Helicobacter pylori infection overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Yamuna Kondapally, M.B.B.S[3]
Overview
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.
Historical Perspective
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.
Pathophysiology
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]
Causes
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.
Differential Diagnosis
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.
Epidemiology and Demographics
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]
Risk Factors
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.
Screening
According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for H. pylori infection.
Natural history, Complications, and Prognosis
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]
Diagnosis
History and Symptoms
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.
Physical Examination
Common physical examination findings associated with H. pylori infection include fatigue, abdominal pain, conjunctival pallor and abdominal tenderness.
Diagnostic Tests
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.
Electrocardiogram
There are no ECG findings associated with H. pylori infection.
X Ray
There are no X ray findings associated with H. pylori infection.
CT
There are no CT findings associated with H. pylori infection.
MRI
There are no MRI findings associated with H. pylori infection.
Ultrasound
There are no ultrasound findings associated with H. pylori infection.
Other Diagnostic Tests
There are no other diagnostic studies associated with H. pylori infection.
Treatment
Medical Therapy
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.
Surgery
Surgical intervention is not recommended for the management of H. pylori infection.
Primary Prevention
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).
Secondary Prevention
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.
References
- ↑ Snow JA, Hatzios SK, Salama NR (2026). "Managing dangerous liaisons: lessons from Helicobacter pylori for understanding bacterial carcinogenesis". J Bacteriol. doi:10.1128/jb.00457-25. PMC 12918743 Check
|pmc=value (help). - ↑ Fock KM, Graham DY, Malfertheiner P (2013). "Helicobacter pylori research: historical insights and future directions". Nat Rev Gastroenterol Hepatol. 10 (8): 495–500. doi:10.1038/nrgastro.2013.96. PMC 3973742. PMID 23752823.
- ↑ 3.0 3.1 3.2 3.3 3.4 Malfertheiner P, Camargo MC, El-Omar E, Liou JM, Peek R, Schulz C, Smith SI, Suerbaum S (2023). "Helicobacter pylori infection". Nat Rev Dis Primers. 9 (1): 19. doi:10.1038/s41572-023-00431-8. PMID 37081005 Check
|pmid=value (help). - ↑ 4.0 4.1 Sundar R, Nakayama I, Markar SR, Shitara K, van Laarhoven HWM; et al. (2025). "Gastric cancer". Lancet. 405 (10494): 2087–2102. doi:10.1016/S0140-6736(25)00052-2.
- ↑ Duan Y, Xu Y, Dou Y, Xu D (2025). "Helicobacter pylori and gastric cancer: mechanisms and new perspectives". J Hematol Oncol. 18 (1): 10. doi:10.1186/s13045-024-01654-2.
- ↑ Wizenty J, Sigal M (2025). "Helicobacter pylori, microbiota and gastric cancer — principles of microorganism-driven carcinogenesis". Nat Rev Gastroenterol Hepatol. 22 (5): 296–313. doi:10.1038/s41575-025-01042-2.
- ↑ De Falco M, Lucariello A, Iaquinto S; et al. (2015). "Molecular mechanisms of Helicobacter pylori pathogenesis". J Cell Physiol. 230 (8): 1702–7. doi:10.1002/jcp.24933.
- ↑ 8.0 8.1 Crowe SE (2019). "Helicobacter pylori infection". N Engl J Med. 380 (12): 1158–1165. doi:10.1056/NEJMcp1710945. PMID 30893536.
- ↑ Chen YC, Malfertheiner P, Yu HT, Kuo CL, Chang YY, Meng FT, Wu YX, Hsiao JL, Chen MJ, Lin KP, Wu CY, Lin JT, O'Morain C, Megraud F, Lee WC, El-Omar EM, Wu MS, Liou JM (2024). "Global Prevalence of Helicobacter pylori Infection and Incidence of Gastric Cancer Between 1980 and 2022". Gastroenterology. 166 (4): 605–619. doi:10.1053/j.gastro.2023.12.022. PMID 38176660 Check
|pmid=value (help). - ↑ Chey WD, Howden CW, Moss SF, Morgan DR, Greer KB, Grover S, Shah SC (2024). "ACG Clinical Guideline: Treatment of Helicobacter pylori Infection". Am J Gastroenterol. 119 (9): 1730–1753. doi:10.14309/ajg.0000000000002968. PMID 39626064 Check
|pmid=value (help). - ↑ Shah SC, Halvorson AE, Lee D, Bustamante R, McBay B, Gupta R, Denton J, Dorn C, Wilson O, Peek R Jr, Gupta S, Liu L, Hung A, Greevy R, Roumie CL (2024). "Helicobacter pylori Burden in the United States According to Individual Demographics and Geography: A Nationwide Analysis of the Veterans Healthcare System". Clin Gastroenterol Hepatol. 22 (1): 42–50.e26. doi:10.1016/j.cgh.2023.05.016. PMC PMC11552088 Check
|pmc=value (help). PMID 37245717 Check|pmid=value (help). - ↑ Suerbaum S, Michetti P (2002). "Helicobacter pylori infection". N Engl J Med. 347 (15): 1175–86. doi:10.1056/NEJMra020542. PMID 12374879.
- ↑ Kusters JG, van Vliet AH, Kuipers EJ (2006). "Pathogenesis of Helicobacter pylori infection". Clin Microbiol Rev. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
- ↑ Ford AC, Yuan Y, Moayyedi P (2020). "Helicobacter pylori eradication therapy to prevent gastric cancer: systematic review and meta-analysis". Gut. 69 (12): 2113–2121. doi:10.1136/gutjnl-2020-320839. PMID 32205420 Check
|pmid=value (help). - ↑ Moss SF, Shah SC, Tan MC, El-Serag HB (2024). "Evolving concepts in Helicobacter pylori management". Gastroenterology. 166 (2): 267–283. doi:10.1053/j.gastro.2023.09.047. PMID 37806461 Check
|pmid=value (help).