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