Topic 23 pathogenesis

Topic 23 pathogenesis - Staph Infection Food Poisoning Dr...

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Staph Infection- Food Poisoning- * Dr. Field said to start with pathogen entry into food 1. Pathogen possibly originally in nasopharynx of carrier is transferred to food by hands 2. Pathogen multiplies in food that is not refrigerated but kept at warm temperatures 3. Toxin is produced and absorbed into food * Toxin heat stable. Pathogen can be killed by heating food but not toxin! 4. Toxin and/or Pathogen (S. aureus) enters host through ingestion of contaminated food 6. Pathogen is killed while enterotoxin reaches GI tract and acts on neural receptors to stimulate vomiting center in brain Watery diarrhea can also be seen 8. Pathology caused by the following: 1. Enterotoxins- responsible for the vomiting and diarrhea 2 .Immunopathology? Exit: Pathogen does not exit Note: It is the toxin NOT the pathogen causing disease 5. The following oropharynx and GI defenses are overcome by toxin but not by pathogen: sIga-located in mucus- binds pathogen Saliva/lysozyme- cleaves peptidoglycan Normal flora of GI tract-compete with pathogen Flushing and peristalsis- helps beat bacteria down and out Low pH of GI tract-inactivates/kills pathogen 7. Adaptive Humoral Response Antibodies facilitate elimination of toxin by the following: Neutralize toxin and prevent attachment of antigen
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Staph Infection- Abscess 1. Pathogen (S. aureus) enters through wound or abrasion 3. Pathogen attaches to epidermal tissues and begins LOCAL colonization using the following: Attachment: Teichoic acid- adhesion to mucosal cells Local Spread /Colonization P protein linked to peptidoglycan coats surface Beta toxin - kills body cells Alpha toxin - forms pores in host cells and phagocytes Staphylokinase -lyses blood clots to promote invasion and spread Hyaluronidase -breaks down polysaccharide ground substance Protease- breaks down protein DNAse- degrades viscous DNA Lipase- breaks down tissue (FAT) *all in red facilitate local spread 5. Pathogen is walled off in abscess but thwarts inflammation and complement effects by using the following: A) to avoid Phagocytosis: P protein- coats surface - conceals pathogen and avoids phagocytosis Capsule-avoids phagocytosis Clumping factor- clotting of plasma and deposition of fibrin protects cells from phagocytosis Beta toxin- kills phagocytes Coagulase- formation of fibrin clots makes it difficult for phagocytes to reach pathogen B. to Avoid Complement: P-protein-coats surface> C3b can’t bind Capsule Coagulase- formation of fibrin clot shields from C3b 2.
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Topic 23 pathogenesis - Staph Infection Food Poisoning Dr...

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