Cross: NON-inflammatory Diarrhea Flashcards

1
Q

causes on Non-Inflammatory D

A

“EEEVVVSB”

ETEC
EPEC
EAEC
Vibrio cholera
Vibrio parahemolyticus
Vibro vulnificus
Staph aureus
Bacillus cereus
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2
Q

define NI diarrhea

A
no cells in stool
watery
LARGER volume
afebrile
SMALL INTESTINE affected
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3
Q

major cause of traveler’s D

A

ETEC
also C jejuni
rarely EAEC

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4
Q

ETEC pathogenesis

1-5 days course of watery D

A

LT and ST
LT=similar to cholera-inc cAMp-inc Cl-secretion from crypts=Na+ and H2O collow=water D
ST=activated cGMPcl secretion-watery D

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5
Q

cGMP activation=water D

A

=heat stabile toxin

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6
Q

cAMP activation=watery D

A

=heat labile toxin

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7
Q

Profuse watery D, Vomitting and dehydration in developing countries= children <6 mos to 2 years old

A

EPEC

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8
Q

pathogenesis of EPEC

A

LEE PAI like EHEC

attachement and effacing through pedastal like strcutures stick it to GI mucosa
NO SHIGA TOXIN PRODUCED-unlike EHEC

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9
Q

does EPEC make a shiga toxin

A

HELL NAW-but it does enter mucosa with LEE like EHEC

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10
Q

EAEC pathogensis

A

NOT UNDERSTOOD

*affects children, HIV pt.’s travellers D

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11
Q

neonatal menigitis

A

E. coli- encapsulated strains (K1 antigen)

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12
Q

90% of UTI (more commonly in females)

A

UPEC
virulence factors incldue
P fimbriae (PAP pilli) and a capsule (K1 antigen)

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13
Q

curved comma shaped GNR-polar flagella

-motile, oxidase positive,

A

vibrio sp.

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14
Q

oxidase positive

A

vibrio

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15
Q

environment for cholera

A

warm months
salt water-SE asia and Africa, SAmerica
-after natural disasters-fecally contaminated water
5-10 million cases annually

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16
Q

main animal reservoir for vibrio cholera

A

shellfish-raw oysters

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17
Q

serogroups responsible for epidemic and pandemic cholera

A

O1 and O139

18
Q

O1 serogroup divided into

A
  • e1 tor

- classic

19
Q

cholera pathogen

A

> High IDose-cant handle stomach acid
-colonizes small bowel-by the help of mucinase enzyme-dissolves glycoprotein over brush border=leads to adherence
secretes cholera toxin (an A/B toxin)-

20
Q

5B (binding) subunit of cholera AB toxin….

A

binds ganglioside R on surface of enterocyte

21
Q

1A (active( subunit of cholera AB toxin…

A

ADP ribosylation of Gs protein-overactive AC-inc. cAMP-loss of CL–>Na+==>H20
=WATERY D

22
Q

clinical course for cholera

mortality rate if untreated is 40%

A

water D=up to 20 L per day “rice water stools”
-high pathogen load in stools-smells like fish
no abdominal pain usually
-no cells in stool

eventually loss of electrolytes= renal failure and cardiac failure
HCO3 loss=acidosis and hypokalemia

23
Q

dx of cholera

A

clnical mostlt

-TCBS, TTGA, MacConkey agar

24
Q

tx of cholera

A
>AGGRESIVE FLUID REPLETION
>TETRACYCLINE
ERYTHROMYCIN
AZITHROMYCIN
CIPRO
VACCINE AVAILABLE
25
Q

RAW OYSTERS

A

VIBRIO-ESP PARAHEMOLYTICUS

26
Q

BACTEREMIA CAN BE SEEN WITH PARAHEMOLYTICUS IF ALSO UNDERLYING

A

LIVER DISEASE

OTHERWISE ITS LIKE A 3 DAYS COURSE AND NOT AS SEVERE AS CHOLERA

27
Q

HAND INFECTION IN ANY WAY DEALING WITH SALT WATER

recreation, oyster shucker-fisherman

A

VIBRIO PARAHEMOLYTICUS

can cause cellulitis if DM, or liver disease

28
Q

tx of parahemolyticus

A

fluid repletion

doxycycline

29
Q

main manifestation is diarrhea and severe skin and soft tissue infections

A

vibrio vulnificus

30
Q

shelfish handers who sustiain hand injusries are at risk

A

virbio vulnificus

31
Q

tc for vulnificus

A

doxy
cefotaxime
recephin

32
Q

most common foodborne illness in japan

A

vibrio vulnificus

33
Q

spore forming GPB
can survive in the envrionment for a while
sustain extremes of temp

A

bacillus cereus

34
Q

REHREATED FRIED RICE
DAIRY
SPICES
BEAN SPROUTS

A

B CEREUS

35
Q

emetic type food poisoning

A

B cereus

36
Q

b cereus diarrheal syndrome

A

caused by diarrheal toxin

8-16 hours after ingestion-vomiting uncommon-resolves in 24 horus

37
Q

b cereus emetic syndrome caused by

A

cerulide toxin-heat stable

38
Q

b cereus emetic syndrome

reheated fried rice

A

1-5 hours after ingestion (preformed)-> Abdominal cramps N/V, D in 1/3 of pt.’s, resolves in 24 hrs

39
Q

S aureus found in

A
potato salad at a picnic
meats eggs
dairy
produce
*when left at room temp
*cross contam by food handler
40
Q

pathogenesis of SA food poisoning

A

acts as a superantigen
within the GI tract=stimulates release fo IL1 and IL2
*within 1-6 hours N/V abdominal cramps
typically done in 24 hours

41
Q

preformed toxins

A

SA and B cereus

42
Q

abundant in soil and freshwater

A

Bacillus cereus