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Helicobacter pylori

By Levi Clancy for Student Reader on

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Helicobacter pylori secretes urease to maintain a basic/neutral environment. Lophotrichous tufted flagella, powered by a proton gradient, give it motility. Helicobacter pylori is extracellular and does not need to be intracellular to replicate. They have a tuft at one end, and this is mediated by that they are encased in a membrane. The structure of VacA is like a flower petal such that it might almost form a pore but it is unclear what it does with pathogenicity.

  • 1881 & 1893: Spiral organisms found in stomach contents of dogs and other mammals

  • 1938: Spiral organisms first described in human gastric mucosa

  • 1975: First attempts to culture gastric bacteria

  • 1982: Helicobacter pylori cultured and shown to cause ulcers

Helicobacter pylori is associated with gastritis, duodenal and gastric ulcers and gastric adenocarcinomas. Gastric adenocarcinomas are the 14th leading cause of death in the world, and are believed to be the 8th leading cause by 2010. This is largely because infection in the lumen of the stomach is not accessible to immunocytes and macrophages.

90% of duodenal ulcers and 70% of gastric ulcers are Helicobacter pylori positive. Presence of gastritis is a risk factor for duodenal ulces and ulcer relapse. Cure of Helicobacter pylori infection leads to a dramatic reduction in ulcer relapse rate. Addition of antibiotics to acid suppressive therapy increases speed of healing of acute ulcers.

Helicobacter pylori and Human Ulcer Diseases

Ancient association with humans. Believed to be present in human stomachs before. Human migration started ~100,000 years ago. Overlap between genetically distinct H. pylori and human populations.

Developing Countries
  • 80% population colonized

  • Colonization during childhood

  • Parent-child transmission (genotyping)

  • Strains persist and re-infection rare

  • Very low rate of ulcers!

 Industrialized Nations
  • 20-50% population colonized

  • Colonization later in life

  • Transmission between spouses rare

  • Rare childhood infection rate (<20%)

Colonizaiton → immunomodulation → host remodeling → symptoms

1. Oral ingestion
2. Transit of gastric environment
a) Adult stomach pH ~ 1-2
b) Infection occurs in early childhood, higher stomach pH
3. Penetrating gastric mucus
a) Thick (viscous), and sloughing action
4. Attachment
a) Allows bacteria to persist in stomach
5. No competition for H. pylori once established on the mucosal
Route of infectionRoute of infection

Interesting genes of Interesting genes of Helicobacter pyloriHelicobacter pylori