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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
- oxidase negative (no cytochrome oxidase; have other cytochromes to allow for ETC)
- members of family commonly associated with human disease:
- – Escherichia
- – Salmonella
- – Shigella
- – Yersinia
- – Klebsiella
- – Serratia
- – Proteus
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
- "Quick" 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:
- --lactose fermentation
- --glucose fermentation
- --H2S production
- --gas production
how are ecoli serotypes grouped? Name the important serotypes for EHEC & ETEC.
- Serotypes based on surface Ag's:
- --O (lipopolysaccharide)
- --H (flagellar)
- --K (capsular)
- O157:H7 = EHEC
- O148:H28 = ETEC
how do you separate the E. coli serotypes?
- E. coli Serotype differentiation via:
- immunologic assay
- culture on MacConkey agar w/sorbitol
- **E. coli O157:H7 does NOT ferment sorbitol (thus colonies are clear not pink)
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?
- found on:
- bacterio phages
- pathogenicity islands
- virulence factors:
- secretion systems
describe the pathogenesis of an EPEC infection. what would be the presenting Sx's/signs?
- Enteropathogenic E. coli (EPEC):
- 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
- V/N: hard to replace fluids
- non-bloody stools
describe the pathogenesity of EHEC.
- aka STEC (shiga toxin-producing E. coli)
- found in U.S. (O157:H7 most diseases)
- -->cattle major reservoir (eat undercooked meat or unpasteurized fluids)
- produces Vero toxin (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?
- Hemorrhagic (hemorrhagic colitis):
- bloody, copious diarrhea
- few leukocyrtes
- usually self-limiting (~1wk)
- in kids can cause hemolytic uremic syndrome (HUS):
- hemolytic anemia
- kidney failure
- 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.
- common strains: 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 (?)
- dehydration, sepsis/shock
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:
- 1000mg azythromycin
- or rifaximin
what Sx's together are defined as dysentery?
- bloody diarrhea +/- mucus w/ PMNs & RBCs
- abd cramps
what is the most common cause of dysentery?
what are diagnostic tests of dysentery?
- Hektoen Enteric Agar:
- --Shigella will be transparent --> no CHO fermentation, no H2S production
- --Salmonella enterica 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 common cause in industrial world, mildest
what are the features of Shigella
- G- bacillus (rod), lactose-, NON-motile,H2S-
- genetically similar to Escherichia
why is there a biphasic diarrheal illness in shigellosis?
- watery diarrhea precedes the dystenteric syndrome b/c of combined action of ShFT-1 enterotoxin resulting in active secretion & abnL water reabsorption.
- dysenteric 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
- Non-typhoid: more common
- --from poultry/eggs, dairy, & contaminated work surfaces
- Typhoid 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:
- left: rectal luminal narrowing & mucosal inflammation (similar to UC)
- right: 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?
- rectal prolapse
- complications generally in kids <10yo:
- Hemolytic uremic syndrome
- thrombotic thrombocytopenic purpura
- microangiopathic anemia
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!