Helicobacter pylori infection is caused by H. pylori which is a gram-negative, microaerophilic, and acidophilic bacterium that infects various areas of the stomach and duodenum. It is one of the most common bacterial infections in humans. It is associated with many gastrointestinal diseases like gastritis, peptic ulcer disease, adenocarcinoma and MALT lymphoma.

Helicobacter pylori was first cultured in April 1982 by pathologist J. Robin Warren and clinical fellow Barry J. Marshall at Royal Perth Hospital, Australia. Their work overturned the long-held view that the stomach was sterile and that peptic ulcer disease was caused by acid, stress, and diet.^[1][2] The findings were published in The Lancet in 1983 and 1984. Causation was then supported by Marshall’s 1984 self-ingestion experiment and by 1990 trials showing that eradication cures duodenal ulcer. Two watershed events followed in 1994: the NIH recommended antibiotic therapy for infected ulcer patients, and the International Agency for Research on Cancer (IARC) classified H. pylori as a group 1 human carcinogen. Warren and Marshall received the Nobel Prize in Physiology or Medicine in 2005.

The precise mode of transmission of Helicobacter pylori is most likely considered to be through fecal-oral and oral-oral routes, largely through intrafamilial spread (particularly mother-to-child). H. pylori is a noninvasive organism. It is found within the mucus layer overlying surface epithelial cells and also deep within gastric glands, where it interacts with gland base stem/progenitor cells. It colonizes gastric-type epithelium only; it does not colonize normal squamous esophagus or normal duodenal mucosa, but can colonize foci of gastric metaplasia. Chronic infection is the strongest risk factor for non-cardia gastric adenocarcinoma and drives gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Pathogenesis of H. pylori infection depends on bacterial, host and environmental factors.

Helicobacter pylori colonization produces gastritis in essentially all infected individuals. Without eradication, chronic–active gastritis persists for life. In a minority of patients it progresses over decades along the Correa cascade: non-atrophic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → intestinal-type gastric adenocarcinoma.^[3][4][5] Several factors determine the outcome of infection:

• Bacterial virulence, mainly the cag pathogenicity island (cag PAI) with CagA, ADP-heptose, and the VacA genotype.
• The host immune response, which is vigorous but ineffective.
• The gastric microenvironment, including the gastric microbiota.^[3][6]

The anatomic distribution of gastritis predicts the dominant complication:

• Antral-predominant gastritis leads to duodenal ulcer.
• Corpus-predominant or multifocal atrophic gastritis leads to gastric ulcer and gastric cancer.^[4][7]

Persistent antigenic stimulation induces mucosa-associated lymphoid tissue (MALT), from which gastric MALT lymphoma can arise.^[3]

Helicobacter pylori is a gram-negative, microaerophilic, and acidophilic bacterium that infects various areas of the stomach and duodenum. Many cases of peptic ulcers, gastritis, duodenitis, and perhaps some cancers are caused by H. pylori infections. However, many who are infected do not show any symptoms of disease. Helicobacter spp. are the only known microorganisms that can thrive in the highly acidic environment of the stomach. H. pylori‘s helical shape (from which the genus name is derived) is thought to have evolved to penetrate and favor its motility in the mucus gel layer.

Helicobacter pylori infection must be differentiated from other diseases that cause nausea, vomiting, abdominal pain, epigastric pain and unexplained weight loss such as atrophic gastritis, GERD, gastrinoma, peptic ulcer disease, gastric adenocarcinoma, stress-induced gastritis and non-Hodgkin’s lymphoma.

H. pylori is one of the most common chronic bacterial infections in humans. It is usually acquired in early childhood and persists for life unless treated.^[8][3] Global adult prevalence fell from 52.6% before 1990 to 43.9% during 2015–2022. Prevalence in children and adolescents has stayed at about 35% and has not declined significantly in any WHO region.^[9] In North America, prevalence is estimated at 30%–40%. Infection is more common in non-White racial and ethnic groups, in people raised in crowded or poor sanitary conditions, and in early-generation immigrants from endemic regions.^[10] In the largest contemporary US cohort, positivity was highest in non-Hispanic Black and Hispanic individuals and lowest in non-Hispanic White individuals.^[11]

Common risk factors in the development of H. pylori infection are contaminated food and water, poor hygiene, overcrowding, lower socio-economic status, smoking, age, and race.

According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for H. pylori infection.

H. pylori infection is usually acquired in childhood and, if it is not treated, persists for life. Almost every colonized person develops chronic active gastritis, although most remain asymptomatic.^[3][8] The pattern of gastritis largely determines the long-term outcome:

• Antral-predominant gastritis predisposes to duodenal ulcer.
• Corpus-predominant or atrophic gastritis predisposes to gastric ulcer, intestinal metaplasia, and non-cardia gastric adenocarcinoma.^[12]

The major complications are peptic ulcer disease (lifetime risk about 10–20%), distal gastric adenocarcinoma (about 1–2%), and gastric MALT lymphoma (<1%).^[13] Overall prognosis is favorable. Confirmed eradication cures most ulcer disease, lowers gastric cancer incidence and mortality, and induces remission in most patients with early-stage gastric MALT lymphoma. Residual cancer risk persists when atrophy or intestinal metaplasia is already established.^[14][15]

Specific areas of focus when obtaining a history from the patient include history of nausea, vomiting, epigastric pain or abdominal pain, bloating, gastrointestinal bleeding, anorexia, weight loss, pallor, a positive history of GI diseases or H. pylori infection, history of medication use (NSAIDS) and food and drinking water hygiene. Majority of patients infected are asymptomatic. Symptoms of H. pylori infection include halitosis, nausea, vomiting, epigatric or abdominal pain, bloating, belching, dark or tarry like stools (melena), fatigue, diarrhea and unexplained weight loss.

Common physical examination findings associated with H. pylori infection include fatigue, abdominal pain, conjunctival pallor and abdominal tenderness.

In developed countries, the use of test and treat strategy is declining for younger patients presenting with dyspepsia. In developing countries, as the rates of ulcer or gastric cancer are high, the more appropriate initial approach in the diagnosis of H. pylori infection in developing countries are an empirical test-and-treat approach or initial endoscopy.

Endoscopic Tests

Endoscopic diagnostic tests are biopsy-based diagnostic methods for H. pylori infection. These include histology, rapid urease testing, culture and polymnerase chain reaction (PCR).

Nonendoscopic Tests

The nonendoscopic diagnostic testing methods for H. pylori include antibody tests, urea breath test, and fecal antigen test.

There are no ECG findings associated with H. pylori infection.

There are no X ray findings associated with H. pylori infection.

There are no CT findings associated with H. pylori infection.

There are no MRI findings associated with H. pylori infection.

There are no ultrasound findings associated with H. pylori infection.

There are no other diagnostic studies associated with H. pylori infection.

Indications for treatment of H. pylori infection include past or present duodenal and/or gastric ulcer, with or without complications, following resection of gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, atrophic gastritis, dyspepsia, patients with first-degree relatives with gastric cancer and patient‘s wishes. Factors involved in choosing treatment regimens include prevalence of H. pylori infection, prevalence of gastric cancer, resistance to antibiotics, availability of bismuth, availability of endoscopy and H. pylori tests, ethnicity, drug allergies and tolerance, previous treatments and outcome, adverse effects, effectiveness of local treatment and recommended dosages and treatment duration.

Surgical intervention is not recommended for the management of H. pylori infection.

Effective measures for primary prevention of the H. pylori infection include hand washing (antibacterial soaps), avoid contaminated food and water, maintain proper hygiene (hand sanitizers, antiseptic washes) and avoid close contact with infected family members ( e.g., kissing, by sharing eating utensils and drinking glasses).

The secondary prevention strategies following H. pylori infection to prevent recurrence of peptic ulcer disease and gastric cancer include the use of antbiotics to prevent recurrence of infection and the post treatment confirmation of H. pylori eradication after treatment using diagnostic tests.