Food/water-borne diseases Flashcards
food intoxication
bacteria grows in food, secretes exotoxin, exotoxin is consumed, consumption of bacteria not required
cause of food intoxication
improper handling and storage
food-borne infection
bacteria contaminated food consumed. bacteria colonizes in intestine and cause disease. most secrete ecotoxin
cause of food borne illness
improper cooking, cross contamination
how does S. aureus food intoxication enter the body
carried in nasal cavity as part of normal flora
how does S. aureus cause food intoxication
food handler contaminates food and leaves it at room temp
how it the exotoxin of S. aureus unusal
it is heat stable. reheating food is not protective. it is a super Ag that stimulates peristalsis. vomiting occurs
Clostridium botulium (gram +ive rod) food intoxication due to
errors in home canning, surviving endospores can generate vegetative cell that prosuces exotoxin
Clostridium botulium can be destroyed by
since it is heat labile exotoxin boiled for 10 mins will denature
describe exotoxin of Clostridium botulium
AB exotoxin. B subunit protects from stomach acid and alllows to bind to specific cell receptor. after uptake of A subunit target nerve cells and prevents muscle contraption. no diarrhea, blurred vision and respiratory paralysis leads to death
Vibrio cholera (gram -ive) is passed by
oral fecal route. ID50 is 10^8 bacteria. or 10^4 if taking antiacids
what must Vibrio cholera do to be virulent
bacteria must be lysogenized by 2 different phage. VP1 phage encodes PAI called VP1. VP1 includs genees for pili, used as adhesin to bind to intestinal epithelium and receptor for ctx phage. ctx phage encodes for cholera exotoxin is a AB5 exotoxin, encoded on an operon
why are more B subuntis synthesized
ribosome binding site for ctxb is 70X stronger than ctxA
what does V. cholera do in the intestine
secretes a neuramindase which removes sialic acid from a glycolipid calleed GM1. bacteria catabolized sialic acid
how does CTXA of V. cholera enter the cell
CTXB subunit adheres to GM1 w/o sialic acid. CTXB forms a pre in intestinal cell, CTXA enters
what does V. cholera do in the intestine
secretes a neuramindase which removes sialic acid from a glycolipid called GM1. bacteria catabolized sialic acid
how does CTXA of V. cholera enter the cell
CTXB subunit adheres to GM1 w/o sialic acid since it has been catabolized. CTXB forms a pre in intestinal cell, CTXA enters
fn of CTX A of V. cholera
ctxA activates a host cell regulatory protein called Gs by ADP ribosylation. in turn activatad Gs activated adenylate cyclaclase whech converts amp to cAMP. nomrally levels of cAMP is regulated but now Gs is also activated. increase levels of cAMP alters fn of Na+ and Cl- transporters
how does an increase in ions in lumen lead to shock and death
ions does not go to the cells. osmotic pressure causes h20 to move out to lumen of intestine, so much fliud leaving leads to shock
fn of CTX A of V. cholera
ctxA activates a host cell regulatory protein called Gs by ADP ribosylation. in turn activated Gs activated adenylate cyclaclase which converts amp to cAMP. normally levels of cAMP is regulated but now Gs is also activated. increase levels of cAMP alters fn of Na+ and Cl- transporters
how does an increase in ions in lumen lead to shock and death
ions does not go to the cells. osmotic pressure causes h20 to move out to lumen of intestine, so much fluid leaving leads to shock
