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74 Cards in this Set

  • Front
  • Back

pathology

study of disease

etiology

cause of disease

pathogenesis

manner in which disease develops

microbial antagonism

competitive exculsion, prevent overgrowth of pathogens by using up nutrients, O2, changing pH (acidic), produce bacteriocidins

commensalism

one organism benefits, the other unaffected


S.epi on skin

mutualism

both organisms benefit


E.coli in intestine, produce Vit K

parasitism

one organism benefits at the expense of other


tapeworm

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

Exceptions to Koch's postulates

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



incidence

Number of ppl in population who develop disease in particular timeframe.


Indicates spread.

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.

sporadic disease

occurs only occasionally

endemic disease

constantly present

epidemic

many ppl infected in an area in a short amount of time

Contact transmission

Direct (person to person)
Indirect (via fomite)
Droplet (Sneeze/cough <1m)


Vehicle transmission


waterborne


foodborne


airborne (>1m)

Vector transmission

many arthropods


Mechanical (fly feet)


Biological (bug bites/bug feces)

HAIs

Lots of microbes


weak hosts


chain of transmission


Resistant strains

EIDs

New or changing, recent or forecast increase


Most zoonotic, new strains, spread to new location, animal control

epidemiology

studies when/where disease occurs and how it spreads

pathogenicity

ability to overcome host defense and cause disease

virulence

degree of pathogenicity

Portals of Entry

Mucous membranes
GI, GU, resp tract, eyes


Skin


breaks in the skin


Parenteral


penetration, injection, bites, surgery

ID50

Infectious dose for 50% of population


How much to cause disease




Allows for comparison of virulence

LD50

Lethal dose for 50%


How much to kill




Allows for comparison of virulence

Virulence factors

Adherence, cell walls, capsules, enzymes

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.

Siderophores

proteins secreted by pathogen to "steal" iron

Direct damage by pathogen

Using nutrients, waste production, host cell lysis

toxins

poisons made by some pathogens

lysogenic conversion

pathogen acquires new DNA from phage with toxins, resistance factors, etc.

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

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

A-B toxins

2-part exotoxin. A - active part that damages specific cell/part of cell. B - binding part that attaches to host cell.

Membrane disrupting toxins

cause host cell lysis by damaging plasma membrane

Superantigens

bacterial proteins, provoke very intense immune response (cytokine storm)

Genotoxins

damage DNA




Helicobacter

Virus cytopathic effects

Visible damage to infected cells. Type/time varies by virus.


Stops synthesis, inclusion bodies, transformation, activate/alter genes, change surface antigens

Innate Immunity

Born with it, fast response but no memory, responds the same to all invaders.

Adaptive Immunity

specific to the invader, slower response, has memory component

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

Innate Immunity


2nd line

Defensive cells that eat pathogens (NKs, neutros, eos, monos/macros, DCs), inflammation, fever, antimicrobial substances

Phagocytosis

1. Adherence
2. Ingestion


3. Formation of phagosome


4. Fusion of phagosome & lysosome


5. Digestion in phagolysosome


6. Discharge of wastes

Pathogenic evasion of phagocytosis

Inhibit adherence (capsules, M proteins)


Lyse phago (MAC)


Kill WBCs (leukocidins)


Escape or Survive phagosome


Prevent fusion of phagolysosome.

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)

Fever

Boosts # of T cells , increases effects of IFN, lowers available iron (transferrin), increases


reactions for faster healing

Complement system


Classical pathway

Antibody-antigen complex activates C1 --> activates C2 & C4 --> C2a & C4b activate C3

Complement system


Alternative pathway

BDP factors bind to microbe surface --> C3 binds to BDP and is activated.

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

Complement results


Cytolysis

C3b --> activates C5 --> activates C6-C9 to form Membrane Attack Complex (MAC), lyse cell

Complement results


Opsonization

C3b binds to microbe surface, enhances phagocytosis

Complement results


Inflammation

C3b -->activates C5 -->C5a & C3a bind to mast cells, stim release of histamine and attract phagocytes.

IFNs

Alpha & beta made by infected cells, stimulate neighbor cells to make antiviral proteins (AVPs)

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

Humoral Immunity

Involves B cells attacking path free floating, not in cells. Antibodies, MHC II

Cellular Immunity

Involves T cells fighting pathogens inside cells. TLRs, MHC I

IgG

monomer, most common in serum (80%), can leave blood stream. Trigger complement, neutralize toxins, attack bacteria and viruses

IgM

5 monomers joined by J chain, 6%, 1st made for infection, stay in bloodstream. Agglutination. Presence may indicate current infection.

IgA

monomer in serum (13%), dimer in secretions. In mucus, tears, milk. Protects mucus membranes

IgD

Monomer, not well-defined. Hangs out on B cells, helps start immune response

IgE

monomer, binds to masts/basos. Allergic reactions, parasitic worms

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

Cytotoxic T lymphocytes (CTLs)

Start as inactive CTLp's, CD8 cells, MHC class II


Attack infected cells with perforin and induce apoptosis.

B cells

Plasma cells - make antibodies


Memory cells hang out, wait for next infection

Live attenuated vaccine

Weakened pathogen, will replicate.


Lifelong immunity usually w/no booster.


Measles.

Inactivated killed vaccine

Dead pathogen. Safer, but doesn't last, need boosters.


Rabies

Subunit vaccine

Only inject antigenic fragments. Hep B

Toxoid vaccine

Subunit vaccine of inactivated toxin


Tetanus

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.

phaeo-

brown

-phyte

plant

sapr-

rotten

rhodo-/rubri-

red

sept-

rotting