Cross: NON-inflammatory Diarrhea Flashcards
causes on Non-Inflammatory D
“EEEVVVSB”
ETEC EPEC EAEC Vibrio cholera Vibrio parahemolyticus Vibro vulnificus Staph aureus Bacillus cereus
define NI diarrhea
no cells in stool watery LARGER volume afebrile SMALL INTESTINE affected
major cause of traveler’s D
ETEC
also C jejuni
rarely EAEC
ETEC pathogenesis
1-5 days course of watery D
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
cGMP activation=water D
=heat stabile toxin
cAMP activation=watery D
=heat labile toxin
Profuse watery D, Vomitting and dehydration in developing countries= children <6 mos to 2 years old
EPEC
pathogenesis of EPEC
LEE PAI like EHEC
attachement and effacing through pedastal like strcutures stick it to GI mucosa
NO SHIGA TOXIN PRODUCED-unlike EHEC
does EPEC make a shiga toxin
HELL NAW-but it does enter mucosa with LEE like EHEC
EAEC pathogensis
NOT UNDERSTOOD
*affects children, HIV pt.’s travellers D
neonatal menigitis
E. coli- encapsulated strains (K1 antigen)
90% of UTI (more commonly in females)
UPEC
virulence factors incldue
P fimbriae (PAP pilli) and a capsule (K1 antigen)
curved comma shaped GNR-polar flagella
-motile, oxidase positive,
vibrio sp.
oxidase positive
vibrio
environment for cholera
warm months
salt water-SE asia and Africa, SAmerica
-after natural disasters-fecally contaminated water
5-10 million cases annually
main animal reservoir for vibrio cholera
shellfish-raw oysters
serogroups responsible for epidemic and pandemic cholera
O1 and O139
O1 serogroup divided into
- e1 tor
- classic
cholera pathogen
> 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)-
5B (binding) subunit of cholera AB toxin….
binds ganglioside R on surface of enterocyte
1A (active( subunit of cholera AB toxin…
ADP ribosylation of Gs protein-overactive AC-inc. cAMP-loss of CL–>Na+==>H20
=WATERY D
clinical course for cholera
mortality rate if untreated is 40%
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
dx of cholera
clnical mostlt
-TCBS, TTGA, MacConkey agar
tx of cholera
>AGGRESIVE FLUID REPLETION >TETRACYCLINE ERYTHROMYCIN AZITHROMYCIN CIPRO VACCINE AVAILABLE
RAW OYSTERS
VIBRIO-ESP PARAHEMOLYTICUS
BACTEREMIA CAN BE SEEN WITH PARAHEMOLYTICUS IF ALSO UNDERLYING
LIVER DISEASE
OTHERWISE ITS LIKE A 3 DAYS COURSE AND NOT AS SEVERE AS CHOLERA
HAND INFECTION IN ANY WAY DEALING WITH SALT WATER
recreation, oyster shucker-fisherman
VIBRIO PARAHEMOLYTICUS
can cause cellulitis if DM, or liver disease
tx of parahemolyticus
fluid repletion
doxycycline
main manifestation is diarrhea and severe skin and soft tissue infections
vibrio vulnificus
shelfish handers who sustiain hand injusries are at risk
virbio vulnificus
tc for vulnificus
doxy
cefotaxime
recephin
most common foodborne illness in japan
vibrio vulnificus
spore forming GPB
can survive in the envrionment for a while
sustain extremes of temp
bacillus cereus
REHREATED FRIED RICE
DAIRY
SPICES
BEAN SPROUTS
B CEREUS
emetic type food poisoning
B cereus
b cereus diarrheal syndrome
caused by diarrheal toxin
8-16 hours after ingestion-vomiting uncommon-resolves in 24 horus
b cereus emetic syndrome caused by
cerulide toxin-heat stable
b cereus emetic syndrome
reheated fried rice
1-5 hours after ingestion (preformed)-> Abdominal cramps N/V, D in 1/3 of pt.’s, resolves in 24 hrs
S aureus found in
potato salad at a picnic meats eggs dairy produce *when left at room temp *cross contam by food handler
pathogenesis of SA food poisoning
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
preformed toxins
SA and B cereus
abundant in soil and freshwater
Bacillus cereus
