cholerae霍乱弧菌课件.ppt

* Penetrate mucus, colonize cells 2)rough trip-drastic changes in env 3)how is intestin bad for bact? Why do bact leave? * 1)No fever—not invasive 2) clever-viable even after exit body—take host’s liquid * 1)Fluid and electrolyte loss 2)Hypokalemia—low levels of K+ in blood a)necessary for proper nerve, muscle, heart function b)cramping, cardiac arrest 2)why sunken eyes? 3)Phosphates move out of cells * 1)Disease runs its course in 2-7 days * 1 * Look up those diseases * Define dark field and phase microscopy! * 1) Treatment depends on severity of dehydration * 1)Distr to cholera inflicted areas 2) Fluid therapy a) electrolyte solution with glucose for energy 3)Add glucose to therapy—elminates need for sterility, IV * 1)Sodium transport coupled to glucose transport in small intestine a)glucose accelerates absorption of glucose and water 2)Glucose Enables small intestine to absorb fluids and salts more efficiently 3)Boil water for at least 10 minutes 4)Bicarbonate—corrects acidosis 5)Sports drinks a)excess sugar—worsen condition bc of osmolosis * 1)Need intuitive system 2)epidemic-local people help each other no medical personel, illiterate 3)Doctors without borders 4) IV drip treatment of cholera victims at Refugee camp mozambique * 1)Saline can be used because it’s better than nothing Pathogenesis: Mechanism of Action cont. Enzymatically, fragment A1 catalyzes the transfer of the ADP-ribosyl moiety of NAD to a component of the adenylate cyclase system. The A1 fragment catalyzes the attachment of ADP-Ribose (ADPR) to the regulatory protein forming Gs-ADPR from which GTP cannot be hydrolyzed. Since GTP hydrolysis is the event that inactivates the adenylate cyclase, the enzyme remains continually activated. CHOLERA Pathogenesis: Mechanism of Action cont. Thus, the net effect of the toxin is to cause cAMP to be produced at an abnormally high rate which stimulates mucosal cells to pump large amounts of Cl- into the intestinal contents. Pathogenesis: Mec