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works to eliminate extracellular antigens in blood stream, B cells responsible for this immunity, once they are activated they differentiate into plasma cells that secrete antibodies |
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deals with antigens residing within a host cell, directed by t-cells |
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Fc region of antibody can attach to its receptor on a phagocyte making antibody coated antigens easier to identify and engulf |
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Antibody dependent cellular toxicity |
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when multiple IgG antibodies bind to infected cell, it becomes a target for natural killer cells, the NK cells bind to the Fc region of IgG and deliver compounds directly |
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present antigens made within the cell, produced by all nucleated cells, antigens recognized by cytotoxic t cells (respond to endogenous antigens) |
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present antigens taken up in a cell, only specialized antigen presenting cells make MHC II molecules, antigens recognized by t helper cells (respond to exogenous antigens) |
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- when b cell receptor binds to t dependent antigen, b cell takes it in by endocytosis and encloses it within an endosome, antigen degraded and delivered to MHC II molecules on surface of b cell where they are presented to Th cells which scan naïve b cell to determine if it has encountered an antigen it can recognize, if Th’s antigen receptor binds to peptide fragments being presented, the t cell activates the b cell by delivering cytokines to b cell and initiating clonal expansion |
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T independent antigens activation |
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- have multiple, repeating epitopes so clusters of b cell receptors bind to antigen simultaneously leading to b cell activation without Th cells |
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dendritic cell detects pathogen, travels to secondary lymph organ and encounters naïve t cell, presents material, if t cell recognizes it, it becomes activated and starts clonal expansion |
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Mechanisms of establishing infection |
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Adherence, colonization, delivering effector proteins to host cell (changing cell’s function/ structure), exploiting antigen sampling, |
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how bacteria overcome Innate immunity |
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- can hide in host cell because innate system doesn’t recognize intracellular invaders, can bind to complement regulatory proteins to avoid complement system activation and postpone MAC formation, preventing encounters with phagocytes, avoiding recognition and attachment by phagocytes, surviving in phagocytes |
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how bacteria overcome Adaptive immunity |
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- overcoming antibodies by producing IgA protease to break down IgA antibodies, antigenic variation so antibodies wouldn’t recognize them, mimicking host cell molecules (capsules, ect.) |
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LPS, integral part of outer membrane, cnnot be converted to an effective toxoid for immunization, only in gram -, it is heat stable, produces an innate immune response (fever, drop in blod pressure) only systematic distribution is dangerous |
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proteins that may or may not be secreted by bacterial cells, found in gram + and – cells, can generally form toxoid and are inactivated by heat, generally potent toxins |
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Virus like particle vaccine |
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Enhances immune response to antigens, includes danger signals (patterns associated with tissue damage or invading microbes) |
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incidence of a disease in a population at risk |
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diseases constantly present in a population |
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indirect- carries microbe on its body from one place to another, flies on food, you eat food and get sick |
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direct- carrier either injects the human with pathogen or it bites human |
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Intrinsic antibioticresistance |
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lack target entirely (cell wall, nucleotides), hidden target (underneath membrane), altered target (deformed) |
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Selected antibiotic resistance |
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altered target (mutation by natural selection), repeat exposure of same antibiotic, incomplete treatment (typically happens with bacteriostatic agents) |
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Acquired antibiotic resistance |
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Definition
- horizontal gene transfer, spontaneous mutation |
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What are the acquired actions through horizontal gene transfer that contribute to resistance? |
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Definition
Enzymatic degradation- encodes enzymes to attack antibacterial cells, changes charge, pH, solubility and prevents it from entering cell Uptake blockage Extrusion- bacteria spit antibodies out |
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Why are antibiotics not effective on viral infections? |
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Definition
Viruses don’t have cell walls or ribosomes and rely on host machinery for replication, therefore it is difficult to target viruses without damaging human cells |
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3 targets that are used to treat fungal infections |
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Cell wall synthesis- chitin Plasma membrane- ergosterol Cell division- tubulin (spindle apparatus) not unique to fungus, has to build up in sytem |
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What are thought to be the main mechanisms for current antiprotozoal and antihelminthic drugs? |
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Inhibit biosynthetic pathways or neuromuscular functions |
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