Helicobacter pylori (H. pylori or HP) is a microaerophilic, flagellated, highly motile, gram-negative spiral bacteria that was first isolated from mucosal biopsies of patients with chronic active gastritis by two Australian investigators, Warren and Marshall, who subsequently received the Nobel Prize in 2005 for their discovery. The organism was first named “Campylobacter pyloris,” then the name was changed to Helicobacter pylori when it was shown genetically that it was not a member of the Campylobacter genus. HP is one of the most common human infectious agents and is causally linked with neutrophilic gastritis, chronic active gastritis, atrophic gastritis, peptic ulcer disease, gastric intestinal metaplasia, gastric adenocarcinoma, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric B-cell lymphoma.

HP infection occurs primarily during childhood and usually persists for life unless the infection is adequately treated. The major risk factor for infection is the socioeconomic status of the family during childhood. The prevalence of HP in the United States has decreased in the white middle- and upper-class population 50 years of age and younger, but the infection is still common among older persons (infected at a younger age), the socially disadvantaged, and the immigrant populations.

HP has been found in water, stool, dental plaque, and saliva. There is strong epidemiologic evidence for waterborne transmission in Peru and Colombia. Primary mode of transmission is person to person, but oral, gastro-oral, and fecal spread is likely.

Acute infection has been demonstrated dramatically by Warren and Marshall, who voluntarily ingested a culture of HP and developed acute HP disease. It is not known how often infection with HP spontaneously clears. In most cases, infection is lifelong. Most infected persons develop chronic active gastritis. Gastritis may be confined mostly to the gastric antrum and/or involve the entire stomach. In
persons with predominately antral involvement, gastric acid secretion may be normal or increased. In such persons, duodenal ulcer and esophagitis secondary to GER may occur. In persons with diffuse HP infection of the entire stomach, gastric atrophy may develop and acid secretion may diminish; in fact, these persons may develop hypoand achlordria and even vitamin B₁₂ deficiency. In advanced cases, intestinal metaplasia and gastric adenocarcinoma may develop. Once patients develop severe atrophy, intestinal HP metaplasia or gastric adenocarcinoma may not be present in these tissues where there is no acid secretion.

Interestingly, in persons treated with proton pump inhibitors (PPIs) chronically, there is usually a shift of HP infection from the antrum to the corpus and accelerated atrophic changes. Thus some experts advise eradication of HP before long-term PPI therapy is instituted in HP-infected individuals.