Bacterial infection of GI3 Flashcards

1
Q

Vibrio species like Vibrio cholera and parahaemolyticus

type, shape, oxygen, where live, pH and temps, what do they require for growth

A
  • gram neg
  • comma, curved shaped
  • facultative anaerobes
  • free living in water
  • broad range of growth -temp/pH (susceptive to stomach acid)
  • require sodium for growth
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2
Q

Vibrio cholera

  • symptoms
  • incubation
  • duration
  • how much diarrhea
  • how does it spread
  • inflammatory?
A
  • asymptomatic to severe watery diarrhea
  • 2-3 day incubation
  • seven day duration
  • 250 mL/kg rate of mucus, electrolyte and water-filled diarrhea
  • spreads via contaminated water
  • No
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3
Q

what’s important about immunity in regard to V. cholerae

A
  • we can become immune to the particular O antigen type we were effected by but
  • if bacteria use a different O antigen type then we are screwed!
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4
Q

what’s different in classic cholera biotype vs El Tor biotype

A

El tor is the current strain (7) that is more resilient and has a longer duration

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5
Q

pathogenesis of cholera toxin

A
  • uses toxin co-regulated pilus to adherence to intestinal epithelial cells
  • uses AB TOXIN to activate adenylate cyclase to increase cAMP and cause massive efflux of electrolytes and water with NO SIGNIFICANT CELL DAMAGE
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6
Q

how are Vibrio cholera diagnosed? Treatment?

A
  • culture

- treat- rehydration-IV/Oral and without rehydration, mortality is 90%

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7
Q

Vibrio parahaemolyticus
symptoms
what causes V. parahaemolyticus

A
  • symptoms- watery diarrhea TO BLOODY DIARRHEA, nausea, vomiting, abdominal cramps, low grade fever
  • virulence is Kanagawa hemolysin- induces chloride secretion thus watery diarrhea
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8
Q

what is vibrio parahaemolyticus associated with eating
inflammatory?
treatment and prevention?

A
  • shellfish and other seafood
  • yes
  • treatment- self limiting
  • prevention- proper cooking of shellfish
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9
Q
Yersinia enterocolitica
type of bacteria
found in?
symptoms?
Inflammatory?
A
  • gram neg coccobacilli
  • found in contaminated water and food (improperly cooked pork)
  • symptoms? FEVER, abdominal cramps and watery to bloody diarrhea
  • last 1-2 wks
  • yes
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10
Q

mechanism of Yersinia entercolitica

A
  • not well understood but invades M cells in the terminal ileum like salmonella but invades via a different mechanism
  • involves T3SS and injection of Yops (Yersinia outer proteins)
  • products heat stable enterotoxin
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11
Q

diagnosis and treatment of Yersinia entercolitica

A

-diagnosis via culture of stool

treatment- self limiting

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12
Q

Clostridium difficile (C. diff)
type-
inflammatory?
symptoms

A

-gram pos anaerobe
-non invasive
-spore forming
-emerging nosocomial pathogen
-inflammation
symptoms-
1) asymptomatic,
2) CDAD (clostridium difficile associated diarrhea)
3) pseudomembrane colitis
4) fulminant colitis with toxic megacolon -which cause plaques on colon that may have to be removed

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13
Q

how does C diff work?

A
  • Toxin AB causes damage to epithelial mucosa and causes host cell cytoskeleton to be damaged = BLOODY diarrhea
  • this occurs when a pt is hospitalized and given many broad spectrum antibiotics that change the gut flora
  • some hospital emplyees could have C diff on hands and touch them and they get c diff
  • if immunosuppressed enough, get CDAD
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14
Q

diagnosis and treatment and prevention of C. diff

A

diagnosis- toxin in stool and culture is not helpful b/c it’s part of our normal biota
treatment- oral vanco and metronidazole
prevention- fecal transplant (EWW)

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15
Q
Enterohemorrhagic e. coli (EHEC)
type
reservoirs
transmitted via
inflammatory?
body part?
A
  • gram negative, facultative anaerobe
  • animals like cattle
  • transmitted via HAMBURGERS (eHec) and vegetables (washed with water from streams)
  • yes
  • large intestine
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16
Q

what disease does EHEC cause

A
  • hemorrhagic colitis -bloody diarrhea
  • no fever, marked ab pain and tenderness
  • sequelae-*hemolytic uremic syndrome (HUS)- anemia and kidney failure
17
Q

how does EHEC work?

A
  • attaches and effaces lesion like EPEC HOWEVER:
  • toxin like shiga toxin (verotoxin)- blocks translation by cleaving part of 60S subunit of the ribosome
  • > attaches to brush border of intestinal mucosa, produces verotoxin that destroys microvilli, verotoxin enters blood causing vascular endothelial damage and increased plt aggregation, plt-fibrin thrombi form causing ischemic damage to colon, kidneys and other tissues =hemorrhagic colitis and hemolytic uremic syndrome (kidney disease) via attaching to GB3 kidney receptors that cows DONT have (so don’t get HUS)
18
Q

diagnosis, treatment and prevention of EHEC?

A

-diagnosis- presumptive- bloody diarrhea WITHOUT fever, culture, PCR (stx gene that encodes the toxin)rapid test

treat- supportive, antibiotics not helpful and maybe hurtful because antibiotics cause bacterial cell damage and initiates a lysogenic phage to start working to get a lytic cycle going which leads to toxin production and increased HUS rate

prevention- cook raw hamburgers and raw vegis

19
Q
Shigella spp
Type?
inflammatory?
body part?
reservoir?
infectious dose 
how spreads?
A
  • intracellular gram neg rod- anaerobe
  • inflammatory
  • large intestine effected
  • res- only humans
  • inf dose- very LOW (<10 organisms)
  • poor sanitary infrastructure, crowded healthcare systems and DAYCARE CENTERS
20
Q

where is shigella soneii found

s. flexneri
s. dysentarie

A

soneii- developed countries
flexneri- developing countries (in the middle-flexible)
dysentarie- underdeveloped countries tropical countries- worst

21
Q

how long post ingestion does shigella toxin have effects?
how long does it last
symptoms

A

-1-3 days
-last 2-5 days post symptoms
-symptoms are strain specific
soneii = fever, malaise, WATERY diarrhea
flexerni and dysentarie- cause DYSENTERY- fever, malaise, watery diarrhea, cramps, bloody and pus filled stools, TENESMUS (NEED TO CONSTANTLY DEFECATE )
S. dysenteriae- POTENTIAL for hemolytic uremic syndrome (HUS)

22
Q

pathogenesis of Shigella

A

acid resistant
1) -adheres selectively to and pass thru M cells
-phagocytosis by macrophages
-rapid escape from phagosome
-rapid induction of macrophage apoptosis = infection
OR
2)enter via another mech to get into M calls and then
- they interact with basolateral portion of enterocytes (small intestine)
-induce uptake via type 3 secretion system- injection of Ipa proteins and cause cytoskeletal rearrangement
-lysis of endocytic vacuole -unknown mech
-jump to neighboring cells via actin polymerization at a pole (evades host defense)- basically gets motile
-ulcers form
-diarrhea via inflammation
-toxin is shiga toxin that binds gb3 receptors and inhibits translation to cause cell death (glomerular endothelial cells rich in gb3 so get HUS)

23
Q

diagnosis and treatment of shigella

A

diagnosis-culture of stool, serological test
treatment- rehydration, antibiotic treatment- ampicillin resistance is common, choice dependent on susceptibility profile
prevention- no vaccine, improve sanitation and hygiene
NOTE: INFECTION DOES NOT CONFER IMMUNITY

24
Q

Enteroinvasive E. coli

mech:

A

-very uncommon
mechanism same as shiga-toxin but no shiga toxin so no HUS
appears that E. coli obtained pathogenicity island from shigella spp via horizontal transfer