Helicobacter

Helicobacter pylori

Characteristics/Epidemiology

Ability to colonise the stomach

Colonise gastric mucosal cells, and metaplastic gastric epithelium in the duodenum or oesophagus.

Found in >95% of duodenal ulcer and almost all gastric ulcers who are not taking anti-inflammatory drugs or aspirin.

Pathogenesis/Transmission

Transmission - person to person

Infection tend to be chronic if untreated.

H. pylori penetrate the mucus lining (attracted to hemin and urea)

   -> Activate inflammatory cells

   -> Release urease -> converts urea to ammonia

      -> Neutralise acid

   -> Cytotoxin and ammonia released

      -> Cause destruction of mucus producing cells

      -> Underlying tissues exposed to acid

Clinical significance

Diseases:

• Acute gastritis
• Duodenal ulcer
• Gastric ulcer

Risk factor for development of:

• Gastric carcinoma
• Gastric B-cell lymphoma

Laboratory identification

Microscopic/biochemical characteristics

• Curved/spiral
• Corkscrew motility
• Microaerophilic
• Produce urease

Serologic test (ELISA for serum antibodies to H. pylori)

Breath test for urease

Endoscopy + biopsy

Treatment

Combination drug: tetracycline+metronidazole+bismuth

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Things to revise/add later:

Bibliography:

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