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M2 GI/Nutrition > Infectious Diarrhea - Noe > Flashcards

Infectious Diarrhea - Noe Flashcards

1
Q

What is the prognosis for most non-infectious diarrheas?

What volume of excrement defines a diarrhea?

A

Even non-infectious diarrheas will typically be self-limited.

>1L per day.

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2
Q

What is the most common cause of gastroenteritis overall?

Of community-acquired diarrhea?

A

Viral infections (mainly norovirus).

Bacterial infections.

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3
Q

Salmonella Typhi

Describe its morphology.

What are its vectors for GI infection?

When does its occurrence peak?

A

Salmonella Typhi

Salmonella are gram-negative encapsulated bacilli.

Poultry, eggs, milk. Pet turtles?

Peak in summer & fall.

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4
Q

Salmonella Typhi

Causes a small bowel or colonic diarrhea?

What is typhoid fever?

What is the consequence of gallbladder colonization?

A

Salmonella Typhi

Small bowel.

Tranlocation from the GI to a systemic infection (fever observed).

Increased gallstones, carrier state (ie Typhoid Mary)

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5
Q

What is the most common cause of osteomyelitis in patients with Sickle-cell disease?

A

Tempted to say Salmonella? They’re more susceptible, yes, but the most common is still Staph Aureus.

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6
Q

Salmonella Typhi

How does it cause disease?

What role do antibiotics play here?

A

Salmonella Typhi

Salmonella is tolerant of acidic conditions and enters gut tissues (survive in the phagolysosome)

Antibiotics are not indicated since they will kill the microbiota that help resist salmonellosis.

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7
Q

Shigella

Describe its morphology.

Who is generally affected?

What is its inoculum?

A

Shigella

Gram negative, unencapsulated bacilli.

Notable for pediatric infection (comparably high death rate).

Very small, as few as 10 organisms.

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8
Q

Shigella

How does it cause disease?

What role do antibiotics play here?

A

Shigella

Produces shiga toxin (impedes host protein synthesis). Note risk of HUS, seizures, or reactive arthritis.

Antibiotics can shorten the clinical course; they are indicated (unlike antidiarrheals)

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9
Q

What is the most common bacterial diarrhea caused by?

What are its transmission factors?

A

Campylobacter Jejuni.

Uncooked poultry, contaminated milk or water. Dog feces?

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10
Q

Campylobacter Jejuni

Bloody or watery diarrhea?

Describe the illness it causes (include sequelae!)

A

Campylobacter Jejuni

Classically bloody, but this only occurs in under half of cases.

Flu-like prodrome with reactive arthritis, E-nodosum, pseudoappendicitis and Guillain-Barre syndrome.

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11
Q

Giardia Lamblia

Describe its morphology.

How is it spread?

Small bowel or colonic?

A

Giardia Lamblia

It is a multiflagellate protozoan (horseshoe crab-shaped)

Fecal-oral contamination of water (or food). Classically in hikers drinking unfiltered stream water.

Small bowel (upper abdominal bloating).

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12
Q

ETEC

How does it cause disease?

What is this disease known as?

A

ETEC

Heat labile (LT) toxin increases intracellular cAMP causing Cl secretion and decreased NaCl absorption. Heat-stable toxin (ST) more or less does the same, but with cGMP.

Traveler’s diarrhea

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13
Q

Describe the illness caused by EIEC.

Contrast it with that caused by EAEC.

A

EIEC invades the gut epithelium, causes bloody diarrhea.

EAEC adheres to the gut using flagella, causes intestinal inflammation.

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14
Q

What is the name given to O157-H7?

What is its transmission factor?

Major disease sequela?

A

EHEC (enterohemorrhagic E. Coli)

Contaminated beef.

Hemolytic uremic syndrome. NOTE: Can be precipitated by antibiotics!

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15
Q

Vibrio Cholerae

Describe its morphology.

Inoculum?

Means of transmission?

A

Vibrio Cholerae

Gram-negative flagellated bacillus.

Large, on the order of millions of organisms.

Contaminated water and seafood (classic: oysters)

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16
Q

Vibrio Cholerae

How does it cause disease?

Describe the illness it causes.

A

Vibrio Cholerae

Cholera toxin - Increases cAMP to open CFTR, etc etc…

Often self-limiting, but sometimes prolific watery diarrhea (1L/hr!). Death occurs without supportive hydration.

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17
Q

Norovirus

How is it spread?

Where?

Symptoms?

A

Norovirus

Fecally contaminated food/water, person-to-person transmission.

Schools, hospitals, nursing homes, cruise ships.

N/V/D (watery), pain. Pretty nondescript and short-lived.

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18
Q

Rotavirus

Who is most vulnerable?

When?

Why it is no longer the most common cause of childhood diarrhea (and diarrheal death?)

A

Rotavirus

Children between 6-24mo.

Winter!

Vaccine is available.

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19
Q

All of the parasitic infections share a common pathway by which they reach the GI tract. What is it?

A

Penetration of the airways in the lungs, migration to the pharynx, then travel (by peristalsis) to the GI tract.

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20
Q

How does Ascaris first gain access to the body?

How does Strongyloides first gain access?

A

Ingestion of the ova from fecally-contaminated food. (Yes; it goes from GI, to lung, back to GI…)

Resides in soil, penetrates uncovered skin.

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21
Q

How do Necator and Ancylostoma gain access to the body?

What is their major sequela?

A

Larval penetration through the skin, like with Strongyloides**.

Hookworm infections are the leading cause of IDA in the developing world.

22
Q

What are some opportunistic GI infections seen in the immunocompromised?

A

Cryptosporidium, Isospora, Cyclospora, Microsporia

MAC (mycobacterium avium complex)

CMV, HSV, Adenovirus

23
Q

Who is at highest risk for nosocomial infections?

What are some usual culprits?

A

Anyone admitted, but worse in the elderly (both incidence and outcome).

C. Diff, tube feeding (osmotic diarrhea), medications, fecal impaction, ischemia.

24
Q

Name some major important elements of the history in assessing diarrhea

A
  • Volume
  • Consistency
  • Frequency
  • Pain (with BM, without BM)
  • Waking at night
  • Gas and bloating
  • Recent Abx or chemotherapy
  • Recent travel
  • Ill family members
  • Nursing home residence or close living quarters
  • Occupational exposure (healthcare, school, daycare)
  • Pets
  • Water supply (well water or municipal treated water?)
  • Diet (unpasteurized, undercooked, organic)
25
Q

Fever with diarrhea carries high suspicion for which two cytotoxic organisms?

What else is associated with fever and diarrhea?

A

C. diff and E. histolytica

Also: invasive bacteria, enteric viruses, ischemia, IBD

26
Q

Timing of food history: what tends to present at…

  • <6 hours?
  • 8-14 hours?
  • > 14 hours?
A
  • <6 hours: toxin ingestion (especially pre-formed, alread on the food), including toxins from S. aureus (potato salad) and B. cereus (Chinese food/rice **think ‘cereal’**)
  • 8-14 hours: C. perfringens
  • >14 hours: non-specific viral or bacterial
27
Q

Is endoscopy usually indicated in acute diarrhea?

What about chronic?

A

Acute: no

Chronic: often, yes

28
Q

Does stool culture have high sensitivity or low sensitivity or bacterial pathogens? Why?

A

High sensitivity (negative culture usually not a false negative)

Bacterial pathogens are shed/excreted continuously - they have a tendency to show up in the stool if they are, in fact, in the GI tract.

29
Q

Give (6) clinical contexts that likely require stool culture

A
  • Severe illness with diarrhea
  • Community outbreaks
  • Diarrhea that requires hospitalization
  • Immunocompromised patients (HIV, transplants, etC)
  • Patients with significant co-morbidities (IBD)
  • Food handlers and daycare providers (negative stool culture often a condition for returning to work following illness)
30
Q

Are stool screenings for O&P (ova and parasites) useful? Why?

When should it be ordered anyway?

What’s a more sensitive/specific test approach (especially for Giardiasis and Cryptosporidium)?

A

Not usually -> useless for most patients!

Ova are shed intermittently - high false-negative rate

It’s time-consuming (collections on 3 consecutive days, 24 hours apart)

When to order:

  • Persistent (>14 days) diarrhea
  • Travel to mountainous regions
  • Exposure to infants in daycare setting
  • Immune-compromise
  • Community waterborne outbreak

More sensitive/specific: ELISA or DFA microscopy to detect antigen in stool

31
Q

What is (pretty much always) the first-line treatment for diarrhea?

A

Hydration (preferably oral)

32
Q

What shoud always be added to oral hydration in the context of diarrhea? Why?

Give some examples.

Is gatorade appropriate for oral rehydration?

A

Glucose and sodium

Intestinal co-transport of sodium and glucose tends to remain intact - adding glucose and sodium to water assists in the uptake of water in the gut

Oral rehydration solutions

  • Pedialyte! Also something called ‘rehydralyte’
  • WHO-ORS (apparently not used much in the US?)
  • Homemade: 1/2tsp salt, 1/2tsp baking soda, 4tbsp sugar, 1L water (yum!)
  • Gatorade: may be adequate for relatively healthy patients. The high carbohydrate load in Gatorade and other sports drinks can worsen diarrhea (therefore, not for severely ill patients)
33
Q

When might IV rehydration be appropriate?

A
  • patient cannot tolerate oral rehydration (vomiting, excessive diarrhea)
  • Electolyte imbalances (infants with immature kidneys, patients on diuretics or cardiac meds)
34
Q

What is the criteria for moderate/severe traveler’s diarrhea?

How should it be treated? What effect does this have on disease course?

A

>4 stools dails, fever, pus and/or mucus in stool

Treat (promptly!): FQ or TMP-SMX

Abx treatment reduces the duration of disease from 3-5 days to 1-2 days

35
Q

Describe the indications for empiric antibiotics in the context of diarrhea

What drugs should be used?

A
  • Fever, bloody diarrhea, occult blood or PMNs in the stool
    • except if EHEC or C. diff are suspected!
  • >8 stools per day, volume depletion
  • Hospitalization or immunocompromised patients

Drugs:

  • FQ for 3-5 days
  • Azithromycin or erythromycin if FQ resistance suspected
36
Q

Are anti-motility agents generally recommended for control of diarrhea? Why?

A

No!

Most of the time this is not needed and may contribute to the development of sever diarrhea-related complications (Bacterial translocation, C. diff toxic megacolon, EHEC-related HUS)

37
Q

If anti-motility agents are absolutely needed, name two drugs that might be appropriate.

A

Loperamide

Diphenoxylate

38
Q

Clindamycin use is closely associated with infection of what organism?

Describe it (gram-stain, oxygen tolerance, spores)

What is the transmission mode?

A

Clostridium difficile

G+, anaerobic, spore-forming

Transmission: fecal-oral

39
Q

List some major risk factors for development of C. diff infection

A
  • Recent Abx use (especially clindamycin) -> risk persists for 2-3 weeks
  • Duration of hospital stay
  • Age (generally not seen in infants)
  • Chemotherapy
  • IBD
  • AIDS
  • GI surgery or G tube
  • Antacids
40
Q

Name and describe the toxins utilized by C. diff

Testing for which one carries a very high sensitivity?

A

Toxin A (Endo A)

  • Enterotoxin
  • Present in most non-epidemic strains

Toxin B (Endo B)

  • Cytotoxin
  • Expressed by 98% of strains (high sensitivity for C. diff) -> or just use PCR
  • Present in most non-epidemic strains

Binary

  • Associated with BI/NAP1/027 strains
  • Unclear role
41
Q

What is C. diff BI/NAP027?

What contributes to its pathogenicity?

A

Hypervirulent strains of C. diff

tcdC gene mutation (toxin regulator) causes expression of 16X toxin A and 23X toxin B compared to more common strains. These strains also express binary toxin and carry a higher resistance to FQ Abx.

42
Q

What was one postulated reason for recent increased reports of C. diff infections in low-risk populations?

A

Colonization in cows -> ground beef

43
Q

Describe the clinical presentation of C. diff infection

What else might be seen in an especially severe presentation?

A
  • Typical:
    • bloody watery diarrhea
    • fever
    • abdominal pain
    • leukocytosis
    • Pseudomembranous colitis
  • Severe:
    • toxic megacolon
    • sepsis/cytokine storm
    • colonic perforation
    • death
44
Q

The attached colonic endoscopy image is characteristic of what type of infection?

A

C. diff pseudomembranous colitis?

45
Q

Give (4) prevention techniques that should be used by healthcare professionals to prevent C. difficile in the healthcare setting

A
  • Glove use
  • Hand hygeine/washing (alcohol hand gels are ineffective against spores! Wash those hands for reals!)
  • Isolation gowns
  • Judicious use of Abx
46
Q

What two antibiotics are the mainstay therapies for C. diff infection?

How are they administered?

Which is for inpatient? Which is for outpatient therapy?

Which has a lower overall relapse rate, higher efficacy, and better side effect profile?

A

Vancomycin and metronidazole (both oral)

Outpatient: metronidazole

Inpatient: vancomycin

Vanco: lower recurrence, higher efficacy, better side effect profile

47
Q

What findings consititute severe C. diff infection? With complications?

A
  • Severe disease
    • Age > 65
    • Cr > 1.5X baseline
    • WBC > 15K
  • Severe with complications:
    • hypotension/shock
    • Ileus
    • Megacolon (this is a surgical emergency!)
48
Q

What complication associated with C. difficile is a surgical emergency?

A

Toxic megacolon (dilation, lack of haustra -> i.e. ‘lead pipe sign’)

49
Q

How many patients experience recurrence of C. diff infection? How does this happen? Give some risk factors.

What is the treatment approach for recurrence?

A

10-35% -> spores may have survived treatment and re-colonized the gut

  • Continued Abx
  • Age
  • Co-morbidities
  • Antacid medication
  • Immunosuppression
  • Immunodeficiency

Treatment:

  • Repeat metronidazole
  • Give vancomycin (if not already tried), longer course with tapering
  • Rifaximin
  • Fidaxomicin
  • Oral IVIG (the shotgun approach)
50
Q

What is Fidaxomicin?

What is its mechanism of action?

Why is it so awesome? If it’s so awesome, why is it not used much?

A

An alternative to vancomycin for the treatment of C. diff

Inhibits RNAP

Great for C. diff because: poor G- specificity (kills G+ only), so it kills C. diff while preserving normal gut flora. Also, it achieves a high fecal concentration while keeping serum levels low (it stays where it’s supposed to be) - fewer systemic effects.

Expensive! ($300/day) -> only used for cases highly refractory to vanco or metro

51
Q

The 2009 film The Human Centipede proposes a unique approach to what promising new type of GI therapy (especially C. diff)?

A

Fecal transplant!

*Bonus: the film also presents an appropriate metaphor for the (ahem) logistical concerns associated with fecal transplant therapy.

M2 GI/Nutrition (43 decks)

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