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
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 to a specific pathogen
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Host Defenses Figure 16.1
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Skin Epidermis consists of tightly packed cells with Keratin, a protective protein Mechanical Factors
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Mucous membranes Ciliary escalator: Microbes trapped in mucus are transported away from the lungs Lacrimal apparatus: Washes eye Saliva: Washes microbes off Urine: Flows out Vaginal secretions: Flow out Mechanical Factors
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Fungistatic fatty acid in sebum Low pH (3-5) of skin Lysozyme in perspiration, tears, saliva, and tissue fluids Low pH ( ) of gastric juice Transferrins in blood find iron NO inhibits ATP production Chemical Factors
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens. Normal Microbiota
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements In Blood Table 16.1
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%
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings 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 White Blood Cells
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phago: eat Cyte: cell Ingestion of microbes or particles by a cell, performed by phagocytes Phagocytosis
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phagocytosis Figure 16.8a
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
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Redness Pain Heat Swelling (edema) Acute-phase proteins activated (complement, cytokine, kinins) Vasodilation (histamine, kinins, prostaglandins, leukotrienes) Margination and emigration of WBCs Tissue repair Inflammation
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
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Inflammation Figure 16.9a, b
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Inflammation Figure 16.9c, d
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) Fever: Abnormally High Body Temperature
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Serum proteins activated in a cascade. The Complement System Figure 16.10
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Effects of Complement Activation Opsonization or immune adherence: enhanced phagocytosis Membrane attack complex: cytolysis Attract phagocytes Figure 16.11
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Effects of Complement Activation Figure 16.12
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Classical Pathway Figure 16.13
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Alternative Pathway Figure 16.14
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Lectin Pathway Figure 16.15
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
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Alpha IFN & Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria Interferons (IFNs)
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Interferons (IFNs) 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.