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GI- Week 2 > Non-Inflammatory Diarrhea > Flashcards

Non-Inflammatory Diarrhea Flashcards

1
Q

What is the definition of acute diarrhea?

A

3 or more loose stools per day lasting less than 2 weeks.

Chronic diarrhea: persists greater than 4 weeks

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2
Q

What is the major difference between inflammatory and non-inflammatory diarrhea?

A

Inflammatory diarrhea is marked by the presence of blood (aka dysentery) while non-inflammatory diarrhea is more marked by watery diarrhea

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3
Q

What are some general characteristics of inflammatory diarrhea?

A

–WBCs and RBCs seen in stool

–Fever is common

–Small volume diarrhea

–Colon is commonly affected

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4
Q

What are some general characteristics of non-inflammatory diarrhea?

A

–No cells in stool

–Usually afebrile

–Large volume diarrhea

–Small intestine is commonly affected

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5
Q

What are the main causes of non-inflammatory diarrhea?

A
  • Enterotoxigenic E. coli
  • Enteropathogenic E. coli
  • Enteroaggregative E. coli
  • Vibrio cholerae
  • Vibrio parahemolyticus
  • Vibrio vulnificus
  • S. aureus
  • Bacillus cereus
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6
Q

Describe Enterotoxigenic E. Coli

A

This infection typically occurs via contaminated food/water and is a major cause of traveler’s diarrhea

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7
Q

How does ETEC present?

A

Watery diarrhea, ranging from mild to severe, and typically lasting 1-5 days

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8
Q

Describe the pathogenesis of ETEC

A

ETEC produces heat-labile toxin (LT) and heat-stabile toxin (ST)

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9
Q

Describe LT of ETEC

A

LT is similar to Cholera toxin. It stimulates adenylate cyclase and increases intracellular cyclic AMP, resulting in secretion of chloride from intestinal crypt cells and inhibition of absorption of sodium chloride at the villous tips. Secretion of free water into the intestinal lumen follows, manifesting clinically as watery diarrhea

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10
Q

Describe ST of ETEC

A

ST activates enterocyte cyclic GMP, also leading to stimulation of chloride secretion and inhibition of sodium chloride absorption. End result again is secretion of free water into the intestinal lumen and watery diarrhea

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11
Q

Describe Enteropathogenic E. Coli (EPEC)

A

This infection produces a profuse, watery diarrhea that can be severe with vomiting and dehydration and is most commonly associated with illness in children under 6 mo.-2 yo in developing countries

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12
Q

Describe the pathogenesis of EPEC

A

•Organism characterized by ability to produce attaching and effacing lesions and formation of pedestal like structures (LEE)

–No Shiga toxin produced

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13
Q

Describe EAEC (enteroaggregative E. Coli)

A

•Cause of diarrhea in children and adults in both developed and developing countries

–Also can affect HIV patients in developing countries (and probably developed countries)

–Can cause traveler’s diarrhea

•Pathogenesis not well understood

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14
Q

What are some other kinds of E. Coli infections?

A
  • Nosocomial (can lead to sepsis)
  • Neonatal meningitis due to encapsulated strains (K1-antigen)
  • Uropathogenic E. Coli (UPEC)
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15
Q

Describe UPEC

A

UPEC causes 90% of UTIs (more common in females) with symptoms including urgency, frequency, fysuria, pyuria, suprapubic pain, and fever

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16
Q

How is UPEC UTI diagnosed?

A

–Diagnosis: bacteria in urine

  • >105 per ml in females
  • >103 per ml in males
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17
Q

What are the virulence factors used by UPEC?

A

–Virulence factors include a P fimbriae (also called PAP pili), and a capsule (K antigen)

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18
Q

Describe vibrio

A

This is a comma-shaped, gram - rod that is motile due to a polar flagellum and is oxidase POSITIVE

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19
Q

Where is vibrio commonly found?

A

In saltwater (disease common in warm months)

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20
Q

What are the significant human vibrio pathogens?

A

–V. cholerae

–V. parahaemolyticus

–V. vulnificus

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21
Q

How is Vibrio cholerae transmitted?

A

Transmitted primarily through fecally contaminated drinking water, less often food and is known for becoming rampant/epidemic in areas devastated by natural/man-made disasters (i.e. earthquakes, etc.) and in areas with poor sanitation, malnutrition, overcrowding, and/or inadequate medical services

•Marked season variation in incidence of infection in most climates due to rapid growth of Vibrio bacteria in warmer temperatures

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22
Q

Epidemiology of Vibrio cholerae

A

5-10 mill cases/yr

Endemic in Asia, Africa, S. America, and Indian subcontinent

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23
Q

What are the reservoirs of Vibrio cholerae?

A

Humans, marine shellfish

24
Q

What is serotyping of Vibrio cholerae based on?

A

200+ serotypes based on the O antigen

25
Q

What Vibrio cholerase serotypes are responsible for epidemic and pandemic cholera?

A

O1 (two biotypes: E1 Tor and Classic) and O139

26
Q

Describe the pathogenesis of Vibrio Cholerae

A

Pathogenesis is dependent on colonization of the small intestine (which requires a LARGE no. of bacteria to be ingested because VC is sensitive to stomach acid- high infectious dose) and secretion of toxins

27
Q

How does VC adhere to small intestine cells?

A

Adherence to cells of brush border of the gut is related to secretion of the bacterial enzyme mucinase which dissolves glycoprotein covering over the intestinal cells.

28
Q

What does VC do once mucinase allows it to adhere to brush border epithelial cells?

A

–Organism then multiplies and secretes cholera toxin – AB toxin

29
Q

Describe Cholera AB toxin

A
  • 5 B (binding) subunits: binds to ganglioside receptor on the surface of the enterocyte.
  • 1 A (active) subunit: inserted into the cytosol and catalyzes addition of ADP-ribose to the Gs (stimulatory G) protein. Causes persistent stimulation of adenylate cyclase.

–As a result, cyclic AMP is overproduced and activates cyclic AMP-dependent protein kinase which phosphorylates ion transporters in the cell membrane, resulting in the loss of water and ions from the cell. Watery efflux enters the lumen of the gut and massive watery diarrhea ensues

30
Q

Mechanism of Cholera AB toxin

A
31
Q

How does VC present?

A

There is a 1-3 day incubation period followed by the onset of large volumes (up to 20L/day) of watery diarrhea without the presence of RBCs or WBCs in stool

Vomiting and dehydration are common and **abdominal pain is usually ABSENT**

32
Q

How is VC stool unique?

A

–Stool is often termed rice water stools – watery stool with flecks of mucous. Often has a fishy odor. Very large number or organisms in the stool

33
Q

What are the consequences of dehydration with VC induced diarrhea?

A
  • Loss of fluid and electrolytes leads to cardiac and renal failure
  • Acidosis and hypokalemia also occur as a result of loss of bicarb and K in the stool.
34
Q

What is the mortality rate of VC without tx?

A

40%

35
Q

How is VC diagnosed?

A

–Most cases diagnosed based on clinical suspicion

–Organism can be isolated from the stool using selective media such as thiosulfate citrate bile sucrose (TCBS) agar, taurocholate tellurite gelatin agar (TTGA), or MacConkey agar (colonies will be colorless)

36
Q

What is the tx of VC?

A

–Mainstay of treatment: aggressive volume repletion

–Antibiotics adjunctive therapy for patients with cholera and moderate-severe volume depletion: Tetracycline, erythromycin, azithromycin, ciprofloxacin are options

37
Q

Note about VC tx

A

In 2002, the World Health Organization (WHO) recommended the use of a reduced osmolar ORS, which has been demonstrated to decrease stool output, vomiting, and the need for supplemental intravenous fluids

38
Q

How can VC be prevented?

A

–Clean water supply, appropriate sanitation

–About 760 million people still lack access to clean water sources

–WHO recommends oral cholera vaccine in cholera control programs in endemic areas

39
Q

Describe Vibrio parahaemolyticus

A

This is a marine organism transmitted by ingesting raw or undercooked seafood, especially shellfish (oysters) and is a major cause of diarrhea in Japan (rare in the US, but more common around the coasts in warm months)

40
Q

How does Vibrio parahaemolyticus present?

A
  • Incubation period about 1 day
  • Mild to severe watery diarrhea, nausea/vomiting, abdominal cramps, fever
  • Self-limited of about 3 days’ duration
41
Q

Bacterema with VP is uncommon, but more common in pts with underlying conditions such as ______

A

liver disease

42
Q

What else can VP cause?

A

Also causes wound infections: associated with marine recreational activities and handling of seafood. Generally mild, however in those with liver disease, diabetes, alcoholism, etc., cellulitis can be severe

43
Q

How is VP diagnosed?

A

culture

44
Q

How is VP tx?

A

Volume repletion. In severe cases antibiotics are warranted: doxycycline.

45
Q

Describe Vibrio vulnificus

A

This is a marine organism that causes a non-inflammatory diarrhea and severe SKIN and SOFT TISSUE infections (especially in those with open wounds- fish handlers)

46
Q

What can Vibrio vulnificus cause in immunocompromised pt who have eaten raw shellfish containing it?

A

a rapidly fatal septicemia

  • Patients most at risk are those with underlying liver disease, alcohol abuse, and some other chronic disease (diabetes, rheumatoid arthritis)
  • 39% mortality rate
  • Bullous skin lesions are characteristic
47
Q

How is VV diagnosed and tx?

A

Diagnosis: culture

Tx: Doxy + Cefotaxime or Ceftriaxone

48
Q

Describe Bacillus cereus

A

Spore-forming gram + bacilli that can survive in the enivronment for extended periods and withstand temperature extremes AND can survive food processing (Has been recovered from rice, dairy products, spices, bean sprouts. Fried rice important cause of emetic-type food poisoning.)

49
Q

Where is bacillus cereus especially abundant?

A

in soil and fresh water

50
Q

What toxins does Bacillus cereus produce?

A

2 enterotoxins: diarrheal enterotoxin and emetic toxin

51
Q

How does Bacillus cereus infection present?

A

There are two syndrome presentations: the diarrheal syndrome and the emetic syndrome

52
Q

How does the diarrheal syndrome of bacllus cereus present?

A

•abdominal cramps, copious diarrhea, 8-16 hours after ingestion, resolves within 24 hours. Vomiting uncommon

53
Q

How does the emetic syndrome of bacllus cereus present? What causes it?

A

caused by direct ingestion of the toxin cereulide (heat stable). Abdominal cramps, nausea/vomiting. Diarrhea occurs in 1/3 of people. Onset within 1-5 hours of ingestion, resolve in 6-24 hours.

54
Q

Describe S. aureus toxins

A

Enterotoxin is heat-stable and acts as a superantigen within the GI tract to stimulate release of IL-1 and IL-2

55
Q

What causes S aureus GI infections?

A

•Associated with consumption of foods prepared by a food handler such as dairy, produce, meats, eggs and salads (potato salad at a picnic).

–Food handler usually contaminates the product.

–Food is left at room temperature and organisms multiply and can produce substantial quantity of toxin

56
Q

What are the symptoms of a S. aureus GI infection?

A

•Symptoms begin within 1-6 hours of ingestion with nausea, vomiting and abdominal cramps

–Fever and/or diarrhea occur in a minority of patients

•Typically lasts for 24 hours or less, but can be longer

GI- Week 2 (27 decks)

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