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PATH30001 - Mechanisms of Disease > Lecture 4 - Infection - Helicobacter pylori > Flashcards

Lecture 4 - Infection - Helicobacter pylori Flashcards

1
Q

What are the main mechanisms of infectious agents causing disease?

A
  1. Entry
  2. Toxins:
    • exotoxin
    • endotoxin
    • enzymes
  3. Immunopathology
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2
Q

How big are bacteria?

A

Generally

1-15 microns

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3
Q

What are the various organisms that can cause disease in human hosts?

A 
Bacteria
Viruses
Fungi
Parasites
(prions)
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4
Q

What are the ‘non sterile’ areas on our body?

What does this mean?

A 
Our body is largely colonised by micro-organisms
This is our microflora
 • skin
 • gut
 • mouth
 • nose
 • vagina
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5
Q

Under which circumstances will microflora cause disease?

A
  • Antibiotic use wipes out microflora, pathogens can now colonise
  • immunocompromise
  • damage to barriers
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6
Q

What factors determine virulence?

A
  • virulence factors
  • ability to evade immune system
  • ability to spread
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7
Q

What are some barriers to infection?

A 
Mechanical:
 • epithelium
 • flushing (urine, tears)
 • mucociliary elevator
Chemical:
 • lysozyme
 • phospholipase
 • pH
 • surfactant
 • mucous
Normal flora
 • occupying the niche
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8
Q

What are the various sections of the stomach?

A
  • Cardia
  • Fundus
  • Corpus
  • Antrum
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9
Q

What is the function of the cardia of the stomach?

A

Mucous secreting cells

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10
Q

What is the function of the fundus of the stomach?

A

Acid and enzyme secretion

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11
Q

What is the function of the corpus of the stomach?

Why is this significant? Explain the consequences

A

Acid and enzyme secretion

  1. Cardia is inflamed
  2. Decreased acid production
  3. Gastric atrophy
  4. Gastric ulceration
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12
Q

What is the function of the antrum of the stomach?

Why is this significant?

A

Mucin and gastrin secretion

  1. Antrum is inflamed
  2. Increased acid production (because these cells produce gastrin)
  3. Risk of duodenal ulcer
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13
Q

What is the tissue structure of the stomach wall?

A 
Mucosa:
 • Epithelium
 • Lamina propria
 • Muscularis mucosae
 • + Gastric pits

Submucosa

Muscularis propria
• Oblique
• Circular
• Longitudinal

Serosa

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14
Q

Which is the most prevalent stomach cancer?

What is another, less common one?

A

Gastric adenocarcinoma (90%)

Gastric lymphoma (a MALToma, 5%)

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14
Q

How were peptic ulcers treated originally?

How did this fall short, and why?

A

Blockage of gastric acid secretion
(blockage of proton pumps in parietal cells)

Ulcers would return unless acid suppression was continued. This is because the cause was not removed

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14
Q

What is the cause of peptic ulcers?

A

Helicobacter pylori

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14
Q

H. pylori was the first bacterium to be classed as a…

A

carcinogen

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14
Q

What diseases does H. pylori cause?

A
  • peptic ulcer
  • chronic gastritis
  • gastric adenocarcinoma
  • gastric lymphoma
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14
Q

Which countries are most affected by H. pylori infection?

A

Unindustrialised countries

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14
Q

How does H. pylori enter the system?

A

Oral ingestion, usually in childhood

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14
Q

How is H. pylori acid resistant?

A

Urase
• produces basic compounds (ammonia, urea)
• buffers the cytoplasm

14
Q

Where does H. pylori hang out in the stomach?

A

• Adheres to the mucosa
(does not invade)
• In the mucous

14
Q

Why is H. pylori so genetically diverse?

A
  • genetic drift
  • v. competent at transformation
  • high mutation rate
14
Q

What are the virulence determinants of H. pylori?

A

vacA
babA
cagA

14
Q

What is babA?

A

Protein allows adhesion of bacterium to gastric epithelium

14
Q

What is cagA?

A

Gene that codes for a protein that is strongly associated with
• peptic ulcers
• gastric cancer
through biochemical pathways in the host cell

The gene is translocated into the host cell

14
Q

What are some of the effects of the biochemical changes in response to cagA?

A
  • paracellular leakage of gastric mucosa
  • motility
  • apoptosis
  • proliferation
  • cytoskeletal changes
14
Q

Describe very generally the immune response to H. pylori

A

Considerable immune response launched

Ineffective at clearing the infection

14
Q

How does H. pylori avoid immune responses?

A
  • altered PAMPs that aren’t recognised by PRRs

* Inhibit respiratory burst by macrophages

15
Q

(General Question)

What are some important PAMPs in bacteria?

A
  • flagellin

* LPS

16
Q

Describe what happens when H. pylori initially adheres to epithelial cells

A

Cytokine release

→ neutrophil infiltration

17
Q

Who discovered the cause of peptic ulcers?

Why is this important?

A

Dr Barry Marshall and Robin Warren

They challenged the accepted dogma despite criticism, and went on to win a Nobel prize for it

18
Q

What is the symbol for macrophages?

A

Mφ

19
Q

What are the later immune responses to H. pylori infection?

A
  • Adaptive (B and T lymphocyte) induction
  • apoptosis of epithelial cells
  • disruption of mucous layer
  • increased gastrin released, increased acidity
20
Q

Is H. pylori intra- or extracellular?

What does this mean for the immune response?

A

Extracellular
• Humoral response is important
• Th2 is important

21
Q

Why don’t all people with H. pylori get peptic ulcers?

A

• different strains
• different host immune responses
• genetic, environmental cofactors
→ NSAID use, smoking, alcohol

22
Q

H. pylori was the first bacterium to be classed as a…

A

Carcinogen

23
Q

What causes gastritis?

A

Disruption of normal balance between mucosal defences and damaging forces

H. pylori is often responsible for this disruption

24
Q

Gastritis often leads to…

A

Peptic ulcers

26
Q

How can host polymorphisms affect predisposition to cancer?

A 
Polymorphisms in genes for immunity
 • HLA
 • cytokines
etc.
affect the host response, and thus affect predisposition
27
Q

What is vacA?

A

Pore proteins that affect endosomal compartments such as vacuoles

Endosomal compartments, such as the mitochondria.
Leads to release of cytochrome c from the mitochondria → apoptosis

28
Q

How does smoking affect predisposition to peptic ulcer?

A

Impairs mucosal blood flow, and thus impairs the healing process

29
Q

How is H. pylori infection treated nowadays?

A
  • Antibiotics

* proton pump blocker to reduce acidity

30
Q

What defences against infection are there in the stomach?

A

Acid
Proteases
Epithelial & mucous barrier

31
Q

What is a peptic ulcer?

A

Breach of the mucosa

Extends from mucosa through to submucosa or deeper

32
Q

What are the symptoms of a peptic ulcer?

A

Epigastric gnawing

Burning pain

33
Q

Where do peptic ulcers occur?

A

Anywhere in the GIT exposed to gastric acid

34
Q

Why is cure of infection a challenge?

A

• Antibiotic activity is altered at stomach pH

36
Q

Where do H. pylori bacteria all attach?

A

They don’t all attach, but some do attach to the gastric mucosa

40
Q

What are the causal factors of Duodenal ulcers?

What are some other sequelae?

A

Increased acid in duodenal portion of small bowel
This is a result of inflamed antrum (see below)

  1. Inflamed antrum
  2. Increased acid production
  3. Acid in duodenum
  4. Metaplasia of duodenal cells to gastric mucosal cells
  5. The cells can be infected: colonisation of duodenum with H. pylori
51
Q

Why does chemotaxis confer stability in the stomach to H. pylori?

A

It can move to the more pH neutral areas (the mucous)

52
Q

H. pylori only bind to…

A

Gastric mucosa (in the stomach)

PATH30001 - Mechanisms of Disease (34 decks)

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