Gastritis and Viral Gastroenteritis Flashcards

1
Q

Mention important properties of Helicobacter pylori

A
  • Gram-negative rods with comma, S-shaped or spiral-shaped
  • Multiple flagella at one pole & motile
  • Microaerophile
  • Oxidase, catalase & urease positive
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2
Q

How is Helicobacter pylori transmitted?

A
  • Natural habitat :
  • human stomach & probably acquired by ingestion
  • Person to- person transmission
  • clustering of infection within families
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3
Q

Pathogenesis of Helicobacter pylori

A
  • It attaches to mucus-secreting cells of gastric mucosa
  • Production of large amounts of ammonia from urea by organism’s urease, coupled with inflammatory response ———> damage to mucosa
  • Loss of protective mucus coating —> gastritis & peptic ulcer
  • Ammonia neutralizes stomach acid, allowing organism to survive
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4
Q

Clinical findings of Helicobacter pylori

A
  1. Gastritis & peptic ulcer with recurrent pain in upper abdomen + frequently accompanied by bleeding into gastrointestinal tract
  2. stimulate B-cell proliferation & B-cell lymphoma—-> Antibiotic treatment directed against organism often causes tumor to regress
  3. No bacteremia or disseminated disease
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5
Q

How B-cell proliferation & B-cell lymphoma is formed in Helicobacter pylori?

A

H. pylori found in gastric mucosa-associated lymphoid tissue (MALT) lymphomas as chronic inflammation induced by organism ——-> stimulate B-cell proliferation & B-cell lymphoma

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6
Q

Diagnosis of H. pylori by non invasive method

A

Non invasive methods:

  1. Urea breath test:
    * Radiolabeled urea is ingested.
    * If organism is present ——> urease cleave ingested urea —-> radiolabeled CO 2 ——> radioactivity detected in breath
  2. H. pylori stool antigen test:
    * by enzyme-linked immunosorbent Assays
    for initial diagnosis or confirmation of eradication
  3. Serum IgG antibodies against H. pylori:
    * Positive result indicates exposure to H. pylori
    * but can not distinguish between past & current infection
    * Antibodies may still be detected after eradication
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7
Q

Invasive methods (require biopsies) to diagnose H.pylori

A
  1. Gram-stained smears of biopsy specimens of gastric mucosa
  2. Rapid urease test
  3. Histological examination (Gold standard)
  4. Immunohistological staining
  5. Culture
  6. PCR of biopsy samples
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8
Q

How Rapid urease test for H.pylori is done?

A
  • Gastric biopsy placed onto —-> urea containing medium with color indicator
  • If H. pylori is present —> urease rapidly splits urea ( 1-2 hrs) —-> ammonia —-> shift in ph —-> color change
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9
Q

Which stains are used in Histological examination of H.pylori ?

A
  1. Hematoxylin
  2. eosin
  3. modified Giemsa stain or Warthin-Starry silver stain
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10
Q

How H.pylori looks like after a gastric biopsy in the gold standard test ?

A

slender, curved bacilli

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11
Q

Why is Immunohistological staining performed?

A

performed to improve sensitivity & specificity of detection

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12
Q

Which antibodies are stained during Immunohistological staining test ?

A

Monoclonal & polyclonal antibodies

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13
Q

H. pylori requires complex media for growth ; which media/s are used in its culture ?

A
  1. Non selective media :
    * Chocolate, brain heart infusion & brucella agars
    * supplemented with horse or rabbit blood
  2. Selective media :
    * Thayer-Martin agar, Pylori agar &
    Dent’s medium
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14
Q

When culture for H.pylori is performed?

A

Culture is performed when patients are not responding to treatment & susceptibility to antibiotics is needed

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15
Q

When colonies appear & how they look like ?

A

When :

  • Colonies appear in 2 to 5 days*at 37°C
  • with low levels of oxygen (5 -10%) & increased levels of carbon dioxide (5 -12%)

Appearance:
* small (1 to 2 mm in diameter), translucent & nonhemolytic

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16
Q

Which test for H.pylori is limited due to accessibility & cost?

A

PCR

17
Q

What does PCR result provide in diagnosis of H.pylori ?

A

Highly sensitive & specific test provide rapid results & information regarding antibiotic resistance
(e.g., identify specific mutations)

18
Q

Important properties of Norwalk virus ( Caliciviruses; Norovirus)

A
  • Nonsegmented, single-stranded, positive polarity RNA genome
  • Nonenveloped virus with icosahedral nucleocapsid
  • No polymerase within virion
  • Electron microscope : 10 spikes & 32 cup-shaped depressions
  • Six genogroups
  • Genogroup II —-> most human infections
19
Q

Transmission of Norovirus

A
  • Fecal–oral route —-> ingestion of contaminated seafood or water
  • Outbreaks occur in group settings :
    such as cruise ships , schools , hospitals etc
  • Person-to-person transmission occurs in group settings
20
Q

When does the New strains of Norwalk virus appear ?

A

every 2 to 4 years —-> widespread infections

21
Q

What are the features of Norwalk virus that helps it in transmission?

A
  1. Low infectious dose
  2. Excretion of virus in stool :
    * both before onset of symptoms & for several weeks after recovery
  3. Resistance to inactivation by chlorination & drying in environment
  • Infectious for several days in water
  • Uncooked food
  • environmental surfaces such as door handles
22
Q

Infection is limited to which type of cell in Norovirus?

A

mucosal cells of intestinal tract

23
Q

Clinical findings of Norovirus

A
  1. Watery diarrhea :
    * without red cells or white cells
  2. Sudden onset of vomiting & diarrhea
  3. low-grade fever & abdominal cramping
  4. chronic gastroenteritis ( in immunocompromised patients)
  5. signs of central nervous system involvement such as headache, meningismus & photophobia ( in outbreaks)
24
Q

Diagnosis of Norwalk virus

A
  • Diagnosis is clinical.

* Polymerase chain reaction (PCR) test on stool

25
Q

Period of illness in Norovirus

A

Illness lasts 2 to 3 days & no long-term sequelae

26
Q

Important properties of Rotavirus

A
  • 11 segments of double-stranded RNA genome surrounded by double-layered icosahedral capsid
  • RNA-dependent RNA
  • 6 serotypes
  • viral hemagglutinin ( Outer surface protein): type-specific antigen & elicits protective antibody
27
Q

Rotavirus transmission

A

Fecal–oral route

28
Q

Pathogenesis of watery diarrhea in rotavirus

A
  • Rotavirus replicates in mucosal cells of small intestine ——> excess secretion of fluids & electrolytes into bowel lumen —-> loss of salt , glucose & water—-> non-bloody watery diarrhea ( stimulation of enteric nervous system)
  • No inflammation
29
Q

Rotavirus virulence pathogenesis

A
  1. Gene governs tissue tropism

2. Gene controls inhibition of cell RNA & protein synthesis

30
Q

Rotavirus IgA

A
  1. Intestinal IgA :
    * directed against specific serotypes protects against reinfection
  2. Colostrum IgA :
    * protects newborns up to age of 6 months
31
Q

What are the laboratory diagnosis of rotavirus ?

A
  1. Detection of rotavirus in stool:
    * Radioimmunoassay or
    * ELISA
    * Practical approach as there are large numbers of viruses in stool
  2. Demonstration of rotavirus in stool by immunoelectron microscopy :
    * Antibody aggregated viruses, allowing them to be visualized
    * Not practical
  3. Fourfold or greater rise in antibody titer
  4. Culture:
    * not routinely done