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
features of vibrio cholerae
- rice watery stool (light or pale in color with small fleck or flakes)
- excretion of 20-30L diarrhea a day –> hypovolemic shock
treatment or management of vibrio cholerae
- 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
how do you diagnose vibrio cholerae
thiosulphate-citrate-bile salts-sucrose (TCBS) agar which is a sucrose differentiating agar
-if sucrose positive then you know it is vibrio cholerae
what does it tell you if thiosulphate-citrate-bile salts-sucrose (TCBS) agar is sucrose negative
vibrio parahemolyticus
vibrio vulnificus
cholera antigens serotype
inaba, ogawa, hikojima
two different disease you can get from clostridium perfringes
- necrotic enteritis (strain C)
- type A food borne infection (strain A)
which one of the clostridium perfringes is more common and how do you get it
- 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
pathogenesis of clostridium perfringes
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
incubation period and symptoms of clostridium perfringes
incubation is 8-24hrs
watery diarrhea and severe abdominal pain
NO FEVER, NAUSEA, VOMITING
how do you diagnose c. perfringes
enterotoxin in feces
large c. perfringes spores in feces
large# vegetative cells in incriminated food
