Pathogen Safety Data Sheets: Infectious Substances – Helicobacter pylori

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Helicobacter pylori

SYNONYM OR CROSS REFERENCE: Known as Campylobacter pylori prior to 1989 Footnote 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 Footnote 1Footnote 2. They are microaerobic and have respiratory metabolic abilities Footnote 2. The bacteria appear as an S-shaped, spiral rod, at about 2.4 – 4.0 µm in length Footnote 3.

SECTION II – HAZARD IDENTIFICATION

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 Footnote 4. This can result in clinical symptoms of infection, such as duodenal ulcer and gastric adenocarcinoma Footnote 5. Other common illnesses as a result of infection include gastroenteritis Footnote 6, diffuse antral gastritis, and gastric carcinoma Footnote 7. H. pylori is a Class I human carcinogen according to the World Health Organization Footnote 8. Infection can last a lifetime in the host if not properly treated, causing chronic gastritis which can lead to peptic gastroduodenal ulcer disease Footnote 9. The rate of mortality varies with country and age, but is generally low, being around 2 – 4% Footnote 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 Footnote 10. Rate of distribution varies according to country, as infection rates can decrease with improvements in industrialization and socioeconomic conditions Footnote 7.

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

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

MODE OF TRANSMISSION: The exact route of transmission is unknown, but acquisition is likely to occur during childhood Footnote 5 through faecal–oral or oral–oral contact (3) or during gastrointestinal tract transit disorders Footnote 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 Footnote 1 Footnote 13.

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

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

SECTION III – DISSEMINATION

RESERVOIR: Humans, houseflies (Musca domestica), old world macaques, dogs, cats and other mammals, water and raw vegetables Footnote 16Footnote 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 Footnote 8.

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

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Sensitivity has been established for clarithromycin, amoxicillin, tetracycline, imipenem, cefaclor, minocycline, simethicone, gabexate mesilate, and ketoconazole Footnote 18Footnote 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 Footnote 19Footnote 21.

SUSCEPTIBILITY TO DISINFECTANTS: Readily inactivated by free chlorine, iodine treatments can inhibit its vacuolation toxin activity Footnote 22, thus practices used for treating drinking water, apart from ozonolysis, should be sufficient for disinfecting H. pylori as well Footnote 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/cm2Footnote 23. Bacteria can be heat-killed by incubating at 70˚C for 10 minutes, followed by 95˚C for 5 minutes Footnote 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 Footnote 25Footnote 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 Footnote 8.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Presence of H. pylori can be confirmed by culture, blood antigen detection, urease detection, or bacterial metabolite detection in the infected individual’s breathFootnote 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 Footnote 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 Footnote 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 Footnote 15.

SECTION VI – LABORATORY HAZARDS

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 Footnote 15.

SOURCES/SPECIMENS: H. pylori may be located in the oral cavity, gastrointestinal and hepatobiliary regions of infected mammals and birds Footnote 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 Footnote 15.

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 Footnote 28.

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 Footnote 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 Footnote 29. Additional precautions should be considered with work involving animals or large scale activities.

SECTION VIII – HANDLING AND STORAGE

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 Footnote 29.

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

STORAGE: In appropriately labelled leak-proof containersFootnote 29.

SECTION IX – REGULATORY AND OTHER INFORMATION

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

Canada

REFERENCES:

Footnotes

Footnote 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.

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Footnote 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.

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Footnote 3

, L. M. (2000). Helicobacter pylori: epidemiology and routes of transmission. Epidemiologic Reviews, 22(2), 283-297.

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Footnote 4

Brock, T. D., Madigan, M. T., Martinko, J. M., & Parker, J. (2000). Biology of Microorganisms (9th ed.). New Jersey, USA: Prentice-Hall, Inc.

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Footnote 5

Hardin, F. J., & Wright, R. A. (2002). Helicobacter pylori: Review and Update., 23-31.

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Footnote 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

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Footnote 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.

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Footnote 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

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Footnote 9

de Boer, W. A., & Tytgat, G. N. J. (2000). Treatment of Helicobacter pylori infection.230, 31-34.

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Footnote 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

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Footnote 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.

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Footnote 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

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Footnote 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.

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Footnote 14

Rabeneck, L., & Graham, D. Y. (1997). Helicobacter pylori: When To Test, When To Treat.(126), 315-316.

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Footnote 15

Matysiak-Budnik, T., Briet, F., Heyman, M., & Megraud, F. (1995). Laboratory-acquired Helicobacter pylori infection. Lancet, 346(8988), 1489-1490.

Return to footnote 15 referrer

Footnote 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.

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Footnote 17

Fox, J. G. (1995). Non-human reservoirs of Helicobacter pylori. Alimentary Pharmacology & Therapeutics, 9 Suppl 2, 93-103.

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Footnote 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.

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Footnote 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.

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Footnote 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.

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Footnote 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

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Footnote 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.

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Footnote 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

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Footnote 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

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Footnote 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.

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Footnote 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

Return to footnote 26 referrer

Footnote 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

Return to footnote 27 referrer

Footnote 28

Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).

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Footnote 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.

Return to footnote 29 referrer

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