Microbal Mechanisms of Pathogenicity – Flashcards
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| superantigens |
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| provoke intense immune response. T cells produce too many cytokines. you hurt yourself. TSS, staph antigens. |
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| diptheria toxin |
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| inhibits protein synthesis. A-B toxin. diptheriae only produces toxin when infected by phage. |
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| erythrogenic toxins |
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| strep. pyogenes synthesizes 3 types of cytotoxins that are superantigens that damage the plasma membranes of blood caililaries. Scarlet fever caused by strep. pyogenes |
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| botulinum toxin |
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| Clostridium botulinum. A-B toxin |
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| tetanus toxin |
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| A-B toxin binds to nervous system controlling skeletal muscles causeing contractions |
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| Vibrio Enterotoxin |
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| vibrio cholerae A-B binds to epithelial cells, causeing them to secrete large amounts of fluids and electrolytes. causes diarrhea and vomiting. E. Coli can produce a similar toxin |
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| Staphlococcal Enterotoxin |
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| staph aureus produces a superantigen in the intestines. |
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| DIC |
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| caused by endotoxins. causes blood clots. |
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| study chart pg. 438 |
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| lacrimal apparatus |
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| system that protects the eyes by flushing them |
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| sebum |
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| prevents hair from drying, protective layer over the skin |
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| leukocytes |
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| white blood cells |
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| granulocytes |
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| type of white blood cells that have large granules. Neutrophils, basophils, eosinphils. |
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| neutrophil |
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| stain in neutral dye, active in initial stage of infection. they can leave teh blood, enter an infected tissue, and destroy microbes. |
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| basophils |
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| stain in basic dye. release histamine for inflammation in allergic responses. |
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| Eosinophils |
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| stain with acidic dye called eosin. produces toxic proteins that fight parasites such as helminths. they can also leave the blood. |
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| agranulocytes |
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| have granules, but you can't see them. 3 types: monocytes, dendritic cells, lymphocytes |
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| monocytes |
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| not actively phagocytic until they leave the blood and mature into macrophages |
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| dendritic cells |
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| found on skin, mucous membranes, thymus, lymph nodes. phagocytosis and initiating adaptive immune response (communicates with T and B cells) |
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| Lymphocytes |
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| include natural killer cells, T cells, and B cells. |
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| natural killer (NK) cells |
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| hunt and kill infected cells using toxic stuff stored in granules. example of toxic stuff: perforin creates channel in membrane causeing cytolysis, granymes cause cells to self destruct |
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| leukocytosis |
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| increase of white blood cells in response to infection |
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| differential white blood cell count |
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| percentage of kinds of white blood cells |
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| platelets |
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| blood clotting |
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| fixed macrophages/ histiocytes |
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| resident in certain tissues and organs of the body. all have different names. the other kind of macrophages wander. |
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| mononuclear phogocytic system |
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| all the macrophages of the body |
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| chemotaxis |
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| attraction of phagocytes to mircobes |
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| opsonization |
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| coating process that promotes phagocytosis |
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| phagolysosome |
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| fusion of phagosome (membrane formed around microbe when it is brought into the macrophage) with a lysosome |
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| lysosome |
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| hydrolyzes peptidoglycan |
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| inflammation |
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| redness, pain, heat, swelling, sometimes loss of function. acute (shoret but severe) or chronic (long but not as bad) |
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| vasodilation |
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| dilation of blood vessels, increasing blood flow to damaged areas and is resonsible for redness and heat associated with inflammation |
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| edema |
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| accumulation of fluid |
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| chemicals released by damaged cells in response to injury |
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| histamine, kinins, prostaglandins, leukotrienes |
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| Complement system |
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| destroys microbes by 1: cytolysis 2:inflammation 3:phagocytosis |
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| opsonization |
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| coating microbe to enhance phagocytosis. makes it easier for phagocyte to bind to a microbe. |
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| MAC membrane attack complex |
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| C5b- C9 in the complement system. causes cytolysis |
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| C3 convertase |
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| C3 |
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| C3a:binds to mast cells with C5a and cause them to relase histamine and other chemicals that increase blood vessel permeability during inflammation. this happens because they release histine. C3b: binds to microbe, causing opsonization |
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| classical pathway |
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| antibodies attach to antigens. C1 binds to antibodies, starts cascade. |
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| alternative pathway |
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| B,D,P factors are surface proteins that bind to C3. |
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| Lectin pathway |
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| lectin binds to mannoose, working as an opsonin and activating C2 and C4, which cascades to C3. |
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| interferons |
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| type of cytokine. interfere with viral replication. alpha and beta (causes uninfected cells to synthesize AVPs), gamma (causes macrophages to produce nitric oxide that appears to kill bacteria). |
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| AVPs (antiviral proteins) |
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| disrupt viral multiplication |
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| iron-binding proteins |
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| Lactoferrin, transferrin, ferritin, hemoglobin |
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| AMPs (antimicrobial peptides) |
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| attract dendritic cells, kill microbes, recruit mast cells. broad spectrum of activity. |
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| perforin/ granzyme |
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| pore-forming protein that lets granzyme into the cell. granzyme then apoptosizes (chops up the DNA) of the cell. |
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| T Cytotoxic cells (CD8+ T cells) |
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| matures into CTL (cyutotoxic T lymphocyte) that destroys cells on contact using perforin and granzymes. |
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| T Regulatory cells |
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| stop T cells from reacting against self. maintains tolerance. |
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| T helper cells |
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| activated when come into contact with APC. produce cytokines and activates all cells related to cell-mediated immunity: mactophages, T cytotoxic cells, and NKs. |
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| Dendritic cells |
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| primary APCs to induce immune responses by T cells. |
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| Macrophages |
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| cell eaters. activated by ingesting antigenic material or by cytokines made by helper T cells. activated macrophages are better phagocytes adn APCs. notable: eat cancer cells. |
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| Natural Killer Cells (NKs) |
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| don't have to be activated by antigen. kill cells that don't display MHC class I slef-antigens |
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| cytokines |
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| chemical messengers. soluble proteins or glycoproteins produced by immune cells in response to a stimulus. communicate between white blood cells. |
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| chemokines |
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| cytokines that bring leukocytes into area of infection important for inflammation |
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| tumor necrosis factor |
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| TNF- alpha. targets tumor cells. factor in inflammatory responses |
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| cytokine storm |
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| harmful overproduction of cytokines caused by a feedback loop. |
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| Humoral immunity |
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| B cells. targets free circulating patogens using antibodies |
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| cellular immunity |
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| t cells- targets infected cells, or intracellular pathogens. mostly uses specialized phagocytic or NK cells |
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| B cells |
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| lymphocytes that mature in bone marrow. involved in humoral immunity. produces Antibodies. mature into plasma cells that make antibodies or memory cells. |
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| T cells |
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| lymphocytes that mature in the thymus. involved in cellular immunity. |
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| antibodies |
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| stem (Fc region)and V region on tips of the Y. V region binds to epitope, Fc region binds to host cell or complement. |
