Infectious Diarrhea - Noe Flashcards Preview

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Flashcards in Infectious Diarrhea - Noe Deck (51):

What is the prognosis for most non-infectious diarrheas?

What volume of excrement defines a diarrhea?

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

>1L per day.


What is the most common cause of gastroenteritis overall?

Of community-acquired diarrhea?

Viral infections (mainly norovirus).

Bacterial infections.


Salmonella Typhi

Describe its morphology.

What are its vectors for GI infection?

When does its occurrence peak?

Salmonella Typhi

Salmonella are gram-negative encapsulated bacilli.

Poultry, eggs, milk. Pet turtles?

Peak in summer & fall.


Salmonella Typhi

Causes a small bowel or colonic diarrhea?

What is typhoid fever?

What is the consequence of gallbladder colonization?

Salmonella Typhi

Small bowel.

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

Increased gallstones, carrier state (ie Typhoid Mary)


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

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


Salmonella Typhi

How does it cause disease?

What role do antibiotics play here?

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.



Describe its morphology.

Who is generally affected?

What is its inoculum?


Gram negative, unencapsulated bacilli.

Notable for pediatric infection (comparably high death rate).

Very small, as few as 10 organisms.



How does it cause disease?

What role do antibiotics play here?


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)


What is the most common bacterial diarrhea caused by?

What are its transmission factors?

Campylobacter Jejuni.

Uncooked poultry, contaminated milk or water. Dog feces?


Campylobacter Jejuni

Bloody or watery diarrhea?

Describe the illness it causes (include sequelae!)

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.


Giardia Lamblia

Describe its morphology.

How is it spread?

Small bowel or colonic?

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).



How does it cause disease?

What is this disease known as?


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


Describe the illness caused by EIEC.

Contrast it with that caused by EAEC.

EIEC invades the gut epithelium, causes bloody diarrhea.

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


What is the name given to O157-H7?

What is its transmission factor?

Major disease sequela?

EHEC (enterohemorrhagic E. Coli)

Contaminated beef.

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


Vibrio Cholerae

Describe its morphology.


Means of transmission?

Vibrio Cholerae

Gram-negative flagellated bacillus.

Large, on the order of millions of organisms.

Contaminated water and seafood (classic: oysters)


Vibrio Cholerae

How does it cause disease?

Describe the illness it causes.

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.



How is it spread?




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

Schools, hospitals, nursing homes, cruise ships.

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



Who is most vulnerable?


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


Children between 6-24mo.


Vaccine is available.


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

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


How does Ascaris first gain access to the body?

How does Strongyloides first gain access?

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

Resides in soil, penetrates uncovered skin.


How do Necator and Ancylostoma gain access to the body?

What is their major sequela?

Larval penetration through the skin, like with Strongyloides.

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


What are some opportunistic GI infections seen in the immunocompromised?

Cryptosporidium, Isospora, Cyclospora, Microsporia

MAC (mycobacterium avium complex)

CMV, HSV, Adenovirus


Who is at highest risk for nosocomial infections?

What are some usual culprits?

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

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


Name some major important elements of the history in assessing diarrhea

  • 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)


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

What else is associated with fever and diarrhea?

C. diff and E. histolytica

Also: invasive bacteria, enteric viruses, ischemia, IBD


Timing of food history: what tends to present at...

  • <6 hours?
  • 8-14 hours?
  • > 14 hours?

  • <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


Is endoscopy usually indicated in acute diarrhea?

What about chronic?

Acute: no

Chronic: often, yes


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

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.


Give (6) clinical contexts that likely require stool culture

  • 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)


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)?

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


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

Hydration (preferably oral)


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

Give some examples.

Is gatorade appropriate for oral rehydration?

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)


When might IV rehydration be appropriate?

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


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

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

>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


Describe the indications for empiric antibiotics in the context of diarrhea

What drugs should be used?

  • 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


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


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


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)


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




Clindamycin use is closely associated with infection of what organism?

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

What is the transmission mode?

Clostridium difficile

G+, anaerobic, spore-forming

Transmission: fecal-oral


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

  • 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


Name and describe the toxins utilized by C. diff

Testing for which one carries a very high sensitivity?

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


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



What is C. diff BI/NAP027?

What contributes to its pathogenicity?

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.


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

Colonization in cows -> ground beef


Describe the clinical presentation of C. diff infection

What else might be seen in an especially severe presentation?

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


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

C. diff pseudomembranous colitis?


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

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


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?

Vancomycin and metronidazole (both oral)

Outpatient: metronidazole

Inpatient: vancomycin

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


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

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


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

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


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

What is the treatment approach for recurrence?

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

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


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


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?

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


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

Fecal transplant!

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