Enteric Infections Flashcards

1
Q

Define: secretory diarrhea

- what are the features?

A
  • Watery diarrhea w/o fever or with minimal fever.
  • Continues despite increasing intake of food and water
  • mid abdominal pain
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2
Q

Define: Inflammatory diarrhea

A
  • mucoid like diarrhea
  • accompanied by fever
  • may often be bloody and have WBC in the stool
  • lower abdominal and rectal pain
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3
Q

Where does secretory diarrhea originate in the GI tract

A

small bowel

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4
Q

What are 5 examples of causative pathogens of secretory diarrhea?

A
  1. Vibrio cholera
  2. Rotavirus
  3. E. coli (ST or LT)
  4. Norovirus
  5. Giardia
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5
Q

What are 5 examples of causative pathogens of inflammatory diarrhea?

A
  1. Shigella
  2. Campylobacter
  3. E. coli (EHEC/STEC)
  4. Entamoeba histolytica
  5. C. difficile
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6
Q

What are the two toxins that C. diff produces? Which is more pathogenic?

A
Toxin A (enterotoxin) and B (cytotoxin)
- Toxin B is more pathogenic
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7
Q

What are 2 medication types that increase risk for C. diff?

A
  1. broad spectrum antibiotics

2. PPIs

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8
Q

What is the diarrhea like with C. difficile?

A

watery and foul smelling (like a barn)

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9
Q

What is the leukemoid reaction?

A

phenomenon of an increase in WBC count that mimics leukemia but is due to infection
- common in C. diff

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10
Q

What is the treatment approach for C. diff?

A
  1. Stop unnecessary antibiotics
  2. Metronidazole (IV or oral) and Vancomycin (oral only)
  3. Stool transplant to replenish to replenish microbiota
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11
Q

what are 3 virulence factors that pathogenic E. coli have?

A
  1. Fibriae: allow for colonization
  2. Adhesions: allow for cell invasion
  3. Toxins: both endo and exo
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12
Q

Shiga toxin is an example for what kind of toxin?

A

Exotoxin = secreted

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13
Q

What is ETEC and what specific pathogenic adaptations does it have?

A

Enterotoxigenic E. coli

  1. fimbriae for attachment
  2. Heat labile (LT) toxin similar to cholera
  3. heat stable toxin (ST)
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14
Q

What is the clinical syndrome for ETEC diarrhea?

A

mild water diarrhea and nausea but no vomiting for 1-4 days

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15
Q

What is the pathogenesis of ETEC diarrhea?

A

ingestion of fecally contaminated food/water with 10^8-10 bacteria needed to cause disease

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16
Q

What is the treatment for ETEC diarrhea?

A

Oral rehydration

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17
Q

What are EHEC and STEC?

A

They’re the same thing

enterohemorrhagic e. coli and shigatoxin producing e. coli

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18
Q

What are the virulence factors specific to EHEC/STEC

A

The shiga toxin (A/B) toxin

  • acts on ribosomes to block protein synthesis leading to cell death
  • has preference for enterocytes and endothelial cells in the kidney
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19
Q

What is the clinical syndrome of EHEC/STEC?

A

vomiting, diarrhea (often bloody), and abdominal pain

for children: 5-10 days later can develop lethargy, anemia, oliguria = hemolytic uremic syndrome

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20
Q

What are the two forms of salmonella?

A

non-typhoidal and typhoidal

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21
Q

What are the forms of non-typhoidal salmonella? What kind of illness do they cause?

A

Enteritidis and thyphimurium

- usually not invasive, self resolving disease

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22
Q

What are the forms of typhoidal salmonella? What kind of illness do they cause?

A

Typhi and parathyphi

- cause invasive disease with fever and bacteremia which is fatal if not treated

23
Q

what are the typical reservoirs of non-typhoidal salmonella?

A

reptiles and chickens

24
Q

What is the clinical picture of non-typhoidal salmonella?

A

Acute diarrhea with fever and abdominal pain that resolves within 4-7 days

25
Q

What is the reservoir of typhoidal salmonella?

A

human only

26
Q

What are the clinical symptoms of typhoidal salmonella disease?

A

Not always diarrhea! Can be constipated
- can lead to ileus and perforation

Long fevers + rash, headache

27
Q

Where can salmonella typhi reside in the body dormant

A

the gallbladder

28
Q

What is the virulence factor of typhoidal salmonella?

A

Vi capsular antigen which prevents phagocytosis

29
Q

What is the treatment for typhoidal salmonella?

A

antibiotics based on local resistance

30
Q

What are 3 adaptations that H. pylori have to increase colonization in the stomach ?

A
  1. urease: converts urea to ammonium to neutralize stomach acid
  2. swimming ability: spiral shape + flagella
  3. Adhesions to bind to epithelial receptors
31
Q

H. pylori is the most common cause of gastritis and also causes what % of duodenal and gastric ulcers?

A

90% of duodenal ulcers

70-80% of gastric ulcers

32
Q

Who should you screen for H. pylori infection ?

A
  1. anyone with dyspepsia symptoms
  2. Anyone with gastric cancer, active or history of peptic ulcer disease
  3. red flag sx: early satiety, bleeding, weight loss, dysphagia, odynophagia
33
Q

What are the 3 tests available to diagnose H.pylori? What are the benefits/issues with each?

A
  1. Urease breath test
    - highly sensitive and specific, can use to test for cure
    - false neg with recent PPI or antibiotics
  2. serology
    - high sensitivity and easy to perform clinically
    - lower specificity = false +
    - still positive post treatment
  3. Endoscopy + biopsy
    - highest sensitivity + specificity, can also diagnose cancer or PUD
    - false neg possible is GI bleed, recent PPI or antibiotics
34
Q

What is the treatment for H. pylori? For how long?

A

“Triple Therapy”

  1. PPI: Lansoprazole…
  2. Antibiotics (pick 2)
    - clarithromycin
    - amoxicillin
    - Metronidazole
    - Tetracycline/doxy

Need to do a urease breath test to confirm

35
Q

What type of virus is Hep A? Where does it replicate?

A

Picornavirus

- replicates in hepatocytes

36
Q

What is the transmission of Hep A ?

A

fecal oral

37
Q

What is the incubation period of Hep A?

A

~ 28 days

38
Q

What is the clinical presentation of Hep A?

A

Typically mild, self limiting illness

  • fatigue
  • nausea
  • diarrhea
  • abdo pain
  • fever

Later develop:

  • jaundice,
  • pruritis
  • dark urine
  • pale stools
39
Q

How common is fulminant liver failure with Hep A

A

Very uncommon (<1%)

40
Q

What is the treatment for Hep A?

A

Supportive

- most people recover in about 2-3 months

41
Q

Is Hep A a chronic infection?

A

No, once it is cleared you are seropositive and immune

42
Q

Dramatic elevations in transaminase levels are hallmarks of…

A

Acute hepatitis infection

- A or B

43
Q

Food poisoning is by definition…

A

disease caused by eating food that has been contaminated with bacterial TOXIN

44
Q

What are two common species that cause “food poisioning?

A
  1. Staph aureus: produces enterotoxin

2. Bacillus cereus: commonly found in soil (rice) and its spores survive cooking and produce enterotoxin at room temp

45
Q

What is the clinical presentation of food poisoning?

A

ACUTE onset nausea, vomiting, and upper GI pain within 1-6 hours of ingestion

  • more vomiting than diarrhea
  • resolves within 24 hrs
46
Q

What kind of bacterial is clostridium botulinum

A

gram positive, spore forming anaerobic rod

47
Q

What kind of toxin does clostridium botulinum produce?

A

neurotoxin

- binds SNARE proteins and prevents Ach vesicles from docking at cleft

48
Q

What is the clinical syndrome of botulism poisoning in adults?

A

“The D’s”

  • double vision
  • drooping eyelids
  • dry mouth
  • dysarthria
  • dizziness
  • dysphagia
  • descending flaccid paralysis
  • diaphragm paralysis
49
Q

What is the clinical syndrome of botulism poisoning in babies?

A

“floppy” baby

  • hypotonia
  • constipation
50
Q

What is an abdominal abscess?

A

A disruption of the bowel wall integrity that allows normal flora to exit into the peritoneum and cause disease

51
Q

What is the management of an abdominal abscess?

A

surgical drainage and antibiotics

  1. Piptazo or cefriaxone + metronidazole
  2. surgical drainage with sample sent for culture at time of drainage
52
Q

What are the two most common pathogens causing bowel abscesses?

A

E. coli and bacteroides

53
Q

What other pathogens should you consider if a patient who is hospitalized with recent abx exposure develops a bowel abscess?

A

candida, enterococcus, and resistant gram negative bacteria