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24 Cards in this Set
- Front
- Back
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Listeria Monocytogenes
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Has membrane bound proteins
Allowing a Protein-Protein interaction with Host allowing it to gain entrance Gram - Often containment of Food and ingested this way also Binds to Actin in epithial cells of GI Spread to the brain causes Meningitis |
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Type 3 secretion appratus
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complex of protein on a microbe that will insert into the Eukaryotic Cell Membrane
Allowing it to shuttle in enzymes that break down this membrane Allowing the organism to bring in the pathogen undetected like a Trojan Horse Control the Cytoskeleton/migration |
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What are 3 ways it can spread in the host?
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Circulating fluids: lymph/blood
Via WBC's (mainly monocytes, but also neutrophils) Direct Spread: open orifice and along skin |
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How do you get systemic spread of an orgainsm?
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Via WBC (monocyte/neutrophils)
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Resistance to Lysozyme and Basic Proteins of the body
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via Defensins
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Resistance to Endocytosis and Phagocytois
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via Capsule
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Granulomas
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Area of necrotic debris arise from the chronic cytokine release (TNF-Alpha, IL-6)
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Extracellular Mechanism for Survival Around Macrophages
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Prevention of Chemotaxis/Cytokine release: Type 3 Secretion
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Intracellular Mechanism for Survival
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Receptors for Internalization
IgG Fc Receptor- triggers oxidative bursts Complement receptors via C3 can enter the cell but DO NOT get oxidative burst |
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Legionella
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No triggering of oxidative burst
Uses the complement receptor, not the IgG Fc |
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M. Tuberculosis
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Modify or abort normal route of phagosome maturation
May modify the pH or secretions |
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Chlamydia and Legionella
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Diversion of phagosome to another pathway and resist phagosomal fusion
Direct the vacuole to another destination |
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Coxiella and Salmonella
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Resist lysosomal degradation
However cannot survive in activated macrophage |
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Listeria, Shigellae and Rickettsiae
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Escape from phagosome
Intially taken in but then go in through he membrane and are free in the cytoplasm Now are subjected to MHC class I pathway of antigen processing/presentation |
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How Coxiella Burnetii has virulence
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Intracellular replication, resists lysomal degradation and formation of immune complexes in chronic disease; get a resistance built up in chronic state
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How Ehrlichia Chaffeenis has virulence
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Intracellular replication with ability to sequester or destroy infected circulating cells
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Virulence of Rickettsia Rickettsii
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Intracellular growth in cell cytoplasm - protects from immune cleance, replicates in endothelial cells giving vasculitis, hypovolemia and hypoproteinemia by loss of plasm in the tissues
results in reduced perfussion of organs and organ failure |
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Virulence of Rickettsia Tsutsugamushi
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Intracellular parasite, replicates in endothelia
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Virulence of Rickettsia Prowazzekii
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Intracellular parasite, replicates in endothelia causes vasculitis
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Key points to Rickettsia
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Intracellular in the cytoplasm
Evade phagosome uptake Mostly in the endothelial cells |
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Virulence of C. Trachomatis
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Intracellualr replication in VACULOES
Prevention of Phagolysosomal fusion survival of EBs resulting form cross linking of membrane proteins Result of re-infectin and host response |
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Virulence of Chlamydia pneumoniae
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Same as for Trachomatis
Destroy epitheial cells and infect the endothelia cells, sm muscle, and macrophages can prevnt apoptosis stays in vacuole and cell is long lived |
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Virulence of Chlamydia Psittaci
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Replication in vacuoles, prevention of of phagolysosomal fusion
Symptoms: pulmonary and CNS |
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When do chronic intracellular organisms change gene and protein expression?
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In the stationary growth phase (enhances survival)
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