TORTORA • FUNKE
• CASE
Microbiology
Nonspecific Defenses of the Host
AN INTRODUCTION
EIGHTH EDITION
B.E Pruitt & Jane J. Stein
Chapter 16
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
(antibodies) to a specific
pathogen
PowerPoint® Lecture Slide Presentation prepared by Christine L. Case
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Host Defenses
Mechanical Factors
• Overview of the body’s defenses
Describe the role of the skin and mucous membranes in
nonspecific resistance.
• Skin (works generally if intact)
• Epidermis consists of tightly packed cells with
• Keratin, a protective protein, waterproof
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Human skin layers
Figure 16.1
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Mechanical Factors
Differentiate between mechanical and chemical factors, and list five
examples of each.
• Mucous membranes (overcome by large numbers)
• Ciliary escalator: Microbes trapped in mucus are
transported away from the lungs
• Lacrimal apparatus: Washes eye, removes microbes
• Saliva: Washes microbes off teeth and gums, tongue
• Mucus traps microbes, moved up and out by ciliary
escalator
• Urine: Flows out
• Vaginal secretions: Flow out
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Ciliary escalator
• Microbes trapped in mucus produced by goblet cells,
then propelled upward by cilia
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Chemical Factors
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Normal Microbiota
• Fungistatic fatty acid (unsaturated) in sebum
• Sweat washes off skin (contains lysozyme)
Describe the role of normal microbiota in nonspecific resistance.
• Low pH (3-5) of skin
• Lysozyme in perspiration, tears, saliva, and tissue
fluids
• Low pH (1.2-3.0) of gastric juice prevents microbe
growth (except Helicobacter pylori)
• Microbial antagonism/competitive exclusion: Normal
microbiota compete with pathogens, preventing their
growth on the host.
• Transferrins in blood bind iron removing this nutrient
• NO (nitrous oxide) inhibits ATP production of microbes
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Phagocytosis
• Phago: eat
• Cyte: cell
Define phagocytosis and phagocyte.
• Ingestion of microbes or particles by a cell, performed
by phagocytes (certain white blood cells)
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Differential White Cell Count
Define differential blood 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%
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White Blood Cells
Principle kinds of leukocytes
• Leukocytes (white blood cells) divided into
granulocytes (neutrophils, basophils, eosinophils),
lymphocytes, and monocytes
• Granulocytes: (dominate early in infection)
• Neutrophils: Phagocytic (most important)
• Basophils: Produce histamine
• Eosinophils: Toxic to parasites, some phagocytosis
• Lymphocytes: Involved in specific immunity
• Monocytes: Phagocytic as mature macrophages
• Fixed macrophages in lungs, liver, bronchi
• Wandering macrophages (enlarged monocytes) roam
tissues
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Lymphatic system
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Macrophage engulfing rod-shaped bacteria
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Phagocytosis
Microbial Evasion of Phagocytosis
• Inhibit adherence: M protein,
capsules
Streptococcus pyogenes, S. pneumoniae
• Kill phagocytes: Leukocidins
Staphylococcus aureus
• Lyse phagocytes: Membrane
attack complex
• Escape phagosome
Listeriamonocytogenes
• Prevent phagosome-lysosome
fusion
• Survive in phagolysosome
HIV
Shigella
Coxiella burnetti
Classify phagocytic cells, and describe the roles of granulocytes and monocytes.
Describe the process of phagocytosis, and include the stages of
adherence
and ingestion.
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Figure 16.8a
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Inflammation – body response to cell damage
• Redness
List the stages of inflammation.
• Pain
• Heat
• Swelling (edema)
• Acute-phase proteins activated (complement, cytokine,
kinins) – short, intense
• Chronic inflammation is a prolonged response
• 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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Inflammation
Describe the roles of vasodilation, kinins, prostaglandins, and
leukotrienes in inflammation.
• Histamine
• Kinins
• Prostaglandins
• Leukotrienes
Vasodilation, increased permeability of blood
vessels
Vasodilation, increased permeability of blood
vessels
Intensity histamine and kinin effect
Increased permeability of blood vessels,
phagocytic attachment
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Figure 16.9a, b
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Inflammation
Phagocyte migration and Phagocytosis
• Phagocytes can stick to lining of blood vessels
• They also can squeeze through blood vessels
• Pus is the accumulation of damaged tissue, dead
microbes, granulocytes, macrophages
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Describe phagocyte migration.
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
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Figure 16.9c, d
Outcomes of Complement Activation System
• Serum proteins
(liquid in blood)
activated in a
cascade.
• Activate one
another in a
cascade to
destroy
invading
microorganisms
• When IL-1 is eliminated, body temperature falls. (Crisis
- sweating)
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Effects of Complement Activation
Figure 16.10
Effects of Complement Activation (inflammation)
List the components of the complement system.
• Cytolysis caused by
complement
• Opsonization or
immune adherence:
enhanced
phagocytosis
• Membrane attack
complex: cytolysis
• Attract phagocytes
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Figure 16.11
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Figure 16.12
5
Classical Pathway of complement activation
• Pathway
initiated by
antigenantibody
reaction
Describe three
pathways of activating
complement.
• Results in
cytolysis,
inflammation,
and
phagocytosis.
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Figure 16.13
Alternative Pathway of complement activation
• Pathway
initiated by
contact
between
proteins and
pathogen
Lectin Pathway of complement activation
• Mannosebinding lectin
binds to
mannose,
enhancing
phagocytosis
via classical
and alternative
pathways
Figure 16.14
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Some bacteria evade complement
• Capsules prevent C activation
• Surface lipid-carbohydrates prevent MAC formation
• Enzymatic digestion of C5a
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Figure 16.15
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Interferons (IFNs) – antiviral action
of alpha and beta interferons
Interferons (IFNs)
2 The infecting
virus replicates
into new
viruses.
Define interferon.
Compare and contrast the actions of α-IFN, β-IFN, and χ-IFN.
• Alpha IFN & Beta IFN: Cause cells to produce antiviral
proteins that inhibit viral replication
• Interferons are host-cell specific, but not virus-specific
• Gamma IFN: Causes neutrophils and macrophages to
phagocytize bacteria
1 Viral RNA from an
infecting virus
enters the cell.
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.
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.
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
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Figure 16.16
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