Shiga toxin-producing Escherichia coli (STEC) infection

Queensland Health Guidelines for Public Health Units

Revision History

 Version  Date  Changes
1.0 June 2013 Full revision of guideline. 
2.0 July 2014 Full revision of guideline.

Infectious Agent

Shiga toxin-producing Escherichia coli (STEC) are defined as strains of E. coli that produce Shiga toxins (stx). Stx are cytotoxic to Vero cells and this is the basis for an alternative nomenclature, verotoxins (VT) and verotoxigenic E. coli (VTEC). Strains of STEC that cause haemorrhagic colitis are commonly referred to as enterohaemorrhagic E. coli (EHEC).

There are many different E. coli serotypes; most are non-pathogenic. The most common STEC serotype reported in Australia between 2001 and 2009 was Escherichia coli O157 (58% ) followed by O111 (14%) and O26 (11%) (1).

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Notification Criteria

Note: Where STEC is isolated in the context of haemolytic uraemic syndrome (HUS), it should be notified as both STEC and HUS.

Laboratory definitive evidence

  1. Isolation of Shiga toxin-producing E. coli from faeces

    OR
  2. Identification of the gene/s associated with the production of Shiga toxin or Vero toxin in E. coli by nucleic acid testing on isolate or fresh faeces.

    Note: The national case definition requires that identification of genes associated with the production of Shiga toxin be from an "isolate or raw bloody diarrhoea" (2).

Community Outbreak Criteria

Two or more associated cases involving more than one household.

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Notification Procedure

Pathology Laboratories

To notify on confirmation of diagnosis by telephone or facsimile.

Attending Medical Practitioners/Medical Superintendents (or Delegates)

Notify two or more possibly linked cases of gastroenteritis by telephone or facsimile.

Reporting to NOCS

Report confirmed cases only

Confirmed case

A confirmed case requires laboratory definitive evidence.

HUS case suspected to be STEC-related (see HUS guideline)

Diarrhoea-associated HUS in which no other pathogen able to cause HUS has been identified. Assume all cases of diarrhoea-associated HUS to be STEC-related until proven otherwise. Report only as a HUS case but manage case and contacts as for confirmed STEC cases.

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Objectives of surveillance

  1. To identify outbreaks of STEC and HUS promptly, so as to enable rapid public health response
  2. To monitor the epidemiology of STEC infections.

Public Health Significance and Occurrence

Most Shiga toxin producing E. coli cases notified in Australia are sporadic infections. Infected individuals usually present with bloody diarrhoea and some may experience kidney failure due to HUS. HUS may occur in 5-10% of individuals during EHEC outbreaks and is more likely to occur among children or the elderly (3). HUS carries a 12% risk of death or end stage renal disease with 25% of survivors suffering long-term renal consequences (4). Therefore, considerable effort is made by public health authorities to investigate and control the spread of STEC infection. In Australia between 2000 and 2010 there were an average of 15 cases of HUS (range 3 to 31) notified annually to NNDSS. In Queensland, an average of two HUS cases (range 0 to 3) were notified annually over the same time period. There were six community STEC outbreaks reported in Queensland between 2001 and 2013. Two outbreaks were caused through zoonotic transmission (both petting zoos), two outbreaks involved person to person transmission and one outbreak was associated with contaminated tank water. No source or mode of transmission was identified in the other outbreak.

Australia’s largest outbreak of STEC infection occurred in Queensland during August 2013 associated with a petting zoo at the RNA (Ekka). There were 57 notified cases of E. coli O157:H- infection including 55 primary infections and 2 secondary infections acquired through transmission from a primary case in the same household. The median age of cases was 9 years (65% cases were children). Bloody diarrhoea was reported among 41% cases but there were no reports of HUS. The median incubation period among primary cases was 4 days (range 1 to 11 days).

A case control study covering six Australian jurisdictions over the period 2003-2007 found risk factors for infection to include consuming hamburgers, eating at restaurants, occupational exposure to raw red meat by the case or a member of their household, occupational exposure to animals, consumption of sliced processed chicken meat, consumption of sliced corned beef, bush camping in Australia and eating at catered events (5).  

A large outbreak of E. coli O111 infection occurred in Australia in 1995 associated with the consumption of contaminated mettwurst (6). Outbreaks have also been associated with environmental exposures including visiting petting zoos and dairy farms.

The most common cause of sporadic infection and outbreaks of E. coli O157:H7 in the United States has been the consumption of undercooked minced beef (7). Other documented causes of infection include consumption of contaminated alfalfa sprouts, salads (lettuce, coleslaw), fermented meat, unpasteurised milk, apple cider and drinking water (8).

A large international outbreak of E. coli O104:H4, associated with more than 3000 cases of infection and over 800 cases of HUS, occurred predominantly in Germany in May and June 2011 (9). Sprouts grown from fenugreek seeds were implicated as the source of infection on the basis of traceback investigation (10).

Clinical Features

STEC causes a wide range of illness. Infection may be asymptomatic. Symptomatic infection can vary from mild non-bloody diarrhoea to haemorrhagic colitis. HUS is typically reported among cases with bloody diarrhoea, though it can also develop in patients with non-bloody diarrhoea. Illness in patients with non-bloody diarrhoea is usually less severe, and these individuals are less likely to develop systemic sequelae. Haemorrhagic colitis is marked by an acute onset of severe abdominal cramps followed by a progression from watery to bloody diarrhoea that lasts for 4-10 days. Stools are usually free of white blood cells. Nausea and vomiting may occur. Fever is comparatively mild, even absent. The infection is normally self-limiting with most patients recovering within 7-10 days of onset. However, in some instances, Shiga toxins are absorbed from the gut and damage vascular endothelial cells in target organs such as the gut and kidney.

The development of fever and leukocytosis may herald complications, which include HUS (more commonly in children), thrombotic thrombocytopenic purpura (more commonly in the aged), and death. HUS usually develops between 2 and 14 days after the onset of diarrhoea (11). By the time HUS develops the STEC organism may no longer be detectable in the stool.

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Reservoir

The lower intestinal tract of ruminants, particularly healthy adult cattle (both beef and dairy) and sheep are the principal reservoirs of STEC. STEC can also colonise birds, dogs and cats. Some strains of STEC cause diarrhoea in young calves.  STEC can survive for months in the environment including animal faeces, soil and water. Humans may also serve as a reservoir for person-to-person transmission.

Mode of Transmission

Transmission occurs via the faecal-oral route. Ingestion of bacteria may occur through:

  • Consumption of contaminated food or water. Most human infections are probably foodborne. Transmission occurs primarily by ingestion of faecally contaminated food, most often inadequately cooked beef, especially minced beef, dried, fermented or ready to eat meat products (e.g. salami), fresh produce (including melons, lettuce, coleslaw, cider and alfalfa sprouts) and also unpasteurised milk and milk products. Waterborne transmission can also occur from contaminated drinking and recreational waters.
  • Direct contact with infected animals or their faeces.
  • Cross contamination from fomites (e.g. contaminated bathroom surfaces).
  • Person-to-person contact with someone who is infectious (particularly in families, childcare settings and residential care facilities).
  • In large outbreaks the risk of secondary transmission of STEC O157 is estimated to be 7-11% (12). A study in Wales calculated the household transmission rate for sporadic STEC O157 infection to be between 4 and 15% (13), while a Scottish study of both sporadic and outbreak cases over a 10 year period in Scotland calculated the secondary transmission rate for E. coli O157 to be 11% (14). This estimate was based on the testing of symptomatic secondary cases only and is therefore likely to be an underestimate. Most secondary cases occurred in the same household as the index case.

Incubation Period

Incubation period is usually 2 to 10 days (with a median of 3-4 days), though may be as long as 14 days. The median incubation period among primary cases from the RNA (EKKA) outbreak in 2013 was 4 days (range 1 to 11 days).

Period of Communicability

Duration of excretion of the pathogen is usually a week or less in adults and up to 3 weeks in children (15) although excretion can extend up to 14 weeks (16). Based on date of onset of diarrhoea and date of last positive stool sample, the median duration of excretion among primary cases from the RNA (EKKA) outbreak in 2013 was 19 days (range 2 to 52 days). For children aged <5 years, the median duration of excretion was 29 days (range 5 to 37 days).

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Susceptibility and Resistance

The infectious dose is reported to be very low (11, 17). Little is known about differences in susceptibility and immunity. Children less than 5 years of age are at greatest risk of developing HUS (18). Old age also appears to be a risk factor for developing HUS (11).

Management

Management of cases and contacts is determined by whether they are symptomatic and their risk category. Groups at higher risk of transmitting infection include:

  • Children under 5 years of age and other people unable to maintain good hygiene
  • Food handlers (where this involves preparing or serving unwrapped food to be served raw or not subjected to further heating)
  • Carers of the following groups: children under 5 years of age, those unable of maintain good hygiene and the elderly
  • Health care workers

Cases (Flowchart 1).

Investigation
All cases should be investigated. Attempt to identify the food vehicle or source of infection, such as ingestion of suspect foods, especially raw or undercooked meat, fermented meats, sprouts, unpasteurised milk and their products, exposure to petting zoos or farms with ruminants, drinking or contact with untreated water, and recent overseas travel. Identify if the case is in a high risk category and whether they attended childcare or worked as a food handler or child carer or health care worker during their exposure and/or infectious period. Microbiological evidence of clearance should be obtained from all cases. This consists of 2 successive negative stool samples obtained at least 24 hours apart and not sooner than 48 hours after the last dose of antimicrobials (if administered). The first clearance sample should not be taken until at least 24 hours after symptoms have ceased.

Restriction
Any case in a high risk group should be excluded from work or high risk setting (e.g. childcare) until microbiological clearance has been obtained.

Cases who are not in a high risk group should be excluded from work and other settings until diarrhoea has ceased for at least 24 hours.

In cases of persistent excretion, consider referral to an infectious diseases physician. Those in high risk occupations may be allowed to return to work in non-high-risk roles. In circumstances where exclusion from childcare may pose significant financial difficulties on families, children under 5 years of age may be considered for individual (solo) childcare in consultation with Department of Communities. However, this would require counselling of the carer on the necessary hygiene precautions and risks, and recommendation for screening following eventual microbiological clearance by case/termination of care of child.

Treatment
While the use of antibiotics has been described both in treatment of cases early in their infection, and in eliminating carriage in asymptomatic individuals (19, 20), the role of antibiotics in the management of STEC is unclear and there is some concern that they may increase the risk of HUS. Where prolonged STEC carriage is causing a significant social or psychological burden, antibiotics may be considered in consultation with an infectious diseases physician and/ or paediatrician on a case by case basis.

Counselling
The case/carers of case should be advised of the nature of the infection, its mode of transmission and the low infectious dose. The importance of good hygiene should be emphasised. Educate about hygiene practices, in particular the importance of washing hands with soap and water for at least 15 seconds, after using the toilet, prior to handling food, or caring for children or patients. Cases should be made aware of the concerns around use of antibiotics in the management of STEC.     

Contacts (see Flowchart 2)

Contact Tracing
Yes

Definition
Contacts include (i) people exposed to the suspected or identified source(s) of infection and (ii) people who are believed to have had significant risk of direct or indirect exposure to the excreta of an infectious person. This includes but is not limited to household members, people who physically care for or are cared by the case, and childcare contacts.        

Investigation
Investigation of contacts should be performed in all cases. Contacts who are symptomatic, in the same household as the case or are in a high risk group should be screened for infection with 2 stool specimens collected at least 24 hours apart.

Restriction
Symptomatic contacts
All contacts with diarrhoea should be excluded from work/school/childcare whilst symptomatic; those in high risk groups should remain excluded until 2 negative stool specimens are obtained. Symptomatic contacts who are not in high risk groups can return to work 24 hours following resolution of symptoms.

Asymptomatic household contacts
All household contacts under 5 years of age and those unable to maintain good hygiene should be excluded from childcare or similar settings until two negative stool specimens collected at least 24 hours apart are obtained. These specimens should be obtained at the same time or following microbiological clearance of the household case. In situations where excretion in the household case is prolonged, in-home/single childcare may be required until clearance of the case. Alternatively, if a risk assessment indicates a low risk of transmission in the household (e.g. case with prolonged carriage is able to practise scrupulous hygiene and to ensure use of separate bathroom to contacts) children who are household contacts of the case may be allowed to return to childcare after their initial clearance, as long as they remain asymptomatic and fortnightly stool specimens remain clear.

Asymptomatic food handlers, childcare workers and health care workers who are household contacts of cases under 5 years of age/people unable to maintain good hygiene, should be excluded until two negative stool specimens collected at least 24 hours apart are obtained. These specimens should be obtained at the same time or following the microbiological clearance of the household case. In situations where excretion in the household case is prolonged, decisions on longer-term exclusion of such contacts should be made on a case by case basis, and if required, on the advice of an expert panel. If cleared to return to work, regular faecal screening (at least every fortnight), should continue until clearance of the case.

Asymptomatic food handlers, childcare workers and health care workers who are household contacts of cases 5 years of age and over (if the case is able to maintain good hygiene) do not require exclusion while being screened. In situations where excretion in the household case is prolonged, regular faecal screening (at least every fortnight) of the contact should continue until the case is cleared.

Asymptomatic non-household contacts:
Asymptomatic non-household contacts who are in a high risk group should be assessed on a case by case basis in regard to exclusion from work/school/childcare while being screened.
Asymptomatic non-household contacts who are not in a high risk group do not need to be excluded.

Counselling
Contacts should be advised of the nature of the infection, its mode of transmission and the low infectious dose. The importance of good hygiene should be emphasised. Educate about hygiene practices, in particular the importance of washing hands with soap and water for at least 15 seconds, after using the toilet, prior to handling food or caring for children or patients. This should be supervised for young children in childcare and similar settings.
 
Other control measures
Consider informing adjacent public health units of the notification.

Special situations

Cases among children in childcare (Flowchart 3)

Undertake a situation specific risk assessment to inform appropriate public health management. The risk assessment should involve a visit to the childcare centre. Points to consider in assessing risk include:

  • the likely source of infection for the case (i.e. from child care or elsewhere)
  • the potential for transmission in that setting, which may include whether the case was continent and symptomatic during their infectious period at childcare, and nappy changing and food preparation practices

If a second case is identified in the same childcare setting, consideration should be given to convening an expert panel to review and advise on further action. Temporary closure of the facility (or part of the facility in which the cases attended) and a full clean may need to be considered in some circumstances.

Whenever a case occurs in a childcare setting, special attention should be paid to personal hygiene practices and cleaning within the setting.

Community outbreaks/epidemics

  • Establish an IMT
  • Determine spread of outbreak (OzFoodNet to monitor for interstate cases)
  • Consider the need for enhanced surveillance (including HUS) through hospitals and diagnostic pathology laboratories
  • Look for common source of infection and the vehicle of transmission
  • If the outbreak is suspected to be foodborne, refer to the Foodborne Illness Outbreak Management Guidelines – 2006 and notify Food Safety Standards & Regulation Team, Environmental Health Unit.

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Preventive Measures

  • Minimise person to person transmission by instructing cases and contacts on the importance of washing hands with soap and water for at least 15 seconds and drying thoroughly, prior to handling food and after using the toilet
  • Educate the public that all beef should be thoroughly cooked. Minced beef should be cooked until all pink colour is gone
  • Encourage good food hygiene practices, such as washing cutting boards, knives and hands after preparing raw meat; using separate cutting boards for foods of animal origin and other foods; not returning cooked meat to the same plate that was used for raw meat; and not using marinade or sauces used on raw meat on cooked meat
  • Educate the public on the risks associated with consuming unpasteurised milk or untreated water
  • Ensure adequate hygiene in childcare centres, especially frequent supervised hand washing with soap and water and cleaning of toys, surfaces

Summary

For community outbreaks, prepare a report of the investigation for the Communicable Diseases Unit and the standard outbreak summary report for OzFoodNet.

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References

    1. Vally H, Hall G, Dyda A, et al. Epidemiology of Shiga toxin producing Escherichia coli in Australia, 2000-2010. BMC Public Health 2012;12:63-74.
    2. Department of Health and Ageing. Australian national notifiable diseases case definitions: Shiga toxin-producing/vero toxin-producing Escherichia coli – STEC/VTEC case definition. Accessed from http://www.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-nndss-casedefs-cd_stec.htm on December 9, 2011.
    3. Mandell GL, Dolin JE, Dolin R, (Eds) 2009. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases, 7th Ed.  Philadelphia: Churchill Livingstone.
    4. Garg AX SR, Barrowman N et al. Long-term renal prognosis of diarrhea-associated hemolytic uremic syndrome—a systematic review, meta-analysis, and meta-regression. JAMA. 2003;290:1360-70.
    5. McPherson M, Lalor K, Coombs B, Raupach J, Stafford R, Kirk MD. Serogroup-specific risk factors for shiga toxin-producing Escherichia coli infection in Australia. Clin Infect Dis. 2009;49:249-56.
    6. Community outbreak of hemolytic uremic syndrome attributable to Escherichia coli O111:NM--South Australia 1995. MMWR Morb Mortal Wkly Rep, 1995. 44(29): p. 550-1, 557-8.
    7. Rangel JM, Sparling PH, et al. Epidemiology of Escherichia coli O157:H7 outbreaks, United States, 1982-2002. Emerg Infect Dis. 2005;11(4):603-609.
    8. Fratamico P.M. and J. Smith, Escherichia coli, in Foodborne infections and intoxications, H. Riemann and D. Cliver, Editors. 2006, Elsevier. p. 224.
    9. Frank C, Werber D, Cramer JP, Asker M, Faber M et al. Epidemic profile of shiga-toxin-producing Escherichia coli O104:H4 outbreak in Germany. NEJM. 2011; published online on October 26, 2011
    10. Buchholz U, Bernard H, Werber D, Bohmer MM, Remschmidt C et al. German outbreak of Escherichia coli O104:H4 associated with sprouts. NEJM. 2011; published online on October 26, 2011
    11. Thorpe C. Shiga toxin-producing Escherichia coli infection. Clin Infect Dis. 2004;38:1298-303.
    12. Parry SM, Palmer SR. The public health significance of VTEC O157. Symp Ser Soc Appl Microbiol. 2000;29:1S-9S.
    13. Parry SM, Salmon RL. Sporadic STEC O157 infection: secondary household transmission in Wales. Emerg Infect Dis. 1998;4:657-61.
    14. Locking ME, Pollock GJ, Allison LJ, Rae L, Hanson MF, Cowden JM. Escherichia coli O157 infection and secondary spread, Scotland, 1999-2008. Emerg Infect Dis. 2011;17:524-7.
    15. Heymann D (Ed) 2008. Control of communicable Diseases Manual, 19th Ed. Washington: American Public Health Association.
    16. O'Donnell J, Thornton L, McNamara EB, Prendergast T, Igoe D, Cosprove C. Outbreak of Vero cytotoxin-producing Escherichia coli 0157 in a child day care facility. Commun Dis Public Health. 2002;5(1):54-8.
    17. Tilden J, Young W, McNamara AM, Custer C, Boesel B, Lambert-Fair MA, Majkowski J, Vugia D, Werner SB, Hollingsworth J, Morris JG. A new route of transmission for Escherichia coli: infection from dry fermented salami. Am J Public Health. 1996;86(8):1142-5.
    18. Proulx F, Seidman EG, Karpman D. Pathogenesis of shiga toxin-associated haemolytic uraemic syndrome. Pediatric Research. 2001;50:163-71.
    19. Jensen C, Schiellerup P, Olsen K, Scheutz F, Petersen E, Gerner-Smidt P, Molbak K. Antimicrobial treatment of asymptomatic carriers of verocytotoxin-producing Escherichia coli: An empiric study. Scand J Infect Dis. 2004;37:61-3.
    20. Panos G, Betsi GI, Falagas ME. Systematic review: are antibiotics detrimental or beneficial for the treatment of patients with Escherichia coli O157:H7 infection? Aliment Pharmacol Ther. 2006;24:731-42.

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Flowcharts

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Last updated: 23 December 2014