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Gastrointestinal - Microbiology > Non-Inflammatory Diarrhea > Flashcards

Non-Inflammatory Diarrhea Flashcards

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1
Q

What are the bacterial causes non-inflammatory diarrhea?

A

Causes of non-inflammatory diarrhea​
ETEC
EPEC
EAEC
Vibrio cholerae, parahemolyticus and vulnificus ​
S. aureus​
Bacillus cereus

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2
Q

What are the bacterial causes of inflammatory diarrhea?

A

Causes of inflammatory diarrhea​
EHEC x​
EIEC x​
Shigella x​
Salmonella enterica and enteritidis x​
Campylobacter jejuni x​
Clostridium difficile x​
Yersinia enterocolitica x​

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3
Q

What is the major cause of traveler’s diarrhea?
• how does it present clinically?
• Duration?

A

Enterotoxogenic E. Coli (ETEC)

Source of Infection:
Contaminated food/water​

​

Clinical presentation​:
Watery diarrhea, ranges from mild to severe​
Duration 1-5 days

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4
Q

What 2 toxins are produced by ETEC?

A

Organism produces heat-labile toxin (LT) and heat-stable toxin (ST)​

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5
Q

How does the heat-labile toxin work in ETEC?

A

LT (heat labile toxin) similar to Cholera toxin. Stimulates adenylate cyclase and increases intracellular cyclic AMP, resulting in secretion of chloride from intestinal crypt cells (via CFTR?) 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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6
Q

How does the heat stable toxin of ETEC work?

A

ST (heat stable toxin) 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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7
Q

Who most commonly is affected by EPEC (Enteropathogenic E. coli)?
• Pathogenesis of this organism?
• Symptoms of infection?
• Production of Shiga-like toxin?

A

• Most commonly associated with illness among children <6 months to 2 years of age in developing countries​

Symptoms
• Profuse, watery diarrhea can be severe with vomiting and dehydration​

Pathogenesis:
• 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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8
Q

Is it possible for EPEC to cause infection in adults?

A

Yes, but this is uncommon

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9
Q

Enteroaggregative E. coli (EAEC)
• Who most commonly gets infected?
• Where is this found?

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

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10
Q

What is a defining microbiological feature of E. coli that causes neonatal meningitis?

A

Neonatal meningitis​ - so it must be encapsulated

Encapsulated strains (K1-antigen)​

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11
Q

Uropathogenic E. coli (UPEC)
• what does it cause?
• How common is it?
• Virulence factors?

A

Uropathogenic E. coli (UPEC)​
UPEC cause 90% of urinary tract infections (UTI) ​
More common in females than males ​

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

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12
Q

What 3 types of Vibrio species cause disease in humans?

A

V. cholerae​

V. parahaemolyticus​

V. vulnificus

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13
Q

Vibrio
• Gram Stain and Morphological Characteristics
• Motility
• Oxidase -/+?
• Common location to see bacteria?

A

Curved (comma-shaped), gram- rods​

Motile, polar flagellum​

Oxidase positive​

Commonly found in saltwater, disease in warm months​

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14
Q

Vibrio cholerae
• Factors that predispose to epidemics?

A

Transmitted primarily through fecally contaminated drinking water, less often food​
Other factors predisposing to epidemics:
• poor sanitation, malnutrition, overcrowding, inadequate medical services ​

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15
Q

What is the main animal reservior of V. cholerae?

A

Main animal reservoirs: marine shellfish. ​
• Ingestion without adequate cooking can ​transmit the disease​

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16
Q

What 2 serogroups are most implicated in epidemic and pandemic cholera?

A

O1 and O139 serogroups responsible for epidemic and pandemic cholera​

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17
Q

What are the two biotypes of the O1 serogroup of V. cholerae?

A

O1 serogroup divided into 2 biotypes​

E1 Tor​

Classic​

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18
Q

T or F: it only takes a small exposure to V. cholorae to come down with an infection.

A

False, this bug has a high infectious dose

19
Q

How is V. cholerae able to hold onto the colonic epithelium so that it can cause infection?

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.​

20
Q

What type of toxin is cholera toxin?

A

AB toxin

21
Q

How does cholera toxin work?

A 
_5 B (binding) subunits:_ 
binds to **ganglioside recepto**r on the surface of the enterocyte.​
_1 A (active) subunit:_
inserted into the cytosol and **catalyzes addition of ADP-ribose to the Gs (s**timulatory 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​

22
Q

How does infection with Vibrio cholerae present clinically?
• Incubation Period
• Appearance of Stools

A

Incubation period
• 1-3 days​

  • Watery diarrhea in large volumes (up to 20 L/day)​ => Dehydration is common
  • No RBCs or WBCs in stool​ (non-inflammatory diarrhea)
  • Stool is often termed rice water stools – watery stool with flecks of mucous. Often has a fishy odor.
  • Vomiting is common​
  • Abdominal pain usually absent​
23
Q

Vibrio cholera
• complications of dehydration?
• Mortality rate

A

Loss of fluid and electrolytes (Acidosis and hypokalemia occur as a result of loss of bicarb and K in the stool)leads to cardiac and renal failure​

• Mortality rate without treatment 40%​

24
Q

What media can Vibrio cholerae be cultured on?

A

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

25
Q

How is a diagnosis of Cholerae made?
• how is this infection treated?

A

Diagnosis ​
• 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)​

Treatment​
• Mainstay of treatment: aggressive volume repletion​
• Antibiotics adjunctive therapy for patients with cholera ​and moderate-severe volume depletion:Tetracycline, ​erythromycin, azithromycin, ciprofloxacin are options​

26
Q

Are oral rehydration salts (ORS) effective in the treatment of cholera infection?

A

reduced osmolar ORS
• Decrease stool output
• Decrease vomiting
• Reduce the need for supplemental intravenous fluids​

27
Q

Vibrio parahaemolyticus
• How is this infection most often acquired?
• Epidemiology?

A
  • Marine organism transmitted by ingesting raw or undercooked seafood, especially shellfish (oysters). ​
  • Major cause of diarrhea in Japan (raw fish eaten in large quantities)​
  • Relatively rare in the United States. Can be seen in the Gulf and Pacific Coasts in warm months​
28
Q

Vibrio parahaemolyticus
• Clinical presentation (incubation period, symptoms, duration)
• Non-GI symptoms?

A

Clinical presentation​
• Incubation period about 1 day​
• Mild to severe watery diarrhea, nausea/vomiting, abdominal cramps, fever​
• Self-limited of about 3 days’ duration
​
Also causes wound infections: associated with marine recreational activities and handling of seafood.

29
Q

Who is at the greatest risk for severe complications of would infections from Vibrio parahaemolyticus?

A

those with:
• liver disease
• diabetes
• alcoholism ​

30
Q

T or F: Vibrio parahaemolyticus is the most common food born illness in Japan

A

True

31
Q

Vibrio parahaemolyticus
• Diagnosis
• Treatment

A

Diagnosis:
• culture​

Treatment:
• volume repletion
• doxycycline

32
Q

Vibrio vulnificus
• How do people acquire this infection?
• Clinical presentation
• How might this present differently in immunocompromised patients?

A

Vibrio vulnificus is acquired by eating undercooked seafood containing the organism or by transmission through and open wound.

Clinical Presentation:
• Diarrhea​
• Severe skin and soft tissue infections​ => BULLOUS Skin lesions
• Can cause a rapidly fatal septicemia in immunocompromised people who have eaten raw shellfish containing the organism​

33
Q

Who is at a high risk of getting a Vibrio vulnificus skin infection?

A

Seafood handlers that sustain wounds while handling the seafood

34
Q

Other than immunocompromised, who is at increased risk of severe infection from vibrio vulnificus?
• Is the rate of mortality high or low with this organism?

A

Patients most at risk are those with
• underlying liver disease
• alcohol abuse
• other chronic disease (diabetes, rheumatoid arthritis)​

39% mortality rate​

35
Q

What is the diagnosis and treatment for Vibrio vulnificus?

A

Diagnosis​
• Culture​

Treatment​
• Doxy plus Cefotaxime or Ceftriaxone​

36
Q

What gram positive SPORE forming bacilli is often a contaminant in FRIED RICE?

A

Bacillus cereus - because this organism is spore forming, it can persist in the soil for prolonged periods of time

37
Q

Bacillis cereus
• What food products OTHER than fried rice can it be found on?
• Where does it exist in the environment?

A

Has been recovered from rice, dairy products, spices, bean sprouts.

Environmental Sources:
• Fresh Water
• Soil

38
Q

What are the two potential outcomes after ingesting Bacillus cereus?
• How do they present clinically (onset after ingestion, duration of illness, symptoms)?
• How do the etiologies of these conditions differ?

A

Diarrheal syndrome:
• abdominal cramps, copious diarrhea, 8-16 hours after ingestion
• Vomitting is UNCOMMON
• resolves within 24 hours.

Emetic syndrome:
• 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. ​

39
Q

What accounts for the difference in time to onset for Vibrio cereus diarrheal and emetic infections?

A

BOTH infections have a rapid onset of symptoms because they are BOTH mediated by TOXINs that are PREFORMED
• Diarrheal syndrome - mediated by diarrheal enterotoxin
• Emetic Syndrome - mediated by emetic toxin

40
Q

What causes the symptoms associated with S. aureus food poisoning?
• Explain how it works.

A

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

41
Q

What types of food is S. aureus food poisoning typically associated with?

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. ​

42
Q

S. aureus food poisoning
• Clinical Presentation (onset, duration, symptoms)

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​
43
Q
A

Gastrointestinal - Microbiology (5 decks)

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