Transcript Chapter 16
TORTORA • FUNKE • CASE Microbiology AN INTRODUCTION EIGHTH EDITION B.E Pruitt & Jane J. Stein Chapter 16 Nonspecific Defenses of the Host Nonspecific Defenses of the Host • Susceptibility • • • • Lack of resistance to a disease Resistance Ability to ward off disease Nonspecific resistance Defenses against any pathogen Specific resistance Immunity, resistance to a specific pathogen Native (innate) species specific immunity Host Defenses Figure 16.1 First line of Defense Mechanical Factors Physical barriers to pathogens • Skin – Epidermis consists of tightly packed cells with – Keratin, a protective protein Mechanical Factors • 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 Chemical Factors • Fungistatic fatty acid in sebum • Low pH (3-5) of skin • Lysozyme in perspiration, tears, saliva, and tissue fluids • Low pH (1.2-3.0) of gastric juice • Transferrins in blood find iron • NO inhibits ATP production Normal Microbiota • Microbial antagonism/competitive exclusion: – Normal microbiota compete with pathogens. Second line of Defense 1. Phagocytosis 2. Inflammation 3. Fever 4. Antimicrobial substances Formed Elements In Blood (note functions) • RBC’s • WBC’s • • Agranulocytes • Monocytes • Lymphocytes Granulocytes • Neutrophils (PMNs) • Basophils • Eosinophils Table 16.1 Differential White Cell Count • Percentage of each type of white cell in a sample of 100 white blood cells Neutrophils 60-70% Basophils 0.5-1% Eosinophils 2-4% Monocytes 3-8% Lymphocytes 20-25% 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 Phagocytosis • Phago: eat • Cyte: cell • Ingestion of microbes or particles by a cell, performed by phagocytes Phagocytosis Figure 16.8a Microbial Evasion of Phagocytosis • Inhibit adherence: M protein, capsules Streptococcus pyogenes, S. pneumoniae • Kill phagocytes: Leukocidins Staphylococcus aureus • Lyse phagocytes: Membrane attack complex Listeriamonocytogenes • Escape phagosome Shigella • Prevent phagosome-lysosome fusion HIV • Survive in phagolysosome Coxiella burnetti and Mycobacteria spp Inflammation • • • • • Redness Pain Heat Swelling (edema) Acute-phase proteins activated (complement, cytokine, kinins) - chemical messengers • Vasodilation (histamine, kinins, prostaglandins, leukotrienes) - bring in more help • Margination and emigration of WBCs • Tissue repair Chemicals Released by Damaged Cells • Histamine Vasodilation, increased permeability of blood vessels • Kinins Vasodilation, increased permeability of blood vessels • Prostaglandins Intensity histamine and kinin effect • Leukotrienes Increased permeability of blood vessels, phagocytic attachment Inflammation Figure 16.9a, b Inflammation Figure 16.9c, d Fever: Abnormally High Body Temperature • 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) The Complement System Serum proteins activated in a cascade. Increasing as previous catalyzes the next step Outcomes of Complement system 1. Opsonization 2. Chemotaxic 3. Cell lysis Figure 16.10 Effects of Complement Activation • Opsonization or immune adherence: enhanced phagocytosis • Membrane attack complex: cytolysis • Attract Figure 16.11 Effects of Complement Activation Figure 16.12 Classical Pathway Figure 16.13 Alternative Pathway Figure 16.14 Lectin Pathway Figure 16.15 Some bacteria evade complement • Capsules prevent C’ activation • Surface lipid-carbohydrates prevent MAC (membrane attack complex C5b - C9) formation • Enzymatic digestion of C5a Interferons (IFNs) Antiviral proteins • 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) 2 The infecting virus replicates into new viruses. 5 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. 1 Viral RNA from an infecting virus enters the cell. 3 The infecting virus also induces the host cell to produce interferon on RNA (IFN-mRNA), which is translated into alpha and beta interferons. 4 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. Figure 16.16