GI 3 Flashcards
in neurologic shellfish poisoning, what is the algae involved
dinoflagellate alage: karenia brevis
compare to the dinoflagellate algae in ciguatera poisoning –> gambierdiscus toxicua aka ciguatoxin
what toxin does karenia brevis make
brevetoxin
why do you get poisoned by this brevetoxin after you prepare your shellfish
it is not denatured by steaming shellfish
incubation period/ duration for neurologic shellfish poisoning and the symptoms
less than 1-3 hours and lasts 24-73 hours
paresthesia, mouth numbness, tingling sensation of mouth and extremities, GI upset
toxin in paralytic shellfish poisoning
saxitoxins
type of dinoflagellate algae that is seen in paralytic shellfish poisoning
Alexandrium spp., Gymnodinium catenatum, Pyrodinium bahamense, Gonyaulax spp
incubation period/duration for paralytic shellfish poisoning and the symptoms
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
what is big difference in symptoms between paralytic and neurologic shellfish poisoning
in paralytic, GI symptoms are less common
type of diarrhea seen in food borne infections
acute watery diarrhea
what is the number one cause of traveler’s diarrhea and what is another name for it
e. coli
montezuma’s revenge
type of bacteria is e. coli
gram negative anaerobes
type of diarrhea is seen in e. coli
dependent on the strain but it is non inflammatory diarrhea
symptoms of e.coli poisoning
rapid onset of profuse watery diarrhea with little or no fever
treatment of e. coli poisoning
fluid replacement therapy
no antibiotics because of resistance
counsel people of better hygiene especially if in food industry
pathogenesis of ETEC (enterotoxigenic e. coli)
- 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
what are the two toxins that e. coli can release and what are their functions
LT toxin which works on adenylate cyclase
ST toxin which works on guanylate cyclase
when does one see enteropathogenic e.coli (EPEC)
childhood diarrhea
seen in developing country
minor cause of traveler’s diarrhea
pathogenesis of EPEC (enteropathogenic e. coli)
- 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
how do you treat EPEC diarrhea
rehydration therapy
trimethoprim/fluoroquinolones
properties of vibrio cholerae
gram negative rods motile with single polar flagellum oxidase positive O and H antigens (serogroup O1 and O139) acid sensitive
what can vibrio cholerae ferment
ferment sucrose and mannose but not arabinose
how does one acquire vibrio cholerae
through food and water with infected human feces
pathogenesis of vibrio cholerae
- 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)
why do you have hypokalemia and metabolic acidosis in vibrio cholerae
because of K+ and HCO3- loss
