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192 Cards in this Set
- Front
- Back
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Adaptive/acquired immunity
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response to antigens. Involves production of antibodies
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Pathogenicity:
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capacity to cause disease. A binary ability-Does/not not
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Passive immunity
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"ready-made antibodies"
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Natural
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maternal antibodies
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Artificial
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antibodies from other sources
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Active Immunity
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Our own antibodies
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Natural
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from exposure to infectious agent
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Artificial
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Immunization
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Virulence
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intensity of disease produced. Can be highly virulent, or not so much
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T independent antigen response
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Determined by the antigen. B cell divides many times, and differentiates into plasma cells. Then produces gobs of IgM. NO memory cells are produced
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T-dependent antigen response
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The B cell acts like a APC. Binds to antigen, 'eats' it, presents it on surface on MHC. T cells will come and bind to MHC.T cells will proliferate into T helper cells. T cells will secrete cytokines that cause B cell to differentiate into more B cells, which produce IgGds and MEMORY cells.
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2 types of B cell response
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T-dependent antigen response, T-independent antigen response
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APC (antigen presenting cells)
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B cells, DCs Ingest the antigen, process it, present it on surface on MHCs. This activates the T cells (the helper cells (MHC II) and the CTL (cytotoxic lymphocytes, MHC II))
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3 groups of WBC (white blood cells)that start response
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B-cells, APCs, and T cells. Most are in lymph nodes and spleen, some circulating in blood.
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Cell-Mediated component
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Refers to mostly T cells, which are effective against intracellular pathogens.
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Humoral component
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Refers to the B cells and the antibodies they produce. These are effective against extracellular pathogens
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Cell mediated immunity
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T cells attack cells that display foreign antigens . Will attack these, cells infected with pathogens,Tumor cells,Transplanted tissue cells
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Septicemia
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Bacteria are present, and reproducing (by far the scariest)
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Bacteremia
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bacteria are present and are not really reproducing in the blood
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Viremia
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Viruses in the blood (they are free viruses, being transported, not really IN cells
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How Microbes Cause Disease (Steps)
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Infect, adhere to cell surfaces/invade tissues, multiply
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Infectious Agents
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Genetic factors, congenital defects, nutritional deficiencies, immunological interaction, neoplasia
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immunological interaction
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any sort of autoimmune disease will make one more susceptible to disease
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neoplasia
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new growth (cancer) (HPV causes neoplasia)
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Contexts on Which Virulence and Pathogenicity are dependent
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Species of pathogen, # of pathogens, Site of infection, Host susceptibility
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virulence factors
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Any characteristics of a microbe that aid in its disease-causing abilities
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Examples of virulence factors
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-Helps increase contact between host and pathogen (ex: spore forming) -Anything that promote adherence (receptor proteins, spikes on viruses) -anything that helps promote invasion -promotes colonization/multiply once they are 'there' -anything that does harm (some enzyme that will punch pores into hosts cell membrane)
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Exotoxins
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Secreted by bacteria
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Exotoxin properties
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Mostly made of protein , highly specific in actions ( remember proteins are specific), Produced by both Gram + and Gram - cells, Highly potent: a little goes a long way, Highly antigenic: immune response is very likely
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Examples of exotoxins
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Botulinum toxin, Hemolysins, Leukocidins
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Endotoxin location
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Bound to Gram - cell wall
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Endotoxin Properties
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A lipopolysaccharide, More generalized action, Less potent , need large doses-body's responses causes most damage , Weakly antigenic
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How Fungi Cause disease
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Gain access via inhalation, digestion, wounds, Fungal spores release digestive enzymes to damage cells and deepen invasion, May produce toxins.
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Ergotism
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gangrenous, convulsive disease
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How protists cause disease
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Destroy cells and interfere with host function
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Stages of infectious disease course
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Incubation, Prodomial, Invasive, Acme, Decline, Convalescence
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incubation period
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microbes present in body, no signs or symptoms
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Prodomal phase
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vague signs and symptoms become present
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invasive phase
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signs/symptoms at most severe
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decline phase
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declining signs/symptoms
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Why haven't we eradicated infectious diseases?
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Limited access to healthcare, development of resistant strains, new diseases, increase in immigration/travel
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Phagocytes
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remove disease and pathogens. Some release chemicals to control circ. System.
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Fixed macrophage
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In tissues, don't move around.
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Monocyte
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move around and differentiate into macrophages *huge*
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Fibroblast
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Set down collagen (makes scars). Walls off inflamed area
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Neutrophils
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The most abundant type of white blood cell. Neutrophils are phagocytic and tend to self-destruct as they destroy foreign invaders, limiting their life span to a few days.
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Free macrophage
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Macrophages that can move around
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Agranulocytes
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WBCs that contain no visible cytoplasmic granules. Although they are found in the bloodstream, they are much more abundant in lymphoid tissue
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Monocyte
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a type of white blood cell that is relatively large and contains a single oval-shaped nucleus; also called mononuclear leukocyte
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B Lymphocyte (function)
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act as phagocytes when acting as APCs, also produce plasma cells
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T Lymphocyte
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cell of specific immune system which matures in the thymus and is responsible for antigen-specific cellular interactions (cytotoxic T cells and helper T cells) (70-85% of lymphocytes in blood)
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NK Cells
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Have two types of protein receptors on surface, one that inhibits killing, and one that promotes it. 'Wander' around body ignoring cells that have MHC I complex (means its part of the body). Will attack cells that do not have it, binding to target cells with its activating receptors.
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Parts of an Inflammatory Response
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blood flow increased, phagocytes activated, capillary permeability increased, complement activated, clotting rxn walls off area, specific defenses activated
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Chronic Inflammation
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Neither pathogen or host are killed, area becomes walled off (granuloma), It becomes a source of infection if immunity is decreased or a sterile abscess if the infection is eradicated
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repair and regeneration of granuloma
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capillaries grow to site, and fibroblasts divide and secrete collagen to create scar tissue
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What do Pyrogens do?
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induce neural secretion of prostaglandins that create fever
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Endogenous
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Body produces fever
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Exogenous
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Something 'else' produces fever (like a bacteria)
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Benefits of fever
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Helps denature 'bad' cell proteins, slows microbial growth, lets host know its sick, causes fatigue so host lays down=more energy to fight infection, Increases heart rate (increased filtration), Increases defensive activity of some enzymes
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What are the types of molecular defenses?
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LEMs, Interferons, Complement system,
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Leukocyte Endogenous Mediator production
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Produced by activated phagocytes
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What do LEMs do?
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Affect cells lining gut, inhibits iron absorption and promotes iron uptake in circulatory system. This keeps pathogens from absorbing iron to further their growth. Also causes fever.
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What are interferons associated with?
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Viral infections
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How do interferons work?
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When a host cell is virally infected, it will produce interferons that bind to receptors on neighboring cells that will break down viral proteins upon injection.
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What are interferons most effective against?
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RNA viruses
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Types of Complement Systems
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Classical, Alternate, and Lectin
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Classical complement system
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activated by C proteins (compliment proteins) binding with Ag-Ab complexes (antigen-antibody complexes)
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Alternate Complement System
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activated by C protein binding to polysaccharides on microbial surfaces.
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Lectin Complement System
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Activated by interaction of acute phase proteins with bacterial surface molecules
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What does the complement system trigger?
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Inflammation, attracts phagocytes, Enhances opsinization, Causes lysis of Gram - bacteria and host cells displaying foreign matter.
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Passive Immunity
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"ready made" antibodies. Contains Natural and Artificial antibodies
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Natural Passive antibodies
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maternal antibodies. (from our mothers)
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Artificial Passive antibodies
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Antibodies from other sources
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Active Immunity
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Our own (body made) antibodies. Natural and Artificial
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Natural active antibodies
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come from exposure to an infectious agent
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Artificial active antibodies
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Come from immunizations
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4 Properties of Adaptive Immune Responses
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1) Distinguish between self and nonself, 2)Specificity 3)diversity, 4)memory
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specificity (adaptive immune response)
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Reacts in a particular way to each foreign substance
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Diversity(adaptive immune response)
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able to respond to more than 1 billion antigens
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memory(adaptive immune response)
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memory cells produced can circulate for more than 1 year, so if reexposed there will be a very vigorous response
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Three types of cells necessary for adaptive immunity
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B cells, T cells, APC's
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APC's
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antigen presenting cells,
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APC function
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B Cells ingest the antigen and present it on the surface of MHCs. Activates the T cells and the CTLs (cytotoxic lymphocytes)
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2 Types of B Cell response
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T-Dependent and T-Independent response.
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T-Dependent Response
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B cell acts like an APC . Binds to the antigen, engulfs it, presents it on the suface of the MHC. T Cells bind to the MHC, and proliferate into the helper T cells. T cells secrete cytokines that cause B cells to divide into more B cells, producing IgGs and memory cells
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T-Independent Antigen Response
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Is determined by the antigen. The B cells divide many times into plasma cells. Produces gobs of IgM. No memory cells are produced.
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Antigens
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A molecule that one can observe an immune response to
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Common immunogenic substances
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Proteins, polysaccharides, glycoproteins.
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Epitopes
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Piece of an antigen that the immune system recognizes. Antibodies bind to epitopes.
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Haptens
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get no response unless they are attached to a protein. Basis for a lot of allergic reactions.
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What does an antibody/antigen complex activate?
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the complement system and will cause opsinization
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Function of Opsinization
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enhances phagocytosis
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IgG
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a monomer. Predominantly found in blood. Some secreted in milk. Can cross placenta. has two binding sites per immunoglobulin (due to it being a monomer)
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IgA
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Secretory globulin. Found in tears, saliva, mucous, gut, etc. Is a dimer (two monomers bound together). Most abundant immunoglobulin found in colostrom from mother's milk.
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IgM
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a pentamer (5 monomers). Has 10 binding sites. Most abundant in blood early in infection. First immunoglobulin produced when infection is present
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T Cell Production/Maturation
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Come form stem cells in bone marrow. Migrate to Thymus as they differentiate into t cells, then migrate to lymph node
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B lymphocyte production/maturation
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Develop in bone marrow, remain in marrow while differentiating into B cells, migrate to lymph nodes
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How cells differentiate between self and nonself
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clonal selection and deletion
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Clonal selection/deletion
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during B lymphocyte development, the DNA will be rearranged that codes for receptor type. lymphocytes that find their (self) antigens during development, will be deleted. Most happens in bone marrow of fetus., The inactivation or destruction of lymphocyte clones that would produce immune reactions against the animal's own body.
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Humoral Component
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Refers to the B cells and the antibodies they produce.
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What are humoral components effective against?
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Extracellular pathogens
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Cell-Mediated component
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Refers to T cells
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What are Cell-Mediated components effective against?
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Intracellular pathogens
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Secondary Response compared to Primary response
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Memory cells are already floating around. Will bind to antigens, and will proliferate/differentiate. Will produce more IgG quicker and it will last longer.
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Effects of opsinization
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enhances phagocytosis
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How antibodies prevents actions of toxins
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bind to all toxin secreting sites. Same principle when preventing viruses from entering cells.
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What foreign antigens will T cells attack?
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Cells infected with pathogens, tumor cells, transplanted tissue cells
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Cell mediated immunity
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T cells attack cells that display foreign antigens
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2 kinds of MHCS
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MHC I and MHC II
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MHC I
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All nucleated cells have it
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MHC II
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APCs have this.
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If antigen is presented on MHC II
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T helper cells are activated.
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If antigen is presented on MHC I
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cytotoxic killer cells are activated.
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Cytotoxic killer cells are...
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cells that can go after cells that are expressing the antigen, and will release membrane-lysing toxins.
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Natural Killer Cells are part of what immunity
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innate immunity and are nonspecific
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What are natural Killer Cells activated by?
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Cytokines released by infected cells, and a constant portion of antibodies
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What do NK cells do
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Destroy target cells by forming pores in cell membranes. Does apoptosis.
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Superantigens bind to
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MCH II of APC and T cell receptors nonspecifically. (Hijacks the immune system).
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Superantigen Immune Response
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Activates T cells up to 100X faster. Causes lots of T cell replication and release of cytokines, aka hyper inflammatory response.
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Examples of superantigens
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MRSA, Influenza A, TSS
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How do superantigens specifically affect T cells?
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A huge percentage of T cells become involved. (Normal response uses.001% of T cells. When a superantigen is present, it uses more than 20% of them )
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What are antibodies produced by?
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Produced by B cells, plasma cells (differentiated B cell)
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Variable regions
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The arms of the "y". Bind to particular Ag, makes Ab specific.
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Constant regions
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The tail of the "y". Determines class of Ab, what self-tissues it can bind to.
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How do antibodies react to bacterial toxins?
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bind to toxin, neutralize it, and then are ingested by a macrophage
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How do antibodies react to extracellular bacteria?
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Bind to/Opsinize pathogen, then ingested by macrophage
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Which antibodies react to bacteria in plasma?
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IgM
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Which antibodies react to bacterial toxins?
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IgA
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Which antibodies react to extracellular bacteria?
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IgG
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Basophil Function
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Releases histamine and other chemicals during inflammation
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Neutrophil function
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Phagocytic Function. Contain oxidative chemicals chemicals to kill internalized microbes.
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Monocyte
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Develop into phagocytic macrophages in tissues.
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dendritic cells
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Phagocytic cells. Responsible for antigen presentation in the lymph node. (AN APC CELL)
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Major histocompatibility complex
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cell surface proteins essential to immune recognition reactions.
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What do APCs activate?
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cytotoxic T cells, Memory T cells, T helper cells
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T helper cells stimulate
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Some stimulate B Cells (humoral response), Some stimulate infected macrophages attack internal bacteria
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Activated macrophages accelerate
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inflammatory response
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NK cells are activated by
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Cytokines released by infected cells, constant portion of antobodies
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Types of active vaccines
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attenuated live, killed, subunit, recombinant DNA, toxoid
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Attenuated live vaccines
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contain a 'treated' microbe, so it is still immunogenic but has low virulence. Higher risk associated with these
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Killed vaccines
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whole microorganism killed and injected, Have more side effects due to extraneous materials
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subunit vaccines
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A group of vaccines that contain only the antigen subunit of the microorganism.Fewer side effects, safer than attenuated and killed, but extremely hard to do.
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Recombinant DNA vaccine
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Uses an antigen that attracts a huge immune response, isolates this gene, and adds it to a non pathogenic organism, which is then injected.
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Toxoid
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Isolate a toxin within a pathogen, change the toxin so it garners an immune response but no toxin is produced.
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Hazards associated with Active vaccines
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in already immunocompromised patients, side effects will make them sicker, rendering the immune response less able to respond. Also increased virulence, possible allergic reactions, risks to fetus in pregnant woman, Live viruses may revert to virulence
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positive aspects of attenuated live vaccines
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polyvalent (more than one antigen)=larger immune response
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antitoxins
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antibodies against specific toxins. (botulism, tetanus)
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passive immunization
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ready-made antibodies are introduced into an unprotected individual. Often called antisera
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immune serum globulin (antisera)
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Made of pooled serum (found in blood) gamma globulin fractions. (mumps, measles, hep A)
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Incubation period
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time from exposure to clinical signs.
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Length of incubation period depends on
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dose of inoculum, severity of wound, length of neural path from wound to CNS
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Precipitin ring test
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detects antibodies or antigens. Antibodies called precipitins react with antigens. Diffuse toward one another and their complexes form a visible ring.
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Immunodiffusion Tests
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Same principle as precipitin, but carried out on a thing layer of agar on glass slide. Used to determine if more than one antigen (therefore more than one antibody) is present in a serum specimen.
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Agglutination tests
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Antibodies binding to antigens on cells/particles causes clumping. Also from antigens binding to antibodies on particles.
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What are agglutination tests used for?
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Organisms difficult to detect/culture in lab
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Latex Agglutination Test for antigens
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Adsorb known antibodies to latex beads, antigen will bind to its antibody if present
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Latex Agglutination Test for Antibodies
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Adsorb known antigen to latex beads. Antibodies will bind to complementary antigen
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Streptococcus Virulence factors
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M protein and lipotechoic acid allow adherence, Capsulated (avoids phagocytosis), enzymes that promote invasion, hemolysins supply iron from red blood cells
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The Complement Fixation Test Detects...
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It was widely used to diagnose infections, particularly with microbes that are not easily detected by culture methods, and in rheumatic diseases.
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Complement Fixation Test Function
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to detect the presence of either specific antibody or specific antigen in a patient's serum.
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When doing diagnostic tests, what is always important to run?
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Positive and Negative controls
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Types of diagnostic Tests
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Precipitin ring test Immunodiffusion test Latex agglutination test Hemagglutination test Hemagglutination inhibition test Complementation fixation test ELISA test
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Morbidity Rate
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number of individuals affected by disease during a set period in relation to total number of population
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calculating morbidity rate
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number of cases per 100,000 people per year
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Mortality rate
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number of deaths due to disease during a set period in relation to total number of population
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Calculating mortality rate
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number of deaths per 100,000 people per year
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Incidence of a disease
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number of NEW cases contracted within a set population during a specific period of time
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How is incidence usually expressed?
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news cases per 100,000 people per year
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Prevalence
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TOTAL number of people infected within a population during any given time
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Endemic
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if an infectious disease agent is continually present in the population of a particular geographic area, but numbers are too low to equal a health problem
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Epidemic
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when a disease suddenly has a higher than normal incidence in a population
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Common Source outbreak
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an epidemic that arises from contact with contaminated substances
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Propagated epidemic
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From direct person to person contact. (horizontal)
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cytotoxic T cells (function)
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destroy infected cells. Dont deactivate viruses, but help stop spread
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What are Dendritic cells?
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APCs
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Macrophages (function)
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Phagocytes. Also can be APCs
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Neutrophils (function)
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Phagocytes
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Where do plasma cells come from?
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B cells
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T helper cell function
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Help make memory cells. Stimulate phagocytes. Stimulate B cells when antigens are T dependent
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What does the Complement System do?
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Lyse cells that have an antibody/antigen complex, or that have a polysaccharide or lectins
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Mucus (function)
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attracts viruses to flush them out of the body
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Inflammation (function)
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increases permeability and activates compliments
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contamination
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presence of microorganisms
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infection
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microorganism reproduction
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disease
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disturbance of state of health where body cannot function normally
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pathogenicity
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capacity to produce disease
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virulence
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intensity of disease produced
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adhesins
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virulence factor that helps bacteria adhere to host
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streptokinase
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virulence factor that promotes invasion by preventing clotting
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hyaluronidase
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holds cells of certain tissues together (spreading factor)
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coagulase
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promotes invasion by accelerating blood clotting
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Mechanisms for antibiotic resistance
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mechanisms antibiotic pumped out bacterium alters targeted molecule bacterial enzyme chemicall alters antibiotic molecule bacterial enzyme degrades antibiotic molecule
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