WEEK 3: Helicobacter pylori and GI disease Flashcards

1
Q

A 45-year-old male from Sudan, the eldest among 5 siblings’ complaints of gnawing or burning pain in the epigastrium for past 6-8 months is seen by a gastroenterologist.

This pain typically occurs when the stomach is empty, between meals and in the early morning hours.

It last from minutes to hours and may be relieved by eating or by taking antacids.

Sometimes he has nausea, vomiting sometimes blood stained, and loss of appetite.

Differential diagnosis?

A

*Gastritis
*Peptic ulcer
*Gastro-esophageal reflux
*Gastric cancer
*Biliary tract disease.
*Food poisoning
*Gastroenteritis

Severe pain
*Perforated or penetrating ulcer
*Pancreatitis

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2
Q

No history of NSAID use.
An endoscopy was done, ulcer noticed, and a gastric biopsy was performed.
Culture- using enriched medium

Describe the culture process for the stomach.

A

Enriched medium: Chocolate agar

  1. This tissue was cultured on Chocolate agar
  2. Incubated in microaerophilic conditions (5% O₂ , 10% CO₂)
  3. At 37⁰C for 5 days.
  4. Colonies appeared by the 5th day.
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3
Q

What is Gram staining for helicobacter pylori?

A

Gram negative curved rods were observed.

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4
Q

Describe Biochemical test for Helicobacter Pylori.

A
  1. TSI-Sugars not fermented
    H₂S not produced
  2. Oxidase positive
  3. Urease positive
  4. Catalase positive
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5
Q

Discuss microbiological characters of Helicobacter pylori.

A
  1. Small Helical (spiral or curved) (0.5-1.0 um X 2.5-5.0 um
  2. Highly motile-rapid cork screw motion
  3. Multiple polar sheathed flagella
  4. Microaerophilic
  5. Gram negative rods (Giemsa, Silver, Acridine stains)
  6. Culture in blood or serum enriched medium and selective medium like Skirrow’s medium.
  7. Colonies visible after 48-72 hours.
  8. Cells become rod-like and coccoid on prolonged culture

NOTE: “Microaerophilic” refers to an organism or microorganism that requires or thrives in environments with low oxygen levels.

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6
Q

Outline clinical features of Helicobacter pylori.

A

Colonization usually asymptomatic.

The most common ulcer symptom is
*Gnawing or burning pain in the epigastrium.
This pain typically occurs when the stomach is empty, between meals and in the early morning hours..

*Less common ulcer symptoms include nausea, vomiting, and loss of appetite.

*Bleeding can also occur
Prolonged bleeding may cause anemia leading to weakness and fatigue.

*hematemesis, melena.

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7
Q

Outline endoscopic tests for Helicobacter pylori.

A
  1. Culture
  2. Urease test
  3. PCR
  4. Histology
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8
Q

Outline non-endoscopic tests for Helicobacter pylori.

A
  1. Urea breath test
  2. Antibody testing
  3. Fecal antigen test
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9
Q

Describe Worldwide prevalence of H. pylori infection.

A

Infection rates in percent. H. pylori infection is highly prevalent in Africa, Asia, and South America
3.6 billion people infected.

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10
Q

Describe EPIDEMIOLOGY OF Helicobacter pylori.

A

Isolated from humans all over the world

Sole reservoir- Human

High prevalence and incidence of colonization

Estimated 50-60% of the world population is infected

Suboptimal sanitary condition (institutions for the mentally retarded and orphanages)

Clusters in family. Associated with large family size and older siblings.

Isolated from the feces in children, dental plaque

Associated with severe inflammation, peptic ulcer disease and gastric cancer

H.pylori listed as Class 1 carcinogen by WHO.

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11
Q

State the mode of transmission of Helicobacter pylori.

A

Person to Person Transmission
*Fecal-oral
*Oral-oral
*Gastro-oral

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12
Q

Outline 3 main increased risk of infection of Helicobacter pylori.

A

Younger age
Underdeveloped countries
Lower socioeconomic status

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13
Q

State the different Helicobacter species found in human beings.

A
  1. Helicobacter pylori: Human stomach
  2. Helicobacter cinnaedi and H. fenneliae: Human intestine
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14
Q

Colonize human intestinal tract
Isolated from homosexual men with proctitis, proctocolitis, enteritis, and bacteremia and are often transmitted through sexual practices

Name the helicobacter species.

A

Helicobacter cinnaedi and fenneliae

NOTE:
*Proctitis is the inflammation of the rectum.
* Proctocolitis refers to the inflammation of both the rectum and the colon.
*Enteritis is the inflammation of the small intestine.
*Bacteremia is the presence of bacteria in the bloodstream.

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14
Q

Discuss Virulence Factors of Helicobacter.

A
  1. Urease: Neutralize gastric acid,
  2. Lipopolysaccharides: They adhere to the host cells and cause inflammation
  3. Outer proteins: They adhere to the host cell.
  4. Flagella: Allows for motility and chemotaxis.
  5. Exotoxins: Vacuolating toxin: Induce gastric mucosal immunity
  6. Secretory enzymes: Mucinase, protease, lipase: Cause gastric mucosal injury
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15
Q

The VacA protein influences cellular processes via different routes, thus assisting in chronic colonization of the gastric mucosa by H. pylori.

Describe them.

A

(1) Surface-bound VacA may be directly delivered to the cell membrane. Secreted VacA may either

(2) bind to a cell membrane receptor and initiate a proinflammatory response,

(3) be taken up directly by the cell and be trafficked to the mitochondria and induce apoptosis,

(4) be taken up by pinocytosis and induce vacuolization,

(5) form a membrane channel, resulting in leakage of nutrients to the extracellular space, or

(6) pass through the tight junctions and inhibit T-cell activation and proliferation. ‏

16
Q

Outline factors contributing to gastric pathology and disease outcome in H. pylori infection.

A
  1. Smoking, alcohol, NSAIDS, PPI result in Low gastric acid which in turn causes Pangastritis and consequently atrophic gastritis and cancer.

NOTE: Pangastritis is a medical term used to describe inflammation affecting the entire stomach lining.

  1. Helicobacter virulence factors can cause Chronic gastritis.
  2. High acid production result in antral predominant gastritis which then results in Peptic ulcer disease.
17
Q

Discuss the Timeline of disease progression in H. pylori-infected persons.

A

All infected individuals develop a superficial gastritis within the first weeks of infection, followed by a chronic active gastritis which develops after months or years.

After decades, patients can develop antral gastritis or pangastritis, depending on the localization of the infection.

The antral inflammation can lead to gastric metaplasia, which supports the growth of duodenal ulcer.

The latter can lead to atrophy and intestinal metaplasia, two prerequisites for the development of gastric cancer or gastric ulcer.

In contrast, constant chronic active gastritis can lead to the growth of MALT lymphomas.

18
Q

Discuss Factors influencing development of clinical disease.

A
  1. Bacterial factors
    cag pathogenicity island
    vacuolating toxin
  2. Host factors
    Gastric acidity
    Immune responses
  3. Environmental factors
    Gender
    Smoking
19
Q

State the beneficial effects of Helicobacter pylori.

A

Decreases the risk of
*Gastroesophageal reflux disease
*Barrett’s oesophagus
*Adenocarcinoma of Oesophagus
*Childhood asthma
*Allergic rhinitis
*Eczema (atopic dermatitis)
*Skin allergies

20
Q

Outline factors that result in decreased incidence of Helicobacter pylori infection.

A

Developed countries
Smaller family sizes
Decreased crowding
Improved sanitation
Widespread use of antibiotics