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NAME: Vibrio cholerae, serogroup O1, serogroup O139 (Bengal)


CHARACTERISTICS: Vibrio cholerae is a gram negative, non-spore forming, curved rod that is oxidase positive(Footnote 1,Footnote 2,Footnote 3). It is very motile and has a single polar flagellum(Footnote 1). The bacterium is 1- 3 µm by 0.5-0.8 µm, is a facultative anaerobe and is part of the Vibronaceae family(Footnote 1,Footnote 3). Serogroups O1 (classical and El Tor biotypes) and O139 are primarily responsible for cholera outbreaks(Footnote 1,Footnote 3). Pathogenic serogroups produce cholera toxin (CT) while non pathogenic strains may or may not produce this toxin(Footnote 2). Recently, V. cholerae serougroup O75 strains possessing the cholera toxin gene were isolated from patients with severe diarrhoea, and serogroup O141 has been associated with sporadic cholera-like diarrhoea and bloodstream infections in the United States(Footnote 4,Footnote 5). Some serotypes may serve as a reservoir for the cholera toxin phage genome(Footnote 6,Footnote 7). Serotypes that do not produce cholera toxin can still cause illness in humans (i.e. enteritis)(Footnote 8).


PATHOGENICITY/TOXICITY: Vibrio cholerae can cause syndromes ranging from asymptomatic to cholera gravis(Footnote 3). In endemic areas, 75% of cases are asymptomatic, 20% are mild to moderate, and 2-5% are severe forms like cholera gravis(Footnote 3). Symptoms include abrupt onset of watery diarrhoea (a grey and cloudy liquid), occasional vomiting and abdominal cramps(Footnote 1,Footnote 3). Dehydration ensues with symptoms and signs such as thirst, dry mucous membranes, decreased skin turgor, sunken eyes, hypotension, weak or absent radial pulse, tachycardia, tachypnea, hoarse voice, oliguria, cramps, renal failure, seizures, somnolence, coma and death(Footnote 1). Death due to dehydration can occur in a hours to days in untreated children and the disease is dangerous for pregnant women and their foetuses during late pregnancy as abortion, premature labor and fetal death may occur(Footnote 3,Footnote 9,Footnote 10). In cases of cholera gravis involving severe dehydration, up to 60% of patients can die; however, less than 1% of cases treated with rehydration therapy are fatal. The disease typically lasts from 4-6 days(Footnote 3,Footnote 11). Worldwide, diarrhoeal disease, caused by cholera and many other pathogens, is the second leading cause of death for children under the age of 5 and at least 120,000 deaths are estimated to be caused by cholera each year(Footnote 12,Footnote 13). In 2002, the WHO deemed that the case fatality ratio for cholera was about 3.95%(Footnote 3).

EPIDEMIOLOGY: In the past 200 years, there have been 8 main cholera pandemics, with the disease being most common in tropical and subtropical areas(Footnote 2,Footnote 14). Most of the cases are in the Indian subcontinent and Africa (in 2002 the WHO estimated that 97% of the cholera cases were in Africa)(Footnote 2,Footnote 3). There are several million cases of cholera each year and in endemic areas, these tend to be most common in children aged 2-9 and in women who are of child-bearing age(Footnote 3,Footnote 12). Epidemics in endemic areas tend to occur during the hot season(Footnote 1).

HOST RANGE: Humans, water birds, shellfish, fish, and herbivores have been found to contain the infectious agent(Footnote 1).

INFECTIOUS DOSE: The infectious dose ranges between 10Footnote 6 and 10Footnote 11 ingested vibrios(Footnote 1). The infectious dose depends on gastric acidity (lower acidity levels reduces the number of vibrios required for infection)(Footnote 1).

MODE OF TRANSMISSION: Cholera is typically spread by consumption of water that is contaminated with infectious feces(Footnote 1,Footnote 2). Epidemics caused by infectious raw fish and seafood have been reported(Footnote 1).

INCUBATION PERIOD: The incubation period can range from a few hours to 5 days after infection(Footnote 1).

COMMUNICABILITY: Symptomatic patients may shed vibrios before clinical signs of illness and up to 2 weeks after, whereas asymptomatic patients typically only shed vibrios for 1 day(Footnote 12). A carrier state (where the patient has the infectious agent without any clinical manifestations) can exist for several weeks where vibrios are shed in small and intermittent quantities (15), (16).


RESERVOIR: Humans are a reservoir for the disease as are animals around aquatic environments(Footnote 1). The bacterium has been found in birds and herbivores surrounding freshwater lakes and rivers as well as in algae, copepods (zooplankton), crustaceans and insects(Footnote 1,Footnote 3).




DRUG SUSCEPTIBILITY: Susceptible to antibiotics. Tetracycline has been the drug of choice, although resistance to this antibiotic is becoming more common(Footnote 17,Footnote 18). Ciproflaxin, doxycycline and co-trimoxazole can also be used(Footnote 1). An outbreak in 1979 in Bangladesh was caused by multi-drug resistant strains of El Tor biotype(Footnote 18). 36% of strains in this outbreak were resistant to tetracycline, ampicillin, kanamycine, streptomycin, and trimethoprim sulfamethoxazole(Footnote 18).

DRUG RESISTANCE: Resistance has been shown to nalidixic acid, furazolidone, and co- trimoxazole, V. cholerae O1 lnaba isolates have been found to be muli-antibiotic resistant, when increasing resistance to ciprofloxacin(Footnote 19).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 2-5% phenol, 1% sodium hypochlorite, 4% formaldehyde, 2% glutaraldehyde, 70% ethanol, 70% propanol, 2% peracetic acid, 3-6% hydrogen peroxide, and 0.16% iodine(Footnote 14).

PHYSICAL INACTIVATION: Vibrio cholerae is sensitive to cold (loss of viability after a cold shock at 0ºC)(Footnote 20).

SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(Footnote 21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(Footnote 21). It has also been found on fomites at room temperature for 1-7 days(Footnote 21).


SURVEILLANCE: Monitor for symptoms. Confirm diagnosis by dark field microscopy of a wet mount of fresh stool, PCR or ELISA(Footnote 1,Footnote 3,Footnote 11).

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

FIRST AID/TREATMENT: Fluid replacement, electrolyte replacement and base i.v. fluid replacement followed by the WHO's oral rehydration solution (Na+ 90 mmol/L, K+ 20 mmol/L, Cl- 80 mmol/L, citrate (10 mmol/L and glucose 110 mmol/L) is the recommended treatment for dehydration(Footnote 1). Administering an antibiotic like ciproflaxin, doxycycline or co-trimoxazole reduces the duration of the illness(Footnote 1).

IMMUNIZATION: Routine vaccination for laboratory workers and travellers is not recommended(Footnote 22,Footnote 23). Traditional parenteral inactivated vaccine strains are available though not recommended for widespread use as they only provide protection for 3-6 months(Footnote 3,Footnote 14). Oral vaccines that provide protection for several years (up to 3) are available but their efficacy in endemic areas has not been confirmed(Footnote 3,Footnote 13).

PROPHYLAXIS: Chemoprophylaxis with antibiotics has not been shown to be effective(Footnote 1). Proper hygiene, sanitary measures, water treatment and careful food preparation are the best prophylactic measures in endemic areas(Footnote 1).


LABORATORY-ACQUIRED INFECTIONS: 12 cases of infection with 4 deaths were reported up to 1979(Footnote 24). The deaths were associated with mouth pipetting, contact with infectious feces and contaminated laboratory laundry(Footnote 24).

SOURCES/SPECIMENS: Feces and naturally or experimentally infected animals are the main specimens which contain the infectious agent(Footnote 22).

PRIMARY HAZARDS: The primary hazards when working with this agent are ingestion and accidental parenteral inoculation(Footnote 9,Footnote 14,Footnote 22). The risk of aerosol exposure is not known(Footnote 22).

SPECIAL HAZARDS: The risk of infection is higher in people who don't have gastric acid (i.e. due to gastrectomy or achlorhydria)(Footnote 2).


RISK GROUP CLASSIFICATION: Risk group 2(Footnote 25).

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 to splashes(Footnote 26).

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. Additional precautions should be considered with work involving animals or large scale activities(Footnote 26).


SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (30 min)(Footnote 26).

DISPOSAL: All wastes should be decontaminated before disposal either by steam sterilization, incineration or chemical disinfection(Footnote 26).

STORAGE: The infectious agent should be stored in a sealed and identified container(Footnote 26).


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: September 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 compiled 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.

Public Health Agency of Canada, 2010


Footnote 1
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (Eds.). (2003). Zoonoses Infectious Diseases Transmissible from Animals to Humans (3rd ed.). Washington: ASM press.
Footnote 2
Ryan, K. J., & Ray, C. G. (Eds.). (2004.). Sherris Medical Microbiology: An Introduction to Infectious Disease. (Fourth Edition. ed.). New York.: McGraw-Hill.
Footnote 3
Bronze, M.S., and Greenfield, R.A (Ed.). (2005). Biodefence Principles and Pathogens horizon bioscience.
Footnote 4
Crump, J. A., Bopp, C. A., Greene, K. D., Kubota, K. A., Middendorf, R. L., Wells, J. G., & Mintz, E. D. (2003). Toxigenic Vibrio cholerae serogroup O141-associated cholera-like diarrhea and bloodstream infection in the United States. The Journal of Infectious Diseases, 187 (5), 866-868. doi:10.1086/368330
Footnote 5
Tobin-D'Angelo, M., Smith, A. R., Bulens, S. N., Thomas, S., Hodel, M., Izumiya, H., Arakawa, E., Morita, M., Watanabe, H., Marin, C., Parsons, M. B., Greene, K., Cooper, K., Haydel, D., Bopp, C., Yu, P., & Mintz, E. (2008). Severe diarrhea caused by cholera toxin- producing vibrio cholerae serogroup O75 infections acquired in the southeastern United States. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 47 (8), 1035-1040. doi:10.1086/591973
Footnote 6
Boyd, E. F., & Waldor, M. K. (2002). Evolutionary and functional analyses of variants of the toxin-coregulated pilus protein TcpA from toxigenic Vibrio cholerae non-O1/non-O139 serogroup isolates. Microbiology (Reading, England), 148 (Pt 6), 1655-1666.
Footnote 7
Udden, S. M., Zahid, M. S., Biswas, K., Ahmad, Q. S., Cravioto, A., Nair, G. B., Mekalanos, J. J., & Faruque, S. M. (2008). Acquisition of classical CTX prophage from Vibrio cholerae O141 by El Tor strains aided by lytic phages and chitin-induced competence. Proceedings of the National Academy of Sciences of the United States of America, 105 (33), 11951- 11956. doi:10.1073/pnas.0805560105
Footnote 8
Farina, C., Marini, F., Schiaffino, E., Luzzi, I., Dionisi, A. M., Leoni, F., Ottaviani, D., & Bordoni, S. (2010). A fatal Vibrio cholerae O37 enteritis. Journal of Medical Microbiology, doi:10.1099/jmm.0.023093-0
Footnote 9
Fleming D & Hunt D (Ed.). (2006). Biological Safety Principles and Practices (4th ed.). Washington: ASM Press.
Footnote 10
Smith, J. L. (1999). Foodborne infections during pregnancy. Journal of Food Protection, 62 (7), 818-829.
Footnote 11
Brock, T. D., Madigan, M. T., Martinko, J. M., & Parker, J. (2000). Biology of Microorganisms (9th ed.). New Jersey, USA: Prentice-Hall, Inc.
Footnote 12
Nelson, E. J., Harris, J. B., Morris, J. G.,Jr, Calderwood, S. B., & Camilli, A. (2009). Cholera transmission: the host, pathogen and bacteriophage dynamic. Nature Reviews.Microbiology, 7(10), 693-702. doi:10.1038/nrmicro2204
Footnote 13
Lopez, A. L., Clemens, J. D., Deen, J., & Jodar, L. (2008). Cholera vaccines for the developing world. Human Vaccines, 4 (2), 165-169.
Footnote 14
Collins, C. H., & Kennedy, D. A. (Eds.). (1983). Laboratory-acquired Infections (4th ed.). Oxford: Butterworth-Heinermann.
Footnote 15
Gangarosa, E. J., Saghari, H., Emile, J., & Siadat, H. (1966). Detection of Vibrio cholerae biotype El Tor by purging. Bulletin of the World Health Organization, 34 (3), 363-369.
Footnote 16
Sinha, R., Deb, B. C., De, S. P., Abou-Gareeb, A. H., & Shrivastava, D. L. (1967). Cholera carrier studies in Calcutta in 1966-67. Bulletin of the World Health Organization, 37 (1), 89- 100.
Footnote 17
Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., & Pfaller, M. A. (Eds.). (2007). Manual of Clinical Microbiology (9th ed.). Washington: ASM Press.
Footnote 18
R. I. Glass, M. I. Huq, J. V. Lee, E. J. Threlfall, M. R. Khan, A. R. M. A. Alim, B. Rowe and R. J. Gross. (1983). Plasmid-Borne Multiple Drug Resistance in Vibrio cholerae Serogroup O1, Biotype E1 Tor: Evidence for a Point-Source Outbreak in Bangladesh. J Infect. Dis, 147, 204.
Footnote 19
Das, S., Saha, R., & Kaur, I. R. (2008). Trend of antibiotic resistance of Vibrio cholerae strains from East Delhi. The Indian Journal of Medical Research, 127 (5), 478-482.
Footnote 20
Adhikari, P. C. (1975). Sensitivity of cholera and El Tor vibrios to cold shock. Journal of General Microbiology, 87 (1), 163-166.
Footnote 21
Felsenfeld, O. (1965). Notes on food, beverages and fomites contaminated with Vibrio cholerae. Bulletin of the World Health Organization, 33 (5), 725-734.
Footnote 22
Richmond, J. Y., & McKinney, R. W. (Eds.). (1999). Biosafety in Microbiological and Biomedical Laboratories (4th ed.). Washington: CDC-NIH.
Footnote 23
Gardner, P., & Schaffner, W. (1993). Immunization of adults. The New England Journal of Medicine, 328 (17), 1252-1258.
Footnote 24
Pike, R. M. (1979). Laboratory-associated infections: incidence, fatalities, causes, and prevention. Annual Review of Microbiology, 33, 41-66. doi:10.1146/annurev.mi.33.100179.000353
Footnote 25
Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57- 58 Elizabeth II, 2009. (2009).
Footnote 26
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.