A bulletin for the Australian Food Industry November 2005
Fresh produce continues to cause illness overseas
Shiga toxin producing Escherichia coli in Australia
Download PDF file of this issueShiga toxin producing Escherichia coli in Australia
Barry Combs, Public Health Officer, OzFoodNet, SA
Introduction
Shiga toxin-producing Escherichia coli (STEC) was first recognised as a significant cause of gastroenteritis in 1982 following two outbreaks in the United States1. Subsequently, STEC infection was associated with haemolytic uremic syndrome (HUS), a serious complication that can result in death. HUS may develop in 5-10 percent of persons infected with STEC 2,3.
It is thought that most STEC infections develop from eating undercooked beef and lamb, or eating agricultural produce and drinking water that have been contaminated with animal manure2. Outbreaks of disease can be quite large, such as one in Scotland in 1996 with 512 cases and 20 deaths4. Apart from the societal costs associated with this disease, the financial costs to food producers can be substantial with one outbreak in the USA resulting in the recall of 18,600 tons of ground beef and beef trimming 5.
STEC Infections in Australia
In Australia, during 1999-2004, there was a mean of 49 reports of STEC each year. The notification rate in Australian States and Territories varies considerably, from an average of 0.07 cases per 100,000 population in NSW, to an average of 2.6 cases per 100,000 population in South Australia (Table 1). South Australia has similar notification rates to the United States, where reported cases range from 2.1-2.9 per 100,000 population6. The differences in notification rates between Australian jurisdictions are likely to be due to the types of diagnostic test used and numbers of samples tested. South Australia has screened all diarrhoeal stools containing blood with a sensitive polymerase chain reaction test for STEC since 1997 in response to a large HUS outbreak in 1995 7.
Table 1. Notification rates of STEC infection in Australian states (mean rates from 1999 to 2003 and rates for 2004)
Data sourced from the 'Communicable Diseases Network Australia - National Notifiable Diseases Surveillance System, personal communication and OzFoodNet Annual Reports11.
| Mean notification rate (per 100,000 population) | |||||
|---|---|---|---|---|---|
| NSW | QLD | VIC | SA | WA | |
| 1999-2003 | 0.07 | 0.19 | 0.07 | 2.6 | 0.10 |
| 2004 | 0.08 | 0.25 | 0.09 | 2.04 | 0.05 |
The majority of cases reported in Australia are sporadic, which is consistent with other countries. In most cases the sources of sporadic infections are never identified. Outbreaks or case control studies of sporadic infection provide the best information on causes. A case control study of sporadic cases in South Australia found an association between the consumption of berries and illness8. Further studies on sporadic STEC infections are being conducted in Australia by OzFoodNet. Overseas studies on sporadic STEC infection have found there is an increased risk from eating undercooked ground beef 9 and contact with farm animals 10.
During 2004, the main serotypes causing infection in Australia were O157 (58 percent), followed by O111 (16 percent) and O26 (13 percent)11. This serotype prevalence is similar to findings in other countries. One study in the US found that O157 was the predominant serotype with other serotypes found in the remaining 54 percent of isolates 12.
STEC serotypes that are commonly found in human infections have also been detected among Australian animals. A large range of STEC serotypes, including serotypes O157, O26, O91, O113, O111 have been isolated from cattle 13.
In Australia, of nine STEC outbreaks investigated between 1995 and mid-2005, (Table 2), five were detected in South Australia, which has enhanced surveillance of bloody stool specimens. A range of different serotypes was associated with the outbreaks, with O111 detected in three outbreaks. In two thirds of the outbreaks, many of the cases developed the serious illness HUS. Australia's largest outbreak occurred in 1995 when 23 children developed HUS. The outbreak investigation implicated Mettwurst, made from a mixture of pork, beef and lamb meat and, whilst other serotypes were detected, O111 was the main serotype associated with this outbreak.
In summary, outbreaks of STEC have occurred in Australia caused by several different serotypes. In Australia, the cause of sporadic STEC cases and many STEC outbreaks is unknown, although some animal sources have been identified. Studies into sporadic STEC infection should, in the future, help to determine what foods or behaviours increase the risk of STEC infection and provide the basis for preventative measures.
Table 2. Outbreaks of STEC in Australia from 1995 to 2005 (year-to-date, 7 October 2005)
| State | Year | Setting | Vehicle of infection | Total no. of outbreak cases | no. HuS cases | STEC serotype | Reference |
|---|---|---|---|---|---|---|---|
| SA | 1995 | Community | Mettwurst | 23a | 23 | O111, O157, O160 | 7 |
| QLD | 1996 | Community | Unknown | 6 | 0 | O157 | 14 |
| SA | 1998 | Community | Unknown | 4 | 3 | O113 | 15 |
| NSW | 1999 | Community | Unknown | 7b | 7 | 16 | |
| NSW | 1999 | Community | Meat pizza | unknown | 1 | O15 | 17 |
| SA | 2002 | Petting zoo | Animals | 6 | 0 | O26 | - |
| SA | 2003 | Aged Care facility | Unknown | 3 | 0 | O111 | 18 |
| QLD | 2004 | Rural community | Unknown | 4 | 2 | O86:H27 | 19 |
| SA | 2005 | Church | Unknown | 3 | 1 | O111 | - |
a Non-HUS cases were not officially documented in this outbreak, although there were unofficial reports of large numbers of people with gastrointestinal illness who had consumed the implicated food.
b STEC was not detected in these cases, although one case had high level of antibodies against
E. coli O157.
Acknowledgements
The author wishes to thank OzFoodNet staff, especially Martyn Kirk and Gerard Fitzsimons, for their contributions to this article.
References
1. Riley LW, Remis RS, Helgerson SD, McGee HB, Wells JG, Davis BR, et al. 1983. Hemorrhagic colitis associated with a rare Escherichia coli serotype. New England Journal of Medicine.308.12.681-685.
2. Mead PS, Griffin PM. 1998. Escherichia coli O157:H7. Lancet 352.9135.1207-1212.
3. Karmali MA, Steele BT, Petric M, Lim C. 1983. Sporadic cases of haemolytic-uraemic syndrome associated with faecal cytotoxin and cytotoxin-producing Escherichia coli in stools. Lancet. 1.8325.619-620.
4. Cowden JM, Ahmed S, Donaghy M, Riley A. 2001 Epidemiological investigation of the central Scotland outbreak of Escherichia coli O157 infection, November to December 1996. Epidemiology and Infection 126.3.335-341.
5. Anonymous. 2002. Multistate outbreak of Escherichia coli 0157:H7 infections associated with eating ground beef-United States, June-July 2002. Morbidity and Mortality Weekly Report 51.29.637-639.
6. Anonymous. 2001. Preliminary FoodNet data on the incidence of foodborne illnesses--selected sites, United States, 2000. Morbidity and Mortality Weekly Report 50.13.241-246.
7. Cameron A, Beers M, Walker C. 1995. Community outbreak of hemolytic uremic syndrome attributable to Escherichia coli 0111:NM-South Australia. Morbidity and Mortality Weekly Report 44.550-558.
8. Hundy R. 2002. Risk factors for sporadic human infection with shiga toxin-producing Escherichia coli in South Australia. South Australia: Communicable Disease Control Branch.
9. Le Saux N, Spika JS, Friesen B, Johnson I, Melnychuck D, Anderson C, et al. 1993. Ground beef consumption in noncommercial settings is a risk factor for sporadic Escherichia coli O157:H7 infection in Canada. Journal of Infectious Diseases 167.2.500-502.
10. Parry SM, Salmon RL, Willshaw GA, Cheasty T.1998. Risk factors for and prevention of sporadic infections with vero cytotoxin (shiga toxin) producing Escherichia coli O157 [comment]. Lancet. 351.9108.1019-1022.
11. OzFoodNet. 2005. Reported foodborne illness and gastrointeritis in Australia: Annual report of the OzFoodNet network, 2004. Communicable Disease Intelligence 29.2.164-190.
12. Fey PD, Wickert RS, Rupp ME, Safranek TJ, Hinrichs SH. 2000. Prevalence of non-O157:H7 shiga toxin-producing Escherichia coli in diarrheal stool samples from Nebraska. Emerging Infectious Diseases 6.5.530-533.
13. Hornitzky MA, Bettelheim KA, Djordjevic SP. 2001. The detection of Shiga toxin-producing Escherichia coli in diagnostic bovine faecal samples using vancomycin-cefixime-cefsulodin blood agar and PCR. FEMS Microbiology Letters 198.1.17-22.
14. McCall B. 1996. An outbreak of Escherichia coli 0157 infection on the Gold Coast. Communicable Disease Intelligence 20.10.236-239.
15. Paton AW, Woodrow MC, Doyle RM, Lanser JA, Paton JC. 1999. Molecular characterization of a Shiga toxigenic Escherichia coli O113:H21 strain lacking eae responsible for a cluster of cases of hemolytic-uremic syndrome. Journal of Clinical Microbiology.37.10.3357-3361.
16. Bartlett M, McAnulty J, Rutherford A, Gupta L, Karalis T, Maywood P, et al. 1999. Haemolytic uraemic syndrome: A cluster of cases in early 1999. NSW Public Health Bulletin 10.9.109.
17. Dalton C, Voetsch A, P. B, Thompson R, Robins-Browne R, Bettelheim KA, et al. 2001. An outbreak of shiga-toxin producing E. coli O15 associated with beef consumption. In: Communicable Disease Control Conference; Canberra; 2001. p. 19.
18. Combs BG, Wise RP, Tribe IG, Mwanri L, Raupach JCA. 2003. Investigation of two clusters of shiga toxin-producing Escherichia coli cases in South Australia. Communicable Disease Intelligence 27.4.517-519.
19. Morgan AK, Piispanen J, Humphreys J, Murphy D. 2005. A cluster of cases of haemolytic uraemic syndrome in north Queensland associated with a novel Shiga-like toxin-producing Escherichia coli. Communicable Disease Intelligence 29.2.193-196.