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ESCHERICHIA COLI

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Escherichia coli, enteropathogenic

SYNONYM OR CROSS REFERENCE: EPEC Footnote 1, Footnote 2, intestinal pathogenic E coli Footnote 3, acute and protracted infant diarrhea Footnote 4.

CHARACTERISTICS: Enteropathogenic Escherichia coli (EPEC) are in the family Enterobacteriaceae Footnote 2. The bacteria are gram negative, rod shaped, non-spore forming, motile with peritrichous flagella or nonmotile, and grow on MacConkey agar (colonies are 2 to 3 mm in diameter and red or colorless) Footnote 5. They can grow under aerobic and anaerobic conditions and do not produce enterotoxins Footnote 1.

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: EPEC cause acute, profuse, watery diarrhea, which rarely becomes persistent Footnote 1. Stools are typically not bloody, mucoid, or dysenteric. Low-grade fever with nausea and vomiting may be present Footnote 1, Footnote 6. EPEC is characterized by the formation of attaching-and-effacing lesions in the involved intestinal areas Footnote 7. Two groups of EPEC are now recognized, typical EPEC and atypical EPEC. Typical EPEC, a leading cause of infantile diarrhea in developing countries, is rare in industrialized countries, where atypical EPEC seems to be a more important cause of diarrhea Footnote 8. Typical and atypical EPEC also differ in genetic characteristics, serotypes, and virulence properties. Atypical EPEC is more closely related to Shiga toxin–producing E. coli (STEC), and like STEC these strains appear to be emerging pathogens Footnote 8. The atypical EPEC strains may be less virulent than the typical ones. One reason may be the lack of the EPEC adherence factor (EAF) plasmid Footnote 8.

EPIDEMIOLOGY: Typical EPEC primarily causes disease in neonates and young children, with most cases occurring in children < 2 years old and particularly in those < 6 months old Footnote 1. Disease may occur in adults if sufficiently high inocula are ingested. Outbreaks have occurred in pediatric wards, nurseries, and day care centers and in adults that have consumed contaminated food from a buffet. In developing countries, EPEC are highly prevalent and are an important cause of childhood diarrheal disease and dehydration-associated deaths. Studies in Brazil, Mexico, and South Africa have shown that 30–40% of infant diarrhea can be attributed to EPEC Footnote 6. Atypical EPEC are prevalent in both developed and developing countries. They appear to cause disease in a broader range of ages and have been associated with outbreaks in developed countries Footnote 9. However, the enteropathogenicity and the role of certain atypical EPEC strains is controversial Footnote 10. At least two case-control studies showed no statistical difference in infection rates between cases and matched controls suggesting they may be part of the normal human flora Footnote 11-Footnote 13. It is likely that EPEC and atypical EPEC in particular, are vastly underreported.

HOST RANGE:Humans Footnote 1 and animals, including cattle and horses Footnote 14.

INFECTIOUS DOSE: The infectious dose of EPEC in healthy adults is estimated to be 106 organisms Footnote 15.

MODE OF TRANSMISSION: Contaminated food, water, and fomites serve as vehicles for the fecal/oral transmission of EPEC Footnote 1, Footnote 16.

INCUBATION PERIOD: The incubation period is between 6-48 hours Footnote 17.

COMMUNICABILITY: Can be transmitted through direct contact with infected persons Footnote 14.

SECTION III - DISSEMINATION

RESERVOIR: Typical EPEC: Humans Footnote 18. Atypical EPEC: dogs, cats, cattle, sheep, rabbits, monkeys and humans Footnote 8, Footnote 9.

ZOONOSIS: Yes. May be transmitted when handling infected cattle, dogs, cats, sheep, rabbits, and horses Footnote 19.

VECTORS: None.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY/RESISTANCE: Susceptible to carbapenem, fosfomycin-trometanol, nitrofurantoin, and bovine apo-lactoferrin. E. coli can be resistant to chloramphenicol, β lactams, nalidixic acid, ampicillin and ciprofloxacin. Fluoroquinolones such as ciprofloxacin enhance toxin production Footnote 3, Footnote 20.

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to a combination of 2,2-dibromo-2-cyanoacetamide (DBA) with sodium iodide (20:80 parts), iodine, 2 % glutaraldehyde, quaternary ammonium (20°C, 0.5 min), hypochlorite (0.525%, 20°C, 0.5 min), phenolics (20°C, 0.5 min), and ethyl alcohol (70%, 20°C, 0.5 min) Footnote 21-Footnote 23.

PHYSICAL INACTIVATION: Ozone can inactivate E. coli Footnote 24. E. coli is also sensitive to heat treatment, especially at temperatures of 70°C or higher Footnote 19, Footnote 25.

SURVIVAL OUTSIDE HOST: E. coli can survive for 1.5 hours to 16 months on dry inanimate surfaces Footnote 26.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Stool culture is a common method used to identify E. coli Footnote 27. DNA probes and techniques such as PCR can be applied directly to clinical samples and food Footnote 3. Both typical and atypical EPEC are most frequently identified by detection of the eae gene encoding the intimin protein. The presence of the eae gene and demonstration of the absence of the verotoxin (enterotoxin) gene are absolutely required for the molecular identification of EPEC Footnote 1. To identify typical EPEC, PCR or DNA hybridization methods can be used for detection of the EAF plasmid and the gene encoding bfp Footnote 1, Footnote 3. Additional tests that may be performed in some situations are the fluorescent actin staining test and adherence tests showing localized adherence (LA).

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

FIRST AID TREATMENT: Treatment with trimethoprim/sulfamethoxazole (TMP-SMX) or quinolones reduces the duration of diarrhea Footnote 28. Treatment of fluid and electrolyte loss is usually achieved through oral rehydration Footnote 19. The use of the World Health Organization Oral Rehydration Salts (ORS) solution has been recommended Footnote 1. Intravenous rehydration may be necessary for infants, individuals with excessive vomiting, or those with severe dehydration. Bismuth subsalicylate may decrease the amount of diarrhea and the duration of disease. Antimicrobial therapy is generally not indicated, because of the self-limited nature of most of these diseases.

IMMUNIZATION: There are currently no vaccines approved for human use against diarrheagenic E. coli Footnote 1.

PROPHYLAXIS: TMP-SMX is recommended for short term use (< 2 weeks) for those at a high risk of disease Footnote 28. Bismuth subsalicylate provides some prophylactic benefit, but should not be used as a substitute for other preventive measures Footnote 1.

SECTION VI - LABORATORY HAZARDS

LABORATORY ACQUIRED INFECTIONS: 12 cases of laboratory acquired infections with E. coli have been reported, the majority of which have been caused by enterohemorrhagic E.coli (EHEC) Footnote 29.

SOURCES / SPECIMENS: Stools and fecally contaminated material Footnote 1, Footnote 6, Footnote 16.

PRIMARY HAZARD: Ingestion Footnote 29.

SPECIAL HAZARD: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 Footnote 30.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures Footnote 31.

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.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC) Footnote 31. 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.

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up Footnote 31.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism by autoclave, chemical disinfection, gamma irradiation, or incineration before disposing Footnote 31.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labeled Footnote 31.

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: December 2011

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, 2011
Canada

REFERENCES:

Footnote 1
Wilson, W. R., Sande, M. A., & Drew, W. L. (2001). Current diagnosis & treatment in infectious diseases. New York: Lange Medical Books/McGraw-Hill. Retrieved from http://online.statref.com/document.aspx?FxId=66&DocID=1&grpalias=

Footnote 2
Nataro, J. P., Bopp, C. A., Fields, P. I., Kaper, J. B., & Strockbine, N. A. (2007). Escherichia, Shigella and Salmonella. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical Microbiology (9th ed., pp. 670-687). Washington, DC, USA: ASM press.

Footnote 3
Baylis, C. L., Penn, C. W., Thielman, N. M., Guerrant, R. L., Jenkins, C., & Gillespie, S. H. (2006). Escherichia coli and Shigella spp. In S. H. Gillespie, & P. M. Hawkey (Eds.), Principles and Practice of Clinical Bacteriology (2nd ed., pp. 347-365). England, UK: John Wiley and Sons Ltd.

Footnote 4
Levine, ,Myron, & Vial, ,Pablo. (1988). Escherichia coli that cause diarrhea. Indian Journal of Pediatrics, (2), 183-190. doi:10.1007/BF02722179

Footnote 5
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: ASM press.

Footnote 6
Stenutz, R., Weintraub, A., & Widmalm, G. (2006). The structures of Escherichia coli O-polysaccharide antigens. FEMS Microbiology Reviews, 30(3), 382-403.

Footnote 7
Pothoulakis, C. (2009). Review article: Anti-inflammatory mechanisms of action of Saccharomyces boulardii. Alimentary Pharmacology and Therapeutics, 30(8), 826-833.

Footnote 8
Trabulsi, L. R., Keller, R., & Tardelli Gomes, T. A. (2002). Typical and atypical enteropathogenic Escherichia coli. Emerging Infectious Diseases, 8(5), 508-513.

Footnote 9
Moura, R. A., Sircili, M. P., Leomil, L., Matte, M. H., Trabulsi, L. R., Elias, W. P., Irino, K., & Pestana de Castro, A. F. (2009). Clonal relationship among atypical enteropathogenic Escherichia coli strains isolated from different animal species and humans. Applied and Environmental Microbiology, 75(23), 7399-7408. doi:10.1128/AEM.00636-09

Footnote 10
Afset, J. E., Bruant, G., Brousseau, R., Harel, J., Anderssen, E., Bevanger, L., & Bergh, K. (2006). Identification of virulence genes linked with diarrhea due to atypical enteropathogenic Escherichia coli by DNA microarray analysis and PCR. Journal of Clinical Microbiology, 44(10), 3703-3711. doi:10.1128/JCM.00429-06

Footnote 11
Jensen, C., Ethelberg, S., Olesen, B., Schiellerup, P., Olsen, K. E., Scheutz, F., Nielsen, E. M., Neimann, J., Hogh, B., Gerner-Smidt, P., Molbak, K., & Krogfelt, K. A. (2007). Attaching and effacing Escherichia coli isolates from Danish children: clinical significance and microbiological characteristics. Clinical Microbiology and Infection : The Official Publication of the European Society of Clinical Microbiology and Infectious Diseases, 13(9), 863-872. doi:10.1111/j.1469-0691.2007.01773.x

Footnote 12
Fujihara, S., Arikawa, K., Aota, T., Tanaka, H., Nakamura, H., Wada, T., Hase, A., & Nishikawa, Y. (2009). Prevalence and properties of diarrheagenic Escherichia coli among healthy individuals in Osaka City, Japan. Japanese Journal of Infectious Diseases, 62(4), 318-323.

Footnote 13
Nishikawa, Y., Zhou, Z., Hase, A., Ogasawara, J., Kitase, T., Abe, N., Nakamura, H., Wada, T., Ishii, E., Haruki, K., & Surveillance Team. (2002). Diarrheagenic Escherichia coli isolated from stools of sporadic cases of diarrheal illness in Osaka City, Japan between 1997 and 2000: prevalence of enteroaggregative E. coli heat-stable enterotoxin 1 gene-possessing E. coli. Japanese Journal of Infectious Diseases, 55(6), 183-190.

Footnote 14
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (2003). Bacterial Zoonoses. Zoonoses: Infectious Diseases Transmissible from Animals to Humans. (3rd ed., pp. 173-252). Washington, DC.: ASM press.

Footnote 15
Todar, K. (2008). Pathogenic E. coli InTodar's Online Textbook of Bacteriology. Retrieved 04,21, 2010, from http://www.textbookofbacteriology.net/e.coli_4.html

Footnote 16
Jay, J. M., Loessner, M. J., & Golden, D. A. (2005). Foodborne Gastroenteritis Caused by Escherichia coli. Modern food microbiology (7th ed., pp. 637-656). NY, USA: Springer Science.

Footnote 17
Chao, H. -., Chen, C. -., Chen, S. -., & Chiu, C. -. (2006). Bacterial enteric infections in children: Etiology, clinical manifestations and antimicrobial therapy. Expert Review of Anti-Infective Therapy, 4(4), 629-638.

Footnote 18
Johnson, T. J., & Nolan, L. K. (2009). Pathogenomics of the virulence plasmids of Escherichia coli. Microbiology and Molecular Biology Reviews, 73(4), 750-774.

Footnote 19
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., Graevenitz, A. V., & Zahner, H. (2003). Bacterial Zoonoses. Zoonoses: Infectious diseases transmissible from animals to humans (3rd ed., pp. 196-200). Washington DC: ASM press.

Footnote 20
Ochoa, T. J., & Cleary, T. G. (2009). Effect of lactoferrin on enteric pathogens. Biochimie, 91(1), 30-34.

Footnote 21
Lehmann, R. H. (2001). Synergism in Disinfectant Formulation. In S. S. Block (Ed.), Disinfectant, sterlization and preservation (5th ed., pp. 459-472). PA, USA: Lipincott Williams and Wilkins.

Footnote 22
Scott, E. M., & Gorman, S. P. (1996). Glutaraldehyde. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 361-381). Philadelphia P.A.: Lipincott Williams and Wilkins.

Footnote 23
Weber, D. J., & Rutala, W. A. (2001). The emerging nosocomial pathogens cryptosporidium, escherichia coli O157:H7, helicobacter pylori, and hepatitis C: Epidemiology, environmental survival, efficacy of disinfection, and control measures. Infection Control and Hospital Epidemiology, 22(5), 306-315.

Footnote 24
Weavers, L. K., & Wickramanayake, G. B. (2001). Disinfection and Sterilization Using Ozone. In S. S. Block (Ed.), Disinfection, Sterilization and preservation (5th ed., pp. 205-214). PA, USA: Lippincott, Williams and Wilkins.

Footnote 25
Zhao, T., Doyle, M. P., Kemp, M. C., Howell, R. S., & Zhao, P. (2004). Influence of freezing and freezing plus acidic calcium sulfate and lactic acid addition on thermal inactivation of Escherichia coli O157:H7 in ground beef. Journal of Food Protection, 67(8), 1760-1764.

Footnote 26
Kramer, A., Schwebke, I., & Kampf, G. (2006). How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infectious Diseases, 6

Footnote 27
Jones, T. F. (2007). Investigation of Foodborne and Waterborne Disease Outbreaks. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical Microbiology (9th ed., pp. 152-169). Washignton, DC: ASM press.

Footnote 28
Ryan, K. J. (2004). Enterobacteriaceae. In K. J. Ryan, & C. G. Ray (Eds.), Sherris Medical Microbiology: Introduction to infectious diseases (4th ed., pp. 343-371). USA: Mcgraw Hill.

Footnote 29
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.

Footnote 30
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).

Footnote 31
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.