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49 Cards in this Set
- Front
- Back
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Normal Flora
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Microorganisms normally found on or in the human body
Sites: skin, upper respiratory tract, gi tract, anterior urethra and vagina |
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Normal Flora
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Knowledge of nml flora is useful in predicting infectious etiologies
ex. aspiration pneumonia: anaerobes in oropharynx lead to anaerobic lung infections (bacteriodes sp) |
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Normal Flora
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UTI: E. coli is a common enteric bacillus that can cause urine infxn
Injection drug users: S. aureus is a common skin organism that can cause cellulitis, abscess or endocarditis |
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Sterile Areas
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Blood, CSF, synovial fluid, deep body tissues
Isolation of bacteria from these sites is diagnostic of infection |
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Host Defense Mechanisms - Non specific physical barriers
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Fluid currents: washes microbes away (ex. cilia, micturition)
Skin: squamous epithelium, sweat and sebum Mucous Membranes: IgA secretion, variable epithelial layers covered with mucus, and normal flora vs. pathogen - competition for local nutrients |
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Host Defense Mechanisms - Chemical barriers
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Inflammatory response:
* Increased blood supply * Increased capillary permeability * Decreased pH * Inflammatory mediators All lead to: acute phase reaction as well as rubor, calor, dolor, tumor |
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Host Defense Mechanisms - Acute phase reaction
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Fever, decreased appetite, increased catabolism
Alterations in hepatic protein synthesis: increased CRP and haptoglobin Increased WBC w/ L shift |
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Host Defense Mechanisms - Innate Immunity
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Natural ability to counter foreign Ag's (ex. complement)
Usually does not req prior exposure to Ag (ex. cytokines) Foreign AG usually recognized by its H2O expression Phagocytosis |
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Complement Cascade
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Final structure made: Membrane Attack Complex (MAC) - punches hole in membrane and allows osmotic gradient to occur and floods cell w/ H2O
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Toll-Like Receptors (TLR)
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Integral proteins on cell membranes that recognize pathogens and activate immune cell responses
Receptors recognize: Pathogen-Associated Molecular Patterns (PAMP) TLR bind w/ PAMP to induce cytokine production, phagocytosis or apoptosis |
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Host Defense Mechanisms - Acquired Immunity
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Immune cells "learn" about specific Ags following exposure and establish "memory"
Distinguishes: self from non-self Includes: Humoral immunity (Abs) and Cellular Immunity (Cells) |
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Humoral Immunity
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Acquired humoral immunity is provided by antibodies
Genetic recombination and somatic mutation make > 6 million specific Ab |
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Ab (immunoglobulin) components
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Fab fragment = Ag-binding site
Fc fragment = targets the bound Ag to a specific fate (ex. binding to macrophage Fc receptor) |
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Ig Classes - IgG
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Major: circulating Ab (secondary response - chronic)
Several subclasses: some activate complement and others bind Fc fragment Responds to bacteria, viruses and fungi Crosses placenta |
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Ig Classes - IgM
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Major: Primary response Ab (acute)
Activates complement Cross-links Ag, shape = pentamer |
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Ig Classes - IgD
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Major role: unclear
Increased concentration w/ some allergies (ex. milk, PCN) |
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Ig Classes - IgA
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Major Ab found in: epithelial secretions (ex. mucous membranes)
IgA is a dimer w/ a j chain |
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Ig Classes - IgE
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Major Ab responsible for: allergic rxns
Fc receptors specific for: mast cells and basophils Plays a role in parasite infections |
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Cellular Immunity - Lymphocytes
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These cells are "pre-committed" in their immune specificity before interaction w/ Ag
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Lymphocytes - Clonal Selection
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Process where the body keeps lymphocytes that recognize foreign Ag
Deletes lymphocytes that recognize self Ag |
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Lymphocytes - Clonal expansion
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Process of increased numbers of lymphocytes that are specific for a certain Ag
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Lymphocytes - B Cells (10%)
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Humoral Immunity
Mature in bone marrow and probably gut-associated lymphoid tissue (GALT) - "bursa of fabricius" - chicken... Cell membrane receptors are Igs that are Ag specific Differentiate into plasma cells which produce Abs |
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Lymphocytes - T Cells (75%)
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Cellular immunity - distinguished from B cells by:
Not having Ig as cell membrane receptors - instead they have "CD" molecules Mature in thymus during fetal and early neonatal growth Establishing self-tolerance Req foreign or abnml Ag to be presented w/ the MHC for recognition |
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Specific T Cells - Cytotoxic T Cells
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Expressure CD8 receptors
Attack host cells that infected w/ viruses or bacteria Cytotoxic mechanisms: * Perforins punches hole in target cell * Granzymes induce apoptosis |
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Specific T Cells - Helper T Cells
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Expressure CD4 receptor
Stimulate proliferation of B-cells and cytotoxic T cells 2 major subtypes: 1. TH1: involved in cellular immunity 2. TH2: interact w/ B cells in humoral immunity |
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Specific T Cells - Suppressor (regulatory) T cells
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Express CD8
These cells appear to help regulate the immune response by preventing over activity of the immune system |
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Specific T Cells - Null/Natural Killer (NK) cells (10%)
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Involved in Ab-dependent and Ab-independent cell-mediated cytotoxicity
They can recognize Ag w/o MCH restricitons Lack immunologic memory |
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Other Immune Response Cells - Macrophages
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Major: antigen presenting cell (APC)
Upon Ag recognition the Ag is phagocytized, processed and then "presented" to T lymphocytes |
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Macrophages
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Secrete:
Proteolytic enzymes Active O2 metabolites Arachidonic acid metabolites Cytokines (IL's, TNF, etc) Nitric oxide |
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Other Immune Response Cells - Neutrophils
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Non-specific phagocytes
Express membrane receptors for: C3b C5a IL-8 Fc Fragment |
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Other Immune Response Cells - Eosinophils
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Found in inflammatory sites
Play a crucial role in host defense against parasites They are phagocytes and cells that release inflammatory mediators |
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Other Immune Response Cells - Basophils
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Play a role in immediate and late phase allergic responses
High affinity for IgE and mediates immediate hypersensitivity reactions Releases: histmain, leukotrienes, prostaglandins, heparin and PAF |
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Major Histocompatibility Complex
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MHC Type 1 and 2:
Cell surface proteins that play a major role in the body's immune repsonse Also called: Human Leukocyte Antigen (HLA) |
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MHC Class 1 Molecules
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Found on cell membranes of all nucleated cells and platelets
Endogenously produced Ag (ex. virus) combined w/ MHC 1 expressed on a cell surface targets that cell for destruction MHC 1 and endogenous Ag binds CD8 receptors on cytotoxic T cells |
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MHC Class 1 Molecules
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Class 1 isotypes:
* HLA-A, HLA-B, HLA-C * HLA "tissue" typing determines a person's MHC genes * Some MHC genes predispose pts to immune dz (ex HLA-B27 - ankylosing spondylitis and Reiter's syndome) |
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MHC Class 2 Molecules
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Presents on APCs
Phagocytized Ag combnines w/ MHC 2 expressed on cell surface and is presented to CD4 bearing: Helper T Cells Activated the immune response by: B-cell differentiation and Cytotoxic T-cell killing |
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Immunodeficiency
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A defect in any part of the immune response mechanism
Can be mild or severe, transient or permanent |
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Immunodeficiency - AIDS
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Human immunodeficiency virus (HIV) targets helper T-cell CD4 Ag which leads to infection and cell death
Therefore, decreases ability of the body to mount an immune response Decreased immune response causes increased infxn susceptibility. |
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Immunodeficiency
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DM: decreased immune response increases infxn susceptibility
Splenectomy: * Spleen = key immunologic organ * Decreased immune response increases infxn susceptibility (ex. pneumococcal pneumonia) |
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Autoimmunity
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Under certain circumstances a host Ag can look like non-self Ag and induce abnml activation of the immune response
Results in immune mediated destruction of body cells, tissues or organs |
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Hypersensitivity Responses
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Inappropriate secondary immune response in a person w/ prior exposure to Ag
Classically there are 4 types (Gell and Coombs) |
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Hypersensitivity Responses - Type 1
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Immediate Hypersensitivity
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Hypersensitivity Responses - Type 2
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Cytotoxic reaction
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Hypersensitivity Responses - Type 3
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Immune Complex Dz
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Hypersensitivity Responses - Type 4
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Delayed Hypersensitivity
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Type1: Immediate Hypersensitivity
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IgE binds w/ Ag and both bind to mast cell Fc receptor
Causes mast cell degranulation and release of histamine and other mediators Ex: allergic asthma, hay fever, urticaria and anaphylaxis |
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Type 2: Cytotoxic Reaction
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Ab binds to cell and causes lysis
This process is mediated by complement and cytotoxic T cells Ex: transfusion rxns and hemolytic anemias |
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Type 3: Immune Complex Dz
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Ag-Ab complexes become deposited in tissues leading to complement mediated cell lysis
Results in organ dysfunction and fever Often involves: kidneys and joints Ex: Serum sickness and some types of nephritis |
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Type 4: Delayed Hypersensitivity
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24-48 hours after Ag exposure:
* T Cells become activated and release lymphokines (lymphocyte cytokines) * Macrophages become activated and cause local inflammation Ex: poison ivy, tuberculin skin test (PPD) and granulomatous dz (TB, leprosy) |
