The Duality of the Immune SysteM Flashcards
(106 cards)
1
Q
Antibody-Mediated Immunity
A
HUMORAL IMMUNITY
2
Q
Humor
A
fluid
3
Q
Antibody production
A
HUMORAL IMMUNITY
4
Q
processes of HUMORAL IMMUNITY
A
- Activation of B cells
- Proliferation
- Differentiation
5
Q
Proteins secreted un response to contact with antigens
A
ANTIBODY
6
Q
ANTIBODY Moves to the
A
GAMMA of globulin
7
Q
Protein migration:
A
Cathode to Anode
8
Q
ANTIBODY STRUCTURE
A
FAB FRAGMENT
Fc FRAGMENT
9
Q
o 1 light chain
o Half of heavy chain
o Binds to antigen
A
FAB FRAGMENT
10
Q
o Crystallizable at 4C
o Half of heavy chain
o Binds to cell or phagocyte
A
Fc FRAGMENT
11
Q
MECHANISM OF ACTION: ANTIBODY
A
- AGGLUTINATION AND PRECIPITATIOMN
- OPSONIZATION
- TOXIN NEUTRALIZATION
- STERIC HINDRANCE
- ACTIVATION OF COMPLEMENT
- ANTIBODY DEPENDENT CELLULAR CYTOXITY
12
Q
Reaction between a SOLUBLE antibody and a PARTICULATE antigen
A
AGGLUTINATION
13
Q
Clumps the antigens together to facilitate phagocytosis
A
AGGLUTINATION
14
Q
Reduces number of infectious units to be dealt with
A
AGGLUTINATION
15
Q
reaction between a Soluble antibody and SOLUBLE antigen
A
PRECIPITATION
16
Q
Coating antigen with antibody to enhance phagocytes
A
OPSONIZATION
17
Q
Causes inflammation and lysis; Serum proteins
A
ACTIVATION OF COMPLEMENT
18
Q
Binding on cell surface before the antigens
A
STERIC HINDRANCE
19
Q
Antibody-antigen complex initiates
A
COMPLEX FIXATION
20
Q
Formation of MAC complex; Cell lysis
A
COMPLEX FIXATION
21
Q
Antibody attached to target cell cause destruction by macrophages, eosinophils and NK cells
A
ANTIBODY DEPENDENT CELLULAR CYTOXITY
22
Q
Cells in CELLULAR IMMUNITY
A
- Macrophages
- Antigen Presenting Cells
- T cells
23
Q
Induce immune response by Tcells
A
Antigen Presenting Cells/Dendritic cell
24
Q
types of T-HELPER CELLS
A
T-Helper Cells (A. Memory T cells; B. Cytokines)
T- Cytotoxic Cells
25
Activation
Secretes perforins
Causes lysis of infected host cell
T- Cytotoxic Cells
26
types of T CELLS
```
T-HELPER (TH1) CELSS
T-HELPER (TH2) CELSS
T-HELPER (TH17) CELSS
Cytotoxic T Lymphocytes (CTL)
T Regulatory (Treg) Cell
Activated Macrophage
Neutral Killer (NK) Cell
```
27
types of T CELLS
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T-HELPER (TH1) CELSS
T-HELPER (TH2) CELSS
T-HELPER (TH17) CELSS
Cytotoxic T Lymphocytes (CTL)
T Regulatory (Treg) Cell
Activated Macrophage
Neutral Killer (NK) Cell
```
28
Activates cells related to cell-mediated immunity: macrophages, Tc cells, and natural killer cells
T-HELPER (TH1) CELSS
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Stimulates production of eosinophils, IgM, and IgE
T-HELPER (TH2) CELSS
30
Recruits neutrophil; stimulates production of antimicrobial proteins
T-HELPER (TH17) CELSS
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Destroys target cells on contact; generated from T cytotoxic cell
Cytotoxic T Lymphocytes (CTL)
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Regulates immune response and helps maintain self-tolerance
T Regulatory (Treg) Cell
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Enhanced phagocytic activity; attacks cancer rolls
Neutral Killer (NK) Cell
34
Attacks and destroys target cell; participates in antibody dependent cell mediated cytotoxity
Neutral Killer (NK) Cell
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TYPES OF ACQUIRED IMMUNITY
NATURAL IMMUNITY
| ARTIFICIAL IMMUNITY
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Transfer of antibodies from mother to her infant; Temporary immunity to newborn
Naturally Acquired Passive Immunity
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Exposure to antigen; Infection
Naturally Acquired Active Immunity
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Injection of antigen
Artificially Acquired Active Immunity
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Vaccination of antigenic preparations:
1. Toxoids
2. Attenuated cell
3. killed organism
4. Capsular Polysaccharide
40
Injection of antibodies
Artificially Acquired Passive Immunity
41
Factors of COLONIZATION AND DISSEMINATION
1. Host defense mechanism
| 2. Pathogenicity and Virulence
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refers to the ability of a microbe to cause disease in the host
Pathogenicity
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disease-causing microbes
Pathogens
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microorganism that does not associate with their host except in the case of disease; may cause disease to normal individual
True pathogens
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microorganism causing disease when one or more of the defense mechanisms designed to restrict them from the usually sterile internal tissues are breached by accident. by intent, or by an underlying metabolic or an infectious disorder
Opportunist
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Degree or intensity of pathogenicity
Virulence
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Refers to the characteristics of the organism that enable them to cause disease
Virulence factors
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shows the two difference between two different SPECIES
PATHOGENICITY
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shows the difference between two STRAINS
VIRULENCE
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MECHANISMS OF INVASIVENESS
1. Adhesins
2. Invasins
3. Aggresins
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MECHANISMS OF TOXIGENESIS
1. Exotoxin
| 2. Endotoxins
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Structures that attach to the host cells or tissues
Adhesins
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- Substances that act locally
- Damages host cells or tissues
- Facilitate growth and dissemination
Invasins
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ENZYMES: Invasins
1. Hylarunonidase
2. Collagenase
3. Kinases
4. Coagulase
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“Spreading factor”
Hyaluronidase
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Digest the “cement” component
Hyaluronidase
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Digest the primary connective tissues
Collagenase
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presence of Collagenase in
Clostridium perfringens
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“Streptokinase” or “Fibrinolysin”
Kinases
60
Acts on fibrinogen
Coagulase
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Refers to bacterial features that allow the organism to resist the host-defense mechanism
Aggresins
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host-defense mechanism
- Against phagocytosis
| - Against Immune response
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Against phagocytosis
1. Inhibition of Chemotaxis
2. Avoiding contact with phagocytes
3. Inhibition of Opsonization
4. Inhibition of Phagolysosome formation
5. Resistance to killing by lysosomal factors
6. Escape from phagosome
7. Killing of phagocytes
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Inhibition of chemotaxis: example
STREPTOLYSIN O
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kills the phagocytes
Inhibition of chemotaxis
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CAPSULES
Avoiding contact with phagocyte
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Inhibition of phagolysosome: example
EXAMPLE: SULFATIDE
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Resistance to lysozymes: example
EXAMPLE: Mycolic Acid
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Escape to the cytoplasm
Escape from phagosome
70
Digestion of the membrane of the phagosome
Escape from phagosome
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Escape from phagosome: example
Example: Phospholipase
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Killing phagocytes
- Streptolysin O
| - Leukocidins
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AGAINST IMMUNE RESPONS
1. Molecular Mimicry
2. Antigenic Disguise
3. Local Interference with Antibody Activity
4. Antibodies absorbed by Soluble Bacterial Antigens
5. Induction of Ineffective Antibodies
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-Mimics the host structures
Molecular mimicry
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Hyaluronic acid in the capsule
Molecular mimicry
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Hides their antigenic surface to the antibodies
Antigenic disguise
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Produces IgA protease that inactivates IgA
Local Interference with Antibody Activity
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Production of antigens that will neutralize the antibodies
Antibodies absorbed by Soluble Bacterial Antigens
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Stimulate production of weak antibodies
| Example: Reduction Modifiable Proteins
Induction of Ineffective Antibodies
80
Modifying their antigenic determinants within a course of disease
ANTIGENIC VARIATION
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Prevents anamnesis and secondary immune response
ANTIGENIC VARIATION
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ability to cause disease due to production of toxins
TOXIGENESIS
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TYPES OF TOXIGENESIS
o Exotoxins
| o Endotoxins
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TYPES OF TOXINS
1. SOURCE
2. LETHAL DOSE
3. CHEMICAL COMPOSITION
4. EFFECT
5. MANNER OF RELEASE
6. HEAT DENATURATION
7. TOXICITY
8. IMMUNOLOGY
85
SOURCE: EXOTOXIN
Elaborated by few Gram-positive and Gram-negative bacteria
86
SOURCE: ENDOTOXIN
Elaborated by Gram-negative bacteria
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CHEMICAL COMPOSITION: EXOTOXIN
Proteins or peptides
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CHEMICAL COMPOSITION: ENDOTOXIN
Lipids or lipopolysaccharides
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MANNER OF RELEASE TOXICITY: EXOTOXIN
Secreted by living cells; Highly toxic
90
MANNER OF RELEASE TOXICITY: ENDOTOXIN
Lysis of bacterial cells; Low toxicity
91
LETHAL DOSE EFFECT ON THE HOST: EXOTOXIN
-Low concentration; Specific for particular structure or function
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LETHAL DOSE EFFECT ON THE HOST: ENDOTOXIN
-High concentration; Generalized and produces the same effects
93
- Heat labile
- Can be converted to toxoids
- Can be neutralized
LETHAL DOSE EFFECT ON THE HOST
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- Heat stable
| - Cannot be converted to toxoids
HEAT DENATURATION
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INFECTIOUS DISEASE CYCLE
a. SOURCE OF THE PATHOGEN
b. TRANSMISSION TO HOST
c. PORTAL OF ENTRY
d. COLONIZATION AND DISSEMINATION
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INFECTIOUS DISEASE CYCLE
a. INFECTION
| b. PREVENTION AND CONTROL
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CLINICAL STAGES OF INFECTION
a. INCUBATION PERIOD
b. PRODROMIUM
c. PERIOD OF ACTIVE INVASION
d. CONVALESCENCE
98
CLINICAL STAGES
INCUBATION
PRODROMIUM
ACTIVE INVASION
CONVALESCENCE
99
TYPES OF INFECTION
```
DURATION
LOCATION
BLOOD
OCCURRENCE
MANIFESTATION
DISEASE DISTRIBUTION
```
100
DURATION
1. ACUTE
| 2. CHRONIC
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LOCATION
1. LOCALIZED
| 2. SYSTEMICFOCAL
102
BLOOD
1. BACTEREMIA
2. SEPTICEMIA
3. TOXEMIA
103
OCCURRENCE
1. PRIMARY INFECTION
2. SECONDARY INFECTION
3. MIXED INFECTION
104
MANIFESTATION
1. ASYMPTOMATIC
2. LATENT
3. SYMPTOMATIC
105
DISEASE DISTRIBUTION
1. ENDEMIC
2. SPORADIC
3. EPIDEMIC
4. PANDEMIC
106
PREVENTION AND CONTROL
1. TREATMENT OF HUMAN RESERVOIR
2. CONTROL OF ANIMAL RESERVOIR
3. CONTROL OF VECTORS
4. REDUCTION OF VEHICLE CONTAMINATION
5. INTERRUPTION OF TRANSMISSION
6. IMMUNIZATION
7. NOTIFICATION OF HEALTH AUTHORITIES
8. PUBLIC EDUCATION
