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
Q

What EC is a problem of developed countries? Reservoir?

A
  • EHEC - enterohemorrhagic

- GIT of cattle

26
Q

Phasic progression of EHEC?

A

watery diarrhea (ileum) - hemorrhagic colitis - HUS

27
Q

Major EHEC serotype in US?

A

O157:H7 - low infective dose + acid resistant

28
Q

When is EHEC shed?

A

warm months

29
Q

What does EHEC infection look like in the beginning?

A

EPEC - A/E lesion via pili

30
Q

What toxins has EHEC acquired?

A

STx1, STx2 or both (on phage)

31
Q

Structure and receptor of Stx?

A
  • AB enterotoxin

- Gb3 - glycolipid; distribution of receptor in tissue causes localization of effects

32
Q

What does the Stx toxin do to protein synthesis?

A
  • removes adenine from 28S rRNA of host ribosome
  • inhibits protein synthesis
  • Intermediate ER stress on endo cells in colon (receptor) produces hypercoaguable state
33
Q

How does Stx cause hemorrhagic colitis?

A
  • 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
Q

What happens in HUS?

A
  • Stx travels through blood to kidney where it binds glomerular endo cells (Gb3 receptor)
  • dec GF, ARF, hemolytic anemia, thrombocytopenia
35
Q

What % of hemorrhagic colitis cases progress to HUS? Who doesn’t get it?

A
  • 5-10% - < 5 yo and elderly

- AA’s do not get it

36
Q

How is HUS treated?

A

aggressive - fluid and kidney dialysis (may be brain manifestation in elderly due to Gb3 on neurons = 50% mortality)

37
Q

When are anti-motility drugs and antibiotics not given?

A

EHEC - want to get Stx out

38
Q

Why are antibiotics not give in EHEC hemorrhagic colitis?

A
  • 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
Q

What is the new EC pathotype that appeared in 2011?

A

Stx-EAEC - shiga producing enteroaggregative EC (EAEC acquired shiga toxin and drug resistance)

40
Q

Who gets Stx-EAEC?

A
  • 90% in young, mid-aged adults

- HUS mostly in women –> 22% of STEAEC cases

41
Q

What two gram positive spore forming organisms are agents of food poisoning in the US?

A

Clostridium perfringens and Bacillus cereus

42
Q

What is the major protozoan cause of persistent diarrhea?

A

Giardia lamblia - adheres in gut and causes persistent water diarrhea (Hiker’s disease in contaminated water)

43
Q

What zoonotic infection is a problem for IC patients and causes persistent diarrhea?

A

Cryptosporidium parvum