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74 Cards in this Set
- Front
- Back
pathology |
study of disease |
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etiology |
cause of disease |
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pathogenesis |
manner in which disease develops |
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microbial antagonism |
competitive exculsion, prevent overgrowth of pathogens by using up nutrients, O2, changing pH (acidic), produce bacteriocidins |
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commensalism |
one organism benefits, the other unaffected S.epi on skin |
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mutualism |
both organisms benefit E.coli in intestine, produce Vit K |
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parasitism |
one organism benefits at the expense of other tapeworm |
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Koch's Postulates |
1. Same path present in every case of disease 2. Path isolated from host, grown pure culture 3. Culture causes same disease on innoculation 4. Path from innoculated same as original |
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Exceptions to Koch's postulates
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M. leprae - cannot culture in artificial media T. pallidum - no virulent str. on artificial media Some diseases have multiple pathogen causes Some pathogens cause different diseases |
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incidence |
Number of ppl in population who develop disease in particular timeframe. Indicates spread. |
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prevalence |
Number of ppl in pop. who develop disease at specified time, regardless of 1st appearance. Indicates how serious/how long disease affects a population. |
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sporadic disease |
occurs only occasionally |
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endemic disease |
constantly present |
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epidemic |
many ppl infected in an area in a short amount of time |
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Contact transmission |
Direct (person to person)
Indirect (via fomite) Droplet (Sneeze/cough <1m) |
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Vehicle transmission
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waterborne foodborne airborne (>1m) |
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Vector transmission |
many arthropods Mechanical (fly feet) Biological (bug bites/bug feces) |
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HAIs |
Lots of microbes weak hosts chain of transmission Resistant strains |
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EIDs |
New or changing, recent or forecast increase Most zoonotic, new strains, spread to new location, animal control |
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epidemiology |
studies when/where disease occurs and how it spreads |
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pathogenicity |
ability to overcome host defense and cause disease |
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virulence |
degree of pathogenicity |
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Portals of Entry |
Mucous membranes Skin breaks in the skin Parenteral penetration, injection, bites, surgery |
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ID50 |
Infectious dose for 50% of population How much to cause disease Allows for comparison of virulence |
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LD50 |
Lethal dose for 50% How much to kill Allows for comparison of virulence |
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Virulence factors |
Adherence, cell walls, capsules, enzymes |
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Pathogen must be able to... |
1. Microbe enters thru preferred portal 2. Reproduce and adhere 3. Penetrate/evade host defenses 4. Damage host cells 5. Exit usually thru same portal as entry to find new hosts. |
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Siderophores |
proteins secreted by pathogen to "steal" iron
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Direct damage by pathogen |
Using nutrients, waste production, host cell lysis |
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toxins |
poisons made by some pathogens |
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lysogenic conversion |
pathogen acquires new DNA from phage with toxins, resistance factors, etc. |
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Exotoxins |
Mostly G+ bact, product of cell metabolism, small amount lethal, highly toxic, proteins (A-B), no fever, unstable (destroyed at 60-80C) Botulism, tetanus |
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Endotoxins |
G - bact, lipid A part of LPS in cell wall, released during division or cell death, requires high long heat to disable, not as toxic, need higher dose to be lethal, cause fever S.pneumoniae |
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A-B toxins |
2-part exotoxin. A - active part that damages specific cell/part of cell. B - binding part that attaches to host cell. |
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Membrane disrupting toxins |
cause host cell lysis by damaging plasma membrane |
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Superantigens |
bacterial proteins, provoke very intense immune response (cytokine storm) |
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Genotoxins |
damage DNA Helicobacter |
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Virus cytopathic effects |
Visible damage to infected cells. Type/time varies by virus. Stops synthesis, inclusion bodies, transformation, activate/alter genes, change surface antigens |
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Innate Immunity |
Born with it, fast response but no memory, responds the same to all invaders. |
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Adaptive Immunity |
specific to the invader, slower response, has memory component |
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Innate Immunity 1st line |
Skin & mucus membranes block things, sweat washes, flow of fluids trap and remove, pH inhibits growth, normal microbiota make unwelcome environment for pathogens |
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Innate Immunity 2nd line |
Defensive cells that eat pathogens (NKs, neutros, eos, monos/macros, DCs), inflammation, fever, antimicrobial substances |
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Phagocytosis |
1. Adherence 3. Formation of phagosome 4. Fusion of phagosome & lysosome 5. Digestion in phagolysosome 6. Discharge of wastes |
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Pathogenic evasion of phagocytosis |
Inhibit adherence (capsules, M proteins) Lyse phago (MAC) Kill WBCs (leukocidins) Escape or Survive phagosome Prevent fusion of phagolysosome. |
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Inflammation |
1. Vasodilation: increase perm. of blood vessels (histamines, prostaglandins, kinins, blood clots) 2. Phago migration/phagocytosis: marginization & diapedesis. 3. Tissue repair: can't complete until all junk gone. Cells from parenchyma (functional) or stroma (scar tissue) |
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Fever |
Boosts # of T cells , increases effects of IFN, lowers available iron (transferrin), increases reactions for faster healing |
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Complement system Classical pathway |
Antibody-antigen complex activates C1 --> activates C2 & C4 --> C2a & C4b activate C3 |
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Complement system Alternative pathway |
BDP factors bind to microbe surface --> C3 binds to BDP and is activated. |
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Complement system Lectin pathway |
Macros release cytokines that stim liver to produce lectins --> lectins bind to mannose on microbe surface --> activates C2 & C4 --> C2a & C4b activate C3 |
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Complement results Cytolysis |
C3b --> activates C5 --> activates C6-C9 to form Membrane Attack Complex (MAC), lyse cell
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Complement results Opsonization |
C3b binds to microbe surface, enhances phagocytosis |
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Complement results Inflammation |
C3b -->activates C5 -->C5a & C3a bind to mast cells, stim release of histamine and attract phagocytes. |
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IFNs |
Alpha & beta made by infected cells, stimulate neighbor cells to make antiviral proteins (AVPs) |
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Antimicrobial proteins (AMPs) |
Short chains w/broad antimicrobial effects. Inhibit cell wall synthesis, poke holes to lyse, damage DNA/RNA of invader, attract phagos/masts. Microbes don't develop resistance |
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Humoral Immunity |
Involves B cells attacking path free floating, not in cells. Antibodies, MHC II |
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Cellular Immunity |
Involves T cells fighting pathogens inside cells. TLRs, MHC I |
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IgG |
monomer, most common in serum (80%), can leave blood stream. Trigger complement, neutralize toxins, attack bacteria and viruses |
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IgM |
5 monomers joined by J chain, 6%, 1st made for infection, stay in bloodstream. Agglutination. Presence may indicate current infection. |
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IgA |
monomer in serum (13%), dimer in secretions. In mucus, tears, milk. Protects mucus membranes |
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IgD |
Monomer, not well-defined. Hangs out on B cells, helps start immune response |
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IgE |
monomer, binds to masts/basos. Allergic reactions, parasitic worms |
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T Helper cells |
CD4 cells that activate B cells & macros, MHC class I TH1 - activate CD8 TC cells & NKs TH2 - stim production IgE, allergies, eos TH17 - inflammation, recruit neutros |
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Cytotoxic T lymphocytes (CTLs) |
Start as inactive CTLp's, CD8 cells, MHC class II Attack infected cells with perforin and induce apoptosis. |
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B cells |
Plasma cells - make antibodies Memory cells hang out, wait for next infection |
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Live attenuated vaccine |
Weakened pathogen, will replicate. Lifelong immunity usually w/no booster. Measles. |
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Inactivated killed vaccine |
Dead pathogen. Safer, but doesn't last, need boosters. Rabies |
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Subunit vaccine |
Only inject antigenic fragments. Hep B |
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Toxoid vaccine |
Subunit vaccine of inactivated toxin Tetanus |
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Conjugated vaccine |
Polysaccharide from capsule combined with proteins to make it work for very young kids whose immune systems won't yet respond to just the polysaccharide. Hib. |
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phaeo- |
brown |
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-phyte |
plant |
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sapr- |
rotten |
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rhodo-/rubri- |
red |
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sept- |
rotting |