Chapter 15 Microbio

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Anonymous
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Chapter 15 Microbio
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2010-07-13 18:38:47
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Microbiology SCC
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First/ Second Line of Defense
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  1. Order of events: Phagocytosis
    • 1. Chemotaxis
    • 2. Adherence
    • 3. Ingestion
    • 4. Digestion
    • 5. Formation of residual body
    • 6. Discharge of waste material
  2. Examples of 2 main phagocytes
    • Monocytes (macrophages)
    • Neutrophils
  3. Phagocytosis: Ingestion
    • By formation vesicle (by pseudopods of phagocyte) and
    • after ingestion called phagosome
  4. Phagocytosis: digestion
    Phagocyte fuses with lysosome (have digestion enzymes) --> Phagolysosome bacteria is digested
  5. Residual body
    Phagolysosome containing undigested components of pathogen
  6. Non specific defense
    Same immune response any type of pathogen

    Quick response time, no memory of previous exposure
  7. First Line of Defense
    • Skin
    • Mucous membranes
    • Secretions
    • Normal Microbiota
  8. Protective Factors of Skin
    • 1. Sebum/oil (lysozyme) rich in fatty acid --> acidic pH on skin
    • 2. Keratinized epidermis keeps skin dry
    • 3. Closely packed cells
    • 4. Periodic shredding of skin cells
    • 5. Sweat- high salt concentration
    • 6. Lysozyme present in sweat (damages peptidoglycan) hurt GM positive bacteria
  9. Protective factors of conjunctiva of eye
    • Tears (rich in salt and lysozyme)
    • Tears flush out eyes
  10. Protective factors of respiratory tract
    Mucous: Ciliary living (ciliary escalator)
  11. Protective factors of GI tract
    • Acidic pH (gastric juice)
    • Movement of food (peristalsis) through GI tract
  12. Genitourinary tract
    • Urine- flushes the urinary tract
    • Vaginal pH and normal floura is acidic (prevents pathogen growth)
  13. gastroferritin
    reduces iron for pathogen to use
  14. microbial antagonism
    Competition among microbes (observed b/w normal microbiota and pathogens)
  15. Normal microbiota protect host by
    • Occupying niches that pathogens might occupy
    • producing acids
    • producing bacteriocins
    • changing oxygen availability
  16. Second Line of Defense
    • Complement System
    • Inflammation
    • Phagocytosis
    • Fever
    • Antimicrobial compounds
  17. Antimicrobial compounds
    • Interferon
    • Transferrin
    • Antimicrobial peptides
  18. Blood
    • Plasma (fluid)
    • Formed elements RBC (Erythrocytes)
    • WBC (Leukocytes defense)
    • Platelets (Thrombocyts) blood clotting
  19. 3 Types of white blood cells
    • Granulocytes
    • Agranulocytes
    • Lymphocytes
  20. 3 Types of Granulocytes
    • Neutrophils
    • Basophils
    • Eosinophils
  21. Neutrophils
    • Granulocyte
    • Phagocytosis
  22. Basophils
    • Granulocytes
    • Produce histamine
  23. Eosinophils
    • Granulocyte
    • Allergic reaction, destroy helminths
  24. Agranulocytes (monocytes) Macrophages
    Large nucleus, mature into macrophages, phagocytosis
  25. 2 categories of agranulocytes (macrophages)
    • Wandering- Can leave blood vessel and reach infection)
    • Fixed- Non motile, localized to specific tissue
  26. Examples of Fixed agranulocytes
    • Microglia cells (nervous tissue)
    • Kupffer cells (liver)
  27. Lymphocytes
    • Natural Killer cells
    • T cells
    • B cells
  28. Helper T Cells
    Secrete cyotkine (chem messenger) and activates other cells (B cells, T cytotxic cells) Cytotoxic T Cells (destroy infected cells)

    tumor specific response
  29. High during viral infections
    Lympohtocytes
  30. Eosinophils
    High during allergies/ helminth infection
  31. HIgh w/ bacterial infection
    Neutrophils
  32. Plasma
    Has blood clotting factor
  33. Serum
    • Not clotting factors present (rich in antibodies)
    • Used to diagnose an infection by detecting presence of specific antibodies
  34. Primary lympoid organs
    • Production and maturation of blood cells
    • Red Bone Marrow (production of all RBCs)
    • Thymus gland (T lymphocytes mature here)
  35. Secondary lymphatic organs
    • Lymph nodes (maturation, storage of WBCs)
    • Spleen
    • Tonsils
    • Pever's patch (small intestine)
  36. Complement System
    Consists of a group of proteins called complement components (C1-C9, P, B, D). One component then triggers another. Present in inactive form in blood serum (no pathogen present)

    When activated, splits into two subcomponents

    All pathways activate C3 component
  37. Classical Pathway of complement activation
    • Mediated by antibodies against protein or polysaccharide angiten
    • (2 sites- antigen binding site; part of cell surface against which antibodies are produced)
  38. Alternative pathway for complement activation
    Mediated by factor B, P (properdin), D, able to recognize LPS (lipopolysaccharide) angitens
  39. Lectin Pathway of complement activation
    Carbohydrate binding proteins that bind to carbohydrate antigen of a pathogen
  40. Three results of complement system
    • Opsonization
    • Inflammation
    • Cytolysis
  41. Opsonization
    • Coat the pathogen, helps phagocyte recognize and ingest pathogen easily
    • C3b- oposonin, coating protein bind to antigens of pathogen
  42. Inflammation (and chemotaxis)
    By release of histamine from some cells (mast cells, ect.)
  43. Cytolysis
    Formation of MAC in plasma membrane of bacteria

    Destroys the pathogen (forms holes in pathogens membrane) C5b+C6+C7+C8+C9 all bind together and form an attacking complex which forms holes in invading pathogens cytoplasm membrane
  44. C3a activates
    C5--> C5a and C5 b
  45. C5a and C3a act as
    Chemotatic factors (attracts phagocytes) also initiates inflammation

    Mast cells have receptors for C3a, C5a, which activate mast cells to release histamine (vasodilator)
  46. Inflammation
    Localized, nonspecific immune response, 2nd defense
  47. Purpose of Inflammation
    • Prevent spread of pathogen
    • Destroy pathogen
    • Tissue repair
  48. Signs and symptoms of inflammation
    Pain, localized heat, redness, swelling
  49. Sequence of events of inflammation
    • 1. Tissue Damage
    • 2. Release of acute phase proteins (histamine, prostaglandins, leukotrienes)
    • 3. Vasodilation: Increase in diameter of blood vessel, supplies WBC's , more O2, clotting factors
    • 4. Phagocytic migration (Chemotaxis) (ex- C3a, C5a, complement componenet, leukotrienes)
    • 5. Phatgocytic margination: attachment of phagocyte to inner lining of blood vessels (endothelium)
    • 6. Phagocytic emigration (diapedesis)- phagocytes are released (squeezed out) between gaps of endothelial cells increased vascular permeability
    • 7. Phagocytosis
    • 8. Tissue Repair (more nutrients and O2)
  50. Examples of vasodilators
    Histamine, Protaglandins
  51. Protaglandin
    Increases vascular permeability
  52. Fever
    A systemic immune response (not localized)
  53. Purpose of fever
    Enhances immune response; helps inhibit growth of bacteria (denatures enzymes)
  54. Interferons
    Proteins produced in response to viral infection

    • Host-cell-specific (species specific) but not virus specific
    • Have to be of human orgin to create disease in humans
  55. Types of interferons
    • Alpha and Beta- Inhibit viral infection
    • Gmmas- activate macrophages and neutrophils (cytokines)
  56. Mechanism of alpha and beta interferons
    • Produced by a
    • viruses infected cells

    Infected cell secretes infereron that bind to receptor on neighboring, uninfected cell.

    • Uninfected cell is stimulated to produce anti-viral
    • protines (AVP’s)

    • AVP’s degrade viral RNA and inhibit
    • protein synthesis
  57. Transferrin
    Iron binding proteins in teh blood, reduces availability of free iron for pathogen
  58. Antimicrobial peptides
    • example: Defensins, 40 amino acids long
    • Broad spectrum of activity; inhibit metabolism, forms holes in membrane of pathogen

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