Foodborne disease in Australia: incidence, notifications and outbreaks. Annual report of the OzFoodNet network, 2002

In 2002, OzFoodNet continued to enhance surveillance of foodborne diseases across Australia and has expanded its network to cover all Australian states and territories. This annual report was published in Communicable Diseases Intelligence Vol 27, No 2, June 2003, and can be viewed as 6 HTML documents and is also available in PDF format.

Page last updated: 30 June 2003

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


Results continued

Gastrointestinal and foodborne disease outbreaks

During 2002, OzFoodNet sites reported 513 outbreaks of gastrointestinal illness affecting 11,791 persons. Ninety-two of the outbreaks were due to transmission from contaminated food or water giving an overall rate of 4.7 outbreaks per million population. Three outbreaks were due to contact with infected animals.

The aetiology of the remaining outbreaks was either difficult to determine or were likely person-to-person transmission. Sites conducted 100 investigations into clusters where the mode of transmission was not determined, or a foodborne source was not identified. Person-to-person transmission was suspected as the cause of 318 outbreaks affecting 8,203 persons. The majority of these outbreaks occurred in aged care facilities and hospitals, and were due to norovirus.

Foodborne disease outbreaks

In 2002, 92 foodborne disease outbreaks affected 1,819 persons, hospitalised 103 persons and caused two deaths (Table 6). Appendix 2 shows a summary description of each outbreak.

Victoria reported the largest number of outbreaks (26/92, 28.3%), followed by New South Wales (23/92, 25%). The reporting rates of foodborne outbreaks for different OzFoodNet sites ranged from 1.5 per million persons in Western Australia to 31.2 per million persons in the Hunter. The Australian Capital Territory and the Northern Territory did not report any outbreaks with a foodborne mode of transmission during 2002. The majority of outbreaks occurred in summer and autumn (Figure 18). There was a peak in December relating to pre-Christmas functions, which was also observed in 2001.

Figure 18. Outbreaks of foodborne disease, Australia, 2001 to 2002

Figure 18. Outbreaks of foodborne disease, Australia, 2001 to 2002

Table 6. Outbreaks of foodborne disease in Australia, 2002, by OzFoodNet site

State
Number of outbreaks Number affected Hospitalised Deaths Mean number of cases per outbreak
Hunter
17
143
8
0
8.4
New South Wales
23
404
21
0
17.6
Queensland
18
205
18
1
11.4
South Australia
4
113
22
1
28.3
Tasmania
1
5
3
0
5.0
Victoria
26
859
29
0
33.0
Western Australia
3
90
2
0
45.0
Total
92
1,819
103
2
20.0


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Aetiological agents
The most common agent responsible for foodborne disease outbreaks was Salmonella, which was responsible for 28 per cent (26/92) of outbreaks (Table 7). These outbreaks affected a total of 543 persons with a hospitalisation rate of 13 per cent (68/543). S. Typhimurium was responsible for 81 per cent (21/26) of Salmonella outbreaks. Two fatalities were reported from two separate outbreaks of S. Typhimurium. There was only one outbreak of campylobacteriosis which affected 24 persons, and one small outbreak of Vibrio parahaemolyticus.

Table 7. Aetiological agents responsible for foodborne disease outbreaks showing number of outbreaks and numbers of persons affected, Australia, 2002

Agent category
Number of outbreaks Number affected Hospitalised Deaths
S. Typhimurium
21
471
61
2
C. perfringens
8
155
1
0
Norovirus
8
378
3
0
Salmonella other
5
72
7
0
Ciguatera
4
14
7
0
S. aureus
2
15
1
0
B. cereus
1
37
0
0
Campylobacter
1
24
6
0
Hepatitis A
1
8
0
0
Mixed toxins
1
272
13
0
Suspected wax esters
1
10
0
0
V. parahaemolyticus
1
2
0
0
Unknown
38
361
4
0
Total
92
1,819
103
2


There were 16 outbreaks of toxin related illness during 2002. The most common was due to Clostridium perfringens (8 outbreaks). There were four outbreaks due to ciguatera fish poisoning, all of which were small (median of 3 persons). Ciguatera fish poisoning had the highest hospitalisation rate of 50 per cent (7/14). There were three outbreaks due to Staphylococcus aureus, one of which was a large outbreak in which Bacillus cereus was also identified. B. cereus was responsible for two outbreaks both involving rice meals.

There were nine outbreaks of known viral aetiology, eight of which were due to norovirus. These outbreaks of norovirus affected 378 persons, but only 0.8 per cent (3/378) were hospitalised. The other outbreak of viral illness was due to hepatitis A and affected eight persons.

There was one outbreak of gastroenteritis suspected to be due to wax esters from escolar or oilfish marketed under the name of rudderfish. Thirty-eight (41%) outbreaks were of unknown aetiology; these affected 361 persons and four cases were hospitalised.

Food vehicles
There was a wide variety of foods implicated in outbreaks of foodborne disease during 2002 (Table 8), although investigators could not identify a source for 34 per cent (31/92) of outbreaks. Fish, poultry and mixed foods were implicated in six outbreaks each. There were six outbreaks associated with red meat and a further six outbreaks associated with seafood. Five outbreaks were associated with eggs. There were two outbreaks associated with Vietnamese pork/beef rolls and two associated with kebabs.

Outbreaks involving cream filled cakes, egg dishes and fish had hospitalisation rates of 20 per cent or higher. Two outbreaks of salmonellosis, one associated with cream cakes and the other with a raw egg dish, resulted in two fatalities.

Table 8. Categories of food vehicles implicated in foodborne disease outbreaks, Australia, 2002

Vehicle category
Number of outbreaks Number affected Hospitalised Deaths
Fish
6
26
7
0
Mixed foods
6
345
22
0
Poultry
6
57
8
0
Red meat/meat products
5
101
0
0
Dessert
4
71
2
0
Cream filled cake
3
61
12
1
Pizza
3
17
0
0
Rice dishes
3
46
1
0
Seafood
3
68
2
0
Suspected egg dishes
3
27
2
1
Suspected seafood
3
12
0
0
Egg dishes
2
23
8
0
Salad dishes
2
99
15
0
Sauces
2
38
0
0
Soup
2
23
0
0
Kebabs
2
49
5
0
Vietnamese rolls
2
52
8
0
Asian foods
1
12
1
0
Bean dish
1
132
1
0
Sandwiches
1
12
0
0
Suspected red meat/meat products
1
4
0
0
Unknown
31
544
9
0
Total
92
1,819
103
2


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Outbreak settings
The most common setting for the occurrence of outbreaks was at restaurants (43%), followed by the home (13%), takeaway venues (11%), and events catered for by professional companies (8%) (Table 9). There were two outbreaks in community settings. Five outbreaks were due to foods purchased from bakeries, two of which were Asian bakeries. There were four small outbreaks (median size: 5 persons) associated with national franchised fast food outlets. There were two outbreaks each at schools, childcare centres, cruises and community fairs.

Table 9. Categories of settings for foodborne disease outbreaks, Australia, 2002

Setting category
Number of outbreaks Number affected Hospitalised Deaths
Restaurant
40
736
23
0
Home
12
120
23
0
Takeaway
8
66
5
0
Commercial caterer
7
154
4
0
Bakery
5
113
20
1
Aged care facility
4
68
4
1
National franchised fast food
4
20
0
0
Fair/festival/mobile service
2
278
14
0
Child care
2
19
1
0
Community
2
29
6
0
Cruise/airline
2
21
1
0
School
2
180
2
0
Hospital
1
13
0
0
Institution
1
2
0
0
Total
92
1,819
103
2


Investigative methods and levels of evidence
States and territories investigated 28 outbreaks using retrospective cohort studies and nine outbreaks using case control studies. Fifty per cent (14/28) of outbreak investigations using cohort studies were of unknown aetiology. Twenty-one per cent (6/28) of investigations using cohort studies were Salmonella outbreaks. Fifty per cent of C. perfringens outbreak investigations used cohort studies. Sixty-seven per cent (6/9) of outbreak investigations using case control studies were due to Salmonella. The remaining 55 outbreaks relied on descriptive information to attribute a foodborne cause or identify a food vehicle.

To attribute the cause of the outbreak to a specific food vehicle, investigators obtained analytical evidence from epidemiological studies for 12 outbreaks. Microbiological evidence of contaminated food was found in eight outbreaks, with a further eight outbreaks investigations obtaining both microbiological and analytical evidence. Investigators obtained analytical and/or microbiological evidence for 52 per cent (14/27) of Salmonella outbreaks. Seventy-two per cent (66/92) of outbreaks relied on descriptive evidence to implicate a food or foodborne transmission.

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Significant outbreaks
Six outbreaks affected 50 persons or more in 2002. Two were due to norovirus, two due to bacterial toxins, and two due to Salmonella Typhimurium. Four of these outbreaks occurred at restaurants, one at a school and one at a community festival. A variety of foods were implicated in these outbreaks, including: a bean dish, Caesar salad, seafood salad, lamb curry and a mixed meal of rice and meats.

The outbreak associated with the Caesar salad was due to S. Typhimurium 8, and occurred in South Australia. Seventy-eight cases were associated with this outbreak and 15 persons were hospitalised. Fifty-eight per cent (45/78) of cases were laboratory confirmed as S. Typhimurium 8. Several salad ingredients tested positive for S. Typhimurium 8 including the dressing, anchovies and parmesan cheese, with a very high organism count detected in the salad dressing (830,000 per gram). A meal of lamb, rice and potatoes contaminated with S. aureus and B. cereus caused an outbreak of gastrointestinal illness at a religious festival. Approximately 45 per cent of 600 persons attending the event became violently ill after eating food that was prepared with inadequate facilities for cold storage and preparation.

There were 20 outbreaks affecting between 20 and 50 persons. Cakes were implicated in four of these, two of which were caused by Salmonella. In one outbreak of S. Typhimurium 99 in South Australia, the bakery used the same piping bag to dispense both sausage meat, and cream for cakes. Two outbreaks were due to Vietnamese rolls containing pork and/or beef contaminated by S. Typhimurium 135 and S. Typhimurium 126.

Queensland reported an outbreak of Campylobacter infections from northern Queensland in August 2002. The public health unit, in conjunction with the Queensland site, interviewed 24 cases who identified chicken as a likely source and no other common exposures. The public health unit investigated a local poultry abattoir that was the main supplier of chickens for the region. Investigators collected samples of raw fresh chicken from the abattoir and from retail outlets representing three different chicken producers in Queensland. Sixty-seven per cent (29/43) of raw chicken samples were positive for the presence of Campylobacter. A specific Campylobacter subtype (Fla type 7) was the predominant subtype among human cases in northern Queensland and in chicken from two Queensland poultry manufacturers. PFGE typing of Fla type 7 isolates found that strains from human cases (Fla type 7; PFGE type P1) were indistinguishable from those obtained from the local abattoir. Fla type 7 Campylobacter isolates obtained from the other southern Queensland chicken manufacturers were distinct from these isolates by PFGE typing.

During February, the Hunter site investigated an outbreak of C. perfringens intoxication affecting 33 persons following a spit roast meal. The company had transported the meats to Newcastle from Sydney without proper temperature controls. At a national surveillance teleconference, it was reported that this outbreak was similar to four others in the Australian Capital Territory prior to Christmas. After investigation, it was identified that the same company supplied all five meals. All Australian jurisdictions reviewed their records to identify other similar incidents. The survey identified that the company had caused a total of 12 separate outbreaks affecting 332 persons in four jurisdictions in the previous five years.

There were two outbreaks associated with imported foods that could have international implications. One outbreak of S. Montevideo in the Hunter affected 47 persons and was linked to a local takeaway kebab shop. A further six associated cases were notified in 2003, which are not included in the outbreak total reported here. The investigation found several products in the kebab shop positive for S. Montevideo including tahini and hommus. Unopened jars of tahini originating from Egypt subsequently tested positive for S. Montevideo and S. Tennessee. This outbreak resulted in nationwide consumer and trade recalls, and an international alert to electronic list servers. Despite the potential for wider spread, New South Wales was the only site to report infections, although there were three cases in interstate visitors. There were no human infections reported overseas.

The other outbreak with potential for international spread occurred in Western Australia in August 2002. Delegates of a mining conference in Kalgoorlie became ill after consuming 'oyster shooters' served at a cocktail party. Over 1,000 persons attended the conference and the attack rate from a cohort study of 700 participants was 23 per cent. The oyster shooters were prepared using bulk oyster meat imported from Japan, and tomato juice. The label on the packet of oysters clearly stated, 'cook before consumption'. Norovirus was suspected as the cause of illness, although no virus was detected in faeces, or in a different batch of the same brand of oysters. There were three outbreaks of confirmed norovirus associated with Korean imported bulk oyster meat in New Zealand at the same time (Gail Greening, Institute of Environmental Science and Research, New Zealand, personal communication, April 2002).

Animal-to-person outbreaks

Sites reported three outbreaks that were transmitted from animal-to-person during 2002. Two of these were Salmonella outbreaks associated with poultry hatching programs in childcare centres. One was an outbreak of S. Agona affecting seven children in the Hunter region associated with ducklings. The other was an outbreak of S. Typhimurium 170 affecting six children in Queensland following hatching of chickens. A trace-back investigation in Queensland identified S. Typhimurium 170 and S. Typhimurium 12 in environmental samples from two poultry breeder sheds operated by the hatchery, which supplied eggs for the hatching program.

The other outbreak of animal-to-person gastroenteritis was due to shiga toxin producing E. coli in South Australia. Six persons were affected after either visiting or having contact with persons visiting a petting zoo located at a regional fair. The predominant E. coli serotype was O26, although some later cases were non-O26. Investigation of the petting zoo revealed a pig with same multiplex polymerase chain pattern for STEC which was negative for E. coli O26.

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Cluster investigations

A cluster is defined as an increase in infections that are epidemiologically related in time, place or person where investigators are unable to implicate a vehicle or determine a mode of transmission for the increase. 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 report, there are a small number of point source outbreaks where the mode of transmission is indeterminate that have been classified as a cluster.

During 2002, states and territories conducted 100 cluster investigations, including three multi-state investigations. These clusters affected 1,751 persons with 65 cases hospitalised and one death. Forty-five per cent (45/100) of these investigations related to clusters of Salmonella. Salmonella clusters affected 601 persons with 53 cases hospitalised and one death. S. Typhimurium was responsible for 38 per cent (17/45) of cluster investigations. Of the remaining 28 investigations, there were 25 other different Salmonella serovars involved. Fifty-three per cent (53/100) of cluster investigations were of unknown aetiology.

There was one investigation of norovirus in a restaurant where the mode of transmission was unable to be determined. The Northern Territory reported a cluster of Cryptosporidium infections in the first six months of 2002. This community-wide increase was linked to infections acquired in a childcare centre and a local pool.

The first multi-state cluster investigation occurred in January 2002 and was related to S. Typhimurium 170.16 Queensland, New South Wales and Victoria jointly investigated cases to generate hypotheses. Many cases were interviewed, although the source of infections was not identified.

The other two cluster investigations in November 2002 were of S. Kottbus and S. Potsdam. States and territories investigated less than 20 cases of S. Kottbus. The S. Kottbus cluster was spread across Australia and no common exposure was identified. The S. Potsdam cluster investigation involved New South Wales, the Australian Capital Territory, Victoria, South Australia and Tasmania. Thirty-four per cent of S. Potsdam cases were New South Wales residents, although the rate in Tasmania (3.2 cases per 100,000 population) was tenfold higher than any other jurisdiction (Figure 19).

Figure 19. Cases of Salmonella Potsdam, Australia, November to December 2002, by date of onset

Figure 19. Cases of Salmonella Potsdam, Australia, November to December 2002, by date of onset

Sites interviewed 50 cases of S. Potsdam using hypothesis-generating questionnaires. Reliable food histories were available for 25 of these cases. The most commonly consumed foods in the three days prior to illness were fresh tomatoes (68%) and chicken (68%). Fifty-two per cent of cases ate tomatoes on the day before onset of illness. Investigators suspected that the source of infection was a type of fresh salad produce, although comparison with food histories from population-based controls indicated that it would be difficult to show this epidemiologically.

Collecting reliable food histories during the Christmas period complicated epidemiological investigations. Food safety agencies were involved in a complicated traceback investigation for produce and other foods. Despite these intensive efforts, no source of infection for the outbreak was identified.

The true number of clusters investigated is difficult to determine, as the figures do not include all cluster investigations conducted in Public Health Units or local government areas. Jurisdictions have different definitions of 'cluster' and triggers for investigating clusters to fit with staff resources and local priorities.


This article was published in Communicable Diseases Intelligence Volume 27, No 2, June 2003.

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