Flashcards in Micro Enteric Bacteria 1 Deck (28):
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shigella bacteriology
-gram -, oxidase - rods
-not lactose fermenting
-not H2S producing
-nonmotile
-facultative anaerobes and facultative intracellular
-human-restricted
-fecal-oral
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how to distinguish lactose fermenter from non lactose fermenter
MacConkey medium - fermenters will be bright pink
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shigella infectious dose
very low ~100IUs
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what does shigella typically cause?
bloody diarrhea, local inflammation, ulceration
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what complications are there a risk for with shigella?
1. reactive arthritis (Reiter's Syndrome - can't pee, can't see, can't climb a tree)
2. HUS
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what is a sign of a poorer prognosis with shigella?
malnourished child (esp with vit A and zinc deficiencies)
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Reactive arthritis autoimmune?
HLA-B27
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shigella virulence factors
1. shiga toxin - plasmid borne
-toxin causes cell necrosis, apoptosis, inflammatory response, and hemorrhage for bloody diarrhea
2. siderophores
3. type III secretion system
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siderophores
iron-chelating moles that allow the bacteria to parasitize enough iron to grow to large numbers
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how does shigella invade?
enters through M cells and infects macrophages - goes into epithelial cells backwards and sideways to infect neighboring cells causing a local infection
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how is entry of shigella mediated?
type III secretory system
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how does shigella cause HUS?
shiga toxin escapes into blood stream setting off an immunologic/hematologic cascade leading to acute hemolysis, uremia, DIC
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diagnosis of shigella
physical: fever, dehydration, severe headache, progression from watery to bloody diarrhea
lab: agglutination, methylene blue (neutrophils) stain of fecal matter
**usually affects very old or very young
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diagnosis of HUS caused by shigella or E. coli
check blood for schistocytes, decreased platelets, increased PMNs, increased lactate dehydrogenase
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shigella treatment
rehydrate, antibiotics if warranted but NOT if suspecting E Coli!!!, HUS dialysis and supportive care, NO antidiarrheal meds
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e coli bacteriology
-straight gram - rod
-facultative anaerobe
-lactose fermenter
-H2S negative, urease negative
-may be mobile or nonmobile
-normal GI fauna
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e coli pathologies
1. enterotoxigenic diarrhea
2. enterohemorrhage diarrhea
3. enteropathogenic, enteroaggregative, enteroinvasive diarrheas
4. UTIs
5. meningitis
6. pneumonia
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is E coli intracellular or extracellular?
EXTRACELLULAR (have fimbriae for adherence or Type III or IV secretion system) with the exception of EIEC which is like shigella with actin-based cell to cell motility
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e coli gastroenteritis
-water diarrhea
-bacteria use fimbrae to attach to gut lining
-enterotoxins force hot cells to release fluids, potassium
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e coli bloody gastroenteritis
-bloody diarrhea
-bacteria adhere to gut lining with some tissue destruction
-strains carrying Shiga plasmid which becomes active inside gut cells, shutting down protein synthesis, destroying some, and causing inflammation
-if toxin reaches bloodstream, risk of HUS
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risk of HUS
shiga toxin in EHEC
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Enterohemorrhagic E coli (EHEC) pathogenesis
includes O157:H7 - carries shiga toxin gene which halts host protein synthesis and kills infected cells causing a bloody diarrhea with 9-30% proceeding to HUS (acute renal failure, microangiopathic hemolytic anemia and thrombocytopenis)
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what is EHEC associated with?
antibiotics to treat bloody diarrhea
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what happens when shiga toxin hits the bloodstream?
Gb2 receptor activated, nephrotoxicity, capillary occlusion (fibrin-platelet thrombi in renal microvasculature), cytokine dysreguation (esp vWF, TNFalpha, IL1, IL6), kidney failure with lactate dehydrogenase marker
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diagnosis e coli
pink on MacConkeys (lactose fermenter), bloody or nonbloody diarrhea, dehydration, recent travel abroad
check for HUS
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e coli treatment
self-limited, rehydrate
EHEC: give NO antimotility agents and antibiotics associated with increased HUS risk
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staph aureus food poisoning
gastroenteritis caused by toxin secreted by staph aureus in room temp food
-onset is fast - intoxication process only takes hours (infectious process would take at least a day)
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