Follow Us

Helicobacter Pylori


Gram negative, helix shaped, microaerophilic bacterium found in the stomach.


To colonize the stomach, must survive the acidic pH of the lumen and use its flagella to burrow into the mucus to reach its niche, close to the stomach's epithelial cell layer.
To avoid being carried into the lumen, H. pylori senses the pH gradient within the mucus layer by chemotaxis and swims away from the acidic contents of the lumen towards the more neutral pH environment of the epithelial cell surface.
It produces adhesins which bind to membrane-associated lipids and carbohydrates and help it adhere to epithelial cells.
H. pylori produce large amounts of the enzyme urease, molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia. The ammonia is converted to ammonium by accepting a proton (H+), which neutralizes gastric acid.
The survival of H. pylori in the acidic stomach is dependent on urease. The ammonia produced is toxic to the epithelial cells and, along with the other products of H. pylori including proteases, vacuolating cytotoxin A (VacA), and certain phospholipases damages those cells.

Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining.
Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances.

Sign and Symptoms

Over 80% of people infected with H. pylori are asymptomatic symptoms.
Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea
Chronic gastritis, the symptoms, if present, is often those of non-ulcer dyspepsia: stomach pains, nausea, and bloating, belching, and sometimes vomiting or black stool.


Blood antibody test, stool antigen test, or with the carbon urea breathe test (in which the patient drinks 14C or 13C labeled urea, which the bacterium metabolizes, producing labeled carbon dioxide that can be detected in the breath)
Most reliable method for detecting H. pylori infection is a biopsy check during endoscopy with a rapid unease test, histological examination, and microbial culture.


The standard first-line therapy is a one week "triple therapy" consisting of proton pump inhibitors such as omeprazole and the antibiotics clarithromycin and amoxicillin
Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin.
There are an increase number of antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies, such as a quadruple therapy, which adds a bismuth colloid, such as bismuth subsalicylate.


The bacterium persists in the stomach for decades in most people. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10–20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers; H. pylori infection is also associated with a 1–2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma.