Acute Gastroenteritis Flashcards

1
Q

Common clinical feature of acute gastroenteritis?

A

acute infectious diarrhea w/ > 12h incubation

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2
Q

Response of SI to infection?

A

secretory diarrhea

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3
Q

Response of LI to infection?

A

dysentery - scant diarrhea, cramps, tenesmus (need to defecate without relief)

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4
Q

What is necessary for inflammatory acute infectious diarrhea?

A
  • invasion or killing of intestinal cells
  • stool contains PMNs, blood due to damage
  • typically fever
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5
Q

Vibrio cholerae morphology and unique cultural characteristic?

A
  • GN motile curved rod (marine)

- acid-sensitive = require selective medium pH 8.6

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6
Q

Two serotypes of V. cholerae? Where are they found?

A
  • O1 (classic and El Tor) - El Tor is causing worldwide pandemic
  • O139 - more recent; Bangladesh and India; resembles O1 El Tor
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7
Q

Reservoirs of V. cholerae?

A
  • coastal waters + fecal contamination
  • copepods (egg sacs) and shellfish (filter water and copepods)
  • asymptomatic human shedding
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8
Q

What organism is associated with reduced gastric acidity and Type O blood risk factors?

A

V. cholerae

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9
Q

What two phages are required for V. chol virulence?

A
  • Tcp pilus

- Ctx (AB enterotoxin) - requires Tcp

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10
Q

How does cholera toxin work?

A
  • ADP ribosylates adenylate cyclase generates inc cAMP
  • activation of apical CFTR Cl- channel
  • results in hypersecretion of Cl-, K+, bicarb and water (hypokalemia, acidosis, hypoglycemia)
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11
Q

Classic cholera stool description?

A

rice water

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12
Q

Treatment for cholera?

A
  • restore fluid and electrolyte balance

- AB’s dec duration/volume of diarrhea

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13
Q

Most commonly isolated vibrio from human disease in US?

A

Vibrio parahaemolyticus

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14
Q

Disease observed with V. parahaemolyticus?

A
  • mild cholera
  • bug has many toxins (hemolysis, proteins)
  • low grade to mild fever
  • wound infections
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15
Q

What is unique about the clinical presentation of cholera?

A

NO FEVER

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16
Q

How is V. parahaemolyticus transmitted?

A

contaminated shellfish in the spring and summer

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17
Q

Leading cause of Traveler’s Diarrhea in US? How?

A
  • ETEC - enterotoxigenic

- imported on produce

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18
Q

Where and how does ETEC adhere?

A
  • covered in pili

- ileum

19
Q

Two toxins associated with ETEC?

A
  • LT = heat-labile (similar to Ctx, inc cAMP)
  • ST = heat-stable (inc cGMP)
  • both cause Cl- mediated fluid loss
20
Q

Which EC causes persistent watery diarrhea for ~ 2 weeks?

A

Enteroaggregative EC (EAEC)

21
Q

How does EAEC adhere?

A

‘stacked brick’ (aggregative) pattern of adherence mediated by pili via formation of BIOFILM –> thick mucus layer (diagnostic)

22
Q

Which EC is an important cause of infant diarrhea in developing countries and can adhere to plant matter?

A

EPEC - enteropathogenic

23
Q

How infective is EPEC?

A
  • VERY - low infective dose
24
Q

Pathogenesis of EPEC?

A
  • “attaching and effacing lesion”
  • attach w/ pili to form microcolonies (pedestal); intimately attach and secrete/inject toxins/proteins
  • destroy microvilli
  • injected proteins and deranged cell signaling cause diarrhea
25
What EC is a problem of developed countries? Reservoir?
- EHEC - enterohemorrhagic | - GIT of cattle
26
Phasic progression of EHEC?
watery diarrhea (ileum) - hemorrhagic colitis - HUS
27
Major EHEC serotype in US?
O157:H7 - low infective dose + acid resistant
28
When is EHEC shed?
warm months
29
What does EHEC infection look like in the beginning?
EPEC - A/E lesion via pili
30
What toxins has EHEC acquired?
STx1, STx2 or both (on phage)
31
Structure and receptor of Stx?
- AB enterotoxin | - Gb3 - glycolipid; distribution of receptor in tissue causes localization of effects
32
What does the Stx toxin do to protein synthesis?
- removes adenine from 28S rRNA of host ribosome - inhibits protein synthesis - Intermediate ER stress on endo cells in colon (receptor) produces hypercoaguable state
33
How does Stx cause hemorrhagic colitis?
- pro-coagulant state due to ER stress results in microvascular thrombosis - thrombosis lyses RBC's - frank bloody diarrhea BUT IT IS NOT INVASIVE! so little to no fever
34
What happens in HUS?
- Stx travels through blood to kidney where it binds glomerular endo cells (Gb3 receptor) - dec GF, ARF, hemolytic anemia, thrombocytopenia
35
What % of hemorrhagic colitis cases progress to HUS? Who doesn't get it?
- 5-10% - < 5 yo and elderly | - AA's do not get it
36
How is HUS treated?
aggressive - fluid and kidney dialysis (may be brain manifestation in elderly due to Gb3 on neurons = 50% mortality)
37
When are anti-motility drugs and antibiotics not given?
EHEC - want to get Stx out
38
Why are antibiotics not give in EHEC hemorrhagic colitis?
- AB's cause stress response in bacteria so bacteriophage enters lytic phase, leaves and produces a ton of Stx - can cause progression to HUS
39
What is the new EC pathotype that appeared in 2011?
Stx-EAEC - shiga producing enteroaggregative EC (EAEC acquired shiga toxin and drug resistance)
40
Who gets Stx-EAEC?
- 90% in young, mid-aged adults | - HUS mostly in women --> 22% of STEAEC cases
41
What two gram positive spore forming organisms are agents of food poisoning in the US?
Clostridium perfringens and Bacillus cereus
42
What is the major protozoan cause of persistent diarrhea?
Giardia lamblia - adheres in gut and causes persistent water diarrhea (Hiker's disease in contaminated water)
43
What zoonotic infection is a problem for IC patients and causes persistent diarrhea?
Cryptosporidium parvum