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TORTORA • FUNKE
• CASE
Microbiology
AN INTRODUCTION
EIGHTH EDITION
B.E Pruitt & Jane J. Stein
Chapter 16
Nonspecific Defenses of the Host
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 to a
specific pathogen
Native (innate)
species specific immunity
Host Defenses
Figure 16.1
First line of Defense
Mechanical Factors
Physical barriers to pathogens
• Skin
– Epidermis consists of tightly packed cells with
– Keratin, a protective protein
Mechanical Factors
• Mucous membranes
• Ciliary escalator: Microbes trapped in mucus
are transported away from the lungs
• Lacrimal apparatus: Washes eye
• Saliva: Washes microbes off
• Urine: Flows out
• Vaginal secretions: Flow out
Chemical Factors
• Fungistatic fatty acid in sebum
• Low pH (3-5) of skin
• Lysozyme in perspiration, tears, saliva, and
tissue fluids
• Low pH (1.2-3.0) of gastric juice
• Transferrins in blood find iron
• NO inhibits ATP production
Normal Microbiota
• Microbial antagonism/competitive
exclusion:
– Normal microbiota compete with
pathogens.
Second line of Defense
1. Phagocytosis
2. Inflammation
3. Fever
4. Antimicrobial substances
Formed Elements In Blood (note functions)
•
RBC’s
•
WBC’s
•
•
Agranulocytes
•
Monocytes
•
Lymphocytes
Granulocytes
•
Neutrophils (PMNs)
•
Basophils
•
Eosinophils
Table 16.1
Differential White 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%
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
Phagocytosis
• Phago: eat
• Cyte: cell
• Ingestion of microbes or particles by a
cell, performed by phagocytes
Phagocytosis
Figure 16.8a
Microbial Evasion of Phagocytosis
• Inhibit adherence: M protein,
capsules
Streptococcus pyogenes, S. pneumoniae
• Kill phagocytes: Leukocidins
Staphylococcus aureus
• Lyse phagocytes: Membrane attack
complex
Listeriamonocytogenes
• Escape phagosome
Shigella
• Prevent phagosome-lysosome
fusion
HIV
• Survive in phagolysosome
Coxiella burnetti and Mycobacteria spp
Inflammation
•
•
•
•
•
Redness
Pain
Heat
Swelling (edema)
Acute-phase proteins activated (complement,
cytokine, kinins) - chemical messengers
• Vasodilation (histamine, kinins, prostaglandins,
leukotrienes) - bring in more help
• Margination and emigration of WBCs
• Tissue repair
Chemicals Released by Damaged
Cells
• Histamine
Vasodilation, increased permeability of blood
vessels
• Kinins
Vasodilation, increased permeability of blood
vessels
• Prostaglandins
Intensity histamine and kinin effect
• Leukotrienes
Increased permeability of blood vessels,
phagocytic attachment
Inflammation
Figure 16.9a, b
Inflammation
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
• When IL-1 is eliminated, body temperature
falls. (Crisis)
The Complement System
Serum proteins
activated in a
cascade.
Increasing as
previous
catalyzes the
next step
Outcomes of
Complement
system
1. Opsonization
2. Chemotaxic
3. Cell lysis
Figure 16.10
Effects of Complement Activation
• Opsonization or
immune
adherence:
enhanced
phagocytosis
• Membrane attack
complex:
cytolysis
• Attract
Figure 16.11
Effects of Complement Activation
Figure 16.12
Classical Pathway
Figure 16.13
Alternative Pathway
Figure 16.14
Lectin Pathway
Figure 16.15
Some bacteria evade
complement
• Capsules prevent C’ activation
• Surface lipid-carbohydrates prevent
MAC (membrane attack complex C5b - C9)
formation
• Enzymatic digestion of C5a
Interferons (IFNs)
Antiviral proteins
• 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)
2 The infecting
virus replicates
into new
viruses.
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.
1 Viral RNA from an
infecting virus
enters the cell.
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.
Figure 16.16