Public Health Agency of Canada
Symbol of the Government of Canada

Share this page

SHIGELLA SPP.

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Shigella spp.

SYNONYM OR CROSS REFERENCE: Serogroup A: S. dysenteriae, serogroup B: S. flexneri, serogroup C: S. boydii, serogroup D: S. sonnei, shigellosis, and bacillary dysentery.

CHARACTERISTICS: Shigella spp., of the Enterobacteriaceae family, are gram-negative rod-shaped pathogenic bacteria (1). They are non-motile, non-encapsulated, and facultative anaerobes that do not ferment lactose, or do so slowly. Different serogroups, considered as species, can be differentiated by their biochemical properties, phage or colicin susceptibility, and polyvanlent antisera can detect specific polysaccharide antigens (2, 3). S. dysenteriae is considered the most virulent, and can produce a potent cytotoxin known as Shigatoxin (4).

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Ingested pathogens can survive gastric acidity and cause illness by infecting the colonic mucosa and multiplying in the colonic epithelial cells, and spreading laterally to adjacent cells (5-7). Infection may be mild and asymptomatic, but it is most commonly characterized by acute intestinal infections upon ingestion, resulting in mild watery diarrhea to severe inflammatory bacillary dysentery or shigellosis, manifested by severe abdominal cramps, nausea and vomiting, fever, tenesmus, anorexia, and stool containing blood and mucus (1, 2, 8). Further complications include Reiter’s syndrome which has been associated with S. flexneri (9, 10), severe dehydration, intestinal perforation, toxic mega colon, bacteremia, toxaemia (11), septicaemia, seizures, toxic encephalopathy with headache and alterations of consciousness, septic shock and convulsions (very rare) (4), and haemolytic uremic syndrome, which have been linked to Shiga toxin (a potent cytotoxin produced by S. dysenteriae that can also cause other neurotoxic effects). Virulence of Shigella is temperature-regulated, as organisms are able to invade HeLa cells at 37°C, and cannot do so in vitro at 30°C (12). Infections are usually self-limiting, but can become life-threatening in immunocompromised patients or if not properly treated. Severity of infection depends on the host, dose, and serotype (2). S. dysenteriae is the most pathogenic species, with a fatality rate up to 20%, whereas S. sonnei usually cause mild forms of shigellosis.

EPIDEMIOLOGY: Worldwide distribution. 5 – 15% of all diarrhea cases can be linked to Shigella spp. infection, where two-thirds of all cases and deaths occur in children younger than 5 years (1). Rate of infection is high during the weaning period due to risk of ingesting contaminated foods; increasing age is associated with decreasing prevalence and severity (13). S. flexneri is most common in developing countries where there is poor hygiene and limited clean drinking water; however, outbreaks are usually caused by S. dysenteriae. S. sonnei is most common in developed countries (14). Infections are most prevalent during summer and early fall in temperate regions and during rainy seasons in tropical regions. High risk groups include children in day-care centers, homosexual men, individuals in custodial institutions, migrant workers, travellers to developing countries, and certain First Nation reserves (6).

HOST RANGE: Humans and higher primates (2).

INFECTIOUS DOSE: Infection can result from ingestion of 10 – 200 organisms (14).

MODE OF TRANSMISSION: Organisms are spread through the fecal-oral route, and transmission is typically through one of three mechanisms: ingestion of contaminated foods (washed with fecally contaminated water, or handled with poor hygiene, commonly in tossed salads, chicken, and shellfish) (2); drinking contaminated water (or in swimming pools); or by person-to-person contact by anal sexual contact (6). Spread of infection linked to flies has also been recorded.

INCUBATION PERIOD: Ranges from 1 – 7 days (6). Acute diarrhea can develop within 1 – 2 days (14). Symptoms and shigellosis may occur within 12 – 50 hours (2).

COMMUNICABILITY: Agents begin to be shed in feces 4 weeks after infection, and it is communicable as long as the organisms are present in excrement (6). Although rare, asymptomatic carriers can also spread the infection for up to some months.

SECTION III - DISSEMINATION

RESERVOIR: Humans are the most common; infections have been observed in primates (2).

ZOONOSIS: None.

VECTORS: Organisms have been found to survive on flies (2).

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Susceptible to ampicillin, trimethoprim, sulfamethoxazole, naldixic acid, ofloxacin, chloramphenicol, fluoroquinolones, and ciprofloxacin (6, 15, 16).

DRUG RESISTANCE: Multidrug-resistant strains are emerging, including those against trimethoprim-sulfamethoxazole (TMP-SMX), ampicillin, and chloramphenicol (15, 17).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde, iodines, phenolics, and formaldehyde (18).

PHYSICAL INACTIVATION: Organisms can be heat-killed by steaming using an autoclave for 1 hour at 100˚C under normal atmospheric pressure (19).

SURVIVAL OUTSIDE HOST: Can survive up to months on dry surfaces (20), up to 10 days in citric juices and carbonated soft drinks, several days on contaminated vegetables (2), over 3 hours on fingers, 2 – 28 days on metal utensils at 15°C or 0 – 13 days at 37°C, in feces for 12 days at 25°C (21), and water for under 3 days (22). Growth is possible at 25°C – 37°C and bacteria can survive at 5°C on MacConkey agar. Flies can carry Shigella for up to 20 – 24 days (23).

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Serological testing of stool isolates can distinguish and confirm serogroups (6).

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

FIRST AID/TREATMENT: Administer appropriate drug therapy. Oral rehydration or electrolyte replacement in dehydrated patients can lead to recovery within days (1). Antibiotics usually are not needed in mild cases, but should be administered for infections involving S. dysenteriae. Antimicrobials may reduce duration of infection, carriage state of the patient, and mortality (2). Other treatments aids for severe cases include mechanical ventilation, anticonvelsants, and inotropics (4).

IMMUNIZATION: No vaccines are currently available; however, live and subunit parental vaccine candidates are under review (24). Live attenuated, conjugate, broad spectrum, and proteosome-based vaccines are also currently being studied (3).

PROPHYLAXIS: None available – hand-washing, strict hygiene control during food preparation, providing safe drinking water, improving toilet facilities and excreta disposal can limit dissemination of the bacteria (6, 23).

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: Shigella species have been recently identified to be the most frequently identified agent of laboratory-acquired infections because of their high virulence and low infectious dose (25).

SOURCES/SPECIMENS: Organisms can be found in stool and rarely in blood samples (4).

PRIMARY HAZARDS: Infection may be acquired through ingestion or accidental parenteral inoculation (4).

SPECIAL HAZARDS: Experimentally infected guinea pigs and other rodents have been previously reported to transmit infection to laboratory personnel, although rare (26).

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 (27). 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. These containment requirements apply to the genus as a whole, and may not apply to each species 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 of exposure to splashes (28).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC) (28). 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 (28).

SECTION VIII – HANDLING AND STORAGE

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 (28).

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration (28).

STORAGE: Properly labelled and sealed containers (28).

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: 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.

Copyright ©

Public Health Agency of Canada, 2010

Canada

REFERENCES

  1. Schroeder, G. N., & Hilbi, H. (2008). Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion. Clinical Microbiology Reviews, 21(1), 134-156. doi:10.1128/CMR.00032-07
     
  2. Downes, F. P., & Ito, K. (Eds.). (2001). Compendium of Methods for the Microbiological Examination of Foods (4th ed.). Washington, DC, USA: American Public Health Association.
     
  3. Kweon, M. N. (2008). Shigellosis: the current status of vaccine development. Current Opinion in Infectious Diseases, 21(3), 313-318. doi:10.1097/QCO.0b013e3282f88b92
     
  4. Erqou, S. A., Teferra, E., Mulu, A., & Kassu, A. (2007). A case of shigellosis with intractable septic shock and convulsions. Japanese Journal of Infectious Diseases, 60(5), 314-316.
     
  5. Formal, S. B., Hale, T. L., & Kapfer, C. (1989). Shigella vaccines. Reviews of Infectious Diseases, 11 Suppl 3, S547-51.
     
  6. Weir, E. (2002). Shigella: wash your hands of the whole dirty business. CMAJ : Canadian Medical Association Journal = Journal De l'Association Medicale Canadienne, 167(3), 281.
     
  7. Niyogi, S. K. (2005). Shigellosis. Journal of Microbiology (Seoul, Korea), 43(2), 133-143.
     
  8. Trevejo, R. T., Abbott, S. L., Wolfe, M. I., Meshulam, J., Yong, D., & Flores, G. R. (1999). An untypeable Shigella flexneri strain associated with an outbreak in California. Journal of Clinical Microbiology, 37(7), 2352-2353.
     
  9. Good, A. E., & Schultz, J. S. (1977). Reiter's syndrome following Shigella flexneri 2a: a sequel to traveler's diarrhea. Report of a case with hepatitis. Arthritis and Rheumatism, 20(1), 100-104.
     
  10. Finch, M., Rodey, G., Lawrence, D., & Blake, P. (1986). Epidemic Reiter's syndrome following an outbreak of shigellosis. European Journal of Epidemiology, 2(1), 26-30.
     
  11. Ovsyshcher, I., Rudnik, L., Alkan, M., & Ilia, R. (1987). Atrio-ventricular block associated with Shigella flexneri infection. European Journal of Clinical Microbiology, 6(4), 504.
     
  12. Yao, R. J., Palmer, K. C., Leon, M. A., & Palchaudhuri, S. (1991). Shigella dysenteriae 60R strain adheres to and invades tissue culture cells in the absence of virulence plasmid. FEMS Microbiology Letters, 67(3), 323-328.
     
  13. Evans, A. S., & Brachman, P. S. (Eds.). (1998). Bacteria Infections of Humans - Epidemiology and Control (3rd ed.). New York, NY, USA: Kluwer Academic / Plenum Publishers.
     
  14. Kurjak, A., & Chervenak, F. A. (Eds.). (2006). Textbook of Perinatal Medicine (2nd ed.). United Kingdom: Informa UK Ltd.
     
  15. Arman, D., Willke, A., & Tural, D. (1994). In vitro activity of eight antibiotics against Salmonella and Shigella species. European Journal of Epidemiology, 10(3), 345-347.
     
  16. DuPont, H. L., Ericsson, C. D., Mathewson, J. J., & DuPont, M. W. (1992). Five versus three days of ofloxacin therapy for traveler's diarrhea: a placebo-controlled study. Antimicrobial Agents and Chemotherapy, 36(1), 87-91.
     
  17. Griffin, P. M., Tauxe, R. V., Redd, S. C., Puhr, N. D., Hargrett-Bean, N., & Blake, P. A. (1989). Emergence of highly trimethoprim-sulfamethoxazole-resistant Shigella in a native American population: an epidemiologic study. American Journal of Epidemiology, 129(5), 1042-1051.
     
  18. Laboratory Safety Manual (1993). (2nd ed.). Geneva: World Health Organization.
     
  19. Mukhopadhaya, A., Mahalanabis, D., Khanam, J., & Chakrabarti, M. K. (2003). Protective efficacy of oral immunization with heat-killed Shigella flexneri 2a in animal model: study of cross protection, immune response and antigenic recognition. Vaccine, 21(21-22), 3043-3050.
     
  20. Kramer, A., Schwebke, I., & Kampf, G. (2006). How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infectious Diseases, 6, 130. doi:10.1186/1471-2334-6-130
     
  21. Islam, M. S., Hasan, M. K., & Khan, S. I. (1993). Growth and survival of Shigella flexneri in common Bangladeshi foods under various conditions of time and temperature. Applied and Environmental Microbiology, 59(2), 652-654.
     
  22. Sorvillo, F. J., Waterman, S. H., Vogt, J. K., & England, B. (1988). Shigellosis associated with recreational water contact in Los Angeles County. The American Journal of Tropical Medicine and Hygiene, 38(3), 613-617.
     
  23. Khalil, K., Lindblom, G. B., Mazhar, K., & Kaijser, B. (1994). Flies and water as reservoirs for bacterial enteropathogens in urban and rural areas in and around Lahore, Pakistan. Epidemiology and Infection, 113(3), 435-444.
     
  24. Niyogi, S. K. (2005). Shigellosis. Journal of Microbiology (Seoul, Korea), 43(2), 133-143.
     
  25. Singh, K. (2009). Laboratory-acquired infections. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 49(1), 142-147. doi:10.1086/599104
     
  26. Fleming, D. O., & Hunt, D. L. (Eds.). (2000). Biological Safety - Procedures and Practices (3rd ed.). Washington, DC, USA: American Society of Microbiology.
     
  27. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).
     
  28. 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.