Helicobacter pylori: Infectious substances pathogen safety data sheet
Section I – Infectious agent
Name
Helicobacter pylori
Agent type
Bacteria
Taxonomy
Family
Helicobacteraceae
Genus
Helicobacter
Species
pylori
Synonym or cross-reference
Campylobacter pylori and Helicobacter nemestrinaeFootnote 1.
Characteristics
Brief description
H. pylori is a Gram-negative, helical or curved-shaped bacterium measuring 2.5 to 5 μm x 0.5 μmFootnote 2. H. pylori has multiple unipolar, sheathed flagella that confer motilityFootnote2. H. pylori is nutritionally fastidious, microaerophilic, and is urease, catalase, and oxidase positive. H. pylori has a circular genome approximately 1.6 Mbp in lengthFootnote 3.
Properties
H. pylori can cause gastritis, peptic (gastric and duodenal) ulcer disease, and gastric cancerFootnote2Footnote 4. H. pylori primarily colonize the surface of gastric epithelium, but are also found in the oral cavityFootnote 5. Virulence factors include CagA, VacA, and OipA, which contribute to gastric inflammationFootnote 6Footnote 7. H. pylori cell may transform into a viable but non-culturable coccoid form under adverse environmental conditionsFootnote2Footnote 8.
Section II – Hazard identification
Pathogenicity and toxicity
H. pylori colonization of the mucosal surface of the stomach/duodenum is generally asymptomatic, but acute acquisition can cause upper gastrointestinal illness with nausea, abdominal pain, and burpingFootnote 9Footnote 10. Symptoms usually last for less than one week, but can persist up to 14 daysFootnote9. H. pylori infection is treatable with appropriate antibioticsFootnote 11. The recurrence rate of infection depends on geographic region and age, however, the rate is about 19% according to H. pylori prevalence up until January 2023Footnote 12. Persistent H. pylori colonization (e.g., for years or decades) can cause chronic gastritis, which can progress to peptic ulcer disease in 5-20% of casesFootnote 13Footnote 14, and/or gastric cancer in 1% to 3% of casesFootnote 15Footnote 16Footnote 17.
H. pylori infection is associated with 90-100% of duodenal ulcers and 60-100% of gastric ulcersFootnote4. Symptoms of peptic ulcer include epigastric pain, bloating, and nausea, and complications can lead to bleeding and perforationFootnote14. Mortality rates after hemorrhage and perforation are approximately 8.6% and 23.5%, respectivelyFootnote 18.
Atrophic gastritis and intestinal metaplasia are precursors to gastric cancer and are strongly associated with H. pylori infection in adultsFootnote13. Gastric cancer types include adenocarcinomas, which account for 95% of gastric cancers, and gastric lymphomas, such as mucosal-associated lymphoid tissue (MALT) lymphomaFootnote17. Gastric adenocarcinoma can be classified according to anatomic site of occurrenceFootnote 19. Cardia adenocarcinomas are located near oesophagus, whereas non-cardia adenocarcinomas occur in the mid and distal region of the stomach. Nearly 90% of non-cardia adenocarcinomas and 72-98% of gastric MALT lymphomas are associated with H. pyloriFootnote17Footnote 20. The 5-year survival rate for gastric cancer in the United States has been reported to be between 31%Footnote19 and 36%Footnote 21, but is variable depending on the cancer stage at the time of interventionFootnote19Footnote21.
Associations between H. pylori infection and development of extra-gastric conditions, including hypertension and strokeFootnote 22Footnote 23, type II diabetes mellitusFootnote 24, metabolic syndromeFootnote 25, fatty acid liver diseaseFootnote 26, chronic idiopathic thrombocytopenic purpuraFootnote 27, idiopathic parkinsonismFootnote 28, iron deficiency anemiaFootnote27Footnote 29, skin conditionsFootnote 30, migraineFootnote 31Footnote 32, and vitamin B12 deficiency, have been drawnFootnote 33Footnote 34.
Epidemiology
H. pylori is prevalent worldwide. Prevalence varies according to geographic region, age, and socioeconomic factorsFootnote 35Footnote 36. Prevalence of H. pylori infection in adults is estimated to be 20-35% in Canada and United States, and tends to be higher (50-90%) in developing countriesFootnote17Footnote35Footnote36.
Over past decades, the declining trend of H. pylori prevalence rates in most countries roughly correlate with decreases in incidence of peptic ulcer disease and gastric cancerFootnote14Footnote 37Footnote 38Footnote 39Footnote 40. Globally, annual incidence of peptic ulcer disease is 58 to 142 per 100,000 populationFootnote 41. There are approximately one million new gastric cancer cases (73% non-cardia) and 783,000 gastric cancer-associated deaths annually worldwideFootnote 42Footnote 43. Roughly 77% of new gastric cancer cases occur in AsiaFootnote 44.
Males as roughly twice as likely to develop gastric cancer compared to femalesFootnote19Footnote42, despite evidence that H. pylori prevalence rates are similar in males and femalesFootnote35. Outcome of H. pylori infection is influenced by polymorphisms in certain host genesFootnote7.
Host range
Natural host(s)
HumansFootnote 7, non-human primatesFootnote 45, catsFootnote 46, ovinesFootnote10Footnote 47, bovinesFootnote 48, caprines, camelsFootnote 49, and buffalo.
Other host(s)
PigsFootnote 50, dogsFootnote 51, gerbilsFootnote 52, rodents, and Caenorhabditis elegansFootnote 53 have been experimentally infected.
Infectious dose
Approximately 105 colony forming units (CFU) via ingestionFootnote 54.
Incubation period
Approximately 3 daysFootnote54.
Communicability
H. pylori can be transmitted via oral-oral, faecal-oral, and gastro-oral routes, since H. pylori is present in saliva, feces, and vomitusFootnote10. Ingestion via waterborne and foodborne (e.g., contaminated raw vegetables, raw milk) routes is possibleFootnote10Footnote17Footnote 55. Iatrogenic transmission via use of inadequately disinfected endoscopes is a possible mode of transmissionFootnote10.
Section III – Dissemination
Reservoir
Primarily humansFootnote 56Footnote 57.
Zoonosis
Animal-to-human transmission via close contact with infected animals or consumption of animal products containing H. pylori is possibleFootnote47Footnote 58Footnote 59Footnote 60. There is a lack of evidence for transmission between humans and domestic catsFootnote 61.
Vectors
Cockroaches and flies have been suggested as vectors of H. pylori transmission, as infected insects excrete H. pylori in fecesFootnote10Footnote 62.
Section IV – Stability and viability
Drug susceptibility/resistance
H. pylori is generally susceptible to penicillins (e.g., amoxicillin, ampicillin, ticardillin, mezlocillin, piperacillin)Footnote 63, cephalosporins (e.g., cefpodoxime, ceftibuten, cefixime, cefoxitin, cefuroxime, ceftizoxime, latamoxef, ceftriaxone)Footnote 64Footnote 65, kanamycinFootnote 66, gentamicinFootnote 67Footnote 68, tetracyclineFootnote68, rifabutinFootnote 69, and sitafloxacinFootnote 70.
H. pylori are generally resistant to polymyxins, trimethoprim, sulphonamides, and vancomycinFootnote67Footnote 71Footnote 72. Rates of resistance to antimicrobials commonly used in first-line therapy (e.g., amoxicillin, clarithromycin, metronidazole, levofloxacin) for H. pylori eradication have been steadily increasing in many areasFootnote 73Footnote 74.
Clarithromycin-resistant H. pylori strains in North America (13-26%)Footnote 75Footnote 76, European region (25-31%), Western Pacific region (30-38%), Eastern Mediterranean region (23-25%), and Southeast Asia region (6-28%) have been reportedFootnote74.
Prevalence of metronidazole-resistant H. pylori is highly variable from 8% in South America to 99% in parts of Africa, 44% in Asia-Pacific region, and 14 to 28% in North AmericaFootnote76Footnote 77.
Levofloxacin resistance rate is approximately 18% in Asia-Pacific region, 30% in North America, less than 10% in Africa and South America, and up to 62% in South KoreaFootnote70Footnote76Footnote77. Resistance to other quinolones (e.g., moxifloxacin) is emerging in some areasFootnote68Footnote 78.
Rates of resistance to tetracycline (<10%) is generally low in most countriesFootnote7Footnote73Footnote74Footnote76Footnote 79Footnote 80. H. pylori resistance to furazolidone and rifampin (<10%) is relatively rareFootnote68Footnote75Footnote80Footnote 81, but resistant strains are emerging in some areasFootnote 82Footnote 83Footnote 84.
H. pylori strains resistant to multiple drugs (amoxicillin, clarithromycin, metronidazole, and levofloxacin) have been reportedFootnote67Footnote72Footnote78Footnote 85. Furthermore the rates of resistance, based on a patient cohort study preformed in 2023, are 17.3% for amoxicillin, 44.2% for clarithromycin, 38.5% for levofloxacin, and 86.5% for metronidazoleFootnote85.
Susceptibility to disinfectants
Glutaraldehyde (2%)Footnote10, chlorineFootnote 86Footnote 87, ozoneFootnote86, ethanol (80%)Footnote 88, chlorhexidine gluconate (1%)Footnote88, benzalkonium chloride (0.1%)Footnote88, and alkyldiaminoethylglycine hydrochloride (0.1%)Footnote88.
Physical inactivation
H. pylori can be inactivated by UV radiationFootnote 89, dry heat treatment (170°C for 1 hour) and moist heat treatment (121°C for 15 minutes)Footnote 90.
Survival outside host
H. pylori remains culturable after 9 to 12 days in milk at 4°CFootnote 91Footnote 92, and 2 to 5 days in food at 4°CFootnote 93. The viable but non-culturable coccoid form can survive for up to 26 months in water at 4°CFootnote 94.
Section V – First aid/medical
Surveillance
H. pylori infection can be detected using the 13C urea breath test, which is a non-invasive test based on detection of urease activity in the stomachFootnote 95. H. pylori can also be detected using a stool antigen testFootnote 96Footnote 97Footnote 98. More invasive testing involves endoscopy with gastric biopsy followed by culture and/or PCRFootnote 99.
Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.
First aid/treatment
H. pylori eradication therapy is typically 2 weeksFootnote 100. Treatment regimes may include a proton pump inhibitor (e.g., rabeparzole, esomeprazole) or other acid blocker (e.g., vonoprazan) in combination with two or more antimicrobial drugsFootnote70Footnote73Footnote100Footnote 101.
In addition, herbal remedy approaches to treatment have been emerging for the H. pylori infectionFootnote 102Footnote 103. Specifically, in experimental settings, herbal remedies such as Metrella kentia, citrus lemon, and Cratoxylum arborescens (Vahl) Blume have shown they can be used by the H. pylori positive individuals to avoid the creation of ethanol-induced stomach ulcersFootnote103.
Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.
Immunization
A vaccine candidate that demonstrates sufficient long-lasting protective immunity has not been developed to dateFootnote 104Footnote 105Footnote 106. In the case of H. pylori, several bacterial antigens have been highlighted as potential vaccine targetsFootnote 107. Currently, vaccine candidates under development are at a very early stage (preclinical or phase I).
Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook, and by consulting the Canadian Immunization Guide.
Prophylaxis
None.
Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.
Section VI – Laboratory hazard
Laboratory-acquired infections
A laboratory worker acquired H. pylori via accidental oral ingestionFootnote 108.
Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.
Sources/specimens
Saliva, vomitus, gastric mucosal biopsy, and fecesFootnote7.
Primary hazards
Ingestion of infectious material is the primary hazard associated with the exposure of H. pyloriFootnote 109.
Special hazards
Work with experimentally or naturally infected hosts of H. pylori may present a special hazard.
Section VII – Exposure controls/personal protection
Risk group classification
H. pylori is a Risk Group 2 human pathogen and Risk Group 2 animal pathogenFootnote 110Footnote 111. H. pylori is a group 1 carcinogen according to the International Agency for Research on CancerFootnote 112.
Containment requirements
Containment Level 2 facilities, equipment, and operational practices outlined in the Canadian Biosafety Standard are required for work involving infectious or potentially infectious materials, animals, or cultures.
Protective clothing
The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. At minimum, use of a labcoat and closed-toe cleanable shoes, gloves when direct skin contact with infected materials or animals is unavoidable, and eye protection where there is a known or potential risk of exposure to splashes.
Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone and work activities must be documented.
Other precautions
A biological safety cabinet (BSC) or other primary containment devices to be used for activities with open vessels, based on the risks associated with the inherent characteristics of the regulated material, the potential to produce infectious aerosols or aerosolized toxins, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.
Use of needles and syringes to be strictly limited. Bending, shearing, re-capping, or removing needles from syringes to be avoided, and if necessary, performed only as specified in standard operating procedures (SOPs). Additional precautions are required with work involving animals or large-scale activities.
Additional information
For diagnostic laboratories handling primary specimens that may contain H. pylori, the following resources may be consulted:
Section VIII – Handling and storage
Spills
Allow aerosols to settle. Wearing personal protective equipment, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (Canadian Biosafety Handbook).
Disposal
All materials/substances that have come in contact with the regulated materials should be completely decontaminated before they are removed from the containment zone or standard operating procedures (SOPs) to be in place to safely and securely move or transport waste out of the containment zone to a designated decontamination area / third party. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the regulated material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook).
Storage
The applicable Containment Level 2 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be labelled, leakproof, impact resistant, and kept either in locked storage equipment or within an area with limited access.
Section IX – Regulatory and other information
Canadian regulatory information
Controlled activities with H. pylori requires a Pathogen and Toxins licence, issued by the Public Health Agency of Canada.
The following is a non-exhaustive list of applicable designations, regulation, or legislation:
- Human Pathogen and Toxins Act and Human Pathogens and Toxins Regulations
- Health of Animals Act and Health of Animals Regulations
- Transportation of Dangerous Goods Act and Transportation of Dangerous Goods Regulations
Last file update
August, 2024
Prepared by
Centre for Biosecurity, Public Health Agency of Canada.
Disclaimer
The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.
Persons in Canada are responsible for complying with the relevant laws, including regulations, guidelines and standards applicable to the import, transport, and use of pathogens in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.
Copyright © Public Health Agency of Canada, 2024, Canada
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