Pathogen Safety Data Sheets: Infectious Substances – Enterobacter spp.



NAME: Enterobacter spp.

SYNONYM OR CROSS REFERENCE: Species include: E. cloacae, E. aerogenes (previously known as Klebsiella mobilis), E. agglomerans (reclassified as Pantoea agglomerans), E. gergoviae, E. sakazakii (also Cronobacter sakazakii ), E. cowanii, E. hormaechei, E. taylorae , E. asburiae, E. intermedius, E. amnigenus, E. dissolvens, E. kobei, E. pyrinus and E. nimpressuralis(1) , E. cancerogenus(2).

CHARACTERISTICS: Enterobacter spp. are in the family Enterobacteriaceae(1). Enterobacter spp. are facultatively anaerobic Gram-negative bacilli, 0.6-1 μm in diameter and 1.2-3 μm long, motile by means of peritrichous flagella and have class 1 fimbriae(1,3,4). They produce acid upon glucose fermentation, are methyl red negative, and Voges-Proskauer positive, with an optimal growth temperature of 30 °C(1). 80 % are encapsulated(1).


PATHOGENICITY/TOXICITY: Enterobacter spp., particularly E. aerogenes and E. cloacae, have been associated with nosocomial outbreaks, and are considered opportunistic pathogens(1,5). Enterobacter spp. can cause numerous infections, including cerebral abscess, pneumonia, meningitis, septicemia, and wound, urinary tract (particularly catheter-related UTI), and abdominal cavity/intestinal infections(6,7). In addition, Enterobacter spp. have been noted in intravascular device-related infections, and surgical site infections (primarily postoperative or related to devices such as biliary stents)(7). Many species can cause extra-intestinal infections(6), for example, Enterobacter sakazakii, has been associated with brain abscesses in infants and with meningitis(3,7). Mortality rates for bacterial meningitis range from 40-80%(5).

EPIDEMIOLOGY: Worldwide distribution(4). E. cloacae and E. aerogenes are responsible for the majority of Enterobacter infections, 65-75% and 15-25 %, respectively(7). Enterobacter spp. are commonly found in intensive care units and are responsible for 8.6 % of nosocomial infections according to the US Centers for Disease Control and Prevention (CDC)(8). Enterobacter spp . are also involved in a considerable proportion of reported bacteremia cases; in one pediatric hospital, Enterobacter spp. were noted to be the most common cause of bacteremia, accounting for 14 % of cases(8), while in adults Enterobacter spp. are responsible for 1.5-6% of bacteremia cases(1). From 1970 to 1971, there was an epidemic of septicemia caused by contaminated IV products that affected 378 patients across the United States(9).

HOST RANGE: Plants(6), humans, and animals(1). Enterobacteriaceae are primarily colonizers of the lower gastrointestinal tract of humans and animals(10).

INFECTIOUS DOSE: There is no experimental or epidemiologic evidence of infectious dose or Enterobacter spp. available; however, approximately 1000 cells have been considered infectious, similar to the infectious dose of the pathogenic bacteria Neisseria meningitidis , Escherichia coli O157, and Listeria monocytogenes 4b(11).

MODE OF TRANSMISSION: Transmission is through direct or indirect contact of mucosal surfaces with infectious agent (e.g. bacteria can transfer from contaminated hands in neonatal units or contaminated urinals)(1) or, in the case of endogenous flora, through transfer to adjacent, susceptible, sterile body sites(10). Enterobacteriaceae can also be spread through the fecal-oral route(12).


COMMUNICABILITY: Person to person transmission can occur through the fecal-oral route(12).


RESERVOIR: Enterobacter spp. are commonly found in soil and water; E. cloacae and E. aerogenes can inhabit the intestines of humans and animals and can also be found in sewage(1). E. aerogenes has also been found in dairy products(2).




DRUG SUSCEPTIBILITY: Most Enterobacter spp . are susceptible to cefepime(7), aminoglycosides, fluoroquinolones, and trimethoprim-sulfamethoxazole(8). Tigecycline has been shown effective in vitro(7).

DRUG RESISTANCE: Enterobacter spp. are resistant to ampicillin; first- and second- generation cephalosporins(7); and cephalothin(6).

SUSCEPTIBILITY TO DISINFECTANTS: While information specific to Enterobacter spp. is not available, most species in the family Enterobacteriaceae are susceptible to 70-80 % ethanol(13) and most vegetative bacteria are also susceptible to 1% sodium hypochlorite, glutaraldehyde, formaldehyde, iodines, hydrogen peroxide, peracetic acid, and quaternary ammonium compounds(14).

PHYSICAL INACTIVATION: Enterobacter sakazakii have been shown to be inactivated by pulsed electric fields and high hydrostatic pressure(15,16). While additional information specific to Enterobacter spp. is unavailable, most vegetative bacteria can be inactivated by moist heat (121 °C for 15 min- 30 min) and dry heat (160-170 °C for 1-2 hours)(17).

SURVIVAL OUTSIDE HOST: Enterobacter spp. are commonly found in the environment (e.g. soil, water, and sewage)(6). Many species of the family Enterobacteriaceae survive readily in nature requiring only water and a minimal energy source(10).


SURVEILLANCE: Monitor for symptoms. Stool specimen should be observed for presence of blood or mucous(3). Enterobacter species can be isolated by plating into MacConkey agar, eosin methylene blue agar or blood agar(6). PCR assays for the detection and identification of Enterobacter spp. have also been developed(6).

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

FIRST AID/TREATMENT: Administer appropriate antibiotics accounting for local antimicrobial susceptibility patterns(1).




LABORATORY ACQUIRED INFECTIONS: There has been 1 reported case of symptomatic laboratory acquired infection with E. aerogenes(18).

SOURCES / SPECIMENS: Infected urine, feces, respiratory secretions, wound exudates, blood, water, soil, and plants(2,6).

PRIMARY HAZARD: Direct or indirect contact of infected specimens with mucous membranes, parenteral inoculation, aerosols, and ingestion(1,10,19,20).



RISK GROUP CLASSIFICATION: Risk Group 2(21). This risk group applies to the genus as a whole, and may not apply to every species within the genus.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures(22). These containment requirements apply to the genus as a whole, and may not apply to each species/subspecies/clonal isolate/strain within the genus.

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(22).

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


SPILLS: Allow aerosols to settle. Wearing protective clothing, gently cover spill with paper towels and apply and appropriate disinfectant, starting at perimeter and working towards the centre. Allow sufficient contact time before clean up(22).

DISPOSAL: Decontaminate before disposal - steam sterilization, incineration, chemical disinfection(22).

STORAGE: In sealed containers that are appropriately labeled.


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 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.

Copyright ©
Public Health Agency of Canada, 2010


  1. Hart, C. A. (2006). Klebsiella. Citrobacter, Enterobacter and Serratia spp .. In S. H. Gillespie, & P. M. Hawkey (Eds.), Principles and practice of Clinical Bacteriology (2nd ed., pp. 377- 386). England, UK: John Wiley and Sons Ltd.
  2. Abbott, S. L. (2007). Klebsiella , Enterobacter , Citrobacter , Serratia , Plesiomonas , and Other Enterobacteriaceae . In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & M. L. Landry (Eds.), Manual of Clinical Microbiology (9 th ed., pp. 698-715). Washington, DC: ASM press.
  3. Summaries of Infectious Diseases. (2009). In L. Pickering, C. J. Baker, D. W. Kimberlin & S. S. Long (Eds.), RED BOOK: 2009 REPORT OF THE COMMITTEE ON INFECTIOUS DISEASES (28th ed., ). Elk Grove Village, IL: American Academy of Pediatrics. Retrieved from
  4. Paterson, D. L., Rossi, F., Baquero, F., Hsueh, P. R., Woods, G. L., Satishchandran, V., Snyder, T. A., Harvey, C. M., Teppler, H., & DiNubile, M. J. (2005). In vitro susceptibilities of aerobic and facultative Gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: the 2003 Study for Monitoring Antimicrobial Resistance Trends (SMART). Journal of Antimicrobial Chemotherapy, 55 (6), 965.
  5. Pagotto, F. J., Nazarowec-White, M., Bidawid, S., & Farber, J. M. (2003). Enterobacter sakazakii: infectivity and enterotoxin production in vitro and in vivo. Journal of Food Protection&# 174;, 66 (3), 370-375.
  6. Farmer, J. J., Boatwright, K. D., & Janda, J. M. (2007). Enterobacteriaceae: Introduction and identification. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical microbiology (9th ed., pp. 649-669). Washington, DC, USA: ASM press.
  7. Russo, T. A., & Johnson, J. R. (2008). Diseases Caused by Gram-Negative Enteric Bacilli. In A. S. Fauci, & A. Fauci (Eds.), Harrison's principles of internal medicine (17th ed., ). New York: McGraw-Hill Medical Pub. Division. Retrieved from
  8. Boyce, T. G., Gruber, W. C., & Fisher, R. G. (2004). Enterobacter. In R. D. Feigin, Cherry, Demmler & Kaplan (Eds.), Textbook of pediatric infectious diseases (5th ed., pp. 1427- 1431). PA, USA: Saunders.
  9. Maki, D. G., Rhame, F. S., Mackel, D. C., & Bennett, J. V. (1976). Nationwide epidemic of septicemia caused by contaminated intravenous products:: I. Epidemiologic and clinical features. The American Journal of Medicine, 60 (4), 471-485.
  10. Ryan, K. J. (2004). Enterobacteriaceae. In K. J. Ryan, C. G. Ray & J. C. Sherris (Eds.), Sherris medical microbiology :an introduction to infectious diseases (4th ed., ). New York: McGraw-Hill, Medical Pub. Division. Retrieved from
  11. Iversen, C., & Forsythe, S. (2003). Risk profile of Enterobacter sakazakii, an emergent pathogen associated with infant milk formula. Trends in Food Science and Technology, 14 (11), 443-454.
  12. Bayda , B., Uslu, H., Yavuz, I., Ceylan, I., & Da suyu, . M. (2007). Effect of a chronic nail- biting habit on the oral carriage of Enterobacteriaceae. Oral Microbiology and Immunology, 22 (1), 1-4.
  13. Widmer, A. F., & Frei, R. (2007). Decontamination, Disinfection and sterilization. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical Microbiology (9th ed., pp. 65-96). Washington, DC: ASM press.
  14. Rutala, W. A. (1996). APIC guideline for selection and use of disinfectants. American Journal of Infection Control, 24 (4), 313-342.
  15. Pérez, M. C. P., Aliaga, D. R., Bernat, C. F., Enguidanos, M. R., & López, A. M. (2007). Inactivation of Enterobacter sakazakii by pulsed electric field in buffered peptone water and infant formula milk. International Dairy Journal, 17 (12), 1441-1449.
  16. Pina Pérez, M. C., Rodrigo Aliaga, D., Saucedo Reyes, D., & Martínez López, A. (2007). Pressure inactivation kinetics of Enterobacter sakazakii in infant formula milk. Journal of Food Protection, 70 (10), 2281-2289.
  17. Pflug, I. J., Holcomb, R. G., & Gomez, M. M. (2001). Principles of the thermal destruction of microorganisms. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 79-129). Philadelphia, PA: Lipincott Williams and Wilkins.
  18. Harding, A. L., & Byers, K. B. (2006). Epidemiology of Laboratory-associated infections. In Fleming, D and Hunt, D. (Ed.), Biological Safety: principles and practices (4th ed., pp. 53- 77). Washington, DC, USA: ASM press.
  19. Xie, H., Gan, X., & Ma, F. (2009). Characteristics of Bacterial and Fungal Aerosol in Gymnasia in China. Paper presented at the 2009 International Conference on Energy and Environment Technology, 19-23.
  20. Zuber, S., Boissin-Delaporte, C., Michot, L., Iversen, C., Diep, B., Brùssow, H., & Breeuwer, P. (2008). Decreasing Enterobacter sakazakii (Cronobacter spp.) food contamination level with bacteriophages: prospects and problems. Microbial Biotechnology, 1 (6), 532-543.
  21. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
  22. 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.
Report a problem or mistake on this page
Please select all that apply:

Privacy statement

Thank you for your help!

You will not receive a reply. For enquiries, contact us.

Date modified: