Pathogenesis Flashcards
Nocardia Pathogenesis
Causes bronchopulmonary disease
Develops after inital colonization of upper respiratory tract by inhalation
Primary cutaneous infections develop from introduction in subcutaneous tissue through trauma
M. Tuberculosis Pathogenesis
Intracellular pathogen that established lifelong infection
Enter lower respiratory tract by inhalation
Phagocytized by alveolar macrophages, prevents fusion of phagosome with lysosomes
Macrophage secretes cytokine which increases local inflammation with recruitment of T cells
Granuloma forms with bacteria inside
Alveolar macrophages and Langhans giant cells surround bacteria
Lesion is walled off (tubercle)
Tubercle in M. Tuberculosis
Small tubercle (bacteria killed off)
Large/caseous tuburcle (bacteria protected and remains dormant)
Can become reactive later when immune system wanes
Lesion liquefies, bacteria coughed up, may spread to other organs
Neisseria Meningitidis Pathogenesis
Inhalation (enter respiratory tract)
Attached to non ciliated columnar cells of nasopharynx (IgA protease assists and pili are key no pili means harder to colonize)
Bacterium internalized in phagocytic vacuole, avoid destruction, replicate and migrate
Exotoxin caused vascular damage
Bacterium enters bloodstream
Travels to meninges and lungs
Neisseria Gonorrhoeae Pathogenesis
Sexually passed
Fimbriated cells attach to intact mucus membrane epithelium
Penetration into and multiplication before passing through mucosal epithelial cells
Establish infection
Sites of inoculation (Cervix/Vagina or Urethra/Penis)
Can be passed anally/orally
Campylobacter Pathogenesis
Infectious dose and host factors influence development (High does and most bacterium killed by gastric acid/Low does with neutralized gastric acid)
Pathogenesis not clearly defined (No good animal model)
Damage to mucosal surface of jejunum, ileum, colon
Non-motile and adhesion lacking strains are avirulent
Seems to be associated with Guillain-Barre Syndrome
Helicobacter pylori
Colonize mucosal lining of stomach and duodenum
Colonization initiated by blockage of acid production by acid inhibitor protein, neutralization of acid by ammonia produced by urease activity
Tissue damage mediate by ureases breaksdown ammonia by-products, Mucinase, Phospholipase, Vaculating cytotoxin
Salmonella Pathogenesis
Ingestion of contaminated food
T3SS mediates invasion into M cells
Located in Peyer’s patches (transport foreign particles to macrophages for clearance)
Cells survive phagosome, replicate and spread
Inflammation confined to GI tract
Systemic disease very serious
Shigella Pathogenesis
Attach to and invaded M cells in Peyer’s patches via fimbriae and T3SS
Survive phagocytic vacuole and replicate
Invade adjacent cells
Induce apoptosis of cells (leads to sloughing of epithelium/colonic ulcers)