What is the pathophysiology of acute bacterial gastritis?

Updated: Jun 13, 2019
  • Author: Mohammad Wehbi, MD; Chief Editor: BS Anand, MD  more...
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Answer

Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H pylori is the most common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The prevalence of H pylori in otherwise healthy individuals varies depending on age, socioeconomic class, and country of origin. The infection is usually acquired in childhood. In the Western world, the number of people infected with H pylori increases with age.

Evidence of H pylori infection can be found in 20% of individuals younger than 40 years and in 50% of individuals older than 60 years. How the bacterium is transmitted is not entirely clear. Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food. This is why the prevalence is higher in lower socioeconomic classes and in developing countries. H pylori is associated with 60% of gastric ulcers and 80% of duodenal ulcers.

H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis.

The acute gastritis encountered with H pylori is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease, an enzyme that catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection.

H pylori also has flagella that enable it to move and help it to penetrate the mucous layer so that it comes into contact with the gastric epithelial cells. It also has several adhesion molecules that help it to adhere to these cells. It produces inflammation by activating a number of toxins and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause acute gastritis.

Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic superficial gastritis. The infection is established within a few weeks after the primary exposure to H pylori. It produces inflammation via the production of a number of toxins and enzymes. The intense inflammation can result in the loss of gastric glands responsible for the production of acid. This is referred to as atrophic gastritis. Consequently, gastric acid production drops. The virulence genotype of the microbe is an important determinant for the severity of the gastritis and the formation of intestinal metaplasia, the transformation of gastric epithelium. This transformation can lead to gastric cancer.


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