Burden and causes of foodborne disease in Australia: Annual report of the OzFoodNet network, 2005

Foodborne disease is a considerable burden on Australian society. In 2005, OzFoodNet sites recorded 25,779 notifications of seven potentially foodborne diseases.

Page last updated: 30 September 2006

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

Introduction | Methods | Results | Discussion | Acknowledgements | References

The OzFoodNet Working Group

Abstract

In 2005, OzFoodNet sites recorded 25,779 notifications of seven potentially foodborne diseases, which was 12.5 per cent higher than the mean for the previous five years. Diseases with significant increases in 2005, when compared to historical reports include: Shiga toxin-producing Escherichia coli, shigellosis, haemolytic uraemic syndrome, salmonellosis and campylobacteriosis. The most significant increases were those due to Salmonella (13.1%) and Campylobacter (5.1%) because of the frequency of these infections. Reports of listeriosis were lower than previous years and there were only four materno-foetal infections compared to seven in 2004. Sites reported 624 outbreaks of gastroenteritis and foodborne disease in 2005. One hundred and two of these were foodborne and affected 1,926 persons, hospitalised 187 and caused four deaths. Among foodborne outbreaks, Salmonella Typhimurium was the most common pathogen and restaurants were the most common place where food implicated in outbreaks was prepared. Outbreaks associated with fish, poultry meat, and mixed meat dishes were common. There were two large outbreaks of salmonellosis, including one associated with dips at a Turkish restaurant, one with alfalfa sprouts, and several due to egg-based dishes. In addition, there were several multi-state investigations of Salmonella infection during 2005, including one large outbreak of S. Typhimurium 135 implicating poultry meat from retail supermarkets. Sites identified a source of infection for 39 per cent (41/104) of investigations into clusters of salmonellosis. Overall, 97.4 per cent of Salmonella notifications on state and territory surveillance databases recorded complete information about serotype and phage type. This report highlights the considerable burden of disease from food sources in Australia and the need to continue to improve food safety. Commun Dis Intell 2006;30:278–300.

Introduction

Foodborne disease is a considerable burden on Australian society with 5.4 million cases annually, costing an estimated $1.2 billion dollars.1 While the majority of cases of foodborne disease are mild and do not require medical attention, the sheer number of affected people taking time from work to recover or care for affected family members make up approximately 60 per cent of these costs. In addition, the costs to food businesses implicated in outbreaks of disease can be significant, although they are difficult to ascertain.1

There are over 200 different types of illness that may be transmitted by food, although only a handful are specifically notifiable to health departments.2 Due to the mild nature of foodborne diseases, most cases do not appear in surveillance statistics collected by health departments. In Australia, for every notification of Salmonella and Campylobacter there are approximately 6.9 (95% credible interval 4.0–16.4) and 9.6 (95% credible interval 6.2–22.4) cases in the community respectively.3 The proportion of cases that are notified varies considerably by disease, as the severity of various illnesses differ markedly.2,3

Health departments use surveillance of infectious diseases for observing trends, preventing further spread of infections, detecting outbreaks and monitoring the effects of interventions.4 The source of infection is difficult to determine in sporadic cases of enteric diseases as they may be acquired from infected persons, animals, contaminated water or foods and other sources within the environment. In outbreaks of enteric diseases the modes of transmission are more likely to be determined. Where these outbreaks are foodborne they can be useful for developing policy to prevent further disease.5

In 2000, the Australian Government Department of Health and Ageing established the OzFoodNet network to enhance surveillance for foodborne disease.6 This built upon an 18-month trial of active surveillance in the Newcastle region of New South Wales. OzFoodNet was modelled on the Centers for Disease Control and Prevention’s FoodNet surveillance system. The OzFoodNet network consists of epidemiologists employed by each state and territory health department to conduct investigations and applied research into foodborne disease. The network involves many different collaborators, including the National Centre for Epidemiology and Population Health, and the Public Health Laboratory Network. OzFoodNet is a member of the Communicable Diseases Network Australia, which is Australia’s peak body for communicable disease control.7 The Australian Government Department of Health and Ageing funds OzFoodNet and convenes committees to manage the network, and a committee to review the scientific basis for various research projects.

This is the fifth annual report of OzFoodNet and covers data and activities for 2005.

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Methods

Population under surveillance

In 2005, the coverage of the network included the entire Australian population, which was estimated to be 20,328,609 persons.8 In 2005, the Hunter New England Area Health Service hosted an OzFoodNet site, which supplemented statewide foodborne disease surveillance across New South Wales.

Data sources

Rates of notified infections

All Australian states and territories require doctors and/or pathology laboratories to notify patients with infectious diseases that are important to public health. Western Australia is the only jurisdiction where laboratory notification is not mandatory under legislation, although most laboratories still notify the health department by agreement. OzFoodNet aggregated and analysed data on patients notified with the following diseases or conditions, a proportion of which may be acquired from food:

  • Campylobacter infections;
  • Non-typhoidal Salmonella infections;
  • Listeria infections;
  • Shiga toxin producing Escherichia coli infections and haemolytic uraemic syndrome;
  • typhoid; and
  • Shigella infections.

To compare notifications in 2005 to historical totals, we compared crude numbers and rates of notification to the mean of the previous five years. Where relevant, we used data from the National Notifiable Diseases Surveillance System (NNDSS) and OzFoodNet sites to analyse data for specific sub-types of infecting organisms.

The date that notifications were received by each jurisdiction was used for analysis notification data. To calculate rates of notification, we used the estimated resident populations for each state or territory as at June 2005.8 For cases of neonatal listeriosis infections we used birth data from the Australian Institute of Health and Welfare.9

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Gastrointestinal and foodborne disease outbreaks

OzFoodNet collected information on gastrointestinal and foodborne disease outbreaks that occurred in Australia during 2005. An outbreak of foodborne disease was defined as an increase in the number of reports of a particular infection or illness associated with a common food or meal. A cluster was defined as an increase in infections that were epidemiologically related in time, place or person where investigators were unable to implicate a vehicle or determine a mode of transmission. An example is a temporal or geographic increase in the number of cases of a certain type of Salmonella serovar or phage type. Another example is a community-wide increase of cryptosporidiosis that extends over some weeks or months. In this category, some outbreaks where the mode of transmission was indeterminate have been included.

OzFoodNet epidemiologists collate summary information about the setting where the outbreak occurred, where food was prepared, the month the outbreak occurred, the aetiological agent, the number of persons affected, the type of investigation conducted, the level of evidence obtained and the food vehicle responsible for the outbreak. To summarise the data, we categorised outbreaks by aetiological agents, food vehicles and settings where the implicated food was prepared. Data on outbreaks due to transmission from animals and cluster investigations were also summarised. The number of outbreaks and documented causes may vary from summaries published by individual jurisdictions.

Surveillance evaluation

OzFoodNet compared the results of surveillance across different sites, including rates of reporting outbreaks, and investigation of clusters of Salmonella. To measure the quality of national surveillance data, OzFoodNet examined the completeness of information on state and territory databases in 2005. The proportions of Salmonella notifications with serotype and phage type information were compared with results for previous years.

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Results

Rates of notified infections

In 2005, OzFoodNet sites reported 25,779 notifications of seven diseases that were potentially foodborne. This was a 12.5 per cent increase from the mean of 22,827 notifications for the previous five years. Reports for these seven diseases make up almost a quarter of notifications to the National Notifiable Diseases Surveillance System.10 A summary of the number and rates of notifications by OzFoodNet sites is shown in Appendix 1.

Salmonella infections

In 2005, OzFoodNet sites reported 8,376 cases of Salmonella infection, which equated to 41.2 cases per 100,000 population and an increase of 13.1 per cent from the mean for the previous five years (Figure 1). The rates ranged from 28.3 cases per 100,000 population in Victoria to 196.8 cases per 100,000 population in the Northern Territory, which traditionally has the highest rates of all jurisdictions.

Figure 1. Notification rates of Salmonella infections, 2005, compared to the mean of the notification rate (2000–2004), by OzFoodNet site

Figure 1.  Notification rates of salmonella infections, 2005, compared to the mean of the notification rate (2000-2004), by OzFoodNet site

Overall, notification rates of salmonellosis for 2005 were increased in all states and territories, particularly in Tasmania (105.3%), Victoria (20.8%) and New South Wales (17.0%) compared to historical means. The major increase in Tasmania was due to large outbreaks of S. Typhimurium 135 in November and December 2005.

The male to female ratio for salmonellosis was 1:1. The highest age-specific rate of Salmonella infection was 200.8 cases per 100,000 population in males aged 0–4 years. Notification rates were also elevated in the 5–9 year age group with a further peak in notification rates in the 20–29 year age group.

Rates of salmonellosis were highest in northern areas of Australia. The highest rate is consistently reported in the Kimberley region of Western Australia.8 Western Australia reported that the Kimberley region had a rate of 262 per 100,000 population, which represents a 17 per cent decrease for the regional notification rate from the previous year. In Western Australia, rates of salmonellosis were higher in Indigenous people in all age groups, particularly in children aged 0–4 years. In the Northern Territory, Indigenous people had 1.8 times the rate of salmonellosis notifications compared to non-Indigenous people with the highest burden amongst the 0-4 year age group who had 1.4 times the rate of non-Indigenous children in the same age group.

During 2005, the most commonly reported Salmonella serotype was S. Typhimurium. There were 836 notifications of Salmonella Typhimurium 135 (including a subgroup locally designated 135a) to OzFoodNet sites making it the most common infection (Table 1). This compared to 578 notifications of this phage type in 2004. Salmonella Typhimurium 197 increased dramatically in 2005 with 536 notifications, which was a 102 per cent increase from 266 notifications in 2004. The highest specific rates for single subtypes reported by OzFoodNet sites were S. Typhimurium 135 and S. Mississippi in Tasmania, and S. Ball and S. Saintpaul in the Northern Territory with rates of 36.3, 12.2, 23.7,and 23.7 per 100,000 population, respectively. These subtype-specific rates were almost as high as the total rate of Salmonella notifications in some other jurisdictions.

Table 1. Numbers, rates and proportions of the top 5 Salmonella infections, 2004 to 2005, by OzFoodNet site*

OzFoodNet site
Salmonella type(sero/phage type)
Top 5 infections
2005
n
Rate Proportion
(%)
2004
n
Rate Ratio§
Australian Capital Territory Typhimurium 170/108
14
4.3
14.6
31
9.6
0.5
Typhimurium 135
13
4.0
13.5
5
1.5
2.6
Typhimurium 9
10
3.1
10.4
6
1.9
1.7
Stanley
5
1.5
5.2
2
0.6
2.5
Hvittingfoss
4
1.2
4.2
0
0.0
Typhimurium 44
4
1.2
4.2
0
0.0
New South Wales Typhimurium 170/108
373
5.5
17.2
351
5.2
1.1
Typhimurium 9
154
2.3
7.1
108
1.6
1.4
Typhimurium 197
109
1.6
5.0
43
0.6
2.5
Typhimurium 135
181
2.7
8.3
178
2.6
1.0
Birkenhead
82
1.2
3.8
77
1.1
1.1
Northern Territory Ball
48
23.7
12.0
50
25.0
1.0
Saintpaul
48
23.7
12.0
48
24.0
1.0
Litchfield
21
10.4
5.3
15
7.5
1.4
Weltevreden
15
7.4
3.8
8
4.0
1.9
Chester
12
5.9
3.0
12
6.0
1.0
Kinondoni
10
4.9
2.5
6
3.0
1.7
Queensland Saintpaul
276
7.0
10.6
225
5.8
1.2
Virchow 8
190
4.8
7.3
247
6.4
0.8
Typhimurium 197
145
3.7
5.6
145
3.7
1.0
Typhimurium 135
137
3.5
5.3
185
4.8
0.7
Aberdeen
135
3.4
5.2
118
3.0
1.1
Hvittingfoss
135
3.4
5.2
110
2.8
1.2
South Australia Typhimurium 9
57
3.7
9.7
46
3.0
1.2
Infantis
48
3.1
8.2
17
1.1
2.8
Typhimurium 64
47
3.0
8.0
4
0.3
11.8
Typhimurium 135
47
3.0
8.0
44
2.9
1.1
Typhimurium 170/108
33
2.1
5.6
70
4.6
0.5
Tasmania Typhimurium 135
176
36.3
58.5
2
0.4
88.0
Mississippi
59
12.2
19.6
63
13.1
0.9
Typhimurium 9
10
2.1
3.3
4
0.8
2.5
Typhimurium 170/108
7
1.4
2.3
3
0.6
2.3
Typhimurium 44
5
1.0
1.7
0
0.0
Victoria Typhimurium 197
279
5.6
19.6
59
1.2
4.7
Typhimurium 135
191
3.8
13.4
137
2.8
1.4
Typhimurium 9
118
2.3
8.3
145
2.9
0.8
Typhimurium 170/108
63
1.3
4.4
88
1.8
0.7
Typhimurium 44
50
1.0
3.5
7
0.1
7.1
Western Australia Oranienburg
63
3.1
8.0
5
0.3
12.6
Typhimurium 135
69
3.4
8.7
74
3.7
0.9
Enteritidis 6A
35
1.7
4.4
21
1.1
1.7
Saintpaul
32
1.6
4.0
46
2.3
0.7
Muenchen
30
1.5
3.8
23
1.2
1.3
Australia Typhimurium 135
836
4.1
10.0
578
2.9
1.4
Typhimurium 197
536
2.6
6.4
266
1.3
2.0
Typhimurium 170/108
535
2.6
6.4
647
3.2
0.8
Saintpaul
434
2.1
5.2
395
2.0
1.1
Typhimurium 9
428
2.1
5.1
360
1.8
1.2

* Where there were multiple fifth ranking Salmonella types all data have been shown, giving more than five categories for some sites.
† Rate per 100,000 population.
‡ Proportion of total Salmonella notified for this jurisdiction in 2005.
§ Ratio of the number of reported cases in 2005 compared to the number reported in 2004.
S. Typhimurium 135 includes a local variant phage type 135a which is not a recognised international classification.

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Salmonella Enteritidis

S. Enteritidis is a serotype that can infect the internal contents of eggs through the oviducts of infected chickens, predominantly with S. Enteritidis phage type 4.11,12 People may often become infected with this serotype after eating raw or undercooked eggs. This phage type has caused major problems in the northern hemisphere where it has become established in commercial egg laying flocks, although the incidence has declined in many countries.11,12 Australia is largely free of S. Enteritidis phage type 4 infections except in people returning from overseas. There are other phage types of S. Enteritidis that are endemic in Australia, although the sources of these local infections are poorly understood.

In 2005, OzFoodNet concluded data collection for a case control study of S. Enteritidis infections to determine the risk factors for infection. OzFoodNet epidemiologists enrolled cases of S. Enteritidis that were acquired in Australia between 2001 and 2005 to assess food-based and zoonotic risk factors for infection and compare them to population-based controls. The results of this study are still being collated for analysis.

During 2005, OzFoodNet sites recorded 387 cases of S. Enteritidis, of which 84 per cent (289/343) had travelled overseas (Table 2). Relevant travel histories were difficult to obtain, as people had often travelled to several countries before returning to Australia. Asian countries were commonly mentioned, and reflect that they are common travel destinations for Australians. In the Asian region, cases of S. Enteritidis infection reported travelling to Bali (37%), Singapore (9%), Indonesia (9%), and Thailand (9%). Travel history could not be determined for 11 per cent (44/387) of cases. The most common infecting phage types were 6a (76 cases), 1b (38), 1 (28) and 4 (21).

Table 2. Number of Salmonella Enteritidis infections, 2005, by travel history and state or territory

OzFoodNet site
History of travel overseas Total
Yes No Unknown
Australian Capital Territory
8
1
 
9
New South Wales
67
6
20
93
Northern Territory
 
 
1
1
Queensland
20
41
19
80
South Australia
20
1
2
23
Tasmania
2
1
 
3
Victoria
71
3
2
76
Western Australia
101
1
 
102
Total
289
54
44
387

Overall, 14 per cent (54/387) of patients infected with S. Enteritidis acquired their infection in Australia. The median age of cases was 29 years (age range 0.3–96 years) and 35 per cent were male. Locally-acquired S. Enteritidis infections predominantly occurred in Queensland, where 76 per cent (41/54) of all locally-acquired infections were reported. Most locally-acquired infections in Queensland were due to phage type 26 (Table 3). Locally-acquired S. Enteritidis infections are strongly seasonal and infections decreased markedly in the winter of 2005 (Figure 2).

Table 3. Number of locally-acquired Salmonella Enteritidis infections, 2005, by phage type and State or Territory

Phage type
State or territory Total
ACT NSW Qld SA Tas Vic WA
1
 
1
 
 
 
 
 
1
4
 
 
1
 
 
 
 
1
7
1
 
 
 
 
 
 
1
13
 
 
1
 
 
 
 
1
26
 
 
29
 
1
 
1
31
14 var
 
 
1
 
 
 
 
1
1B
 
1
 
 
 
 
 
1
21B var
 
 
 
1
 
 
 
1
26 var
 
 
 
 
 
2
 
2
26 var/26
 
 
 
 
 
1
 
1
4B
 
1
 
 
 
 
 
1
6A
 
3
 
 
 
 
 
3
RDNC*
 
 
3
 
 
 
 
3
RDNC/12
 
 
1
 
 
 
 
1
Untypable
 
 
5
 
 
 
 
5
Total
1
6
41
1
1
3
1
54

* ‘Reaction Does Not Conform’ (RDNC) represents phage type patterns that are not yet assigned.

Figure 2. Salmonella Enteritidis infections acquired in Australia, 2003–05, by phage type and month of notification

Figure 2.  Salmonella Enteritidis infections acquired in Australia, 2003-05, by phage type and month of notification
Salmonella clustering

In total, state and territory health departments conducted 104 investigations into clusters and point source outbreaks of salmonellosis during 2005. A source of infection was identified for 39 per cent (41/104) of these investigations. Approximately 61 per cent (63/104) of these outbreaks were due to various phage types of S. Typhimurium.

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Campylobacter infections

In 2005, OzFoodNet sites reported 16,479 cases of Campylobacter infection, equating to a rate of 121.6 cases per 100,000 population. This rate represented a five per cent increase over the mean for the previous five years (Figure 3). Tasmania, experienced the greatest increase, with the notification rate in 2005 being 27 per cent above the mean of the previous five years. The only state to experience a decrease in notification rate was South Australia (-11%). The highest and lowest rates of Campylobacter notification were in Tasmania (157.9 cases per 100,000 population) and in Queensland (111.7 cases per 100,000 population). Data for campylobacteriosis were not available for New South Wales.

Figure 3. Notification rates of Campylobacter infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site excluding New South Wales

Figure 3.  Notification rates of Campylobacter infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site excluding New South Wales

Rates of Campylobacter infection were consistently high in all age groups in all jurisdictions. The highest rate of notifications was in males in the 0–4 year age group (268 cases per 100,000 population), with a secondary peak in the 20–29 year age group for both males and females. Fifty-five per cent of notified cases were male. There were 12 identified outbreaks of Campylobacter during 2005, nine of which were suspected to be foodborne.

Listeria

OzFoodNet sites reported 56 cases of listeriosis in 2005, which represents a notification rate of 0.3 cases per 100,000 population (Figure 4). This was a 17 per cent decrease in the notification rate compared to the five-year historical mean. South Australia investigated a common source outbreak of listeriosis associated with cold meats. The Australian Capital Territory investigated three cases during 2005, although no common source was identified.

Figure 4. Notification rates of Listeria infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

Figure 4.  Notification rates of Listeria infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

Four materno-foetal infections were reported during 2005, giving a rate of 1.6 cases per 100,000 births. The rate of materno-foetal infections has been steadily declining in recent years. Victoria, Western Australia, New South Wales and Queensland each reported single cases in neonates during 2005. Twenty-five per cent (1/4) of infected neonates died during 2005 (Figure 5).

Ninety-three per cent (52/56) of infections during 2005 were reported in persons who were either elderly and/or immunocompromised. Among non-pregnancy related cases, the male to female ratio was approximately 1:1. The highest age specific rate was 1.6 cases per 100,000 population, reported in males in the 60–64 years age group and females over the age of 75 years. Twenty-seven per cent (11/52) of non-pregnancy associated cases died, which was similar to previous years. However, it is difficult to establish the level of attribution of listeriosis to the cause of death as many cases have terminal illness due to immunocompromising conditions.

Figure 5. Notifications of Listeria showing non-pregnancy related infections and deaths, and materno-foetal infections and deaths, Australia, 2000 to 2005

Figure 5.  Notifications of Listeria showing non-pregnancy related infections and deaths, and materno-foetal infections and deaths, Australia, 2000 to 2005

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Shigella

OzFoodNet sites reported 721 cases of shigellosis during 2005, which equated to a notification rate of 3.5 cases per 100,000 population (Figure 6). This was a 26 per cent increase in the rate of notification compared with historical averages, after adjusting for the introduction of notifications from New South Wales in January 2001.

Figure 6. Notification rates of Shigella infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site*

Figure 6.  Notification rates of Shigella infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

* Shigellosis became notifiable in New South Wales from 2001 onwards.

The highest rate of notification was in the Northern Territory (96 cases per 100,000 population), which was almost 30 times higher than the overall Australian rate. Rates of shigellosis are considerably higher in Indigenous communities, which is reflected in the rates of states and territories with higher proportions Indigenous people in the general population. In Western Australia, the rates of shigellosis were in excess of 300 cases per 100,000 population in Indigenous people aged 0–4 years and 75 years or older.

Overall, the notification rate for shigellosis was elevated in all jurisdictions, except for Queensland which had 7.2 per cent fewer notifications than the previous five years. The male to female ratio of shigellosis cases was approximately 1:1. The highest age specific notification rates were in males and females in the 0–4 year age group, with 19.1 and 16.6 cases per 100,000 population, respectively. There was one small outbreak of shigellosis of unknown mode of transmission in New South Wales in July 2005.

In 2005, Shigella sonnei biotypes a and g were the most common strains infecting people, with 167 and 136 notifications respectively. Mannitol negative Shigella flexneri 4a also increased in Central Australia during February and March 2005. These increases were particularly noted in South Australia and the Northern Territory. In Australia, the mode of transmission for the majority of shigellosis infections was through person-to-person transmission or were acquired overseas.

Typhoid

OzFoodNet sites reported 52 cases of typhoid infection during 2005, representing an overall notification rate of 0.3 cases per 100,000 population (Figure 7). The notification rate decreased 22 per cent when compared to the five year historical mean. The highest rates were reported in New South Wales and Western Australia with rates of 0.4 and 0.3 cases per 100,000 population respectively. Tasmania, the Northern Territory and the Australian Capital Territory did not report any cases.

Figure 7. Notification rates of typhoid infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

Figure 7.  Notification rates of typhoid infections, Australia, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

Where travel status was known, sites reported that 96 per cent (45/47) of typhoid cases had recently travelled overseas (Table 4). Thirty per cent (14/47) of these cases had recently travelled from Indonesia or Bali where the predominant phage types were A (3 cases), D2 (2 cases) and E2 (2 cases). Twenty cases had travelled to the Indian subcontinent and the predominant phage type of S. typhi was E1a (5 cases). The two non-travelling cases were either long-term carriers or infected by close contact with a known carrier. Travel status was unknown for five cases. Information on phage type was reported for 81 per cent (42/52) of isolates.

Table 4. Travel status for notified typhoid cases, Australia, 2005

Country
Number of cases
Predominant phage type (cases)
Africa
1
A (1)
Locally acquired
2
E1a (1), untypable (1)
Bali
1
Degraded (1)
Bangladesh
4
E1 (1), E1a (1), E7 (1), unknown (1)
Cambodia
1
E1A (1)
China
1
Unknown (1)
Guinea
1
A (1)
India
12
A (1), E1 (1), E1a (4), E9 (1), E2 (1), untypable (1), degraded (1), Unknown (2)
Indonesia
13
A (3), D2 (2), E2 (2), degraded (1), untypable (2), unknown (3)
Malaysia
1
D2 (1)
Nepal
1
Unknown (1)
Pakistan
3
M1 (2), unknown (1)
Samoa
3
E1a (1), E1 (1), E7 (1)
South America
1
A (1)
Sri Lanka
1
Degraded (1)
Tanzania
1
A (1)
Unknown
5
D2 (1), E1a (2), E2 (1), unknown (1)

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Shiga toxin-producing Escherichia coli infections

OzFoodNet sites reported 78 cases of Shiga toxin-producing E. coli (STEC) infection during 2005, compared to 50 for 2004. These numbers do not include cases of haemolytic uraemic syndrome (HUS) where an STEC organism was isolated or detected in stool samples, as they are reported separately under the category of HUS. The notification rate of 0.4 cases per 100,000 population was a 50.8 per cent increase over the mean rate for previous years (Figure 8). The elevated number of cases reported in 2005 was the result of enhanced screening for STEC in bloody stools in some jurisdictions, such as Western Australia, Victoria, and the Hunter - New England area of New South Wales. Previously, only South Australia has had a program of testing stools containing blood for STEC, which accounts for the consistently high rate of notification in this State.

Figure 8. Notification rates of Shiga toxin-producing Escherichia coli infections, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

Figure 8.  Notification rates of Shiga toxin-producing <em>Escherichia coli</em> infections, 2005, compared to mean rates for 2000 to 2004, by OzFoodNet site

South Australia (35 cases) reported the majority of cases and had the highest rate of notification of 2.3 cases per 100,000 population. All sites reporting cases had significant increases in the number of cases notified, except for Queensland and South Australia where the notification rates were similar to previous years. There were no cases reported from Tasmania, the Australian Capital Territory or the Northern Territory during 2005. The male to female ratio of cases was 0.8:1, contrasting with a male:female ratio of 0.5:1 in 2004. In 2005, the highest rate of reported infection was in females aged 5–9 and 45–49 years, with a rate of 0.8 cases per 100,000 population in both these age groups. The highest rate reported for males was 0.7 per 100,000 population in the 20–24 years age group.

E. coli serotype O157 was responsible for 39 per cent (15/38) of infections where serotype information was available in 2005, compared to 52 per cent in 2004. E. coli O111 was the second most common serotype and was responsible for 26 per cent (10/38) of reports compared to 15 per cent (5/33) in 2004 (Table 5). In 2005, twice as many notified cases of E. coli O157 were female compared to males.

There were two clusters of cases investigated during 2005, both of which occurred in the community in South Australia. The mode of transmission and source were not identified for either cluster. In the first cluster, three serotype O111 cases with similar pulsed-field gel electrophoresis (PFGE) patterns attended the same church, but other links were not identified. One of these cases had HUS and another was a sibling of the HUS case. In a cluster of nine cases in November, there were a range of different serotypes including two O111 isolates with identical PFGE patterns.

The serotype was not identified in 51 per cent (40/78) of cases as polymerase chain reaction (PCR) tests are commonly used for diagnosis. These PCR tests detect the presence of toxin producing genes, and serotype-specific PCR tests only detect serotypes O157, O111 and O113. Culture of E. coli is not routinely carried out. In South Australia, the Hunter and Western Australia only stools containing macroscopic blood were screened for Shiga toxins 1 and 2 genes, unless specifically requested by the treating doctor. ‘H’ typing information was available for only 34 per cent (16/47) of isolates that were serotyped in 2005. There were six infections due to E. coli O157:H-, five due to E. coli O26:H11, two due to E. coli O157:H7, one each of serotypes O111:H-, O166:H15, and O77:H28.

Table 5. Number of notified cases of Shiga toxin-producing Escherichia coli, 2005, by state and serotype

Serotype
State Total
NSW Qld SA Vic WA
O157
2
2
5
4
2
15
O111
1
1
7
0
1
10
O26
0
3
1
2
0
6
O113
0
0
3
0
0
3
O103
0
0
1
0
0
1
O77
0
0
0
1
0
1
O112
0
0
1
0
0
1
O166
0
1
0
0
0
1
Non-O157 non-O111
0
0
0
0
9
9
Unknown
11
2
17
1
0
31
Total
14
9
35
8
12
78

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Haemolytic uraemic syndrome

There were 17 cases of haemolytic uraemic syndrome reported during 2005, which was a rate of 0.1 case per 100,000 population. This compared to 16 cases of HUS in 2004. New South Wales reported six of these cases, Victoria and Queensland both reported three cases each, Queensland and Tasmania both reported two cases each, and Western Australia reported 1 case in 2005(Figure 9).

Sixty-five per cent of cases were male. The highest rates of notification were in males and females aged 0–4 years, with rates of 1.2 and 0.7 cases per 100,000 population respectively. Sites reported that STEC were detected in the faeces of 53 per cent (9/17) of cases. Three cases were infected with serotype O111, two cases were infected with O157; one was OR:H- and three cases were STEC positive by PCR. One notified case was due to a non-enteric pathogen—Streptococcus pneumoniae. There was some clustering of HUS cases in 2005, with Tasmania investigating two apparently linked cases of E. coli O157:H- 54(var) in November and December, although no source was identified.

Figure 9. Numbers of notified cases of haemolytic uraemic syndrome, Australia, 2001 to 2005, by month of notification and state or territory

Figure 9.  Numbers of notified cases of haemolytic uraemic syndrome, Australia, 2001 to 2005, by month of notification and state or territory

Gastrointestinal and foodborne disease outbreaks

During 2005, OzFoodNet sites reported 624 outbreaks of gastrointestinal illness affecting 10,865 persons. The mode of transmission for 57 per cent (358/624) of outbreaks was suspected to be person-to-person transmission (Figure 10).

These person-to-person outbreaks were responsible for 66 per cent (7,222/10,865) of all persons affected by outbreaks and three deaths. Forty-six per cent (163/358) of the person-to-person outbreaks occurred in aged care facilities, while 23 per cent (84/358) and 12 per cent (42/358) of outbreaks occurred in childcare and hospital settings, respectively. Thirty-seven per cent (134/358) of person-to-person outbreaks were caused by norovirus, while 51 per cent (183/358) were of unknown aetiology, many of which were suspected to be due to a viral pathogen.

Sites conducted investigations into 147 different clusters or point source outbreaks where the mode of transmission was not determined, including 63 clusters due to various strains of Salmonella. Four outbreaks were suspected to be due to animal-to-person infection, three of these were due to Salmonella and one was due to Cryptosporidium.

Figure 10. Foodborne and gastroenteritis outbreaks reported by OzFoodNet sites, Australia, 2005, by mode of transmission (n=624 outbreaks)

Figure 10.  Foodborne and gastroenteritis outbreaks reported by OzFoodNet sites, Australia, 2005, by mode of transmission

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Foodborne disease outbreaks

In 2005, there were 102 foodborne disease outbreaks giving an overall rate of 5.0 outbreaks per million population. These outbreaks affected 1,975 persons, hospitalised 166 persons and caused four deaths. A summary description of all foodborne outbreaks is shown in Appendix 2.

Queensland reported the largest number of outbreaks (31%, 32/102 of all outbreaks reported) (Table 6). The reporting rates of foodborne outbreaks for different OzFoodNet sites ranged from 0.7 per million population in New South Wales to 15.4 per million population in the Australian Capital Territory. The majority of outbreaks occurred in summer and autumn (Figure 11).

Table 6. Outbreaks of foodborne disease in Australia, 2005, by OzFoodNet site

State or territory
Number of outbreaks Persons affected Mean: persons affected Hospitalised Fatalities Outbreaks per million population
Australian Capital Territory
5
51
10.2
4
0
15.4
New South Wales
19
246
12.9
24
1
0.7
Northern Territory
2
9
4.5
1
0
9.9
Queensland
32
292
9.1
69
3
8.1
South Australia
6
163
27.2
5
0
3.9
Tasmania
6
205
34.2
10
0
12.4
Victoria
27
808
29.9
40
0
5.4
Western Australia
5
198
39.6
13
0
2.5
Total
102
1,975
19.4
166
4
5.0

Figure 11. Outbreaks of foodborne disease, Australia, 2001 to 2005, by selected aetiological agents

Figure 11.  Outbreaks of foodborne disease, Australia, 2001 to 2005, by selected aetiological agents
Aetiological agents

The most common agent responsible for foodborne disease outbreaks was Salmonella, which caused 32 per cent (33/102) of outbreaks (Table 7). These outbreaks affected a total of 1,200 persons with a hospitalisation rate of 13 per cent (150/1,200). S. Typhimurium was responsible for 79 per cent (26/33) of foodborne Salmonella outbreaks. Four fatalities were reported from three separate outbreaks of Salmonella, two of which occurred in aged care homes and one other occurred in an institutional setting. The highest hospitalisation rate was for listeriosis although this was only one small outbreak.

Table 7. Aetiological agents responsible for foodborne disease outbreaks, number of outbreaks and persons affected, Australia, 2005

Agent category
Number of outbreaks Persons affected Mean outbreak size (persons) Hospitalised Fatalities
Campylobacter sp.
9
93
10.3
2
0
Ciguatera
10
57
5.7
2
0
Clostridium perfringens
4
76
19.0
0
0
Histamine poisoning
5
12
2.4
0
0
Listeria monocytogenes
1
3
3.0
3
Norovirus
4
91
22.8
2
0
Salmonella other
7
180
25.7
24
4
Salmonella Typhimurium
26
1,020
39.2
126
0
Staphylococcus aureus
2
4
2.0
0
0
Vibrio parahaemolyticus
1
2
2.0
0
0
Unknown
33
437
13.2
7
0
Total
102
1,975
19.4
166
4

Fifteen of the 21 outbreaks of illness due to toxins in 2005 were related to contaminated fish. Outbreaks of ciguatera and histamine poisoning, were small with a mean of 5.7 and 2.4 persons affected respectively. There were four outbreaks of Clostridium perfringens intoxication and two of Staphylococcus aureus intoxication. There were nine outbreaks of Campylobacter affecting 93 people, and one outbreak of vibriosis affecting two people. There were four outbreaks of norovirus affecting 91 people. Thirty-two per cent (33/102) of outbreaks were of unknown aetiology, which affected 437 persons including seven cases who were hospitalised.

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Food vehicles

There was a wide variety of foods implicated in outbreaks of foodborne disease during 2005 (Table 8), although investigators could not identify a specific food vehicle in 30 per cent (31/102) of outbreaks. Contaminated fish was the most common food vehicle and was responsible for 16 per cent (16/102) of outbreaks. Ten were due to ciguatera fish poisoning and five due to small outbreaks of histamine poisoning. Queensland reported nine of the ciguatera outbreaks from locally-caught fish, with Victoria reporting one ciguatera outbreak caused by fish sourced from Fiji. Four out of five outbreaks of histamine poisoning were associated with the consumption of tuna, with the remaining outbreak associated with an unknown species of fish.

Poultry and mixed meat dishes were responsible for nine outbreaks each. Sauces and gravies were implicated as the cause of six outbreaks, which included four outbreaks relating to eggs. Egg-based dishes caused two outbreaks, and a further three outbreaks were suspected as being due to eggs. In addition, there were two outbreaks due to desserts containing raw eggs; and two due to cakes and one due to sandwiches where cross contamination from eggs was suspected. In total, investigators identified 14 outbreaks of salmonellosis where eggs were suspected or proven to be the actual source of contamination of the implicated food.

There were two outbreaks associated with drinking water, one of which was associated with a municipal water supply. There were three outbreaks due to dips, including one very large outbreak associated with food served at a Turkish restaurant in Victoria. Outbreaks due to desserts had the highest hospitalisation rate, with 61 per cent (34/56) of people affected in three outbreaks being admitted to hospital.

Table 8. Categories of food vehicles implicated in foodborne disease outbreaks, Australia, 2005

Agent category
Number of outbreaks Persons affected Hospitalised
Fish
16
80
2
Mixed meat dish
9
152
19
Poultry
9
76
4
Sauces and gravy
6
125
11
Mixed dish
4
38
4
Cakes
3
129
13
Dessert
3
56
34
Dips
3
475
26
Sandwiches
3
123
0
Seafood
3
57
22
Suspected eggs
3
28
2
Egg-based dishes
2
11
2
Salad dishes
2
162
12
Water
2
34
2
Pizza
1
9
0
Pork
1
25
1
Suspected water
1
22
0
Unknown
31
373
12
Total
102
1,975
166

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Outbreak settings

The most common settings where food was prepared in outbreaks was at restaurants (33%), followed by the home (12%), events catered for by professional companies (11%) and aged care homes (8%) (Table 9). Foods that were contaminated in primary production environments, such as fish contaminated with ciguatoxin, were classified as ‘primary produce’ and were responsible for 12 per cent of outbreaks. Food prepared in bakeries and at takeaway stores were responsible for five outbreaks each, while food prepared at school camps was responsible for three outbreaks. The setting where people ate the food was similar to where it was prepared. There were 11 outbreaks in aged care homes, two of which were due to food prepared elsewhere and one was suspected to be due to contaminated tank water.

Table 9. Settings where food implicated in disease outbreaks was prepared, Australia, 2005

Setting category
Number of outbreaks Persons affected Hospitalised
Restaurant
34
956
73
Private residence
12
136
12
Primary produce
12
184
12
Commercial caterer
11
218
10
Aged care
8
117
3
Takeaway
5
19
4
Bakery
5
141
13
Camp
2
24
2
Hospital
2
14
3
Institution
2
40
4
Other
2
36
4
Grocery store/delicatessen
2
6
0
Not applicable
1
8
0
School
1
36
1
Child care facility
1
33
0
Unknown
2
7
2
Total
102
1,975
166

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Investigative methods and levels of evidence

States and territories investigated 24 outbreaks using retrospective cohort studies and 10 outbreaks using case control studies, with one investigation using both methodologies. Forty-two per cent (10/24) of cohort studies were used for outbreaks of unknown aetiology, which is similar to previous years. Thirty-eight per cent (9/24) of investigations using cohort studies were for Salmonella outbreak investigations. Sixty-five outbreaks relied on descriptive information to attribute a foodborne cause or identify a food vehicle, while no individual patient data was collected in two outbreaks.

To attribute the cause of the outbreak to a specific food vehicle, investigators obtained analytical evidence from epidemiological studies of 19 outbreaks. Microbiological evidence of contaminated food was found in 12 outbreaks, with a further five outbreak investigations obtaining both microbiological and analytical evidence. Investigators obtained analytical and/or microbiological evidence for 39 per cent (13/33) of Salmonella outbreaks, which was similar to 33 per cent for 2004. Sixty-three per cent (66/102) of outbreaks relied on descriptive evidence to implicate a food or foodborne transmission. These were mainly smaller outbreaks or were in settings where patient interviews were difficult to collect such as aged care facilities.

Significant outbreaks

There were five outbreaks affecting 50 or more persons in 2005, which is similar to previous years. Four were due to Salmonella Typhimurium and one was due to Salmonella Oranienburg. Two of the outbreaks occurred at restaurants, two in the community and one was associated with a bakery. The largest outbreak was due to S. Typhimurium 197 in Victoria during January. This outbreak affected in excess of 448 people and was related to dips served at a Turkish restaurant.

Two large outbreaks of S. Typhimurium 135 occurred in Tasmania during October and December, and affected a total of 184 people. These outbreaks were associated with cakes prepared at a bakery and raw egg sauces from a restaurant. A common egg-farm supplied eggs to both of the implicated premises. Eggs from this farm were associated with two additional smaller outbreaks in Tasmania.

In November, the Western Australian Department of Health investigated an outbreak of Salmonella Oranienburg. The outbreak extended into the first four months of 2006, and affected at least 125 people. The Health Department conducted a case control study that implicated commercially produced alfalfa sprouts, which was later confirmed microbiologically. The other outbreak affecting more than 50 people occurred in South Australia and involved 81 people with 46 of them diagnosed with S. Typhimurium 64 after eating rolls with various fillings from a restaurant.

There were 20 outbreaks affecting between 20 and 50 persons. Six of these outbreaks occurred in association with food prepared at restaurants and five with food prepared by commercial caterers. A wide range of food vehicles were responsible for these outbreaks. Six outbreaks were due to Salmonella, of which serotype Typhimurium was responsible for five of these.

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Cluster investigations

During 2005, states and territories conducted 82 investigations of clusters of enteric diseases that affected 1,076 people and hospitalising at least 65 people. Investigators were unable to determine the mode of transmission or source of infections for these clusters, which were due to organisms such as Salmonella, Campylobacter, Shiga toxin-producing E. coli and hepatitis A. These clusters do not include all investigations conducted at the state, territory or public health unit level, but the number is indicative of the effort to investigate enteric diseases in Australia. Seventy-seven per cent (63/82) of these investigations related to clusters of Salmonella, where the mean number of cases was 10.8 and the total number of persons affected was 683. S. Typhimurium was responsible for 49 per cent (31/63) of cluster investigations. Investigations of clusters of S. Typhimurium involved more cases with a mean of 13.5 persons than for non-Typhimurium strains with a mean of 8.3 persons. Of the remaining 32 investigations, 24 other different Salmonella serovars were involved.

During 2005, there were major increases in Cryptosporidium infections in eastern States of Australia. This was reflected in 53 per cent (10/19) of cluster investigations relating to Cryptosporidium. The mean size of Cryptosporidium cluster investigations was 33.1 persons, which was considerably larger than that for other pathogens. Five of the investigations of Cryptosporidium infection were related to contaminated swimming pool water, and the source was unknown for the remaining five outbreaks.

There were three investigations into clusters of campylobacteriosis, two each of Giardia and STEC infections, and one each of Shigella and hepatitis A infections. The true number of clusters investigated is difficult to ascertain, as public health units or local governments do not record all cluster investigations they conduct. States and territories may also have different definitions and triggers for investigating clusters.

In 2005, OzFoodNet investigated several multi-state clusters of Salmonella, including:

  • cases of S. Typhimurium 135 in the Australian Capital Territory, and New South Wales associated with a yum cha meal in Sydney;
  • S. Hvittingfoss infections in eastern States of Australia in June and July;
  • S. Havana cases in New South Wales, Western Australia, South Australia and Victoria in November; and
  • S. Typhimurium phage types 44 and 135 in all Australian states and territories, except the Northern Territory, in November and December.

OzFoodNet site epidemiologists and state and territory investigators conducted case control studies for two of these multi-state investigations. In June, the source of S. Hvittingfoss infections were investigated using a case control study, although no source was identified.13 In the investigation of S. Typhimurium phage types 135 and 44, OzFoodNet initiated a case control study investigating the association between infection with these two phage types and consumption of chicken or eggs. Phage type 135 was significantly associated with consumption of chicken purchased from retail supermarkets. The findings of the case control study for S. Typhimurium 44 were equivocal, although 62 per cent (8/13) of point source outbreaks of this phage type occurring during this investigation were suspected to be associated with consumption of eggs.

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Surveillance evaluation

Australian surveillance of infectious diseases notified under legislation to state and territory health departments is very effective. The high quality of the data is due to the quality of laboratory services, including reference testing, and awareness of the medical community about the need to notify. In the past 10–15 years, there have been progressive improvements in the capacity of health departments to detect and investigate foodborne diseases at state and territory and national levels. To improve surveillance, OzFoodNet regularly evaluates surveillance and compares data collected at different sites.

National information sharing

In 2005, all jurisdictions contributed to a fortnightly national report to identify clusters of foodborne illness that were occurring across state and territory boundaries. The cluster report was useful for identifying common events affecting different parts of Australia. The cluster report supplemented information sharing on a closed list server, teleconferences and at quarterly face-to-face meetings. In addition, all jurisdictions contributed data to the NNDSS for several diseases that were potentially transmitted by food. In 2005, OzFoodNet made greater use of NNDSS data on specific serotypes and phage types of Salmonella, which allowed the detection of clusters and outbreaks at the national level.

Outbreak reporting and investigation

During 2005, the Australian Capital Territory site reported the highest reporting rate of outbreaks of foodborne disease (15.4 outbreaks per million population), along with Tasmania (12.4 outbreaks per million population). Tasmania also reported the highest rate of foodborne salmonellosis outbreaks (8.2 outbreaks per 100,000 population). The rates of other sites reporting foodborne Salmonella outbreaks ranged between 0.5–4.9 outbreaks per million population. Queensland investigated the largest number of foodborne disease outbreaks (32 outbreaks; 8.1 per million population). States and territories conducted 36 analytical studies (cohort or case control studies) to investigate foodborne disease outbreaks, which was slightly less than that of the previous year.

Completeness of Salmonella serotype and phage type reports

Overall, 97.4 per cent (8,153/8,371) of Salmonella notifications on state and territory surveillance databases in 2005 contained information about serotype and/or phage type (Figure 12). This was an increase of 0.7 per cent from 2004.

Phage type recording on the four most prevalent serotypes—Typhimurium, Bovismorbificans, Enteritidis and Virchow—were all greater than 95 per cent complete for phage type information on surveillance databases. Phage type recording was lowest for serotypes Heidelberg and Hadar, with 18.0 per cent (6/43) and 8.0 per cent (2/25) of reports on databases missing the phage type, respectively (Figure 13). Queensland had the highest proportion of complete Salmonella notification (99.8%), while six sites reported 95 per cent or higher.

Figure 12. Proportion of Salmonella infections notified to state and territory health departments with serotype and phage type information available, Australia, 2000 to 2005

Proportion of Salmonella infections notified to state and territory health departments with serotype and phage type information available, Australia, 2000 to 2005

Figure 13. Proportion of Salmonella infections for six serotypes notified to state and territory health departments with phage type information available, Australia, 2000 to 2005

Figure 13.  Proportion of Salmonella infections for six serotypes notified to state and territory health departments with phage type information available, Australia, 2000 to 2005

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Discussion

This report highlights the rates of diseases due to microbiologically contaminated food in Australia. In particular the increasing notification rates of Salmonella and Campylobacter are concerning. For Salmonella in 2005, reports of several phage types of S. Typhimurium were increased and health departments conducted at least 63 investigations of S. Typhimurium illness clustered in time, place or person. The rate of campylobacteriosis was particularly high despite health departments conducting relatively few investigations. If we extrapolate using estimated rates of under-reporting, there may have been as many as 153,000 to 554,000 cases of Campylobacter occurring in the community during 2005.2,3 It is likely that approximately 75 per cent of these Campylobacter infections would be foodborne in origin.14

The notification rates of Campylobacter and Salmonella in Australia are ten and three times higher respectively than for FoodNet sites in the United States of America (USA).15,16 The reasons for this are unclear, but are currently being explored. The USA has observed declining incidence of campylobacteriosis in recent years.16,17 In comparison to New Zealand, Australia has similar rates of salmonellosis and lower rates of campylobacteriosis.18 New Zealand has seen progressively increasing rates of campylobacteriosis for several years.19 The reasons for the elevated rates in New Zealand are unclear, but local risk factors for infection include consumption of under-cooked poultry and contact with animals. Australian case control studies of campylobacteriosis have also found that these are important risk factors for infection.20

The overall rate of typhoid infections decreased in 2005 and there were fewer locally-acquired typhoid infections. In contrast, the rate of travel-acquired Salmonella Enteritidis remained similar to previous years. The number of locally-acquired S. Enteritidis infections in 2005 was similar to previous years, and were predominantly reported from Queensland. It was concerning to see an outbreak of S. Enteritidis 26var in an aged care home in January 2005 in Victoria, although this was an isolated event. Human surveillance of S. Enteritidis infections is very important to monitor for the incursion of this serotype into egg-laying flocks of poultry.20,21

In previous years' reports we have noted the considerable variation of the rates of STEC notifications in different Australian states and territories.23 During 2005, Western Australia, Victoria and the Hunter enhanced surveillance for STEC, which was reflected in increased rates in these regions. Internationally, E. coli O157:H7 is the predominant strain reported from surveillance data.16 In Australia, E. coli O157 was also the most common, but the rates were much lower than those observed overseas and many other strains were also common in Australia.Jurisdictions investigated clustering of cases for both STEC and HUS, although they were unable to identify common sources of infection.

While notifications of enteric infections provide information on the burden of disease they are hard to interpret due to the difficulties in establishing the sources of transmission. Summaries of foodborne disease outbreaks provide a systematic way to assess information for the development of food safety policy.5,24 Australian outbreak data for 2005 highlights several areas where continued vigilance or improvements in food safety are needed, including: fish-related outbreaks, alfalfa sprout production, and poultry and egg-associated salmonellosis.

Fish is the most common food vehicle for identified outbreaks in Australia, although they usually only affect small numbers of people.25 The two most common intoxications associated with fish—ciguatera and histamine poisoning—are poorly recognised by clinicians and often not reported to health departments. Ciguatera outbreaks in Australia occur almost exclusively in Queensland where amateur fishermen catch fish on affected reefs. However during 2005, three outbreaks of ciguatera occurred where people purchased contaminated fish from retailers. The outbreaks of histamine poisoning in 2005 were almost all associated with tuna. Some of these investigations implicated tuna imported from Asia, although these were unable to be traced back to a common source (personal communication,C Shadbolt, New South Wales Food Authority, July 2006). It was encouraging to see that there were no outbreaks associated with escolar fish in 2005, which has previously caused outbreaks of oily diarrhoea or histamine poisoning.26

There were nine outbreaks related to consumption of poultry, making it the second most common food vehicle following fish. Salmonella was the aetiological agent in two of these outbreaks, Campylobacter in two, Clostridium perfringens in one and the aetiology was not determined for the remaining four outbreaks. In addition to these nine outbreaks, OzFoodNet coordinated investigations into a large multi-state cluster of S. Typhimurium 135 in November and December 2005. In this investigation microbiological and epidemiological evidence indicated that poultry from retail stores was the likely cause for the outbreak. Food Standards Australia New Zealand are preparing a primary production standard for poultry meat in cooperation with industry and other stakeholders, which will aim to reduce human illness associated with poultry meat.

During 2005, there were four outbreaks of S. Typhimurium 135 in Tasmania linked to the same egg farm. Eggs are a common cause of foodborne disease outbreaks, despite Australia not having S. Enteritidis endemic in layer flocks.25 OzFoodNet found that eggs may be responsible for 14 per cent of all foodborne disease outbreaks in 2005, which is higher than previous years. The predominant cause of these outbreaks was S. Typhimurium, which has a lower potential for trans-ovarian transmission in layer flocks than S. Enteritidis.27 Outbreaks in Australia may be occurring from surface contamination of eggs or through very low rates of trans-ovarian transmission.25 Food Standards Australia New Zealand are in the process of establishing a committee to develop a national standard for the primary production of eggs.

The outbreak of S. Oranienburg associated with contaminated alfalfa sprouts in Western Australia was the first well-documented outbreak associated with sprouts in Australia. There have been many outbreaks of sprout-associated illness overseas, some of which have implicated seed originating from Australia.28 These overseas outbreaks traced back to Australian seed have been due to a variety of pathogens, including: E. coli O157:NM; S. Kottbus; S. Bovismorbificans; and S. Saintpaul.28–31 The National Enteric Pathogen Surveillance Scheme records 26 isolations of various serotypes of Salmonella from sprouts over the last 20 years (personal communication, Joan Powling, March 2006). The Western Australian outbreak highlighted several areas where alfalfa seed production may be vulnerable to contamination, including growing lucerne pasture and processes within sprouting facilities.28 Following the outbreak, the Implementation Sub-Committee of the Food Regulation Standing Committee formed a working group to consider ways to improve food safety of these products.

Forty-four per cent of foodborne outbreaks occurred in association with foods prepared at restaurants and commercial caterers, which is similar to previous years. Aged care homes were also common settings for foodborne disease outbreaks and resulted in three of the four outbreak-associated deaths in 2005. Foodborne outbreaks constituted only 6 per cent (11/189) of all outbreaks in aged care homes, but the risk of residents dying was significantly higher for foodborne transmission when compared to other modes of transmission (relative risk 10.2, 95 per cent confidence interval 2.0–58.2). Outbreaks in aged care settings are very difficult to investigate due to the poor recall of food consumption by patients, meaning that a food vehicle was identified in only three outbreaks.

It is important to recognise some of the limitations of the data in this report. Surveillance data are inherently biased and require careful interpretation. These biases include the higher likelihood that certain population groups will be tested, and different testing regimes may be used in different states and territories, resulting in different rates of disease.3 Some of the numbers of notifications are small, as are populations in some jurisdictions. This can make rates of notification unstable and meaningful interpretation difficult. Importantly, some of the most common enteric pathogens are not notifiable, particularly norovirus and enteropathogenic E. coli. There are some pathogens, such as Campylobacter, that are very common but are not often recognised as causing outbreaks. This means relying on outbreak data to set food safety policy will under-estimate the importance of certain pathogens and food vehicles as a cause of human illness and over-estimate others.5 There can also be considerable variation in assigning causes to outbreaks depending on investigation methods, number of cases and circumstances of the outbreak.

Health agencies conducting surveillance for foodborne disease must constantly improve their practices and evaluate their efforts. This should involve stakeholders such as laboratories, clinicians, and other government departments. The number of analytical studies that health departments used to investigate outbreaks is evidence of robust inquiry into the causes of these diseases. During 2005, OzFoodNet coordinated or participated in the investigation of several multi-state outbreaks. For these multi-state investigations, outbreak investigation team members entered de-identified data into a web-based database—NetEpi—for hypothesis generation and case control studies.13 This method of data collection was very rapid compared to other methods. Using the Internet to collect information in outbreak settings is a powerful tool for widely dispersed outbreaks and will become routine in the future.32

OzFoodNet has shown the benefits of regular communication about surveillance data for detecting national outbreaks. In May 2005, OzFoodNet and the NSW Health Department held an advanced outbreak investigation workshop to improve Australian epidemiologists' abilities to respond to foodborne disease outbreaks. This follows a consultation that OzFoodNet held in 2004, which identified that training and capacity building in disease investigation were important for national preparedness.

It is important that this report assist with the development of food safety policy for Australia. In previous years we have identified similar food vehicles and settings where food is prepared, which indicate that current controls may be inadequate. National surveillance of foodborne diseases is critical to provide data to evaluate these efforts. Ideally, these data would be compared in a timely fashion with data arising from surveillance of hazards in foods and pathogens in animals, as many foodborne diseases have a zoonotic origin.33,34

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Acknowledgements

We would like to thank epidemiologists, project officers, interviewers and research assistants at each of the OzFoodNet sites who contributed to this report. We also acknowledge the work of various public health professionals and laboratory staff around Australia who interviewed patients, tested specimens, typed isolates and investigated outbreaks. We would like to thank jurisdictional laboratories, the Microbiological Diagnostic Unit Public Health Laboratory, Australian Salmonella Reference Laboratory, and the National Enteric Pathogen Surveillance Scheme. The high quality of their work is the foundation of this report. OzFoodNet is an initiative of the Australian Government.

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References

1. Abelson P. The cost of foodborne illness in Australia. Australian Government Department of Health and Ageing, Canberra 2006.

2. Mead PS, Slutsker L, Dietz V, McCraig LF, Bresee JS, Shapiro C, et al. Food-related illness and death in the United States. Emerg Infect Dis 1999;5:607–625.

3. Hall G, Raupach J, Yohannes K. An Estimate of under-reporting of foodborne notifiable diseases: Salmonella, Campylobacter, Shiga toxin-producing E. coli (STEC). National Centre for Epidemiology Working Paper No. 52, Australian National University, 2006.

4. Allos BM, Moore MR, Griffin PM, Tauxe RV. Surveillance for sporadic foodborne disease in the 21st Century: the FoodNet perspective. Clin Infect Dis 2004;38 Suppl 3:S115–S120.

5. O'Brien SJ, Gillespie IA, Sivanesan MA, Elson R, Hughes C, Adak GK. Publication bias in foodborne outbreaks of infectious intestinal disease and its implications for evidence-based food policy. England and Wales 1992–2003. Epidemiol Infect 2006;134:667–674.

6. Ashbolt R, Givney R, Gregory JE, Hall G, Hundy R, Kirk M, et al. Enhancing foodborne disease surveillance across Australia in 2001: the OzFoodNet Working Group. Commun Dis Intell 2002;26:375–406.

7. Lindenmayer P. Networking for health protection: the Communicable Diseases Network Australia. Commun Dis Intell 2001;25:266–269.

8. Australian Bureau of Statistics. 3201.0 – Population by Age and Sex, Australian States and Territories, June 2005. Canberra, 2005.

9. Australian Institute of Health and Welfare. Australia’s mothers and babies 2002. Canberra 2004.

10. Yohannes K, Roche PW, Roberts A, Liu C, Firestone SM, Bartlett M, et al. Australia's notifiable diseases status, 2004, annual report of the National Notifiable Diseases Surveillance System. Commun Dis Intell 2006;30:1–79.

11. Braden CR. Salmonella enterica serotype Enteritidis and eggs: a national epidemic in the United States. Clin Infect Dis 2006;43:512–517.

12. Doorduyn Y, Van Den Brandhof WE, Van Duynhoven YT, Wannet WJ, Van Pelt W. Risk factors for Salmonella Enteritidis and Typhimurium (DT104 and non-DT104) infections in The Netherlands: predominant roles for raw eggs in Enteritidis and sandboxes in Typhimurium infections. Epidemiol Infect 2006;134:617–626.

13. Oxenford CJ, Black AP, Bell RJ, Munnoch SA, Irwin MJ, Hanson RN, et al. Investigation of a multi-state outbreak of Salmonella Hvittingfoss using a web-based case reporting form. Commun Dis Intell 2005;29:379–381.

14. Hall G, Kirk MD, Becker N, Gregory JE, Unicomb L, Millard G, et al. Estimating foodborne gastroenteritis, Australia. Emerg Infect Dis 2005;11:1257–1264.

15. Vally H, Kirk MD, Scallan E, Angulo FJ, Hall GV. Higher Incidence of Campylobacter infection in Australia compared with the United States in 2001. Communicable Disease Control Conference 2005, Sydney, 2–3 May 2005.

16. Centers for Disease Control and Prevention. Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food—10 States, United States, 2005, MMWR Morb Mortal Wkly Rep 2006;55;392-395.

17. Samuel MC, Vugia DJ, Shallow S, Marcus R, Segler S, McGivern T, et al. Epidemiology of sporadic Campylobacter infection in the United States and declining trend in incidence, FoodNet 1996-1999. Clin Infect Dis 2004;38 Suppl 3:S165–S174.

18. Notifiable and other diseases in New Zealand: Annual Report 2005. Institute of Environmental Science and Research Limited, Porirua 2006.

19. Baker MG, Sneyd E, Wilson NA. Is the major increase in notified campylobacteriosis in New Zealand real? Epidemiol Infect 2006:1-8 [Epub ahead of print].

20. Stafford R, Unicomb L, Ashbolt R, Kirk M, OzFoodNet Working Group. The burden of Campylobacter infections in Australia. Communicable Disease Control Conference 2005, Sydney, 2–3 May 2005.

21. Kirk M. Foodborne surveillance needs in Australia: harmonisation of molecular laboratory testing and sharing data from human, animal, and food sources. N S W Public Health Bull 2004;15:13–17.

22. ESG Sergeant, TM Grimes, CAW Jackson, FC Baldock, IF Whan. Salmonella Enteritidis surveillance and response options for the Australian egg industry. Rural Industries Research and Development Corporation, RIRDC Publication No 03/006 RIRDC Project No AUV-1A, January 2003.

23. Combs BG, Raupach JC, Kirk MD. Surveillance of Shiga toxigenic Escherichia coli in Australia. Commun Dis Intell 2005;29:366–369.

24. Adak GK, Meakins SM, Yip H, Lopman BA, O'Brien SJ. Disease risks from foods, England and Wales, 1996-2000. Emerg Infect Dis 2005;1:365–372.

25. Dalton CB, Gregory J, Kirk MD, Stafford RJ, Givene R, Kraa E, et al. Foodborne disease outbreaks in Australia 1995 to 2000. Commun Dis Intell 2002;28:211–224.

26. Shadbolt C, Kirk M, Roche P. Diarrhoea associated with consumption of escolar (rudderfish). Commun Dis Intell 2002;26:436–438.

27. Okamura M, Kamijima Y, Miyamoto T, Tani H, Sasai K, Baba E. Differences among six Salmonella serovars in abilities to colonize reproductive organs and to contaminate eggs in laying hens. Avian Dis 2001;45:61–69.

28. Ferguson DD, Scheftel J, Cronquist A, Smith K, Woo-Ming A, Anderson E, et al. Temporally distinct Escherichia coli 0157 outbreaks associated with alfalfa sprouts linked to a common seed source—Colorado and Minnesota, 2003. Epidemiol Infect 2005;133:439–447.

29. O'Mahony M, Cowden J, Smyth B, Lynch D, Hall M, Rowe B, et al. An outbreak of Salmonella Saint-paul infection associated with beansprouts. Epidemiol Infect 1990;104:229-235.

30. Ponka A, Andersson Y, Siitonen A, de Jong B, Jahkola M, Haikala O, et al. Salmonella in alfalfa sprouts. Lancet 1995;345:462–463.

31. Winthrop KL, Palumbo MS, Farrar JA, Mohle-Boetani JC, Abott S, Beatty ME, et al. Alfalfa sprouts and Salmonella Kottbus infection: a multistate outbreak following inadequate seed disinfection with heat and chlorine. J Food Prot 2003;66:13–17.

32. Srikantiah P, Bodager D, Toth B, Kass-Hout T, Hammond R, Stenzel S, et al. Web-based investigation of multistate salmonellosis outbreak. Emerg Infect Dis 2005;11:610–612.

33. O'Brien SJ. Foodborne zoonoses. BMJ 2005;331:1217–1218.

34. Kahn LH. Confronting zoonoses, linking human and veterinary medicine. Emerg Infect Dis 2006;12:556–561.

Appendix 1. Number of cases and rates per 100,000 population of potentially foodborne diseases reported to OzFoodNet sites, Australia, 2005

Condition
  ACT NSW NT Qld SA Tas Vic WA Aust
Campylobacter cases
393
NN
250
4,427
2,113
766
6,108
2,422
16,479
rate
120.9
NN
123.3
111.7
137.0
157.9
121.6
120.5
121.6
Salmonella cases
96
2,174
399
2,607
586
301
1,422
791
8,376
rate
29.5
32.1
196.8
65.8
38.0
62.0
28.3
39.4
41.2
Shiga toxin Escherichia coli cases
0
14
0
9
35
0
8
12
78
rate
0.0
0.2
0.0
0.2
2.3
0.0
0.2
0.6
0.4
Haemolytic uraemic syndrome cases
0
6
0
3
2
2
3
1
17
rate
0.0
0.1
0.0
0.1
0.1
0.4
0.1
0.0
0.1
Typhoid cases
0
28
0
3
2
0
12
7
52
rate
0.0
0.4
0.0
0.1
0.1
0.0
0.2
0.3
0.3
Shigella cases
7
134
195
80
47
4
103
151
721
rate
2.2
2.0
96.2
2.0
3.0
0.8
2.1
7.5
3.5
Listeria cases
3
25
0
7
6
0
11
4
56
rate
0.9
0.4
0.0
0.2
0.4
0.0
0.2
0.2
0.3

NN Not notifiable.

Appendix 2. Outbreak summary for OzFoodNet sites, Australia, 2005

State
Month of outbreak
Setting prepared
Agent category
Number affected Hospitalised Evidence* Epidemiological study
Responsible vehicles
ACT Jan Commercial caterer Unknown
7
0
A
C
Strawberries, smoked salmon & grapes
Mar Restaurant S. Hessarek
5
2
AM
C
Hollandaise sauce
Apr Restaurant Campylobacter
11
1
A
C
Chicken salad & chicken pasta
Jun Commercial caterer Norovirus
25
1
A
CCS
Pork bruschetta & duck tart
Jul Restaurant Unknown
3
0
A
CCS
Unknown
NSW Jan Private residence S. Typhimurium 197
43
13
A
CCS
Lambs liver
Mar Commercial caterer Unknown
13
0
A
CCS
Beef casserole
Mar Restaurant Unknown
3
2
D
D
Chicken Caesar salad burger
Apr Restaurant Unknown
5
0
D
D
Lamb & beef
Apr Restaurant Unknown
2
0
D
D
Chicken
May Institution Unknown
37
1
D
CCS/C
Self serve salad bar
May Restaurant Unknown
2
0
D
C
Chicken
Jul Restaurant S. Typhimurium 9
16
D
D
Suspected raw egg dishes
Aug Aged care Unknown
12
D
N
Unknown
Aug Restaurant Unknown
3
0
D
D
Suspected coleslaw
Sep Restaurant Unknown
9
0
A
C
Ham pizza
Oct Child care facility S. Typhimurium 197
33
0
D
C
Unknown
Oct Takeaway Campylobacter
5
0
D
D
Unknown
Oct Institution S. Birkenhead
3
3
D
D
Suspected pureed food
Nov Restaurant C. perfringens
23
0
D
C
Suspected yellow rice
Nov Restaurant S. Typhimurium 44
8
2
D
D
Caesar salad dressing
Nov Takeaway S. Typhimurium 9
4
3
D
D
Chicken, rice, coleslaw, potatoes
Nov Private residence Histamine poisoning
4
0
M
N
Tuna steak
Unk Restaurant Unknown
24
0
D
D
Pasta + pizza
NT May Private residence Unknown
5
0
D
D
Vietnamese pork rolls
Jul Private residence S. Typhimurium RDNC
4
1
D
D
Vietnamese rice paper rolls
Qld Jan Aged care C. perfringens
36
0
M
D
Braised steak & gravy
Jan Not applicable Mixed Salmonella
8
0
M
D
Rainwater
Jan Primary produce Ciguatera
4
0
D
D
Mackerel
Jan Primary produce Ciguatera
2
0
D
D
Black trevally
Feb Other S. Typhimurium 12
10
2
D
D
Unknown
Mar Primary produce Ciguatera
2
0
D
D
Yellowtail kingfish
Apr Primary produce Ciguatera
17
2
D
D
Spanish mackerel
Apr Commercial caterer Unknown
11
0
D
C
Unknown
Apr Grocery store/ delicatessen S. aureus
2
M
D
Custard filled dumplings
May Bakery S. Typhimurium 197
13
7
D
D
Egg based bakery products
May Private residence Campylobacter
5
0
D
D
Unknown
May Takeaway S. Typhimurium 170/108
2
1
D
D
Chicken meat
Jul Restaurant S. Typhimurium 9
40
29
A
C
Bread and butter pudding
Jul Restaurant C. perfringens
3
0
M
D
Beef rendang
Jul Restaurant Histamine poisoning
2
0
D
D
Yellowfin tuna
Sep Primary produce Ciguatera
5
0
D
D
Black kingfish
Sep Aged care Campylobacter
3
0
D
D
Unknown
Sep Unknown Campylobacter
2
0
D
D
Unknown
Sep Primary produce Ciguatera
2
0
D
D
Spanish mackerel
Sep Primary produce Ciguatera
2
0
D
D
Trevally
Sep Takeaway S. aureus
2
M
D
Chips and gravy
Oct Other S. Chester/ Saintpaul
26
2
AM
CCS
Municipal water
Oct Commercial caterer S. Potsdam
6
4
D
D
Unknown
Nov Restaurant Unknown
18
0
A
CCS
Seafood mornay & rice
Nov Restaurant C. perfringens
14
0
M
D
Chicken and lamb guvec
Nov Restaurant Unknown
5
0
D
D
Unknown
Nov Private residence S. Typhimurium 44
3
0
D
D
Egg and bacon roll
Nov Camp S. Typhimurium 44
2
0
D
D
Unknown
Dec Private residence S. Typhimurium 44
23
22
D
D
Prawn soup
Dec Primary produce Ciguatera
10
0
D
D
Barracuda
Dec Primary produce Ciguatera
8
0
D
D
Yellowtail kingfish
Dec Grocery store/ delicatessen Campylobacter
4
0
D
D
Chicken kebabs
SA Feb Restaurant S. Typhimurium 9
13
0
A
CCS
Unknown
May Restaurant S. Typhimurium 170/108
9
A
CCS
Marinated chicken roll
Jun Restaurant S. Typhimurium 64
81
A
C
Bread roll with fillings
Nov School Campylobacter
36
1
D
C
Unknown
Nov Hospital Listeria
3
3
M
D
Cold meats
Dec Restaurant Norovirus
21
1
D
D
Dips
Tas Feb Restaurant Histamine poisoning
2
0
D
D
Yellowfin tuna
May Private residence Vibrio
2
0
D
D
Suspected seafood
Oct Bakery S. Typhimurium 135
107
6
AM
C
Bakery products
Oct Restaurant S. Typhimurium 135
11
2
D
D
Sauces/dressings containing raw egg
Nov Bakery S. Typhimurium 135
6
0
D
D
Salad rolls/sandwiches
Dec Restaurant S. Typhimurium 135
77
2
AM
C
Mayonnaise & tartare sauce
Vic Jan Restaurant S. Typhimurium 197
448
25
M
D
Dips
Jan Commercial caterer Unknown
40
0
A
CCS
Veal rolls & red curry
Jan Aged care Unknown
30
0
D
D
Unknown
Jan Commercial caterer Unknown
29
0
A
C
Chicken vol-au-vents
Jan Private residence Unknown
10
1
D
D
Unknown
Jan Aged care S. Enteritidis 26var
7
2
D
D
Suspected eggs
Jan Private residence S. Typhimurium 126 var 4
5
0
D
D
Suspected eggs
Feb Camp Campylobacter
22
0
M
C
Suspected water
Feb Restaurant Unknown
16
0
A
C
Seafood platter, baked fish & octopus
Feb Bakery Unknown
6
0
D
D
Suspect pork rolls
Mar Private residence S. Typhimurium 12
15
0
D
C
Unknown
Mar Commercial caterer S. Typhimurium 9
14
5
D
C
Chocolate mousse
Mar Restaurant S. Typhimurium 9
13
5
M
D
Hollandaise sauce
Mar Aged care Unknown
11
0
D
D
Unknown
Mar Takeaway Unknown
6
0
M
D
Hommus dip
Jul Restaurant Histamine poisoning
2
0
A
D
Tuna
Jun Commercial caterer Unknown
17
0
A
C
Gravy & pork
Jun Hospital Unknown
11
0
D
D
Unknown
Aug Primary produce Ciguatera
5
0
D
D
Fijian snapper
Sep Restaurant Unknown
11
0
A
C
Suspected Spanish mackerel
Oct Commercial caterer Norovirus
36
0
A
C
Sandwiches
Oct Aged care Unknown
6
0
D
D
Unknown
Nov Aged care Unknown
12
1
D
D
Unknown
Nov Bakery Norovirus
9
0
D
D
Cakes
Nov Unknown Campylobacter
5
0
D
D
Unknown
Nov Primary produce Histamine poisoning
2
0
D
D
Fish
Dec Restaurant S. Typhimurium 170/108
20
1
D
C
Suspected pork
WA Apr Commercial caterer Unknown
20
0
D
D
Unknown
Jun Private residence Unknown
17
1
D
D
Unknown
Oct Restaurant Unknown
21
1
D
C
Unknown
Oct Restaurant Unknown
15
0
D
C
Unknown
Nov Primary produce S. Oranienburg
125
11
AM
CCS
Alfalfa sprouts

* A=analytical epidemiological evidence; D=descriptive evidence: M=microbiological evidence.
† C=cohort study; CCS=case control study; D=descriptive study; N=individual patient data not collected.
† All four outbreaks of S. Typhimurium 135 in Tasmania were due to the local variant phage type 135a, which is not a recognised international classification.

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Author affiliations

In 2005, the OzFoodNet Working Group was (in alphabetical order): Rosie Ashbolt (Tas), Jenny Barralet (Qld), Robert Bell (Qld), Kylie Begg (ACT), Phillipa Binns (NT), Dennis Bittisnich (DAFF), Andrew Black (ACT), Barry Combs (SA), Christine Carson (WA), Scott Crerar (FSANZ), Craig Dalton (HNE Health), Gerard Fitzsimmons (DoHA), Robyn Gibbs (WA), Joy Gregory (Vic), Gillian Hall (NCEPH), Geoff Hogg (MDU), Melissa Irwin (NSW), Martyn Kirk (DoHA), Karin Lalor (Vic), Deon Mahoney (FSANZ), Tony Merritt (HNE Health), Roseanne Muller (NT), Sally Munnoch (HNE Health), Jennie Musto (NSW), Lillian Mwanri (SA), Leonie Neville (NSW), Chris Oxenford (DoHA, NCEPH), Rhonda Owen (DoHA), Raj Patil (DAFF), Nevada Pingault (WA), Jane Raupach (SA), Mohinder Sarna (WA), Mark Salter (FSANZ), Cameron Sault (Tas), Craig Shadbolt (NSWFA), Russell Stafford (Qld), Nicola Stephens (Tas), Barbara Telfer (NSW) Hassan Vally (NCEPH, WA), Tory Worgan (HNE Health), Kefle Yohannes (DoHA)

Correspondence: Mr Martyn Kirk, Coordinating Epidemiologist, OzFoodNet, Office of Health Protection, Australian Government Department of Health and Ageing, GPO Box 9848, MDP 137, Canberra, ACT 2601. Telephone: +61 2 6289 9010. Facsimile: +61 2 6289 7100. Email: martyn.kirk@health.gov.au

 

This report was published in Communicable Diseases Intelligence Vol 30 No 3, September 2006.


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