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40 Cards in this Set
- Front
- Back
Viroids
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All Nucleic Acids
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Prions
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All proteins
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Viruses
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Obligated to be parasites, have no organelles need a host to survive and replicate
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Fungi
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Eukaryotic cells
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Prokaryotic
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Bacteria, some have lost the ability to grow on their own
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Virulence factors
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Components of the structure of bacteria which contribute to the ability of the bacteria to cause disease.
FIMBRIA--allow attachment Toxins which contribute to disease. Some secrete enzymes. REALLY DEPENDS ON structure and what it it is capable of doing |
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Bacterial structure
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A. No organelles
B. Cell Wall C. Gram + or - D. Some antibiotics do not work on G+ wall or vice versa due to inability to get pass the wall |
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Gram - Bacteria
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Lipopolysaccarides, external component that is associate with FEVER, ACTIVATIOn OF LYMPHOCYTES,
CAUSE OF ENDOTOXIN |
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Gram Stains
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Crystal violet stain which gets into cells colors them blue the Gram + will stay blue while the - will be red since the when alcohol is added it is washed out
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Pili
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Help in colonization, they grip to the enviroment that they land in
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Capsules
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Genetically produced by bacteria
Immune systems will not be able to digest or remove efficiently Bacteria consists of the plasmid and other **** that it can pick up to influence activity |
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Biofilms
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ARTIFICIAL IMPLANTATIONS
Colonies form and communicate with eachother and form layers! Cause problems like infection caused by bacteria occurs in vivo |
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Generational time
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Replication occurs at different rates,
Abscess bacteria cannot grow as fast, if you give a static drug it will not be effective due to slow growth rate |
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Anaerobes
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Superoxid Dimutase present and eliminates radical, uses fermentation route,
uses derivative of pyruvate to grow, slow growening, make certain fermentation products that tell you what they are |
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Facilitative Bacteria
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Grow Aerobically and anaerobically
Anaerobically is slower than aerobic prefer aerobically. |
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Conjunction
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Mediated by F factor
1. F+ factor moves in from another cell(F+ to F- cell) via a sex pili thingy. Then integrates into other cell's genome. 2. Enters F- cell with some other component first then has HFR come last. THe HFR activates host chromosomoe and integrates. 3. This is the result of biological exchange TRANSFER OF RESISTANCE |
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Transformation
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Bacteria has lysed DNA floating around
Pick up floating DNA by competence factor add to it's genome, this may make it more virulent or allow it to be resistant to something |
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Transduction
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Bacteria have phages
Phages can kill other bacteria by 2 methods Lytic: Enter Cell, replicate, lyse cell, don't play a role in virulence, use medically. Lysogenic-genetic material enters cell, depending on synthesis of repressor gene stops the ability of the host for totall replication. Sets phage genetic material for integration into host chroms. Can also lyse the cell if integration fails. |
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Specialized transduction
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Transfer of host DNA sements near site of prophage integration contains viral and Host DNA
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Generalized Transduction
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Randomly packages host DNA in a bacteriophage coate and may transfer any gene
Transducing particle contains only host DNA |
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Plasmid
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Dna Pieces that self replicat. Can carry antibiotic resistance, toxic genes and transposons
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Transposons
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Movable genetic elements incapable of independent replication. Inserts int chrom.
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Integrons
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mobile genetic element consist of an integrase gene, resistance genes, and insertion sequence. NO SELF REPLIC.
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Pathogenicity islands
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Genes code for unique secreation systems, toxins adhesion, etc, contains integrase and transponse genes.
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Bacterial Pathogenesis
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Transmission
Evasion of 1* host defenses Adherence to mucase membranes by pili or capsules, adherins mediate adherence. BIOFILMS FORM Colonization by growth Disease sympoms caused by toxin production Host response nospecific and specific Progression or resolution of disease |
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Exotoxins
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polypeptides relased by cell highly toxic both gram + and -
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Endotoxins
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lipopolysaccarides, intergal part of gram -,
cause SMALL AMOUNTS::: Fever, Vasodialation, Increased Antibody Synthesis, Inflammation LARGE AMOUNTS::: SHock, intravascular coagulation |
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Pyogenic
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Pus producing where neutrophils are predominant
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Granulomatous
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Macrophages and t cell predominate
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Survival of Host Defenses
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1. Invactivation of antibody
2. Inhibition of complement action (keeps complement from binding to cell 3.Antigenic (phase) variation- alteration of epitopes on major bact. surface molecules avoiding antibodies. 4. Molecular mimicry-Pathogens mimic host factors and allow evasion of adaptive host impun system. 5. Lipopolysac. Modification- changes stop phago. or membrane attack complexes. IE MAC forms to far from the cell when modified to damage cell. |
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LIVE Vaccines In U.S.
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Measles, mumps, Rubella, Varicella, Polio, Yellow Fever, smallpox, influenza, TB, Typhloid
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Killed Vaccines in US
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Polio, Hep A, flu, polio, rabies, cholera, pertuss, plague, typhoid.
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Exotoxin subunits??
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A-active does harm to cell
B-Binder binds to cell surface. |
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5 Class of Antibacterial Attack
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Inhibit cell wall synthesis,
Inhibit NA synthesis Protein synthesis at 30S subunit and 50S Alteration of cell membrane function to target gram negative bacteria |
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Innate Immunity
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Skin, resporitory epithelia, saliva
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Active (Adaptive) Immunity
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B Cells respond by making antibodies specific to virus receptors and have the ability to bind to our own cell receptors to keep viruses away from them.
IgM=first antibody that comes up when comes across antigenes IgG- antibodies stored from past encounters T-lymophcytes, compliments, |
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Compliment-
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binds to antibody which binds to cell which then puts holes in bacteria cell, this then attracts phagocytes to eat it
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Lukocydins
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Made to kill macrophages
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Super antigens
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Super stimulate cells of the body to secrete cytokines which shocks the body
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Sialic Acid
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Added to endotoxin by lipopolysaccharide to hide it from host defenses in gram negative cells.
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