infectedBlood donations screened for HIVBlood and blood products heat treated to prevent virus infectingDrug treatment to prevent HIV replicating in cells and slow AIDS development
17 Problems with controlLimited success changing sexual practices and increasing condom use by education programsLimited success with preventing drug users sharing needlesLong latent period when HIV+ person can continue to pass on virus to othersNo successful vaccine yet, HIV mutates quickly, hides inside body cellsDrugs to delay onset of AIDS are expensiveLack of funds in LEDCs for education programs and drug treatmentReluctance to know if HIV+ due to discrimination
18 Learning OutcomesDescribe 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 macrophagesLymphocytes eg:B cells, plasma cells, B memory cellsT 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 classPhagocytesNeutrophilsMonocytesMacrophagesB plasma cellsT killer cellsT helper cellsT and B memory cells
22 Functions of White Blood Cells Phagocytesengulf pathogens (usually a non-specific response)NeutrophilsMulti-lobed nucleus, travel in blood, may migrate to tissue fluid between cells. Short-lived, take part in phagocytosis, attracted to sites by histamine and monokines (released by macrophages and monocytes)MonocytesMade in bone marrow, travel in blood and become macrophages. Take part in phagocytosis and release monokinesMacrophages:large phagocytes permanently in lymph nodes and organs, long lived, may become APCs (antigen presenting cells) after ingesting a pathogen. Release monokines to attract neutrophils and stimulate B cells to turn into plasma cellsB plasma cellsdifferentiate from B cells (made and mature in bone marrow) produce antibodies specific to an antigen from a pathogenT killer cellsMade in bone marrow mature in thymus,kill infected body cells and destroy pathogen at same timeT helper cellsRelease cytokines that cause B cells to turn into plasma cells and stimulates phagocytosis by phagocytesT and B memory cellsRemain in blood long-term to react swiftly to second infection by same pathogen
24 Describe in detail and illustrate the 4 stages of phagocytosis (use AS vocabulary and knowledge of cell ultrastructure)RecognitionEngulfingDigestingRelease of waste productsDescribe and illustrate what happens at the end of phagocytosis if the phagocyte becomes an APC (Antigen Presenting Cell)
25 Immune responseThe 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 DefinitionsANTIGENAny molecule that can stimulate an immune response. Usually proteins, carbohydrates or glycoproteins of cell membranes or virus coatsANTIBODYMolecules 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 bondsConstant region that helps the antibody be recognised by and attach to phagocytesVariable region that is specific and complementary to each antigen. Millions of different ones are possible due to the huge variability of protein structuresHinge region that allows flexibility and attachment to more than one antigen moleculeA polypeptide is a long chain of amino acids joined by peptide bonds (ref to other module of AS spec)
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 flagellaBind to pathogens “flagging them up” to phagocytesBind 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 cellsLarge 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 RESPONSEFew cells with specific receptors for antigenSlow growth of specific lymphocyte populationSlow production of required antibodySlow elimination of pathogenSymptoms of infectiondevelopSECONDARY RESPONSEMany cells with specific receptors for antigen (memory cells from previous infection)Fast production of antibodyFast elimination of pathogenSymptoms of infection rarely develop