Chapter 15 Revised
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Transcript of Chapter 15 Revised
MicrobiologyWith Diseases by Taxonomy
Second Edition
PowerPoint® Lecture Slides
Copyright © 2007 Pearson Education, Inc. publishing as Benjamin Cummings
15InnateImmunity
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Innate Resistance
Innate (Immunity) Resistance – that which present at birth; before contact with microbes or their products
Nonspecific – not directed against a particular agent, but against anything foreign (not part of the body)
Resistance to most plant and animal PathogensResistance due to physiological processes of humans
that are incompatible with those of the Pathogen Correct chemical receptors not present on human cells. Temperature and pH may be incompatible with those
necessary for the Pathogens survival.
Pathogens for which humans don’t have Innate Resistance to can cause disease.
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First Line of Defense
Structures, chemicals, processes that work to prevent pathogens entering the body
Nonspecific Defenses Includes the Skin and Mucous Membranes of the
Respiratory, Digestive, Urinary, and Reproductive Systems
PLAYPLAYAnimation: Host Defenses
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Skin – Physical Components of Defense
Two major layers Epidermis
Outer layer composed of multiple layers of tightly packed cells Few Pathogens can penetrate these layers Shedding of dead skin cells removes attached
microorganisms Epidermal Dendritic Cells
Also termed Langerhans Cells Phagocytize Pathogens, and important in
Adaptive (Specific) Immunity
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Skin – Physical Components of Defense
Dermis Contains protein fibers of Collagen
Give skin strength and pliability to resist abrasions that could introduce microorganisms
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Skin – Chemical Components of Defense
Perspiration secreted by Sweat Glands Salt – inhibits growth of Pathogens by drawing water
from their cells Antimicrobial Peptides – Sweat Glands secret
Dermicidins Lysozyme – destroys cell wall of many bacteria
Sebum secreted by Sebaceous (Oil) Glands Helps keep skin pliable and less likely to break or tear Lowers the pH of the skin to a level inhibitory to many
bacteria
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Mucous Membranes
Line all body cavities open to the outside environmentTwo distinct layers
Epithelium Deeper Connective Tissue layer that supports the
Epithelium
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Epithelium
Thin, outer covering of the Mucous MembranesUnlike surface Epidermal Cells of Skin, Epithelial
cells of Mucous Membranes are living.Tightly packed to prevent entry of PathogensContinual shedding of cells carries attached
microorganisms away.
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Respiratory System
Figure 15.2
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Microbial Antagonism
Normal Microbiota help protect the body by competing with potential Pathogens.
Various activities of the Normal Microbiota make it hard for Pathogens to compete. Consumption of nutrients makes them unavailable to
Pathogens Create an environment unfavorable to other
microorganisms by changing pH
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Microbial Antagonism
Helps stimulate the body’s Second Line of Defense Promote overall health by providing vitamins to host
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Other First-Line Defenses
Many body organs secrete chemicals with antimicrobial properties
Lacrimal (Tear) Glands that bathe the eye
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Lacrimal Apparatus
Figure 15.3
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Second Line of Defense
Operates when pathogens succeed in penetrating the Skin or Mucous Membranes
Nonspecific DefenseComposed of cells, antimicrobial chemicals, and
processes, but no physical barriers Many of these components are contained or originate
in the Blood.
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Blood
Composed of cells and portions of cells within a fluid called Plasma Plasma mostly water containing Electrolytes, dissolved
gases, nutrients, and proteins Serum – Plasma from which the Clotting Factors, a
group of Plasma Proteins, have been removed Include Iron-binding compounds Other Plasma Proteins include Complement
Proteins and Antibodies Formed Elements -- the cells and cell fragments in the
Plasma
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Formed Elements
Three types of Formed Elements Erythrocytes (Red Blood Cells) – carry oxygen and
carbon dioxide in the blood Platelets (Thrombocytes) – cell fragments involved in
Blood Clotting Leukocytes (White Blood Cells) – involved in
defending the body against invaders Two groups
Granulocytes Agranulocytes
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Granulocytes
Their cytoplasm contains visible granules that stain different colors based on the dye used
Three types Basophils – stain dark blue or purple with the Basic
Dye Methylene Blue Eosinophils – stain red/orange with the Acidic Dye
Eosin Neutrophils – stain pink with a mixture of Acidic and
Basic DyesNeutrophils and Eosinophils can phagocytize
PathogensNeutrophils and Eosinophils are capable of Diapedesis
– changing shape to squeeze through blood vessel walls
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Diapedesis
Figure 15.6
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Agranulocytes
Cytoplasm appears uniform under a Light Microscope; lack visible cytoplasmic granules
Two types Lymphocytes – most involved in Adaptive Immunity Monocytes – leave the blood and mature into
Macrophages which phagocytic and involved in Adaptive (Specific) Immunity
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Macrophages
Phagocytic cells of the Second Line of DefenseWandering Macrophages leave the blood via
Diapedesis and phagocytize throughout the body.Fixed Macrophages do not move throughout the body,
and often phagocytize within a specific organ. Include Alveolar Macrophages (in lungs), Microglia
(in Central Nervous System), Küpffer Cells (in liver)
All Macrophages, plus Monocytes attached to Endothelial Cells; constitute the Mononuclear Phagocytic System
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Lab Analysis of Leukocytes
Differential White Blood Cell Count test can signal signs of disease. Increased Eosinophils can indicate allergies or
parasitic worm infection. Bacterial diseases often show increase in leukocytes
and in Neutrophils Viral infections show increase in Lymphocytes
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Components of the Second Line of Defense
PhagocytosisExtracellular killing by LeukocytesNonspecific Chemical Defenses InflammationFever
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Phagocytosis
Phagocytes – cells capable of phagocytosisPhagocytosis is not completely understoodCan be divided into five stages
Chemotaxis Adherence Ingestion Killing Elimination
PLAYPLAYAnimation: Phagocytosis
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Phagocytosis (continued)
Chemotaxis – movement in response to a chemical stimulus Phagocytes move toward chemical stimulus (Positive
Chemotaxis) via Pseudopodia Phagocytes attracted to chemicals released by
microbes, damaged host cells, activated Leukocytes, and components of Complement
Adherence –binding of Phagocyte to microbe by attaching to complementary molecules on its surface (such as Glycoproteins) Bacterial Capsule or M Protein (in Streptococcus
pyogenes) may interfere with Adherence. Opsonins (Antibodies or Complement Proteins) that
coat microbe facilitate it; thus enhance Phagocytosis
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Phagocytosis (continued)
Ingestion – envelopment of microbe by Phagocyte via its Pseudopodia, and taking it in by Endocytosis Microbe contained within Phagosome (membrane of
which was originally part of Phagocyte’s Cytoplasmic Membrane)
Killing – enzymatic destruction of microbe within Phagocyte’s Lysosomes which fuse with Phagosome forming Phagolysosome Digestive Enzymes from Lysosomes usually kill and
break down microbial cell. M Protein (in S. pyogenes) and waxy cell walls (in
Mycobacterium tuberculosis) may prevent Lysosome activity.
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Phagocytosis (continued)
Elimination – excretion of microbial cell remnants from Phagocyte by Exocytosis In some Phagocytes (Dendritic Cells and
Macrophages) microbial cell surface markers may remain attached to phagocytic cell’s Cytoplasmic Membrane to help activate Lymphocytes.
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Phagocytosis
Figure 15.8
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Host Cell Protection
The host’s cells are protected from destruction by the Phagocytes. Some Phagocytes have receptors for bacterial surface
components, such as flagellar proteins or cell wall components, that are lacking on the body’s cells.
Opsonins such as Complement and Antibody attached to microbial cell provide a signal to the Phagocyte.
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Extracellular Killing by Leukocytes
Three Cell types that kill extracellularly Eosinophils
Mainly attack parasitic Helminths (worms) by attaching to their surface, or to Antibodies attached to worm’s surface
Secrete toxins that weaken or kill the Helminth Eosinophilia -- elevated Eosinophil levels;
often indicative of a Helminth infestation
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Extracellular Killing by Leukocytes (cont.)
Natural Killer Lymphocytes (NK Cells) – large Lymphocytes that attack foreign (those that are not part of body) and abnormal body cells, but do not target specific microbes, as do other Lymphocytes Secrete toxins onto the surface of virus-infected
cells and tumors Differentiate normal body cells because they have
membrane proteins similar to the NK Cells
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Extracellular Killing by Leukocytes (cont.)
Neutrophils Produce chemicals that kill nearby invaders
Enzymes that form Superoxide Radicals and Hydrogen Peroxide (Oxidants)
An Enzyme that converts these Oxidants into Hypochlorite (active ingredient in bleach)
Generate Extracellular Fibers that bind to and kill bacteria
Extracellular Fibers composed of DNA and Histones, and formed into NETs (Neutrophil Extracellular Traps) to bind microbes and expose them to high concentrations of antimicrobial chemicals
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Nonspecific Chemical Defenses
Augment Phagocytosis Some attack Pathogens directly Some enhance other features of Innate Immunity
Includes various chemicals Lysozyme Complement Interferon Defensins
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Complement System (Complement)
Set of Serum Proteins designated numerically according to the order of their discovery
Complement activation results in Lysis of the foreign cells
Complement can be activated in several ways Classical Pathway Alternate Pathway
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The Classical Pathway
Complement named for the events of this originally discovered pathway
Various complement proteins act nonspecifically to “complement” the action of Antibodies
In this Pathway: binding of Antibodies to Antigen activates Complement
Complement Enzymes split Complement Molecules into Fragments which
1) combine to form new enzymes, or 2) dilate blood vessels and increase their
permeability, enhancing Diapedesis, or 3) increase Inflammation, or 4) attract Phagocytes by Chemotaxis, or
5) are Opsonins
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The Classical Pathway (continued)
This Pathway followed by the Complement Cascade – sequence of reactions involving Complement Proteins in which product of one reaction is the enzyme that catalyzes the next reaction
Membrane Attack Complexes (MACs) – end products of Complement Cascade which punch holes in foreign cells’ cytoplasmic membrane, allowing water to flow into cells and lyse them
Gram (-) Bacteria more sensitive to MACs than Gram (+) due to their exposed Outer Membrane
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The Alternate (Properdin) Pathway
Activation occurs independent of Antibodies; instead occurs when Complement Proteins (B, D, and Properdin) bind to Endotoxins or Glycoproteins in Cell of Bacteria or Fungi
Useful in early stages of infection before Antibodies have formed
Complement Cascade also follows this Pathway, resulting in formation of MACs and Cell Lysis
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Complement – Two Pathways
Figure 15.10
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Classical Complement Cascade
Figure 15.11
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Inactivation of Complement
Complement System nonspecific and MACs can form on most cells’ exposed cell membrane
Body’s own cells can withstand Complement Cascade Membrane-bound Proteins on normal body cells bind
to and break down activated Complement Proteins This stops Complement Cascade before cell damage
occurs
PLAYPLAYAnimation: The Complement System
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Interferons (IFNs)
Protein molecules secreted by virus-infected host cells to nonspecifically inhibit the spread of viral infections
Cause many symptoms typically associated with viral infections (malaise, headache, muscle aches, chills, and fever)
Three Classes produced by different cell types Alpha Interferon from Monocytes, Macrophages, and
some Lymphocytes Beta Interferon from Fibroblasts Gamma Interferon from activated T Lymphoytes and
NK Lymphocytes (NK Cells)
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Interferons (continued)
Interferons do not protect virus-infected cells that secrete them, but neighboring cells by interfering with viral replication in them, and by activating NK Lymphocytes
Not specific; Interferon secretion stimulated by one type of virus can help protect against other viruses
Alpha and Beta Interferons have same action They bind to receptors on other cells’ cytoplasmic
membrane stimulating them to produce Antiviral Proteins (AVPs) which activated when they bind to viral nucleic acids
Some AVPs breakdown cells’ mRNA; others block protein synthesis at ribosomes – both preventing viral replication in cell
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Interferons (continued)
AVPs stop all protein synthesis in cell (for both virus and host cell) for 3-4 days.
This often enables cell to rid itself of virus, and yet survive brief period without protein synthesis.
Gamma Interferon (Macrophage Activating Factor) stimulates activity of Phagocytes – both Macrophages and Neutrophils
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Interferons (continued)
Alpha and Beta Interferons are present early in the infection.
Interferon Gamma appears later in the course of infection, since T Lymphocyte activation is part of the Specific Immune Response which occurs after the Nonspecific Response
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The Characteristics of Human Interferons
Table 15.3
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Interferon Therapy
It was thought that this might be a good antiviral treatment.
Recombinant DNA Technology used to produce various Interferons Synthetic Genes for Human Interferons inserted into
genomes of Escherichia coli and Saccharomyces cerevisiae
Interferons produced in this way are pure and can be made in large quantities.
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Inflammation
Nonspecific Localized Response to tissue damage resulting from various causes – chemicals, heat, UV, trauma, and Pathogens
Characterized by Redness, Heat, Swelling, and Pain; sometimes also loss of function
Two types Acute Inflammation Chronic Inflammation
PLAYPLAYAnimation: Inflammation
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Acute vs. Chronic Inflammation
Acute Inflammation Develops quickly and is short lived Is usually beneficial, since results in elimination of what caused
it Important in the Second Line of Defense; it involves
Dilation and Increased Permeability of the Blood Vessels (due to release of Inflammatory Chemicals by Macrophages, Basophils, Mast Cells, Platelets, and damaged cells))
Migration of Phagocytes [involves Chemotaxis, Margination (sticking to blood walls), and Diapedesis (squeezing between cells in blood vessel wall)]
Tissue Repair (by Stem Cells or Fibroblasts) Chronic Inflammation
Develops slowly and lasts a long time Can cause damage to tissues, resulting in disease
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Inflammatory Chemicals (Mediators)
Vasodilators: Histamine, Serotonin, Prostaglandins, Bradykinin
Increase Capillary Permeability: Prostaglandins and Leukotrienes
Chemotactic Factors: Collagen, Fibrin, Mast Cell secretions, Bacterial Peptides
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Events in Inflammation
Figure 15.17.1
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Events in Inflammation
Figure 15.17.2
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Chemical Mediators of Inflammation
Table 15.4
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Fever
A body core temperature over 37CResults when chemicals called Pyrogens trigger the
Hypothalamus to increase the body’s core temperatureVarious types of Pyrogens stimulate production of
Interleukin 1 (IL-1). These include: Bacterial Toxins Cytoplasmic contents of bacteria released by Lysis Antibody-Antigen Complexes
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Fever Production
IL-1 production causes the Hypothalamus to secrete Prostaglandin which resets Hypothalamic “Thermostat”.
Communication with brain initiates temperature ↑ by 1) Muscle Contractions, 2) Increased Metabolic Activity, and 3) Constriction of Blood Vessels (reduce heat loss).
Chills associated with Fever are due to the reduced blood flow of constricted vessels – signal Fever onset.
↓ in IL-1 production results in the body’s temperature returning to normal by 1) Sweating, 2) Vasodilation, and 3) ↓ in Metabolic Rate
Aspirin & Acetaminophen ↓ Fever by blocking Prostaglandin Synthesis.
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Benefits of Fever
Enhances the effects of Interferons Inhibits growth of some microorganisms (when above
their Optimum Temperature range)May enhance the performance of
1) Phagocytes, and 2) Cells of Specific ImmunityMay also accelerate the process of Tissue Repair
Adverse Effects of Fever: 1) Denature Proteins 2) Inhibit Nerve Impulses
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A Summary of Some Nonspecific Components of the First and Second Lines of Defense
Table 15.5