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GI, Liver, GallBladder, Pancreas > M- Viral Infections of the Gut and Nosocomial Diarrhea > Flashcards

M- Viral Infections of the Gut and Nosocomial Diarrhea Flashcards

1
Q

What are the 2 main viral causes of gastroenteritis?

What are the 2 other frequent viral causes?

A
  1. Rotavirus (peds>adults)
  2. Norovirus (older kids and adults > pediatrics)

Adenovirus (pediatric)
Astrovirus (pediatric)

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2
Q

What populations are most affected by Rotavirus? What disease presentation is in each?

A
  1. Children - acute, severe, dehydrating diarrhea
  2. Nursing home residents, other adults
  3. Immunocompromised - chronic diarrhea
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3
Q

An HIV + man comes in with chronic diarrhea. What is the likely cause?

A

Rotavirus- causes chronic diarrhea in the immunocompromised

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4
Q

What family of virus is rotavirus?
What is the structure and genome?
How is the structure protective?

A

It is a member of the reovirus family.

Structure: It is non-enveloped which makes it resistant to drying, gastric acid, detergent, and disinfectants and thus able to survive in the environment.

Genome: dsRNA with 11 segments coding 12 proteins. It CAN go through reassortment (like influenza but much more rare and less viral variation from year to year.)

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5
Q

Describe what is in the 3 concentric shells of the Rotavirus.
Which is used for classification and serology?

A

Inner- 1 major protein, polymerase, genome
Middle- VP6 major antigen
Outer (used for classification and serology):
1. surface glycoprotein VP7
2. protease-cleaved protein VP4

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6
Q

There are 7 serogroups for Rotavirus. Which 3 cause disease in humans? Which is primarily associated with children? Adults?

A

Serogroups A, B and C cause disease in humans.

A = children
B,C = adults
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7
Q

What is the infectious dose of Rotavirus?
How is it spread?
What is the seasonal distribution?

A 
Infectious dose : 10 virions
It is spread by fecal-oral transmission:
- person to person
-fomites
- fecally infected water and food

There is a winter peak in temporal climates
(year round infection in tropical climates)

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8
Q

Your child goes to a day care and now is having diarrhea. What is your first instinct on the cause?

A

It is probably from secondary spread of rotavirus.
I
nfectious dose is low (10 virion) and high dose comes out per ml of stool (10^11)

This makes spread easier in:

  • families
  • day care centers
  • adult caregivers get sick from their kids
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9
Q

How long is the incubation period for Rotavirus?
How long does vomiting usually last?
What other symptoms are present?
What is the duration of the disease?

A

The incubation period for Rotavirus is 1-3 days and lasts 3-4 days.
The vomiting only lasts for the first day because the rotavirus is a primarily diarrheal disease.

Other symptoms:

  1. watery diarrhea - 20 stools per day (stool leukocytes in a small proportion of patients)
  2. dehydration
  3. mild URI symptoms
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10
Q

What is the pathogenesis of rotavirus?
Where specifically in the GI tract does it infect?
What are the 3 mechanisms by which it causes diarrhea?

A

It infects cells at the villus tip in the small intestine.

  1. lytic destruction of absorptive cells –> fluid leakage from barrier disruption
  2. Damaged cells are replaced by immature crypt cells –> malabsporption–> carbs in the lumen–> osmotic diarrhea
  3. NSP4 (non-structural protein 4) is a secretagogue–> secretory diarrhea
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11
Q

Describe immunity to rotavirus.

What 2 antibodies appear to be protective?

A

Immunity is transient and requires repeated exposures to get good immunity.
Immunity is serotype specific, so if a different strain infects you, you will get sick again.

Intestinal IgA appears to be protective
Maternal antibody in breast milk is protective

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12
Q

How do you make the diagnosis of rotavirus?

A

It is unneccessary to make etiologic diagnosis.

For epidemiological studies or special hosts you could:

  • EM
  • ELISA (chronic diarrhea in immunocompromised)
  • PCR
  • Latex agglutination
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13
Q

What is treatment for Rotavirus?

A

Symptomatic and supportive care like rehydration

There are no antiviral treatments

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14
Q

What is the criteria to receive IV therapy for Rotavirus?

A
  1. intractable vomit
  2. altered mental status (unable to follow directions)
  3. loss of >10% body weight
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15
Q

How do you prevent rotavirus?

A
  1. handwashing, barrier precautions, isolation of cases
  2. adequate sanitation/water treatment
  3. Vaccine - RotaTeq and Rotarix
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16
Q

To what viral family does Norovirus belong?
What is the structure and genome?
How does the structure protect the virus?
What is the prototype strain?

A

It is a Calicivirus.

Structure: it does not have an envelope so it is resistant to detergents, drying out, etc allowing it to spread environmentally.

Genome: ssRNA (+)

The prototype strain is Norwalk virus

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17
Q

What is the infectious dose of norovirus?
How is it spread?
What places are likely to have epidemic outbreaks?

A

Infectious dose is 10 virion (same as rotavirus)
It is spread by the fecal-oral route
-undercooked food/water
- person to person

First exposure as children but there are secondary and tertiary spread.

Epidemic outbreaks in :

  • nursing homes
  • hospitals
  • cruise ships
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18
Q 
Describe the disease manifestation of norovirus. 
What is the incubation?
What is the most predominant symptom?
What are the other symptoms?
How long does it last?
A

Norovirus has an incubation of 1-2 days and disease manifestations last about 2-3 days.

The most predominant symptom is VOMIT

Other symptoms: fever, myalgia, diarrhea (8 stool a day vs. 20 with rotavirus)

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19
Q

What is the pathogenesis of Norovirus?

A
  1. shortening/atrophy of villi in prox. small bowel
  2. inflammatory infiltrate
  3. carb malabsorption –> osmotic diarrhea
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20
Q

What is immunity for Norovirus?

A

It is short-lived (4 to 6 months) and requires re-exposure to get any type of protection.

Immunity is strain specific, but 50% of adults are immune suggesting high exposure rate

21
Q

What is diagnosis for Norovirus?

A

It is usually only presumptive based on clinical grounds and epidemiological context of outbreaks.

Immune serum can agglutinate particles for EM and PCR can be used for epidemiology.

22
Q

How can rotavirus and norovirus be distinguished clinically?

A

Rotavirus- diarrheal prominent

Norovirus- vomiting prominence

23
Q

What is treatment and prevention of norovirus?

A

Treatment:

  1. rehydration
  2. analgesics, antiemetics

Prevention:

  1. provide uncontaminated food/water
  2. handwashing & disinfection procedures
  3. isolation if necessary

-NO VACCINE-

24
Q

How does prevention of getting rotavirus and norovirus different?

A

Rotavirus has an effective vaccine, norovirus does not

25
Q

Who typically gets viral gastroenteritis from adenovirus?
What is incubation and how long does disease presentation last?
What 2 serotypes cause gastroenteritis?

A

Children in a hospital/institutionalized setting tend to get infected with serotypes 40, 41.

The incubation is about a week and the disease symptoms last 8-12 days

26
Q

Who is typically infected by astrovirus? What is incubation and duration of the illness?

A

Astrovirus affects extremes of life : children and elderly

Incubation is 1-4 days and the disease last 1-4 days

27
Q

What are the major causes of diarrhea in the hospital setting?
What is the most significant?

A
  1. non-infectious vs. infectious
  2. Viral (rotavirus, norovirus)
  3. Antibiotic associated
  4. C. difficile ** this is the most significant bc it has increased morbidity, mortality, hospital stay and healthcare costs
28
Q

How does C. difficile look on gram stain?

A

It is a spore forming gram + rod that is strictly anaerobic.
The rods will be purple with dark spots on the ends (the spores)

29
Q

There are endogenous and exogenous sources of C. difficile. What is meant by this?

What is required for someone to actually get disease from C. difficile?

A
  1. Endogenous- 4% of adults have it in their normal flora (and it can cause problems if it outcompetes)
  2. Exogenous- spores can survive for a long time in the environment.

Presence of the toxin is necessary to cause disease

30
Q

Where are outbreaks likely to occur for:

  1. Rotavirus
  2. norovirus
  3. C. difficile
A
  1. daycares (nursing homes, children’s hospitals)
  2. cruise ships (nursing homes , hospitals)
  3. hospitals, nursing homes, on the shoes hands and clothing of health care workers
31
Q

What is the pathogenesis of CDAD?

A
  1. antibiotic therapy
  2. alteration of colonic microflora
  3. C. difficile exposure and colonization
  4. Release of toxin A and B
  5. Colonic mucosa injury and inflammation
  6. diarrhea
32
Q

What is the biggest risk factor for CDAD?

What are other risk factors?

A

This biggest risk factor is:
Previous or concurrent antibiotic therapy

Other risks:
old age
severity of underlying disease
NG tubes
GI procedures
H2RB and PPI
ICU 
duration of hospital stay
33
Q

What 4 antibiotics have a strong increased risk of developing CDAD?

What 2 have mild association?

A
  1. clindamycin ** notorious for C. difficile
  2. ampicillin
  3. cephalosporin
  4. fluoroquinolone

Mild association: pipercillin and ticarcillin

34
Q

What toxins are associated with C. difficile?
What is their mode of action?
Which is more potent?

A

It has 2 toxins: A and B
They both bind Rho GTP-binding proteins, dysregulate the cytoplasm by depolymerizing actin, round up, detachmrny apoptosis and cytopathic effects

Toxin B is 10x more potent and is a cytotoxin
Toxin A is a cytotoxin AND enterotoxin (causes secretory diarrhea)

35
Q

What is the spectrum of clinical entities of CDAD from least bad to worst?

A
  1. asymptomatic
  2. antibiotic-associated diarrhea
  3. psuedomembranous colitis
  4. toxic megacolon
36
Q

What are three clinical manifestations that should make you think about C. difficile?

A
  1. Elevated peripheral WBC (even before diarrhea)
  2. stool positive for occult blood
  3. stool leukocytes present
37
Q

What symptoms are associated with toxic megacolon?

A
  1. ileus - lack of propulsion
  2. abdominal distension
  3. hypotension
  4. severe pain
  5. radiologic evidence of acute dilation
38
Q

What causes pseudomembranous colitis?
What is the gross pathology?
What is the microscopic pathology?

A

C. difficile has cytopathic effects causing friable red mucosa with ulcerations and hemorrhage.

Gross:
-multiple, elevated whitish-yellow plaques

Microscopic:
mucin, fibrin, PMNs and dead enterocytes

39
Q

How does the patient history differ from CDAD and other antibiotic-associated diarrhea?

A

CDAD- no relevant history of antibiotic intolerance

Other: history of antibiotic intolerance

40
Q

How is the diarrhea different from CDAD and other antibiotic-associated diarrhea?

A

CDAD- colitis, cramps, fever, fecal leukocytes

Other: moderate w/o evidence of colitis

41
Q

What complications are associated with CDAD that are not associated with other antibiotic associated diarrhea?

A

CDAD- psedomembranous colitis, toxic megacolon, hypoalbuminemia, relapses

Other: maybe dehydration

42
Q

When you withdraw implicated antibiotics, what happens if it was CDAD? What happens if it is antibiotic-associated diarrhea from another cause?

A

CDAD- often persists and progresses

Other: usually resolves

43
Q

What drugs are contraindicated for CDAD?

A

antiperistasis drugs

44
Q

What is the current method used at UTSW for diagnosis of C. difficile?
What are the problems with the method?

A

PCR

  1. false + because dead c. difficile will test + but are not secreting toxin
  2. has to be in clinical context
45
Q

What is the treatment for C. difficile?
Which drug is more preferred?
Which drug is used for more severe disease?

A
  1. discontinue antibiotics
  2. oral metronidazole (preferred because cheaper and no vanc resistance)
  3. oral vancomycin - better for more severe disease
46
Q

When is vancomycin given over metronidazole for C. difficile?
How is vancomycin delivered?

A
  1. pregnant
  2. lactating
  3. intolerance to metronidazole
  4. failure to respond to metronidazole after 3-5 days

It must be given orally. IV vancomycin cannot penetrate the gut mucosa to get to the site of infection

47
Q

What are treatments for relapsed or recurrent C. difficile?

A
  1. cholestyramine- binds toxin
  2. probiotics
  3. IVIG to toxin
  4. Stool transplant **
  5. colectomy
48
Q

What are the guidelines for controlling nosocomial C. defficile infection?

A
  1. frequent hand washing with soap and water *** (need to be mechanical so alcohol sanitizer doesnt work)
  2. gloves
  3. cleaning with sporicidal agents
  4. isolation
  5. avoid rectal thermometers
49
Q

What is allowing outbreaks of C. difficile to continue?

A
  1. new strain (NAP1) that has a mutation in a toxin repressor gene leading to constitutive activation
  2. New toxin (binary toxin)

GI, Liver, GallBladder, Pancreas (24 decks)

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