Cross: Inflamamtory Diarrhea Flashcards
Causes of inflammatory D
****SEESSCCY**** Shigella EHEC EIEC Salmonella enterica Salmonella enteritidis** C. jejuni C. difficile Yersinia enterocolitica
90% of infectious D=
viral etiology
D lasting longer than 10-14 days=
likely from a parasite
acute diarrhea
3 or more loose stools per day lasting less than 2 weeks
chronic diarrhea
more than 4 weeks-consider HIV status
bugs that cause D in HIV patients
MAI
CMV
define inflammatory D
- small volume
- often bloody (dysentery)
- WBC/RBC’s in stool
- fever is COMMON
- most often affects colon
define non-inflammatory D
- large volume
- watery
- non-bloody
- no cells in stool
- afebrile
- SMALL INTESTINE USUALLY AFFECTED
general characters for Shigella, E. coli, Salmonella
>Gram Negative >glucose fermenting with acid production? >Oxidase negative >reduce nitrates to nitrites ALL MOTILE EXCEPT SHIGELLA
flagellar antigens
H antigen
polysaccharide side chain on LPS
O antigen
Gram negative, NON-motile, NON-lactose fermenting, DOES Not PRODUCE H2S
Shigella
Strain of Shigella most commonly affecting US-school aged/day care children
Shigella sonnei-70% cases
DAYCARE CENTERS migrant workers, nursing homes, traveler to developing countries,
most common shigella strains worldwide
- Shigella dysenteriae
2. Shigella flexneri
how is shigella transmitted
fecal oral route-very low ID
shigella pathogenesis
EIEC has a similar mechanism
> taken up by M cells (resistant to gastric acid)
escape into LP-taken up by macs-> cause apoptosis
HOST INFLAMMATORY RESPONSE KILLE THE CELL IN WHICH IT IS MUTLIPLYING-ALLOWING IT TO ESCAPE
SPREADS FROM CELL TO CELL VIA MEMBRANE BOUND PROTRUSIONS -FORMINS-DEPENDENT ON HOST CELLULAR ACTIN POLYMERIZATION-LYSES MEMBRANES THAT SURROUNDS IT AND NOW IS FREE IN ADJACENT CELL
complications from Shigellosis
- reiter’s syndrome
2. HUS- from shiga toxin (AB toxin) more common with S. dysenteriae
TX for Shigellosis
Ceftriaxone
Ciprofloxacin
Azithromycin
*shortens course and reduces duration of organism shedding in tools
this bug can cause inflammatory and non-inflammatory diarrhea
E. coli
5 strains we are discussing here
how does shiga toxin work>
cleaves a base on the 28s of 60S subunit in Ribosomal subunit thus inhibiting protein synthesis
shiga toxin seen in
Shigella dysenteria
EHEC (Shiga toxigenic e coli) which include O157:H7
and O104: H4
*these are really “SHIGA-TOXIN-LIKE”
cannot ferment sorbitol-colonies white on culture
DISTINGUISHING FEATURE
EHEC-aka STEC
SOURCE OF EHEC
INADEQUATELY COOKED MEAT (HAMBURGERS)-CONTAM VEGGIES AND MIK-ALSO HUMAN-TO HUMAN
CAUSES HEMORRHAGIC COLITIS- HOSPITAL STAY IN 50%-SHIG TOXIUN LIKE S. DYSENTERIAE
EHEC
ehec Is grouped into
O157:H7-like and
non O157: H7
locus of enterocyte effacement (LEE)
PAI within EHEC that contains a TYPE III secretion system-aids in attachment and effacement of the bug onto colonic mucosa via a pedestal formation and delivery of the e coli receptor to the host cell
responsible for the diarrhea in EHEC
LEE pathogenicity island
little fever, acute onset cramps and WATERY D-becomes bloody (hemorrhagic colitis) within 24 hours-lasts up to 8 days
EHEC
EHEC strain more likely to cause outbreaks, dysentery, HUS, ischemic colitis
O157:H7
which bugs use LEE for entry
EHEC and EPEC
feared complication of EHEC and Shigellosis (less common)
5-10 days after diarrhea
HUS from SHIGA TOXIN IN BLOOD STREAM 90% of cases in children but only complicated 9% of EHEC cases 5% mortality rate 50% require dialysis-most regain function
main cause of AKI in children
HUS following EHEC infection