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Micro Post Midterm > GI 3 > Flashcards

GI 3 Flashcards

1
Q

in neurologic shellfish poisoning, what is the algae involved

A

dinoflagellate alage: karenia brevis

compare to the dinoflagellate algae in ciguatera poisoning –> gambierdiscus toxicua aka ciguatoxin

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2
Q

what toxin does karenia brevis make

A

brevetoxin

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3
Q

why do you get poisoned by this brevetoxin after you prepare your shellfish

A

it is not denatured by steaming shellfish

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4
Q

incubation period/ duration for neurologic shellfish poisoning and the symptoms

A

less than 1-3 hours and lasts 24-73 hours

paresthesia, mouth numbness, tingling sensation of mouth and extremities, GI upset

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5
Q

toxin in paralytic shellfish poisoning

A

saxitoxins

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6
Q

type of dinoflagellate algae that is seen in paralytic shellfish poisoning

A

Alexandrium spp., Gymnodinium catenatum, Pyrodinium bahamense, Gonyaulax spp

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7
Q

incubation period/duration for paralytic shellfish poisoning and the symptoms

A

less than 2 hours with 3 day duration
tingling and numbness of mouth spreading to extremities, GI symptoms less common, ataxia,

if severe, muscular paralysis and respiratory paralysis

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8
Q

what is big difference in symptoms between paralytic and neurologic shellfish poisoning

A

in paralytic, GI symptoms are less common

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9
Q

type of diarrhea seen in food borne infections

A

acute watery diarrhea

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10
Q

what is the number one cause of traveler’s diarrhea and what is another name for it

A

e. coli

montezuma’s revenge

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11
Q

type of bacteria is e. coli

A

gram negative anaerobes

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12
Q

type of diarrhea is seen in e. coli

A

dependent on the strain but it is non inflammatory diarrhea

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13
Q

symptoms of e.coli poisoning

A

rapid onset of profuse watery diarrhea with little or no fever

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14
Q

treatment of e. coli poisoning

A

fluid replacement therapy
no antibiotics because of resistance
counsel people of better hygiene especially if in food industry

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15
Q

pathogenesis of ETEC (enterotoxigenic e. coli)

A
  • bacteria must colonize the small intestine with specialized fimbrae called CFA (colonization factor antigen)
  • CFA allows e. coli to adhere to epithelial cells then release one or both of 2 plasmid encoded enterotoxin
  • both toxins are AB - five binding units surrounding a single A active subunit
  • B binding subunit attaches to GM1 ganglioside receptor on the brush border which allows A to enter into the cell
  • entry –> activated Gs protein adenylate cyclase –> ↑cAMP –> hypersecretion of electrolytes and water outside the cell –> distension and watery diarrhea
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16
Q

what are the two toxins that e. coli can release and what are their functions

A

LT toxin which works on adenylate cyclase

ST toxin which works on guanylate cyclase

17
Q

when does one see enteropathogenic e.coli (EPEC)

A

childhood diarrhea
seen in developing country
minor cause of traveler’s diarrhea

18
Q

pathogenesis of EPEC (enteropathogenic e. coli)

A
  • you have a plasmid borne (EAF - enteric adherence factor) bundle forming pilus (BFP)
  • effacement of microvilli –> leads to loss of absorptive area of the small intestine –> outflux of sodium and chloride –> watery diarrhea
19
Q

how do you treat EPEC diarrhea

A

rehydration therapy

trimethoprim/fluoroquinolones

20
Q

properties of vibrio cholerae

A 
gram negative rods
motile with single polar flagellum
oxidase positive
O and H antigens (serogroup O1 and O139)
acid sensitive
21
Q

what can vibrio cholerae ferment

A

ferment sucrose and mannose but not arabinose

22
Q

how does one acquire vibrio cholerae

A

through food and water with infected human feces

23
Q

pathogenesis of vibrio cholerae

A
  • vibrio cells align close to the microvilli of SI
  • cholera toxin is released which is a very potent enterotoxin
  • bacteriophage encoded
  • AB toxin which is used to bind and get into the cell
  • ganglioside GM1 –> activates adenylate cyclase (similar to LT toxin in e. coli) –> increase cAMP –> outflux of water and electrolytes (hypokalemia and metabolic acidosis) –> watery diarrhea (dehydration)
24
Q

why do you have hypokalemia and metabolic acidosis in vibrio cholerae

A

because of K+ and HCO3- loss

25
Q

features of vibrio cholerae

A
  • rice watery stool (light or pale in color with small fleck or flakes)
  • excretion of 20-30L diarrhea a day –> hypovolemic shock
26
Q

treatment or management of vibrio cholerae

A
  • oral or admin IV glucose
  • replace ionic loss –> rehydration therapy
  • antibiotic like tetracycline to reduce the duration of diarrhea
  • vaccine (not recommended because it only last 3-6 months)
  • sanitation and hygiene
27
Q

how do you diagnose vibrio cholerae

A

thiosulphate-citrate-bile salts-sucrose (TCBS) agar which is a sucrose differentiating agar
-if sucrose positive then you know it is vibrio cholerae

28
Q

what does it tell you if thiosulphate-citrate-bile salts-sucrose (TCBS) agar is sucrose negative

A

vibrio parahemolyticus

vibrio vulnificus

29
Q

cholera antigens serotype

A

inaba, ogawa, hikojima

30
Q

two different disease you can get from clostridium perfringes

A
  • necrotic enteritis (strain C)

- type A food borne infection (strain A)

31
Q

which one of the clostridium perfringes is more common and how do you get it

A
  • necrotic enteritis is less common and you get from improperly cooked pork
  • type A food borne infection is more common and you get it from meat or meat products like gravy
32
Q

pathogenesis of clostridium perfringes

A

spore former so it survives cooking and germinates in meat or meat products –> then we eat it –> spores colonize SI –> produce and release CPE (clostridium perfringes enterotoxin) –> affects permeability of epithelial membrane –> watery diarrhea

33
Q

incubation period and symptoms of clostridium perfringes

A

incubation is 8-24hrs
watery diarrhea and severe abdominal pain
NO FEVER, NAUSEA, VOMITING

34
Q

how do you diagnose c. perfringes

A

enterotoxin in feces
large c. perfringes spores in feces
large# vegetative cells in incriminated food

Micro Post Midterm (31 decks)

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