Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Bacteriology and epidemiology of Helicobacter pylori infection

Section Editor
Mark Feldman, MD, MACP, AGAF, FACG
Deputy Editor
Shilpa Grover, MD, MPH, AGAF


Gastric organisms were first observed more than 100 years ago and their association with gastritis has been recognized since the 1970s [1]. The true implication of these microbes was not fully realized, however, until 1982 when Marshall and Warren identified and subsequently cultured the gastric bacterium, Campylobacter pyloridis, later reclassified as Helicobacter pylori (H. pylori) [2]. This organism is now known to cause chronic gastritis, most peptic ulcers, and gastric adenocarcinoma and lymphoma. (See appropriate topic reviews.)

The bacteriology and epidemiology of H. pylori will be reviewed here. Understanding its bacteriology and the unique features that enable it to survive in an environment as hostile as the stomach are important in appreciating how H. pylori causes tissue injury and clinical disease (see "Pathophysiology of and immune response to Helicobacter pylori infection"). The epidemiology of this infection sheds light on the geographic, ethnic, and racial differences in prevalence of H. pylori-associated diseases and the changing incidence of these conditions throughout the world.


Microbiology — H. pylori is a spiral shaped, microaerophilic, gram negative bacterium measuring approximately 3.5 microns in length and 0.5 microns in width (picture 1). In vitro, it is a slow growing organism that can be cultured on blood agar or selective media such as Skirrow's media incubated at 37ºC in a 5 percent oxygen atmosphere for three to seven days [3]. Small, uniformly sized, translucent bacterial colonies form and the organisms can be morphologically characterized by Gram stain and their typical spiral or rod shaped appearance. High power microscopy reveals that the organism has two to seven unipolar sheathed flagella which enhance its mobility through viscous solutions.

If the growth environment is less than ideal, coccoid forms of H. pylori can occasionally be seen in culture [3]. These coccoid forms are thought to represent an adaptation to hostile surroundings; they appear to be more resistant and may enable the organism to survive for periods of time outside the human host in feces or in drinking water.

In addition to morphologic characterization, the organism can be biochemically characterized as catalase, oxidase, and urease positive. Urease appears to be vital for its survival and colonization; it is produced in abundance, making up more than 5 percent of the organism's total protein weight. Bacterial urease activity is clinically important because it forms the basis for several invasive and noninvasive tests to diagnose infection. (See "Indications and diagnostic tests for Helicobacter pylori infection".)

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: May 11, 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Marshall BJ. History of the discovery of C. pylori. In: Campylobacter Pylori in Gastritis and Peptic Ulcer Disease, Blaser MJ (Ed), Igaku-Shoin, New York 1989. p.7.
  2. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 1:1311.
  3. Goodwin CS, Worsley BW. Microbiology of Helicobacter pylori. Gastroenterol Clin North Am 1993; 22:5.
  4. Amieva MR, El-Omar EM. Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology 2008; 134:306.
  5. Mobley HL. Defining Helicobacter pylori as a pathogen: strain heterogeneity and virulence. Am J Med 1996; 100:2S.
  6. Rain JC, Selig L, De Reuse H, et al. The protein-protein interaction map of Helicobacter pylori. Nature 2001; 409:211.
  7. Ernst PB, Peura DA, Crowe SE. The translation of Helicobacter pylori basic research to patient care. Gastroenterology 2006; 130:188.
  8. Mobley HL. The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration. Aliment Pharmacol Ther 1996; 10 Suppl 1:57.
  9. Weeks DL, Eskandari S, Scott DR, Sachs G. A H+-gated urea channel: the link between Helicobacter pylori urease and gastric colonization. Science 2000; 287:482.
  10. Kawakubo M, Ito Y, Okimura Y, et al. Natural antibiotic function of a human gastric mucin against Helicobacter pylori infection. Science 2004; 305:1003.
  11. Logan RP. Adherence of Helicobacter pylori. Aliment Pharmacol Ther 1996; 10 Suppl 1:3.
  12. Wadström T, Hirmo S, Borén T. Biochemical aspects of Helicobacter pylori colonization of the human gastric mucosa. Aliment Pharmacol Ther 1996; 10 Suppl 1:17.
  13. Cave DR. Transmission and epidemiology of Helicobacter pylori. Am J Med 1996; 100:12S.
  14. Pounder RE, Ng D. The prevalence of Helicobacter pylori infection in different countries. Aliment Pharmacol Ther 1995; 9 Suppl 2:33.
  15. Linz B, Balloux F, Moodley Y, et al. An African origin for the intimate association between humans and Helicobacter pylori. Nature 2007; 445:915.
  16. Torres J, Leal-Herrera Y, Perez-Perez G, et al. A community-based seroepidemiologic study of Helicobacter pylori infection in Mexico. J Infect Dis 1998; 178:1089.
  17. Smoak BL, Kelley PW, Taylor DN. Seroprevalence of Helicobacter pylori infections in a cohort of US Army recruits. Am J Epidemiol 1994; 139:513.
  18. Everhart JE, Kruszon-Moran D, Perez-Perez GI, et al. Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States. J Infect Dis 2000; 181:1359.
  19. Parsonnet J. The incidence of Helicobacter pylori infection. Aliment Pharmacol Ther 1995; 9 Suppl 2:45.
  20. Rowland M, Daly L, Vaughan M, et al. Age-specific incidence of Helicobacter pylori. Gastroenterology 2006; 130:65.
  21. Parsonnet J, Shmuely H, Haggerty T. Fecal and oral shedding of Helicobacter pylori from healthy infected adults. JAMA 1999; 282:2240.
  22. Perry S, de la Luz Sanchez M, Yang S, et al. Gastroenteritis and transmission of Helicobacter pylori infection in households. Emerg Infect Dis 2006; 12:1701.
  23. Hunt RH, Sumanac K, Huang JQ. Review article: should we kill or should we save Helicobacter pylori? Aliment Pharmacol Ther 2001; 15 Suppl 1:51.
  24. Webb PM, Knight T, Greaves S, et al. Relation between infection with Helicobacter pylori and living conditions in childhood: evidence for person to person transmission in early life. BMJ 1994; 308:750.
  25. Kivi M, Johansson AL, Reilly M, Tindberg Y. Helicobacter pylori status in family members as risk factors for infection in children. Epidemiol Infect 2005; 133:645.
  26. Nouraie M, Latifi-Navid S, Rezvan H, et al. Childhood hygienic practice and family education status determine the prevalence of Helicobacter pylori infection in Iran. Helicobacter 2009; 14:40.
  27. Zajacova A, Dowd JB, Aiello AE. Socioeconomic and race/ethnic patterns in persistent infection burden among U.S. adults. J Gerontol A Biol Sci Med Sci 2009; 64:272.
  28. Asaka M, Kimura T, Kudo M, et al. Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. Gastroenterology 1992; 102:760.
  29. Tsugane S, Tei Y, Takahashi T, et al. Salty food intake and risk of Helicobacter pylori infection. Jpn J Cancer Res 1994; 85:474.
  30. Fox JG, Dangler CA, Taylor NS, et al. High-salt diet induces gastric epithelial hyperplasia and parietal cell loss, and enhances Helicobacter pylori colonization in C57BL/6 mice. Cancer Res 1999; 59:4823.
  31. Lee SA, Kang D, Shim KN, et al. Effect of diet and Helicobacter pylori infection to the risk of early gastric cancer. J Epidemiol 2003; 13:162.
  32. Machida-Montani A, Sasazuki S, Inoue M, et al. Association of Helicobacter pylori infection and environmental factors in non-cardia gastric cancer in Japan. Gastric Cancer 2004; 7:46.
  33. Graham DY, Malaty HM, Evans DG, et al. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States. Effect of age, race, and socioeconomic status. Gastroenterology 1991; 100:1495.
  34. Malaty HM, Engstrand L, Pedersen NL, Graham DY. Helicobacter pylori infection: genetic and environmental influences. A study of twins. Ann Intern Med 1994; 120:982.
  35. Riccardi VM, Rotter JI. Familial Helicobacter pylori infection. Societal factors, human genetics, and bacterial genetics. Ann Intern Med 1994; 120:1043.
  36. Mégraud F. Transmission of Helicobacter pylori: faecal-oral versus oral-oral route. Aliment Pharmacol Ther 1995; 9 Suppl 2:85.
  37. Fox JG. Non-human reservoirs of Helicobacter pylori. Aliment Pharmacol Ther 1995; 9 Suppl 2:93.
  38. Handt LK, Fox JG, Dewhirst FE, et al. Helicobacter pylori isolated from the domestic cat: public health implications. Infect Immun 1994; 62:2367.
  39. Dore MP, Sepulveda AR, El-Zimaity H, et al. Isolation of Helicobacter pylori from sheep-implications for transmission to humans. Am J Gastroenterol 2001; 96:1396.
  40. Dore MP, Bilotta M, Vaira D, et al. High prevalence of Helicobacter pylori infection in shepherds. Dig Dis Sci 1999; 44:1161.
  41. Hulten K, Han SW, Enroth H, et al. Helicobacter pylori in the drinking water in Peru. Gastroenterology 1996; 110:1031.
  42. Bellack NR, Koehoorn MW, MacNab YC, Morshed MG. A conceptual model of water's role as a reservoir in Helicobacter pylori transmission: a review of the evidence. Epidemiol Infect 2006; 134:439.
  43. Queralt N, Bartolomé R, Araujo R. Detection of Helicobacter pylori DNA in human faeces and water with different levels of faecal pollution in the north-east of Spain. J Appl Microbiol 2005; 98:889.
  44. Goodman KJ, Correa P, Tenganá Aux HJ, et al. Helicobacter pylori infection in the Colombian Andes: a population-based study of transmission pathways. Am J Epidemiol 1996; 144:290.
  45. Thomas JE, Gibson GR, Darboe MK, et al. Isolation of Helicobacter pylori from human faeces. Lancet 1992; 340:1194.
  46. Malaty HM, Graham DY, Klein PD, et al. Transmission of Helicobacter pylori infection. Studies in families of healthy individuals. Scand J Gastroenterol 1991; 26:927.
  47. Goodman KJ, Correa P. Transmission of Helicobacter pylori among siblings. Lancet 2000; 355:358.
  48. Bamford KB, Bickley J, Collins JS, et al. Helicobacter pylori: comparison of DNA fingerprints provides evidence for intrafamilial infection. Gut 1993; 34:1348.
  49. Vincent P, Gottrand F, Pernes P, et al. High prevalence of Helicobacter pylori infection in cohabiting children. Epidemiology of a cluster, with special emphasis on molecular typing. Gut 1994; 35:313.
  50. Schwarz S, Morelli G, Kusecek B, et al. Horizontal versus familial transmission of Helicobacter pylori. PLoS Pathog 2008; 4:e1000180.
  51. Hardo PG, Tugnait A, Hassan F, et al. Helicobacter pylori infection and dental care. Gut 1995; 37:44.
  52. Kignel S, de Almeida Pina F, André EA, et al. Occurrence of Helicobacter pylori in dental plaque and saliva of dyspeptic patients. Oral Dis 2005; 11:17.
  53. Malaty HM, Evans DJ Jr, Abramovitch K, et al. Helicobacter pylori infection in dental workers: a seroepidemiology study. Am J Gastroenterol 1992; 87:1728.
  54. Axon AT. Review article: is Helicobacter pylori transmitted by the gastro-oral route? Aliment Pharmacol Ther 1995; 9:585.
  55. Tytgat GN. Endoscopic transmission of Helicobacter pylori. Aliment Pharmacol Ther 1995; 9 Suppl 2:105.
  56. Borody TJ, Andrews P, Mancuso N, et al. Helicobacter pylori reinfection rate, in patients with cured duodenal ulcer. Am J Gastroenterol 1994; 89:529.
  57. Archimandritis A, Balatsos V, Delis V, et al. "Reappearance" of Helicobacter pylori after eradication: implications on duodenal ulcer recurrence: a prospective 6 year study. J Clin Gastroenterol 1999; 28:345.
  58. Mitchell HM, Hu P, Chi Y, et al. A low rate of reinfection following effective therapy against Helicobacter pylori in a developing nation (China). Gastroenterology 1998; 114:256.
  59. Rowland M, Kumar D, Daly L, et al. Low rates of Helicobacter pylori reinfection in children. Gastroenterology 1999; 117:336.