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NAME: Helicobacter pylori

SYNONYM OR CROSS REFERENCE: Known as Campylobacter pylori prior to 1989 (1), chronic gastritis, peptic ulcer disease.

CHARACTERISTICS: The extracellular H. pylori, of the Helicobacteraceae family, are gram-negative, microaerophilic, motile, and they are the only species in the Helibacter genus to have multiple unipolar-sheathed flagella (1, 2). They are microaerobic and have respiratory metabolic abilities (2). The bacteria appear as an S-shaped, spiral rod, at about 2.4 – 4.0 µm in length (3).


PATHOGENICITY/TOXICITY: H. pylori are not invasive, but colonize in the human stomach’s antral region and gastric mucosal surfaces where they release pathogenic proteins that induce cell injury and inflammation (4). This can result in clinical symptoms of infection, such as duodenal ulcer and gastric adenocarcinoma (5). Other common illnesses as a result of infection include gastroenteritis (6), diffuse antral gastritis, and gastric carcinoma (7). H. pylori is a Class I human carcinogen according to the World Health Organization (8). Infection can last a lifetime in the host if not properly treated, causing chronic gastritis which can lead to peptic gastroduodenal ulcer disease (9). The rate of mortality varies with country and age, but is generally low, being around 2 – 4% (10).

EPIDEMIOLOGY: Worldwide – H. pylori is has one of the highest global prevalence for a human pathogen with more than 50% of the world’s population infected, especially in developing countries where those chronically infected can reach up to 90% by adulthood (10). Rate of distribution varies according to country, as infection rates can decrease with improvements in industrialization and socioeconomic conditions (7).

HOST RANGE: Humans and animals, including non-human primates, pigs, cattle, dogs, cats, rodents, birds (8, 11), (2).

INFECTIOUS DOSE: Unknown for humans. Infection in the Rhesus monkey occurred with a minimum of 104 H. pylori bacteria intake by orogastrical inoculation (12).

MODE OF TRANSMISSION: The exact route of transmission is unknown, but acquisition is likely to occur during childhood (5) through faecal–oral or oral–oral contact (3) or during gastrointestinal tract transit disorders (6). Transmission may also occur through food-borne, airborne, or waterborne pathways, as the water sewage system has been found to be an agent of dissemination (1, 13).

INCUBATION PERIOD: Unclear as symptoms usually do not appear until adulthood and observable symptoms may never develop (known as silent infections) (14). Major symptoms such as abdominal pain, heartburn, and nausea have been observed 3 – 4 days after ingestion of the bacteria (15).

COMMUNICABILITY: Transmission from person–to-person may occur, usually through oral–oral routes (7).


RESERVOIR: Humans, houseflies (Musca domestica), old world macaques, dogs, cats and other mammals, water and raw vegetables (16, 17).

ZOONOSIS: The bacteria are able to be transmitted from animals and humans, and vice versa. This has been found to be especially common between humans and cats (8).

VECTORS: Houseflies can carry viable H. pylori on their bodies, in their intestinal tracts, and in excreta (16).


DRUG SUSCEPTIBILITY: Sensitivity has been established for clarithromycin, amoxicillin, tetracycline, imipenem, cefaclor, minocycline, simethicone, gabexate mesilate, and ketoconazole (18-20).

DRUG RESISTANCE: Strains have been found to show resistance to antibodies such as clarithromycin, erythromycin, ofloxacin, and metronidazole, and show low levels of resistance to tetracycline, amoxicillin, fluoroquinolones, and rifabutin (19, 21).

SUSCEPTIBILITY TO DISINFECTANTS: Readily inactivated by free chlorine, iodine treatments can inhibit its vacuolation toxin activity (22), thus practices used for treating drinking water, apart from ozonolysis, should be sufficient for disinfecting H. pylori as well (13). Exposing H. pylori to 1.1mg/L residual chlorine for 45 minutes is enough to eradicate the pathogen (biocidal properties of chlorine are optimized at lower pH levels, such as around <pH 7 or 6).

PHYSICAL INACTIVATION: Inactivated by low pressure UV light at fluences (UV dose) of less than 8 mJ/cm2 (23). Bacteria can be heat-killed by incubating at 70˚C for 10 minutes, followed by 95˚C for 5 minutes (24).

SURVIVAL OUTSIDE HOST: Unknown. As culturing H. pylori in the laboratory is difficult as it needs adequate conditions of desiccation, air supply, and temperature, it is likely that it does not survive well outside of its host (25, 26); however, in its coccoid form, it can survive up to one year in a river-water microcosm, and remains culturable for more than 10 days in 4˚C water (8).


SURVEILLANCE: Presence of H. pylori can be confirmed by culture, blood antigen detection, urease detection, or bacterial metabolite detection in the infected individual’s breath (2).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Administer appropriate drug therapy. H. pylori is rapidly developing antibiotic resistance, so antibiotics can be applied with a proton pump inhibitor or a bismuth compound (9). Such dual, triple or quadruple treatments have been found to be more effective than administering one antibiotic alone.

IMMUNIZATION: Recombinant urease (rUrease) and parenteral vaccine containing H. pylori antigens (CagA, VacA, and NAP) in combination with aluminum hydroxide as an adjuvant have been found to be effective vaccines against H. pylori (27), although they cannot prevent re-infection.

PROPHYLAXIS: Omeprazole, clarithromycin, and metronidazole can be administered if early symptoms of infection such as heartburn, nausea, or severe epigastic cramps are experienced (15).


LABORATORY-ACQUIRED INFECTIONS: There have been at least three reports of accidental infection, one of them being accidental ingestion of H. pylori. A female gastroenterologist with no history of gastrointestinal diseases or other symptoms was using a strain of H. pylori to infect a filter-grown intestinal cell layer, which had been incubating for 48 hours. After touching the filter, she had put her fingers in her mouth, and experienced upper abdominal pain, heartburn, and nausea 3 – 4 days after ingestion. The infection appeared to be cured after treatment with omeprazole, clarithromycin, and metronidazole (15).

SOURCES/SPECIMENS: H. pylori may be located in the oral cavity, gastrointestinal and hepatobiliary regions of infected mammals and birds (2). They can also be found in tissues of the small intestine, saliva, gastric juice, and faeces.

PRIMARY HAZARDS: Accidental ingestion poses the most common hazard (15).




CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes (29).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited (29). Additional precautions should be considered with work involving animals or large scale activities.


SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (29).

DISPOSAL: Decontaminate all wastes before disposal; steam sterilization, chemical disinfection, and/or incineration (29).

STORAGE: In appropriately labelled leak-proof containers (29).


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions, and recommendations contained in this Pathogen Safety Data Sheet are complied from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©

Public Health Agency of Canada, 2010



  1. Velazquez, M., & Feirtag, J. M. (1999). Helicobacter pylori: characteristics, pathogenicity, detection methods and mode of transmission implicating foods and water. International Journal of Food Microbiology, 53(2-3), 95-104.
  2. Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., Pfaller, M. A., & Yolken, R. H. (Eds.). (2003). Clinical Microbiology (8th ed.). Herdon, VA, United States of America: American Society for Microbiology.
  3. Brown, L. M. (2000). Helicobacter pylori: epidemiology and routes of transmission. Epidemiologic Reviews, 22(2), 283-297.
  4. Brock, T. D., Madigan, M. T., Martinko, J. M., & Parker, J. (2000). Biology of Microorganisms (9th ed.). New Jersey, USA: Prentice-Hall, Inc.
  5. Hardin, F. J., & Wright, R. A. (2002). Helicobacter pylori: Review and Update., 23-31.
  6. Laporte, R., Pernes, P., Pronnier, P., Gottrand, F., & Vincent, P. (2004). Acquisition of Helicobacter pylori infection after outbreaks of gastroenteritis: prospective cohort survey in institutionalised young people. BMJ (Clinical Research Ed.), 329(7459), 204-205. doi:10.1136/bmj.329.7459.204
  7. Bardhan, P. K. (1997). Epidemiological features of Helicobacter pylori infection in developing countries. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 25(5), 973-978.
  8. Meng, J., & Doyle, M. P. (1997). Emerging issues in microbiological food safety. Annual Review of Nutrition, 17, 255-275. doi:10.1146/annurev.nutr.17.1.255
  9. de Boer, W. A., & Tytgat, G. N. J. (2000). Treatment of Helicobacter pylori infection.230, 31-34.
  10. Torres, J., Lopez, L., Lazcano, E., Camorlinga, M., Flores, L., & Munoz, O. (2005). Trends in Helicobacter pylori infection and gastric cancer in Mexico. Cancer Epidemiology, Biomarkers & Prevention : A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology, 14(8), 1874-1877. doi:10.1158/1055-9965.EPI-05-0113
  11. Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (2003). Zoonosis – Infectious Diseases Transmissible from Animals to Humans (3rd ed.) American Society for Microbiology.
  12. Solnick, J. V., Hansen, L. M., Canfield, D. R., & Parsonnet, J. (2001). Determination of the infectious dose of Helicobacter pylori during primary and secondary infection in rhesus monkeys (Macaca mulatta). Infection and Immunity, 69(11), 6887-6892. doi:10.1128/IAI.69.11.6887-6892.2001
  13. Johnson, C. H., Rice, E. W., & Reasoner, D. J. (1997). Inactivation of Helicobacter pylori by chlorination. Applied and Environmental Microbiology, 63(12), 4969-4970.
  14. Rabeneck, L., & Graham, D. Y. (1997). Helicobacter pylori: When To Test, When To Treat.(126), 315-316.
  15. Matysiak-Budnik, T., Briet, F., Heyman, M., & Megraud, F. (1995). Laboratory-acquired Helicobacter pylori infection. Lancet, 346(8988), 1489-1490.
  16. Grubel, P., Hoffman, J. S., Chong, F. K., Burstein, N. A., Mepani, C., & Cave, D. R. (1997). Vector potential of houseflies (Musca domestica) for Helicobacter pylori. Journal of Clinical Microbiology, 35(6), 1300-1303.
  17. Fox, J. G. (1995). Non-human reservoirs of Helicobacter pylori. Alimentary Pharmacology & Therapeutics, 9 Suppl 2, 93-103.
  18. Lwai-Lume, L., Ogutu, E. O., Amayo, E. O., & Kariuki, S. (2005). Drug susceptibility pattern of Helicobacter pylori in patients with dyspepsia at the Kenyatta National Hospital, Nairobi. East African Medical Journal, 82(12), 603-608.
  19. Nakae, M., Sugahara, Y., Sasaki, H., Yasui, H., Imai, C., Hasegawa, Y., Osaka, K., & Shibasaki, K. (1998). Drug susceptibility of clinically isolated Helicobacter pylori. The Japanese Journal of Antibiotics, 51(4), 281-285.
  20. Ansorg, R., von Recklinghausen, G., & Heintschel von Heinegg, E. (1996). Susceptibility of Helicobacter pylori to simethicone and other non-antibiotic drugs. The Journal of Antimicrobial Chemotherapy, 37(1), 45-52.
  21. Megraud, F. (2004). H pylori antibiotic resistance: prevalence, importance, and advances in testing. Gut, 53(9), 1374-1384. doi:10.1136/gut.2003.022111
  22. Ma, F., Zhao, W., Kudo, M., Aoki, K., & Misumi, J. (2002). Inhibition of vacuolation toxin activity of Helicobacter pylori by iodine, nitrite and potentiation by sodium chloride, sterigmatocystin and fluoride. Toxicology in Vitro : An International Journal Published in Association with BIBRA, 16(5), 531-537.
  23. Hayes, S. L., White, K. M., & Rodgers, M. R. (2006). Assessment of the effectiveness of low-pressure UV light for inactivation of Helicobacter pylori. Applied and Environmental Microbiology, 72(5), 3763-3765. doi:10.1128/AEM.72.5.3763-3765.2006
  24. Gnad, T., Feoktistova, M., Leverkus, M., Lendeckel, U., & Naumann, M. (2010). Helicobacter pylori-induced activation of beta-catenin involves low density lipoprotein receptor-related protein 6 and Dishevelled. Molecular Cancer, 9, 31. doi:10.1186/1476-4598-9-31
  25. Goodman, K. J., & Correa, P. (1995). The transmission of Helicobacter pylori. A critical review of the evidence. International Journal of Epidemiology, 24(5), 875-887.
  26. Megraud, F., & Lehours, P. (2007). Helicobacter pylori detection and antimicrobial susceptibility testing. Clinical Microbiology Reviews, 20(2), 280-322. doi:10.1128/CMR.00033-06
  27. Kabir, S. (2007). The current status of Helicobacter pylori vaccines: a review. Helicobacter, 12(2), 89-102. doi:10.1111/j.1523-5378.2007.00478.x
  28. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).
  29. Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.