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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings PowerPoint ® Lecture Slide Presentation prepared by Christine L. Case Microbiology.

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Presentation on theme: "Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings PowerPoint ® Lecture Slide Presentation prepared by Christine L. Case Microbiology."— Presentation transcript:

1 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings PowerPoint ® Lecture Slide Presentation prepared by Christine L. Case Microbiology B.E Pruitt & Jane J. Stein AN INTRODUCTION EIGHTH EDITION TORTORA FUNKE CASE Chapter 16 Nonspecific Defenses of the Host

2 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Nonspecific Defenses of the Host SusceptibilityLack of resistance to a disease Resistance Ability to ward off disease Nonspecific resistanceDefenses against any pathogen Specific resistanceImmunity, resistance (antibodies) to a specific pathogen

3 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Host Defenses Figure 16.1 Overview of the body’s defenses

4 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Skin (works generally if intact) Epidermis consists of tightly packed cells with Keratin, a protective protein, waterproof Mechanical Factors Describe the role of the skin and mucous membranes in nonspecific resistance.

5 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Human skin layers

6 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Mucous membranes (overcome by large numbers) Ciliary escalator: Microbes trapped in mucus are transported away from the lungs Lacrimal apparatus: Washes eye, removes microbes Saliva: Washes microbes off teeth and gums, tongue Mucus traps microbes, moved up and out by ciliary escalator Urine: Flows out Vaginal secretions: Flow out Mechanical Factors Differentiate between mechanical and chemical factors, and list five examples of each.

7 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

8 Ciliary escalator Microbes trapped in mucus produced by goblet cells, then propelled upward by cilia

9 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Fungistatic fatty acid (unsaturated) in sebum Sweat washes off skin (contains lysozyme) Low pH (3-5) of skin Lysozyme in perspiration, tears, saliva, and tissue fluids Low pH ( ) of gastric juice prevents microbe growth (except Helicobacter pylori) Transferrins in blood bind iron removing this nutrient NO (nitrous oxide) inhibits ATP production of microbes Chemical Factors

10 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens, preventing their growth on the host. Normal Microbiota Describe the role of normal microbiota in nonspecific resistance.

11 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

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13 Phago: eat Cyte: cell Ingestion of microbes or particles by a cell, performed by phagocytes (certain white blood cells) Phagocytosis Define phagocytosis and phagocyte.

14 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Percentage of each type of white cell in a sample of 100 white blood cells Differential White Cell Count Neutrophils60-70% Basophils0.5-1% Eosinophils2-4% Monocytes3-8% Lymphocytes20-25% Define differential blood cell count.

15 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Leukocytes (white blood cells) divided into granulocytes (neutrophils, basophils, eosinophils), lymphocytes, and monocytes Granulocytes: (dominate early in infection) Neutrophils: Phagocytic (most important) Basophils: Produce histamine Eosinophils: Toxic to parasites, some phagocytosis Lymphocytes: Involved in specific immunity Monocytes: Phagocytic as mature macrophages Fixed macrophages in lungs, liver, bronchi Wandering macrophages (enlarged monocytes) roam tissues White Blood Cells

16 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Principle kinds of leukocytes

17 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Lymphatic system

18 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Macrophage engulfing rod-shaped bacteria

19 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phagocytosis Figure 16.8a Describe the process of phagocytosis, and include the stages of adherence and ingestion.

20 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Microbial Evasion of Phagocytosis Inhibit adherence: M protein, capsules Streptococcus pyogenes, S. pneumoniae Kill phagocytes: LeukocidinsStaphylococcus aureus Lyse phagocytes: Membrane attack complex Listeriamonocytogenes Escape phagosomeShigella Prevent phagosome-lysosome fusion HIV Survive in phagolysosomeCoxiella burnetti Classify phagocytic cells, and describe the roles of granulocytes and monocytes.

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22 Redness Pain Heat Swelling (edema) Acute-phase proteins activated (complement, cytokine, kinins) – short, intense Chronic inflammation is a prolonged response Vasodilation (histamine, kinins, prostaglandins, leukotrienes) Margination and emigration of WBCs Tissue repair Inflammation – body response to cell damage List the stages of inflammation.

23 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Chemicals Released by Damaged Cells HistamineVasodilation, increased permeability of blood vessels KininsVasodilation, increased permeability of blood vessels ProstaglandinsIntensity histamine and kinin effect LeukotrienesIncreased permeability of blood vessels, phagocytic attachment Describe the roles of vasodilation, kinins, prostaglandins, and leukotrienes in inflammation.

24 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Inflammation Figure 16.9a, b

25 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Inflammation Figure 16.9c, d Describe phagocyte migration.

26 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phagocyte migration and Phagocytosis Figure 16.9c, d Phagocytes can stick to lining of blood vessels They also can squeeze through blood vessels Pus is the accumulation of damaged tissue, dead microbes, granulocytes, macrophages

27 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Hypothalamus normally set at 37°C Gram-negative endotoxin cause phagocytes to release interleukin 1 Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature Body increases rate of metabolism and shivering to raise temperature When IL-1 is eliminated, body temperature falls. (Crisis - sweating) Fever: Abnormally High Body Temperature

28 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Serum proteins (liquid in blood) activated in a cascade. Activate one another in a cascade to destroy invading microorganisms Outcomes of Complement Activation System Figure 16.10

29 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Effects of Complement Activation Cytolysis caused by complement Opsonization or immune adherence: enhanced phagocytosis Membrane attack complex: cytolysis Attract phagocytes Figure List the components of the complement system.

30 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Effects of Complement Activation (inflammation) Figure 16.12

31 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Classical Pathway of complement activation Figure Pathway initiated by antigen- antibody reaction Results in cytolysis, inflammation, and phagocytosis. Describe three pathways of activating complement.

32 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Alternative Pathway of complement activation Figure Pathway initiated by contact between proteins and pathogen

33 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Lectin Pathway of complement activation Figure Mannose- binding lectin binds to mannose, enhancing phagocytosis via classical and alternative pathways

34 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Some bacteria evade complement Capsules prevent C activation Surface lipid-carbohydrates prevent MAC formation Enzymatic digestion of C5a

35 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Alpha IFN & Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication Interferons are host-cell specific, but not virus-specific Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria Interferons (IFNs) Define interferon. Compare and contrast the actions of  -IFN,  -IFN, and  -IFN.

36 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Interferons (IFNs) – antiviral action of alpha and beta interferons Figure Viral RNA from an infecting virus enters the cell. The infecting virus replicates into new viruses. The infecting virus also induces the host cell to produce interferon on RNA (IFN-mRNA), which is translated into alpha and beta interferons. Interferons released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on uninfected neighboring host cells, inducing them to synthesize antiviral proteins (AVPs). These include oligoadenylate synthetase, and protein kinase. New viruses released by the virus-infected host cell infect neighboring host cells. 6 AVPs degrade viral m-RNA and inhibit protein synthesis and thus interfere with viral replication.


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