Micro Enteric Bacteria 1 Flashcards Preview

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Flashcards in Micro Enteric Bacteria 1 Deck (28):
1

shigella bacteriology

-gram -, oxidase - rods
-not lactose fermenting
-not H2S producing
-nonmotile
-facultative anaerobes and facultative intracellular
-human-restricted
-fecal-oral

2

how to distinguish lactose fermenter from non lactose fermenter

MacConkey medium - fermenters will be bright pink

3

shigella infectious dose

very low ~100IUs

4

what does shigella typically cause?

bloody diarrhea, local inflammation, ulceration

5

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

6

what is a sign of a poorer prognosis with shigella?

malnourished child (esp with vit A and zinc deficiencies)

7

Reactive arthritis autoimmune?

HLA-B27

8

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

9

siderophores

iron-chelating moles that allow the bacteria to parasitize enough iron to grow to large numbers

10

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

11

how is entry of shigella mediated?

type III secretory system

12

how does shigella cause HUS?

shiga toxin escapes into blood stream setting off an immunologic/hematologic cascade leading to acute hemolysis, uremia, DIC

13

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

14

diagnosis of HUS caused by shigella or E. coli

check blood for schistocytes, decreased platelets, increased PMNs, increased lactate dehydrogenase

15

shigella treatment

rehydrate, antibiotics if warranted but NOT if suspecting E Coli!!!, HUS dialysis and supportive care, NO antidiarrheal meds

16

e coli bacteriology

-straight gram - rod
-facultative anaerobe
-lactose fermenter
-H2S negative, urease negative
-may be mobile or nonmobile
-normal GI fauna

17

e coli pathologies

1. enterotoxigenic diarrhea
2. enterohemorrhage diarrhea
3. enteropathogenic, enteroaggregative, enteroinvasive diarrheas
4. UTIs
5. meningitis
6. pneumonia

18

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

19

e coli gastroenteritis

-water diarrhea
-bacteria use fimbrae to attach to gut lining
-enterotoxins force hot cells to release fluids, potassium

20

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

21

risk of HUS

shiga toxin in EHEC

22

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)

23

what is EHEC associated with?

antibiotics to treat bloody diarrhea

24

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

25

diagnosis e coli

pink on MacConkeys (lactose fermenter), bloody or nonbloody diarrhea, dehydration, recent travel abroad
check for HUS

26

e coli treatment

self-limited, rehydrate
EHEC: give NO antimotility agents and antibiotics associated with increased HUS risk

27

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)

28

foodborne botulism

gastroenteritis and descending flaccid paralysis caused by neurotoxin secreted by clostridium botulinum into airtight-packed food
-onset is fast (not as fast as staph)