GI_Final_Session 8 Cont'd
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GI_Final_Session 8 Cont'd
GI gastrointestinal westernu
GI final session 8 westernu
Describe the general features of Enterobacteriaceae. what members of this family cause disease in humans?
ubiquious - soil, water, vegetation, normal intestinal flora
Gram negative, facultative anaerobic rods
(no cytochrome oxidase; have other cytochromes to allow for ETC)
members of family commonly associated with human disease:
what is the best assay to help distinguish GI nL flora from the GI bacterial pathogens?
what are diagnostic tests for suspected traveler's diarrhea? describe the outcomes of the tests
" biochem test to separate nL from pathogenic:
To isolate G-:
--lactose + streaks will be purple; E.coli will "disperse" purple; lactose (-) is clear
or Eosin-Methylene blue agar
--"green sheen; black nucleated centers" = E coli (?)
TSI = triple sugar iron assay
(not routinely used) tests for:
how are ecoli serotypes grouped? Name the important serotypes for EHEC & ETEC.
Serotypes based on surface Ag's:
O157:H7 = EHEC
O148:H28 = ETEC
how do you separate the E. coli serotypes?
Serotype differentiation via
culture on MacConkey agar w/sorbitol
does NOT ferment sorbitol
(thus colonies are
Describe the pathogenesis of ETEC in traveler's diarrhea.
ETEC has 2 toxins clinically indistinguishable
NON-invasive so, NO PMN's or RBC's in stool
heat labile toxin (LT):
--similar to cholera toxin (not as severe)
--binds epithelial cells of SI
an A-B type toxin
"A" increases cAMP --> secretion Cl- and decrease absorption Na+ -->watery diarrhea
heat stable toxin (ST):
--increases cGMP (also affects Cl- secretion)
= fluid hypersecretion; NO inflammation
where are pathogenic strains of E. coli's virulence factors found? what are the virulence factors?
describe the pathogenesis of an EPEC infection. what would be the presenting Sx's/signs?
attchment & effacement via type III secretion system which alters the actin, then form pedestals
--> descruction of surface microvilli
STEPS in pathogenesis
1. BFP (bundle forming pili)
: used for initial attachment to host cell
2. Secretion of bacterial factors
: type III secretion systems--enter host cell & cause damages
3. bacteria releases factors that insert into host cell & allow for "infimate" attachment--see changes in host cell actin (formation of actin pedestals effacement damage) of host cell surface
-->-->loss of mivrovilli
common in kids of developing countries
diarrhea (infantile) b/c malabsorption of fluids
: hard to replace fluids
describe the pathogenesity of EHEC.
aka STEC (shiga toxin-producing
found in U.S. (O157:H7 most diseases)
major reservoir (eat undercooked meat or unpasteurized fluids)
(VTEC) = "shiga-like"
--an AB-type; "A"
inactivates 28S rRNA
= stop protein synthesis -->death of epithelial cells
low infectious dose, like shigella (~100cells)
SORBITOL NON-fermenter on S-MAC
what would be the presenting features of an EHEC infection?
bloody, copious diarrhea
usually self-limiting (~1wk)
in kids can cause hemolytic uremic syndrome (HUS)
5-10% of kids infected w/EHEC
what are features of EIEC? pathogenesis?
persistant watery diarrhea (esp infants) >14d, can progress to dysentery
may be as important as ETEC in traveler's D
rare in U.S.
: O124, O143, O164
invade & destroy colonic epithelium
--replicates in cytoplasm
--form "actin tail" allow spread b/w cells
--Macrophages can also spread b/w cells
what are the freatures of EAEC?
persistent watery diarrhea >14d (esp. infants)
also another cause of traveler's diarrhea
bacterial fimbriae for attachment --> mucus&biofilm
what are potential complications of taveler's diarrhea?
increased risk for IBS
yeast infection (?)
what is the management of traveler's diarrhea?
w/o systemic illness
Sxic w/ loperamide & rehydration
+single dose ciprofloxacin, levofloxacin or ofloxacin cures most cases
w/systemic or severe illness
what Sx's together are defined as
bloody diarrhea +/- mucus w/ PMNs & RBCs
what is the most common cause of dysentery?
what are diagnostic tests of dysentery?
Hektoen Enteric Agar:
will be transparent --> no CHO fermentation, no H2S production
will be BLACK (H2S producers)
except Typhi is a weak H2S producer
what are the major species of Shigella?
S. dysenteriae--(grpA) MOST pathogenic
S. flexneri--(grp B) common in developing cntry
S. boydii--(grp C) india
S. sonnei--(grp D) MOST
cause in industrial world,
what are the features of Shigella
G- bacillus (rod), lactose-, NON-motile,H
genetically similar to
why is there a biphasic diarrheal illness in shigellosis?
diarrhea precedes the dystenteric syndrome b/c of combined action of ShFT-1 enterotoxin resulting in active secretion & abnL water reabsorption.
syndrome is result of invasion of mucosa (Type III secretion system & actin filaments)
what is the pathogenesis of shigella?
direct fecal oral contamination
*resistance to low-pH allows passage through GI (partly why only 100-200CFU required to cause infection)
ShET-1 (shigella enterotoxin) causes watery diarrhea & mucosal inflammation --> invasion of mucosa
encodes type III secretion system that inserts into membrane to allow effectors to transit --> bacteria induce their own uptake
once inside, effectors trigger cytosckeletal rearrangements to further induce bacteria uptake
intracellular shigellae use cytoskeleton to propel themselves inside infected cell --> allows cell-to-cell spread
CK's released by infected cells attract more PMNs thus exacerbating the inflammation --> acute colitis
describe features of Salmonella
G- bacilli, lactose-, motile, H2S producer
2400 serotypes; based on:
--somatic O ag (LPS outer sugars)
--surface Vi an (only some) = capsule ag's
--flagella H ag's
: more common
--from poultry/eggs, dairy, & contaminated work surfaces
form is RARE in U.S.
what is the pathogenesis of salmonella infection?
ingestion contaminated food/water
enters SI --> enters M cells --> basolateral surface
Macrophages often ingest bacteria, but bacteria can prevents lysosomal enzymes of macrophage from degrading bacteria
--bacteria disseminated by macrophages to liver, spleen, lymph nodes, bone marrow
alters host cell (like shigella)
describe the image:
: rectal luminal narrowing & mucosal inflammation (similar to UC)
: severe inflammatory infiltrate of PMNs & macrophages, glands are straight w/o architectural distortion or branching b/c it is ACUTE process
describe biopsy of colon:
PMNs in lamina propria w/focal crypt destruction
what are potential complications of dysentery?
complications generally in kids <10yo
Hemolytic uremic syndrome
thrombotic thrombocytopenic purpura
what is the management?
Cipro = "best researched drug"
avoid anti-motility agents b/c can precipitate toxic megacolon
**don't forget to check Pum's drug document!