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Yet Again another Pandemic threat. http://www.who.int/csr/disease/avian_influenza/phase/en/index.html.
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Yet Again another Pandemic threat http://www.who.int/csr/disease/avian_influenza/phase/en/index.html
An influenza pandemic occurs when a new influenza virus appears against which the human population has no immunity, resulting in epidemics worldwide with enormous numbers of deaths and illness.
Outbreaks of influenza in animals, especially when happening simultaneously with annual outbreaks of seasonal influenza in humans, increase the chances of a pandemic, through the merging of animal and human influenza viruses.
During the last few years, the world has faced several threats with pandemic potential, making the occurrence of the next pandemic a matter of time.
Some Links • Timeline for vaccine • A fact sheet on swine flue • who Now list this a N1H1 post pandemic period, N1H1 becomes pare of our seasional flue
Some Numbers • Many Millions get flue • Each year 200,000 hospitalized • 35,000 die • Mortality rate 0.1% • SARS 10% • Bird flue up to 90% • Swine flue? Is it really 10%?
Nonspecific Immunity Resistance don’t get it Susceptibility get it
Nonspecific immunity (innate immunity) are the defenses that protect the body against any pathogen. • Are not normally set up against any particular pathogen. • Adaptive immunity: Immunity, resistance to a specific pathogen
An Overview of the Body’s Defenses ANIMATION Host Defenses: The Big Picture Figure 16.1
The Concept of Immunity • Host Toll-like receptors (TLRs) attach to Pathogen-associated molecular patterns (PAMPs) • TLRs induce cytokines that regulate the intensity and duration of immune responses
The skin • Mechanical • Skin Structure • Saliva washes • Mucus traps and ciliary escalator • Urine, vaginal flows out • Chemical • Sebum w/ unsaturated fatty acids • Perspiration • Lysozyme • Acid conditions stomak(1.2-3pH) skin (3-5pH) • Normal microbiota • Transferrins, and NO
Physical Factors • Skin • Epidermis consists of tightly packed cells with • Keratin, a protective protein Figure 16.2
Ciliary Escalator Figure 24.7
Ciliary Escalator Figure 16.4
Phagocytosis • Define. • What does this look like? • What does this do?
Chemical Factors • Fungistatic fatty acid in sebum • Low pH (3–5) of skin • Lysozyme in perspiration, tears, saliva, and urine • Low pH (1.2–3.0) of gastric juice • Low pH (3–5) of vaginal secretions
Normal Microbiota and Innate Immunity • Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens or alter the environment • Commensal microbiota: One organism (microbe) benefits and the other (host) is unharmed • May be opportunistic pathogens
Differential White Cell Count • Percentage of each type of white cell in a sample of 100 white blood cells
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
Components of Lymphatic System Figure 16.5a
The Lymphatic System ANIMATION Host Defenses: Overview Figure 16.5b–c
Phagocytosis • Phago: From Greek, meaning eat • Cyte: From Greek, meaning cell • Ingestion of microbes or particles by a cell, performed by phagocytes Figure 16.6
Phagocytosis Figure 16.7
Phagocytosis ANIMATION Phagocytosis: Overview ANIMATION Phagocytosis: Mechanism
Actions of phagocytic cells • Neutrophils (granulocyte) phagocyte • Increase in number during infection (leukocytosis) • Neutrophils are most important • Can act as antigen presenting cells (APC) • Important in specific resistance
Mechanism of phagocytosis • Chemotaxis to pathogen • Adherence • Engulfment • Killing • Resistance of microbes can be seen in some ability to live even after phagocytosis.
Inflammation • Redness • Pain • Heat • Swelling (edema) • Acute-phase proteins activated (complement, cytokine, kinins) • Vasodilation (histamine, kinins, prostaglandins, leukotrienes) • Margination and emigration of WBCs • Tissue repair
Fever • Body temp is controlled by the brain • High temp in response to IL-1 • Caused by • Bacterial endotoxins • Interleukin-1 • Chills indicate rising body temp (crisis)
Disadvantages Tachycardia Acidosis Dehydration 44–46°C fatal Fever • Advantages • Increases transferrins • Increases IL–1 activity • Produces Interferon
Antimicrobial substances • IFN- and IFN-: Cause cells to produce antiviral proteins that inhibit viral replication • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria • Lysozyme • Acids on skin • Complement
Antiviral Actions of Interferons (IFNs) Figure 16.15
Antimicrobial peptides Lyse bacterial cells Innate Immunity • Transferrins • Bind serum iron
Deficiencies in complement can result in an increased susceptibility to disease
The Complement System • Serum proteins activated in a cascade • Activated by • Antigen-antibody reaction • Proteins C3, B, D, P and a pathogen ANIMATION Complement System: Overview ANIMATION Complement System: Activation
The Complement System • C3b causes opsonization • C3a + C5a cause inflammation • C5b + C6 + C7 + C8 + C9 cause cell lysis ANIMATION Complement System: Results
The Complement System Figure 16.9
Effects of Complement Activation • Opsonization or immune adherence: Enhanced phagocytosis • Membrane attack complex: Cytolysis • Attract phagocytes Figure 16.10
Inflammation Stimulated by Complement Figure 16.11
Classical Pathway of Complement Activation Figure 16.12
Alternative Pathway of Complement Activation Figure 16.13
Lectin Pathway of Complement Activation Figure 16.14
Some Bacteria Evade Complement • Capsules prevent C activation • Surface lipid-carbohydrates prevent membrane attack complex (MAC) formation • Enzymatic digestion of C5a