GI 5 Flashcards

1
Q

4 genera of norwalk virus

A

NOROVIRUS, SAPOVIRUS, lagovirus, vesivirus

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2
Q

feature of norwalk virus

A
  • naked, + ssRNA

- amorphous surface with feathery ragged outline

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3
Q

causes 66% of gastroenteritis outbreaks in long term facilities

A

sapovirus (family of calciviridae)

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4
Q

types of patients you see sapovirus

A

children and adults (elderly)

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5
Q

sapovirus is common in older children and adults. why is it becoming popular in children less than 5 years

A

because of vaccination to rotavirus

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6
Q

what time of the year is norovirus common

A

winter

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7
Q

transmission of norwalk virus/norovirus

A

primarily fecal oral route

but can be air and food borne

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8
Q

food is norovirus commonly seen in

A

raw shellfish

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9
Q

pathogenesis of norovirus

A

virus multiplies in the SI –> produces transient lesion of the mucosa –> spares the large intestine –> shed in feces

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10
Q

importance of norovirus sparing the large intestine

A

there is NO FECAL LEUKOCYTES

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11
Q

clinical manifestation of norovirus: include incubation period, duration, and symptoms

A
  • incubation - it is mild and brief so 24-48 hrs
  • duration: lasts 24-60 hours
  • abdominal cramps, myalgias, malaise, headache, nausea, low grade fever & 1-2 days diarrhea
  • fatalities are rare
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12
Q

how do you diagnose norovirus

A
  • mean duration of 12-60hrs
  • mean incubation is 24-48hrs
  • greater than 50% of people with vomiting
  • no bacterial agent previously found
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13
Q

how do you detect norovirus

A

not sensitive so must difficult to culture

-virus peaks in stool at about day 2-5 so you can do RT-qPCR assay

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14
Q

where do you commonly see norovirus outbreaks

A

cruise ships

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15
Q

how do you treat norovirus

A
  • Ligolyte

- 2 doses of IM vaccine taken 3 weeks apart

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16
Q

describe adenovirus

A
  • icosahedral
  • naked ds DNA
  • 12 vertices pentons with fibers on the end
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17
Q

two serotypes of adenovirus

A

40 and 41 (Group F)

18
Q

pathogenesis of adenovirus

A
  • main target is the respiratory tract but infects epithelial cells of pharynx, conjuctiva, SI, and other organs
  • if in SI, it will replicate and present in the stool
19
Q

symptoms of adenovirus

A

diarrhea with or without vomiting

20
Q

features of astrovirus

A

small, naked +ssRNA that has smooth or slight indented outer shell

21
Q

when are people infected with astrovirus

A

throughout the year but peak in the winter

22
Q

feature of Hep A

A

icosahedra, naked +ssRNA

23
Q

how is Hep A virus spread

A

fecal oral route, person to person, poor sanitation, and overcrowding

24
Q

Hep A is the common cause of what condition and what are the first symptoms

A

acute hepatitis
nausea, vomiting, and fever
jaundice comes later on and does not subside until all the other symptoms are gone

25
Q

features of Hep E

A

naked, symmetrical +ssRNA

26
Q

where do you find Hep E and what is its incubation period

A

found in Indian subcontinent

6 weeks which is longer than Hep A

27
Q

what are inflammatory diarrhea

A
– Bacterial
• Shigella spp.
• E. coli (EIEC)
• Salmonella Serotypes
• Campylobacter spp.
• Yersinia spp.
• V. parahaemolyticus & V. vulnificus
• EAEC & STEC (EHEC) (Non invasive organisms - cytotoxin)

– Parasitic
• Entamoeba histolytica
• Balantidium coli

28
Q

what is the symptomology of inflammatory diarrhea

A

bloody diarrhea

29
Q

how do you get the microbes associated with inflammatory diarrhea and what are the type of toxins released

A

food borne infection

release enterotoxin and cytotoxins

30
Q

what are the 4 groups of O antigen of shigella and classify them according to their severity

A

shigella dysenteriae (most severe)
shigella flexneri
shigella boydii
shigella sonnei (mildest form) –> water diarrhea instead of bloody diarrhea

31
Q

what is the virulence factors of shigella

A
  • endotoxin (O antigen)
  • exotoxin: enterotoxin that act as neurotoxin
  • NAD glycohydrolase
32
Q

what does the enterotoxin and NAD glycohydrolase in shigella do

A
  • enterotoxin which acts as a neurotoxin causes meningismus and coma and ulceration
  • NAD glycohydrolase destroys all NAD in human cells hence shutting down metabolism and then cell death
33
Q

what are the clinical manifestation of shigella sonnei and flexneri

A
  • flexneri: severe abdominal pain and dysentery

- sonnei: vomiting and watery diarrhea common

34
Q

pathogenesis of shigellosis

A
  • ingest small amount which invades epithelial and M cells in large intestine via invasive induce endocytosis
  • multiplies in the cytoplasm
  • then spreads to adjacent epithelial cells by actin polymerization –> cell destruction via apoptosis
35
Q

what is bacillary dysentery

A

shigella dysenteriae type 1 (shiga bacillus)

36
Q

what is so important about shigella dysenteriae type 1 (shiga bacillus)

A

the only species to produce the shiga toxin –> which is a cytotoxin that inhibits protein synthesis leading to cell death

37
Q

what does the shiga toxin act as?

A

enterotoxin –> produces diarrhea
exotoxin –> inhibits sugar and AA absorption in SI
neurotoxin –> affects CNS

38
Q

common population that you see the shigellas in

A

shigella sonnei - children less than 5 years in day care
shigella flexneri - men who have sex with other men
shigella boydii - rare

39
Q

pathogenesis of shigella

A

transmitted the fecal oral route: sanitation break downs (4 Fs - fingers, food, flies, feces)

40
Q

treatment of shigella

A

antibiotics
tetracycline - most common
chloramphenicol
ampicillin

41
Q

how do you diagnose shigella

A

take sample of stool or water or food

use MacConkey’s agar or S-S agar (salmonella-shigella agar)

42
Q

what would you see on the S-S agar for shigella – why?

A

it will grow as colorless or pale due to no lactase fermentation

shigella is non motile, gram negative, no fermentation lactose, no utilization of citric acid, no H2S production (except S. flexnieri), no gas from glucose