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34 Cards in this Set
- Front
- Back
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Frank Pathogen
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-primary
-cause disease in host with normal immune system |
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Opportunistic Pathogen
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-commonly present in normal flora
-take opportunity to infect us when our immune system is down |
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Subclinical Infection
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-not highly virulent=attenuated
-too few=below the infectious dose |
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Clinical Infection
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enough virulence to cause signs and symptoms
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Infectious Dose (ID50)
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infectious dose at the 50th percentile
-idea that people have high and low thresholds |
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Signs and symptoms
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signs=apparent upon examination
symptoms=effects only patient notices i.e pain, nausea |
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Balanced Pathogenicity
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-goal of pathogen->opportunistic native flora
-does not want to kill its host before the pathogen can replicate and spread -i.e myxomatosis virus in rabbits |
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Localized Infection
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-disease only affects immediate area of infection
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Disseminated Infection
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-disease affects other locations
-commonly disseminated in blood and lymphs |
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Septicemia
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-acute illness caused by pathogens in blood
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Acute illness
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incubation period->illness->organism dies
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Chronic Illness
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incubation period-> illness-> illness persists or recurs over a long period
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Latent Illness
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incubation period->illness-> dies down but still small amount of bacteria -> recurrence when immunity is weak
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Koch's Postulate
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1) bacteria must be present in most disease cases
2) bacteria DNA must be isolated from the disease case and grown in pure culture 3)specific disease must be reproduced from pure culture in healthy model host i.e animal models 4)bacteria DNA must be recoverable from the susceptible host 5)number of infections are polymicrobial=multiple bacteria cause infection |
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Infection vs. Intoxication
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Infection:
-multiplication of organism causes disease -severity is related to number of organisms -killing organisms cures disease Intoxication: -toxin produced by organism causes disease -organism does not have to be present -antibiotics have no effect so use antitoxins (passive immunity) |
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Fimbrial Adhesin
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-pili with special adhesin proteins at the tip (fimbriae) which is what our cells recognize
-bind to receptors on host cell, this is specific -receptor normally serves another purpose |
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IgA protease
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destorys IgA which is the antibody so allows for colonization on mucous membranes
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Siderophore
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iron siderophores compete with our lactoferrin for Fe
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Type 3 effector
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-needle complex
-secrete bacteria directly into our cells |
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Membrane Ruffles
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effector causes our cytoskeleton to be rearranged so instead of flat surface we get folds in which the bacteria can slip in
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Horizontal Gene Transfer
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-passing of virulence factors which enhance invasion and colonization on pathogenicity island to another bacterial cell
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Pathogenicity Island
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unit of virulence factors and get transferred all at once
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M cells
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-microfold cells
-uptake bacteria and pass them across the cell and show it to the macrophages on the other side -some bacteria can live in the macrophages or some escape before and go in through the basal membrane and to other cells |
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Activated Macrophage
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-Th cells bind antigen on MHC 2 and the CD28/B7 signal
-enhanced oxidative burst and digestive capabilities |
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Apical Membrane
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-harder to penetrate by bacteria
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Basal Membrane
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-easier for bacteria to enter into epithelial cells
-like slipping in the backdoor |
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Actin rockets
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-push the pathogen into next cells i.e shigella
-polymerized by the antigens |
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Serum Resistance
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-avoidance of the complement system
-C3b floating in blood stream tags a bacterial cell and doesn't do this to our cells because we have a protein called CRP which blocks C3b interaction -bacteria steals CRP receptor so C3b will not bind to bacteria and complement system will not be activated |
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C3b regulatory protein
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-regulatory protein that binds to bacterial cells to tag for opsonization and activation of the compliment system but gets blocked by CRP
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C5a peptidase
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-prevents PMN recruitment
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Lysin (leukocidin)
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kill phagocytes
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Fc binding protein
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-staph protein A
-bind Fc part of antibody to the bacteria so now it looks like a B cell and our immune system doesnt recognize it |
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Staphylococcal Protein A
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-what binds Fc part of antibodies
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Pilus Switching
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antigenic variation
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