Flashcards in Micro Enteric Bacteria 1 Deck (28)
-gram -, oxidase - rods
-not lactose fermenting
-not H2S producing
-facultative anaerobes and facultative intracellular
how to distinguish lactose fermenter from non lactose fermenter
MacConkey medium - fermenters will be bright pink
shigella infectious dose
very low ~100IUs
what does shigella typically cause?
bloody diarrhea, local inflammation, ulceration
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)
what is a sign of a poorer prognosis with shigella?
malnourished child (esp with vit A and zinc deficiencies)
Reactive arthritis autoimmune?
shigella virulence factors
1. shiga toxin - plasmid borne
-toxin causes cell necrosis, apoptosis, inflammatory response, and hemorrhage for bloody diarrhea
3. type III secretion system
iron-chelating moles that allow the bacteria to parasitize enough iron to grow to large numbers
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
how is entry of shigella mediated?
type III secretory system
how does shigella cause HUS?
shiga toxin escapes into blood stream setting off an immunologic/hematologic cascade leading to acute hemolysis, uremia, DIC
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
diagnosis of HUS caused by shigella or E. coli
check blood for schistocytes, decreased platelets, increased PMNs, increased lactate dehydrogenase
rehydrate, antibiotics if warranted but NOT if suspecting E Coli!!!, HUS dialysis and supportive care, NO antidiarrheal meds
e coli bacteriology
-straight gram - rod
-H2S negative, urease negative
-may be mobile or nonmobile
-normal GI fauna
e coli pathologies
1. enterotoxigenic diarrhea
2. enterohemorrhage diarrhea
3. enteropathogenic, enteroaggregative, enteroinvasive diarrheas
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
e coli gastroenteritis
-bacteria use fimbrae to attach to gut lining
-enterotoxins force hot cells to release fluids, potassium
e coli bloody gastroenteritis
-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
risk of HUS
shiga toxin in EHEC
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)
what is EHEC associated with?
antibiotics to treat bloody diarrhea
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
diagnosis e coli
pink on MacConkeys (lactose fermenter), bloody or nonbloody diarrhea, dehydration, recent travel abroad
check for HUS
e coli treatment
EHEC: give NO antimotility agents and antibiotics associated with increased HUS risk
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)