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33 Cards in this Set
- Front
- Back
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pathogenicity |
degree of disease virulent- destructive in path of disease disease- actively have signs and symptoms |
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host entry portal of entry |
entry site of microorganisms most microorg have preferred entry |
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mucous membranes portal of entry |
resp tract, GI tract, genitourinary tract, conjuctiva most popular entry lines almost every tract in the body, get in inhalation or ingestion conjuctiva- exposed all times, tears-antibodies |
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skin portal of entry |
not that hospitable healthy skin is hard to penetrate enter through open cuts and knicks |
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parental route portal of entry |
bruises, iv |
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number of invading organisms |
ID50- (infection dose), # of org to cause infection in 50% microrg LD50- (lethal dose), # org to cause death to 50% microorg bac varies in # required to cause infection |
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pathogen attachment |
surface molecules on pathogen (adhesin) bind to complementary surface receptors on cells of host tissue adhesins are on any part of bac cell |
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capsule bac pathogen penetrate host cell |
ability to invade immune system, prevent phagocytosis streptococcus pneu- pneu in kids, older adults klebsiella pneu- resp tract inf, young children haemophilia pneu- resp tract inf, meningitis bacillus anthracis- can cause disease |
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cell wall components bac pathogen penetrate host cell |
M protein- resist immune system, prevent phagocytosis fimbriae/opa protein- GI tract infection organisms, work together, facilitate attachment my colic acid- gives TB bac resistance enzymes |
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enzymes bac pathogen penetrate host cell |
coagulases- clots blood, keeps bac protected from immune system (staph) kinases- dissolve clots, organisms spread faster to tissues Hyaluronidase- unglues tissue, help org penetration IgA proteases- prim defense, inactivates antibodies secreted by imm sys, body fluids collagenases- dissolve tissue, in human body |
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antigenic variation bac pathogen penetrate host cell |
change structure and surface components |
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penetration in host cell cytoskeleton bac pathogen penetrate host cell |
active fibers in cell invasins/ cadherin- glycoprotein, disrupt cytoskeleton membrane ruffling- enlarges membrane, make cell ruffled, use center to enter into tissue |
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siderophore damage to host cell |
iron binding molecule enters cell and takes iron |
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direct damage damage to host cell |
use all nutrients and resources cause cell to die |
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production of toxins (toxigenicity) damage to host cell |
affects gram + and gram - bac endotoxin and exotoxin |
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exotoxin |
proteins secreted by gram + and - specific target organs heat sensitive need small amount
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toxoids and antitoxin (exotoxin) |
toxoids- modified toxins, used by immunizations in body antitoxin- antibodies produced by immune system against specific toxin |
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A-B toxins (type of exotoxin) |
bac secretes toxin, A and B component B binds to host cell within body, taken into cell once inside, A and B seperate B is released out of cell A is toxic, causes cell damage A- functioning B- binding |
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membrane disrupting toxins |
affect membrane of cell Leukocidins- toxin disrupt WBC membrane Hemolysins- toxin disrupt RBC membrane Streptolysins- oxygen sensitive, flesh eat bac |
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superantigens |
stimulate/enhance immune response level cause nonspecific activation of T cells resulting in polyclonal T cell activation
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examples of exotoxins |
dipheria- enters resp tract, stay in throat (localized), produce A-B model, inhibit protein synthesis (kill cells), can spread to body botulism- target nerve cells, flaccid paralysis (relaxed muscles), cosmetic, muscle spasms, need small amount tetanus- muscles contracted, prevent transmission of neurotransmitter, do not relax |
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example of exotoxins |
vibrio- causes colera (fecal contamination), life threatening, GI tract entrance, small intestine secrete large amounts water staphylcoccal- stomach flu, contaminate food, staphylococcus |
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endotoxin |
lipid, only gram - LPS layer- outer membrane Lipid A- responsible for endotoxic effect heat resistant, no specific target- general effect in body chills, fever, shock intorvas coagulation-clotting |
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cytokine (endotoxin) |
released by cells too much=destructive cytokine storm- released by various cells |
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interleukin 1 tumor necrosing factor |
pyrogens- fever inducing when released dilates capillaries, goes from circulatory system to nervous system to hypothalamus (brain) causes heat regulation, reset hypothalamus temp, increase body temp |
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shock |
decrease in blood pressure antifilactant shock- allergic reaction septic shock- bac stock from infection toxic shock- induced by toxins |
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LAL limulus amebocyte lysate |
detects endotoxin in drugs, body fluids, and medical devices amebocyte- cells, sensitive to presence of endotoxin (coagulates), horseshoe crab
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plasmids, lysogeny, and pathogenicity R factors, virulence factors, lysogenic conversion |
plasmid/prophage- production of toxins R factor- resistance virulence factors- cause disease pathogenicity- degree of disease lysogeny- viral reproduction
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cytopathic effects or pathogenic effects of viruses |
1. DNA/RNA of host inhibited, protein synthesis effected change components, no transcription/translation 2. cell lysosome damaged=cell death helps destroy bac virus and host cell |
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cytopathic effects |
3. inclusion bodies (character of virus cell, particles together), damaged organelles, masses of viruses negri bodies- brain tissue by rabies virus 4. fusion of many cells (synctyia), certain inf viral infection of 1 cell, all others around fuse AIDS, mumps, chicken pox |
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cytopathic effects |
5. change in host cell function virus takes over, no normal function 6. interferon- antiviral substance produced by immense cells helps against viral infection 7. antigenic changes- virus changes outside of cell
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cytopathic effects |
8. chromosomal disruptions integrate as prophage instead of infection, become part of host cell DNA 9. transformation into malignant cells Herpes, Hepatitis B |
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portals of exit |
similar to portal of entry preferred method for each |
