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					Koch’s Postulate

 Organism should be constantly associated with the lesions of the disease  Should be possible to isolate the organism in pure culture from the lesions of the disease  The isolated organism when inoculated in suitable laboratory animals should reproduce the same disease  Should be possible to re-isolate the organism in pure cultre from the lesions produced in the experimental animals.  Antibodies should be demonstrable in the serum of patients.

Father of Microbiology Father of Bacteriology

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Louis Pasteur Robert Koch - bacteriology

1st Vaccine

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Small pox vaccine – Edward Jenner

Initial Immune Response

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Neutrophils IgM antibodies & IgA (in saliva, sweat, tears, etc. Prolonged  macrophages & IgG IgE in allergic reactions & parasites.

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Intracellular Phagocytosis Pathways

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Oxygen Dependent o Lysozyme o Cathepsin o Lactoferrin Oxygen Independent o Hypochlorus Acid & singlet Oxygen o Superoxide anion & hydrogen peroxide

Inflammation Clinical Features

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Rubor Dolor Tumor Calor Loss of Function

Acute Phase Proteins

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C-Reactive Protein Alpha-1-antitrypsin Haptoglobin Ceruloplasmin Normal serum proteins-synthesized in liver  ↑levels w/ inflammation, infection & trauma.  Aid innate immunity

Defensins

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Innate immunity component Highly cationic peptides that create pores in bacterial wall  death Alpha  GIT & Beta  Lower respiratory tract.

Pyrogenic Proteins

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Interleukin 1 & 6 Prostoglandins

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T-Cells

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Lymphocytes that carry TCR, CD2 & CD3 marker. CD 3  transmembrane signal transduction. T-Helper = CD4  MHC class II(HLA-DR/DQ) (presented by Antigen Presenting Cell) T-Killer = CD8  MHC class I Natural Killer  CD16 & 56 – innate immunity. Secrete perforins (TNF-β) Killer Cells  Fc Portion of IgG. Antibody dependent cytotoxicity Lymphokine Activated Killer cells  NK + IL=2. Cytotoxic to tumor cells. T-Suppressor cells  CD8  suppress/block immune response via Th cells or B cells Delayed hypersensitivity T-Cells  CD4 + (Th cell) Differentiation occurs in Thymus  In cortex 2x (-)  2x (+)  medulla  differentiation  blood Act in Cell Mediated Immunity & Antibody mediated immunity.

B-Cells

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No thymus required for maturation. Ssurface immunoglobulin (IgM & IgD)  definitive for B-cells Also have CD19, CD20, CD21, & CD22 Secondary dev.  Antigen dependent. Helper T-Cell  Activated B-cells  pasma cells producing Abs to specific Ag.

DiGeorge Syndrome

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Abscence of a thymus  ↓T-cellls  potentially lethal wasting disease Pts. prone to chronic infections with viral, bacterial, fungal or protozoal agents.

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Haptens

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Non-immunogenic substances that become immunogenic when linked to a carrier protein. Simple: No precipitate is produced whn comiined with specific antibodies as they are univalent in nature Complex: Combine with specific antibodies to form ppts. As they are polyvalent.

T-Cell Independent Antigens

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Can directly stimulate antibody formation by β-lymphocyte cells w/o involving T-cells. IgM & IgG3 No immunological memory Don’t require processing by macrophages Metabolized slowly

T-Cell Dependent

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TD – antigens Need T-Cell Produce immunological memory Require processing by macrophage.

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Hypersensitivity Types & Mechanism

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Type 1: Anaphylaxis  IgE + Ag  Fc receptors on mast cells & basophils  rapid degranulation(1⁰ inflammatory mediator + release of IL3,4,5,&6)  acute inflammatory reaction (↑ vaso perm.; smooth muscle contraction; granulocyte chemotaxis and extravasation)  2⁰ mediators. o Ag pres to Th2 cells –(IL-4, IL-13)B-cell IgE prodction Type 2: Cytotoxic  IgG (rarely IgM)  mediated by complement classic cascade or cellular mechanisms.--> attaches via Fab. Bridges to complement via Fc region.  complement-mediated lysis. (goodpasture’s, myasethenia gravis, graft rejection, autoimmune hemolytic anemia & thrombocytopenic purpura) Type 3: Immune complex  Ag-Ab complexes deposited in tissue  complement mediated  PMN infiltration (arthus rxn, serum sickness, arthritis, vasculitis, nephritis, pneumonitis) Type 4: Delayed/Cell Mediated – sensitized T-Cells  On contact w/ specific Ag releases lymphokines  Macrophages, leukocytes & tissue cells delayed hypersensitivity (tuberculin test, contact hypersensitivity (chemicals, plants, topically applied drugs, cosmetics soaps, Haptens)

Type I Hypersensitivity Treatment

Symptomatic  Receptor blockers: Antihistamine, antileukotriene  Bronchodialtors: β-agonists(inhalants Prevent Mast Celll Degranulation  Ca++ influx inhibitor (chrmolyn sodium)  Phosphodiesrease (thephylline) Immunotherapy  Hyposensitization  Anti-IgE(Fc) Antibody

Types of Complement Deficiency

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C1 esterase inhibitor deficiency  hereditary angioedema C3 deficiency – impaired opsonisation – infections by capsulated bacteria C5 deficiency – impaired chemotaxis MAC deficiency – recurrent and severe Niesseria infection C1,2,4 deficiency – reduced clearance of immune complexes.

Phagocytic Disorders

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Chronic granulomatous diseases G6PD deficiency Myeloperoxidase deficiency Chediak Higashi disease Job’s syndrome Tuftsin deficiency Adhesion deficiency

B-Cell Deficiency

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Lack of Stem cells – SCID Maturation Deficiency– x-linked agamma globiulinemia (Bruton’s D) o Common variable ID – affects antibodies Class switching deficiency – Hyper IGM syndrome Transient Hypogammaglobulinemia of infancy  ↓CD4 help Secretory component deficiency - IgA deficiency

T-Cell Deficiency

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Congenital athymia – DiGeorge’s Syndrome Chronic mucocutaneous candidiasis – reduced macrophage MIF Bare lymphocyte syndrome – defective expression of MHC II CF: recurrent viral, bacterial, fungal, mycobacterial & protazo

Combined Immunodeficiency

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SCID – X-linked/autosomal recesive  lymphoenia & thymic hypolasia  enzyme defects Nazelofs Syndrome Wiskott Aldrich Syndrom Ataxia Telangiectasia -

Consequences of Antibody Binding

Auto Immune Affiliated Genes

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HLA-DR2 & HLA-DR3 – SLE – Anti-Nuclear Ab. HLA-DR2 – Goodpasture’s Syndrome HLA-DR4 – Rheumatoid arthritis –Synovial fluid  TNF, IL-1 & IL-8  Rheumatoid Factor (IgM) in serum HLA-B27 – Ankylosing Spondylitis, Reiter’s Syndrom (reactive arthritis, conjunctivitis, urethritis  w/ bacterial infection like shigella, salmonella, campylobacter, or Chlamydia)

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Carinoembryonic Antigen

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Found in embryonic gut & associated orgains during 1st & 2nd trimesters. ↑levels of this Ag in pts w/ carcinoma of the colan, pancrease, breast or liver. Good prognostic marker

α-fetoprotein

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Fetal liver produces & is present in high concentrations Marker for hepatoma Non-specific –found in several other malignant & non-malignant dis. In chemically induced tumors – tumor Ag are tumor specific In virus induced tumors – tumor Ags are virus specific

Sialomucin

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Mucoprotein that masks tumor antiges  not recognized as foreign by immune system.

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Mechanisms of Tumor Immunity

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Modulation of surface Ag. (stop expressing  immunologically invisible) Masking tumor antigens – Sialomucin  not recognized as foreign Production of blocking antibodies Fast rate of proliferation of malignant cells  tumor cells sneak through and proliferate so fast that immune system is overcome. Suppression of Cell Mediated Immunity– TGF-b suppresses CMI

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posted:11/22/2008
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