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Pathogenesis - Coggle Diagram
Pathogenesis
Definitions
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ID50: Infectious dose. # of pathogens required to cause infection in 50% of host population (lower #, more virulence)
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Toxin
Biological poisons that assist in their ability to invase, cause damage to tissues
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Endotoxin: Lipopolysaccharide (lipid) found on outer membrane of gram (-) bacteria (inflammation / fever, heat stable, high LD50)
Exotoxin: Protein produced by wide variety of living pathogenic bacteria (specific damage to cells, effected by heat
Exoenzymes
Glycohydrolases: E (Hyaluronidase S in staphylococcus aureas) F (Degrades hylauronic acid that cements cell together to promose spreading through tissues)
Nucleases: E (DNase produced by S. aureus). F (Degrades DNA released by dying cells that can trap bacteria, promoting spread)
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Phospholipases: E (Phospholipase C of bacillus anthracis). F (Degrades phospholipid bilayer of host cells, causes cellular lysis, degrades membrane of phagosomes to enable escape into cytoplasm)
Stages
1. Exposure/contact: Portal of entry (skin, mucosa, placenta)
2. Adhesion: Attachement to cells (adhesins, biofilms)
3. Invasion: Spread of pathogens throughout tissues and body (exoenzymes, toxins-colonize/damage host tissues) (membrane ruffling)
4. Infection: Multiplication of pathogen. Local (boils or abcess). Focal (dental work). Systematic (chx pox). Primary vs. secondary (one infection leads to another, HIV)
Exotoxins
Intracellular targeting toxins (cholera, tetanus, botulinum, diptheria)
B component responsible for cellular specificity of toxin and mediates initial attachment of toxin to specific cell surface receptors. Once A-B toxin binds to host cell, it's brought into cell by endocytosis, entrapped in a vacuole. A and B subunits separate as vacuole acidifies. A subunit enters cell cytoplasm, interferes w/ specific internal cellular function that it targets.
Diptheria: Inhibits protein synthesis. A subunit inactivates elongation factor 2 by trasferring ADP-ribose. Stops protein synthesis and kills cell
Neurotoxin
Tetanus toxin binds to inhibitory interneurons, responsible for release of the inhibitory neurotransmitters glycine and GABA.
These neurotransmitters bind to neurons at neuromuscular junction, resulting in inhibition of acetylcholine release.
Tetanus/Botulinum toxin inhibits release of glycine and GABA from the interneuron, resulting in permanent muscle contraction. First symptom stiffness of the jaw (lockjaw). Violent muscle spasms in other parts of body, typically with respiratory failure and death.
Collagenase
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Degrades collagen between endothelial cells, allowing bacteria to enter bloodstream.