Yet Again another Pandemic threat

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Yet Again another Pandemic threat

• http//www.who.int/csr/disease/avian_influenza/pha
  se/en/index.html

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• 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.

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• 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.

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• 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.

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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

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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?

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Nonspecific Immunity

• Resistance ? dont get it
• Susceptibility ? get it

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• 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

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An Overview of the Bodys Defenses
ANIMATION Host Defenses The Big Picture
Figure 16.1
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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

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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

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Physical Factors

• Skin
• Epidermis consists of tightly packed cells with
• Keratin, a protective protein

Figure 16.2
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Ciliary Escalator
Figure 24.7
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Ciliary Escalator
Figure 16.4
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Phagocytosis

• Define.
• What does this look like?
• What does this do?

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Chemical Factors

• Fungistatic fatty acid in sebum
• Low pH (35) of skin
• Lysozyme in perspiration, tears, saliva, and
  urine
• Low pH (1.23.0) of gastric juice
• Low pH (35) of vaginal secretions

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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

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Formed Elements in Blood
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Formed Elements in Blood
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Formed Elements in Blood
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Differential White Cell Count

• Percentage of each type of white cell in a sample
  of 100 white blood cells

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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

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Components of Lymphatic System
Figure 16.5a
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The Lymphatic System
ANIMATION Host Defenses Overview
Figure 16.5bc
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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
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Phagocytosis
Figure 16.7
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Phagocytosis
ANIMATION Phagocytosis Overview
ANIMATION Phagocytosis Mechanism
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Microbial Evasion of Phagocytosis
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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

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Mechanism of phagocytosis

• Chemotaxis to pathogen
• Adherence
• Engulfment
• Killing
• Resistance of microbes can be seen in some
  ability to live even after phagocytosis.

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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

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Chemicals Released by Damaged Cells
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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)

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Fever

• Advantages
• Increases transferrins
• Increases IL1 activity
• Produces Interferon

• Disadvantages
• Tachycardia
• Acidosis
• Dehydration
• 4446C fatal

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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

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Antiviral Actions of Interferons (IFNs)
Figure 16.15
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Innate Immunity

• Transferrins
• Bind serum iron

• Antimicrobial peptides
• Lyse bacterial cells

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• Deficiencies in complement can result in an
  increased susceptibility to disease

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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
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The Complement System

• C3b causes opsonization
• C3a C5a cause inflammation
• C5b C6 C7 C8 C9 cause cell lysis

ANIMATION Complement System Results
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The Complement System
Figure 16.9
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Effects of Complement Activation

• Opsonization or immune adherence Enhanced
  phagocytosis
• Membrane attack complex Cytolysis
• Attract phagocytes

Figure 16.10
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Inflammation Stimulated by Complement
Figure 16.11
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Classical Pathway of Complement Activation
Figure 16.12
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Alternative Pathway of Complement Activation
Figure 16.13
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Lectin Pathway of Complement Activation
Figure 16.14
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Some Bacteria Evade Complement

• Capsules prevent C activation
• Surface lipid-carbohydrates prevent membrane
  attack complex (MAC) formation
• Enzymatic digestion of C5a