A guide for health professionals working with
immigrant and refugee children and youth

Helicobacter pylori Infections

Key points

  • Helicobacter pylori (H. pylori) is a common bacterial infection in humans. It is transmitted by the fecal–oral and oral–oral routes.
  • Infection prevalence, which ranged anywhere between 7% and 87% globally in 2010, is highest in Asia, Eastern Europe and South America.
  • Approximately 70% of infected people are asymptomatic. Symptoms of abdominal pain, loss of appetite, weight loss, bloody vomit and dark stools are suggestive but not predictive of infection.
  • The risk of infected people developing peptic ulcer disease during their lifetime is estimated at 10% to 15%. Their risk of developing gastric cancer is <3%.
  • Targeted screening and treatment for H. pylori infection is recommended for children who have a primary relative with gastric cancer, and may be considered for newcomer children who are in a high risk group for gastric cancer (e.g. immigrants from resource-limited countries or areas with high rates of gastric cancer, or who have unexplained iron deficiency anemia.
  • In the U.S., Australia and Canada, routine screening of all recently arrived immigrants and refugees for H. pylori infection is not currently recommended.
  • Treatment may not eradicate H. pylori due to antibiotic resistance or poor compliance with multiple drug therapy for 14 days. In addition, the re-infection rate in the pediatric population ranges from 2% to about 13% per year. Reinfection can occur in Canada or while travelling abroad.
  • There is currently no vaccine to prevent infection with H. pylori.



Helicobacter pylori (H. pylori) is one of the most common bacterial infections in humans, with an estimated 1 billion people infected worldwide.


H. pylori is a small curved motile gram-negative rod shaped microaerophilic bacterium that inhabits the submucosa of gastric epithelium. Urease production enables the bacteria to adapt to the acidic gastric environment.1


H. pylori organisms are transmitted from infected humans by the oral–oral and fecal–oral routes. Humans appear to be a natural reservoir for infection, but H. pylori has also been identified in other primates, pigs, cattle, dogs, cats, rodents and birds. Environmental sources of H. pylori infection, such as municipal water sources, have been confirmed in Peru and Mexico.1  

There may be an ethnic or genetic predisposition to infection.2 The importance of additional co-factors, such as environmental exposures (e.g., living in crowded conditions, with substandard sanitation or a sharing a bed with siblings)3 or bacterial virulence factors has also been suggested.

Prevalence is generally <40% in children and youth in Europe and North America, although it has been shown to be higher in Canadian indigenous populations.4 In a study of African immigrants to Australia, H. pylori was detected in 80% of participants.5 A study of prevalence and risk factors for H. pylori infection in Ontario found that  the relative risk of infection was 2.9 times greater for individuals  born out of country who immigrated to Canada after they were 20 years of age.4

The variable prevalence of H. pylori infection globally – by age, region, within and among countries – is clearly presented in the World Gastroenterology Organisation Global Guideline on Helicobacter pylori.

Approximately 70% of infected people are asymptomatic.7 The risk of infected people developing peptic ulcer disease during their lifetime is estimated at 10% to 15%, and the risk of developing gastric cancer is about 0.1% to 3% of H. pylori infected persons.3 The inflammatory response with the gastric mucosa that is observed in individuals infected with H. pylori infection likely contributes to the risk of neoplasia.1 H. pylori infection is a necessary, but not the only cause of adenocarcinoma, the most common type of gastric cancer,3 although host genetic factors, heavily salted food, tobacco use and a high alcohol intake are also associated with individual risk.8,9 Gastric mucosa associated lymphoid tissue lymphoma (MALT) (rare in children) may show complete regression after treatment to eradicate H. pylori.1

Globally, the incidence of gastric cancer incidence has decreased significantly in recent decades, dropping from first to the fifth most common type of cancer  between 1975 and 2010.10 In Canada, stomach cancer in men and women is the eleventh and sixteenth most common type of cancer, respectively.8

The International Agency for Research on Cancer of the World Health Organization provides detailed data on worldwide cancer incidence, mortality and prevalence.10

Age-standardized incidence rates are about twice as high in men as in women, ranging from 3.3 per 100,000 in Western Africa to 35.4 in Eastern Asia for men, and from 2.6 in Western Africa to 13.8 in Eastern Asia for women.10

Figure 1. Trends in incidence of stomach cancer in men in selected countries (age standardized rate per 100,000 men)

Source, Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray, F. GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013. Available from: http://globocan.iarc.fr, accessed on 5 February 2014. http://globocan.iarc.fr/Pages/fact_sheets_cancer.aspx#

Figure 2. Trends in incidence of stomach cancer in women in selected countries (age standardized rate per 100,000 women)

Source, Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray, F. GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013. Available from: http://globocan.iarc.fr, accessed on 5 February 2014. http://globocan.iarc.fr/Pages/fact_sheets_cancer.aspx#

Clinical Manifestations

Approximately 70% of people infected with H. pylori are asymptomatic, and the association between the infection and gastrointestinal symptoms in childhood is unclear. However, symptoms may include bloating, burping, nausea and vomiting, loss of appetite, weight loss, bloody vomit and dark stools from bleeding in the stomach or duodenum.  All these symptoms can occur with other conditions,7 making it more difficult to know when testing is indicated. For the 10% to 15% of individuals who develop a peptic ulcer, common symptoms are a burning or gnawing stomach pain which may come and go, often happening a few hours after eating or during the night, but actually subsiding while eating food and drinking water.

The differential diagnosis in immigrant and refugee children with chronic abdominal pain, early satiety or anorexia, in addition to H. pylori infection, includes other infections such as tuberculosis, intestinal helminths, schistosomiasis, or other gastrointestinal disorders such as inflammatory bowel disease, eosinophilic gastroenteritis, somatic manifestations of post-traumatic stress disorder, and unfamiliarity with Western food.

Screening for H. Pylori

In Australia, the United States and Canada, routine screening of all recently arrived immigrants and refugees for H. pylori infection is not currently recommended.

The first Asia-Pacific Gastric Cancer Consensus group recommended screening for H. pylori infection in high-risk populations (i.e., where the incidence of gastric cancer is estimated to be > 20/100,000 population).9 However, screening in childhood was not recommended because of the increased risk of reinfection and the fact that children are at very low risk of clinically relevant disease.9, 11 The estimated number of asymptomatic subjects needed to  treat to prevent one from developing gastric cancer is estimated at 227 in countries with a high incidence of gastric cancer.12

The decision to not include H. pylori among routine screening recommendations for immigrant/refugee children is based on:

  • Lack of a clear association between H. pylori infection and gastrointestinal symptoms in children.13
  • Inadequate evidence to support immigrant/refugee H. pylori population screening in children and adolescents.5
  • Countries of birth of immigrants and refugees is in constant flux.  Consequently, the epidemiology of diseases in these children shifts.14

However, screening in high risk individuals may be useful, depending on the child’s country of origin or specific risk factors. Screening for and treatment of H. pylori infection has been recommended for children or adolescents:7

  • with at least one primary relative with gastric cancer
  • immigrating from resource-limited countries or countries with high rates of gastric cancer, or
  • with unexplained iron-deficiency anemia.

Diagnostic tests

In Canada, the gold standard for diagnosing H. pylori infection in symptomatic children and youth is culture of the organism from gastric biopsy samples for histologic review obtained by endoscopy. Alternatively, histological detection of H. pylori by urease testing of a gastric specimen can give a rapid and specific diagnosis. While cultures are important, especially considering the increase in antibiotic resistance, performing an endoscopy can be especially problematic in children. The procedure is invasive and expensive, requires hospital admission and sedation, and families may need to travel long distances for testing. 

Some noninvasive tests for detecting infection are available commercially but are not currently recommended for initial diagnosis of H. pylori infection, as the goal is to detect the cause of symptoms and not simply the presence of infection. Non-invasive tests include breath tests that detect labeled carbon dioxide released by H. pylori in expired air after oral administration of isotopically labeled urea. In 2012, the U.S. Food and Drug Administration (FDA) approved the first H. pylori breath test to detect and monitor infection in children ≥3 years of age.7 Urea breath testing is useful for both initial diagnosis and determination of successful treatment because the results rapidly return to normal after eradication. However, urea breath testing is often impractical and availability for children in the primary care setting is limited.5

Fecal antigen testing is also available, using highly sensitive/specific laboratory-based monoclonal enzyme immunosorbent assays (ELISA) of fecal specimens. (The rapid in-office tests to detect H. pylori using an immunochromatographic technique have limited accuracy).15 Testing accuracy is maintained, even if specimens are stored at room temperature for 5 days or frozen for months or years.5 The fecal test detects the presence of antigen, thus providing evidence of active infection for both primary diagnosis or proof of cure. Fecal testing  appears to be as accurate as the urea breath test,13 and each test has demonstrated high sensitivity and specificity.7 The stool antigen test can be used for children of any age.

Tests based on the detection of antibodies (IgG, IgA) against H. pylori in serum, whole blood and saliva are not considered reliable in the clinical setting.16 IgG can persist for years after resolution of infection. One study in African refugee children found a lower sensitivity and specificity (58%/77%) compared to fecal antigen testing.5  

It is important to recognize that proving that the child has H. pylori infection does not prove that H. pylori is the cause of their symptoms as most infected children are asymptomatic.

When the goal is to screen for and treat H. pylori-positive asymptomatic persons from high-risk countries to prevent gastric cancer (a ‘test and treat’ strategy), the Maastricht IV/Florence Consensus  group recommends using the 13C-Urea Breath Test or stool antigen testing rather than invasive endoscopy.15  


The eradication of H. pylori decreases the risk of peptic ulcer disease and, if initiated before the development of precancerous changes, may prevent gastric cancer.17 However, because the risk for developing cancer cannot be predicted accurately and most children with H. pylori infection have no clinical symptoms, there is no current rationale for treating all children infected with H. pylori.1

Treatment is recommended for infected patients who have:7

  • peptic ulcer disease (present or within the past 5 years),
  • persisting iron deficiency anemia (where causes have been ruled out),  or
  • a first-degree relative with gastric cancer, gastric mucosa-associated lymphoid tissue-type lymphoma (MALT), or early gastric cancer. Also see the Screening section of this document. 

Eradication therapy for H. pylori consists of at least 7 to 14 days of antibiotic treatment, with eradication rates higher for regimens of 14 days. Nonadherence to therapy and antibiotic resistance are the two main reasons for noneradication.

Consulting with a specialist in paediatric infectious diseases and/or a gastroenterologist is recommended before commencing therapy.

Current recommended treatment regimens for children include:

  • 2 antimicrobial agents (e.g., clarithromycin* plus either amoxicillin or metronidazole**) plus a proton-pump inhibitor (i.e., lansoprazole or omeprazole), OR
  • Sequential treatment which includes a 5-day period with a proton-pump inhibitor plus amoxicillin, followed by a 5-day period with a proton pump inhibitor plus clarithromycin plus metronidazole.

Alternate therapies in people 8 years of age and older include:

  • Bismuth subsalicylate*** plus  metronidazole plus tetracycline**** plus either a proton-pump inhibitor or an H2 blocker (e.g., cimetidine or ranitidine), OR
  • Bismuth subcitrate potassium plus metronidazole plus tetracycline**** plus omeprazole.

*If the child has previously been exposed to clarithromycin or comes from an area with a high clarithromycin resistance rate, clarithromycin should not be used.
**Children may not like the taste of metronidazole, resulting in decreased compliance.
***Salicylate containing products such as bismuth subsalicylate are not recommended in children due to the association with Reye’s Syndrome.
****Tetracycline products are not recommended in patients 8 years of age and younger.

Clinical follow-up is recommended to check for resolution of symptoms and successful eradication of H. pylori.  A reliable non-invasive test for eradication (i.e., the C13 urea breath test or stool antigen detection) is recommended at least 4 to 8 weeks after completing therapy. The stool antigen may test positive for up to 90 days after treatment.1

One report from the European paediatric treatment registry found an overall eradication rate of 65% in individuals with peptic ulcers (80% in children) following standard regimens. However, antibiotic resistance remains a key factor in the failure of eradication therapy and recurrence of H. pylori infections. The prevalence of H. pylori clarithromycin-resistance is increasing: in central, western and southern Europe resistance is >20%, compared with <10% in northern Europe.15 There are guidelines and flow charts for optimal therapy in areas of low (<20%) and high (>20%) clarithromycin resistance.15 Antibiotic resistance rates of H. pylori to amoxicillin and metronidazole also vary geographically and are higher in developing countries.6

The rate of H. pylori reinfection after treatment in the paediatric population ranges from 2% to about 13% per year. Living in an area of high prevalence of H. pylori can entail a fourfold higher risk of reinfection.1


Targeted H. pylori screening for recent immigrants to Canada who are asymptomatic but come from high prevalence areas has been advocated.4 There is no recommendation in Canada for universal screening of new immigrants or refugees for H. pylori, but clinicians may in the meantime choose to follow the recommendation by experts from other countries to screen only those children and youth specified above, until further information becomes available.

A vaccine to prevent H. pylori infections is currently under study.


  1. Maspons A, Gilger MA. Helicobacter pylori. In: Cherry J, Demmler-Harrison GJ, et al (eds.) Feigin and Cherry’s Textbook of Paediatric Infectious Diseases, 7th edn. Elsevier/Saunders, 2014:1691-9.2.
  2. Rosenberg JJ. Helicobacter pylori. Pediatr Rev;2010; 31(2):85-6.  
  3. McColl KE. Clinical Practice: Helicobacter pylori infection. N Engl J Med 2010;362(17):1597-1604.
  4. Jones N, Chiba N, Fallone C, et al. Helicobacter pylori in First Nations and recent immigrant populations in Canada. Can J Gastroenterol 2012; 26(2): 97-103.
  5. The Royal Children’s Hospital in Melbourne, Australia. Helicobacter pylori. Immigrant Health Services, January 2012: http://www.rch.org.au/immigranthealth/clinical/Helicobacter_pylori/
  6. Hunt RH, Xiao SD, Megraud F et al, Helicobacter pylori in developing countries, World Gastroenterology Organisation Global Guidelines, August 2010
  7. American Academy of Pediatrics. Helicobacter pylori. In: Pickering LK, Baker CJ, Kimberlin DW, et al (eds.). Red Book: 2012 Report of the Committee on Infectious Diseases. Elk Grove Village, IL: AAP, 2012:354-6.
  8. Canadian Cancer Statistics 2013, Public Health Agency of Canada, Statistics Canada, Canadian Cancer Society:19:  www.cancer.ca/en/cancer-information/cancer-101/canadian-cancer-statistics-publication/?region=bc
  9. Talley NJ, Fock KM, Moayyedi P. Gastric Cancer Consensus conference recommends Helicobacter pylori screening and treatment in asymptomatic persons from high-risk populations to prevent gastric cancer. Am J Gastroenterol 2008 103(5):510-14.
  10. Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray, F., GLOBOCAN 2012 v1.0., Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013. Available from:  http://globocan.iarc.fr, accessed on 02/26/2014  http://globocan.iarc.fr/old/FactSheets/cancers/stomach-new.asp
  11. K.M. Fock et al, Asia-Pacific Consensus Guidelines on Gastric Cancer Prevention, Journal of Gastroenterology and Hepatology 23 (2008) 351-365
  12. Malfertheiner P. Author’s response: Helicobacter pylori eradication and gastric cancer prevention. Gut 2013;62(5):950-1.  
  13. Murray RJ, Davis JS, Burgner DP; Australasian Society for Infectious Diseases Writing Group in Australia. The Australasian Society for Infectious Diseases guidelines for the diagnosis, management and prevention of infections in recently arrived refugees: An abridged outline. Med J Aust 2009;190(8):37-41: www.asid.net.au/resources/clinical-guidelines. (Currently in revision.)
  14. Howard CR, John CC. International adoption. In: The Yellow Book – CDC Health Information for International Travel, 2014. New York, NY: Oxford University Press, 2014.
  15. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection – the Maastricht IV/Florence Consensus Report. Gut 2012;61(5):649.
  16. Koletzko S, Jones NL, Goodman KJ, et al. Evidence-based guidelines from ESPGHAN  and NASPGHAN  for Helicobacter pylori infection in children.  J Pediatr Gastroenterol Nutr 2011; 53(2): 230-43.
  17. Jones NL, Chiba N, Fallone C, et al. Helicobacter pylori and immigrant health. CMAJ 2012:184(1):74-5.



  • Heather Onyett, MD


Last updated: May, 2014

Also available at: http://www.kidsnewtocanada.ca/conditions/hpylori
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Caring for Kids New to Canada is a resource for health professionals. The information here is not a substitute for medical advice, nor does it indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate.

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