Chapter 13 Nonspecific Defenses of the Host. SusceptibilityLack of resistance to a disease...
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![Page 1: Chapter 13 Nonspecific Defenses of the Host. SusceptibilityLack of resistance to a disease Resistance Ability to ward off disease Nonspecific resistanceDefenses.](https://reader036.fdocuments.in/reader036/viewer/2022062304/56649f505503460f94c727e5/html5/thumbnails/1.jpg)
Chapter 13
Nonspecific Defenses of the Host
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• 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
TERMS
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Host Defenses
Figure 16.1
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• Skin
• Epidermis: tightly packed cells with outer layer of dead cells with keratin, a protective protein
• Sloughing off dead cells
• Dry environment
Mechanical Factors
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• Mucous membranes
• Microbes trapped in mucus are transported away from the lungs
• Washes eye
• Saliva: Washes microbes off
• Urine: Flows out
• Vaginal secretions: Flow out
Mechanical Factors
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• Bacteriostatic and fungistatic fatty acid in sebum
• Low pH (3-5) of skin
• in perspiration, tears, saliva, and tissue fluids
• Low pH (1.2-3.0) of gastric juice
• in blood bind iron
Chemical Factors
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• Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens.
• nutrients
• antimicrobials
Normal Microbiota
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• Percentage of each type of white blood cell in the WBC population.
Differential White Cell Count
Neutrophils 60-70%
Basophils 0.5-1%
Eosinophils 2-4%
Monocytes 3-8%
Lymphocytes 20-25%
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• Neutrophils:
• Basophils: Produce
• Eosinophils: Toxic to parasites (i.e. helminths), some phagocytosis
• Monocytes: Phagocytic as mature macrophages
White Blood Cells
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White Blood Cells• are found in various
tissues such as the liver, lungs and nervous tissue
• roam tissues
• Involved in specific immunity
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
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Phagocytosis
Figure 16.8a
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• Caused by immune system participants
• Vasodilation
• Margination and emigration of WBCs
• Acute-phase proteins activated (complement, cytokine, vasodilators)
Inflammation
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Inflammation• Redness
• Pain
• Heat
• Swelling (edema)
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Chemicals Released by Damaged Cells
• Histamine Vasodilation, increased permeability of blood vessels
• Kinins Vasodilation, increased permeability of blood vessels
• Prostaglandins Intensify histamine and kinin effect
• Leukotrienes Increased permeability of blood vessels, phagocytic attachment
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Inflammation
Figure 16.9a, b
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Inflammation
Figure 16.9c, d
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• Serum proteins activated in a cascade.
• C3a
• C3b
• C5a
• C5b, C6, C7, C8, C9
The Complement System
Figure 16.10
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Effects of Complement Activation• Membrane attack
complex: cytolysis
• Opsonization: enhanced phagocytosis
Figure 16.11
Cytolysis via complement activation
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Effects of Complement Activation• Inflammation: and attraction of
phagocytes via
vasodilation Chemotaxis
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Classical Pathway
Figure 16.13
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Alternative Pathway
Figure 16.14
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Lectin Pathway
Figure 16.15
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Some bacteria evade complement• may prevent complement activation
• Capsule lipid-carbohydrates may prevent MAC formation and
• Enzymatic digestion of C5a (inhibits inflammation and chemotaxis)
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• 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)
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Interferons (IFNs)
Figure 16.16
1
2
3
4
5
Viral RNA from an infecting virus enters the cell.
The infecting virus replicates into new viruses.
The infecting virus also induces the host cell to produce alpha and beta interferons.
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).
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.