Investigation of two clusters of shiga toxin-producing Escherichia coli cases in South Australia

This report published in Communicable Diseases Intelligence Volume 27, No 4, December 2003 describes an outbreak of Shiga toxin-producing Escherichia coli in South Australia.

Page last updated: 03 December 2003

A print friendly PDF version is available from this Communicable Diseases Intelligence issue's table of contents.

Barry G Combs,1 Rolf P Wise,2 Ingrid G Tribe,3 Lillian Mwanri,1 Jane CA Raupach1

Shiga toxin-producing Escherichia coli (STEC) is an important cause of gastrointestinal illness in developed countries, and outbreaks have been reported in many countries including Australia.1,2 STEC infection can cause bloody diarrhoea, with 3-7 per cent of sporadic cases developing haemolytic uraemic syndrome (HUS), a serious condition, defined by thrombocytopenia, anaemia and renal failure, which can result in death.1,2,3 In Australia, the number of reported STEC cases, was 38, 48 and 52 in the years 2000, 2001 and 2002 respectively.4 South Australia reported 38 (73%) of the 52 cases in 2002. Current surveillance STEC practices in South Australia involves screening of all bloody stools with a polymerase chain reaction (PCR) test for the toxin genes, which contributes to the number of cases reported from this state. Samples positive for toxin are tested for virulence and serotype genes.5 This procedure complements standard epidemiological practices.

Relatively few STEC outbreaks have been reported in Australia.2 This report describes the investigation of two clusters of STEC cases in South Australia, observed in February and March 2003.

The first cluster

Between 3 and 6 March 2003, four STEC cases from Adelaide suburbs were notified to the Communicable Disease Control Branch (CDCB). Of the four cases, three were PCR positive for serotype O157 and toxin gene STX2 and negative for toxin gene STX1. One O157 case was also positive for virulence genes eae (codes for intimin) and hlya (codes for enterohemolysin). The other two cases were negative for these genes possibly due to a low number of STEC in the stool sample. These typing results suggested that the cases may be epidemiological linked.5

These three cases were interviewed with a hypothesis generating questionnaire, which included a 10 day food history prior to illness, food purchasing habits and social activities undertaken during this period.

Of the three cases, one was male and two were females and all were aged 61 years or more. All three cases had bloody diarrhoea with dates of onset of 25, 27 and 28 February 2003. Two were hospitalised for a week and there were no reports of cases developing HUS.

These cases had no contact with each other and the food history revealed no common food vehicle or other exposure. However, the male case and a female case reported eating Hawaiian pizza. In addition, both female cases purchased meat and small goods including fruit and vegetables from the same supermarket.

The stool samples were cultured and E. coli isolates screened for STEC toxin genes. Unfortunately, isolates were only recovered from the male case and one of the female cases, who did not eat pizza. These isolates were subjected to PFGE using restriction enzyme Xba1 (New England Biolabs), and analysed using the software GelCompar 4.1 (Applied Maths, Sint-Martens-Latem, Belgium). The PFGE gel was interpreted according to Tenover criteria for strain identification.6 Results showed that the isolates from community cases 1 and 2 had different patterns from each other (Figure) and from other STEC control isolates (community case 3). Overall, the molecular and descriptive epidemiology suggests that the two cases were unrelated. As an isolate was not cultured from one of the female cases it is unclear if the two female cases were associated with a common food source or other exposure. There were no further reports of STEC O157 with similar dates of onset.

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Figure. Dendogram of Pulsed Field Patterns of STEC isolates from a community cluster and a nursing home cluster

Figure. Dendogram of Pulsed Field Patterns of STEC isolates from a community cluster and a nursing home cluster

The second cluster/outbreak

On 20 March 2003, two STEC cases from a nursing home were notified to the CDCB and epidemiological, environmental and microbiological investigations were initiated. At the nursing home there were 115 residents and approximately 112 staff members. Investigations revealed 12 residents and one staff member had gastrointestinal illness. Stools from all people who were ill were screened for enteric pathogens. All were negative except for one more resident having a stool positive for STEC toxin genes.

The three laboratory confirmed cases, were aged 79 to 87 years, and all experienced diarrhoea. Two of these cases experienced bloody diarrhoea and were hospitalised. The dates of onset were 13, 14 and 16 March 2003.

The cases lived in different sections of the nursing home but staff reported occasionally working across all sections. There was a set menu for residents and two cases may have had contact with each other at lunch times in the dining room. The third case required feeding assistance and did not attend the dining room. Each section of the nursing home had a kitchen where kitchen staff prepared main meals, including snacks. The food safety methods and food hygiene practices in these kitchens were found to be satisfactory. Ingredients for meals were supplied by an external food manufacturing facility, which was reported to be well maintained and had good systems in place for food preparation. At the manufacturing facility there was no evidence of gastrointestinal illness among staff or among people at other locations that the facility supplied. In the 10 day period prior to illness there were no social activities when all three cases could have interacted.

STEC isolates were recovered from the three cases and were serotyped O111, which is a common STEC serotype within South Australia.2 The isolates were PFGE typed and were found to have a common banding pattern (Figure), further confirming that the cases were epidemiologically linked. From the epidemiological and environmental investigations no common foodborne vehicle of infection was found. The only hypothesis that the descriptive epidemiology suggested was person-to-person transmission, perhaps via staff members.

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STEC continues to be an important cause of gastrointestinal illness in South Australia. Most infections are sporadic cases with occasional outbreaks identified. In 2002, there was an outbreak of STEC associated with children visiting a petting zoo.7

In the O157 cluster and nursing home outbreak, only people over 60 years of age were involved. STEC outbreaks in nursing homes have also been reported in Canada and the USA.9,10 This emphasizes the need for high levels of food hygiene and infection control procedures in institutions caring for the elderly, who are at a higher risk for STEC infection. At the South Australian nursing home, the CDCB and local government officers reinforced infection control procedures, which included the need for regular hand washing, food handling procedures, environmental cleaning and correct linen handling procedures. Intensive surveillance of the nursing home continued for four weeks and residents continued to have stools screened for STEC toxin genes.


The authors acknowledge the efforts and valuable assistance of Rod Givney, Director of Communicable Disease Control Branch, and Ian Miller, an Environmental Health Officer from the City of Onkaparinga.

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1. Mead PS, Griffin PM. Escherichia coli O157:H7. Lancet 1998;352:1207-1212.

2. Cameron A, Beers M, Walker C. Community outbreak of hemolytic uremic syndrome attributable to Escherichia coli 0111:NM-South Australia. MMWR Morb Mortal Wkly Rep 1995;44:550-558.

3. Beutin L, Zimmermann S, Gleier K. Human infections with Shiga toxin-producing Escherichia coli other than serogroup O157 in Germany. Emerg Infect Dis 1998;4:635-639.

4. Communicable Diseases Network Australia. National Notifiable Diseases Surveillance System. Notifications of STEC/VTEC, Australia, 1996-2002. Canberra; 2003.

5. Paton AW, Paton JC. Direct detection and characterization of shiga toxigenic Escherichia coli by multiplex PCR for stx1, stx2, eae, ehxA, and saa. J Clin Microbiol 2002;40:271-274.

6. Tenover FC, Arbeit RD, Goering RV, Mickelsen PA, Murray BE, Persing DH, et al. Interpreting chromosomal DNA restriction patterns produced by pulsed-field gel electrophoresis: criteria for bacterial strain typing. J Clin Microbiol 1995;33:2233-2239.

[<p>7. Communicable Disease Control Branch, South Australian Department of Human Services. Shiga toxin-producing <em>Escherichia coli</em> 026. <em>Communicable Disease Control Bulletin</em>2003;11:9. Available from: </p>]

8. Swaminathan B, Barrett TJ, Hunter SB, Tauxe RV, CDC PulseNet Rask Force. PulseNet: the molecular subtyping network for foodborne bacterial disease surveillance, United States. Emerg Infect Dis 2001;7:382-389.

9. Ryan CA, Tauxe RV, Hosek GW, Wells JG, Stoesz PA, McFadden HW Jr, et al. Escherichia coli O157:H7 diarrhea in a nursing home: clinical, epidemiological, and pathological findings. J Infect Dis 1986;154:631-638.

10. Carter AO, Borczyk AA, Carlson JA, Harvey B, Hockin JC, Karmali MA, et al. A severe outbreak of Escherichia coli O157:H7-associated hemorrhagic colitis in a nursing home. N Engl J Med 1987;317:1496-1500.

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Author affiliations

1. OzFoodNet, Communicable Disease Control Branch, Department of Human Services, South Australia

2. Institute of Medical and Veterinary Services, South Australia

3. Disease Surveillance and Investigation Unit, Communicable Disease Control Branch, Department of Human Services, South Australia

Corresponding author: Dr Barry Combs, Public Health Officer, OzFoodNet, Communicable Disease Control Branch, Department of Human Services, PO Box 6, Rundle Mall, SA 5000. Telephone: +61 8 8226 6318. Facsimile: +61 8 8226 7187. Email:

This article was published in Communicable Diseases Intelligence Volume 27 No 4, December 2003.

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This issue - Vol 27 No4, December 2003