Food/water-borne diseases Flashcards

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1
Q

food intoxication

A

bacteria grows in food, secretes exotoxin, exotoxin is consumed, consumption of bacteria not required

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2
Q

cause of food intoxication

A

improper handling and storage

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3
Q

food-borne infection

A

bacteria contaminated food consumed. bacteria colonizes in intestine and cause disease. most secrete ecotoxin

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4
Q

cause of food borne illness

A

improper cooking, cross contamination

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5
Q

how does S. aureus food intoxication enter the body

A

carried in nasal cavity as part of normal flora

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6
Q

how does S. aureus cause food intoxication

A

food handler contaminates food and leaves it at room temp

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7
Q

how it the exotoxin of S. aureus unusal

A

it is heat stable. reheating food is not protective. it is a super Ag that stimulates peristalsis. vomiting occurs

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8
Q

Clostridium botulium (gram +ive rod) food intoxication due to

A

errors in home canning, surviving endospores can generate vegetative cell that prosuces exotoxin

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9
Q

Clostridium botulium can be destroyed by

A

since it is heat labile exotoxin boiled for 10 mins will denature

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10
Q

describe exotoxin of Clostridium botulium

A

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

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11
Q

Vibrio cholera (gram -ive) is passed by

A

oral fecal route. ID50 is 10^8 bacteria. or 10^4 if taking antiacids

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12
Q

what must Vibrio cholera do to be virulent

A

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

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13
Q

why are more B subuntis synthesized

A

ribosome binding site for ctxb is 70X stronger than ctxA

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14
Q

what does V. cholera do in the intestine

A

secretes a neuramindase which removes sialic acid from a glycolipid calleed GM1. bacteria catabolized sialic acid

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15
Q

how does CTXA of V. cholera enter the cell

A

CTXB subunit adheres to GM1 w/o sialic acid. CTXB forms a pre in intestinal cell, CTXA enters

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16
Q

what does V. cholera do in the intestine

A

secretes a neuramindase which removes sialic acid from a glycolipid called GM1. bacteria catabolized sialic acid

17
Q

how does CTXA of V. cholera enter the cell

A

CTXB subunit adheres to GM1 w/o sialic acid since it has been catabolized. CTXB forms a pre in intestinal cell, CTXA enters

18
Q

fn of CTX A of V. cholera

A

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

19
Q

how does an increase in ions in lumen lead to shock and death

A

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

20
Q

fn of CTX A of V. cholera

A

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

21
Q

how does an increase in ions in lumen lead to shock and death

A

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