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Yet Again another Pandemic threat

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  1. Yet Again another Pandemic threat http://www.who.int/csr/disease/avian_influenza/phase/en/index.html

  2. An influenza pandemic occurs when a new influenza virus appears against which the human population has no immunity, resulting in epidemics worldwide with enormous numbers of deaths and illness.

  3. Outbreaks of influenza in animals, especially when happening simultaneously with annual outbreaks of seasonal influenza in humans, increase the chances of a pandemic, through the merging of animal and human influenza viruses.

  4. During the last few years, the world has faced several threats with pandemic potential, making the occurrence of the next pandemic a matter of time.

  5. Some Links • Timeline for vaccine • A fact sheet on swine flue • who Now list this a N1H1 post pandemic period, N1H1 becomes pare of our seasional flue

  6. Some Numbers • Many Millions get flue • Each year 200,000 hospitalized • 35,000 die • Mortality rate 0.1% • SARS 10% • Bird flue up to 90% • Swine flue? Is it really 10%?

  7. Nonspecific Immunity Resistance  don’t get it Susceptibility  get it

  8. Nonspecific immunity (innate immunity) are the defenses that protect the body against any pathogen. • Are not normally set up against any particular pathogen. • Adaptive immunity: Immunity, resistance to a specific pathogen

  9. An Overview of the Body’s Defenses ANIMATION Host Defenses: The Big Picture Figure 16.1

  10. The Concept of Immunity • Host Toll-like receptors (TLRs) attach to Pathogen-associated molecular patterns (PAMPs) • TLRs induce cytokines that regulate the intensity and duration of immune responses

  11. The skin • Mechanical • Skin Structure • Saliva washes • Mucus traps and ciliary escalator • Urine, vaginal flows out • Chemical • Sebum w/ unsaturated fatty acids • Perspiration • Lysozyme • Acid conditions stomak(1.2-3pH) skin (3-5pH) • Normal microbiota • Transferrins, and NO

  12. Physical Factors • Skin • Epidermis consists of tightly packed cells with • Keratin, a protective protein Figure 16.2

  13. Ciliary Escalator Figure 24.7

  14. Ciliary Escalator Figure 16.4

  15. Phagocytosis • Define. • What does this look like? • What does this do?

  16. Chemical Factors • Fungistatic fatty acid in sebum • Low pH (3–5) of skin • Lysozyme in perspiration, tears, saliva, and urine • Low pH (1.2–3.0) of gastric juice • Low pH (3–5) of vaginal secretions

  17. Normal Microbiota and Innate Immunity • Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens or alter the environment • Commensal microbiota: One organism (microbe) benefits and the other (host) is unharmed • May be opportunistic pathogens

  18. Formed Elements in Blood

  19. Formed Elements in Blood

  20. Formed Elements in Blood

  21. Differential White Cell Count • Percentage of each type of white cell in a sample of 100 white blood cells

  22. White Blood Cells • Neutrophils: Phagocytic • Basophils: Produce histamine • Eosinophils: Toxic to parasites, some phagocytosis • Monocytes: Phagocytic as mature macrophages • Fixed macrophages in lungs, liver, bronchi • Wandering macrophages roam tissues • Lymphocytes: Involved in specific immunity

  23. Components of Lymphatic System Figure 16.5a

  24. The Lymphatic System ANIMATION Host Defenses: Overview Figure 16.5b–c

  25. Phagocytosis • Phago: From Greek, meaning eat • Cyte: From Greek, meaning cell • Ingestion of microbes or particles by a cell, performed by phagocytes Figure 16.6

  26. Phagocytosis Figure 16.7

  27. Phagocytosis ANIMATION Phagocytosis: Overview ANIMATION Phagocytosis: Mechanism

  28. Microbial Evasion of Phagocytosis

  29. Actions of phagocytic cells • Neutrophils (granulocyte) phagocyte • Increase in number during infection (leukocytosis) • Neutrophils are most important • Can act as antigen presenting cells (APC) • Important in specific resistance

  30. Mechanism of phagocytosis • Chemotaxis to pathogen • Adherence • Engulfment • Killing • Resistance of microbes can be seen in some ability to live even after phagocytosis.

  31. Inflammation • Redness • Pain • Heat • Swelling (edema) • Acute-phase proteins activated (complement, cytokine, kinins) • Vasodilation (histamine, kinins, prostaglandins, leukotrienes) • Margination and emigration of WBCs • Tissue repair

  32. Chemicals Released by Damaged Cells

  33. Fever • Body temp is controlled by the brain • High temp in response to IL-1 • Caused by • Bacterial endotoxins • Interleukin-1 • Chills indicate rising body temp (crisis)

  34. Disadvantages Tachycardia Acidosis Dehydration 44–46°C fatal Fever • Advantages • Increases transferrins • Increases IL–1 activity • Produces Interferon

  35. Antimicrobial substances • IFN- and IFN-: Cause cells to produce antiviral proteins that inhibit viral replication • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria • Lysozyme • Acids on skin • Complement

  36. Antiviral Actions of Interferons (IFNs) Figure 16.15

  37. Antimicrobial peptides Lyse bacterial cells Innate Immunity • Transferrins • Bind serum iron

  38. Deficiencies in complement can result in an increased susceptibility to disease

  39. The Complement System • Serum proteins activated in a cascade • Activated by • Antigen-antibody reaction • Proteins C3, B, D, P and a pathogen ANIMATION Complement System: Overview ANIMATION Complement System: Activation

  40. The Complement System • C3b causes opsonization • C3a + C5a cause inflammation • C5b + C6 + C7 + C8 + C9 cause cell lysis ANIMATION Complement System: Results

  41. The Complement System Figure 16.9

  42. Effects of Complement Activation • Opsonization or immune adherence: Enhanced phagocytosis • Membrane attack complex: Cytolysis • Attract phagocytes Figure 16.10

  43. Inflammation Stimulated by Complement Figure 16.11

  44. Classical Pathway of Complement Activation Figure 16.12

  45. Alternative Pathway of Complement Activation Figure 16.13

  46. Lectin Pathway of Complement Activation Figure 16.14

  47. Some Bacteria Evade Complement • Capsules prevent C activation • Surface lipid-carbohydrates prevent membrane attack complex (MAC) formation • Enzymatic digestion of C5a