Food Safety Scheme Risk Assessment

Food Safety Risk
Assessment of NSW
Food Safety Schemes
March 2009
NSW/FA/FI039/0903
Food Safety Risk Assessment
of New South Wales
Food Safety Schemes
Table of contents
Executive summary .........................................................................................................6
Introduction ................................................................................................................. 12
Dairy food safety scheme............................................................................................... 16
Meat food safety scheme ............................................................................................... 39
Plant products food safety scheme ................................................................................. 70
Seafood safety scheme.................................................................................................. 87
Vulnerable persons food safety scheme......................................................................... 109
Egg food safety scheme (draft) .................................................................................... 126
Risk Assessment - Conclusion....................................................................................... 144
Appendix 1: Microbiological and chemical hazards of concern.......................................... 145
Appendix 2: Australian food recalls (2004 to 2008) ........................................................ 179
Appendix 3: Australian foodborne illness outbreaks (1995-2008) ..................................... 184
Food Safety Scheme Risk Assessment Page 1 of 214

Table of tables
Dairy food safety scheme
Table 1 –
Pathogenic microorganisms detected in raw milk............................................... 17
Table 2 –
Microbiological hazards in dairy products .......................................................... 18
Table 3 –
Consumption of dairy products ........................................................................ 21
Table 4 –
Summary of foodborne illness outbreaks attributed to dairy products and foods
including dairy as an ingredient...................................................................... 23
Table 5 – NZFSA risk profile outcomes examining hazards in dairy products ....................... 28
Table 6 – Risk ranking for dairy products contaminated with Listeria monocytogenes .......... 30
Table 7 – Risk ranking of dairy products.......................................................................... 31
Meat food safety scheme

Table 8 – Microbiological hazards in livestock and poultry ................................................. 41
Table 9 – Consumption of meat and meat products in Australia ........................................ 45
Table 10 – Consumption of processed meats in Australia .................................................. 45
Table 11 – Summary of foodborne illness outbreaks attributed to all meat (including poultry,
game meat and processed meat products)...................................................... 46
Table 12 – Prevalence of microbiological hazards in Australian beef and sheep meat........... 48
Table 13 – Prevalence of microbiological hazards on chicken meat in NSW......................... 50
Table 14 – Foodborne illness outbreaks of listeriosis from processed meats........................ 52
Table 15 – Prevalence of Listeria monocytogenes in processed meats................................ 53
Table 16 – NZFSA risk profile outcomes examining hazards in meat................................... 55
Table 17 – Risk ranking for meat and meat products........................................................ 56
Table 18 – Risk ranking for processed poultry meat products ............................................ 58
Table 19 – NZFSA risk profile outcomes examining hazards in poultry meat ....................... 58
Table 20 – NZFSA risk profile outcomes examining hazards in processed meats.................. 61
Table 21 – Risk ranking for processed meat products ....................................................... 62
Table 22 – Risk ranking for L. monocytogenes-contaminated processed meats ................... 64
Plant products food safety scheme

Table 23 – Microbiological hazards associated with plant products..................................... 70
Table 24 – Consumption of fruits and vegetables in Australia ............................................ 74
Table 25 – Summary of foodborne illness outbreaks attributed to plant products ................ 77
Table 26 – Risk ranking for plant products contaminated with Listeria monocytogenes ........ 81
Seafood safety scheme

Table 27 – Hazards in seafood and seafood products ....................................................... 87
Table 28 – Summary of international hazard identification studies for seafood.................... 89
Table 29 – Production volumes for seafood in Australia and NSW 2006/07 ......................... 91
Table 30 – Consumption of fish and seafood products in Australia ..................................... 92
Table 31 – Failure rate for imported seafood products (1998 – 2003) ................................ 93
Table 32 – Summary of Australian seafood testing results ................................................ 94
Table 33 – Summary of high mercury levels in NSW seafood ............................................ 95
Table 34 – Prevalence of L. monocytogenes in UK retail smoked fish ................................. 95
Table 35 – Summary of foodborne illness outbreaks attributed to seafood ......................... 96
Table 36 – Risk ranking for seafood products contaminated with Listeria monocytogenes .. 103
Table 37 – Seafood consumption required to reach reference doses for methylmercury..... 105

Vulnerable persons food safety scheme
Table 38 – Summary of foodborne illness outbreaks attributed to food served to vulnerable
persons...................................................................................................... 115
Table 39 – Institutional foodborne illness outbreaks as a percentage of all outbreaks........ 115
Table 40 – Relative susceptibility to listeriosis for different sub-groups............................. 118
Table 41 – Estimated cases of listeriosis for vulnerable population sub-groups for each food
category .................................................................................................... 119
Egg food safety scheme

Table 42 – Hazards in the production of shell eggs and egg products .............................. 127
Table 43 – Prevalence of chemical residues in eggs........................................................ 129
Table 44 – Consumption of eggs and egg products in Australia ....................................... 132
Table 45 – Summary of foodborne illness outbreaks attributed to eggs ............................ 133
Table 46 – Prevalence of Salmonella in Australian eggs .................................................. 133
Table 47 – Risk ranking for type and use of eggs ........................................................... 136
Appendix 1
Table 48 – Top Salmonella serovars from major sources................................................. 147
Table 49 – Characteristics of Salmonella........................................................................ 149
Table 50 – Characteristics of Campylobacter .................................................................. 151
Table 51 – Characteristics of Staphylococcus aureus ...................................................... 153
Table 52 – Characteristics of Clostridium perfringens ...................................................... 155
Table 53 – Characteristics of Bacillus cereus .................................................................. 156
Table 54 – Characteristics of Listeria monocytogenes ..................................................... 159
Table 55 – Characteristics of Vibrio parahaemolyticus ..................................................... 162
Table 56 – Characteristics of Shigella spp. ..................................................................... 163
Table 57 – Characteristics of pathogenic Escherichia coli ................................................ 165
Table 58 – Characteristics of Clostridium botulinum........................................................ 167
Table 59 – Characteristics of Yersinia enterocolitica ........................................................ 168
Table 60 – Important Aspergillus, Fusarium and Penicillium species and their mycotoxins.. 175
Appendix 2
Table 61 – Recalls of dairy products between 2004 and 2008.......................................... 179
Table 62 – Recalls of meat products between 2004 and 2008 ......................................... 181
Table 63 – Recalls of plant products between 2004 and 2008 ......................................... 183
Table 64 – Recalls of seafood products between 2004 and 2008 ..................................... 183
Appendix 3
Table 65 – Foodborne illness outbreaks attributed to milk, dairy products and dairy
products used as an ingredient .................................................................... 185
Table 66 – Foodborne illness outbreaks attributed to meat, meat products and meat products
used as an ingredient.................................................................................. 187
Table 67 – Foodborne illness outbreaks attributed to plant products ................................ 196
Table 68 – Foodborne illness outbreaks attributed fish and seafood products ................... 198
Table 69 – Foodborne illness outbreaks attributed to foods served to vulnerable persons .. 207
Table 70 – Foodborne illness outbreaks attributed to eggs, egg products and eggs used as an
ingredient .................................................................................................. 210

Abbreviations
aw Water activity
ABARE Australian Bureau of Agricultural and Resource Economics
ABS Australian Bureau of Statistics
ACMF Australian Chicken Meat Federation
ACMSF Advisory Committee on the Microbiological Safety of Food (UK)
AECL Australian Egg Corporation Limited
ANZDAC Australia New Zealand Dairy Authorities Committee (formerly
ADASC)
AMRA Australian Milk Residue Analysis Survey
APL Australian Pork Limited
APVMA Australian Pesticide and Veterinary Medicines Authority
ASP Amnesic Shellfish Poisoning
ASQAP Australian Shellfish Quality Assurance Program
ATDS Australian Total Diet Survey/Study
APVMA Australian Pesticides and Veterinary Medicines Authority
AQIS Australian Quarantine and Inspection Service
BSE Bovine Spongiform Encephalopathy
BTEC Brucellosis and Tuberculosis Eradication Campaign
CAC Codex Alimentarius Commission
cfu Colony forming unit
CFR Code of Federal Regulation (US)
CJD Creutzfeldt-Jakob Disease
DAFF Department of Agriculture Fisheries and Forestry (Australian
Government) (formerly AFFA)
DFSV Dairy Food Safety Victoria
DSP Diarrhoetic Shellfish Poisoning
EFSA European Food Safety Agency
EHEC Enterohaemorrhagic E. coli
ERL Extraneous Residue Limit
EU European Union
FAO Food and Agricultural Organization of the United Nations
FDA Food and Drug Administration (US)
FRDC Fisheries Research and Development Corporation
FRSC Food Regulation Standing Committee
FSA Food Science Australia
FSAI Food Safety Authority of Ireland
FSANZ Food Standards Australia New Zealand (formerly ANZFA)
FSIS Food Safety and Inspection Service (US)
GAP Good Agricultural Practices
GBR Geographical BSE Risk
GHP Good Hygienic Practices
GMP Good Manufacturing Practices
HACCP Hazard Analysis Critical Control Point
HAV Hepatitis A virus
HTST High Temperature Short Time pasteurisation
HUS Haemolytic Uremic Syndrome
ICMSF International Commission on Microbiological Specifications for Foods
JECFA Joint FAO/WHO Expert Committee on Food Additives
KP Kanagawa phenomenon
MAP Modified atmosphere packaging
MeHg Methylmercury
ML Maximum Level
MLA Meat & Livestock Australia

MMWR Morbidity and Mortality Weekly Report
MRL Maximum Residue Limit
NARM National Antibacterial Residue Minimisation program
NEPSS National Enteric Pathogen Surveillance Scheme
NGSP National Granuloma Submission Program
NRS National Residue Survey
NZFSA New Zealand Food Safety Authority
OC Organochlorine
OP Organophosphate
PHLS Public Health Laboratory Service, UK
PIRSA Primary Industries and Resources South Australia
PISC Primary Industries Standing Committee
PSP Paralytic Shellfish Poisoning
PTWI Provisional Tolerable Weekly Intake
REPFEDS Refrigerated processed foods of extended durability
RIRDC Rural Industries Research and Development Corporation
RIS Regulatory Impact Statement
RTE Ready-to-eat
SARDI South Australian Research and Development Institute
SSOP Sanitation Standard Operating Procedures
STEC Shiga toxigenic E. coli
SWG Sector Working Groups
TFAP Tuberculosis freedom assurance program
TVC Total Viable Count
UCFM Uncooked comminuted fermented meats
UHT Ultra Heat Treated
USDA US Department of Agriculture
WHO World Health Organization
YMT Yolk Mean Time

Executive summary
The NSW Food Regulation 2004 contains food safety schemes that outline the
regulatory requirements for dairy, meat, plant products, seafood businesses and
businesses serving food to vulnerable persons in NSW. A draft egg food safety
scheme is currently being finalised for inclusion in the Regulation.
The regulatory requirements in the food safety schemes have been introduced over a
number of years, either by the NSW Food Authority or its predecessor organisation
SafeFood Production NSW. Dairy and meat food safety schemes were carried over
from previous legislation. Individual risk assessments were carried out prior to the
introduction of both the seafood and plant products food safety schemes. The
development of the vulnerable persons food safety scheme occurred following the
introduction of Standard 3.3.1 - Food Safety Programs for Food Service to Vulnerable
Populations of the Australia New Zealand Food Standards Code. In respect to the
egg food safety scheme, the NSW Food Authority conducted a risk assessment prior
to developing requirements for the scheme.
Within each sector covered by the food safety schemes there are a wide variety of
hazards that may potentially be present and cause illness in the consumer. The
degree of illnesses caused by these hazards can range from mild illness through to
severe and life threatening disease. In general, it is the microbiological hazards
associated with foods that are considered more significant, as chemical and physical
hazards are rarely detected in food.
This risk assessment document summarises the known information from previous
risk assessments, risk profiles and hazard assessments, and includes new or updated
information where it is available and applicable to food businesses in NSW.

In 2006/2007 there were 684 million litres of milk sold in NSW and ACT, with the
average person consuming in excess of 100 L of pasteurised milk each year.
A wide variety of bacteria may be present in raw milk with the microbial status of
milk being influenced by animal health, the farm environment and production
methods. Pasteurisation was successfully introduced to eliminate tuberculosis and
brucellosis from milk and nowadays the main microbiological hazards associated with
milk and dairy products include Salmonella, Listeria monocytogenes, pathogenic
Escherichia coli, Staphylococcus aureus, Campylobacter spp., Yersinia enterocolitica
and Enterobacter sakazakii.
Between 1995 and 2008 there were 14 Australian outbreaks attributed to dairy
products, none occurring in NSW. Nine of these outbreaks were associated with
consumption of unpasteurised milk. Internationally foodborne outbreaks associated
with dairy products have been attributed to the use of unpasteurised milk,
contaminated non-dairy ingredients, faulty pasteurisation process and poor hygiene.
Controlling the safety of milk and dairy products relies on using raw materials (milk
and non-dairy ingredients) of good quality, ensuring correct formulation, effective

processing, prevention of recontamination and maintenance of temperature
throughout the cold chain. Dairy products identified as high risk include
unpasteurised milk, soft cheese, dairy desserts, fresh cheeses and dairy dips, as
these products may support the growth of pathogenic microorganisms.
Two critical steps in controlling pathogens in milk and dairy products are effective
pasteurisation, followed by good manufacturing practices to ensure post-
pasteurisation contamination does not occur. Food safety programs targeting these
controls have been an effective mechanism for controlling microbial hazards in milk
and dairy products.
There are several potential sources of chemical contamination associated with milk
production including agricultural and veterinary chemicals, environmental
contaminants and chemicals from animal feed. The implementation of on-farm food
safety programs has managed these risks, and the risk is considered low as surveys
of dairy products have not detected significant levels of chemicals in Australian milk
and dairy products.

It has been estimated that Australians each consume 38.2 kg beef and veal, 11.4 kg
lamb, 2.7 kg mutton and 14.4 kg bacon and ham products each year. Various
microbiological hazards are associated with different types of meats, with
Salmonella, pathogenic E. coli, Clostridium perfringens, Campylobacter jejuni and the
parasite Toxoplasma gondii associated with beef and sheepmeat, while the primary
pathogen of concern in pigmeat is Yersinia enterocolitica.
Livestock and poultry can serve as a reservoir for pathogenic microorganisms and
within the abattoir environment these pathogens can be transferred from the gut to
the external surfaces of the carcase and contaminate equipment and workers.
Currently the risk associated with red meat is considered low, due to the control
measures implemented by the meat industry, such as the Australian Standards for
the hygienic production of meat and game meat. However, cross-contamination of
raw meat with ready-to-eat (RTE) foods is considered a potential issue of concern. It
has been estimated that if the cross-contamination rate of Salmonella increased from
1% to 10% there would be an extra 5000 cases of foodborne illness, while an
increase to 50% would result in more than 29,000 cases of salmonellosis across
Australia each year.
Poultry is the most widely consumed meat in Australia, with each person consuming
39.5kg of poultry each year. The primary hazards of concern in poultry meat are
Salmonella and Campylobacter spp. Contamination of poultry can occur on farm
through breeding stock, contaminated water, litter, insects, rodents, wild birds and
farm workers. Surveys have identified poultry meat as a significant source of
foodborne illness, with 46 confirmed outbreaks and 1170 cases of illness between
1995 and 2002. Due to significant under-reporting, it is estimated that cases of
foodborne illness due to processed chicken products may be as high as 79,000 cases
per year. A through chain approach is the preferred option to reduce contamination
of poultry meat, with estimates that this could reduce levels of poultry-related
foodborne illnesses by between 74% and 93% each year.

Processed meat products have also been identified as high risk, with the pathogens
of concern including pathogenic E. coli, Salmonella and L. monocytogenes. There
have been a large number of recalls of processed meats due to L. monocytogenes,
and a significant number of foodborne illness outbreaks. Between 1991 and 2000,
323 cases of illness and one death were attributed to consumption of processed
meats with a total cost to the community estimated to be $77 million.
Controlling pathogens in processed meats include effective cooking, curing or
fermentation with starter culture, and implementation of good hygienic practices
(GHP) to limit the potential for post-processing contamination with
L. monocytogenes. Food safety programs have been widely implemented in the
processed meat sector to ensure control measures are in place. However, it was
estimated that if these programs are not complied with, and poorly controlled or
unreliable processing was allowed to occur in the production of uncooked
comminuted fermented meats, this could lead to a significant increase in risk, with
estimates the number of foodborne illness cases in Australia due to pathogenic
E. coli could be up to 604 cases per year.
Plant products food safety scheme

Previous risk assessment work conducted on the risk associated with plant products
found that fresh cut fruit and vegetables, seed spouts, vegetables in oil and
unpasteurised juice present a high risk. This was due to a history of foodborne illness
outbreaks in Australia, mainly due to Salmonella, in addition to a number of
outbreaks overseas. Annual NSW consumption of these products has been estimated
as being 11,000 tonnes of fresh cut vegetables, 150 tonnes of fresh cut fruits, 2,600
tonnes of seed sprouts, 1000 tonnes of vegetables in oil products, and 100,000 L of
unpasteurised juice.
Surveys of plant products have shown the potential for these high risk plant products
to be contaminated with L. monocytogenes, Aeromonas spp., B. cereus and
Salmonella.
Contamination of fresh cut fruit and vegetables can occur during growth, harvest or
processing with the main pathogens of concern being L. monocytogenes and
C. botulinum in modified atmosphere packaged product. These products are
considered high risk when they are consumed raw.
Seed sprouts can become contaminated with B. cereus, Salmonella and pathogenic
E. coli during growth and harvest of the seeds and also during the sprouting process,
which provides a near perfect environment for the growth of microorganisms.
The oxygen reduced environment provided by vegetables immersed in oil allows for
the growth of anaerobic microorganisms including C. botulinum, the cause of
botulism. To reduce the risk, the vegetables or fruits are usually cooked and acidified
prior to placement in oil.
Unpasteurised fruit juices may become contaminated during the juicing process,
either due to contamination on the exterior of the fruit or the use of damaged and
mouldy fruit. Because the juice is not heat treated, any pathogenic microorganisms
present are able to survive, and acid tolerant strains of pathogenic E. coli and
Salmonella may grow.

Annual consumption of seafood has been estimated at approximately 15.1 kg per
person. The hazards associated with seafood vary depending on the type of seafood
and processing methods employed.
Shellfish, particularly oysters, as filter feeders can accumulate contaminants from the
growing environment. The hazards of concern for shellfish include pathogenic
bacteria and viruses, algal toxins and chemical contaminant from the growing
environment. Viral contamination of shellfish is recognised as the highest risk for all
seafood and is effectively managed by the implementation of shellfish safety
programs that manage the waterway and harvesting of the shellfish. Algal toxins in
shellfish are generally considered low risk where harvest management programs
manage the risk. Where no programs are in place, the risk associated with algal
toxins increases to medium. Severe illness has been associated with the consumption
of oysters contaminated with V. vulnificus.
Wild caught prawns particularly those caught in estuarine waters are susceptible to
contamination from the environment, such as naturally occurring Vibrio spp. present
in the waterway. Prawns treated with metabisulphite may present a problem to
consumers who suffer from asthma-related conditions. The on-board cooking and
cooling of prawns also has the potential to introduce bacterial contamination when
water from the waterway is used to cool the prawns.
Hazards associated with wild caught finfish include ciguatera and histamine,
depending on the type of fish caught. Ciguatera poisoning is generally regarded as
medium risk, with most illnesses occurring with fish caught near tropical reefs.
Histamine poisoning is usually associated with certain fish such as tuna, swordfish,
mahi mahi and blue grenadier and can be controlled by effective temperature control
through out the supply chain. If the fish are to be consumed raw, hazards such as
parasites and Vibrio spp. become significant. Mercury in finfish presents a risk to
pregnant women or women planning to become pregnant. Because mercury is
naturally present in the marine environment, management strategies have relied on
education of the consumer, in particular advising pregnant women to avoid
consuming large predatory fish which are known to contain higher levels of mercury.
Processed, ready-to-eat (RTE) seafood products (including smoked seafood) can
support the growth of L. monocytogenes, however contamination is thought to occur
during the handling and packaging of the finished product. Strict hygiene and
sanitation programs can reduce the likelihood of contamination. The packaging of
smoked seafood under modified atmosphere packaging may allow the growth of
C. botulinum. While botulism poisoning associated these products is rare, the illness
is severe and is considered a medium risk.
Vulnerable persons food safety scheme

Certain population sub-groups are more at risk of foodborne illness or can develop
more severe conditions due to foodborne illness when compared to the general
population. The degree of vulnerability depends on the susceptibility of the individual
and the pathogenicity of the pathogenic microorganism. In general terms, the

vulnerable population group includes children under five years of age, people over 65
years old, pregnant women and persons with depressed immunity.
It is estimated that the number of meals served to vulnerable persons in NSW
facilities such as hospitals, aged-care facilities, hospices, day care establishments and
childcare centres is approximately 133 million meals per year. It is estimated that up
to one million meals per year served at these facilities may be contaminated with a
foodborne pathogen.
Since 1995 there have been 65 foodborne illness outbreaks in Australian aged-care
facilities, childcare centres and hospitals with 758 illnesses and 75 fatalities. The
pathogens implicated have included Salmonella, C. perfringens, L. monocytogenes
and Campylobacter. The prevalence of foodborne-related illness and deaths in the
elderly living in nursing homes is far greater than the baseline level of illness in
general population, while children appear more at risk to Salmonella due high
salmonellosis rate in children seen both in Australia and overseas.
The major hazard of concern to vulnerable persons is L. monocytogenes, with some
sub-groups within the vulnerable population being 100 times more susceptible to
listeriosis than the general population. Other hazards of concern include infants
exposed to C. botulinum through consumption of contaminated honey, neonatal
infants consuming E. sakazakii contaminated infant formula and individuals with liver
dysfunction exposed to Vibrio vulnificus via raw oysters. Other organisms that may
result in more severe illness in vulnerable sub-groups include pathogenic E. coli,
S. aureus and C. perfringens.
When assessing the risk associated with foods, it is important to consider food
preparation and hazardous scenarios. Businesses catering to vulnerable persons
need to consider the susceptibility of their consumers when designing menus and
sourcing, preparing and serving foods. Under the Food Standards Code, these
establishments are required to implement a food safety program including,
substitution of high risk foods with lower alternatives; effective cleaning and
sanitation of fruits and vegetables to be consumed raw; limiting the storage of
reconstituted infant formula; minimising storage times/temperatures for RTE foods;
ensuring foods are cooked properly and effective cleaning and sanitation of
equipment.
Egg food safety scheme (draft)

The average Australian consumes approximately 137 eggs per year, equating to over
800 million eggs being consumed in NSW each year. The primary hazard of concern
is Salmonella, in particular Salmonella Typhimurium which may contaminate the egg
shell through environmental contamination and through contact with bird faeces.
Overseas foodborne illness outbreaks attributed to eggs have been predominantly
due to Salmonella Enteritidis, however Australia layer flocks remain free of
Salmonella Enteritidis.
While Salmonella may be present in the farm environment, surveys have found the
prevalence of Salmonella on shell eggs to be very low. However, eggs and egg
products can also become contaminated during the grading and processing due to
improper crack detection, incorrect washing of eggs and poor hygiene and sanitation
during the processing of eggs into pulp and other products. Although egg products

such as liquid pulp are pasteurised, the heat treatment is only mild and therefore it is
important to limit the level of microbiological contamination.
There is significant epidemiological evidence to suggest that a major contributing
factor of salmonellosis in Australia is the use of dirty and cracked eggs, especially in
products that receive minimal or no cook step. The Food Standards Code limits the
sale of cracked eggs to businesses where the egg will be further processed and
receive a heat treatment.
Depending on the hygienic practices on farm and proper grading, processing and
storage of eggs, the potential number of egg-related illnesses was estimated up to
1800 cases per year across Australia. Current industry practices to address these
issues include strict biosecurity on farm, implementation of quality assurance
systems during grading and processing and effective supply chain management.
Potential sources of chemical contamination of eggs on farm include contaminated
soil, insecticide spray, incorrect use of medication and inappropriate egg washing
solutions and concentrations. However, in general, only low levels of chemicals have
been detected in eggs and previous risk assessment has assessed the risk of
chemicals in eggs as low. The exception to this are specialty eggs such as Balut,
salted and century eggs, where surveys have detected the unauthorised use of lead
as an additive, leading to chemical contamination of some products. These products
may also become contaminated with pathogens due to the extensive handling during
processing.
Conclusion
This review has illustrated that across the food safety schemes there are many
potential hazards that can impact on human health with microbiological hazards
considered the most significant. It concludes that for food businesses within these
schemes, mitigating food safety risks requires the development and implementation
of reliable, systematic and preventative procedures. Such procedures are the core
elements of food safety programs, introduced either due to regulatory requirements
or through industry sponsored Codes of Practices. The review acknowledges that
mitigating food safety risk necessitates a multi-factorial approach extending beyond
the controls implemented by a food business operating under a food safety scheme.

Introduction
Purpose
Under current legislation, the NSW Food Authority (the Authority) can establish food
safety schemes in respect to different type or classes of foods, food businesses or
food activity (Food Act, 2003). The food safety schemes aims to assist in improving
the safe production and handling food by outlining the regulatory requirements for
the food, food businesses or food activity (or activities) covered by the scheme.
Currently food safety schemes exist for dairy, meat, plant products and seafood
businesses operating in NSW, as well as businesses serving food to vulnerable
persons. In addition to these schemes that have already been implemented, an egg
food safety scheme is currently being finalised.
These commodities have been identified as containing high risk products that may
potentially cause outbreaks of foodborne illness, and where the cost benefit analysis
justified a regulatory presence, and the use of regulatory tools such as the
implementation of food safety programs based on principles of Hazards Analysis
Critical Control Point (HACCP).
Current legislation also requires a risk assessment be undertaken when establishing a
new food safety scheme. The risk assessment provides the science to underpin the
food safety scheme and is required to be based on national or international
standards.
The Authority or its predecessor SafeFood Production NSW, previously commissioned
risk assessment prior to the introduction of food safety schemes relating to seafood
and plant products. In addition, risk assessments were conducted on the proposed
scheme for egg and egg products and during the review of the dairy food safety
scheme. The requirements under the meat food safety scheme were carried over
from a previous legislation which did not require a risk assessment to be conducted
and as such the Authority has not previously conducted a risk assessment in relation
to meat. The vulnerable populations food safety scheme was introduced following
the gazettal of Standard 3.3.1 - Food Safety Programs for Food Service to Vulnerable
Populations of the Australia New Zealand Food Standards Code. Food service to
vulnerable populations were identified as high risk in the National Risk Validation
Project (Food Science Australia and Minter Ellison, 2002)
The purpose of this risk assessment document is to provide a scientific review of
hazards and their associated risks for food businesses covered by the food safety
schemes. This risk assessment summarises the known information from previous risk
assessment and where new or updated information is available, this has been
incorporated into the information.
Scope
This risk assessment will review the hazards associated with food businesses
regulated under the food safety schemes of the NSW Food Regulation 2004 and
includes:
♦ Dairy

♦ Meat
♦ Plant products – fresh cut fruits and vegetables, unpasteurised juice and
vegetables in oil
♦ Seafood
♦ Food service to vulnerable persons
♦ Eggs and egg products (draft food safety scheme currently being finalised)
Overview of risk assessment

Risk assessment forms part of an overall process, called risk analysis. Risk analysis is
used by governments and industry to assess, manage and communicate the risk
associated with particular food or food groups and in turn aims to reduce the
potential for foodborne illness. The Codex Alimentarius Commission divides risk
analysis into three components (CAC, 1999):
♦ Risk assessment – a process by which the potential risk posed by food safety
hazard(s) is determined
♦ Risk management – the process of determining alternatives for control the
hazards identified in the risk assessment and
♦ Risk communication – the exchange of information on risk and risk management
amongst interested parties.
Further, CAC (1999) has identified four components of risk assessment:
♦ Hazard identification – the process of identifying potential hazards associated
with the food
♦ Exposure assessment – an estimation of the potential human exposure to the
hazard and includes the use of data such as the occurrence in the food and/or
potential consumption rates of the food
♦ Hazard characterisation – the evaluation of the potential illness associated with
the hazard
♦ Risk characterisation – the process of determining the probability of occurrence
and severity of the adverse health effects based on the information collected in
the hazard identification, exposure assessment and hazard characterisation.
Previous risk assessment work

When developing a food safety scheme, the NSW Food Authority has previously
commissioned risk assessments or sourced information from risk assessments
performed by other government and non-government organisations. These risk
assessments have included:
♦ Ross, T. & Sanderson, K. (1999). A risk assessment of selected seafoods in NSW.
♦ Food Science Australia (2000). Final report – Scoping study on the risk of plant
products.

♦ Food Science Australia & Minter Ellison Consulting (2002). National risk validation
project. Final report.
♦ Miles, D. (2004). Risk assessment of the NSW dairy industry.
♦ Miles, D. and Chan, C. (2007). Risk profile and risk management of eggs and egg
products in NSW.
In addition, risk assessments have been conducted in Australia by other government
and non-government organisations. These include:
♦ Sumner, J. (2002). Food safety risk profile for primary industries in South
Australia. Department of Primary Industries and Resources SA, Adelaide.
♦ FSANZ [Food Standards Australia New Zealand] (2002). Final assessment report
proposal P263. Safety assessment of raw milk very hard cooked-curd cheeses.
Food Standards Australia New Zealand Report.
♦ FSANZ (2006). A risk profile of dairy products in Australia. Food Standards
Australia New Zealand Report.
♦ MLA [Meat & Livestock Australia] (2003). Through chain risk profile for the
Australian red meat industry Part 1: Risk Profile.
♦ FSANZ (2005). Scientific assessment of the public health and safety of poultry
meat in Australia
♦ FSANZ (2006). Public health and safety of poultry meat in Australia. –
Explanatory summary of the scientific assessment, Canberra.
♦ MLA (2006) Listeria monocytogenes in smallgoods: Risks and controls.
♦ Ross, T. Walsh, P. and Lewis, T. (2002). Risk assessment of fish cold smoking
and marination processes used by Australian businesses. Biodevelopment
Consulting Pty. Ltd for SafeFood Production NSW.
♦ FSANZ (2005). Final assessment report, P265, primary production and processing
standard for seafood (Attachment 10).
♦ Daughtry, B., Sumner, J. Hooper, G., Thomas, C. Grime, T., Horn, R., Moses, A.
& Pointon, A. (2005). National food safety risk profile of egg and egg products. A
report for the Australian Egg Corporation Limited (AECL) Publication No 05/06
Project SAR-47.
♦ Thomas, C., Daughtry, B., Padula, D., Jordan, D., Arzey, G., Davey, K., Holds, G.,
Slade, J., & Pointon, A. (2006). An egg: Salmonella quantitative risk assessment
model. AECL publication.
Current approach
As there has been a considerable amount of risk assessment work already
undertaken on industries covered by the food safety schemes, the approach taken in
this document was to provide a review of previous work conducted. This information
has been supplemented with other more recently published information where
necessary (CAC, 2007). To minimise repetition, information common to the different
food safety schemes has been placed in the appendices to the document:

♦ Appendix 1 - Common microbiological and chemical food safety hazards
♦ Appendix 2 - Food recalls in Australia
♦ Appendix 3 - Foodborne illness outbreaks in Australia
A number of methods have been used to estimate the level of exposure to hazards.
The approaches used include production data, consumption data, imported foods
testing failures, recalls, epidemiological data and results of food surveys. When
considering exposure the fate of the hazard during processing and preparation must
be taken into account.
References
CAC [Codex Alimentarius Commission] (1999). Principles and guidelines for the conduct of
microbiological risk assessment. CAC/GL-30. Retrieved 14 October 2008, from
http://www.codexalimentarius.net/download/standards/357/CXG_030e.pdf.
CAC [Codex Alimentarius Commission] (2007). Working principles for risk analysis for food
safety for application by governments. CAC/GL 62/2007. Retrieved 22 December 2008, from
http://www.codexalimentarius.net/download/standards/10751/CXG_062e.pdf.
Food Act 2003, New South Wales Government (2008).
Food Regulation 2004, New South Wales Government (2008).
Food Science Australia & Minter Ellison Consulting (2002). National risk validation project.
Final report 2002.

Hazard identification
The safety of milk and milk products has been extensively reviewed by regulatory
agencies in Australia and internationally. A large number of risk assessments and risk
profiles have been undertaken, examining the risks across the entire dairy supply
chain and conducting in-depth evaluations of specific pathogen-product
combinations. This risk assessment will summarise the major body of relevant work
undertaken to date.
In 1999, the former NSW Dairy Corporation commissioned Food Science Australia to
review the food safety systems that had been implemented in the NSW dairy
industry (Jansson et al, 1999). The report included a brief risk assessment and
endorsed the preventative approach to food safety through the implementation of
Hazard Analysis Critical Control Point (HACCP)-based food safety programs
throughout the dairy supply chain. This was later updated in 2004, when the NSW
Food Authority completed a qualitative risk assessment of the NSW dairy industry
which examined the microbiological and chemical hazards along the dairy supply
chain (Miles, 2004). This was developed as an internal document to provide scientific
rigour to the updated dairy food safety scheme and provide a basis for determining
the priority classification for segments of the industry. In 2002, Primary Industries
and Resources South Australia (PIRSA) commissioned a food safety risk profile on
primary production, including milk and dairy products (Sumner, 2002). This report
highlighted consumption of raw (unpasteurised) milk as a high risk activity.
In 2006, Food Standards Australia New Zealand (FSANZ) undertook a comprehensive
risk profile of dairy products in Australia to inform the development of the Primary
Production and Processing Standard for dairy products (FSANZ, 2006). The FSANZ
risk profile examined both microbiological and chemical hazards. The findings of the
FSANZ risk profile are reported here.
Microbiological hazards
A wide range of microbiological hazards may be introduced into milk during primary
production and processing. Raw milk may have a diverse range of bacteria present in
it, either shed directly into the milk from the udder as a result of illness or disease, or
through contamination from the external surface of the cow and the milking
environment. FSANZ (2006) highlighted the on-farm factors that most significantly
impact on the microbiological quality of raw milk as:
♦ animal-related factors (eg animal health, herd size, age and production status)
♦ environmental factors (eg housing, faeces, feed, soil, and water)
♦ method of milking, operation of milking and storage equipment (eg cleanliness of
equipment and lines, appropriate storage temperature to limit pathogen growth)
The initial levels of bacteria in raw milk can vary considerably, dependent on the
level of control over these factors. Boor (1997) reviewed the different types of
pathogenic microorganisms that have been detected in raw milk (Table 1).

Table 1 – Pathogenic microorganisms detected in raw milk
Microorganism Disease
Enterobacteriaceae
pathogenic Escherichia coli (eg EHEC, STEC) Gastroenteritis, other complications
involve Haemolytic uraemic
syndrome (HUS) and Thrombotic
thrombocytopenic purpura (TTP)
Salmonella Gastroenteritis, typhoid fever
Shigella Dysentery
Yersinia enterocolitica Gastroenteritis
Vibrionaceae and Campylobacter
Campylobacter jejuni Gastroenteritis
Aeromonas hydrophila Gastroenteritis
Other Gram-negatives
Pseudomonas aeruginosa Gastroenteritis
Brucella spp. Brucellosis (Bang’s Disease)
Gram-positive sporeformers
Bacillus cereus Gastroenteritis
Bacillus anthracis Anthrax
Clostridium perfringens Gastroenteritis
Clostridium botulinum Botulism
Gram-positive cocci
Staphylococcus aureus Emetic intoxication
Streptococcus agalactiae Sore throat
Streptococcus pyogenes Scarlet fever/sore throat
Streptococcus zooepidemicus Pharyngitis, nephritic sequelae
Miscellaneous Gram-positives
Listeria monocytogenes Listeriosis (various manifestations)
Corynebacterium spp. Diphtheria
Mycobacterium bovis Tuberculosis
Mycobacterium tuberculosis Tuberculosis
Mycobacterium paratuberculosis Johne’s disease (ruminants)
Crohn’s disease (unproven in
humans)
Rickettsia
Coxiella burnetii Q fever
Viral
Enteroviruses, including polioviruses and Coxsackie Enteric infection
virus, Rotaviruses
Foot and mouth disease virus Foot-and-mouth disease
(not a human disease)
Hepatitis virus Infectious hepatitis
Fungi
Mould (and associated aflatoxins) Mycotoxicoses
Protozoan parasites
Cryptosporidium parvum Cryptosporidiosis
Entamoeba histolytica Amoebiasis
Giardia lamblia Giardiasis
Toxoplasma gondii Toxoplasmosis
adapted from Boor (1997)

In the past, prior to the introduction of mandatory pasteurisation for milk in
Australia, the most important human diseases disseminated by the consumption of
raw milk were tuberculosis and brucellosis. These diseases have now been
eradicated in Australian dairy cow herds. As a result, the FSANZ risk profile (FSANZ,
2006) went on to identify the most significant pathogenic microorganisms to public
health and safety for the Australian dairy industry (Table 2). Further details on these
microbiological hazards are available in Appendix 1.
Table 2 – Microbiological hazards in dairy products
Pathogens Significance in dairy products

pathogenic Escherichia coli Pathogenic strains of E. coli can be found in cattle and may enter milk
through faecal contamination. Is destroyed by pasteurisation
Salmonella Salmonella is occasionally present in raw milk but is destroyed by
pasteurisation. Can contaminate products after pasteurisation, with non-
dairy ingredients a source of contamination. Frequently isolated in milk
powder
Yersinia enterocolitica Y. enterocolitica is destroyed by pasteurisation and its presence in heat
treated milk products is due to environmental contamination after heat
treatment. Y. enterocolitica is able to grow in dairy products held at
refrigeration temperatures and therefore may be considered as a hazard
in prolonged shelf-life products
Campylobacter spp. Campylobacter spp. is destroyed by pasteurisation and its presence in
milk products is due to environmental contamination after heat treatment.
Not normally able to grow in foods
Bacillus cereus Vegetative cells of B. cereus do not survive pasteurisation, however
spores will survive. B. cereus is rapidly outgrown by psychrotrophic
bacteria at refrigeration temperatures. However, in the absence of a
competitive microflora, growth to levels of concern is possible
Clostridium botulinum Vegetative cells of C. botulinum do not survive pasteurisation, however
spores will survive. Will only grow under anaerobic conditions
Staphylococcus aureus May enter raw milk through udder infection. S. aureus is destroyed by
pasteurisation, however toxins are heat stable. S. aureus does not grow
well at refrigeration temperatures or compete with starter cultures
Listeria monocytogenes L. monocytogenes is destroyed by pasteurisation. Its presence in dairy
products is due to post-pasteurisation contamination. Can grow in milk
products at refrigeration temperatures
Enterobacter sakazakii E. sakazakii will not survive pasteurisation. Recontamination of powdered
infant formula during manufacture is a risk. E. sakazakii cannot grow in a
dry substrate, but it can survive for long periods of time and is a potential
hazard when the powder is reconstituted and held at favourable
temperatures. Contamination and subsequent growth may occur during
reconstitution and preparation
adapted from FSANZ (2006)
These hazards were considered significant due to either:

♦ association with reported incidents of foodborne illness (including overseas
outbreaks)
♦ the potential to contaminate dairy products after pasteurisation.

This conclusion is supported by other work, such as that by Todd & Harwig (1996) in
a risk analysis of Canadian food, who stated that although 21 microbial hazards have
been reported to occur in Canadian milk, only eight of those presented a significant
risk to the human population, with Campylobacter jejuni, Salmonella spp. and E. coli
O157:H7 identified as the most important hazards. Johnson et al (1990) identified
Salmonella, Listeria monocytogenes and pathogenic E. coli as the three high risk
organisms to the cheese industry in the USA.
Chemical hazards
Chemicals are used by the dairy industry for a number of purposes, including pest
and weed control on farm, animal health and sanitising equipment. As a result, milk
may be susceptible to chemical contamination if proper controls are not in place. The
FSANZ risk profile evaluated the following potential chemical hazards (FSANZ, 2006):
♦ agricultural and veterinary chemical used in dairy primary production
♦ environmental contaminants, including heavy metals, organic contaminants and
micro nutrients
♦ naturally-occurring chemicals found in plants or in fungi or bacteria associated
with plants which may be ingested by grazing cattle
♦ food processing by-products
♦ food additives, processing aids, and those chemicals that may migrate from
packaging into dairy products.
Dairy products must comply with Standard 1.4.1 - Contaminants and Natural
Toxicants and Standard 1.4.2 - Maximum Residue Limits of the Food Standards
Code. These Standards sets out the Maximum Levels (MLs) of specified metal, non-
metal contaminants and natural toxicants and the Maximum Residue Limits (MRLs)
for agricultural and veterinary chemical residues present in food respectively.
Agricultural and veterinary chemical hazards

Without appropriate controls and the observance of appropriate withholding periods
for treated dairy cattle, it is possible for residues of these chemicals to occur in raw
milk. In Australia, the Australian Pesticide and Veterinary Medicines Authority
(APVMA) is responsible for registering agricultural and veterinary chemical products,
granting permits for use of chemical products and regulating the sale of agricultural
and veterinary chemical products. Veterinary chemicals administered to dairy cattle
are mainly antimicrobials and endo- and ectoparasiticides. Other veterinary chemical
uses include reproductive therapy and use of anti-inflammatory drugs or
anaesthetics. If the cow is lactating, then the product must specifically state that it
can be used in lactating dairy cows, and a milk withholding period may be specified.
The use of environmentally persistent pesticides, such as organochlorines, still poses
a potential problem for grazing animals. Potential hazards include excessive levels of
herbicides, pesticides or fungicides. Cereals and treated seeds used as animal feed
supplement are the most likely source of these contaminants, with the most
significant hazard to human health being those chemicals that can accumulate in
animal tissues or are excreted in the milk.

Aflatoxins
Grain crops can become contaminated with biological toxins, such as aflatoxins, a
group of extremely toxic metabolites produced by the fungi Aspergillus flavus and
Aspergillus parasiticus. When these moulds are allowed to germinate and grow on
harvested seed crops, the aflatoxins can be formed and ingested by dairy cattle
during feeding, eventually contaminating the milk. Aflatoxin contamination of milk is
more common in Europe where intensive supplementary feeding of dairy herds is
conducted. In Australia, where herds predominantly graze on pasture, aflatoxin
contamination has not been reported (ANZFA, 2001).
Cleaning chemicals
Milking premises and equipment must be cleaned and sanitised to prevent the risk of
contaminating the milk with microbiological pathogens. However, overuse of these
chemical can in itself create a hazard with the risk of chemical residues being left on
equipment. All chemicals used in detergents and sanitisers have the potential to
leave a residue on the dairy equipment surface if not used in the correct manner.
Physical hazards
The probability of introducing physical hazards on-farm, which ends up in the final
products is thought to be minimal. Any physical hazard contamination that may be
introduced on farm should be removed at the farm level. Most dairy farms include a
filter ‘sock’ through which the milk passes prior to entering into the farm vat. This
filter will remove most gross physical contaminants.
The introduction of physical hazards at the processing level has occasionally
happened in the past, with pieces of equipment ending up in a dairy product. The
instances of this occurring are very rare, and the preventative maintenance of
equipment means the risk is very low.
Exposure assessment
Consumption of pasteurised milk and dairy products
Consumption of milk and milk products forms a significant part of the average
Australian’s diet. Standard 4.2.4 – Primary Production and Processing Standard for
Dairy Products of the Food Standards Code requires all milk for human consumption
(including milk used to make dairy products) to be pasteurised at a minimum of 72°C
for 15 seconds (or equivalent), unless an applicable law of a State or Territory
provides an exemption 1. There is no such exemption for cow’s milk in NSW,
therefore all dairy products commercially sold in NSW are made from pasteurised
milk. In 2006/07, 684 million litres of milk were sold in NSW/ACT, including modified
and flavoured milk. Data from Dairy Australia shows the average consumption of
dairy products in Australia each year is 103.6 L milk, 11.9 kg cheese, 6.8 kg yoghurt
and 3.9 kg butter/blends per person (Dairy Australia, 2007). A closer analysis of
consumption trends is shown in the Australian National Nutrition Survey (ABS, 1995),
1
Standard 4.2.4A – Primary Production and Processing Standard for Specific Cheeses of the Food Standards Code
does allow imported Gruyere, Sbrinz, Emmental and Roquefort to be made from raw milk.

which showed that 84% of people surveyed consumed dairy products at an average
amount of 347 g/day with the quantity ranging from 209-471 g/day (Table 3).
Consumption of dairy products varies with age, declining from 98% of children aged
2-3 years to 90% of adults aged 19-24 years and then increasing again to 95% of
persons aged 65 years and over.
Liquid milk accounts for approximately 70% of the mean daily intake of dairy
products for persons of all ages. However, the trend of milk consumption within
Australia has been changing to more specialty types. Whole milk accounts for around
56% of milk sales, with lower fat lines increasing to 26%, long life or ultra high
temperature (UHT) treated milk 8.5%, and the remainder as flavoured and specialty
milks (Dairy Australia, 2007). Cheese consumption in Australia has jumped more
than 20% in the past decade. The recent consumer trend has been away from
cheddar cheeses to non-cheddar cheese types, and this is also being reflected in
Australia’s cheese exports, where the non-cheddar share of total export sales has
increased from 45% to 57% over the past seven years.
Table 3 – Consumption of dairy products
Sex Age Proportion of persons Median daily intake per consumer

consuming milk products and of milk products and dishes
dishes 2 (g/day)
(%)
Male 2-3 98.2 471.8
Male 4-7 95.5 365.0
Male 8 - 11 90.9 401.4
Male 12 - 15 92.8 424.0
Male 16 - 18 94.2 392.2
Male 19 - 24 89.1 323.0
Male 25 - 44 93.7 263.2
Male 45 - 64 91.3 258.0
Male 65+ 94.5 255.0
Female 2-3 98.1 394.3

Female 4-7 96.0 280.5
Female 8 - 11 93.3 312.0
Female 12 - 15 90.8 297.7
Female 16 - 18 87.3 258.0
2
Milk products and dishes are defined in the National Nutrition Survey (ABS, 1995) as including the following:
- Dairy milk
- Yoghurt
- Cream
- Cheese
- Frozen milk products (eg ice -cream)
- Other dishes where milk or a milk product is the major component
- Milk substitutes (eg soy-based milk)
- Flavoured milks

Sex Age Proportion of persons Median daily intake per consumer
consuming milk products and of milk products and dishes
dishes 2 (g/day)
(%)
Female 19 - 24 90.1 251.3
Female 25 - 44 94.3 209.3
Female 45 - 64 94.7 216.6
Female 65+ 95.6 225.8
adapted from National Nutrition Survey (ABS, 1995)
Consumption of raw milk

The current Dairy food safety scheme in the Food Regulation 2004 does not provide
an exemption from the requirement to pasteurise cow’s milk sold for human
consumption. However, no such limit exists on the private consumption of raw cow’s
milk. This is believed to be limited to small communities in NSW, such as farm
families. The amount of raw milk consumed on farm within NSW is difficult to
estimate, but is considered to be extremely small when compared to the volume of
pasteurised milk. The US Food and Drug Administration (FDA) and US Department of
Agriculture (USDA) quantitative risk assessment on listeriosis estimated raw milk
consumption to be less than 0.5% of total milk consumption in the USA (FDA/USDA,
2003). Todd & Harwig (1996) made the assumption that ‘farm families’ were the
people most likely to consume unpasteurised dairy products and consequently be
exposed to the microbiological hazards that may contaminate raw milk.
The Dairy food safety scheme does provide an exemption to allow the sale of
unpasteurised goats milk in NSW. This was initially a continuation of the permit
system implemented by NSW Health, however, the former SafeFood NSW
commissioned a risk assessment (AgriQuality New Zealand, 2002), but the authors
could not fully determine the risk from unpasteurised goats milk due to a lack of
data. Recommendations from the report included the implementation of HACCP-
based food safety programs and a microbiological survey of unpasteurised goat’s
milk to generate data to provide the basis for a risk assessment. The National
Nutrition Survey (ABS, 1995) estimated that less than 1% of respondents consumed
goat’s milk and there is no evidence to suggest this has increased in recent years. In
fact the number of licensed goat milk producers in NSW has declined.
Recently ‘cosmetic’ and ‘bathing’ raw milk products have become available for sale in
NSW and other states. Although marketed for non-food use, it is believed these
labelling terms are being used to bypass the Food Standards Code, and that these
products are being consumed. While the volume consumed is considered to be very
small, the products are potentially unsafe. As such, the NSW Food Authority has
taken enforcement action when these products have been identified in the
marketplace, as they do not comply with the Food Standards Code requirements for
pasteurisation of cows milk for human consumption.
FSANZ are currently considering Proposal P1007 - Primary Production & Processing
Requirements for raw milk products. The outcome of that process could influence the
volumes of unpasteurised dairy product offered for sale in Australia.

Hazard characterisation
Foodborne illness outbreaks from milk and dairy products
Australian dairy products enjoy a reputation for high standards of quality and safety.
There have been few reported failures leading to incidents of foodborne illness
attributed to dairy products in the market place in recent years. FSANZ reviewed the
foodborne illness data associated with milk and milk products in Australia. This data
is summarised in Table 4, with more detailed information on each outbreak included
in Table 65 (Appendix 3). Between 1995 and 2008 there were 14 reported outbreaks
directly attributed to specific dairy products, affecting 284 people. Of these, nine
were associated with consumption of unpasteurised milk and none occurred in NSW.
In addition, there were 12 outbreaks identified involving a food product that
contained dairy products as an ingredient. However, because dairy products are an
ingredient in many foods, it is often difficult to determine whether they are the actual
cause of an outbreak.
There have been a number of reports of outbreaks associated with consumption of
dairy products overseas. While unpasteurised dairy products have been a common
cause of dairy-associated outbreaks of illness, pasteurised dairy products have also
been implicated where there have been poor food safety control measures in place,
including the use of contaminated non-dairy ingredients, faulty pasteurisation
process, poor hygiene or contamination post pasteurisation.
Table 4 – Summary of foodborne illness outbreaks attributed to dairy products

and foods including dairy as an ingredient
Hazard Australian Cases Hospitalisations Deaths
outbreaks
(1995-2008)
Salmonella spp. 7 226 5 0
Campylobacter 6 85 0 0
Norovirus 3 123 0 0
C. perfringens 1 27 0 0
Chemical contamination 1 23 0 0
Cryptosporidium 1 8 3 0
S. aureus 1 2 0 0
Unknown 6 86 1 0
Total 26 582 10 0
While there is little corresponding evidence in Australia linking consumption of

pasteurised dairy products to foodborne illness, the widespread consumption of dairy
foods has been demonstrated by some large scale foodborne illness outbreaks
overseas. In 2000, over 15,000 people were sick and 165 people hospitalised in
Japan from dairy products made by the Snow Brand Milk Products Co. that were
contaminated with S. aureus enterotoxin. In addition, the 2008 deliberate
adulteration of Chinese milk with melamine resulted in worldwide recalls of dairy

products and a wide range of other foods where milk powder was used as an
ingredient. The broad distribution of Chinese milk powder graphically demonstrated
that a food safety incident in one country can have international repercussions and
encompass a broad spectrum of products.
Pathogenic Escherichia coli in raw milk

Cattle have been identified as an important reservoir for pathogenic E. coli, and
although pasteurisation does eliminate E. coli, outbreaks of E. coli O157:H7
infections overseas have been attributed to contaminated raw milk and some
pasteurised dairy products. A 1998 Australian study examined the incidence of
pathogenic E. coli in dairy cattle on four farms, with evidence of shiga toxigenic
E. coli (STEC) detected in the faeces of 39% of the 843 cattle tested (Desmarchelier,
1998). The prevalence rates varied between farms, although generally milking cows
had a lower rate (24%) than younger animals (33-41%). The STEC isolated from
dairy cattle included E. coli O157:H7 (0.9%) and E. coli O26 (0.16%), both known
pathogenic strains.
However, when the prevalence of pathogenic E. coli in Australian raw milk was
assessed, it was found to be relatively low (Desmarchelier, 1998), with STEC isolated
from 27 of 1,802 samples (1.5%). It was hypothesised that low level carriage may
normally be present in the dairy herd and this is periodically stimulated by some host
or environmental factor. It appears that during these episodes of increased faecal
shedding, there is an increase in environmental contamination and associated
increased risk of milk becoming contaminated.
Salmonella in dairy products

The first significant case of Salmonella in an Australian milk product occurred in 1943
in Victoria. A typhoid-carrying farm worker contaminated raw milk, which was then
distributed for public consumption, resulting in over 400 cases of typhoid fever and
23 deaths (Merrilees, 1943). Since that time, there has been only one other major
incident involving Salmonella in pasteurised dairy products. This occurred in Victoria
during the 1970’s and was traced to milk powder becoming contaminated due to
contaminated lining of the spray dryer. The former Australian Dairy Authorities’
Standards Committee (now ANZDAC) produced the Australian Manual for control of
Salmonella in the dairy industry (ADASC, 1999b) to specify control measures for
limiting the risk of dried milk products becoming contaminated with Salmonella. In
addition, unpasteurised milk contaminated with Salmonella has been the responsible
for several reported outbreaks in South Australia where, until recently, the sale of
raw cow’s milk was allowed for human consumption.
Yersinia enterocolitica in milk

Y. enterocolitica has been isolated from raw and pasteurised milk in various parts of
the world. Although some strains occasionally associated with human disease have
been isolated from raw milk, the main pathogenic types generally do not
predominate. Milk has been associated with sporadic cases and outbreaks of
Y. enterocolitica infections overseas, but not in Australia.

Campylobacter spp. in milk
Both Campylobacter jejuni and Campylobacter coli are found in the faeces of cattle
and can cause cases of subclinical mastitis. Hutchinson et al (1985) reported a milk-
borne outbreak resulting from the consumption of raw milk from cows exhibiting no
outward evidence of illness. Healthy lactating cows can carry C. jejuni in the
intestinal tract, providing an extrinsic source of contamination. In one US study of
193 healthy dairy cows at three dairies, 77 (40%) had positive rectal cultures (Martin
et al, 1983).
Overseas surveys of Campylobacter in raw milk have shown a prevalence of 1 to 6%
(Wallace, 2003), however, these organisms are unlikely to grow in milk or dairy
products. Nevertheless, several outbreaks of Campylobacter food poisoning from
consumption of raw milk in Australia have been reported among children who were
taken on a class trip to a dairy and given raw milk to drink.
Bacillus cereus in liquid milk

Raw milk is frequently contaminated with Bacillus spores, with the milk often
contaminated at the farm. Sanitation of the teats prior to milking was able to reduce
the incidence of B. cereus in raw milk (Christiansson et al, 1999). The presence of
B. cereus in processed dairy product is often associated with the ability of the spores
to survive pasteurisation, which may then colonise pipes, tanks and filling machines
(Lin et al, 1998).
Notermans et al (1997) examined the risk from B. cereus in pasteurised liquid milk in
the Netherlands. The study estimated that up to 7% of pasteurised milk may contain
B. cereus, with levels up to 105/mL. However, pasteurised milk has not figured as a
cause of B. cereus food poisoning in Australia. One reason for this is the germination
of B. cereus spores and its growth in pasteurised milk leads to the development of
“off flavours” and an appearance discouraging consumption.
Clostridium botulinum in dairy products

Dairy products have not traditionally been associated with outbreaks of botulism.
Since 1912 fewer than 20 outbreaks associated with dairy products worldwide have
been recorded. However, spores of C. botulinum survive the normal milk
pasteurisation process, and therefore control factors such as aw (water activity),
redox potential, pH and temperature must be used in dairy products such as cheeses
and dairy-based spreads and sauces to reduce the risk of botulism.
In 2007, one case of botulism was reported in Victoria and was associated with the
consumption of nationally distributed ready-to-eat nachos meal. The neurotoxin was
detected in discarded remains of that meal pathogen (OzFoodNet Working Group,
2007). One of the components was a cheese sauce and subsequent laboratory
testing showed that the sauce provided an environment that would support growth
of the organism. This case is not included in Appendix 3 data as it was not classed as
an outbreak, affecting only one person.
Botulism in dairy herds is caused by ingestion of preformed toxins produced by the
growth of C. botulinum in decaying crops, vegetation or carcase material, or by the
animal acquiring a gastrointestinal infection with the organism. The presence of

neurotoxin in milk from animals diagnosed with botulism is periodically raised as a
concern. When these incidents occasionally occur in dairy herds in Australia, farmers
voluntarily remove affected animals from supplying milk. There is little evidence in
the scientific literature to suggest the transfer of botulinum neurotoxins or the
organism itself to milk occurs from either symptomatic or asymptomatic animals in
affected herds.
Staphylococcus aureus in milk

S. aureus can be frequently found in raw milk from cows with undetected mastitis.
Even in subclinical cases of mastitis up to 105 cfu/mL of S. aureus can be shed into
the milk. S. aureus is a poor competitor, and will not grow well in the presence of
other bacteria commonly present in raw milk, however it is believed that toxin can be
produced under any conditions that permit growth. The Snow Brand Milk Products
Co. outbreak in Japan was suspected to be due to poor cleaning of distribution pipes
in the production facility, leading to the opportunity for S. aureus to grow to high
levels and produce toxin.
Listeria monocytogenes in dairy products

L. monocytogenes has a history of causing large outbreaks overseas from dairy
products, with a 1985 outbreak in the USA from Mexican-style soft cheese affecting
142 people and causing 48 deaths and an outbreak in Switzerland from Vacherin
Mont D'Or cheese affecting 122 people and causing 34 deaths (Ryser, 1999).
The FDA/USDA risk assessment on Listeria monocytogenes examined 11 categories
of dairy products (FDA/USDA, 2003), while the New Zealand Food Safety Authority
(NZFSA) commissioned a series of risk profiles examining the risk of
L. monocytogenes contamination in ice-cream, low moisture cheese and soft
cheeses.
The worldwide incidence rate for Listeria spp. in raw milk is estimated to be around
3-4% (Sutherland et al, 2003), while in Australian raw milk the incidence also
appears low. A NSW Dairy Corporation survey of 600 raw milk samples failed to
detect L. monocytogenes, however, 0.4% of samples were positive for Listeria spp.
(Sutherland & Porritt, 1995).
The organism is eliminated by pasteurisation, therefore the primary concern is post-
pasteurisation contamination with L. monocytogenes , as it is a common inhabitant
of dairy processing facilities. In dairy factories, the major areas that have been
identified as sources of the organism are drains, floors, conveyors, refrigerated
storage areas and crate wash lines (Sutherland et al, 2003).
Enterobacter sakazakii in infant formula

E. sakazakii is a rare, but life threatening cause of neonatal meningitis, sepsis, and
necrotising enterocolitis. In general, the reported case-fatality rate varies from 33-
80% among newborns diagnosed with this type of severe infection (Lai, 2001).
Premature infants and those with underlying medical conditions may be at highest
risk for developing an E. sakazakii infection, however it should be noted that healthy

infants may not always be immune to E. sakazakii infections (Nazarowec-White &
Farber, 1997).
In 2002 the US FDA issued an alert to health care professionals regarding the risk
associated with E. sakazakii infections among neonates fed milk-based, powdered
infant formulas (FDA, 2002). There have been several E. sakazakii outbreaks
reported among infants fed milk-based powdered formula in neonatal intensive care
units in England, Netherlands, Iceland, Belgium, Greece, U.S. and Canada (Biering et
al, 1989; Lai, 2001; Van Acker et al, 2001; Himelright et al, 2002). These outbreaks
have involved several deaths and were associated with temperature abuse of
reconstituted powdered infant formula. In addition, there have been cases in
premature babies in New Zealand (NZ Ministry of Health, 2005):
♦ in 1986, a premature infant contracted E. sakazakii septicaemia, but survived,
apparently without serious sequelae
♦ in 1991, premature twins contracted E. sakazakii meningitis one twin suffered
serious permanent neurological effects, and the other recovered fully
♦ in 2004, a premature infant contracted E. sakazakii meningitis, and died.
At the time of writing, there have been no reported cases of neonatal illnesses
associated with E. sakazakii in infant formula in Australia, however it must be noted
that the organism is not a notifiable disease in Australia.
Powdered infant formula is not a commercially sterile product, unlike liquid formula
which is subjected to sufficient heat to render it commercially sterile. Powdered
infant formula may be subject to contamination by opportunistic pathogens such as
E. sakazakii through improper cleaning of production lines. While the pathogen does
not grow in the powder it can survive for many months.
Chemicals
The prevalence of chemical in dairy products is assessed by several surveys
conducted each year in Australia to detect chemical residues. The Australian Milk
Residue Analysis (AMRA) survey, the Australian Total Dietary Survey (ATDS), the
National Antibacterial Residue Minimisation (NARM) program, and other targeted
testing programs provide an indication of the potential for chemical contaminants
ending up in dairy products.
The AMRA survey from 1998 to 2005 showed the following:
♦ 89,121 analyses for antimicrobials showed 99.997% compliance with the
maximum residue limit (MRL) for veterinary chemicals residues in milk (there was
one detection of Cloxacillin at a level at the MRL of 0.01 mg/kg in June 2002 in a
bulk milk sample in NSW)
♦ 33,382 analyses for agricultural chemical residues, including organochlorines,
organophosphates and synthetic pyrethroids, showed no detections
Targeted testing of milk in areas subject to locust plagues has also shown very high
compliance rates for organochlorines, organophosphates and Fipronil (a broad
spectrum insecticide). In 2000/2001 123 samples were tested in NSW, with no
residues detected (DFSV, 2002).

The NARM program conducts tests on bobby calves and cull dairy cows that are
presented to abattoirs. Testing on NSW cull dairy cows from 2000 to 2002 showed
that 44 from 455 (9.7%) were positive. Of these positive trace results, eight were
shown to be greater than MRL with Neomycin, and Sulphadiazine found in dairy cull
cows, and Oxytetracycline and Sulphadiazine in the export calves. Chemical residues
persist in meat much longer than milk, and this is reflected in recommended
withholding periods. Traceback investigations where residues were detected showed
that causes ranged from not obeying the withholding period, use of the wrong
withholding period (milk rather than meat) and accidental feeding of medicated milk
to calves (NSW Agriculture, 2001 NSW Agriculture, 2002).
The ATDS detected no agricultural chemical residues in milk and milk products
available on retail shelves. Naturally occurring aflatoxins are not considered a high
risk, as a small survey of 40 dairy products by the NSW Food Authority in 2005
detected aflatoxin M1 in trace levels in only one sample, all others were below the
limit of detection.
Risk characterisation
Risk ranking dairy products
The NZFSA commissioned risk profiles to examine various hazards on hazards in
dairy products, predominantly L. monocytogenes and STEC. The conclusions are
summarised in Table 5. In addition, the FDA/USDA (2003) estimated the risk per
serving and risk per annum of listeriosis for 11 RTE dairy products, based on the
predicted number of annual illnesses associated with the consumption of these
foods. The predictions were based on the estimate of US population used in the
FDA/USDA (2003) risk assessment of 260 million and extrapolated to the Australian
population of approximately 21.6 million (ABS, 2009) by dividing by a factor of 12
(see Table 6). These estimates are approximate, as it is acknowledged that may be
differences in the consumption levels of particular dairy products between American
and Australian consumers.
Table 5 – NZFSA risk profile outcomes examining hazards in dairy products

Hazard Risk
Listeria monocytogenes in soft Data on the prevalence of L. monocytogenes indicate that
cheeses contamination rates are very low, most likely to occur post-
(Lake et al, 2005b) pasteurisation. Current risk to the general is considered low,
although susceptible populations will have a greater risk
Listeria monocytogenes in ice- Found no evidence to link consumption of ice-cream with cases of
cream L. monocytogenes infection in New Zealand
(Lake et al, 2003)
Listeria monocytogenes in low Contamination with L. monocytogenes is unlikely unless
moisture cheese introduced post-pasteurisation from environmental sources, added
(Lake et al, 2005a) ingredients or further processing such as grating. Surveys of low
moisture cheese suggest that contamination with
L. monocytogenes is infrequent and that growth in product is
unlikely. Even taking into account the high consumption of low
moisture cheese, the available data indicates that
L. monocytogenes in low moisture cheese does not represent a
significant risk to human health

Hazard Risk
Shiga-toxin producing Escherichia Approximately 10% of notified human cases of STEC infection
coli in raw milk (mostly E. coli O157:H7) in New Zealand reported consumption of
(Gilbert et al, 2007) raw milk. E. coli O157 has been reported, albeit rarely, in faecal
samples from dairy and beef cattle. However, there is insufficient
data on the prevalence and numbers of STEC in raw milk to
robustly estimate the risk from consumption of raw milk in New
Zealand
Dairy products likely to support the growth of pathogens and prone to contamination
after pasteurisation may be categorised as higher risk than other dairy products.
Alternatively, dairy products that do not support the growth of pathogens, if correctly
formulated, can be classified as low risk.
FSANZ ranked the degree of risk based on (FSANZ, 2006):
♦ intrinsic properties of the product (ie the impact of aw, pH, salt concentration,
and their effect on the growth of contaminating microorganisms)
♦ extent to which food is exposed to factory environment or handling after heat
treatment
♦ hygiene and control during distribution and retail sale
♦ degree of reheating or cooking before consumption (many dairy products are
RTE, so this is rarely a factor).

Table 6 – Risk ranking for dairy products contaminated with Listeria monocytogenes
Dairy product Risk ranking Predicted cases of listeriosis Risk ranking Predicted annual number of
(per serve) per serve (per annum) listeriosis cases
(in Australia) 3 (in Australia) 4
Unpasteurised fluid milk High 7.1 x 10-9 Moderate 0.25
-9
High fat and other dairy products (eg butter, cream, other Moderate 2.7 x 10 High 4.7
miscellaneous milk products)
Soft unripened cheese, >50% moisture (eg cottage Moderate 1.8 x 10-9 Moderate 0.6
cheese, cream cheese, ricotta)
Pasteurised fluid milk Moderate 1.0 x 10-9 High 7.5
-10
Fresh soft cheese Low 1.7 x 10 Low 0
Semi-soft cheese, 39-50% moisture (blue, brick, Low 6.5 x 10-12 Low 0
monterey, muenster)
Soft ripened cheese, >50% moisture (brie, camembert, Low 5.1 x 10-12 Low 0
feta)
Ice-cream and other frozen dairy products Low 4.9 x 10-14 Low 0
-14
Processed cheese (cheese foods, spreads, slices) Low 4.2 x 10 Low 0
-14
Cultured milk products (yoghurt, sour cream, buttermilk Low 3.2 x 10 Low 0
Hard cheese, <39% moisture (cheddar, Colby, parmesan) Low 4.5 x 10-15 Low 0
adapted from FDA/USDA (2003)
3
The risk per serving is inherent to the particular food category, and is therefore assumed to be the same in Australia as that calculated for the USA (FDA/USDA, 2003). This is based on the
assumption that consumption patterns for these foods are identical in Australia and the USA.
4
The risk per annum has been adapted from USA population data contained in the FDA/USDA (2003) risk assessment of 260 million and extrapolated to Australian population data of
approximately 21.6 million (ABS, 2009) by dividing by a factor of 12

Table 7 provides a relative risk ranking for categories of dairy products (FSANZ,
2006), however the ranking can be quite variable. For example, once a shelf-stable
UHT product is opened, it may become contaminated via cross-contamination and
when subjected to temperature abuse it could become a high-risk food. In contrast,
the low pH and low water activity of extra hard cheese means it is unlikely to support
the growth of any pathogen that contaminates the surface. Dried milk powders and
infant formulae are inherently stable products due to their low water activity,
however these products may be prone to contamination, and upon reconstitution
become higher risk, especially if improperly reconstituted and stored.
Table 7 – Risk ranking of dairy products

Risk Dairy product Risk characterisation
ranking
Higher risk Unpasteurised milk No pathogen reduction step
Soft cheeses Mild pH, long shelf life allowing growth of
Listeria monocytogenes (Bemrah et al,
1998)
Dairy desserts Mild pH, fermentable carbohydrate, long
shelf-life
Fresh cheese Dependent on variety - some have low
acid, high moisture
Dairy dips Dependent on variety – some have low
acid, high moisture, added ingredients
Intermediate Unsalted butter Absence of salt, high moisture content

risk
Low fat spreads Absence of salt, high moisture content
Pasteurised milk Storage temperature only hurdle to
control post-pasteurisation contamination
Ice-cream Stored frozen, but soft serve may allow
growth of Listeria monocytogenes
Low risk Yoghurt Low pH does not allow growth of

pathogens
Salted butter High salt concentration
Hard cheese Low water activity, low pH
Extra hard cheeses Low water activity, low pH
UHT milk Commercially sterile
Dried milk powder Low water activity, however prone to
contamination
adapted from FSANZ (2006)
Consumption of raw milk

The consumption of unpasteurised milk appears to represent a significant risk on a
per serving basis, with the FDA/USDA risk assessment categorising unpasteurised
milk as high risk for listeriosis (FDA/USDA, 2003), and the majority of foodborne
illness attributed to dairy products worldwide due to the consumption of
unpasteurised milk and dairy products made from unpasteurised milk. However, the
predicted number of annual illnesses is very low because of the low levels of

consumption of raw milk. FSANZ consumption data tends to estimate the
consumption of raw milk as less than 1% of overall milk consumption (FSANZ, 2006),
while the FDA/USDA risk assessment estimated consumption to be less than 0.5%
(FDA/USDA, 2003).
Primary Industries and Resources South Australia (PIRSA) commissioned a food
safety risk profile on primary production, including milk and dairy products. This
report highlighted consumption of raw milk as a high risk activity and predicted much
higher rates of foodborne illness. It was predicted the risk of illness from all
foodborne pathogens associated with raw milk to be in the order of 36 illnesses per
annum among the 1000 consumers, compared with one illness in 20 years for
pasteurised milk (Sumner, 2002).
Control measures
FSANZ found that the factors having the most significant impact on the safety of
processed Australian dairy products are (FSANZ, 2006):
♦ the quality of raw materials
♦ correct formulation
♦ effective processing
♦ the prevention of recontamination of product
♦ maintenance of temperature control through the dairy supply chain.
While pathogenic microorganisms may contaminate raw milk supplies, pasteurisation
is a very effective Critical Control Point (CCP) in eliminating pathogens, good
manufacturing practices must also be employed to ensure that post-pasteurisation
contamination does not occur.
Prevalence of pathogens in milk

The effectiveness of pasteurisation is dependent upon the microbiological status of
the incoming raw milk. Control measures at the primary production level involve
minimising the likelihood of microbiological hazards contaminating the raw milk. This
is achieved through the implementation of a food safety program incorporating good
agricultural practices (GAP). These measures are effective in reducing the microbial
load of milk being sent for processing.
However, should microbial contamination of raw milk occur, it is critical that milk is
stored at a temperature that minimises the opportunity for the bacteria to multiply.
Temperature abuse of the milk may allow growth of pathogenic bacteria to the
extent where the pasteurisation process may not eliminate all pathogenic bacteria
and/or toxins.
Chemical hazards
Milk from multiple farms may be batched together, either within a milk tanker, or
within a silo at a processing facility, therefore the potential exists for chemically
tainted milk from a single farm to contaminate a large volume of milk within a tanker
and silo at the processing factory. However, the implementation of on-farm food
safety programs has also minimised the presence of chemicals in milk.

In addition to these testing programs, processing factories receiving milk from farms
test incoming batches of milk for the presence of chemical hazards, such as
antibiotics which can adversely affect starter cultures during cheese production.
Correct formulation
Ingredients used in the manufacture of dairy products that are added post
pasteurisation must be of a high microbiological standard. Many non-dairy
ingredients added to ice-cream mix after heat treatment include fruits (canned,
fresh, or frozen and usually in concentrated sugar syrups), nuts, chocolate, pieces of
toffee and biscuit, colours and flavours. These ingredients and those added to other
dairy products such as yoghurt, dairy desserts, dairy dips and cheese may introduce
pathogens into the product (ICMSF, 1998). This is readily illustrated by a botulism
outbreak involving a yoghurt product in the UK. In this outbreak it was not the
yoghurt itself but hazelnut purée added to the yoghurt that was the source of the
intoxication. The hazelnut purée was under processed, had a pH (between 5.0 and
5.5) and a high aw conducive to the growth of the pathogen. Previous batches were
sweetened with sugar but the producer had recently switched to aspartame. The
subsequent rise in aw was not compensated for by additional processing changes. A
total of 27 people were affected and one died (Critchley et al, 1989).
This addition of ingredients added after pasteurisation was identified as a high risk
factor by Jansson et al (1999) who recommended that dairy products with these
additions (eg ice-cream and cheeses) be moved into the high risk category and the
finished product be subject to additional end product microbiological analysis.
The microbial quality of dry-blended ingredients into infant formula was identified as
a significant source of contamination by FSANZ, as there is no heat treatment to
destroy bacteria in the final product (FSANZ, 2006).
Effective processing (pasteurisation)

Dairy processing facilities primarily use High Temperature Short Time (HTST)
pasteurisation (minimum 72°C for 15 seconds) or batch pasteurisation (minimum
65°C for 30 minutes) to eliminate the pathogens of concern in milk. The minimum
times and temperatures for pasteurisation are stated in Standard 4.2.4 – Primary
Production and Processing Standard for Dairy Products of the Food Standards Code.
However, most factories actually heat the milk to higher temperatures and hold it for
a longer time period as an in-built safety margin.
Juffs & Deeth (2007) undertook an extensive evaluation of the effectiveness of
pasteurisation in reducing pathogens in milk and milk products. They concluded that
Australian consumers can be assured that pasteurisation does destroy the pathogens
of concern in milk and dairy products. They also observed that:
♦ literature data indicate that the most significant milk-borne pathogens are
destroyed by pasteurisation with a reasonable margin of safety
♦ the pasteurisation times and temperatures used by Australian processors meets
the minimum requirements prescribed in the Food Standards Code, and in many
cases products are heated to a temperature and/or a time often well in excess of
the prescribed minimums
♦ lack of epidemiological data indicating that pasteurised milk products have been
implicated in foodborne illness outbreaks in Australia in recent years, in contrast

outbreaks have been associated with consumption of raw milk, in Australia and
overseas.
♦ in most cases, milk and dairy products are consumed as RTE foods and will
readily support the growth of any contaminating microorganisms. In the past, the
dairy industry has been subjected to a high level of food safety regulation,
ensuring high levels of hygiene and sanitation are maintained.
The pasteurisation process eliminates all pathogenic bacteria found in raw milk, with
the exception of the spore forming bacteria B. cereus and C. perfringens. However,
neither of these organisms has been identified in incidents of foodborne illness from
dairy products. It is improbable that C. perfringens can germinate and multiply under
the normal conditions of milk storage, while spoilage bacteria will outgrow B. cereus
at refrigeration temperatures.
The prevention of recontamination of product

Post-pasteurisation contamination can pose a major problem where good
manufacturing practices are not employed (Zottola & Smith, 1991). Pathogenic
microorganisms can be introduced into a dairy processing environment with raw
milk. Once these organisms gain access to the processing plant, the presence of
nutrients and moisture can allow not only for survival, but multiplication of these
organisms. The application of food safety programs including elements of Good
manufacturing practice (GMP) and Good hygienic practice (GHP) are critical to limit
the potential for pathogens to contaminate dairy products after pasteurisation.
The primary organisms of concern are Listeria monocytogenes for most dairy
products and Salmonella in dried milk products. A large number of dairy products
have been recalled due to contamination with L. monocytogenes, with nine recalls
between 2004-2008 (Table 65 in Appendix 2).
In 1999, the state dairy regulatory authorities introduced two manuals for the control
of post-pasteurisation contamination with Listeria (ADASC, 1999a) and Salmonella
(ADASC, 1999b). These manuals highlight steps to control entry of these organisms
into dairy processing areas, as well as recommend frequencies for finished product
and environmental testing, and clearance programs if the organisms are detected.
Maintenance of temperature control through the dairy supply chain

The intrinsic nature of many dairy products means they will support the growth of
pathogenic bacteria that may contaminate the product. This categorises these
products as ‘potentially hazardous foods’ under the definition in Standard 3.2.2 -
Food Safety Practices and General Requirements of the Food Standards Code. The
exception to this are products such as yoghurt and hard cheeses (low pH) and ice-
cream (stored frozen). As potentially hazardous foods, maintenance of temperature
control through the dairy supply chain is critical to ensure these foods remain safe
and suitable.

Conclusion
The FSANZ risk profile concluded that (FSANZ, 2006):
♦ a wide range of microbiological hazards may be associated with raw milk and
dairy products, but these do not represent a significant problem under current
management practices which:
o control animal health
o ensure adherence to good milking practices
o require effective heat treatment (eg pasteurisation) and
o have controls to prevent post-pasteurisation contamination in the
dairy processing environment
♦ current risk management measures ensure that pathogenic microorganisms are
unlikely to be present in high numbers in raw milk
♦ pasteurisation provides the kill step to effectively eliminate all but the spore-
forming bacteria
♦ there are extensive regulatory and non-regulatory measures in place along the
dairy industry primary production chain resulting in minimal public health and
safety concerns regarding the use or presence of chemical in dairy products
♦ extensive monitoring of chemical residues in milk over many years has
demonstrated a high level of compliance with the regulations
♦ Australian dairy products have an excellent reputation for food safety, and this is
supported by the lack of evidence attributing foodborne illness to dairy products
and
♦ continuation of the current management practices, particularly monitoring
programs for chemical along the primary production chain, will ensure that the
dairy industry continues to maintain a high standard of public health and safety.
The NSW Food Authority and its predecessor organisations have taken a proactive
role in implementing HACCP-based food safety programs along the dairy supply
chain, a position that may well have contributed to the excellent safety record of
dairy products in NSW. This, when combined with improvements in primary
production practices that effectively manage animal health, adherence to good
milking practices, and improvements in the hygiene of milking equipment and
buildings have been important in reducing the microbial load in raw milk entering
NSW dairy processing facilities. The adoption of industry codes of practice and the
extensive implementation of food safety programs in the dairy industry has helped to
underpin these regulatory control measures.

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The Meat food safety scheme under the Food Regulation 2004 regulates food safety
practices across broad sections of the meat industry, from harvesting of game meat
in the field, through to primary processing at the abattoir and further processing into
ready-to-eat (RTE) meat products. In order to effectively assess the risks, and
consider the different production systems and inherent hazards associated with
different sectors of the meat industry, the following definitions have been used to
categorise the data:
Meat the dressed carcase and carcase parts of an animal (bovine,
bubaline, camelidae, caprine, cervidae, ovine, porcine and soliped
species)
Poultry meat the edible part of any poultry (fowl, duck, geese, turkeys,
pigeons, pheasants, quails, guinea fowls and other avian species)
intended for human consumption. For the purposes of this report,
this also includes processed poultry meat
Game meat the edible part of any wild game animal (any vertebrate animal of
a species that is not farmed, but is killed in the field and can be
legally harvested, excluding fish)
Processed meat meat that is further processed (such as curing, heat treated,
dried, canned, fermented, rendered) to form a meat product with
different characteristics and flavours.
Meat
In Australia, the most comprehensive work has been funded by the meat industry
itself, through Meat and Livestock Australia (MLA), who commissioned a risk profile
of the red meat industry to identify (MLA, 2003):
♦ public health hazards that enter any point of the food chain for meat products
produced in Australia and rank them in terms of risks to the consumer
♦ hazard:product combinations in which further risk analysis might be performed.
From a regulatory viewpoint, FSANZ will be undertaking a scientific assessment of
the hazards that occur for meat, due to be completed in mid 2009. This work will be
used to underpin the broadening the scope of Standard 4.2.3 – Primary Production
and Processing Standard for Meat of the Food Standards Code to include
requirements for primary production. The standard currently only contains
requirements for producers of RTE meat products.
Beef and sheepmeat

There are a significant number of pathogens that may be associated with livestock
(Table 8). Bacterial pathogens such as Salmonella spp. and pathogenic E. coli can
persist for extended periods of time in the farm environment, where they may
contaminate feed, water, pasture, farm equipment through to individual animals or
entire herds. It is well established that cattle are a major reservoir for pathogenic

organisms such as Clostridium perfringens, Campylobacter jejuni, pathogenic
Escherichia coli and Salmonella spp. in their gut, but pathogens have also been
isolated from the rumen, caecum, colon and rectum (McEvoy et al, 2004). From
these locations, pathogens are frequently transferred to the exterior, such as the
hide and hooves. In addition, sheep, cattle and pigs grazing on contaminated
pastures can become infected with the encysted form of the parasite Toxoplasma
gondii.
Because livestock may serve as a reservoir for pathogens, it is not surprising that a
number of these animals will carry pathogens into the abattoir environment. While
the muscle tissue of healthy live animals is essentially sterile at the time of slaughter,
the external surfaces of carcases may become contaminated during de-hiding and
dressing, and if the intestinal tract is punctured and the gut contents escape. This
can also lead to direct or indirect contamination of equipment and workers during
dressing and processing, which may further contribute to carcase cross
contamination.
Internationally, risk assessment work on the meat industry has tended to
concentrate on specific hazards such as E. coli O157:H7 in hamburgers (Cassin et al,
1998) and in tenderised meat (FSIS, 2002). Although a hazard of concern
internationally, in particular the USA, the prevalence of E. coli O157:H7 on Australian
carcases appears to be very low and it does not appear to be a significant source of
foodborne illness in Australia.
In addition to the traditional bacterial pathogens, world-wide attention became
acutely focussed on the possible acquisition of variant Creutzfeldt-Jakob Disease
(CJD) from Bovine Spongiform Encephalopathy (BSE) infected animals. However,
under the assessment of Geographical BSE Risk (GBR), Australian livestock are
considered “highly unlikely” as having BSE (EFSA, 2007). The potential risk factors
for BSE have been addressed through the implementation of appropriate control
measures within Australia, and therefore, BSE will not be further considered in this
risk assessment.
Pigmeat
Pigs are often associated with the carriage of Yersinia enterocolitica, appearing to be
the primary source of Yersinia infections in humans caused by bioserotype 4,O:3
(Barton & Robins-Browne, 2003). The pork tapeworm Taenia solium (larval stage
Cysticercus cellulosae) and the nematode worm Trichinella spiralis are often
associated with pork overseas. However these organisms are not present in
Australian pigs (DAFF, 2004), and are therefore are not further considered in this risk
assessment.

Table 8 – Microbiological hazards in livestock and poultry
Livestock Poultry
Pathogenic bacteria
pathogenic Escherichia coli Salmonella spp.
Salmonella spp. Campylobacter jejuni
Brucella
Campylobacter jejuni
Yersinia enterocolitica
Coxiella burnetii
Listeria monocytogenes
Staphylococcus aureus
Bacillus anthracis
Clostridium spp.
Mycobacterium bovis
Streptococcus spp.
Parasites
Cysticercus bovis
Cysticercus ovis
Onchocerca spp.
Taenia saginata
Toxoplasma gondii
Prions
Bovine Spongiform Encephalopathy (BSE)
adapted from Sumner (2002); FSANZ (2005)
The rate of carriage of the pathogenic organisms in the gut by livestock may be
affected by factors such as animal handling, husbandry techniques and other on-
farm practices that can affect animal health. Practices such as co-mingling of
animals, intensive rearing methods and stress (such as starvation and transport)
have been shown to increase the shedding and transmission of pathogens in
animals.
Chemical hazards in the red meat industry were assessed as part of the risk profile
conducted by the MLA. This work found that the current system for registering and
monitoring the use of chemicals in the meat industry to be well managed. The
incidence and levels of residue contamination reported by the National Residue
Survey (NRS) and the Australian Total Diet Survey (ATDS) are very low. In instances
where chemical residues have been detected in meat, the levels found have been too
low to be considered a public health risk
The MLA risk profile could find no data on physical hazards.

Poultry meat
Internationally, a huge amount of resources have been employed to undertake risk
assessment work on poultry. This work has concentrated on the pathogens
considered to be most significant, namely Salmonella (FAO/WHO, 2001; WHO/FAO,
2002) and Campylobacter (FAO/WHO, 2003).
While in Australia, FSANZ has undertaken a comprehensive scientific assessment of
the poultry meat industry to underpin the development of Standard 4.2.2 - Primary
Production and Processing Standard for poultry meat (FSANZ, 2005). This work
considered:
♦ the extent of food safety risk associated with the consumption of poultry meat
and poultry meat products in Australia
♦ the factors along the poultry meat supply chain that have the greatest impact on
public health and safety.
A range of microbiological hazards may be introduced to poultry meat during the
primary production stages. These include bacterial pathogens that may contaminate
breeding stock, feed, water and the environment. The FSANZ scientific assessment
considered Salmonella spp., Campylobacter spp., pathogenic E. coli, Staphylococcus
aureus, Clostridium perfringens and L. monocytogenes as potential hazards in poultry
meat.
Poultry are exposed to Salmonella via sources such as feed or through environmental
contamination. Once infected, a bird will excrete large numbers of salmonellae in its
faeces which can lead to rapid spread throughout the flock. Salmonella positive birds
at the time of slaughter have high numbers of organisms in their intestines as well as
on external surfaces. Slaughtering and processing operations have the potential to
contaminate the poultry carcase with faecal material and to facilitate cross-
contamination between pathogen-positive birds and pathogen-negative birds, leading
to increased prevalence of Salmonella in finished products. This may occur at various
stages of processing including unloading of birds, scalding, plucking, evisceration,
washing and chilling. Care must be taken during evisceration to ensure the viscera is
not damaged or ruptured as this can lead to significant contamination of the carcase.
The means by which broiler chickens become exposed to contamination with
Campylobacter during primary production is multi-factorial (FSANZ, 2005). Numerous
factors in combination result in the introduction and spread of the organism within a
flock. Campylobacter will colonise individual birds at two or three weeks of age, and
usually within a week virtually all birds in the flock will become infected. Horizontal
transmission is mainly through contaminated water, litter, insects, rodents, and wild
birds and by farm workers via their boots (Wallace, 2003). The implication of this is
that unless a flock is Campylobacter free, virtually all birds in a positive flock will be
carrying Campylobacter in their intestinal tract at the time of slaughter in high
numbers.
The FSANZ risk assessment concluded that although poultry meat may occasionally
be contaminated with other pathogens, Salmonella and Campylobacter are the
primary pathogens of concern and risk management strategies should be targeted to
controlling these organisms (FSANZ, 2005). These two organisms are the leading
causes of foodborne illness in Australia each year and are frequently isolated from
raw poultry meat. They become associated with poultry during primary production
and their prevalence and/or levels may be amplified during primary processing and
further handling through to consumption.

The FSANZ risk assessment found that the risk associated with the other pathogens
was primarily a concern during the production of processed poultry meat products
and temperature abuse of RTE poultry products (FSANZ, 2005). The hazards
associated with further processing of poultry meat are outlined in the sections on
processed meat.
Game meat
The main species harvested as game meat are kangaroo and pigs. Very little data
exists for hazards in game meat, however kangaroo meat has been studied in some
depth as the industry attempts to market the product to increase consumption rates
in the general population. Kangaroo meat is anecdotally stated as being a particular
risk for toxoplasmosis and salmonellosis, however it appears as if there is little
evidence to substantiate that kangaroo meat has Salmonella rates higher than other
animals, and there is no known case of toxoplasmosis being transmitted by eating
kangaroo meat in Australia.
There is a risk of physical hazards in game meat, however strict guidelines exist for
the harvesting of product. The animal must be head shot, not only to ensure a quick
kill but also to prevent damage to the skin, carcase and internal organs which are
required for inspection purposes, and to limit the potential for shot to contaminate
the meat.
Processed meats
The risk posed by processed meats, such as manufactured and fermented meats was
highlighted in the National Risk Validation Project (Food Science Australia & Minter
Ellison Consulting, 2002), with these products classified as a high risk and earmarked
for the introduction of food safety programs. The pathogens of significance for
processed meats were identified as L. monocytogenes, Salmonella and pathogenic
E. coli, as these had been previous causes of foodborne illness outbreaks in
Australia.
The primary sources of contamination for processed meats includes the
contaminants associated with raw meat (eg pathogenic E. coli, Clostridium spp.),
other ingredients such as spices (eg Salmonella spp.) and from the processing
environment (eg L. monocytogenes), especially for products that are subject to
further processing such as slicing.
Control of these organisms is normally through appropriate processing with Critical
Control Points (CCPs) to inactivate these pathogens, such as cooking, fermentation
with starter cultures and curing. However, this does not eliminate any contamination
that occurs post-processing, and as such L. monocytogenes has been the cause of
many recalls of processed meats (Table 62 in Appendix 2) and responsible for
several very large outbreaks overseas from RTE processed meat products.
A potential chemical hazard with processed meat is the inclusion of preservatives
such as sorbate and nitrate salts, particularly for cured products, in exceedance of
limits in the Food Standards Code.

Exposure assessment
Consumption of meat
Daily consumption of meat and meat products was assessed during the National
Nutrition Survey (ABS, 1995), which examined overall consumption of meat,
including poultry and processed meats. The survey showed that approximately three
quarters of the Australian population regularly consume meat and meat products,
with males consuming slightly higher levels than females (Table 9). Consumption of
specific types of meat was estimated in the ABARE report (ABARE, 2007) and by MLA
through production statistics (MLA, 2008a; MLA 2008b).
Beef
Consumption of beef and veal in 2006 was estimated by ABARE at 38.1 kg per
person per year, while MLA estimates beef consumption alone at 35.6 kg beef per
year (MLA, 2008a). Consumption of beef and veal has been steadily decreasing since
the peak consumption period of the late 1970s.
Sheepmeat
Australians are among the highest consumers of lamb in the world, consuming
11.4kg of lamb and 2.7kg of mutton per person every year (MLA, 2008b).
Pigmeat
A considerable amount of the 23.5 kg pork consumed by each person per year is
eaten as processed product (see consumption of processed meats). Consumption of
fresh pork in 2006 was estimated at 11.1 kg per person (APL, 2008).
Consumption of poultry meat

Annual per capita consumption of poultry meat in 2006 was estimated at 39.5 kg
(ABARE, 2007). Chicken consumption accounts for approximately 95% of all poultry
consumed, with the annual consumption of turkey and duck in Australia estimated at
1.6 kg and 0.5 kg per person respectively (FSANZ, 2005). FSANZ estimated the total
number of poultry servings in Australia annually to be 2,880,000,000, with an
average serving size of 250g.
Consumption of game meat

Very little consumption data specific to game meat is available, and when compared
to the major meat categories, forms a very small part of the average persons diet.
Ampt & Owen (2008) surveyed consumer attitudes towards the consumption of
kangaroo meat and found that 58.5% of respondents had tried the meat, with
14.5% having eaten kangaroo meat at least 4 times in the past year (classed as
“medium to high” consumers). In NSW/ACT there were 549 respondents surveyed,
with 14.2% were classified as medium to high consumers, 19.5% were non
consumers, 43.9% were one-off or low consumers and 22.4% objected to eating
kangaroo meat. Men were marginally more likely to consume kangaroo than women.
Ampt & Owen (2008) went on to report that although there had been considerable
changes in the kangaroo industry over the past 10 years, with the widespread
availability of kangaroo in domestic supermarkets, the industry still remains reliant on
export markets.

Table 9 – Consumption of meat and meat products in Australia
Sex Age Proportion of persons Median daily intake for consumers

consuming meat, poultry, of meat, poultry, game products
5 and dishes
game products and dishes
(%) (g/day)
Male 2-3 76.7 62.7

Male 4-7 72.4 84.3
Male 8 - 11 77.0 115.6
Male 12 - 15 78.8 143.0
Male 16 - 18 80.9 196.0
Male 19 - 24 84.1 224.0
Male 25 - 44 84.4 191.8
Male 45 - 64 87.6 168.0
Male 65+ 84.7 126.5
Female 2-3 71.7 52.3

Female 4-7 73.6 77.9
Female 8 - 11 78.3 95.3
Female 12 - 15 80.2 113.1
Female 16 - 18 74.5 131.0
Female 19 - 24 74.0 141.4
Female 25 - 44 76.9 126.0
Female 45 - 64 77.5 114.3
Female 65+ 79.7 83.0
Table 10 – Consumption of processed meats in Australia

Product category Daily serving size (grams per person)
Processed meats 28 – 58
(hams, whole muscle cooked meats)
Cooked sausages (frankfurters, saveloys) 63 – 108
Pâté and meat paste 40 - 56
adapted from MLA (2006)
5
Meat, poultry and game meat products and dishes are defined in the National Nutrition Survey (ABS, 1995) as
including the following:
- muscle meat,
- poultry and other feathered game,
- organs meats and offal, products and dishes,
- sausages, frankfurts and saveloys,
- processed meat,
- mixed dishes where beef or veal is the major component,
- mixed dishes where lamb or pork, bacon or ham is the major component,
- mixed dishes where poultry or game is the major component

Consumption of processed meats
The MLA (2006) reported consumption data for categories of processed meats, on
any given day between 20 and 50% of the population consume processed meats.
The amounts consumed are shown in Table 10. Consumption of processed pig meat,
as bacon and ham, contributes approximately 14.4 kg per person per year (APL,
2008).
Foodborne illness outbreaks from meat and meat products
Table 11 summarises the foodborne illness outbreaks attributed to all meat and meat
products, including poultry, game meat and processed meat. This data also includes
outbreaks where meat was an ingredient in an implicated food (more detailed
information on each outbreak is included in Table 66 in Appendix 3).
Meat
The European Food Safety Agency (EFSA, 2008) evaluated the relative contribution
of different meat categories to cases of foodborne salmonellosis infections in humans
and found that poultry was more often implicated than beef, pork and lamb. Adak et
al (2005) used data from foodborne illness outbreaks in England and Wales to
attribute to source of various types of meats. In this study the most important cause
of foodborne illness was chicken (398,420 cases, 141 deaths) while red meat was
also a very significant source (287,485 cases, 164 deaths).
Table 11 – Summary of foodborne illness outbreaks attributed to all meat

(including poultry, game meat and processed meat products)
outbreaks
(1995-2008)
Campylobacter spp 14 106 2 0
Toxin 6 520 0 0
Norovirus 5 201 5 0
Viral 5 175 0 0
S. aureus 4 51 5 0
B. cereus 2 20 0 0
L. monocytogenes 1 32 0 0
Pathogenic E. coli 1 173 0 1
Shigella spp. 1 13 0 0
Unknown 63 766 5 0
Total 203 4690 114 3

Three major microbiological baseline surveys have been undertaken by MLA of red
meat processed in Australian abattoirs (MLA, 2000; MLA, 2005). These surveys
provide a useful indication of the prevalence and levels of hygiene indicators such as
Total Viable Count (TVC), as well as pathogens such as Escherichia coli O157:H7 and
Salmonella spp. on carcases and in boneless meat (see Table 12). The surveys have
shown an improvement in both the prevalence and levels of microbiological
contamination every 5-6 years that the surveys have been conducted. This has been
attributed to significant improvements in hygiene and sanitation during primary
processing and efficient cooling of carcases.
A baseline survey of NSW abattoirs by the NSW Food Authority (Bass et al, 2008)
found a strong commitment to food safety and that facilities were managing food
safety issues well. Surveys of carcase and meat portion load-out temperatures found
that 96% of product complied with temperature requirements, however only 38% of
offal samples complied. The microbiological hygiene of beef carcases sampled were
categorised as excellent 6 or good, with TVC counts ranging from 0.48 log cfu/cm2 to
3.95 log cfu/cm2. One quarter of the beef carcases sampled tested positive for
E. coli. This prevalence is higher than that found in the national MLA surveys, but the
levels detected were quite low, with counts ranging from -0.89 log cfu/cm2 to 0.69
log cfu/cm2. Almost all sheep carcases (lamb/hogget/mutton) were rated as excellent
or good for TVC and E. coli respectively. The sheep TVC counts ranged from 0.30 log
cfu/cm2 to 5.47 log cfu/cm2. Just over half (53%) of the sheep carcases tested were
positive for E. coli, counts ranging from -0.48 log cfu/cm2 to 2.24 log cfu/cm2. The
hygiene results for pig carcases showed that 80% were rated as excellent or good
for TVC, and 91% rated as excellent or good for E. coli. The pig TVC counts ranged
from 0.85 log cfu/cm2 to 5.03 log cfu/cm2. The percentage of carcases testing
positive for E. coli was 63%, with counts ranging from -1.10 log cfu/cm2 to 1.30 log
cfu/cm2.
European surveillance schemes have found the proportion of fresh beef positive for
Salmonella spp. to be below 0.6% at slaughter, with higher levels at retail (8.3%)
(EFSA, 2008). Despite worldwide consumption of lamb and mutton, these products
have rarely been associated with salmonellosis in humans.
There has been a two pronged approach to controlling hazards in the meat industry.
Hazards related to zoonotic diseases have been controlled through the application of
preventative programs, such as the Brucellosis and Tuberculosis eradication
campaign (BTEC), which was aimed at eradicating brucellosis and tuberculosis from
all Australian cattle. As a result, Australia has been free of brucellosis caused by
Brucella abortus since 1989 and bovine tuberculosis-free status was achieved in
1997, which is now assessed through the Tuberculosis Freedom Assurance Program
(TFAP) and National Granuloma Submission Program (NGSP).
6
Meat Standards Committee (2002) – Microbiological testing for process control in the meat industry - guidelines
defined the following categories:
- Total Viable Count (TVC)
Excellent (<103 cfu/cm2)
Good (103-104cfu/cm2)
Acceptable (104–105cfu/cm2)
Marginal (105-106cfu/cm2)
- E. coli
Excellent (not detected)
Good (>0-10 cfu/cm2)
Acceptable (10-100cfu/cm2)
Marginal (100-103cfu/cm2).

Table 12 – Prevalence of microbiological hazards in Australian beef and sheep
meat
1993-93 survey 1998 survey 2004 survey
Beef carcases
Number of samples 1043 1268 1155
TVC (mean log cfu/g) 3.02 2.43 1.33
E. coli (%) 19 11 4.9
S. aureus (%) 128/465 (27.5%) 3.9 20.1
Salmonella (%) 4/1043 (0.38%) 0.6 0
E. coli O157:H7 (%) 4/1036 (0.38%) not detected 0.1
Listeria 4/190 (2.1%)
Campylobacter 2/753 (0.26%) 0
Boneless beef
E. coli (%) 16.7 5.1 1.1
S. aureus (%) n/a 17.5 2.6
Salmonella (%) 6/921 (0.65%) 0.1 0.1
E. coli O157:H7 (%) 0/804 (not detected) not detected 0
Boneless sheepmeat
E. coli (%) 47.7 24.5 4.3
S. aureus (%) n/a 38.6 14.1
Salmonella (%) 27/415 (6.5%) 1.3 0.5
E. coli O157:H7 (%) 1/342 (0.3%) 1.3 0.2
adapted from MLA (2000); MLA (2005)
NSW legislation requires that any abattoir processing meat must comply with the
AS4696:2007 the Australia Standard for the hygienic production and transportation
of meat and meat products for human consumption (FRSC, 2007c). As part of
compliance with this standard, all abattoirs must have qualified meat safety
inspectors (meat safety officer) to conduct ante-mortem inspections of livestock prior
to slaughter. This is used to identify any stock suspected of carrying infectious
zoonotic diseases, which may then be culled to prevent spread to healthy stock. On-
line post-mortem inspection in abattoirs is used to identify and excise diseased
tissues and organs and/or to exclude diseased carcases from human consumption.
Many studies have been undertaken to assess the influence of different processing
practices in contributing to microbial contamination of carcases. Widders et al (1995)
showed that the level of microbial contamination meat was influenced by the level of
carcase contamination at boning, and by the boning process itself. If carcases were
heavily contaminated, the contamination of processing surfaces was irrelevant in

determining eventual microbial loads on meat. However, where carcase
contamination was at low to moderate levels, cutting boards were a major source for
microbial dissemination during the boning process. It was shown that improved
sanitation of cutting surfaces in the boning room could result in a significant
reduction in microbial contamination on the surface of meat.
Special control measures have also been implemented to target specific hazards of
concern in pigs. In order to minimise pig carcase contamination with Y. enterocolitica
during slaughter, the tongue and pharynx are removed early in the slaughter process
to reduce the leakage of saliva and contaminated material from the tongue and
tonsils onto the carcase (Barton & Robins-Browne, 2003).
The NRS and Australian Total Diet survey results show that misuse of agricultural
and veterinary chemicals within the meat industry is low, with most analyses
returning either no detectable residues or residues well below established legal limits.
As a result, the Australian dietary exposure to pesticides and contaminants falls well
within acceptable health standards (MLA, 2003).
Poultry meat
The FSANZ poultry risk assessment summarised OzFoodNet data for foodborne
illness outbreaks in Australia from poultry meat products (FSANZ, 2005). Between
1995 and 2002 they reported 46 outbreaks involving 1170 cases. The data in Table
66 of Appendix 3 includes and updates the outbreaks from the FSANZ report. From
1995-2008, 94 outbreaks were attributed to products containing chicken, affecting
1815 people and 54 requiring hospitalisation. In addition to these outbreaks, another
6 outbreaks were observed in institutional settings serving vulnerable persons.
Details on these outbreaks are included in Table 69 of Appendix 3. A case control
study conducted on foodborne illness outbreaks in New Zealand concluded that
consumption of raw and undercooked chicken was the most important source of
human campylobacteriosis (Eberhart-Phillips et al, 1995).
The EFSA (2008) reported prevalence of Salmonella in EU member countries at
slaughter ranging from 5.7% to 21.5%, while prevalence in fresh turkey meat varied
from 0 to 11%, fresh duck meat from 15 to 39% and 10% in fresh geese meat.
Although data is not readily available for contamination rates at slaughter for
Australian birds, a survey of retail chicken in NSW found 47.7% of poultry samples
contained low levels of Salmonella. However, of the Salmonella serovars
approximately 65% were the serovar S. Sofia, considered of very low virulence to
humans. In addition, 87.8% of poultry samples were found to be contaminated with
Campylobacter (Pointon et al, 2008, summarised in Table 13.
All facilities slaughtering and processing poultry in NSW are required to comply with
AS 4465:2005 the Australian Standard for the Construction of Premises and Hygienic
Production of Poultry Meat for Human Consumption (FRSC, 2007a). This requires
ante-mortem inspection of poultry presented for slaughter to reject any moribund,
unhealthy or diseased birds and post-mortem inspection to identify and apply a
disposition to any carcase and parts that are not considered wholesome for human
consumption.
In addition to the regulatory requirements, there are various industry codes of
practice and guidelines, such as the National Biosecurity Manual Contract Meat
Chicken Farming (ACMF, 2003), Model Code of Practice for the Welfare of Animals -

Land Transport of Poultry (PISC, 2006). These Codes of Practice concentrate on
prevention of animal disease and welfare aspects, with potential implications for food
safety. The extent of compliance with these control measures varies within the
poultry industry, depending on whether it is a legislative requirement or a voluntary
scheme.
Table 13 – Prevalence of microbiological hazards on chicken meat in NSW

Retailer Product Salmonella Campylobacter
Number Mean Non- Number Mean
positives / concentration Sofia positives / concentration
total ± SD (%) total ± SD
samples samples
(%) (%)
Butcher Skin off 18/28 (64.3) -1.31 ± 0.58 7.1 27/28 (96.4) 1.14 ± 0.57
Skin on 29/47 (61.7) -1.18 ± 0.70 44.7 40/47 (85.1) 1.24 ± 0.64
Whole 7/9 (77.8) -1.70 ± 0.95 0.0 8/9 (88.9) 1.11 ± 1.00
bird
Supermarket Skin off, 21/37 (56.8) -1.41 ± 0.33 13.5 35/37 (94.6) 1.06 ± 0.35
bulk
Skin off, 39/106 -1.38 ± 0.41 16.0 95/106 0.90 ± 0.27
tray (36.8) (89.6)
Skin on, 28/50 (56.0) -1.43 ± 0.47 18.0 42/50 (84) 0.82 ± 0.23
bulk
Skin on, 63/150 -1.48 ± 0.67 9.3 124/150 0.66 ± 0.36
tray (42.0) (82.7)
Whole 11/37 (29.7) -1.75 ± 0.76 5.4 34/37 (91.9) 0.61 ± 0.53
bird
Specialty Skin off 14/28 (50.0) -1.33 ± 0.58 21.4 25/28 (89.3) 1.04 ± 0.35
store
Skin on 28/47 (59.6) -1.38 ± 0.60 21.3 44/47 (93.6) 0.90 ± 0.35
Whole 4/10 (40.0) -2.05 ± 0.04 10 8/10 (80) 0.77 ± 0.37
bird
TOTAL 262/549 -1.42 ± 0.60 15.8 482/549 0.87 ± 0.45

(47.7) (87.8)
adapted from Pointon et al (2008)
The high risk factors for poultry becoming contaminated with Salmonella or
Campylobacter were identified in the FSANZ scientific assessment (FSANZ, 2005).
The development of Standard 4.2.2 - Primary Production and Processing Standard for
poultry meat in the Food Standards Code aims to reduce the contamination of
poultry, poultry carcases and poultry meat by pathogenic Salmonella and
Campylobacter through the implementation of control measures on farm, as well as
maintain existing control measures during processing at abattoirs.

Game meat
NSW legislation requires that harvesting facilities, primary processing and storage
facilities and vehicles comply with AS4464:2007the Australian Standard for the
hygienic production of wild game meat for human consumption (FRSC, 2007b). This
requires that all carcases are subject to inspection by a qualified meat safety
inspector and temperature control of the carcase is maintained. There is no data to
indicate that game meat has been the subject of any foodborne illness outbreaks or
recalls. There is also no recent data to indicate prevalence of microorganisms on
game meat carcases, although it is assumed that with similar control measures in
place to the broader meat industry, that the prevalence of pathogens may be similar.
The incidence of zoonoses and other public health risks from kangaroo meat was
investigated and summarised by Andrew (1988), quoted in Pople & Grigg (1999).
The work summarised the records of inspections between 1980 and 1987 made of
carcases by AQIS officers at export game meat establishments. Of the 204,052
kangaroo carcases harvested, 196,104 were passed as fit for human consumption
and 7,948 were rejected. Of those rejected, 81% were rejected for reasons not
associated with parasites or pathology, mainly poor handling, particularly inadequate
refrigeration. Of the rest, 1,452 were rejected because of a nematode parasite,
Pelicitus roemeri, which is harmless to humans but is considered unsuitable for
human consumption.
Processed meat products

Processed meat products have been implicated in several large scale food poisoning
outbreaks, both overseas and within Australia (see Table 14; Table 66 of Appendix
3). For the period 1991-2000, the National Risk Validation Project identified greater
than 323 cases of foodborne illness and one death attributed to the consumption of
fermented meats, with a further 97 cases and two deaths attributed to manufactured
meat products. The pathogens implicated in these outbreaks were pathogenic E. coli,
L. monocytogenes and Salmonella and the total cost of foodborne illness associated
with fermented and manufactured meats was calculated to $77 million per year
(Food Science Australia & Minter Ellison Consulting, 2002)
The most significant outbreak from a processed meat product occurred in 1995 in
South Australia from Garibaldi-brand Mettwurst, with over 150 people ill and the
death of a young child. Well controlled fermentation and maturation should achieve a
low pH and water activity to eliminate any pathogens present in the raw meat
ingredient, however uncontrolled fermentation, as was the case with the Garibaldi
product, can lead to survival of pathogens. This outbreak led to changes to the Food
Standards Code and regulations regarding the manufacture of uncooked comminuted
fermented meats.
An outbreak of listeriosis from Conroy’s smallgoods occurred in South Australia in
2005, resulting in three deaths of hospital patients. Listeria was isolated from the
slicing machines in the factory used to slice the deli meats. Details are included in
Table 69 in Appendix 3, as the food was served to vulnerable persons. The cost of
the subsequent recall by Conroy’s was in the order of $2 million. A Canadian
outbreak in 2008 from Maple Leaf Foods Inc. resulted in 20 deaths, and the resultant
recall of more than 220 product lines and settlements from class action lawsuits was
in the order of $27 million (AUS$ 33 million).

The manual handling associated with preparing and packaging processed meat
products tend to lend themselves to contamination with L. monocytogenes. Surveys
have shown a significant number of RTE processed meat products are contaminated
with this organism (
Table 15). Sliced meats in particular tend to have high contamination rate with
L. monocytogenes, although actual numbers of organisms are quite low. The long
shelf life associated with these products (~ 6 weeks) can allow growth of the
organism to occur. Advice provided to susceptible persons, such as pregnant women,
is to avoid consuming pre-packaged sliced meats. Table 62 of Appendix 2 shows the
number of recalls from RTE processed meats from 2004-2008, during which time
there have been 33 recalls, mostly due to contamination with L. monocytogenes.
NSW legislation requires that any facility producing processing meat must comply
with AS4696:2007 the Australia Standard for the hygienic production and
transportation of meat and meat products for human consumption (FRSC, 2007c). In
addition to this, there are industry produced documents such as Guidelines for the
safe manufacture of smallgoods (MLA, 2003) and Listeria monocytogenes in
smallgoods: Risks and controls (MLA, 2006) which provide information on hygiene
and sanitation and CCPs for controlling hazards.
Table 14 – Foodborne illness outbreaks of listeriosis from processed meats

Year Country Processed meat Cases Deaths
1987-89 United Kingdom Pâté 366 94
1990 WA Pâté 11 6
1992 France Jellied pork 279 85
tongue
1993 France Pork rillettes, pâté 39 11
1996 SA Diced chicken 5 1
1998-99 USA Hot dogs and deli 101 21
meats
1999 France Ham rillettes >6 2
1999 USA Pâté 11 3
1999 France Jellied pork 23 7
tongue
2000 New Zealand Corned beef 2 -
2000-01 USA Turkey franks >29 >7
2002 USA Deli meats >50 11
(poultry)
2005 SA Corned beef 5 3
2008 Canada Deli meats 50 20
adapted from MLA (2006); Doolittle (2008)

Table 15 – Prevalence of Listeria monocytogenes in processed meats
Product category Contamination rate (%)
Processed meats (hams, whole muscle cooked 4.8
meats)
Cooked sausages (Frankfurters, saveloys) 2.8
Pâté and meat paste 1.2
adapted from MLA (2006)

Meat
The MLA risk profile examined the risk of fresh meats consumed in the home and
found that meat consumed as cuts, roasts, chops, steak are low risk (MLA, 2003).
These products normally receive a cooking step by the end consumer that will
reliably eliminate most pathogenic bacteria. However, the importance of cross
contamination from pathogens in raw and undercooked meat across to RTE foods
was highlighted by Lake et al (2004) as a potential source of infection from Yersinia
in pork (Table 16), and as a potential source for large numbers of Salmonella food
poisoning cases (Table 17). It was predicted that if the cross contamination rate of
Salmonella from raw meat increased from 1% to 10% would result in almost an
extra 4800 case, while an increase to a 50% cross contamination rate would result in
more than 26,000 cases of foodborne illness in Australia each year, where fresh
meat was the cause (MLA, 2003).
Another hazard categorised as high risk by the MLA risk profile was consumption of
undercooked sheep meat or liver contaminated with Toxoplasma gondii, particularly
for pregnant women (MLA, 2003). This area was identified as a data gap in work
undertaken on the New Zealand meat industry by Lake et al (2002b). While it was
predicted there may be more than 600 cases of illness due to infection Toxoplasma
gondii per annum (200 in pregnant women), further work was required to fully
understand the risk factors involved.
Undercooked meat and hamburgers is associated with survival of pathogenic E. coli
being ranked as a medium hazard in some instances. However, a study by the FSIS
(2002) in the USA calculated the probability of illness occurring as extremely low.
This work estimated that the probability of E. coli O157:H7 surviving in a piece of
cooked steak was 0.000026% (2.6 of every 10 million servings), given normal
cooking practices. It was shown that even inadequate cooking of meat would still
reduce the numbers of pathogenic E. coli present on the meat, albeit to a lesser
degree than proper cooking. The predicted number of food poisoning cases from
E. coli O157:H7 in cooked steaks was calculated to be 1 case for every 15.9 million
servings (FSIS, 2002). The risk of illness from pathogenic E. coli in New Zealand
meat was considered low by Lake et al (2002a), as there was no data to link illness
to pathogenic E. coli in that country. The risk from comminuted meat such as
hamburgers is considered greater, as the contamination may be spread throughout
the product, as opposed to just the surface on an intact steak. The MLA risk profile
estimated that if all hamburgers were appropriately cooked, there would be no
illness, however if 20% of hamburgers were undercooked, there would be 6 illnesses
per annum (MLA, 2003).
The NZFSA also commissioned risk profile work on tuberculosis (Cressey et al, 2006)
and Campylobacter (Lake et al, 2007c) from red meat, and both were considered low
risk (Table 16). These were not examined in the MLA risk profile, as Australia has
been declared tuberculosis free and a definitive association of Campylobacter with
red meat could not be established (MLA, 2003).
The risk from C. perfringens from meat consumed in the home was considered
medium (Table 17), with poor cooling and reheating the main contributing factors.
Problems with C. perfringens have arisen more in large scale catering-type

operations than in the home, where the spore forming bacteria have been allowed to
germinate and grow due to poor cooling of meat-based dishes.
Table 16 – NZFSA risk profile outcomes examining hazards in meat

Hazard Risk
Shiga toxin-producing Escherichia Overseas studies have consistently linked human cases of STEC
coli in red meat and meat products infection and particularly E. coli O157:H7 to consumption of red
(Lake et al, 2002a) meat in the form of undercooked hamburgers, not one case in
New Zealand has been associated with regulated foods.
Toxoplasma gondii in red meat Toxoplasma gondii is a protozoan parasite that causes disease in
and meat products humans with a range of outcomes including, at worst,
(Lake et al, 2002b) miscarriages. Cysts in the muscle tissue of meat animals may
result in infection when eaten. The significance of human
infections, especially congenital toxoplasmosis, in New Zealand is
unknown and has been identified as a knowledge gap
Yersinia enterocolitica in pork Pigs are known to be frequently contaminated with
(Lake et al, 2004) Y. enterocolitica, but effective cooking or pasteurisation will
eliminate Y. enterocolitica from foods. Pork consumption has
consistently been associated with yersiniosis in studies in New
Zealand and overseas, with cross contamination from uncooked
meats to RTE foods a potential source of infection.
Mycobacterium bovis in red meat A proportion of human tuberculosis cases have been caused by
(Cressey et al, 2006) Mycobacterium bovis. While transmission of tuberculosis to
humans through consumption of M. bovis-infected meat is
possible, no cases of this have been confirmed in New Zealand
and it is considered low risk.
Campylobacter jejuni/coli in red Seventeen outbreaks of campylobacteriosis in New Zealand from
meat 1999 to 2004 have been associated (weakly) with red meat
(Lake et al, 2007c) consumption. Data in New Zealand indicates there is low but
consistent contamination across pork, beef, and sheep meat. On
this basis it is identified as a minor risk factor for exposure to
Campylobacter in New Zealand.

Table 17 – Risk ranking for meat and meat products
Meat product Hazard Severity 7 Probability Growth Effect of Consumer Epidemiological Risk Predicted
required production, does link rating annual
to cause processing, pathogen number of
illness handling on reduction illnesses (in
the hazard ↓↑→ step Australia) 8
Retail meats consumed in the home (steak, mince, chops, roast, fresh sausages)
Consumed Toxoplasma gondii IB Medium No ↓freezing, → Yes/No Yes High 715 (242 in
undercooked/raw pregnant
women)
Consumed EHEC IB Low Yes ↓→ Yes Yes Medium No estimate
undercooked
Reheated roasts C. perfringens III Low Yes ↓↑ No Yes Medium No estimate
Reheated roasts S. aureus III Medium Yes ↓↑ No Yes Low No estimate
Aeromonas III Low Yes ↓↑ Yes No Low No estimate
Potential pathogen Mycobacterium III/IB Low N/A ?? ?? ?? Low No estimate
paratuberculosis
Poor cooling Bacillus III Low? Yes ↓↑ Yes ??No Low No estimate
Yersinia enterocolitica III Low?? Yes ↓↑ Yes ? Low No estimate
7
ICMSF (2002) defines the level of severity as follows:
− IA – Severe hazard for general population, life threatening or substantial chronic sequelae or long duration
− IB – Severe hazard for restricted populations, life threatening or substantial chronic sequelae or long duration
− II – High hazard incapacitating but not life threatening sequelae rare moderate duration.
− III – Moderate, not usually life threatening no sequelae normally short duration symptoms are self limiting can be severe discomfort.
8
Data from Sumner (2002) predicted annual numbers of illness per annum for the South Australia population (1.5 million), the MLA Risk Profile (MLA, 2003) used an Australian population figure
of 19.7 million. These estimates have been extrapolated to the current population of Australia estimated by ABS (2009) as approximately 21.6 million, by multiplying by a factor of 14.4 and 1.1
respectively.

Meat product Hazard Severity 7 Probability Growth Effect of Consumer Epidemiological Risk Predicted
required production, does link rating annual
the hazard ↓↑→ step Australia) 8
Retail meats consumed in the home (steak, mince, chops, roast, fresh sausages)
Assume 1% cross Salmonella II/IB Low Yes ↓↑ Yes Yes Medium 583
contamination rate
Assume 10% cross Salmonella II/IB Low Yes ↓↑ Yes Yes High 5,830
contamination rate
Assume 50% cross Salmonella II/IB Low Yes ↓↑ Yes Yes High 29,370
contamination rate
Enterohaemorrhagic E. coli in hamburger
Hamburgers EHEC IA/IB Low No ↓→ Yes - Yes Low 0
Hamburgers - assume EHEC IA/IB Low No ↓→ Yes Yes Low 7
50% undercooked
Hamburgers Salmonella II/IB Low Yes ↓→ Yes Yes Low 0
adapted from Sumner (2002); MLA risk profile (MLA, 2003)

Table 18 – Risk ranking for processed poultry meat products
Processed Hazard Severity Probability Growth Effect of Consumer does Epidemiological link Risk Predicted
meat required to production, pathogen rating annual
product cause processing, reduction step number of
illness handling on the illnesses
hazard ↓↑→ (in
Australia) 9
Processed Salmonella II/IB Low Yes ↓ No Yes High 864
chicken
Processed Campylobacter IB Low Yes ↓↑ No Yes High 86,400
chicken
adapted from Sumner (2002)
Table 19 – NZFSA risk profile outcomes examining hazards in poultry meat

Hazard Risk
Salmonella (non-typhoid) in poultry (whole and pieces) Salmonellosis is the second most frequently notified enteric disease in New Zealand. Poultry meat is regarded as an
(Lake et al, 2004) important source of infection
Campylobacter jejuni/coli in poultry Campylobacter is the most frequently notified cause of enteric disease in New Zealand. Consumption of chicken was
(Lake et al, 2007a) linked with Campylobacter infection and several outbreaks of campylobacteriosis identified undercooked chicken as
the transmission vehicle
Campylobacter jejuni/coli in mammalian and poultry The consumption of poultry and mammalian offal is low in comparison to other meat types. However the high
offals prevalence of Campylobacter in raw sheep and chicken livers is of concern, especially when some advice to
(Lake et al, 2007b) consumers is to cook chicken livers "until they're pink in the middle" or "lightly sautéed". Offal for pet food is
frequently contaminated and handling may provide a risk of infection
9
Data from Sumner (2002) predicted annual numbers of illness per annum for the South Australia population (1.5 million). These estimates have been extrapolated to the current population of
Australia estimated by ABS (2009) as approximately 21.6 million, by multiplying by a factor of 14.4.

Poultry meat
In the FSANZ scientific assessment of poultry meat, it was found that on the basis of
epidemiological data, results from microbiological surveys of raw poultry carcase and
outputs from a probabilistic model, there is reasonable evidence to indicate poultry is
the vehicle for a significant proportion of campylobacteriosis and salmonellosis cases
in Australia (FSANZ, 2006). Sumner (2002) estimated large numbers of foodborne
illness cases to be due to processed chicken products, in the order of 79,000 cases
per annum from Salmonella and Campylobacter (Table 21). Work commissioned by
the New Zealand Food Safety Authority has also found the presence of these
organisms on poultry to be a significant source of infection (Table 19).
Management of both Salmonella and Campylobacter requires an approach across
both primary production and processing. Good hygienic practices and good
agricultural practices are necessary prerequisites for the management of Salmonella
and Campylobacter, and appropriate hygiene and sanitation is required during
processing to minimise cross contamination between birds. Surveys of poultry pieces
available for retail sale show that a large proportion of poultry carries these
organisms, creating a risk of foodborne illness from consuming undercooked chicken,
but also the risk of cross contamination occurring in food preparation areas. FSANZ
(2005) found that the implementation of control measures to reduce the prevalence
and levels of Salmonella and Campylobacter by ten-fold at the end of processing
could result in a 74% and 93% reduction in the number of predicted cases of illness
respectively.
FSANZ identified the significant factors contributing to contamination of poultry meat
with Salmonella and Campylobacter as:
♦ On-farm contamination with Salmonella is mainly due to contaminated feed and
water, environmental sources and transmission from contaminated eggs
♦ Important on-farm risk factors for Campylobacter are the age of the birds and
environmental factors
♦ The presence and amount of Salmonella on a chicken after processing largely
determines the likelihood of salmonellosis
♦ Inadequate hand washing and food handling practices determine the likelihood of
human illness from Campylobacter
♦ Adequate cooking is the main means of minimising the risk to human health from
both pathogens.
The FSANZ scientific assessment found little evidence of public health risks
associated with chemical hazards from Australian poultry meat. The report concluded
that the current regulatory measures appear to adequately protect public health and
safety with respect to chemical hazards (FSANZ, 2006).
Game meat
Evidence suggests that the consumption of kangaroo meat and other game meat
present little risk as a source of foodborne illness when compared to other forms of
meat.

Processed meats
Sumner (2002) stated that the highest risk products in the meat industry are
smallgoods, predominantly due to pathogenic E. coli, Salmonella and
L. monocytogenes. The risk of L. monocytogenes from processed RTE meats was
examined by Lake et al (2002), who found that these products were a significant
route of infection in New Zealand. The FDA/USDA risk assessment for
L. monocytogenes identified processed meats products or ‘deli meats’ as the highest
risk food from the 23 RTE foods examined (FDA/USDA, 2003). Deli meats were the
only food to be ranked as very high risk and when extrapolated to the Australian
population are predicted to be responsible for 133 cases of listeriosis per annum (see
Table 22). In addition, frankfurters that were not reheated were ranked as high risk.
However it is not believed that this practice is as common in Australia as in the US.
Pâté and meat spreads were ranked as high risk on a per serving basis,
predominantly due to the probability of contamination with L. monocytogenes post
cooking, but this did not correlate with a high number of predicted illnesses due to
low consumption rates.
The MLA risk profile examined different scenarios for processed meat products and
provided risk rankings and predicted numbers of illness (MLA, 2003, summarised in
Table 21). It was predicted that processed meat were responsible for 43 cases of
listeriosis in Australia per annum. Although there are 50-60 cases of listeriosis
reported each year in Australia, it is estimated that due to under-reporting, the true
number is closer to 120 per year. Therefore, processed meats were considered to be
the source of approximately one third of listeriosis cases in any one year (MLA,
2006).
The MLA guideline Listeria monocytogenes in smallgoods: risks and controls (MLA,
2006) proposes measures to control post processing contamination with
L. monocytogenes in processed meat:
♦ install effective GMPs and sanitation standard operating procedures (SSOPs),
particularly in post-cooking operations such as slicing/portioning and packing
♦ incorporate antimicrobials into formulations of products which are intended for
slicing and packing as long shelf-life products
♦ employ technologies for in-pack pasteurisation.
In late 2008, the NSW Food Authority implemented national testing requirements for
sliced pre-packaged RTE meat products (Meat Standards Committee, 2008). This
Listeria management program involved the introduction of minimum finished product
and environmental testing to any facilities manufacturing these products (NSW Food
Authority, 2008).
The MLA risk profile and the work of Gilbert et al (2007) considered the risk of
pathogenic E. coli (STEC and EHEC) from UCFM products such as salami. Both
studies found that well controlled processes, including efficient fermentation and a
maturation producing a low pH and water activity, effectively controlled the hazard
(Table 20 and Table 21), with a 2-3 log reduction in E. coli. As a result, with a well
controlled process, it was predicted that no illnesses would result from these
products. However, if contaminated meat was used, and an unreliable process was
not able to reduce the hazard, then there may be up to 604 illnesses in a year (see
Table 21). In addition, if susceptible members of the population consumed product

with high levels of pathogenic E. coli present there may be up to 114 cases per
annum. It was predicted that Salmonella may cause 11 illnesses per from UCFM
products, while green runners used for casings of sausages and salami would not
cause any illness. Given the level of specialist skills and knowledge required to safely
make these products, specific requirements for the production of UCFM products are
included in Standard 4.2.3 – Primary Production and Processing Standard for Meat of
the Food Standards Code. Salmonella was considered a medium risk, while the risk
from L. monocytogenes in UCFM products was considered low, as it will not grow in
the product, however it may survive for extended periods. The risk from Toxoplasma
in UCFM products was also considered low, as the risk can be considerably if the
meat is frozen before use, as this will kill the organism.
Kebabs were predicted to be a significant source of illness if allowed to be
recontaminated in the drip tray after cooking, with approximately 25,000 illnesses
per annum. Under normal conditions for cooking kebabs, or even when an extra cook
step was added, it was modelled that in 1% of cases, there may still be an element
of undercooking or some other mishandling to allow survival of Salmonella. In this
scenario, there were still 25 illnesses per annum predicted with kebabs as the cause.
A survey of NSW kebab retail outlets (Jansson et al, 2008) showed that 92% of
outlets undertook an extra cooking step after slicing the meat from the kebab.
Table 20 – NZFSA risk profile outcomes examining hazards in processed meats

Hazard Risk
Listeria monocytogenes in Several notified cases in New Zealand and an outbreak of non-
processed ready-to-eat meats invasive listeriosis in February/March 2000 associated with corned
(Lake et al, 2002) silverside and ham indicate that processed RTE meats are a route
of infection for listeriosis in New Zealand.
Shiga-like toxin producing While uncooked comminuted fermented meat (UCFM) products
Escherichia coli in uncooked might appear to be a higher risk, well controlled processing to
comminuted fermented meat lower the pH and water activity control STECs.
products
(Gilbert et al, 2007)

Table 21 – Risk ranking for processed meat products
Processed meat Hazard Severity Probability Growth Effect of Consumer Epidemiological Risk Predicted
product required production, does link rating annual
the hazard step Australia) 10;
↓↑→
Deli meats L. monocytogenes IB Low Yes ↓↑ No Yes High 43

Terrines L. monocytogenes IB Low Yes ↓↑ No Yes Medium 0.8
Fresh sausage L. monocytogenes IB Low Yes ↓→ Yes No Low >0.01
Cooked sausages L. monocytogenes IB Low Yes ↓ No No Low 0.04
Green runners Salmonella II/IB N/A Yes ↓ Yes No Low 0
Kebabs
Kebabs - Salmonella II/IB Low Yes ↓→ Yes Yes High 27,500
contaminated in
drip tray
Kebabs – Salmonella II/IB Low Yes ↓→ Yes Yes Medium 28
normal
Kebabs - finished Salmonella II/IB Low Yes ↓→ Yes Yes Medium 28
with extra cook
step
10
Data from Sumner (2002) predicted annual numbers of illness per annum for the South Australia population (1.5 million), the MLA Risk Profile (MLA, 2003) used an Australian population figure
of 19.7 million. These estimates have been extrapolated to the current population of Australia estimated by ABS (2009) as approximately 21.6 million, by multiplying by a factor of 14.3 and 1.1
respectively.

Processed meat Hazard Severity Probability Growth Effect of Consumer Epidemiological Risk Predicted
product required production, does link rating annual
the hazard step Australia) 10;
↓↑→
Uncooked comminuted fermented meat (UCFM) products

Salami - general EHEC IA/IB Low No ↓ No Yes Medium 1
population
Salmonella II/IB Low Yes ↓ No Yes Medium 12
L. monocytogenes IB Low Yes ↓ No No Low >0.01
Toxoplasma gondii IB Low No ↓freezing No No Low 0
Salami – EHEC IA/IB Low No ↓ No Yes – high level Medium 125

vulnerable contamination
population
Salami – EHEC IA/IB Low No ↓ No Yes High 604
unreliable process
adapted from Sumner (2002); MLA risk profile (MLA, 2003)

Table 22 – Risk ranking for L. monocytogenes-contaminated processed meats
Processed meat Risk Predicted cases of Risk ranking Predicted annual

product ranking listeriosis per serve (per annum) number listeriosis
(per serve) (in Australia) 11 cases
(in Australia) 12
-8
Deli meats High 7.7 x 10 Very high 133
Frankfurters, not High 6.5 x 10-8 High 2.5
reheated
Pâté and meat High 3.2 x 10-8 Moderate 0.3
spreads
Frankfurters Low 6.3 x 10-11 Low 0.03
reheated
Dry / semi-dry Low 1.7 x 10-11 Low 0
fermented
sausage
Conclusions
The production and processing of meat has a long history of successful regulation.
The preventative programs implemented by government and industry have improved
animal health to the point that many diseases are no longer present in Australian
animals. The meat food safety scheme under the Food Regulation 2004 requires
compliance with national meat standards, leading to ante-mortem and post mortem
inspections at abattoirs that have been effective in ensuring that meat produced in
NSW is safe and suitable for human consumption. The microbiological surveys of
meat production have shown a steady increase in the quality of meat produced.
However, epidemiological data suggests that the prevalence of Salmonella and
Campylobacter on raw poultry significantly contributes to the burden of foodborne
illness within the community, not only from the consumption of contaminated poultry
itself but the added potential for the introduction of these pathogens from poultry
into food preparation areas where they may be a source of cross contamination onto
RTE foods. Currently the food safety scheme requires compliance with the national
poultry meat standard, however this only provides control measures for the
processing sector. A whole chain approach is considered necessary, with control
measures introduced at the primary production level to reduce the prevalence of
these foodborne pathogens. With this aim in mind, FSANZ are currently finalising the
development of Standard 4.2.2 - Primary Production and Processing Standard for
poultry meat into Chapter 4 of the Food Standards Code. When finalised, this will be
adopted into NSW legislation. The contamination of processed meats with
11
The risk per serving is inherent to the particular food category, and is therefore assumed to be the same in
Australia as that calculated for the USA (FDA/USDA, 2003). This is based on the assumption that consumption
patterns for these foods are identical in Australia and the USA. One significant difference would be that
frankfurters are not commonly eaten without reheating in Australia, with MLA (2003) estimating that only 5%
are eaten without further cooking
12
The risk per annum has been adapted from USA population data contained in the FDA/USDA (2003) risk
assessment of 260 million and extrapolated to Australian population data of approximately 21.6 million (ABS,
2009) by dividing by a factor of 12

L. monocytogenes continues to cause issues for meat processors, including a
substantial number of product recalls. Additional hygiene and sanitation measures,
including mandating the testing of finished product and food contact surfaces in high
risk processing facilities, such as those packaging sliced RTE meats, aims to minimise
contamination of this organism in product.

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Plant products food safety
scheme
In 2000, the former SafeFood Production NSW commissioned Food Science Australia
to determine the relative food safety risks for various plant products produced and/or
marketed in NSW (FSA, 2000a). This work resulted in six products being ranked as
high risk due to microbiological hazards (Table 23), and formed the scientific basis
for the introduction of the Plant products food safety scheme into the Food
Regulation 2004. The scheme was developed to introduce minimum regulatory
requirements for businesses producing high risk plant products, and to implement
control measures to minimise the risks from the microbiological hazards associated
with these products.
Table 23 – Microbiological hazards associated with plant products

Plant product High risk ranking Medium risk ranking
Fresh cut vegetables – may be Pathogenic E. coli
consumed raw
Salmonella spp.
L. monocytogenes
Fresh cut vegetables – chilled, L. monocytogenes
MAP or extended shelf life
C. botulinum
Vegetables in oil C. botulinum
Seed sprouts Pathogenic E. coli B. cereus
Salmonella spp. L. monocytogenes
Fresh cut fruit Pathogenic E. coli Cryptosporidium parvum
Salmonella spp. Enteric viruses
L. monocytogenes
Fruit juice / drink Salmonella spp.
(unpasteurised)
Pathogenic E. coli
adapted from FSA (2000a)
Fresh cut vegetables

Fresh cut fruits and vegetables are raw agricultural products that have been
processed by means of washing, trimming, cutting or slicing to make them ready for
consumption. Contamination of vegetables may occur during growth, harvest, or
processing. Under certain conditions microorganisms can also become internalised
within the vegetables. Conditions that promote internalisation of microorganisms
include damage to the natural structure (eg punctures, stem scars, cuts, splits) and
placing warm produce into cooler, contaminated wash water.
The actual process of cutting and/or removing the protective outer surfaces of the
plants may increase the potential for pathogenic bacteria to survive and/or grow.

Many vegetable products do not undergo a kill step that will completely eliminate
pathogens, however measures such as sanitising washes may be used to reduce
microbial contamination of pathogens.
Many fresh cut vegetables are packaged under modified atmosphere packaging
(MAP) and refrigerated to extend the shelf life. This form of processing may lead to
an increased risk with pathogens such as L. monocytogenes and psychrotrophic
strains of C. botulinum by enhancing the conditions for their survival and allowing
additional time for growth. MAP products may become fully anaerobic if the plant
tissue is actively respiring and uses up all the oxygen. As any competition from
aerobic spoilage organisms is inhibited, this may increase the opportunity for
anaerobic or facultative anaerobic pathogens to grow.
Fresh cut fruit

Fresh fruit are normally perceived as low risk foods, as they tend to have a thicker
protective skin than most vegetables and most are harvested from trees or bushes.
The notable exceptions are melons and strawberries, which are considered higher
risk because they grow close to the ground and their surfaces may become
contaminated with soil.
Contamination of fruit may occur at any point from growing (soil, fertilisation,
irrigation water, animal/bird waste), through to harvesting, processing (including
washing), distribution, marketing and consumption. Many microbial pathogens
cannot survive or grow on most fruit due to the low pH environment. However,
melons and strawberries have relatively high pH which makes them more likely to be
a food safety hazard. In addition, the skin of rockmelon tends to be porous which
may allow the penetration of pathogens and agricultural chemicals into the fruit.
Melons are often dipped in a sanitising solution after harvest (FSA, 2000a).
Fresh cut fruits may be value added by peeling, chopping, slicing and packaging
(FSA, 2000a). Many fresh cut fruit are packaged under MAP and refrigerated to
extend the shelf life. With additional time, this can lead to an increased risk from
pathogens that are adapted to the acidic environment of fruit and are able to survive
and grow in these foods.
A range of bacterial and viral pathogens and enteric parasites have been identified as
being of concern in fresh cut fruit. The actual process of cutting and/or removing
protective outer surfaces of the fruit may increase the potential for pathogens to
survive and/or grow. Fruit pickers and handlers with infections are also an important
source of contamination.
Vegetables in oil
This product category includes a diverse range of vegetables and mixtures of
vegetables and herbs that may be used fresh, dried, roasted or acidified. Oil is added
to exclude air, which prevents discolouration of the vegetable. Although immersion of
vegetables in oil reduces the available oxygen in the container, contrary to popular
belief, it does not preserve the food. Some pathogenic bacteria are able to survive
and grow in reduced levels of oxygen and even under anaerobic conditions in the
absence of oxygen.

C. botulinum is the main pathogen of concern because of its ability to grow
anaerobically and it has been linked to outbreaks of illness from the consumption of
vegetables in oil. Vegetables may be contaminated by C. botulinum spores, which
are frequently associated with soil and processes such as cooking and acidification
may be insufficient to inactivate the spores or prevent their germination and growth.
Seed sprouts
Seed sprouts are usually consumed raw and include alfalfa, mung bean, chickpeas,
cress, fenugreek, soy, lentils, sunflower, onion and radish. Seeds for sprouting
generally do not receive any special treatment during harvesting and transport and
so may become contaminated with pathogenic organisms in the field or during
harvesting, handling, processing and distribution. While some bean sprouts may be
cooked prior to consumption, many others are consumed raw, for instance with
salads.
The microbiological pathogens frequently found associated with seeds for sprouting
include B. cereus, Salmonella spp., and E. coli and these organisms have also been
implicated in foodborne illness outbreaks. The rough surfaces and cracks in the seed
may protect the pathogens from microbiocidal treatments and may make detection
during routine analysis difficult. High levels of organic matter also reduce the
effectiveness of chlorine treatments during seed washing and seed sprouting.
Bacterial populations of 102-107 cfu/g have been observed on seeds for sprouting
and this natural population can rapidly increase under the high moisture and
moderate temperature conditions used in sprouting facilities. Microorganisms may
also become internalised in the sprout during growth so sanitising wash treatments
of sprouted seeds are not likely to be effective (FSA, 2000a).
Unpasteurised fruit juice

Fruit juices are made by extracting fruit (citrus juices) or by macerating fruit (grape,
cherry, berry, apple juice, etc.). This may be followed by clarification, filtration,
pasteurisation, and/or other processes to reduce the microbial load. In recent years
there has been a trend to produce ‘natural’ fruit juices containing no preservatives
and receiving little or no heat treatment.
Any microorganisms present on the surface of fruit may potentially contaminate the
juice made from it. Bacterial, viral or protozoan pathogens are unlikely to grow due
to the low pH but may be able survive for extended periods. The length of time the
microorganism may survive is dependent on the pH of the juice, storage temperature
and the physiological state of the microorganism. Some Salmonella spp. and strains
of pathogenic E. coli are known to be particularly acid tolerant, with this response
thought to be activated by previous exposure to sub lethal pH values.
Apple and pear juice are can become contaminated by the mycotoxin patulin which is
produced by several Penicillium and Aspergillus species. P. expansum appears to be
the main patulin producer in apples and apple products. Since patulin is concentrated
in the rotting tissue of fruit, it is a good indicator of the quality of fruit used to make
the juice.
The acidic nature of fruit juices makes them corrosive to metals. To avoid potential
chemical contamination, only stainless steel or corrosion resistant vessels should be

used to store these products. Other metals such as copper can leach into the
beverage during storage.
Exposure assessment
Production data
Leafy salad vegetables, such as lettuce, rocket and baby spinach are the most
common products in the fresh cut category, contributing towards an estimated
national production value of $44 million for the year 1997/98 (Szabo & Coventry,
2001).
The Regulatory Impact Statement (RIS) prepared for the Food Regulation 2004,
based on limited industry information, estimated annual NSW consumption of the
fresh cut fruit and vegetables (NSW Food Authority, 2004) as:
♦ 11,000 tonnes fresh cut vegetables, with a high proportion imported from
Victoria and Queensland
♦ 150 tonnes of fresh cut fruit
♦ Approximately 1000 tonnes of vegetables in oil, with the vast majority imported
from overseas and interstate and
♦ Between 2100 and 2600 tonnes of seed sprouts.
Subsequent recent surveys by the NSW Food Authority of the NSW sprout industry
suggest that 2007/08 production was in the order of 3630 tonnes, with some of this
product being sold interstate. NSW fruit juice suppliers suggest that manufacture of
unpasteurised fruit juices occurs at relatively low volume, about 100,000 L/year, not
including juices prepared in retail premises (NSW Food Authority, unpublished).
Consumption of plant products

Consumption data for fruits and vegetables from the National Nutrition Survey are
summarised in Table 24 (ABS, 1995). During the period 1997-98 and 1998-99, fruit
and fruit products (including fruit juices), consumption increased by 8.3% from 124.7
kg per capita to 135.0 kg. In the same period, imports for oranges and other citrus
fruit rose by more than 62% (ABS, 2000).
Consumption of vegetables has shown a steady 9.4% increase over the last decade.
Per capita consumption of tomatoes showed a significant increase from 20.9 kg in
1997-98 to 24.9 kg in 1998-99, a rise of 19%. The category of other vegetables
showed an increase in consumption in 1998-99 of 4.6% to 25.1 kg per person.
Data from the Australian 1995 National Nutrition Survey (ABS, 1995) indicates that
fruit juices and drinks are consumed in significant amounts by a large proportion of
the population. Approximately 35% of all respondents consumed fruit juices and
drinks with the mean consumption being 250mL per day.
The consumption data does not provide information on how much unpasteurised
juice is consumed, however the Australian Fruit Juice Association believes that
approximately 95% of juice sold has undergone some form of pasteurisation process.

Table 24 – Consumption of fruits and vegetables in Australia
Sex Age Proportion of Median daily Proportion of Median daily

persons intake for persons intake for
consuming consumers of consuming consumers of
fruit products fruit products vegetable vegetable
and dishes 13 and dishes products and products and
(%) (g/day) dishes 14 dishes (g/day)
(%)
Male 2-3 77.6 153.6 68.1 92.1
Male 4-7 65.6 168.0 72.7 118.0
Male 8 - 11 56.4 166.0 77.0 165.0
Male 12 - 15 49.9 167.2 78.8 223.0
Male 16 - 18 39.9 172.0 83.1 253.6
Male 19 - 24 31.9 179.2 84.7 271.3
Male 25 - 44 45.8 210.0 86.6 263.0
Male 45 - 64 59.5 229.0 91.0 297.8
Male 65+ 69.6 202.0 91.7 280.4
Female 2-3 75.4 140.0 79.2 95.2

Female 4-7 72.8 166.0 79.7 122.5
Female 8 - 11 62.5 150.8 77.0 158.0
Female 12 - 15 58.0 172.0 85.9 180.8
Female 16 – 18 41.1 191.0 85.8 185.0
Female 19 - 24 41.4 166.0 86.5 220.5
Female 25 - 44 55.0 188.4 88.0 216.1
Female 45 - 64 69.8 192.0 91.0 258.5
Female 65+ 75.6 196.0 91.5 239.3
13
Fruit products and dishes are defined in the National Nutrition Survey (ABS, 1995) as including the following:
- Pome fruit, berry fruit, citrus fruit, stone fruit, tropical fruit, other fruit
- Mixtures of two or more groups of fruit
- Dried fruit, preserved fruit
- Mixed dishes where fruit is the major component
14
Vegetable products and dishes are defined in the National Nutrition Survey (ABS, 1995) as including the
following:
- Potatoes, cabbage, cauliflower and similar brassica vegetables, carrot and similar root vegetables, leaf
and stalk vegetables, peas and beans, tomato and tomato product, other fruiting vegetables
- Other vegetable and vegetable combinations
- Dishes where vegetable is the major component

Prevalence of hazards in plant products
There have been a small number of surveys of Australian plant products. Arnold &
Cable (1995) in a broad survey of NSW food found 1/54 samples (1.9%) of RTE
salads and vegetables positive for L. monocytogenes.
Szabo et al (2000) tested 120 minimally processed, cut and packaged lettuce
samples. Three samples (2.5%) were positive for L. monocytogenes, 66 samples
(55%) were positive for Aeromonas hydrophila or A. caviae and 71 samples (59%)
were positive for Yersinia enterocolitica.
The Victorian Department of Human Services (DHS) surveyed the microbiological
quality of freshly squeezed juices from retail businesses across the state (Victorian
DHS, 2005). L. monocytogenes was detected in 1/291 samples (0.3%), but the level
was sufficient to classify the sample as potentially hazardous. E. coli was detected in
7/291 samples (2.4%). Salmonella and coagulase positive S. aureus were not
detected.
The Western Australian Department of Health (WA Health, 2006) tested 261 samples
of sprouted seeds from retail stores. E. coli was detected in 7 samples (2.7%), while
Listeria and Salmonella were not detected in any samples.
The NSW Food Authority undertook a small survey in 2006 to determine the safety of
fresh cut vegetables sold in NSW. E. coli was detected in 1/119 samples (0.8%),
while Salmonella, L. monocytogenes and verotoxigenic E. coli were not detected in
any samples (NSW Food Authority, unpublished).
The Authority has also undertaken several surveys of seed sprouts. In 2005, all 30
samples were found to be microbiologically acceptable. In 2006, 1/36 samples
(2.7%) was found to be potentially hazardous due to the presence of verotoxigenic
E. coli (VTEC) and a further two samples were categorised as unsatisfactory due to
elevated levels of E. coli. A more extensive survey in 2008 of 122 samples found
99.2% of samples were microbiologically acceptable, with a single sample
categorised as unsatisfactory due to B. cereus at a level of 5500 cfu/g (NSW Food
Authority, 2008).
There has been considerable international interest in the safety of plant products.
O’Brien et al (2000) prepared a discussion paper on the microbiological status of RTE
fruit and vegetables for the UK Advisory Committee on the Microbiological Safety of
Food (ACMSF). The report provided a summary of foodborne illness outbreaks and
surveys of plant products. The report concluded that while contamination of raw
vegetables usually occurs at low prevalence, it is pervasive.
The Food Safety Authority of Ireland (FSAI) surveyed the bacteriological safety of a
range of plant products as part of a European Commission coordinated program
(FSAI, 2003). Pre-cut fruit and vegetables had samples classed as
unacceptable/potentially hazardous due to the presence of Salmonella in 1/529
samples (0.2%) and L. monocytogenes in 1/344 samples (0.3%). Qualitative tests
found 21/513 samples (4.1%) positive for L. monocytogenes. No sprouted seeds
samples were classed as unacceptable or potentially hazardous. L. monocytogenes
was detected in 1/26 samples (3.8%). No problems were detected with
unpasteurised fruit and vegetable juices.
A similar European Commission program surveyed pre-packed mixed salads from
retail premises in the UK for L. monocytogenes (Little et al, undated).
L. monocytogenes was detected in 4.8% of samples collected. A parallel survey by

the FSAI included Salmonella testing in the survey design (FSAI, undated).
Qualitative analysis showed L. monocytogenes was present in 19/714 samples
(2.7%). Quantitative analysis detected two samples with L. monocytogenes at levels
exceeding 100 cfu/g, however Salmonella was not detected in any sample.
Little & Gillespie (2008) summarised microbiological results of surveys of prepared
salads and fruit examined in the UK. No isolations of E. coli O157 or Campylobacter
were reported. Five of 3852 samples (0.1%) of bagged salad vegetables were
positive for Salmonella but other commodities were negative. L. monocytogenes and
E. coli were detected in most commodities surveyed, usually at low incidence.
Crepet et al (2007) used statistical techniques on 165 prevalence studies and
concentration data from 15 studies of L. monocytogenes in fresh vegetables to
estimate an overall probability of significant counts being found in the products.
Their mathematical method required a minimum of one positive sample in each
survey. However, as some survey sets had no actual detections, this change was
made to data sets to accommodate the statistical analysis. Acknowledging this
deliberate overestimation, the authors calculated the probability of sample
contamination with L. monocytogenes exceeding 10 cfu/g as 1.4%, exceeding 100
cfu/g as 0.6% and exceeding 1000 cfu/g as 0.2%.
Foodborne illness outbreaks from plant products
An indication of the exposure to hazards in plant products is provided by an
examination of the Australian foodborne illness outbreaks between 1995 and 2008
attributed to fresh produce and plant products, summarised in Table 25 (details of
each outbreak are included in Table 67 of Appendix 3). Prior to this, two other
Australian outbreaks of significance brought plant products into the spotlight as a
significant source of foodborne illness. In NSW in 1989 there were three separate
outbreaks from fruit salad due to Salmonella Bovismorbificans traced to a single NSW
salad manufacturer (Biffin & McCarthy, pers comm), while in 1991 a nationwide
outbreak from Norwalk-like virus (norovirus) was attributed to the consumption of
unpasteurised orange juice. The juice was served on airline flights and was
responsible for more than 3000 cases of illness (Foodlink, 2002). In addition, the risk
of listeriosis from plant products was highlighted by an outbreak of listeriosis from
contaminated fruit salad in NSW aged care facilities and hospitals in the Hunter
Valley area. Through 1998-1999, six deaths of elderly patients occurred and nine
were affected (this outbreak is included in outbreak data for the section on the
Vulnerable persons food safety scheme).
Internationally, there have been many examples of outbreaks that have been
attributed to plant products. Sivapalasingham et al (2004) summarised the outbreaks
attributed to fresh produce in the USA from 1993 to 1997. The authors identified 190
produce-associated outbreaks, resulting in 16,058 illnesses, 598 hospitalisations and
eight deaths. They report that produce-associated outbreaks were an increasing
proportion of all reported foodborne outbreaks with a known food cause, rising from
0.7% in the 1970s to 6% in the 1990s. Salad, lettuce, juice, melon, sprouts, and
berries were the fresh produce most frequently implicated. Sivapalasingham et al
(2004) also recognised Cyclospora and E. coli O157:H7 as novel causes of foodborne
illness from plant products.

Table 25 – Summary of foodborne illness outbreaks attributed to plant products
outbreaks
(1995-2008)
Campylobacter spp. 2 128 0 0
Norovirus 1 18 0 0
Shigella spp. 1 55 0 0
Viral 1 61 0 0
Unknown 10 192 2 0
Total 26 1395 35 1
DeWall & Bhuiya (2007) also reviewed outbreaks in the USA from fruit and
vegetables for the period 1990 to 2005. They reported greens-based salads
contaminated with norovirus as the most common cause of outbreaks, followed by
lettuce with norovirus, sprouts with Salmonella, fruit with norovirus, greens-based
salads with Salmonella and melon with Salmonella. Produce-related outbreaks
resulted in an average of 47.8 cases, which is higher than reported for outbreaks
from poultry, beef and seafood.
Doyle & Erickson (2008) presented an overview of the problems associated with
fresh produce. Four further outbreaks that occurred in 2006 were discussed; an
outbreak traced to fresh spinach contaminated with E. coli O157; salmonellosis
traced to tomatoes and two outbreaks linked to lettuce contaminated with E. coli
O157:H7.
Little & Gillespie (2008) reviewed outbreaks related to prepared salads in England
and Wales in the period 1992 to 2006. The authors reported 82 outbreaks from
prepared salads with 3434 people affected, 66 hospitalisations and one death.
Peck et al (2008) reviewed the potential for growth and neurotoxin formation by –
non-proteolytic C. botulinum in short shelf-life foods designed to be chilled. Their
foodborne illness examples included seven outbreaks of botulism in products of plant
origin. The implicated products were commercial garlic-in-oil, hazelnut yoghurt
(attributable to the hazelnut conserve, see the section on the Dairy food safety),
restaurant potato dip, restaurant aubergine dip, commercial black bean dip,
commercial hummus and commercial refrigerated carrot juice. Temperature abuse
was suspected to be contributing factor in four of the outbreaks.
The following international outbreaks warrant individual mention because of either
their size or novel cause:
♦ In 1996 an outbreak of E. coli O157:H7 infection occurred among schoolchildren
in Sakai City, Osaka, Japan. The outbreak was attributed to white radish sprouts
served in a centralised luncheon program servicing 56 schools. Over 8000
children developed symptoms and 398 children were hospitalised. Two further
incidents of E. coli O157:H7 in neighbouring areas were also related to white
radish sprouts. All the implicated sprouts were traced back to one farm (Michino
et al, 1999). This illustrates the size of an outbreak that can result when a hazard
becomes a reality in a centrally processed and is a widely distributed product.

♦ In 1998 an outbreak of cyclosporiasis (a gastrointestinal illness caused the
parasite Cyclospora) occurred in Ontario, Canada. A further 12 clusters of
cyclosporiasis were identified with a total of 192 cases. The investigation linked
the clusters to raspberries imported from Guatemala. Outbreaks of cyclosporiasis
in North America during the spring of 1996 and 1997 were also linked to
Guatemalan raspberries. This is an example of repeated outbreaks attributable to
parasites due to failures in the growing and handling of raspberries (MMWR,
1998).
♦ In 2003 an outbreak of Hepatitis A was traced to a restaurant in Pennsylvania,
USA and linked to the consumption of green onions (similar to shallots). Early in
the outbreak 555 cases had been identified and three people died. The report
noted that green onions require extensive handling during harvesting and
preparation for packing. Contamination by Hepatitis A virus (HAV) could occur by
contact with infected workers or contaminated workers (MMWR, 2003). This is a
large outbreak of viral illness attributable to fresh produce.
♦ In 2006 a multi-state outbreak of E. coli O157:H7 attributed to consumption of
fresh bagged spinach occurred in the USA. By January 2007, 205 cases had been
reported with 103 hospitalisations and 31 cases of haemolytic uraemic syndrome
(HUS) and 3 deaths confirmed. Contamination was traced back to one farm.
While no definitive determination of how the pathogens contaminated the
spinach could be made, the presence of wild pigs near the growing fields and the
irrigation wells were determined to be environmental risk factors. Processing of
the spinach included washing, did not eliminate the problem and may have
facilitated the spread of pathogens from contaminated to uncontaminated
spinach (California Food Emergency Response Team, 2007). This is an example
of a widespread outbreak of severe bacterial illness attributable to hygiene
failures in the growing and processing of spinach.
♦ In 2007, 55 cases of Salmonella Senftenberg infection in England and Wales
were linked to fresh basil. Scotland, Denmark, the Netherlands and the USA
reported 19 further cases with the outbreak strain. Eight samples of fresh packed
basil from Israel tested positive with the same strain. Microbiological evidence
suggested an association between contamination of fresh basil and the cases of
Salmonella Senftenberg infection, leading to withdrawal of basil from all
potentially affected batches from the UK market (Pezzoli, 2008).
♦ In 2008 a large outbreak of Salmonella Saintpaul in the USA and Canada was
associated with multiple raw produce items. As at August 2008, 1442 people had
been affected, with at least 286 hospitalisations and the outbreak might have
contributed to 2 deaths. The epidemiological data suggested the major vehicle
for the spread of the pathogen was jalapeno peppers. However, serrano peppers
were also considered to be a vehicle, and early in the outbreak tomatoes were
considered a source. Contamination of produce may have occurred on the farm
or during processing or distribution. The outbreak strain of Salmonella has been
found in one growing area and an associated packing facility in Mexico (MMWR,
2008). This is the largest culture confirmed outbreak in the USA in the last
decade. As many persons with Salmonella illness do not seek care or have stool
specimens tested, many more unreported illnesses may have occurred.
As previously discussed, the Food Science Australia plant products scoping study
ranked five specific plant product as high risk due to specific pathogens (FSA,
2000a), these are discussed as follows:

Fresh-cut vegetables and fresh cut fruit
Survey data shows that L. monocytogenes occurs in cut vegetables at low prevalence
and usually at low levels. Lake et al (2005) presented data showing that
L. monocytogenes can grow in a range of vegetables, however growth is typically
slow at refrigeration temperatures but numbers can increase by several logs in some
commodities stored at 10°-15°C for 7-10 days. The potential for growth in
refrigerated short shelf-life products would seem to be low. These products have no
final cooking process to eliminate contamination. Where product is packaged in MAP,
the potential longer shelf life increases the potential for pathogen growth.
Pathogenic Escherichia coli

The potential exists for pathogenic E. coli to be present on vegetables from
contamination with ruminant faeces or from food handlers that carry the organism in
their gut. However, surveys of pre-cut vegetables and salads, other than in Mexico,
rarely, if ever, detect pathogenic E. coli.
Gilbert et al (2006) reviewed the dose response estimates for E. coli O157:H7 and
original estimates of infectious dose were less than a few hundred cells. Later work
estimated the probability of infection from exposure to differing numbers of cells.
One model predicted a dose of 5.9 x 105 organisms would result in infection in 50%
of consumers, while the probability of illness from 100 organisms was 2.6 x 10-4. A
second study calculated a median dose (50% of people exposed become
symptomatic) of 1.9 x 105 and a probability of 6 x 10-2 of infection when exposed to
100 cells. An analysis of data from the Sakai City elementary school outbreak with
E. coli O157:H7 indicates much higher probabilities of infection at lower doses than
previous models. Gilbert et al (2006) also reported dose-response for E. coli O111
and O55. The dose for infection of 50% of the exposed population was 2.6 x 106
organisms. The probability of illness when exposed to 100 cells was 3.5 x 10-4.
Gilbert et al (2006) state that the organism will grow on leafy vegetables at
temperatures above 7°C. However, due to the low infectious dose of the organism in
food, growth may not be required to cause illness.
Salmonellae
Jay et al (2003) included data on the incidence of salmonellae in fruit, vegetables
and spices with the prevalence shown to be below 10%. They note that numbers of
salmonellae on raw vegetables are usually <1 cfu/g, but numbers as high as 240
cfu/g have been found on Dutch endive. Jay et al (2003) also includes information
about an outbreak in Germany traced to paprika and paprika powdered potato chips
which resulted in an estimated 1000 cases of Salmonellosis. The numbers of
salmonellae detected in the food were very low, around 2.5 Salmonella cfu/g in the
paprika and 0.04-0.45 Salmonella cfu/g of chips.
Clostridium botulinum
The risk of botulism is increased for products packaged in MAP, with the longer shelf
life increasing the potential for spore germination and pathogen growth. Food
Science Australia rated the risk of this pathogen / product pair as high (FSA, 2000a).
The contributing factors were the severity of the illness, the fact that processing
increases the risk and the existence of an epidemiological link. That rating remains

appropriate, particularly as longer shelf life vegetable products are becoming more
available.
Vegetables in oil
The US Food and Drug Administration (FDA, undated) lists a history of botulism
attributed to inadequately acidified foods and notes that products processed by 29
firms were found to be inadequately acidified. The FDA concluded that the evidence
demonstrated that certain manufacturers of acidified foods did not realise the
importance of adequate pH control. This resulted in the development of a specialised
regulation for acidified foods in Title 21 of the Code of Federal Regulation (21 CFR
114).
Despite the acidified foods regulation being published in 1979, two serious outbreaks
of botulism were reported in the 1980s in Canada and the USA. Chopped garlic in oil
was clearly identified as the source of botulism toxin (St Louis et al, 1988). The
concern about vegetables in oil and botulism remains current. The products are
popular and home production is common. According to Food Science Australia (FSA,
2000b), two false assumptions persist about vegetables in oil:
♦ That the addition of oil has a preservative effect
o Incorrect. The only function of the oil is to prevent oxidation from air
in the container which can lead to discolouration of some foods. By
excluding air from the surface, this establishes anaerobic conditions
which actually favour the growth of some types of bacteria, including
C. botulinum.
♦ That some herbs and spices, and especially garlic, have significant anti-microbial
properties
o Incorrect. The preservative effect of these materials is slight and
inconsistent as outbreaks of botulism in Canada and the USA have
demonstrated.
Seed sprouts
Outbreak investigations have identified several factors that affect the microbiological
safety of sprouted seeds. To date, contaminated seeds have been the likely source
for most outbreaks. Seed contamination could have occurred at the farm, seed
processor, or sprouting facility. The hydrophobic surface of seeds makes sanitation
and removal of contaminating microorganisms difficult. Conditions during sprouting
(time, temperature, aw, pH and nutrients) are ideal for growth of pathogenic bacteria
leading to an increased risk.

The majority of outbreaks caused by consumption of juice have been attributed to
the use of fruit that has been contaminated by animal faeces. Orchards are often
located near livestock or wildlife with the potential for microbial contamination.
Contamination of juice is more likely to occur where the skin or peel of the fruit is in
contact with the juice during processing.

Fresh-cut vegetables and fresh cut fruit
To date, there has been no epidemiological evidence to link cases of
L. monocytogenes infection in Australia with fresh cut vegetables. As such, there is
sparse outbreak data to support the high risk rating allocated by Food Science
Australia (FSA, 2000a). The FDA/USDA (2003) quantitative risk assessment on
L. monocytogenes assigned low relative risk rankings to fruits, vegetables and deli-
type salads (Table 26). The report acknowledged the diversity of the product group
and supported further study. While it appears the probability of infection is low, even
for persons vulnerable to listeriosis, the consequences of the illness remain severe.
This was graphically demonstrated by the Hunter Valley outbreak where six persons
died from consumption of Listeria-contaminated fruit salad. The high risk rating is
also applied to modified atmosphere products (MAP) that are stored for extended
periods. The potential for growth in storage increases the ranking for MAP
vegetables and salads.
Table 26 – Risk ranking for plant products contaminated with Listeria

monocytogenes
Plant product Risk Predicted cases of Risk Predicted annual
ranking listeriosis per serve ranking number of listeriosis
(per serve) (in Australia) 15 (per cases
annum) (in Australia) 16
Vegetables Low 2.8 x 10-12 Low 0.02
-11
Fruits Low 1.9 x 10 Low 0.08
-13
Deli-type salads Low 5.6 x 10 Low 0
Pathogenic Escherichia coli

There have been a number of E. coli outbreaks attributed to this group of products
around the world. Consequences of illness are potentially severe with high rates of
hospitalisation and long terms effects such as HUS and kidney problems. Food
Science Australia (FSA, 2000a) rated the risk as high, while Gilbert et al (2006)
placed pathogenic E. coli in the highest severity category but lowest incidence
category for New Zealand foods. It was concluded that it is essential that efforts
continue to prevent the likelihood of foodborne transmission from this group of
organisms.
15
patterns for these foods are identical in Australia and the USA.
16

Salmonellae
Food Science Australia rated the risk of Salmonella in these products as high risk,
based on the severity of the illness and no consumer cooking step to eliminate the
hazard (FSA, 2000a). Basset & McClure (2008) rated Salmonella spp. as a significant
hazard for both fruit and vegetables based on similar criteria to Food Science
Australia, but note that growth in the product is not required for illness to eventuate.
This appears consistent with the many outbreaks attributed to products in which
Salmonella might survive but not grow.
Food Science Australia (FSA, 2000a) rated the risk of C. botulinum in these products
as high. The contributing factors were the severity of the illness, the fact that
processing and packaging in MAP may increase the risk and the existence of an
epidemiological link. There is no domestic epidemiological evidence to support the
high risk ranking but, to date, longer shelf life vegetable products have had limited
availability.
Vegetables in oil
There appears clear potential for products prepared without appropriate control
measures to result in a poorly acidified product, with potential to cause severe illness
from pathogens such as C. botulinum. These products are sometimes prepared by
small and medium enterprises, which is considered to increase the risk if knowledge
of food safety controls is not adequate.
Seed sprouts
The conditions during sprouting (time, temperature, water activity, pH and nutrients)
are ideal for growth of pathogenic bacteria such as Salmonella and pathogenic E. coli
leading to seed sprouts to be considered a high risk product (FSA, 2000a). The
potential for growth of pathogenic organisms during sprouting increases the risk
substantially, and there is epidemiological evidence to demonstrate that
contamination does occur. The implementation of control measures, such as
sanitation of seeds prior to sprouting, may lower the prevalence of pathogens.

The Food Science Australia high risk ranking of unpasteurised juice is appropriate
(FSA, 2000a). The potential sources of contamination are virtually identical as for
fresh cut fruit, and there is strong epidemiological evidence to justify the risk. The
two large scale outbreaks in Australia in 1991 and 1999, due to contamination of
unpasteurised juice with Salmonella spp. have clearly demonstrated the potential for
unpasteurised juice to cause illness.
Conclusion
The introduction of a plant products food safety scheme into the Food Regulation
2004 targeted the five plant products categorised as high risk by the Food Science
Australia scoping study (FSA, 2000a). Minimum food safety control measures were

introduced with the aim of avoiding outbreaks of foodborne illness from these
products.
While plant products such as fresh cut fruit and vegetables generally have an image
as healthy foods and form an important part of a healthy nutritious diet, the
occurrence of several large scale outbreaks of foodborne illness in the US affecting
thousands of consumers highlights the potential risks associated with these products.
Due to the increasing demand for convenience foods from consumers, the market
share of pre-packed fresh cut fruits and vegetables on supermarket shelves has
increased dramatically in the last several years, therefore it is important that food
safety control measures are in place to ensure that the consuming public is
protected.
In addition to pre-packaged salads, there has been a history of unpasteurised juice
causing two large outbreaks in Australia, while seed sprouts have a history of
causing foodborne illness outbreaks overseas and within Australia. While the history
associated with vegetable in oil products does not involved large outbreaks, there
exists the potential for severe illness, from pathogens such as C. botulinum, if these
products are not produced in a controlled manner. The food safety scheme
requirement for businesses producing plant products to implement a food safety
program means that appropriate control measures are applied, and that verification
of those controls occurs at regular intervals through testing of finished product.

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The food safety hazards of seafood have been extensively studied. The former
SafeFood Production NSW (predecessor organisation of the NSW Food Authority)
commissioned several studies in preparation for the introduction of the Food
Production (Seafood safety scheme regulation) 2001. Subsequent studies have been
undertaken by NSW, South Australian and Australian Governments and by
international agencies. Walsh & Grant (1999) identified hazards as shown in Table
27.
Table 27 – Hazards in seafood and seafood products

Priority Sector Hazard
High Wild caught finfish Histamine/Scombroid ;
Ciguatera ;
Mercury ;
Bivalve molluscs Pathogenic bacteria ;
Viruses ;
Algal toxins: Paralytic shellfish poisoning (PSP),
Diarrhoetic shellfish poisoning (DSP), Amnesic shellfish
poisoning (ASP), Neurotoxic shellfish poisoning (NSP) ;
Cold smoked fish RTE Listeria monocytogenes ;
Hot smoked fish RTE L. monocytogenes ;
Smoked fish vacuum packed Clostridium botulinum ;
or modified atmosphere
packaged (MAP)
Medium Bivalve molluscs Vibrio spp.
High
Medium Wild caught finfish (raw) Parasites ;
Bivalve molluscs Agrichemicals
Aquaculture crustaceans Vibrio spp. ;
Raw fish – vacuum packaged C. botulinum
or MAP
Surimi RTE L. monocytogenes
Cooked whole prawns Post-cooking contamination by pathogenic bacteria
Cooked peeled prawns or L. monocytogenes, Staphylococcus aureus, general
crabmeat pathogens
Salted seafood S. aureus
adapted from Walsh & Grant (1999)
; Those marked were subsequently evaluated by Ross & Sanderson (2000).

Ross & Sanderson (2000) prepared a risk assessment of selected seafood in NSW.
The seafood selected for their study were extracted from the lists developed by
Walsh & Grant (1999). The report noted that the incidence of foodborne illness due
to most hazards was low, but recognised that oysters and other shellfish have
repeatedly been involved in outbreaks. Ciguatera and histamine poisonings are also
relatively common, but are generally less severe in their outcomes (Ross &
Sanderson, 2000).
On behalf of SafeFood Production NSW, Woods & Ruello (2000) facilitated five
industry Sector Working Groups (SWG) to examine the food safety hazards
associated with the five high priority seafood sectors shown in Table 27, and to
recommend practical risk mitigation measures.
Ross, Walsh & Lewis (2002) studied the food safety risks associated with cold
smoking and marination processes used by Australian businesses. This report
identified and ranked hazards with L. monocytogenes, C. botulinum, scombroid and
parasites identified as most significant.
Sumner (2002) undertook a risk profile on seafood and aquaculture products in
South Australia, and based on outbreak data and recalls the report identified
ciguatera, scombroid, viruses, bacterial pathogens and algal toxins as the hazards of
concern.
Huss, Ababouch & Gram (2004) considered the management of seafood safety and
quality from an international viewpoint. The risks they identified were based on cases
of foodborne illness traced to seafood and rejections of seafood imports (Table 28).
During development of Standard 4.2.1 – Primary Production and Processing Standard
for Seafood, to underpin the standard A Risk Ranking of Seafood in Australia was
prepared (FSANZ, 2005). The report identifies hazards along the seafood supply
chain and also includes details on imported food testing failures and epidemiological
data. The identified hazards were consistent with those mentioned in other risk
assessment work. Some detailed description on the nature of the hazards is included
below:
Bivalve molluscs (oysters, pipis, mussels)
Bivalve molluscan shellfish are filter feeders, extracting marine algae, bacteria and
nutrients from surrounding waters. Because of this they are prone to contamination
from the growing environment. Some pathogenic bacteria, especially Vibrio spp. are
endogenous to aquatic environments and can survive and grow in oysters,
presenting a risk to health if ingested.
Bacterial pathogens may also be introduced into shellfish growing areas through
pollution from sewage and animal waste. These organisms can multiply quickly,
particularly at higher temperatures, potentially rendering oysters unsafe. Pathogenic
viruses may be introduced into shellfish growing waters through sewage pollution
and can survive for long periods in shellfish.
Oysters can extract chemical contaminants from their growing waters and
bioaccumulate them to hazardous concentrations in their flesh. Certain species of
toxin-producing algae present a food safety risk from shellfish consumption. Toxins
can accumulate to high levels in shellfish especially, particularly during periods of an
algal bloom.

Table 28 – Summary of international hazard identification studies for seafood
Data analysed Hazard
USA, fish, foodborne illness Scombroid
Ciguatera
C. botulinum
Bacterial pathogens
Norwalk virus
Poisonous fish (puffer fish)
Chemical contaminants
USA, molluscan shellfish, foodborne illness Vibrio spp.
Norwalk virus
Algal toxin
Bacterial pathogens
Scombroid
Ciguatera
Parasite
UK, seafood, foodborne illness Scombroid
Algal toxin
Virus
Bacterial pathogens
Unknown
USA, seafood, import refusals Bacterial pathogens
Scombroid
Poison
Other
EU, seafood, import rejection/detention Vibrio spp.
Bacterial pathogens
Hepatitis virus
Algal toxins
Pesticides
Metal contaminants
Antibiotics
Other chemical contaminants
Parasites
adapted from Huss, Ababouch & Gram (2004)

Prawns – wild caught
Prawns are also potentially exposed to a range of indigenous microbial contaminants
from the water environment. Vibrios are known to utilise the chitinous exoskeleton of
crustacea as points of attachment and to metabolise it as a carbon/energy source
(Karunasagar et al, 1986). V. parahaemolyticus, V. vulnificus and V. cholerae are
considered part of the indigenous microflora of estuarine prawns. Enteric pathogens
derived from faecal contamination may become established as environmental
contaminants in water from which prawns are harvested and have the potential to
contaminate free-living prawns prior to catch.
During on-board processing, dipping of prawns in metabisulphite to inhibit formation
of blackspot can present a risk to asthmatics. Prawns may also be exposed to
chemical hazards from the environment, including the metals arsenic and mercury.
Other chemical residues may be present in wild-catch crustacea due to industrial
pollution and agricultural run-off. This will be a greater risk in estuarine prawns than
those caught in open marine waters (Ross & Sanderson, 2000).
Processing of prawns can lead to the potential for contamination with marine
pathogenic bacteria, other pathogenic bacteria or chemical contaminants. Cooked
prawns can be subject to cross-contamination between raw and cooked prawns.
Finfish
At the point of harvest, hazards potentially present in finfish include metals (eg
arsenic and mercury) and indigenous pathogens from the marine or estuarine
environment which are naturally present in live fish. Marine toxins such as ciguatoxin
may be a significant hazard in tropical reef fish. Ciguatoxin is heat stable, and is not
inactivated by normal cooking. Histamine/scombroid is a hazard in certain species of
fish, particularly if the fish are harvested from warmer waters, die before landing or
are subject to time/temperature abuse after landing. Histamine is heat stable.
A number of parasites may be associated with fish species harvested from particular
locations. This is particularly significant for finfish sourced from overseas locations
and have been associated with illness in humans after ingestion of raw or
undercooked fish. C. botulinum (type E non-proteolytic strains), which causes
botulism, is commonly associated with the marine environment. As spores tend to be
associated with the gut of the fish, evisceration will reduce the risk of exposure.
Other strains may also be present in the processing environment. Cold smoked fish
have a number of significant hazards. Processing temperatures are too low to ensure
freedom from pathogens or parasites. L. monocytogenes may occur post-harvest and
during processing and prolonged storage may allow numbers to increase.
With sushi, the primary concern is related to product prepared in advance and stored
without refrigeration. Hazards include vibrios, other bacterial pathogens and viruses.
Sashimi hazards of concern are parasites and V. parahaemolyticus.

Exposure assessment
Consumption of seafood
Production data for seafood in Australia is summarised in Table 29. From these
figures, the estimated annual consumption of seafood in Australia is about 396,000
tonnes or 18-19 kg per person. This equates to about 10kg of edible weight when
the conversion factor used by Walsh & Grant (1999) is applied. The Fisheries
Research and Development Corporation (FRDC, 2002) estimated the yearly per
capita seafood consumption, expressed as edible weight, to be 15.1 kg in Sydney
and 14.7 kg in Perth. Data on the consumption of fish and seafood products by sex
and age from the National Nutrition Survey (ABS, 1995) is shown in Table 30. This
data showed that seafood was consumed by approximately 20% of the population,
with consumption levels varying between different age groups.
Table 29 – Production volumes for seafood in Australia and NSW 2006/07

Sector Australia NSW
Tonnes (gross) Value ($000) Tonnes (gross) Value ($000)
Wild caught 185,925 1,429,328 15,462 80,657
Aquaculture 59,663 793,039 5200 45,975
Seafood imports 198,602 1,184,394
Seafood exports 48,010 1,157,909
adapted from Australian Fisheries Statistics 2007 (ABARE, 2008)
Prevalence of hazards in seafood

The FSANZ (2005) risk ranking report includes statistics on failed tests for seafood
tested upon entry to Australia. These are summarised in Table 31. In addition,
information from FSANZ (2005) on Australian and international surveys of seafood
used to rank risk is included in Table 32.

Table 30 – Consumption of fish and seafood products in Australia
Sex Age Proportion of persons Median daily intake for

consuming fish and seafood consumers of fish and seafood
products and dishes 17 products and dishes
(%) (g/day)
18
Male 2-3 9.6* 63.3*
Male 4-7 10.6 71.0
Male 8 - 11 11.8 100.5
Male 12 - 15 12.8 148.0
Male 16 - 18 8.8 114.8*
Male 19 - 24 16.0 134.6
Male 25 - 44 16.6 120.0
Male 45 - 64 20.8 120.0
Male 65+ 20.3 95.2
Female 2-3 13.3 47.5*

Female 4-7 16.8 48.0
Female 8 - 11 11.5 90.4
Female 12 - 15 11.2 105.0
Female 16 – 18 16.7 95.0
Female 19 - 24 15.8 99.0
Female 25 - 44 17.2 86.3
Female 45 - 64 20.5 96.0
Female 65+ 18.8 74.5
17
Fish and seafood products and dishes are defined in the National Nutrition Survey (ABS, 1995) as including the
following:
- Fin fish (excluding canned)
- Crustacea and molluscs (excluding canned)
- Other sea and freshwater foods
- Packed (canned and bottled) fish and seafood
- Fish and seafood products
- Mixed dishes with fish or seafood as the major component
18
Results marked with * had a relative standard error of 25 – 50% due to small sample size

Table 31 – Failure rate for imported seafood products (1998 – 2003)
Commodity Hazard Failure Rate (%)
Molluscs Mercury 1.0
Salmonella 0.5
V. cholerae 0.2 (Oysters 1.0)
E. coli 2.4 (Oysters 4.8)
L. monocytogenes 0.8
Standard plate count 3.5
Crustacea Sulphur dioxide 1.9
Salmonella 0.8
V. cholerae 1.3
E. coli 0.9
Staphylococcal enterotoxins 0.3
Standard plate count 5.4
Chloramphenicol 5.3
Antibiotics 5.9
Finfish Mercury 1.3
L. monocytogenes 15.1
Scombroid/Histamine 1.6
E. coli 6.5
Standard Plate Count 1.7
adapted from Imported Foods Inspection Scheme data (FSANZ, 2005)

Table 32 – Summary of Australian seafood testing results
Hazard Commodity Detected/Sampled
V. parahaemolyticus Marine fish at market 39/66 (59%)
Unopened oysters 16/16 (100%)
Opened oysters 13/14 (93%)
Pacific oysters (69-74%)
Scallops, mussels, oysters, fish 20/80 (25%)
V. vulnificus Oysters Detected at low numbers
L. monocytogenes Smoked salmon fillets & slices 1/285 (0.4%) 2/433 (0.4%)
Salmon pâté 8/61 (29.5%) sic
Smoked fish and mussels 2/49 (4.1%)
Marina mix (31%)
Smoked fish (10%)
Seafood salad (3%)
Flake (1.5%)
19
Smoked salmon* 10/56 (17.9%)
Other smoked fish* 0/11
Salmon cheese* 3/5 (60%)
Salmon dip* 10/21 (47.6%)
Salmon mousse/ pâté* 2/8 (25%)
Cooked prawns 12/380 (3.2%)
Histamine Retail seafood 1/11 (9%) <100mg/kg
Smoked fish 0/13
Dried fish 3/5 (60%) <100mg/kg
1/5 (20%) 653 mg/kg
Canned fish 1/7 (15%) <100mg/kg
Canned tuna 3/107 (2%) 50-100mg/kg
Mercury Several species exceed the regulatory limit – see Table 33
adapted from (FSANZ, 2005)
A sampling program undertaken by the NSW Food Authority from 2004 to 2007
tested 658 samples spanning 60 species to gauge the extent of exposure to mercury
from NSW retail seafood (NSW Food Authority, unpublished). The higher level results
summarised in Table 33 do not necessarily imply non-compliance with Standard 1.4.1
– Contaminants and Natural toxicants of the Food Standards Code. The Maximum
level (ML) is applicable to the mean of results for a prescribed number of sampling
units (determined by the size of the sample lot). Overall 85% of individual samples
were below the appropriate ML but the results suggest that limiting intake of some
fish types remains a valid risk management strategy.
19
Results marked with * is data is from a NSW retail survey. The report includes international information on
Hepatitis A virus and the parasite Anisakis simplex

Table 33 – Summary of high mercury levels in NSW seafood
Fish Type Number of samples Maximum (mg/kg) 20 Mean (mg/kg) 21
Angel fish 5 1.002 0.712*
Flake 41 3.35 0.880
Ling 5 1.03 0.503
Marlin 22 1.682 0.851
Shark 23 3.47 0.690
Swordfish 37 4.092 1.454*
adapted from NSW Food Authority (unpublished)
Listeria monocytogenes in smoked fish

The UK Food Standards Agency recently surveyed L. monocytogenes in smoked fish
(UKFSA, 2008) and the results are summarised in Table 34. Detection of Listeria and
L. monocytogenes were relatively common in cold smoked fish. Detections were less
common in hot smoked fish but L. monocytogenes at levels greater than 100cfu/g
were only found in hot smoked fish. These results are consistent with Ross &
Sanderson (2000) who reported that cold smoked fish were more prone to
contamination by L. monocytogenes but, due to lower levels of background flora,
there is potential for growth to higher numbers in hot smoked fish.
Table 34 – Prevalence of L. monocytogenes in UK retail smoked fish

Cold smoked fish Hot smoked fish
Number of samples 1,344 1,878
Listeria spp. detected 282 (20.5%) 96 (5.2%)
L. monocytogenes detected 236 (17.4%) 66 (3.4%)
L. monocytogenes > 100cfu/g 0 3 (0.06%)
adapted from UKFSA (2008)
Algal biotoxins
The Shellfish program of the NSW Food Authority averaged 15-16 oyster harvest
areas closures each year attributable to biotoxin issues from July 2004 to June 2008
(unpublished data). The closures were based on either very high levels of potentially
toxic phytoplankton or positive results from screening tests for algal biotoxins.
The NSW pipi industry also experiences closures due to potential biotoxin issues,
typically in summer or early autumn. Six biotoxin closures were recorded for the
period July 07 to June 08. Pipi biotoxin management plans were introduced following
the 1997 and 1998 diarrhoetic shellfish poisoning (DSP) outbreaks and there have
been no subsequent reports of DSP attributed to NSW pipis.
20
Results for individual samples exceed the maximum level (ML) specified in Standard 1.4.1 – Contaminants and
Natural toxicants of the Food Standards Code
21
Results marked with *, the mean exceeds the ML specified by Standard 1.4.1 – Contaminants and Natural
toxicants of the Food Standards Code, which is generally 0.5 mg/kg for most fish and 1mg/kg for some fish, rays
and sharks

Fate of hazards
A number of hazards are of additional concern because they are not eradicated by
further processing or cooking. These include:
♦ Histamine / scombroid ♦ Clostridium botulinum spores
♦ Ciguatera ♦ Agrichemicals
♦ Mercury contamination ♦ S. aureus toxin.
♦ Algal toxins
Certain commodities are of additional concern because they may be consumed
without adequate cooking and bacterial pathogens or viruses, if present, are not
eliminated.
♦ Oysters
♦ RTE cold smoked and hot smoked fish
♦ Fish intended for consumption raw (eg in sushi and sashimi)
♦ Cooked prawns and other crustaceans
Foodborne illness outbreaks from seafood
OzFoodNet annual reports for 2002-2006 tabulated 85 foodborne illness outbreaks
attributed to seafood, with 558 people affected and 77 hospitalisations. Table 35
includes an updated summary of Australian foodborne illness outbreaks attributed to
fish and seafood products from 1995 to 2008, while more details of these outbreaks
are provided in Table 68 of Appendix 3.
Table 35 – Summary of foodborne illness outbreaks attributed to seafood

outbreaks
(1995-2008)
Ciguatoxin 85 449 83 0
Scombroid 32 126 17 0
Norovirus 9 303 1 0
Wax ester 6 72 0 0
Hepatitis A 5 517 64 1
Vibrio spp. 3 15 3 0
B. cereus 2 41 0 0
DSP 2 115 0 0
Toxin 2 11 0 0
Unknown 23 208 9 0
Total 180 1979 207 0

Several large food poisoning outbreaks related to consumption of oysters occurred in
NSW:
♦ in the mid 1980’s there were a series of outbreaks of Norwalk virus from oysters
harvested from the Georges River, the largest outbreak affected over 2000
people and
♦ in 1997, an outbreak of Hepatitis A virus (HAV) from Wallis Lake oysters affected
around 467 people with one death.
It is estimated the cost to the industry from the Wallis Lake outbreak was around
$30 million and was the catalyst for the introduction of the NSW Shellfish Quality
Assurance Program, the forerunner to the current NSW Shellfish Program operated
by the NSW Food Authority. Prior to 1997, there was some voluntary monitoring by
shellfish farmers, but no consistent testing of water quality in harvest areas. The
implementation of harvest area management plans has gone a long way to
minimising the risk from shellfish (Food Science Australia & Minter Ellison Consulting,
2002).
The National Risk Validation Project highlighted producers, harvesters, processors
and vendors of raw ready-to-eat seafood (including shellfish) as one of five high risk
foods (Food Science Australia & Minter Ellison Consulting, 2002). FSANZ (2005)
reports that 3 outbreaks (with 102 people affected) of shellfish poisoning occurred in
Australia in the period 1990-2000. Mussels with levels of paralytic shellfish poisoning
(PSP) toxin exceeding regulatory limits were detected in Victoria in 1988 and every
year between 1990 and 1995. PSP toxins exceeding regulatory limits have been
reported in Tasmanian mussels, oysters and scallops. Outbreaks of DSP were caused
by NSW pipis in 1997 and 1998. There has been a detection of amnesic shellfish
poisoning (ASP) toxin (domoic acid) above regulatory limits in scallop viscera from
Victoria.
Ross & Sanderson (2000) prepared detailed risk assessments on 10 hazard/product

pairs. Current national and international data suggests that their selections remain
appropriate. The extracts below are from their report and the FSANZ risk ranking.
Viral contamination of shellfish.
Enteric viruses can be introduced into aquatic environments through contamination
with sewage. They may persist longer than enteric bacteria in marine environments
and can be accumulated in bivalve molluscs. As a consequence, their presence in
shellfish does not always correlate with bacterial indicators of faecal pollution in
marine environments. Viruses may also take longer to depurate from contaminated
shellfish than enteric bacteria and viruses are more resistant to inactivation during
cooking than bacteria. Outbreaks of viral food poisoning associated with shellfish
continue to occur in Australia and worldwide. In general, the incidence of seafood-
borne viral food poisoning is low, suggesting that existing control strategies are
effective. Australian outbreaks have been associated with failures or non-
implementation of control strategies.
Noroviruses (previously known as Norwalk-like viruses) cause human gastrointestinal
illness. Symptoms in children are generally mild and self-limiting. A more severe
gastroenteritis with dehydration as the result of vomiting or diarrhoea may occur.

Mortality in the absence of other compromising factors is extremely rare. Infections
in adults typically manifest as explosive projectile vomiting and/or diarrhoea.
Incubation times are dose dependant, typically 15 – 50 hours with a mean of 24 – 48
hours (Ross & Sanderson, 2000).
Hepatitis A (HAV) is usually a mild illness characterised by sudden onset fever,
malaise, nausea, anorexia and abdominal discomfort followed in several days by
jaundice. The incubation period for HAV varies from 10 to 50 days (mean 30 days),
and is dependent upon the number of infectious particles consumed. Many infections
with HAV do not result in clinical illness, especially in children. When illness does
occur, it is usually mild and recovery is complete in one or 2 weeks. Occasionally the
symptoms are severe and convalescence can take several months. Patients suffer
from chronic tiredness during convalescence, and their inability to work can cause
financial loss. Less than 0.4% of the reported cases in the U.S. are fatal. These rare
deaths are usually in the elderly (Ross & Sanderson, 2000).
Algal toxins in shellfish

Shellfish poisoning is caused by a group of toxins elaborated by planktonic algae
upon which the shellfish feed. The toxins are accumulated and sometimes
metabolised by the shellfish. Since shellfish toxins are heat stable, the form in which
shellfish are consumed does not affect the level of the hazard. All individuals are
susceptible to shellfish toxins, although the elderly may be more severely affected,
particularly by amnesic shellfish poisoning (ASP).
There are about 20 toxins responsible for PSP, and all are chemical derivatives of
saxitoxin, but differ in the type and localisation of the derivation. PSP toxins are also
produced by species of cyanobacteria found in Australian freshwater rivers and lakes.
PSP toxins block the sodium channels of excitable membranes of the nervous system
and associated muscles. The extreme potency of PSP toxins has, in the past, resulted
in an unusually high mortality rate. In humans 120-180 µg of PSP toxin can produce
moderate symptoms, 400-1060 µg can cause death, but 2000-10,000 µg is more
likely to constitute a fatal dose.
DSP is caused by a group of high molecular weight polyethers, including okadaic
acid, the pectenotoxins and yessotoxin produced by the armoured dinoflagellate
algae including Dinophysis spp. and Prorocentrum spp. These species are
omnipresent but their toxicity is variable and unpredictable. Dense blooms can
sometimes be completely non-toxic, but at other times shellfish can become toxic
even when only sparse dinoflagellate populations are present.
No human fatalities have been reported due to DSP and patients usually recover
within 3 days. Recovery is generally complete with no after effects and the poisoning
is generally not life threatening. In extreme cases chronic exposure may promote
tumour formation in the digestive system.
ASP is caused by the unusual amino acid, domoic acid, produced by chain-forming
diatoms of the Pseudonitzschia spp. The toxicosis is particularly serious in elderly
patients. All fatalities (up to a report date of 2003) had involved elderly patients.
During an outbreak in Canada, the affected people had consumed mussels
containing 300-1200 µg/g of domoic acid.

Vibrio parahaemolyticus in molluscs and crustaceans
Illness is caused when the ingested organism attaches itself to an individual’s small
intestines and secrets a toxin. Not all strains of the organism are pathogenic. There
appears to be a lack of correlation between pathogenicity and serotype of
V. parahaemolyticus isolates. Virulence correlates with the ability to produce a
thermostable direct haemolysin termed the Kanagawa Phenomenon (KP) haemolysin.
KP negative strains appear to be non-pathogenic (Sanyal & Sen, 1974).
Human volunteer studies have established an infectious dose for KP positive strains
between 2 x 105 and 3 x 107 cfu. V. parahaemolyticus can multiply rapidly in seafood
at permissive temperatures. In a study numbers of V. parahaemolyticus on octopus
stored at 30°C increased from 102/g to 108/g in 6 hours.
Listeria monocytogenes in RTE smoked fish products.

Indications of the nature of foodborne listeriosis have emerged from outbreak data,
animal studies and mathematical modelling of illness. Knowledge is incomplete
because of difficulties such as: some strains of L. monocytogenes are pathogenic but
others are not; the determinants of pathogenicity are not well understood and so the
distribution of pathogenic strains in food is not known.
However, there is general acceptance of some elements of the disease process (Ross
& Sanderson, 2000):
♦ The infectious dose of L. monocytogenes cannot be stated with precision but it
appears that human listeriosis does not usually occur in the absence of a
predisposing risk factor (such as compromised immunity)
♦ Most commentators consider doses of <1000 organisms are highly unlikely to
cause illness in normal individuals, and this has been reflected in food safety
regulations
♦ Attempts to link exposure to the organism to observed levels of illness suggest
the infective dose is much higher than 1000 organisms – but it appears in some
cases fewer than 1000 organism may cause illness
♦ This difference between observed and predicted cases of illness suggests that the
human population susceptible to listeriosis is actually a much smaller sub-group
of the immunocompromised population. However, it could also be an artefact of
under-reporting of listeriosis cases, due to some cases only developing mild flu-
like symptoms.
Clostridium botulinum in vacuum-packed RTE fish products

Foodborne botulism results from eating food contaminated with preformed botulinum
toxin due to the presence and growth of Clostridium botulinum bacteria. Botulism
varies from a mild illness to an acute disease which can be fatal. With treatment,
death due to respiratory failure or airway obstruction is rare. The case fatality rate in
North America has fallen from 60% to 20% due to the availability and prompt
administration of antitoxin. Provision of artificial respiration greatly increases the
chances of recovery from intoxication. Nonetheless, recovery may take many
months.

Internationally, the aquatic environment of fish is frequently contaminated with
C. botulinum spores and so fish will often be contaminated also. The organism only
grows in the absence of air, and represents a risk only in those products which
exclude oxygen by virtue of their packaging (eg vacuum packaged, MAP) or contain
anaerobic regions (eg gut left intact). The toxin is heat labile, so the hazard is
primarily limited to RTE seafoods that are stored in vacuum or anaerobic packaging.
For seafoods, botulism is most commonly associated with C. botulinum type E. This
type is capable of growth and toxin production at refrigeration temperatures but
generally needs weeks of growth to produce amounts of toxin to cause foodborne
illness. This is significantly greater than the shelf life generally observed for seafood
and seafood products. Botulism is a concern in extended shelf life products and thus
the concern with vacuum packaging and canning.
Ciguatera poisoning
Ciguatera is a form of human poisoning caused by the consumption of subtropical
and tropical marine finfish which have accumulated naturally occurring toxins
through their diet. In the US, ciguatera intoxication is considered to be one of the
two most common sources of seafood-borne food poisoning associated with finfish.
Human populations of tropical and subtropical marine regions have a much higher
incidence of ciguatera intoxication.
A relatively high incidence of ciguatera poisoning has been reported in Queensland.
Only a small volume of reef fish from Queensland or other problem areas is on sale
in NSW. There have been several large scale outbreaks in NSW involving scores of
victims. The true incidence of ciguatera poisoning in NSW is unknown. The illness
has only recently become known to the general medical community and there is a
concern that the incidence is largely under-reported because of the general non-fatal
nature and short duration.
The ciguatoxins are lipid-soluble toxins that are relatively inert molecules and remain
toxic after cooking and exposure to mild acidic and basic conditions. The minimum
toxic dose is estimated to be about 1ng/kg body weight. In one incident 6 US
soldiers became ill after eating fish containing approximately 20ng ciguatoxin/g flesh.
Scombroid / Histamine poisoning

Scombroid poisoning (histamine poisoning) is associated with the ingestion of foods
that contain high concentrations of histamine and possibly other vasoactive amines
and compounds. Histamine is the physiological amine involved in allergic reactions
and is the main toxin involved in histamine fish poisoning. A “missing factor” might
be required to produce illness.
Due to uncertainty about its aetiology, it is difficult to determine the susceptible
population for scombroid poisoning. A wide range of histamine concentrations in
implicated foods, particularly the increasing number of incidents associated with low
histamine concentrations, suggests that some individuals are more susceptible to the
toxin than others. Symptoms can be severe for the elderly and for those taking
medications such as isoniazid, a potent histamine inhibitor.

Mercury in seafood
The commentary provided by Ross & Sanderson (2000) on mercury in NSW seafood
has not lost currency. “Based on acute mercury food poisonings in Japan and Iraq, it
is known that high levels of dietary mercury may cause measurable deficits in mental
and physical development of young children exposed during gestation. Low levels of
mercury are naturally present in the environment and in all foods. Inorganic mercury
is poorly absorbed via the diet, however, in aquatic environments bacteria can
convert inorganic mercury to methylmercury (MeHg) which is readily absorbed by the
human body. MeHg is bioaccumulated in aquatic food chains, so all fish contain small
amounts of mercury in their muscle tissue. Predatory fish or mammals such as
whales at the top of the food web have the highest amounts. Mercury levels in most
commercially harvested oceanic fish in the US and Australia are <0.5 mg/kg MeHg,
but some large predators such as sharks, marlin and swordfish may have higher
levels. Numerous studies have shown that nearly all the human exposure to MeHg
occurs via seafood (predominately finfish) consumption. Therefore individuals who
regularly consume large amounts of fish (particularly those fish with high mercury
levels) could be exposed to dangerous levels of mercury”.
Corbett & Poon (2008) reported on cases in NSW where elevated mercury levels
were found in three infants, who had eaten fish congee (a rice and fish porridge) as
a weaning food and ate fish regularly as toddlers. The parents had sought medical
advice as a result of the children displaying either developmental delay or
neurological symptoms. Fish congee is a common weaning food in coastal regions of
southern China and South-East Asia. The authors recommended the development of
multilingual information about fish and mercury be made available to pregnant
women and mothers, especially targeting groups who are likely to be frequent
consumers of fish and who use fish in weaning and infant foods.
Viral contamination of shellfish
There is very little information on levels of enteric viruses in shellfish available on
which to base a risk characterisation. The greatest uncertainties in assessing the risk
are the levels of the viruses of concern (HAV and norovirus) in contaminated
shellfish, the frequency of shellfish contamination and the rate of loss of infectivity of
the viruses in the environment and the oyster (Ross & Sanderson, 2000).
FSANZ concluded that the overall public health risk for bivalve molluscs is relatively
high for products harvested in polluted waters and/or waters not subject to a
monitoring scheme such as the Australian Shellfish Quality Assurance Program
(ASQAP). The relative risk ranking is not significantly reduced where these products
are lightly cooked or steamed prior to consumption (FSANZ, 2005).
Where the implementation of shellfish safety management schemes, such as ASQAP,
is taken into account, the relative risk ranking for oysters and other bivalves is
reduced to medium. The Seafood safety scheme requires shellfish harvesters to
comply with the harvest area management plans developed by the NSW Food
Authority. These plans are established to ensure compliance with ASQAP
requirements.

Algal toxins in shellfish
Ross & Sanderson (2000) assessed the risk of algal biotoxins as low from commercial
harvest areas and medium from recreational harvest areas. The difference was due
to the algal monitoring and area management that occurs in commercial harvest
areas.
FSANZ found the relative risk is medium for waters that are subject to pollution, but
where harvesting of shellfish is controlled under an effective management system.
The risk rating is elevated to high if there is no effective management system in
place (FSANZ, 2005).
Vibrio parahaemolyticus in molluscs and crustaceans

Levels of V. parahaemolyticus in Australian seafood are similar to that found in other
parts of the world. It has been estimated that a meal of raw shellfish would contain
no more than 104 cfu KP positive cells, based on typical numbers of
V. parahaemolyticus present in fish and shellfish and the low incidence of KP positive
isolates in the marine environment. For an infectious dose to be reached,
mishandling of food at temperatures allowing the growth of the bacterium would be
required.
As Vibrio spp. are sensitive to heat, it is raw or inadequately cooked product that
poses the greatest risk of vibriosis. However, several documented cases have
involved post processing contamination. The rapid growth rate of the organism at
ambient temperatures exacerbates the consequences of post-processing
contamination.
Although pathogenic Vibrio spp. are often found in bivalve molluscs and on
crustaceans, the incidence of illness is low. For healthy individuals, doses of
organisms higher than those normally found on food are required. The risk of
contamination is seasonal, corresponding to the increased levels of Vibrio spp. in
growing areas as water temperatures rise. The risk of thermal abuse also increases
during summer.
The FSANZ relative risk ranking for V. parahaemolyticus is low but V. vulnificus and
V. cholerae are rated medium based on severity of illness. The ranking for
V. parahaemolyticus might change if the pandemic O3:K6 strain naturalises in
Australian waters.
Listeria monocytogenes in RTE smoked fish products.

Based on models developed overseas Ross & Sanderson (2000) estimated that 6-7
cases of listeriosis in NSW per annum would be attributable to smoked salmon. This
estimate is about the same order of magnitude as the overall level of incidence
observed from all potential avenues of exposure. The estimate was noted to be
conservative because Australian regulations are tighter than those countries on
which the models were based. Their revised estimate was, at most, a few cases of
listeriosis from smoked vacuum packed seafood per annum in NSW. The outcome of
the FDA/USDA (2003) risk assessment for L. monocytogenes predicted cases of
listeriosis from RTE seafood products to occur very rarely (Table 36), however the
risk per serving for cooked RTE crustaceans was considered high.

Ross & Sanderson (2000) then estimated the likely affect of a single, high
contamination event. Depending on the assumptions used for different scenarios, a
single batch of contaminated product was predicted to impact <1, about 20 or 65
immunocompromised consumers.
FSANZ found that contamination of cold smoked products with L. monocytogenes at
levels representing a health risk to the general population is considered unlikely. This
rose to ‘likely’ where there is insufficient management of risk through the food chain
and for susceptible sub-populations. This rises further to ‘very likely’ when both
conditions apply.
Other than scrupulous factory hygiene, there is no critical control point (CCP)
available to prevent contamination of RTE cold smoked seafood products. Hot
smoking can reduce the levels of L. monocytogenes on the product, but post-
processing contamination can occur. It appears that some factories are able to
achieve very low levels of contamination relatively consistently, but others are not
and rapidly become recolonised.
Table 36 – Risk ranking for seafood products contaminated with Listeria

monocytogenes
Plant product Risk Predicted cases of Risk Predicted annual
ranking listeriosis per serve ranking number of listeriosis
(per serve) (in Australia) 22 (per cases
annum) (in Australia) 23
Cooked RTE High 5.1 x 10-9 Moderate 0.2
crustaceans
Smoked seafood High 6.2 x 10-9 Moderate 0.1
-11
Raw seafood Low 2.0 x 10 Low 0
Preserved fish Low 2.3 x 10-11 Low 0
Clostridium botulinum in vacuum-packed RTE fish products

On the basis of the low incidence of spores in products likely to be available in the
Australian market, and in particular the typical salt levels in these products, type E
botulism risk from these products is considered to be negligible. Product shelf lives
also mitigate against the risk of sufficient growth of C. botulinum potentially present
to reach toxic doses. Ross & Sanderson (2000) note that other products (including
those with the gut intact) and products from other regions (where C. botulinum
spores could be more frequent) may represent a greater risk.
22
patterns for these foods are identical in Australia and the USA
23

FSANZ (2005) ascribes a medium relative risk rating for C. botulinum in smoked fish
products. This reflects the balance between severity (severe) and likelihood
(unlikely).
Ciguatera poisoning
Ciguatoxins are responsible for many outbreaks of foodborne illnesses due to fish
consumption in Australia. In the period 1995 to June 2002, outbreaks were recorded
in all states except South Australia and Tasmania. Queensland and NSW accounted
for the great majority of outbreaks, reflecting both the linkage of the illness with fish
caught near tropical reefs in Queensland and the role of Sydney as the hub for
marketing seafood on the east coast of Australia. A number of fish species were
involved, with coral trout, queenfish, Spanish mackerel and cod species predominant.
FSANZ (2005) rates the relative risk as medium for tropical fish species (in particular
larger members of particular species from certain fishing areas).
Scombroid / Histamine poisoning

Time-temperature abuse during transport, processing, storage or display will
potentially allow formation of histamine. Scombroid species of fish, which have high
levels of histadine, are more likely to accumulate high concentrations of histamine
under conditions of temperature abuse, but many non-scombroid species have also
been involved in outbreaks of histamine fish poisoning. Data from testing samples at
retail and results from testing imported fish products indicate a low level of histamine
in whole fish and fish fillets available in Australia. However, epidemiological data
shows a significant number of outbreaks in commercial and restaurant settings,
indicating potential problems in the cold chain and resultant time-temperature abuse.
Tuna, blue grenadier and mahi mahi have been identified as species involved in
these outbreaks.
FSANZ allocated a relative risk rating of low, due to a moderate severity of disease
and the probability of occurring as ‘likely’ (FSANZ, 2005).
Mercury in seafood
Ross & Sanderson (2000) approached a risk assessment for mercury in seafood by
calculating the weight of fish required to equal the provisional tolerable weekly intake
(PTWI) of methylmercury for consumers of varying body weights and various
mercury levels. Their tables are reproduced in Table 37, except that the Joint
FAO/WHO Expert Committee on Food Additives (JECFA) Provisional tolerable weekly
intake (PTWI) estimate has been reduced following a review (JECFA, 2004).
Estimates in Table 37 are based on the JECFA PTWI and US EPA reference dose, for
comparison.

Table 37 – Seafood consumption required to reach reference doses for
methylmercury
Mercury Body weight
level
mg/kg 13 kg 40 kg 60 kg 70 kg 13 kg 40 kg 60 kg 70 kg
Weekly consumption (g) required to Weekly consumption (g) required to
reach JECFA PTWI of 1.6ug/kg body reach to USEPA reference dose of
weight/week 0.7ug/kg body weight/week
0.15 146 449 674 786 63 196 295 344

0.5 44 135 202 236 19 59 88 103
1.0 22 67 101 118 10 29 44 52
1.5 15 45 67 79 6 20 29 34
adapted from Ross & Sanderson (2000) JECFA (2004)

Table 37Table 37 shows that for non-predatory fish (average mercury level 0.15
mg/kg - Ross & Sanderson 2000) significant consumption is required to exceed the
PTWI. Average consumption figures quoted above equate to 200-300g of seafood
per week. Consumers who predominately consume predatory fish or those
consuming above average levels of fish are at risk.
JECFA noted the existing PTWI of 1.6 µg/kg body weight was set in 2003 based on
the most sensitive toxicological end-point (developmental neurotoxicity) in the most
susceptible species (humans). However life-stages other than the embryo and foetus
may be less sensitive to the adverse effects of methylmercury (JECFA, 2006).
In the case of adults, intakes of up to about two times higher than the existing PTWI
of 1.6 µg/kg body weight would not pose any risk of neurotoxicity. Although in the
case of women of childbearing age, the intake should not exceed the PTWI, in order
to protect the embryo and foetus.
JECFA’s data did not allow firm conclusions to be drawn regarding the sensitivity of
infants and children compared to that of adults. While it is clear that they are not
more sensitive than the embryo or foetus, they may be more sensitive than adults
because significant development of the brain continues in infancy and childhood. The
joint committee could not identify a level of intake higher than the existing PTWI that
would not pose a risk of developmental neurotoxicity for infants and children (JECFA,
2006).
Conclusion
The Wallis Lake Hepatitis outbreak in 1997 graphically demonstrated the need for
tighter food safety controls on commercial harvesting of shellfish for human
consumption. Since that time, the implementation of a Seafood safety scheme and
the NSW Shellfish Program has significantly improved the safety of shellfish through
the classification of harvest areas and the implementation of harvest area
management plans which identify high risk events such as heavy rainfall and holiday
periods which may contribute to pollution of the waterways and compromise shellfish
safety. As coastal populations continue to increase and place additional pressure on
local infrastructure such as sewage treatment plants, it is considered that the future
role of the NSW Shellfish Program in ensuring the continued safety of shellfish is
vital. This was acknowledged by FSANZ when it ranked shellfish harvested from
managed areas as a medium risk, as opposed to high risk when these controls were
not in place.
The management of other food safety hazards associated with seafood, such as
minimising the risk of histamine poisoning, requires general food safety control
measures such as hygiene and sanitation and the application of appropriate storage
temperatures. The seafood safety scheme requires businesses processing seafood to
implement a food safety program, to ensure appropriate control measures are
implemented for hazards such as L. monocytogenes and C. botulinum.
Because it naturally occurs in seafood, the issue of mercury is addressed through
consumer education campaigns, particularly targeting high risk consumers such as
pregnant women.

References – Seafood
ABARE [Australian Bureau of Agricultural Resource] (2008). Australian Fisheries Statistics
2007. Australian Bureau of Agricultural Resources. Retrieved 30 September 2008, from
http://www.abare.gov.au/publications_html/fisheries/fisheries_08/08_fishstats.pdf
January 2009, from
D460/$File/48040_1995.pdf
Corbett, S.J. & Poon, C.C.S. (2008). Toxic levels of mercury in Chinese infants eating fish
congee. Medical Journal of Australia. 188(1), 59-60.
Final Report.
FRDC (Fisheries Research and Development Corporation] (2002). Retail Sale and
Consumption of Seafood (Revised Edition). Ruello and Associates for the Fisheries Research
and Development Corporation. Retrieved 14 January 2009, from
http://www.frdc.com.au/bookshop/Seafood_report.pdf
FSANZ (2005). Final Assessment Report, P265, Primary Production and Processing Standard
for Seafood (Attachment 10). Retrieved 3 September 2008, from
http://www.foodstandards.gov.au/_srcfiles/P265_Seafood_PPPS_FAR.pdf#search=%22risk%
20ranking%20seafood%22
Huss, H.H., Ababouch, L. & Gram, L. Assessment and management of seafood safety and
quality. FAP Fisheries technical Paper 444. Retrieved 30 September 2008, from
ftp://ftp.fao.org/docrep/fao/006/y4743e/y4743e00.pdf
JECFA [Joint FAO/WHO Expert Committee on Food Additives] (2004), WHO Food Additives
Series 52, Safety Evaluation of Certain Additives and Contaminants. Retrieved 21 November
2008, from http://whqlibdoc.who.int/publications/2004/924166052X.pdf
JECFA [Joint FAO/WHO Expert Committee on Food Additives] (2006), Joint FAO/WHO Expert
Committee on Food Additives Summary and Conclusions of the 67th Meeting. Retrieved 21
November 2006, from http://www.who.int/ipcs/food/jecfa/summaries/summary67.pdf
Karunasagar, I, Venugopal, M.N., Karunasagar, I. & Segar, K. (1986). Role of chitin in the
survival of Vibrio parahaemolyticus at different temperatures. Canadian Journal of
Microbiology 32, 889-891.
OzFoodNet (2002 to 2006). Annual Report of the OzFoodNet Network (5 individual annual
reports). Retrieved 30 September 2008, from
http://www.ozfoodnet.org.au/internet/ozfoodnet/publishing.nsf/Content/reports-1
Ross, T. & Sanderson, K. (2000). A Risk Assessment of Selected Seafoods in NSW (Final
report December 2000). SafeFood Production NSW.
Ross, T. Walsh, P. & Lewis, T. (2002). Risk Assessment of Fish Cold Smoking and marination
Processes Used by Australian Businesses. Biodevelopment Consulting Pty. Ltd for SafeFood
Production NSW.
Sanyal, S.C. & Sen, P.C. (1974). Human volunteer study on the pathogenicity of Vibrio
parahaemolyticus. In T. Fujino, G. Sakaguchi, R. Sakazaki, Y. Takeda (Eds) International
Symposium on Vibrio paramhaemoylticus (pp. 227-230) Saikon Publishing Co. Tokyo.
UK Food Standards Agency (2008). A microbiological survey of retail smoked fish with
particular reference to the presence of Listeria monocytogenes, Food Survey Information
sheet 05/08. Retrieved 30 September 2008, from
http://www.food.gov.uk/multimedia/pdfs/fsis0508.pdf

Walsh, P. & Grant, N. (1999). Consultancy for Researching the Business Profile of the NSW
Seafood Industry & Food Safety Hazards of Seafood in NSW (Final Report). Food Factotum.
Woods, J. & Ruello, N. (2000). Report of Seafood Sector Working Groups’ Development of
Model Food Safety Programs. Ruello and Associates Pty. Ltd. For SafeFood Production NSW.

Vulnerable persons food safety
scheme
From time to time certain population subsets within the community are more at risk
to foodborne illness or can develop more serious complications from foodborne
illness than the general population (Acheson & Lubin, 2008). Exactly defining who is
vulnerable can be problematic. This is predominately due to the differing degree of
vulnerability from one person to the next and the varying degrees of virulence of
some pathogenic microorganisms to different vulnerable sub-populations (Acheson &
Lubin, 2008). Acheson & Lubin (2008) provides an overview of the different factors
that influence vulnerability and in general terms vulnerability is due to a suppressed
immune system, either due to age, pregnancy, disease or pharmacologic therapy (ie
chemotherapy or immunosuppressive drug use after an organ transplant). As such it
is common to include the following sub-groups within the vulnerable population
group:
♦ Children under 5 years old
♦ People over 65 years of age
♦ Pregnant women and
♦ Persons with depressed immunity due to either some underlying condition,
therapy treatment or medication.
The increased risk posed by the vulnerable populations require businesses that cater
specifically to these groups to consider the risk when deciding on the types of foods
and how they prepare, store and serve these foods. In developing Standard 3.3.1 -
Food Safety Program for Food Service to Vulnerable Populations of the Food
Standards Code, Food Standards Australia New Zealand (FSANZ) defined the
vulnerable population by considering the types of businesses likely to serve food to
these people (FSANZ, 2006). Standard 3.3.1 of the Food Standards Code (FSANZ,
2008) includes a list of these businesses to which the standard applies, these
include:
♦ Hospitals
♦ Nursing homes
♦ Hospices
♦ Certain day care establishments and
♦ Childcare centres.
In performing a risk assessment on businesses catering to vulnerable populations, it
is acknowledged that the businesses can supply a variety foods to these groups and
the methods for preparation will vary from complete preparation and assembly within
the business through to purchase of ready-to-eat (RTE) foods. To avoid duplication
this section should be ready in conjunction with other sections within this risk
assessment in respect to the risk posed by different foods. Information will be
provided to illustrate areas of concerns and elaborate on other foods not covered in
other sections of this document.

This section will focus on microbiological hazards, only as the risks posed by chemical
and physical hazards are not known to be influenced by a decreased immunity. It
should be noted that most of the risk assessments conducted do not specifically
address establishments serving to vulnerable populations. Where they do examine
specific hazards that affect the vulnerable population (eg L. monocytogenes ) the
context is usually within that of the general population and includes both those
situated in care-type establishments and those living outside these establishments.
Wherever possible, this risk assessment will attempt to focus on the risks associated
with those people within care-type establishments, although due to the lack of
information specific to these establishments this may not always be possible.
When considering the food safety hazard presented to vulnerable populations, the
hazards can be separated into two groups:
♦ Specific hazards – those hazards that present a unique risk to vulnerable
populations and
♦ General hazards – those hazards that, due to a decrease in immunity of an
individual, can result in a greater prevalence in illness when compared to the
general population or result in more serious illnesses.
General information concerning the hazards included in this section can be found in
Appendix 1.
Specific hazards
It is well documented the importance of controlling L. monocytogenes in foods
consumed by the vulnerable population. While the exact dose needed to cause illness
in the vulnerable populations is ill-defined and open for much debate, it is generally
agreed that lower infective doses are needed for illness to occur within the
vulnerable population. However, the type and severity of illness may be dependent
on virulence of the pathogen, host susceptibility and the food matrix (FDA/USDA,
2003). Sutherland et al. (2003) notes that while the infective dose is not clearly
defined, some studies suggest infective doses as low as 102 to 103 cfu/g may cause
illness.
L. monocytogenes is of concern in any RTE food or foods not likely to receive a heat
treatment prior to consumption. This is predominately due to the organism being
ubiquitous in nature, the potential for cross-contamination after cooking and the
ability of the organism to grow at refrigeration temperatures. In their risk
assessment, the FDA/USDA (2003) ranks the potential risk posed by some RTE
foods. Those of very high to high risk include:
♦ Deli meats and uncooked frankfurters
♦ Pâté and meat spread
♦ Unpasteurised milk
♦ Smoked seafood

♦ High fat and other dairy milk
♦ Pasteurised milk and
♦ Soft unripened cheese
Others which present a low risk include cooked crustacean, salads, fermented
smallgoods, other soft cheese and fruits and vegetables.
In general terms, any foods that can support the growth of L. monocytogenes and
does not include a cook step prior to consumption can potentially present some level
of risk to the vulnerable populations.
Infant botulism has been reported in many countries including Australia. It is caused
by the ingestion of C. botulinum spores which subsequently germinate, multiply and
produce toxin in the infant’s gastrointestinal tract. It usually occurs in infants aged
one year or less. Symptoms include constipation followed by weak sucking and
crying ability. The illness affects the nervous system and while death can occur,
mortality rates are generally low due to good intensive car facilities. In cases of
infant botulism, the cause is often unknown, however the presence of C. botulinum
in honey is thought to be one cause of infant botulism (Szabo & Gibson, 2003).
Enterobacter sakazakii
E. sakazakii, recently reclassified into the genus Cronobacter, is a pathogenic
microorganism that has been linked to foodborne illness outbreaks predominately
affecting infants (Lenhner & Stephan, 2004). While there is limited surveillance data,
FAO (2008) reports at least 120 cases worldwide with 27 deaths. Powdered infant
and follow-on formula have been identified as the main food vehicle, with practices
such as reconstitution with warm water and holding bottles at room temperature
increasing the risk of foodborne illness (FAO, 2007 FAO, 2008). Other factors thought
to increase the risk of illness include: age of the infant, nutritional status, HIV status,
other clinical conditions, pharmaceutical treatmen,t low birth weight and premature
birth (FAO, 2008). As with other Enterobacter species, E sakazakii isolates are
thought to have a high rate of antibiotic resistance (Lehner & Stephan, 2004).
Vibrio vulnificus
A specific sub-group within the vulnerable population are at risk from infection by
V. vulnificus is found in the marine environment and can contaminate seafood.
V. vulnificus infections normally affect people with liver dysfunctions (eg cirrhosis,
hepatitis) and also patients with malignancies or those who have undergone
gastrectomy (ICMSF, 1996). Symptoms of infection from V. vulnificus include fever,
chills and nausea (Desmarchelier, 2003). While infections are rare, mortality rates
are high. Most illnesses have been linked to consumption of raw seafood,
predominately raw oysters (Desmarchelier, 2003).
General hazards
When vulnerable populations are exposed to other pathogenic microorganisms the
resulting illnesses are like to be more prevalent and more severe than in the general
population. Buzby (2002) attributed this in elderly people to age related factors (eg
decreased immune function and stomach acid production, digestive orders,

medication and altered sense of smell and taste) and a decrease in stomach and
intestinal contractions resulting in a longer time required to eliminate pathogens and
allowing a greater time for toxin formation and damage. Buzby (2002) also reports
that in the US, rates of foodborne illness can be 10 to 100 times greater for elderly
people within nursing homes when compared to the general population and that the
elderly are more vulnerable to gastroenteritis-induced deaths.
Other sub-groups within the vulnerable population exhibit increased sensitivity to
foodborne illnesses due to decreased immunity. Acheson & Lubin (2008) contribute
this increased risk due to many factors including the use of antibiotics that, while
they aim to treat illnesses caused by certain pathogens, they can also eliminate from
the intestinal tract certain microorganisms that inhibit or suppress the growth of
pathogenic microorganisms. Cancer and transplant patients also have greater
susceptibility to foodborne illness due to their treatments lowering the immune
system, with mortality rates from foodborne illness higher than the general
population (Acheson & Lubin, 2008).
Jay et al (2003) also suggests that the immunocompromised or those with
underlying disease are at a greater risk of infection from Salmonella and the infection
is likely to result in more serious illness. It is thought that the lower gastric acidity
and immature immune response may influence the sensitivity of children to
salmonellosis (Jay et al, 2003). This appears to be supported by a higher number of
reported Salmonellosis infections in children aged four or under, at least three times
higher than other age groups (NSW Health, 2008).
Other pathogens where increased prevalence or severity has been observed in the
vulnerable population include:
♦ Enteropathogenic E. coli – strains of shiga toxigenic E. coli (STEC) are known to
cause severe illness in infants and the elderly and can result in death
(Desmarchelier & Fegan, 2003)
♦ Staphylococcus aureus – while for the healthy populations staphylococcal food
poisoning is rarely fatal, fatalities have been reported in infants and the elderly
(Stewart, 2003)
♦ Clostridium perfringens – fatal cases of C. perfringens food poisoning are
generally associated with the elderly in institutionalised settings (Bates &
Bodnaruk, 2003) in the general population fatalities are rare and
♦ Bacillus cereus – fatal cases are very rare, when reported they have been linked
to children with liver failure (Dierick et al, 2005)
Exposure assessment
Estimating the exact portion of the vulnerable population who are in care-type
establishment that provide food, and the number of meals served by these facilities
is difficult, although there is some information that may be used to estimate potential
numbers of both.
Population figures from the Australian Bureau of Statistics surveys (ABS, 2005; ABS,
2008) indicate that in NSW:
♦ In June 2008 there were 225,945 children aged 4 years old or younger and

♦ In 2005, there were 17.5% and 35.8% of children aged 0 to 2 years old and 3 to
4 years old respectively in long day care.
Using these figures it could be assumed that approximately 26.6% of children aged
less than 5 years old are in long day care, which would correlate to 60,214 children
in long day care facilities. It should be noted that not all these children would be
served meals prepared by the facility and the number of meals each facility serves
may differ.

A survey conducted by the NSW Food Authority (2008a) indicates that:
♦ 1,856 childcare centres in NSW provide food for approximately 79,808 children
each day and
♦ Approximately 26,815,488 meals are served in childcare centres each year.
ABS data (ABS, 2008) also indicate that in June 2007, there were 422,656 people
aged 65 or older. The NSW Food Authority (2008b) surveyed other businesses
included in the definition of Standard 3.3.1 - Food Safety Program for Food Service
to Vulnerable Populations of the Food Standards Code and found that:
♦ there are 1867 facilities in NSW as defined by Standard 3.3.1 (excluding childcare
facilities) and
♦ these facilities serve approximately 106,824,172 meals each year
Therefore in total “food service to vulnerable populations” facilities would serve
approximately 133 million meals per year in NSW. It would be expected that some of
the components of these meals may present a risk to sub-groups within the
vulnerable population.
Foodborne illness outbreaks involving food service establishments for
vulnerable populations
Table 38 provides a summary of foodborne illness outbreaks in food served to
vulnerable persons in Australian institutions (Table 69 of Appendix 3 provides more
detailed information on each outbreak). Since 1995 there have been 67 foodborne
illness outbreaks across Australia involving establishments that serve food to
vulnerable populations, with 1138 illnesses, 64 hospitalisations and 12 fatalities.
These outbreaks occurred in aged-care facilities, childcare centres and hospitals and
the most common organism implicated was Salmonella, others organisms involved
include C. perfringens, L. monocytogenes and Campylobacter.
An outbreak in 1998-1999 in aged-care facilities and hospitals in the Hunter Valley,
NSW highlighted the risks of listeriosis from foods served in these establishments.
The implicated food was fruit salad and the outbreak affected 9 patients, with 6
deaths resulting. All patients were elderly, and some had underlying conditions
making them more susceptible to infection with L. monocytogenes. All the
establishments served food prepared in a central catering facility (Food Science
Australia & Minter Ellison Consulting, 2002). One sample of fruit salad subsequently
tested positive for low levels (<50 cfu/g) of L. monocytogenes, a level considered
unlikely to cause illness, even in immunosuppressed individuals.
Vulnerability to foodborne illness

Previous sections of this chapter provide some insight into the factors why some
groups within the population are more vulnerable to foodborne illness than others.
This can be further illustrated by reviewing foodborne illness surveillance data. Table
39 provides a breakdown on the percentage of outbreaks reported to have occurred
in facilities serving food to the vulnerable populations.

Table 38 – Summary of foodborne illness outbreaks attributed to food served to
vulnerable persons
outbreaks
(1995-2008)
Campylobacter spp. 7 101 6 0
L. monocytogenes 5 24 5 7
Norovirus 4 111 0 0
Toxin 3 44 1 0
Viral 3 38 0 0
B. cereus 1 19 0 0
St. aureus 1 7 0 0
Cryptosporidium 1 4 0 0
Pathogenic E. coli 1 2 0 0
Unknown 8 126 8 0
Total 67 1138 64 12
Table 39 – Institutional foodborne illness outbreaks as a percentage of all

outbreaks 24
Year Outbreaks Cases Hospitalisation Deaths
(% of total) (% of total) (% of total) (% of total)
2001 5.8% 2.9% 1.4% NR 25
2002 8.7% 5.6% 4.8% 50%
2003 15.1% 16.2% 32.4% 66.7%
2004 9.3% 8.1% 24.1% NR
2005 12.7% 10.3% 6.0% NR
2006 6.1% 6.4% 24.6% NR
adapted from outbreak data from OzFoodNet 2002-2006 (OzFoodNet Working Group, 2003; 2004;
2005; 2006; 2007)
Based on NSW Food Authority research (2008) and ABS data (ABS 2005 ABS 2008a
ABS, 2000b), the percentage of the NSW population within facilities catering to
vulnerable populations is approximately 2.5%. When this is compared to the figures
in Table 39, it can be seen that foodborne illness affecting individuals in facilities
24
Institutions include aged-care facilities, child-care, hospitals and institutions
25
NR – not reported

catering to vulnerable populations are over-represented compared to the entire
population which may be an indication of their increased vulnerability.
Prevalence of pathogens
Very little information is available on the prevalence of pathogens or other
microorganisms in foods served to vulnerable populations. Other chapters within this
document provide some general information on the prevalence of microorganisms in
certain commodities some of which would be served to vulnerable populations.
A study conducted by Gillespie et al (2001) looked at the microbiological quality of
sliced cold RTE meats from catering establishments. They found that 26% of
samples were categorised as unsatisfactory when compared to UK Public Health
Laboratory Services microbiological guidelines, with 0.4% of samples categorised as
unacceptable or potentially hazardous. Gillespie et al (2001) also compared the
results of various food handling practices and found:
♦ A higher level of unsatisfactory or unacceptable results with product made
external to the kitchen when compared to product made in-house
♦ A higher level of unsatisfactory or unacceptable results with product purchased
pre-sliced when compared to product sliced in-house.
A review of ready-to-use vegetables from health-care facilities found
L. monocytogenes in 5/135 samples (3.7%) and also found total bacterial levels
similar to samples that had been subjected to temperature abuse scenarios
(Odumeru et al, 1997).
During 2005 and 2006, Little et al (2008) undertook a study on the microbiological
safety of sandwiches served in hospitals and other health care establishments in the
UK. In this study they found L. monocytogenes in 2.7% of 88 samples which
included samples collected from wards. They also found a higher frequency of
L. monocytogenes in sandwiches prepared outside the establishment, where the
filling included poultry meat or contained salad ingredients, soft cheese and/or
mayonnaise.
Food service operations

Food service operations by establishments preparing foods for vulnerable populations
can undertake a variety of methods to prepare these foods. The types of operations
can include:
♦ Preparation and plating of raw or RTE foods
♦ Preparation and plating of previously cooked foods without further heating
♦ Preparation and plating of freshly cooked foods
♦ Reheating and plating of foods previously cooked using:
o Cook chill for short shelf life or
o Cook chill for extended shelf life.
There are also some other specific operations for certain sub-groups that present
specific hazards and will influence the risk to the vulnerable populations. Examples of
these include:

♦ Visitors to some establishments (eg hospitals, aged-care facilities) bringing food
to patients or residents, some of which can present a risk to the sub-population
(Wall, 2008)
♦ Texture-modified or puréed foods provide the opportunity for recontamination of
cooked foods due to improperly cleaned and sanitised equipment (Tallis et al,
1999)
♦ Extended storage and handling of reconstituted infant formula can increase the
risk of foodborne illness in infants due to E. sakazakii (Lehner & Stephan, 2004).
In addition to these operations, food establishments may also purchase some foods
or meals ready cooked, which then require little or minimal handling by the
establishment.
The hazard and subsequent risks associated with the foods served to the vulnerable
populations will be influenced by the type of operations they undertake. For
example:
♦ Inadequate control of the cook chill process (eg poor cooling rates, improper
storage temperatures and inadequate reheating) can result in the growth and
survival of pathogenic microorganisms (Cox & Bauler, 2008)
♦ Improper storage time and temperature of RTE foods that require no further heat
treatment can result in the growth of L. monocytogenes (ILSI, 2005)
♦ Inadequate cooking and poor post-cooking temperature growth can result in the
survival and subsequent growth of pathogenic microorganisms (Cox & Bauler,
2008) and
♦ For foods served raw, inadequate control steps to minimise the presence of
pathogenic microorganisms and inhibit their growth during storage
(Desmarchelier & Fegan, 2003; Sutherland et al, 2003).
Risk of listeriosis
The high risk associated with listeriosis in establishments serving foods to the
vulnerable population has also been noted in the National Risk Validation Project
(Food Science Australia & Minter Ellison Consulting, 2002). In this report the authors
ranked L. monocytogenes and foodservice operations for sensitive populations as the
highest risk rating due to the ability of the pathogen to grow at refrigeration
temperatures and the high mortality and hospitalisation rates associated with the
listeriosis infection.
The main hazard affecting the vulnerable population that has been studied is
L monocytogenes. FAO (2004) published a risk assessment on L. monocytogenes in
RTE foods that assessed the relative susceptibility of different groups within the
population to listeriosis (Table 40). From this table it can be seen that the sub-
groups within the vulnerable population are more susceptible to listeriosis and in turn
the food served to them presents a greater risk of foodborne illness than the food
consumed by the general population.
In their risk assessment on L. monocytogenes in RTE foods, the FDA/USDA (2003)
estimated the number of cases of listeriosis per serving and per annum for different

food categories for certain sub-groups of the vulnerable population. Assuming similar
consumption rates in Australia and using Australian population figures, the potential
number of listeriosis cases per year within Australia for each food category can be
estimated (Table 41). It can be seen from this data that the risk of contracting
listeriosis from any single serving of food is extremely rare, even for the highest risk
foods (eg deli meats, estimated cases are 3.0 x 10-7 per serve for the elderly,
therefore 30 million serves of deli meats would result in 1 case of listeriosis).
However, when combined with the number of meals consumed by the elderly each
year (not only those residing in facilities), there is the potential for 70 cases of
listeriosis each year. Due to the control measures initiated by establishments serving
vulnerable populations, the number of people actually exposed to L. monocytogenes
is likely to be much lower.
Table 40 – Relative susceptibility to listeriosis for different sub-groups

Condition Relative susceptibility
Transplant 2584
Cancer – blood 1364
AIDS 865
Dialysis 476
Cancer – pulmonary 229
Cancer – gastrointestinal and liver 211
Non-cancer liver disease 143
Cancer – bladder and prostate 112
Cancer – gynaecological 66
Diabetes, insulin dependant 30
Diabetes, non-insulin dependant 25
Alcoholism 18
Over 65 years old 7.5
Less than 65 years, no other condition (reference 1
or general population)
adapted from FAO (2004)
Risk of foodborne illness associated with C. perfringens

A risk profile published by Meat and Livestock Australia (2003) examined the risk
posed by C. perfringens in institutional meals for the aged where food safety
programs have been implemented. In determining the risk, factors such as severity,
probability, and the effect of processing and handling were considered. From this
information it was concluded that the risk rating of C. perfringens in institutional
meals for the aged was high with an estimated of 250 cases of C. perfringens
foodborne illness in Australia per year. The ABS (2008) estimates that 33.8% of the
population aged over 65 reside in NSW. Assuming the proportion of elderly within
aged-care facilities is similar, it can be estimated that the number of cases of
foodborne illness due to C. perfringens in facilities in NSW would be 84.5 per annum.

Table 41 – Estimated cases of listeriosis for vulnerable population sub-groups for each food category
Product Intermediate age 26 Elderly Perinatal
27 Per annum 28
Per serve Per annum Per serve Per annum
Per serve
Dairy
Pasteurised fluid milk 4.4 x 10-10 2.6 3.4 x 10-9 4.2 1.5 x 10-7 0.7
-9 -9
High fat and other dairy products 1.0 x 10 1.4 8.3 x 10 2.9 3.2 x 10-7 0.3
-10 -9 -7
Soft unripened cheese 5.8 x 10 0.2 4.9 x 10 0.4 2.0 x 10 0.04
Unpasteurised fluid milk 2.9 x 10-9 0.09 2.2 x 10-8 0.1 9.9 x 10-7 0.03
-10 -9 -8
Fresh soft cheese 1.2 x 10 <0.01 1.0 x 10 <0.01 4.2 x 10 <0.01
-14 -14 -12
Ice-cream/frozen dairy products 1.3 x 10 <0.01 9.2 x 10 <0.01 6.5 x 10 <0.01
Processed cheese 1.4 x 10-14 <0.01 9.3 x 10-14 <0.01 6.7 x 10-12 <0.01
-15 -15 -13
Hard cheese 3.4 x 10 <0.01 9.2 x 10 <0.01 8.1 x 10 <0.01
Cultured milk products 9.5 x 10-15 <0.01 5.6 x 10-14 <0.01 4.7 x 10-12 <0.01
-12 -11 -9
Soft ripened cheese 2.1 x 10 <0.01 2.2 x 10 <0.01 1.3 x 10 <0.01
-12 -11 -9
Semi-soft cheese 2.9x 10 <0.01 3.0 x 10 <0.01 1.6 x 10 <0.01
Meat
Deli meats 3.3 x 10-8 49.1 3.0 x 10-7 70.8 1.2 x 10-5 13.4
-8 -7
Pâté and meat spreads 1.2 x 10 0.1 1.1 x 10 0.2 4.5 x 10-6 0.03
-11 -10 -8
Frankfurters (reheated) 2.7 x 10 <0.01 2.7 x 10 0.02 1.6 x 10 <0.01
Dry/Semi-dry fermented sausages 6.0 x 10-12 <0.01 6.2 x 10-11 <0.01 3.7 x 10-9 <0.01
26
Intermediate age includes susceptible populations not captured in other groups (eg cancer, AIDS and transplant patients).
27
The risk per serving is inherent to the particular food category, and is therefore assumed to be the same in Australia as that calculated for the USA (FDA/USDA, 2003). This is based on the
assumption that consumption patterns for these foods are identical in Australia and the USA
28
The risk per annum has been adapted from USA population data contained in the FDA/USDA (2003) risk assessment of 260 million and extrapolated to Australian population data of
approximately 21.6 million (ABS, 2009) by dividing by a factor of 12

Product Intermediate age 26 Elderly Perinatal
27 Per annum 28 Per serve Per annum Per serve Per annum
Per serve
Plant Products
Fruit 5.0 x 10-12 0.02 5.1 x 10-11 0.05 2.8 x 10-9 <0.01
-13 -12 -10
Vegetables 8.4 x 10 <0.01 8.2 x 10 <0.01 4.8 x 10 <0.01
Deli type salads 1.7 x 10-13 <0.01 1.4 x 10-12 <0.01 8.8 x 10-11 <0.01
Seafood
Cooked RTE crustacean 2.2 x 10-9 0.08 1.9 x 10-8 0.1 7.4 x 10-7 0.03
-9 -8 -7
Smoked seafood 2.1 x 10 0.03 1.9 x 10 0.07 8.4 x 10 <0.01
-11 -10 -9
Raw seafood 1.3 x 10 <0.01 1.3 x 10 <0.01 6.7 x 10 <0.01
Preserved seafood 6.4 x 10-12 <0.01 6.7 x 10-11 <0.01 4.1x 10-9 <0.01

Risk based on meals served and prevalence rates
The potential risk can also be calculated using the information collected on the
number of meals served within establishments catering to the vulnerable population
and studies undertaken on the prevalence of pathogens in foods from these
establishments. As reported by Gillespie et al (2001), 15/3494 (0.4%) of cold sliced
RTE meats where found to be of unacceptable / potentially hazardous, due to the
presence of high levels of E. coli, S. aureus, Listeria and C. perfringens 29. Using the
information collected by the NSW Food Authority on meals served and assuming one
meal per day consists of sliced cold meat then it could be expected that:
♦ 35,753 meals per annum served in childcare facilities that include sliced cold
meats could be potentially hazardous and
♦ 142,432 meals per annum served in other establishments catering to the
vulnerable population could be potentially hazardous.
As mentioned previously, the contamination rate of L. monocytogenes in RTE
vegetables and sandwiches from health care facilities were found to be 3.7% and
2.5% respectively (Odumeru et al, 1997; Little et al, 2008). Again, assuming these
foods were served at one meal per day, the number of meals potentially
contaminated with L. monocytogenes would be:
♦ 330,724 meals per annum containing RTE vegetables at childcare facilities
♦ 1,137,498 meals per annum containing RTE vegetables at other facilities serving
to vulnerable populations
♦ 241,339 sandwiches served per annum at childcare facilities
♦ 961,417 sandwiches served per annum at other facilities catering to vulnerable
populations.
These figures are likely to be an over estimation as exact information on meal types
is not known and it is likely that establishments will have risk managements
strategies in place to minimise the risks associated with food service to vulnerable
populations.
Characterising the risk associated with other hazards within food service for
vulnerable populations is problematic due to the lack of information on the types of
meals served within these establishments. Other chapters within this document
provide an estimation of the risk for certain potentially hazardous foods and the risk
posed is likely to be similar for establishments serving food to the vulnerable
population.
Control measures in food service for vulnerable populations

The risk characterisation and predicted number of listeriosis cases stated previously
are generally not observed due to the risk management strategies or control
measures implemented by establishments serving food to vulnerable populations.
The main strategy to assist in reducing the risk of foodborne illness at these
establishments is the effective development and implementation of a food safety
program. Woody & Benjamin (2008) provide an overview of the practicalities of
implementing a food safety program in healthcare settings. In addition, in
29
Unacceptable / potentially hazardous was defined from categories in the Public Health Laboratory Service (PHLS)
Guidelines for the microbiological quality of some ready-to-eat foods at the point of sale (PHLS, 2000)

implementing the requirements of Standard 3.3.1 - Food Safety Program for Food
Service to Vulnerable Populations of the Food Standards Code, the NSW Food
Authority developed guidance material to assist industry meet the requirements
(NSW Food Authority, 2008c). These documents provide some potential control
measures for establishments serving vulnerable populations including:
♦ Substitution of high risk foods with lower risk alternatives
♦ Effective cleaning and sanitation of fruits and vegetables to be consumed raw
♦ Limited storage of pre-prepared infant formula
♦ Minimise storage times of foods to be consumed without further heat treatment
♦ Proper cooking of foods
♦ Effective cleaning and sanitation of equipment, in particular those used for foods
that will not receive a further heat treatment.
Conclusion
A small sub-group within the population are known to be more susceptible to
foodborne illness. This group is generally referred to as the vulnerable population
and includes children under five years of age, the elderly over 65 and those with
underlying immune suppressant conditions. The hazards affecting the vulnerable
population can be unique to certain groups such as L. monocytogenes and
E. sakazakii or may involve well known foodborne pathogens such as Salmonella
resulting in more severe illness in the vulnerable persons.
This tends to be reflected in epidemiological data, where institutional outbreaks are
over-represented in the number of foodborne illness outbreaks, cases of illness and
deaths from food sources. Based on prevalence data for bacterial pathogens, it is
estimated that over one million of the 133 million meals served at institutions
catering to vulnerable populations in NSW each year may be potentially
contaminated with a food pathogen. This emphasises the importance in
implementing control measures such as food safety programs at establishments
catering to the vulnerable populations, to ensure the safety of their consumers.

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sliced meats from catering establishments in the United Kingdom. Journal of Applied
Microbiology, 88(3), 467-474.
Goulet, V., Hedberg, C., Le Monnnier, A. & de Valk, H. (2008). Increasing incidence of
listeriosis in France and other European countries. Emerging Infectious Disease, 14(5), 734-
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ILSI Research Foundation/Risk Science Institute (2005). Achieving continuous improvement
in reductions in foodborne listeriosis – a risk-based approach. Journal of Food Protection.
68(9), 1932-1994.
Microorganisms in Foods 5: Microbiological specifications of food pathogens. Roberts, T.A.,
Baird-Parker, A.C. & Tompkin, R.B. (Eds.). Blackie Academic & Professional, London.
Jay, S., Davos, D., Dundas, M., Frankish, E. & Lightfoot, D. (2003). Salmonella. In Hocking,
A.D. (Ed.) Foodborne Microorganisms of Public Health Significance (pp. 207-266). Australian
Lehner, A. & Stephan, R. (2004). Microbiological, epidemiological and food safety aspects of
Enterobacter sakazakii. Journal of Food Protection, 67(12), 2850-2857.
Little, C.L., Barrett, N.J., Grant, K. & McLauchlin, J. (2008). Microbiological safety of
sandwiches from hospitals and other health care establishments in the United Kingdom with a
focus on Listeria monocytogenes and other Listeria species. Journal of Food Protection, 71(2),
309-318.
MLA [Meat & Livestock Australia] (2003). Through chain risk profile for the Australian red
meat industry, PRMS.038c, part 1: risk profile. North Sydney: Meat & Livestock Australia.
NSW Food Authority (2008a). Regulatory impact statement: food amendment (child care
centres) regulation 2008. Sydney: NSW Food Authority.
NSW Food Authority (2008b). Regulatory impact statement: food amendment (vulnerable
persons food safety scheme) regulation 2008. Sydney: NSW Food Authority.
NSW Food Authority (2008c). Vulnerable persons food safety scheme manual: policy and
information to help businesses comply with the food service to vulnerable populations food
safety scheme under the food regulation 2004. Retrieved 11 December 2008, from
http://www.foodauthority.nsw.gov.au/_Documents/industry_vp_pdf/vulnerable_persons_food
_safety_scheme_manual_compl.pdf.
NSW Health (2008). Salmonellosis notification in NSW residents. Retrieved 15 October 2008,
from http://www.health.nsw.gov/data/diseases/salmonellosis.html.
O’ Brien, S.J. (2008). Foodborne Disease Outbreaks in Healthcare Setting. In Lund, B.M. &
Hunter, P.R. (Eds.), The microbiological safety of food in healthcare settings (pp. 251-289).
Oxford: Blackwell Publishing Ltd.
Odumeru, J.A., et al. (1997). Assessment of the microbiological quality of ready-to-use
vegetables from health-care food services. Journal of Food Protection, 60(8), 954-960.
OzFoodNet Working Group (2003). Foodborne disease in Australia incidence, notifications and
outbreaks. Annual report of the OzFoodNet network, 2002. Communicable Diseases
Intelligence, 27(20), 209-243
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report of the OzFoodNet network, 2003. Communicable Diseases Intelligence, 28(3), 359-
389.
OzFoodNet Working Group (2005). Reported foodborne illness and gastroenteritis in
Australia: Annual report of the OzFoodNet network, 2004. Communicable Diseases
Intelligence, 29(2), 164-190.
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annual report of the OzFoodNet network, 2005. Communicable Diseases Intelligence, 30(3),
278-300.

OzFoodNet Working Group (2007). Monitoring the incidence and causes of disease potentially
transmitted by food in Australia: Annual report of the OzFoodNet, 2006. Communicable
Disease Intelligence, 31(4), 345-365.
PHLS [Public Health Laboratory Service, UK). (2000). Guidelines for the microbiological quality
of some ready-to-eat foods samples at the point of sale. Communicable Disease and Public
Health 3(3), 163-167.
Stewart, C. (2003). Staphylococcus aureus and staphylococcal enterotoxins. In Hocking, A.D.
Sutherland, P., Miles, D. & Laboyrie, D. (2003). Listeria monocytogenes. In Hocking, A.D.
Szabo, E. A. & Gibson, A. M. (2003). Clostridium botulinum. In Hocking, A.D. (Ed.) Foodborne
Microorganisms of Public Health Significance (pp. 505-542). Australian Institute of Food
Tallis, G., et al. (1999). A nursing home outbreak of Clostridium perfringens associated with
pureed food. Australian and New Zealand Journal of Public Health. 23(40), 421-423.
Wall, P. (2008). Overview. In Lund, B.M. & Hunter, P.R. (Eds.), The microbiological safety of
food in healthcare settings (pp. 1-11). Oxford: Blackwell Publishing Ltd.
Woody, J-M. & Benjamin, D.L. (2008). Practical implementation of food safety management
systems in healthcare setting. In Lund, B.M. & Hunter, P.R (Eds.), The microbiological safety
of food in healthcare settings (pp. 351-380). Oxford: Blackwell Publishing Ltd.

Egg food safety scheme (draft)
The NSW Food Authority previously undertook a risk profile on the NSW egg industry
(Miles & Chan, unpublished) and proposed several risk management strategies to
underpin the incorporation of an Egg food safety scheme into the Food Regulation
2004. As SafeFood NSW, the Authority also commissioned Food Science Australia to
provide a scoping study on plant products, which also examined eggs (FSA, 2000).
This report identified potential hazards associated with the production of eggs and
egg products, shown in Table 42.
In addition the egg industry’s peak body, the Australian Egg Corporation Ltd (AECL)
commissioned the South Australian Research and Development Institute (SARDI) to
complete two sections of work, a risk profile on eggs and egg products to examine
all potential hazards (Daughtry et al, 2005), and a quantitative risk assessment
concentrating on evaluating the risks from Salmonella spp. (Thomas et al, 2006)
All bodies of work include comprehensive assessments of both microbiological and
chemical hazards in eggs and egg products.
Risk assessment work on the Australian egg industry is currently being undertaken
by Food Standards Australia New Zealand (FSANZ) to underpin the development of a
Primary Production and Processing Standard for Eggs, Proposal P301 (FSANZ, 2006).
Microbiological hazards
In an assessment of microbiological standards for eggs and egg products, the former
Australia New Zealand Food Authority (now FSANZ) identified the following
microorganisms of concern in relation to the commercial production, processing and
distribution of eggs (ANZFA, 1999):
♦ Salmonella spp.
♦ Bacillus cereus
♦ Listeria monocytogenes
♦ Staphylococcus aureus
It is recognised that pathogenic organisms may contaminate the shell of the egg,
through environmental and faecal contamination. Bacillus cereus (van Netten et al,
1990), Listeria monocytogenes (McKellar, 1993) and Staphylococcus aureus
(Papadopoulou et al, 1997) have all been detected during analysis of eggs and/or
egg products. However, an analysis of foodborne illness attributed to eggs in
Australia shows that virtually all outbreaks have been due to Salmonella spp., with
Salmonella Typhimurium the dominant serovar responsible for illness associated with
egg consumption.
A risk profile undertaken by the New Zealand Food Safety Authority (NZFSA)
concentrated on non typhoidal Salmonella in and on eggs as the main hazard (Lake
et al, 2004) and the AECL quantitative risk assessment work focused on Salmonella
as the primary hazard of concern.

Table 42 – Hazards in the production of shell eggs and egg products
Product Hazard
Shell eggs Contamination with Salmonella spp.
Growth of Salmonella spp.
Contamination with other pathogens
Penetration of pathogens during egg production and handling
Pathogen survival due to undercooking
Development of antibiotic resistant pathogens
Mycotoxins
Pyrrolizidine alkaloids from feed transferred to eggs
Heavy Metals
Agricultural and veterinary chemicals
Pesticide residues (eg organochlorine residues) in free range and ‘backyard’ eggs
Polychlorinated biphenyls
Potential contamination of eggs or egg products from packaging
Egg products Contamination with Salmonella spp. or other pathogens

Pathogen survival due to inadequate process treatment
Contamination of raw and processed product with heavy metals, chemicals
(including agricultural compounds and veterinary medicines) or other toxicants
adapted from FSA (2000)
Overseas, the focus of egg safety assessment has been slightly different, as
Salmonella Enteritidis has become endemic in overseas laying flocks since the 1980s.
This has provided a major problem for the overseas egg industry as Salmonella
Enteritidis has the unusual ability to colonise the ovarian tissue of hens and this
causes Salmonella cells to be present within the contents of newly laid intact shell
eggs. Contamination of eggs and of egg products with Salmonella Enteritidis is
believed to be the cause of the large increase in human infections in Europe and
North America. The Centre for Disease Control in the USA attributed 77-82% of
Salmonella Enteritidis-related foodborne outbreaks to eggs and egg products. In
many of these cases the outbreaks were associated with the consumption of ‘Grade
A’ shell eggs (WHO, 2002).
Currently Australian layer flocks remains free of Salmonella Enteritidis, and it has
been estimated that this is worth around $48 million per annum to the Australian egg
industry (Sergeant et al, 2003). Given this, there is a strong push from the industry
peak body, the AECL, for the implementation of quality assurance programs and
codes of practice in the industry, including biosecurity measures on farm to ensure
the maintenance of the Salmonella Enteritidis-free status (AECL, 2005a, AECL,
2005b). However, other Salmonella serotypes are intrinsic in the Australia poultry
industry and form part of the microbiota in the intestinal tract of chickens.
The external surfaces of eggs may become contaminated with faecal material,
including Salmonella bacteria between when the egg is laid and when it is collected.
However, if the egg is kept dry it is likely that the bacteria will die on the outside of
the shell. In a survey of Australian farms that included testing of faecal samples and
egg pulp, Cox et al (2002) found that S. Singapore was the dominant organism. This

was thought to be related to the high numbers of Salmonella found in the feed
intended for the chickens, which in turn showed in the numbers found in the faecal
specimens. Survival of Salmonella on the egg surface may be enhanced by high
relative humidity and the organism may penetrate the egg shell if it is wet, as the
shell becomes more porous. Cox et al (2002) showed that S. Infantis,
S. Typhimurium, S. Heidelberg and S. Singapore were all capable of migrating into
the egg under favourable conditions.
Normally the contents of an intact shell egg are essentially sterile when laid and the
intrinsic structure of an egg, with the cuticle, shell and shell membranes combining
to form a protective barrier against bacteria penetrating into the egg. However, if the
egg is cracked (the shell is cracked but the shell membrane is intact) or broken (shell
is cracked and shell membrane is also broken), this can facilitate access of
pathogenic bacteria into the egg contents, where they may be able to increase in
numbers in the nutrient-rich yolk.
Standard 2.2.2 – Egg and egg products of the Food Standards Code prohibits
cracked eggs being made available for retail sale or for catering purposes, due to the
increased risk of bacterial contamination. However, there is anecdotal evidence to
suggest that cracked eggs are being sold at a substantially reduced price for use in
restaurants and for catering purposes. A Canadian risk assessment on the use of
cracked eggs stated that any country producing eggs has to recognise that, despite
regulations controlling the use of cracked eggs, economics will dictate that some of
these will be consumed as whole eggs and a management plan is desirable to limit
hazardous practices associated with these eggs (Todd, 1996).
Chemical hazards
Dawson et al (2001) listed the possible sources of chemical contamination of eggs
including:
♦ free range birds feeding on contaminated soil
♦ insecticide sprays used while birds are present
♦ water medication at incorrect rate
♦ eggs washed in inappropriate solutions
♦ egg washing compound mixed at wrong concentrations
♦ systemic pesticides used in grower sheds
♦ shed fumigation while birds are present
♦ chemical feed additives included at wrong rate
♦ use of antibiotics or other veterinary medicines
Survey results from the National Residue Survey (NRS), and Market Basket Survey
have shown occasional detections of heavy metals. Dieldrin residues have also been
found in free range eggs (FSA, 2000). Free range hens are considered a higher risk
for coming into contact with environmental chemical contaminants because they
have the opportunity to source their own food outside, thus increasing the potential
for eating contaminated vegetation or soil. However, all detections have been at
levels well below the Maximum Residue Level (MRL), and the health risk to humans
was concluded to be low.

There have been detections of veterinary chemical residues in eggs above the MRL,
in the past several years (Table 43). The use of antiprotozoals is common to control
coccidiosis in the hens, and is mainly used as a feed additive. The traceback
investigations of positive detections on farm have tended to indicate mix ups with
feed. The use of cages has reduced the need for veterinary chemical usage because
the hens are housed off the floor and parasitic infections are less of a problem (FSA,
2000).
The AECL risk profile concluded that there was no evidence that pesticides,
veterinary medicines or other chemical contaminants, present a food safety or public
health risk (Daughtry et al, 2005). Despite occasional low level detections, in general
eggs are residue free and no egg samples have been found to contain chemical
residues which would present an immediate health risk.
Table 43 – Prevalence of chemical residues in eggs
National Number of Number with Number of residues above MRL

Residue analyses residues
Survey
1991 617 21 (3.4%) 1 (0.16%)
1992 564 30 (5.3%) 2 (0.35%)
1997 228 1 (0.44%) 0
National Number of Number of Residues above Residues above
Residue samples analyses MRL/ERL ML
Survey
1998 248 703 0 0 30
1999 83 1190 0 0 31
1999-2000 158 3242 0 1 32
2000-2001 122 1683 0 0
2001-2002 92 1387 0 0
No testing of eggs was conducted in 2002-2003 or 2003-2004
2004-2005 75 1000 2 33 0
2005-2006 75 1000 2 34 0
35
2006-2007 75 1025 2 0
adapted from BRS (1996); BRS (1998); AFFA (1999); AFFA (2000); AFFA, (2001); AFFA (2002); DAFF
(2003); DAFF (2005); DAFF (2006); DAFF (2008)
30
1998 - two Dieldrin residues detected in free-range eggs, at concentrations of less than 20% MRL
31
1999 - one residue of Dieldrin in free-range eggs, at concentrations of less than 20% MRL
32
1999-2000 – one residue of copper above the ML was detected
33
2004 -2005 - both residues were due to anticoccidials. One sample containing Lasalocid was thought to be the
result of a mix-up with feed. The traceback for sample containing Nicarbazin was not complete when the NRS
report was published.
34
2005-2006 - two samples showed residue levels of Nicarbazin (anticoccidial) above the Australian Standard and
were found to be the result of a mix-up with feed.
35
2006-2007 – two samples showed residue levels of Nicarbazin (anticoccidial) above the Australian Standard and
were found to be the result of a mix-up with feed.

Physical hazards
Due to the protection offered by the shell of the egg, there is a very small likelihood
of physical contaminants affecting eggs. The main physical hazards present on farm
are blood spots, rodent droppings and insects. Blood spots may be present in eggs
when they are laid and may reach the consumer if the eggs are not carefully checked
during grading. The candling process used for crack detection of commercial eggs
should prevent eggs containing physical contaminants from entering the market.
FSANZ concluded that physical hazards are no a significant issue for eggs and egg
products (FSANZ, 2006).
Other eggs
The Australian egg industry is primarily based on eggs and egg products produced
from hens. Other egg-producing avian species, such as ducks, quails, pheasants,
pigeon, geese, turkey and guinea fowl form a very minor part of the egg market.
There is little detailed information is available about the national production of eggs
and egg products from these species (FSANZ, 2006), or on the microbiological and
chemical status of these products. There is some evidence to suggest that duck eggs
may be more highly contaminated with Salmonella spp. than chicken eggs. Overseas
studies have shown up to 14% of duck eggs contaminated with Salmonella spp. This
is possibly due to the added potential for external contamination of the eggs from
less on-farm controls, but also through an increased probability of vertical
transmission, particularly of Salmonellae with ducks (Jay et al, 2003).
Most duck eggs are processed into specialty products, such as salted eggs, century
eggs and Balut egg. While the primary microbiological hazard of concern remains
Salmonella spp., the manual handling associated with specialty egg production could
possibly lead to contamination with other pathogens such as S. aureus and E. coli.
The NSW Food Authority has detected high level of lead in century eggs made from
duck eggs (McCreadie et al, 2007). Traditional practices involved the use of lead
oxide in the pickling solution, believed to modify the porosity of the egg shell, and
thus influence the rate of ingress of the alkaline pickling solution into the egg. This
was thought essential to produce century eggs with the desirable semi-solid yolk
texture. The Authority survey found a single NSW processor adding lead oxide to the
brine the eggs were soaked in.
Lead oxide can be extremely poisonous and is not permitted as a food additive in
Australia. Given the traditional use of lead salts in specialty egg products, there may
be a need to monitor the lead content of these products periodically in case of
processors go back to a “proven” traditional technique.
Exposure assessment
Consumption of shell-eggs (‘table eggs’)
In NSW, it is estimated there are 139 egg producers with annual production of
almost 58 million dozen eggs worth an estimated $90 million per annum (ABS,
2006). While egg consumption has been steadily declining, consumption data
indicates that the Australian population consumes an average 137 eggs per person
each year (ABS, 2000). The National Nutrition Survey (ABS, 1995) reported that
16.1% of the NSW population consumed eggs and egg products (see Table 44).

Overall results showed that rates of consumption ranged from 8.5% (females aged
16 to 18) to 20.5% (males aged 45 to 64). Of those males consuming eggs and egg
products, average daily consumption varied from 27.8 g/day (2 to 3 years) to 74.0
g/day (12 to 24 years), while for females average daily consumption varied from
43.0 g/day (2 to 3 years) to 50.0 g/day (25 to 44 years).
The consumption data only recorded the consumption levels of eggs (eg fried egg,
poached egg) and dishes where egg was the major ingredient (eg omelette, soufflé,
scrambled eggs). It did not record consumption of foods where egg may be included
as one of many ingredients (eg mayonnaise, desserts).
The national consumption data reveals that between 12-13% of infants (2-3 yrs) and
14-17% of the elderly (65+ yrs) regularly consume eggs. No distinction was made in
what form the eggs were consumed, whether they were served lightly or thoroughly
cooked. This demonstrates that a significant proportion of the vulnerable population
are regular consumers of eggs.
Use of shell eggs

It is estimated that 87% of all egg production is sold at retail as shell eggs, with the
remaining 13% being further processed into egg products such as pasteurised liquid
egg (ABS, 2000). Where egg products are processed, they must meet prescribed
microbiological criteria under Standard 1.6.1 – Microbiological Limits for Food of the
Food Standards Code. Of those eggs sold at retail, it is estimated that 30% are used
as an ingredient in a food where it will be thoroughly cooked.
There is little data on the consumption patterns of eggs by Australian consumers, but
an American survey estimated that 27% of all egg dishes consumed in the US are
lightly cooked (Lin et al, 1997), translating to each person on average consuming
lightly cooked eggs 20 times a year. Lightly cooked eggs are described as "runny",
"runny yolk" or "runny white” and may allow the survival of any pathogenic bacteria
that are present within the egg. Eggs fried "over easy" and "sunny side up"
accounted for almost half (49%) of the lightly cooked eggs eaten. Of instances
where raw eggs were consumed as an ingredient in an uncooked or very lightly
cooked food, 52% was in frosting, salad dressing (18.5%), blended milk beverages
(16%), homemade ice-cream (6%), and hollandaise sauce. Although Australian
consumption patterns may be different to the American data cited here, this does
provide an indication of the potential exposure to pathogens from undercooked eggs.
Consumption of specialty duck egg products and quail eggs

Production data on specialty egg products is limited, and it is assumed that the level
of consumption forms a very small portion of overall egg consumption. Moreover,
they are likely to be consumed by specific minority groups and/or as delicacies only
occasionally rather than as part of routine diet. A per capita consumption figure is
not available for these products.

Table 44 – Consumption of eggs and egg products in Australia
Sex Age Proportion of persons Median daily intake for consumers

consuming egg products and of egg products and dishes
dishes 36 (g/day)
(%)
Male 2-3 12.6 27.8
Male 4-7 11.1 50.0
Male 8 - 11 14.0 58.0
Male 12 - 15 12.3 74.0
Male 16 - 18 18.1 74.0
Male 19 - 24 15.7 74.0
Male 25 - 44 17.9 62.5
Male 45 - 64 20.5 57.0
Male 65+ 17.6 72.0
Female 2-3 13.9 43.0

Female 4-7 12.2 50.0
Female 8 - 11 10.7 50.0
Female 12 - 15 8.7 50.0
Female 16 - 18 8.5 49.0
Female 19 - 24 12.8 50.0
Female 25 - 44 15.2 50.0
Female 45 - 64 16.8 50.0
Female 65+ 14.2 50.0
Foodborne illness outbreaks from eggs
A summary of foodborne illness outbreaks attributed to eggs, or where egg was used
as an ingredient in the implicated food is shown in Table 45 (more detailed
information on these outbreaks is included in Table 70 of Appendix 3). It is clear
from epidemiological data and the literature that Salmonella spp. is the primary
pathogen of concern in relation to foodborne illness associated with eggs.
Prevalence of Salmonella in Australian eggs

Survey data included in the AECL risk assessment provides the best prevalence data
of Salmonella spp. on and within Australian eggs (Thomas et al, 2006). The external
surface of 11,036 eggs from various sources (caged, free range and barn-laid) and
the internal contents of 20,000 caged egg samples were sampled (see Table 46).
36
Egg products and dishes are defined in the National Nutrition Survey (ABS, 1995) as including the following:
- Eggs;
- Dishes where egg is the major ingredient;
- Egg substitutes and dishes.

Table 45 – Summary of foodborne illness outbreaks attributed to eggs
outbreaks
(1995-2008)
Streptococcus pyogenes 1 72 0 0
Toxin 1 16 0 0
Norovirus 1 11 0 0
Campylobacter 1 2 1 0
Unknown 3 32 0 0
Total 110 3941 266 0
Table 46 – Prevalence of Salmonella in Australian eggs
Egg type Number of samples tested Salmonella detected

(estimated prevalence)
Shell eggs – ungraded

Caged (shell) 2160 0 (0 – 0.2%)
Free range (shell) 1200 0 (0 – 0.3%)
Barn laid (shell) 1200 0 (0 – 0.3%)
Shell eggs - graded

Caged (shell) 6476 0 (0 – 0.06%)
Caged (internal contents) 20,000 0 (0 – 0.02%)
adapted from Daughtry et al (2004)
Based on comparable prevalence of external contamination to overseas data

(0.21%), Thomas et al. (2006) concluded that the prevalence of internal
contamination by Salmonella in Australian eggs is likely to be close to the overseas
reported rate of 0.004%, roughly equivalent to one egg every 25,000 being
contaminated with Salmonella. This prevalence must be considered in the context
that there are over 800 million eggs consumed in NSW each year, both as shell eggs
and as an ingredient in food. At this prevalence, there may be 32,000 eggs
contaminated with Salmonella consumed each year in NSW.
Effect of yolk mean time (YMT) on exposure to Salmonella

While it appears inevitable that Salmonella will penetrate into a small proportion of
eggs, the bacteria will not begin to increase in numbers immediately. Studies have
shown that Salmonella will not grow in the iron restricted environment of the
albumen (egg white), and is only able to grow after a considerable period of time. As
the egg ages, the vitelline membrane surrounding the yolk breaks and allows the
Salmonella to enter the yolk and utilise the rich iron supply within the yolk to grow
and rapidly increase in numbers. This length of time for the membrane to break
down is determined by the yolk mean time (YMT) and is affected by the temperature

the egg is stored at. Humphrey (1994) observed large numbers of Salmonella in both
the yolk and albumen after the resolution of YMT.
Thomas et al. (2006) estimated that 75% of eggs in Australia are consumed before
resolution of YMT, based on average industry practices and storage temperatures
throughout the production, distribution and retail chain. In effect, this minimises the
opportunity for Salmonella to proliferate to high numbers within the egg and results
in eggs being a low risk food. However, where eggs are stored at elevated
temperatures for extended periods of time, this can allow the YMT to resolve and
provide the conditions for any Salmonella which may be present in the egg to grow.
Under these conditions, the risk of foodborne illness is increased unless the egg is
fully cooked prior to consumption to eliminate the Salmonella.
Grading and processing of eggs

Several processes used in the grading and processing of eggs may lead to cross
contamination of eggs and egg products if sufficient food safety controls are not in
place. Efficient crack detection is required when the eggs are graded to ensure that
cracked eggs are identified and are re-directed for further processing where they will
be pasteurised. To ensure the efficacy of the crack detection method, it should be
validated and verified.
Washing of eggs is sometimes undertaken by graders and processors to remove any
gross faecal or environmental contamination from the shell of the eggs prior to sale.
However, if not carefully controlled, the washing process has the potential to
damage the shell cuticle and actually increase the risk of microbial penetration into
the egg. Inadequate control of temperature, pH and insufficient changes in wash
water can result in a build up of microorganisms and lead to cross contamination of
eggs. In addition, the incorrect use of chemicals has the potential to cause
unacceptable levels of chemical residues in the egg. Eggs must be dried after
washing as inadequately dried eggs can allow microbial growth and any remaining
bacteria may be aspirated into the egg.
The design and hygiene of equipment used in the processing of eggs is of
considerable importance to avoid niches for bacterial growth (Jones et al, 2003). The
method used to separate the egg contents from the shell for further processing into
liquid pulp can have a major impact on the microbiological content of the resulting
pulp. The risk of bacterial contamination is markedly worsened by the use of dirty
eggs. Liquid egg pulp made from cracked or broken eggs is more likely to be
associated with pathogens or increased pathogen numbers than pulp prepared from
intact shell eggs.
Industry practice is to discard broken eggs, as they are considered a microbiological
risk for both safety and quality. The exception to this appears to be where eggs may
be broken just prior to where they are pulped. The production of egg products must
involve pasteurisation, with the minimum times and temperatures defined in
Standard 1.6.2 – Processing Requirements of the Food Standards Code, or an
equivalent treatment may be used. Pasteurisation of egg pulp must deliver a
sufficient heat treatment to ensure the finished product complies with the
microbiological standards specified in Standard 1.6.1 – Microbiological Limits for Food
of the Food Standards Code. The pasteurisation process for egg pulp is relatively
mild as coagulation of the egg protein needs to be avoided (ICMSF, 1998). The
effectiveness of the pasteurisation process is influenced by the microbial load, so the
higher the bacterial load prior to pasteurisation, the higher the bacterial population

remaining after processing. Thomas et al. (2006) demonstrated that the
pasteurisation parameters set by the Food Standards Code delivers a relatively small
log reduction of Salmonellae for liquid egg yolk and albumen and the presence of
viable Salmonellae in processed products has been demonstrated (NEPSS, 2003). To
ensure the effectiveness of the pasteurisation process, the process must be
monitored and verified through end product testing and additional control measures
implemented to limit the extent of contamination, and the opportunity for growth of
contaminating organisms in the raw material.
Hygienic handling of pasteurised product must be undertaken to ensure pasteurised
product is not recontaminated. Egg pulp remains vulnerable to further contamination
post pasteurisation if good manufacturing practices (GMP) are not implemented.
Salmonella spp. are able grow rapidly in egg yolk under both aerobic and anaerobic
conditions (ICMSF, 1998), unless the product is stored under appropriate
temperature control or kept in a frozen state.
Specialty duck egg products

Production of processed duck eggs exposes the eggs to greater risks of invasion by
pathogens likely to be found in the prevailing environment (eg Salmonella serovars).
The extensive manual handling these products receive may also introduce pathogens
such as S. aureus and E. coli. However, reported cases of illness implicating these
pathogens in processed duck eggs are rare.
Salted duck eggs and Balut eggs are intended to be eaten cooked. The one
documented case of Salmonella poisoning implicating salted eggs was probably an
example of uninformed use of that product (Campbell, pers comm.). There is a high
risk of chemical contamination with the use of non food grade chemical such as lead
oxide, if processors resort to traditional methods for making century eggs.
The primary hazard to human health from eggs and egg products are Salmonella
serovars. This is evident from the epidemiological data, with Salmonella spp.
determined as the cause for the majority of foodborne illness cases attributed to
eggs in Australia. While it is possible that other pathogens may also contaminate the
shell of the egg through faecal and environmental contamination, this is not reflected
in foodborne illness data across Australia.
In the AECL-funded risk profile, Daughtry et al (2005) examined 33 different
scenarios of egg production and storage and final usage. An estimate was made of
how many eggs were captured by each scenario, and an estimate made of the risk
per serving and predicted annual number of illnesses attributable to each (see Table
47). It is acknowledged that there are a number of assumptions made in generating
such predictions, however this information can provide a useful indication of the
highest risk practices and be used to focus risk management strategies.

Table 47 – Risk ranking for type and use of eggs
Scenario Cracked/Intact Salmonella Salmonella kill step Risk Predicted cases Predicted
growth 37 38 39 ranking of Salmonellosis annual number
MR , SR , RE ,
per serve of Salmonellosis
(YMT resolved) NE 40
(in Australia) cases (in
Australia) 41
Eggs subjected to pathogen reduction step (eg cooking)
1. Commercial eggs Intact None MR Low 4 x 10-11 3.34 x 10-2

2. Commercial eggs Intact None SR Low 4 x 10-14 3.34 x 10-5
3. Commercial eggs Intact None RE Low 0 0
-6
4. Commercial eggs Intact 5-log MR Medium 4 x 10 772
-9
5. Commercial eggs Intact 5-log SR Low 4 x 10 7.72 x 10-1
6. Commercial eggs Intact 5-log RE Low 0 0
-11
7. Non-commercial eggs Intact None MR Low 4 x 10 3.43 x 10-3
8. Non-commercial eggs Intact None SR Low 4 x 10-14 3.43 x 10-6
9. Non-commercial eggs Intact None RE Low 0 0
10. Non-commercial eggs Intact 5-log MR Medium 4 x 10-6 79
11. Non-commercial eggs Intact 5-log SR Low 4 x 10-9 7.92 x 10-2
12. Non-commercial eggs Intact 5-log RE Low 0 0
-9
13. Non-commercial eggs Cracked None MR Low 4 x 10 1.32 x 10-3
14. Non-commercial eggs Cracked None SR Low 4 x 10-12 1.32 x 10-6
37
MR – moderate reduction – 100-fold decimal reduction in Salmonella (eg light cooking, fried “sunny side up”, microwave, boiled where liquid yolk remains)
38
SR – substantial reduction – 10,000 fold decimal reduction in Salmonella (eg fried “easy over”, lightly scrambled or omelette, pasta)
39
RE – reliably eliminates – 1,000,000,000 fold decimal reduction in Salmonella (eg hard boiled or scrambled, cakes, biscuits)
40
NE - no effect – no reduction in Salmonella (eg raw egg drinks, some desserts)
41
Data from Daughtry et al (2005) used an Australian population figure of 19.5 million. These estimates have been extrapolated to the current population of Australia estimated by ABS (2009) as
approximately 21.6 million, by multiplying by a factor of 1.1, for consistency with other sections of this risk assessment.

Scenario Cracked/Intact Salmonella Salmonella kill step Risk Predicted cases Predicted
growth 37 38 39 ranking of Salmonellosis annual number
MR , SR , RE ,
per serve of Salmonellosis
(YMT resolved) NE 40
(in Australia) cases (in
Australia) 41
15. Non-commercial eggs Cracked None RE Low 0 0
16. Non-commercial eggs Cracked 5-log MR Medium 4 x 10-4 66
-7
17. Non-commercial eggs Cracked 5-log SR Low 4 x 10 6.60 x 10-2
18. Non-commercial eggs Cracked 5-log RE Low 0 0
Consumed without pathogen reduction step in raw egg drinks and cold desserts
19. Commercial eggs Intact None NE Low 4.0 x 10-9 2.57 x 10-1
-5
20. Commercial eggs Intact 5-log NE Medium 4 x 10 643
-9
21. Non-commercial eggs Intact None NE Low 4.0 x 10 7.92 x 10-2
22. Non-commercial eggs Intact 5-log NE Medium 4 x 10-5 198
-7
23. Non-commercial eggs Cracked None NE Low 4 x 10 1.32 x 10-2
24. Non-commercial eggs Cracked 5-log NE Medium 4 x 10-4 13
-6
25. Non-commercial eggs Cracked eggs in egg butter 3-log NE High 4 x 10 10
Commercial liquid egg pulp
26. Commercial eggs Unpasteurised pulp 1-log NE Medium 2.5 x 10-4 11

-6
27. Commercial eggs Unpasteurised pulp 1-log SR Medium 2.5 x 10 2.15 x 10-1
28. Commercial eggs Unpasteurised pulp 1-log RE Low 2.50 x 10-9 2.68 x 10-4
29. Commercial eggs Unpasteurised pulp 1-log MR Low 0 0
-7
30. Commercial eggs Pasteurised pulp None NE Low 2 x 10 10
-9
31. Commercial eggs Pasteurised pulp None SR Low 2.00 x 10 1.29 x 10-1
32. Commercial eggs Pasteurised pulp None RE Low 2.00 x 10-12 1.29 x 10-4
33. Commercial eggs Pasteurised pulp None MR Low 0 0
adapted from Daughtry et al (2005)

The highest risk per serving was for scenarios where the storage conditions of the
eggs allowed the YMT to be resolved and therefore allowed the numbers of
Salmonella to significantly increase (scenario 16, 24 from Table 47), resulting in a
risk per serving of 400 predicted illnesses per million servings. However, this did not
necessarily translate to a large number of predicted illnesses, as the number of eggs
actually captured by the particular scenario may not be that large. These two
particular scenarios looked at non-commercially produced eggs, which account for a
very small portion of overall egg production.
The largest number of actual predicted illnesses was from scenario 4, where the
storage conditions for the eggs allowed the resolution of the YMT, and final use only
involved a moderate kill step. Thomas et al (2006) estimated that as many as 25%
of shell eggs in Australia are consumed after resolution of YMT, and although the risk
per serving was predicted to be 4 illnesses per million servings, because of the large
number of eggs captured by this scenario, it results in a prediction of 772 illnesses
each year when extrapolated to the current Australian population. Total numbers of
predicted illnesses from all scenarios was greater than 1800 cases per annum.
The final estimate for the level of illness was shown to be dependent on a number of
factors, namely:
♦ the quality of hygienic practices on-farm (ie level and prevalence of
contamination with Salmonella)
♦ hygienic practices during processing
♦ time and temperature of egg storage (ie whether this allowed the resolution of
YMT and subsequent increase in levels of Salmonella in the egg) and
♦ end use of the eggs (level of cooking and subsequent reduction in Salmonella)
The risk profile undertaken previously by the NSW Food Authority (Miles & Chan,
unpublished) identified that the significant control measures to manage
microbiological and chemical hazards were as follows:
Biosecurity measures on farm
Continued strict biosecurity measure will be necessary on commercial farms to
maintain the S. Enteritidis-free status. Because of the small number of breeder flocks
in Australia, and the already high level of biosecurity on these flocks, it is concluded
that the probability of a breeding flock becoming infected with S. Enteritidis is low.
However, should a breeding flock become infected and remain undetected, there
would be significant spread to a large number of layer flocks throughout Australia
(Arzey, 2002). If this should happen it is believed there would be significant increase
in the number of human cases of S. Enteritidis -related illness from eggs (Sergeant et
al, 2003), as has been observed in other countries where S. Enteritidis has become
endemic.
To ensure laying hens and breeding stock remain free from S. Enteritidis the
Australian egg industry has proactively initiated and developed various generic egg
quality Codes of Practice and food safety programs to manage relevant food safety
and quality risks at specific stages of the supply chain for both eggs and egg
products (AECL, 2005a; AECL, 2005b). However the uptake of these by industry is
voluntary. Through-chain regulatory control and implementation of food safety
controls and traceability on farm may aid in maintaining the S. Enteritidis-free status.

Control measures for grading and processing of eggs and egg products
Higher risk operations, including grading and washing of eggs, handling and
processing of egg pulp, and processing of specialty duck eggs, should be carried out
with adequate control through the implementation of HACCP-based food safety
program. The revised Codex Code of Hygienic Practice for Eggs and Egg products
emphasises the use of the Hazard Analysis Critical Control Point (HACCP) approach
wherever appropriate to minimise food safety hazards (Codex, 2006).
Pasteurisation of all liquid egg preparations should be monitored, recorded and
periodically verified. Monitoring should include evidence of the effectiveness of the
process.
Thomas et al (2006) stated that the epidemiological data shows that few foodborne
outbreaks in Australia can be attributed to the ingestion of clean intact shell eggs
that are produced under a quality control system, graded and retailed commercially.
Effective management of the supply chain

The time and temperature that eggs are stored at determines the length of time to
resolve the YMT. Resolution of the YMT can allow significant growth of Salmonella
within the egg, with Daughtry et al (2005) demonstrating that this was a significant
factor in increasing the risk of illness from egg consumption. While Thomas et al
(2006) estimated that 75% of eggs are consumed before the YMT is resolved,
management of the supply chain should ensure that a realistic shelf life is applied to
shell eggs, according to the expected storage conditions through the distribution,
wholesale and retail supply chain.
Prohibition on sale of cracked eggs

The Food Standards Code prohibits the sale of eggs with cracked shells unless those
eggs are sold for further processing. Crack detection forms a significant food safety
control for eggs, and as stated previously this should be undertaken with an
implemented food safety program in place. There is epidemiological evidence
pointing to the use of ungraded eggs and dirty, cracked/seconds eggs being sold
direct off-farm leading to outbreaks of Salmonellosis. A requirement for egg farms to
notify of their operation to the NSW Food Authority would ensure greater ability to
trace back to the potential sources of foodborne illness.
Use of unpasteurised liquid egg preparations

Risk assessment work demonstrates that consumption of uncooked, or lightly cooked
foods containing raw eggs represent an increased risk for foodborne illness. Use of
unpasteurised liquid egg preparations, where sold, should be clearly identified as an
ingredient only for foods that will receive adequate heat treatment to destroy
Salmonella. Due to the potential for survival and growth of Salmonella spp. in
unpasteurised egg pulps, these are unsuitable for use in processed foods unless the
foods receives a sufficient heat treatment to ensure any Salmonella that may be
present are inactivated.

Food service to vulnerable populations
Epidemiological data from foodborne outbreaks consistently points to the use of raw
eggs in foods where it will not be well cooked, and/or the use of cracked and/or dirty
eggs in catering situations. Education of food service to vulnerable populations
should be undertaken on the risks of using raw eggs in foods or drinks that will not
be cooked. As an alternative, these institutions should look to use pasteurised egg
pulp that has been tested and certified as pathogen free.
Conclusions
The risk assessment work undertaken on eggs and egg products consistently
demonstrates that Salmonella is the primary hazard of concern. This is clearly
evident from the epidemiological evidence from outbreaks around Australia where
eggs have been implicated as the cause.
However, prevalence data indicate that the use of clean intact eggs before the
resolution of YMT, and/or consumed either well cooked or used as an ingredient
where the egg will be well cooked should present very little risk to the consuming
public.
But with the number of outbreaks attributable to eggs appearing to increase in the
past few years, there continues to be issues with the management of hazards
throughout the egg supply chain. This risk assessment has identified a number of
areas that may, if not addressed through the implementation of appropriate control
measures, potentially contribute to the contamination of eggs and egg products with
Salmonella and lead to further increases in the outbreaks of foodborne illness
attributable to eggs. The development of a draft egg food safety scheme aims to
implement control measures across the egg supply chain to minimise further
foodborne illness attributable to eggs.

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Risk Assessment - Conclusion
Risk is a function of the probability of a hazard occurring, multiplied by the severity
of the outcome. It is dependent on the food, the potential sources of contamination,
the hazard of concern, the type of processing, eventual use of the food product, and
the resulting illness. The latter can range from mild illness through to severe and life
threatening illnesses.
This risk assessment document provides a scientific review of the hazards and their
associated risks for food businesses covered by the food safety schemes of NSW
Food Regulation 2004. The document summarises the information from previous risk
assessments or risk profiles and supplements it with new and updated information as
available.
The review has illustrated that across the food safety schemes there are many
potential hazards that can impact on human heath. In general, microbiological
hazards were considered the most significant, as chemical and physical hazards were
rarely detected in foods, or where chemical hazards were detected, they were at
levels that do not cause adverse health effects.
The review notes that mitigating the risk presented by such hazards involves a multi-
factorial approach that often extends beyond the controls implemented by a food
business operating under a food safety scheme of NSW Food Regulation 2004. The
implementation of control measures along the entire food chain, from on-farm
controls through to retail, is seen as being the most effective strategy for mitigating
risks.
It is concluded that for food businesses covered by the food safety schemes of NSW
Food Regulation 2004 mitigating food safety risks requires the development and
implementation of reliable, systematic and preventative procedures. Such procedures
are the core elements of food safety programs, which are either introduced due to
regulatory requirements or through industry sponsored Codes of Practice.

Appendix 1: Microbiological and
chemical hazards of concern
This Appendix provides additional information on selected microbiological and
chemical hazards, as a supplement to the information included the main part of this
risk assessment.
The information included in this Appendix is limited to key points that have particular
relevance to the food commodities covered by the food safety schemes discussed in
previous chapters.
In-depth descriptions of the microbiological hazards and extensive reference lists are
available in the reference documents listed at the end of this Appendix.

Salmonella
Nature of the illness
Salmonellosis is one of the most important public and animal health disease
problems, causing worldwide morbidity and mortality of humans and animals.
Salmonellosis is a communicable disease readily transmissible from animals to man,
either directly or through contaminated products of plant or animal origin (Jay et al,
2003).
Gastroenteritis is caused by the penetration and passage of Salmonella cells from the
gut lumen into the epithelium of the small intestine where inflammation occurs.
Acute symptoms include nausea, vomiting, abdominal cramps, diarrhoea, fever and
headache. The onset time varies between 6-48 hours after consumption of
contaminated food. In some cases, chronic arthritis follows 3-4 weeks after the onset
of acute symptoms (FDA, 1992).
Salmonella spp. are important causes of gastrointestinal illness in humans.
Salmonella Enteritidis and S. Typhimurium are the most frequently reported non-
typhoidal serotypes in many countries and outbreaks have been associated with a
diverse range of food. However, a wide variety of serotypes have been associated
with outbreaks involving fresh produce. Although most Salmonella infections are self-
limiting, in a small proportion of cases these may lead to bacteraemia. The case
fatality rate in industrialised countries is less than 1% (EU SCF, 2002).
The infective dose for causing foodborne Salmonellosis in humans was, for decades,
believed to be high, that is 100,000 to one million cells. However, a number of
outbreaks have now occurred where the infective dose was found to be much lower,
for example <10—100 cells. This is particularly the case where products containing a
high fat level are involved, such as chocolate, cheese and salami (Bell & Kyriakides,
2002).
Associated foods
Salmonellosis has been associated with many foods including raw meats, poultry,
eggs, dairy products, fish, yeast, coconut, salad dressings, cake mixes, dried
gelatine, peanut butter, cocoa and chocolate (FDA, 1992).
Salmonellae reside in the intestinal tract of infected animals. They are shed in the
faeces and can be readily transmitted to other animals or man. Most colonised
individuals become healthy excreters, resulting in contamination of the environment.
Contamination is spread amongst animals during transport, holding in confined
quarters and slaughter. Foods of animal origin become contaminated following faecal
contamination of the environment and equipment (ICMSF, 1996).
Table 48 is a recent history of common isolates of salmonellae from major animal
sources.
Cross-contamination is produced by contaminated raw foods during further
processing and preparation. Salmonellae can also become established and multiply in
the environment and equipment of a variety of food-processing facilities (ICMSF,
1996).

Contamination of eggs, and particularly of egg contents, is believed to be a cause of
the large increase in human infections with S. Enteritidis in Europe and North
America since the 1980s. Contamination of intact eggs with S. Enteritidis is mainly
the result of infection of the hen’s reproductive system. Australia has been an
exception to the S. Enteritidis problem. Poultry and eggs in Australia have remained
free of S. Enteritidis (Jay et al, 2003).
Table 48 – Top Salmonella serovars from major sources

Source 2007 2006 2005
Number of isolates Number of isolates Number of isolates
Serovar & incidence Serovar & incidence Serovar & incidence
Human 2185 1792 1713
Typhimurium 34.3% Typhimurium 34.3% Typhimurium 34.3%
Enteritidis 6.7% Bovismorbificans 15.0% Enteritidis 8.8%
Bovine 313 280 293
Bovismorbificans 33.5% Bovismorbificans 43.9% Bovismorbificans 48.8%
Dublin 13.7% Dublin 10.0% Dublin 10.9%
Porcine 118 226 208
Derby 27.1% Derby 51.3% Infantis 34.1%
Johannesburg 16.9% London 11.9% Derby 23.6%
Typhimurium 10.2% Johannesburg 10.2% Anatum 13.0%
Raw meats 236 98 501
London 24.4% Heidelberg 29.6% Johannesburg 29.1%
Derby 22.9% Bovismorbificans 7.1% London 15.2%
Stanley 13.6% Chester 7.1% Derby 13.4%
Ovine 131 297 66
Bovismorbificans 48.9% Bovismorbificans 52.2% Bovismorbificans 54.5%
Chicken – 3842 4386 6011
broilers
II Sofia 33.8% II Sofia 43.3% II Sofia 49.8%
Typhimurium 14.8% Typhimurium 16.2% Infantis 11.1%
Infantis 10.2% Infantis 6.6% Typhimurium 7.8%
Chicken – 631 791 364
layers
Typhimurium 17.3% Mbandaka 20.9% Typhimurium 13.5%
Virchow 13.3% Typhimurium 15.8% Kiambu 11.8%
Mbandaka 10.5% Agona 10.7% Mbandaka 10.4%
Eggs 102 63 84
Typhimurium 30.4% Anatum 36.5% Typhimurium 38.1%

Source 2007 2006 2005
Number of isolates Number of isolates Number of isolates
Serovar & incidence Serovar & incidence Serovar & incidence
Agona 12.7% Montevideo 19.0% Anatum 22.6%
Anatum 10.8% Ohio 19.0% Singapore 10.7%
adapted from Australian Salmonella Reference Centre 2007 Annual Report (Davos, 2007)

Table 49 – Characteristics of Salmonella
Minimum Optimum Maximum
Temperature (°C) 5.2* 35-43 46.2
pH 3.8 7-7.5 9.5
aw 0.94 0.99 >0.99
Limits for growth of Salmonellae when other conditions are near optimum
* Most serotypes fail to grow at <7°C
Survival in food Survive for long periods in foods 10 week in butter, 28 days in refrigerated
vegetables and very stable in chocolate
Survival in environment Survive well on ceramic, glass and stainless steel surfaces. Survive on
human skin. Can become established and multiply in a food processing
environment, where they become a source of contamination
Controls ♦ A kill step, such as cooking, to assure destruction of Salmonellae in
contaminated foods, especially raw meats
♦ Prevention of contamination (cross-contamination) of RTE foods
♦ Low or high temperature storage of foods to prevent growth
♦ Control of contamination in food processing areas
adapted from ICMSF (1996)

Campylobacter
Campylobacter is now recognised as an important enteric pathogen. Surveys have
shown that Campylobacter jejuni is the leading cause of bacterial diarrhoea in the
USA. It causes more illness than Shigella spp. and Salmonella spp. combined (FDA,
1992). Symptoms of campylobacteriosis (also known as campylobacter enteritis or
gastroenteritis) often include fever abdominal pain, nausea, headache, and muscle
pain as well as diarrhoea. The illness usually occurs 2-5 days after ingestion of the
contaminated food or water. Illness generally lasts 7-10 days but relapses are not
uncommon, occurring in about 25% of cases (FDA, 1992).
Complications are relatively rare, but infections have been associated with reactive
arthritis, haemolytic uraemic syndrome, and following septicaemia, infections of
nearly any organ. Meningitis, recurrent colitis, acute cholecystitis and Guillain-Barre
syndrome are very rare complications (FDA, 1992).
Associated foods
Campylobacter frequently contaminates raw chicken, with surveys showing that 20-
100% of raw retail chickens are contaminated. Raw milk is also a source of
infections. The bacteria are often carried by healthy cattle and by flies on farm. Non-
chlorinated drinking water may also be a source of infections.
Campylobacter from raw meat may contaminate work areas and the hands of kitchen
staff before being transferred to RTE foods or causing self-infection.
Raw milk was the most frequently reported vehicle in food related outbreaks of
Campylobacter (Wallace, 2003; ICMSF, 1996). Those references also noted evidence
that sporadic (as opposed to outbreak) illness was linked to poultry consumption. A
more recent case-control study of Campylobacter infection found that consumption
of chicken at restaurant was the largest attributable factor, followed by consumption
of non-poultry meat at a restaurant (Friedman et al, 2004).

Table 50 – Characteristics of Campylobacter
Temperature (°C) 32 42-43 45
pH 4.9 6.5-7.5 ~9
aw >0.987 0.997
Limits for growth of Campylobacter when other conditions are near optimum
The organisms are do not tolerate high levels of oxygen and grow best with 5-6% oxygen and 10%
carbon dioxide
Survival in food Growth usually does not occur in foods due to the minimum temperature
requirement not being met. The organism is relatively fragile and is
inactivated by oxygen, drying, heating, disinfectant and acid conditions.
Despite declining numbers, the organism does survive in moist foods for
variable lengths of time
Survival in environment Survival on surfaces is prolonged by blood and the fluid obtained from the
thawing of frozen meat
Controls ♦ A kill step, such as cooking, to assure destruction of Campylobacter in
contaminated foods, especially raw meats and raw milk
♦ Prevention of contamination (cross-contamination) of RTE foods
♦ Prevention of infection of flocks has been proposed as a control
measure

Staphylococcus aureus
Some strains of Staphylococcus aureus are capable of producing a highly heat stable
protein toxin that causes illness in humans. Onset of symptoms of food poisoning
occurs between 1 and 7 (usually 2-4) hours after the ingestion of food containing
staphylococcal enterotoxins. The most common symptoms are nausea, vomiting,
retching, abdominal cramps and diarrhoea. In severe cases, headache and collapse
may occur. Recovery is rapid, usually within two days (ICMSF, 1996).
A toxin dose of less than 1.0 microgram in contaminated food will produce symptoms
of staphylococcal intoxication. This toxin level is reached when S. aureus populations
exceed 100,000 per gram (FDA, 1992).
Associated foods
Foods that require considerable handling during preparation and that are kept at
slightly elevated temperatures after preparation are frequently involved in
staphylococcal food poisoning. Frequently implicated foods include meat and meat
products; poultry and egg products; salads such as egg, tuna, chicken, potato and
macaroni; bakery products such as cream-filled pastries, cream pies and chocolate
éclairs; sandwich fillings; and milk and dairy products.
Staphylococci are wide-spread in the environment. Humans and animals are the
primary reservoir. Staphylococci are present in the nasal passages and throats and
on the hair, and skin of 50% or more of healthy individuals. Although food handlers
are the main source of food contamination in food poisoning outbreaks, equipment
and environmental surfaces can also be sources of contamination with S. aureus
(FDA, 1992).

Table 51 – Characteristics of Staphylococcus aureus
Growth Growth Toxin Toxin Range
Optimum Range Optimum
Temperature (°C) 37 7-48 40-45 10-48
pH 6-7 4-10 7-8 4.5-9.6
aw 0.98 0.83->0.99 0.98 0.87->0.99
Limits for growth and toxin production for S. aureus when other conditions are near optimum and
aerobic
Survival in food Bacteria are easily killed by heat but are salt tolerant and resistant to
drying and can survive for extended periods in food. The toxins are very
resistant to heat and will survive cooking
Survival in environment Bacteria survive well under most environmental conditions and can persist
for some time in food-production areas
Controls ♦ Protect foods from contamination
♦ Avoid conditions (mainly temperatures) where S. aureus growth can
occur
♦ For products such as salami and cheese that are held at
temperatures where S. aureus can grow, it is very important to
exercise control over the raw materials as well as the fermentation
and maturation stages

Clostridium perfringens
Food poisoning caused by Clostridium perfringens continues to be an important
cause of morbidity in the community. Large outbreaks are still common in Australia
(Bates & Bodnaruk, 2003). Spores of the organism persist in soil, sediments, and
areas subject to human or animal faecal pollution. From the natural environment it is
easily spread to foods. All foods are considered potential sources of the organism,
however according to Bates & Bodnaruk (2003) only about 2-5% of C. perfringens
isolated from food and animals produce C. perfringens enterotoxin (CPE).
The common form of perfringens food poisoning is characterised by intense
abdominal cramps and diarrhoea which begins 8-22 hours after consumption of
foods containing large numbers of C. perfringens. More than 108 vegetative cells are
required and the strain of C. perfringens must be capable of producing the food
poisoning toxin. This illness is a food infection or toxicoinfection only one episode has
ever implied the possibility of intoxication (ie illness from preformed toxin). Toxin
production occurs in the digestive tract and is associated with sporulation (FDA,
1992).
Associated foods
Diarrhoea due to C. perfringens is most commonly associated with the consumption
of cooked, uncured meat products that have been cooled slowly or stored under
inadequate refrigeration and then consumed without thorough reheating.
C. perfringens is commonly found on all meats, but in relatively low numbers. It is
largely derived from the intestines of the animal. C. perfringens produces a spore
which helps it survive harsh environmental conditions. The spores of food poisoning
strains are more heat resistant and can survive cooking.

Table 52 – Characteristics of Clostridium perfringens
pH 5.5-5.8 7.2 8.0-9.0
aw 0.93* 0.95-0.96
Limits for growth of C. perfringens when other conditions are near optimum
* Reports vary depending on the humectant
Survival in food The bacterial spore survives well in food
Survival in environment C. perfringens is widely distributed in the environment where it survives
well. It frequently occurs in the intestines of humans and many domestic
and feral animals
Controls ♦ Control relies almost entirely on cooking and cooling procedures. An
effective control measure is to cool the product rapidly, particularly
through the temperature range 55 to 15°C
♦ Vegetative cells are readily killed by heat and an effective reheating
process will ensure that large numbers of vegetative cells are not
consumed

Bacillus cereus
Foodborne illnesses associated with Bacillus cereus may occur as two distinct
syndromes: diarrhoeal and emetic. The diarrhoeal illness has a typical incubation
period of 10-13 hours. The gastroenteritis is usually mild with abdominal cramps,
profuse watery diarrhoea, rectal spasms and moderate nausea, usually without
vomiting. Evidence indicates that diarrhoeal illness is caused by the consumption of
moderate to high numbers of organisms and production of toxin in the gut.
The emetic illness usually has an onset from 1-5 hours after consuming the
implicated food. Acute nausea and vomiting are the major symptoms with diarrhoea
being uncommon. The symptoms of the emetic syndrome are toxin mediated. The
emetic toxin is a heat stable peptide that appears to produced when B. cereus grows
on particular substrates such as those containing starch or other farinaceous
materials (Jenson & Moir, 2003).
Associated foods
A wide variety of foods including meats, milk, vegetables and fish have been
associated with the diarrhoeal type food poisoning. The vomiting type outbreaks
have generally been associated with rice products, however other starchy foods such
as potato, pasta and cheese products have also been implicated. Food mixtures such
as sauces, puddings, soups, casseroles, pastries, and salads have frequently been
incriminated in food poisoning outbreaks (FDA, 1992).
Every well-documented report of B. cereus intoxication has described
time/temperature abuse that allowed relatively low (innocuous) levels of B. cereus in
foods to greatly increase.
Table 53 – Characteristics of Bacillus cereus

pH 5.0 6.0-7.0 8.8
aw 0.93
Limits for growth of B. cereus when other conditions are near optimum
Survival in food The bacterial spore survives well in food including cooked foods
Survival in environment B. cereus is widely distributed in nature. It is readily isolated from soil,
dust, cereal crops, vegetation, animal hair, fresh water and sediments.
Consequently, it is not surprising to find the organism on virtually every
raw agricultural commodity

Controls ♦ Prevention of illness requires the control of spore germination and the
growth of vegetative cells in cooked RTE food. Cell multiplication
during inadequate cooling of cooked cereal-based or protein-containing
foods is a major concern
♦ Food to be stored should be cooled rapidly to a temperature that
prevents the growth of B. cereus
♦ Food that is to be held warm should be maintained above 60°C
♦ Once formed in a food the emetic toxin is heat stable and can
withstand normal cooking or reheating temperatures

Foodborne listeriosis presents in three ways (Sutherland et al, 2003):
♦ Infection during pregnancy acquired following the consumption of food
contaminated with Listeria monocytogenes. This is a mild flu-like illness or
asymptomatic in the mother but with serious implications for unborn infants
including spontaneous abortion, foetal death, stillbirth and meningitis. Infection is
more common in the third trimester.
♦ Infection of non-pregnant adults acquired following the consumption of
contaminated food. Asymptomatic or mild illness which might progress to central
nervous system infection such as meningitis. Most common in the
immunocompromised or elderly.
♦ Listeria food poisoning following consumption of food with exceptionally high
levels of L. monocytogenes (>107/g). Vomiting and diarrhoea, sometimes
progressing to bacteraemia but usually self resolving.
The onset time to serious forms of listeriosis is unknown but may range from a few
days to three weeks. The onset time to gastrointestinal symptoms is unknown but is
probably greater than 12 hours. When listeric meningitis occurs, the overall mortality
may be as high as 70% from septicaemia 50% from perinatal/neonatal infections
greater than 80%. The mother usually survives infections during pregnancy (FDA,
1992).
Lake et al (2005) comments that it is becoming increasingly realised that the only
completely safe dose of L. monocytogenes is zero, even in healthy people. However,
the probability of invasive disease following exposure to even moderate levels of cells
is very low. The probability of illness for a given dose is about 100 times higher for
‘at risk’ populations (the elderly, the immunocompromised and the perinatal). The
dose response model used by Lake et al (2005) for a significant L. monocytogenes
dose of 106 cells generates probabilities of illness of about 10-6 for the ‘more at risk’
and approaching 10-8 for the general population. When compared with probabilities
of illness in generated in the FDA/USDA (2003) risk assessment on RTE foods, this
appears to be a conservative.
Associated foods
L. monocytogenes has been associated with such foods as raw milk, supposedly
pasteurised milk, cheese (particularly soft-ripened varieties), ice-cream, raw
vegetables, fermented raw-meat sausages, raw and cooked poultry, raw meats and
raw and smoked fish. Its ability to grow at low temperatures permits multiplication in
refrigerated foods.
The vast majority of cases are sporadic, making epidemiological links to food very
difficult.

Table 54 – Characteristics of Listeria monocytogenes
Temperature (°C) -0.4* 37 45
pH 4.39 7.0 9.4
aw 0.92
Limits for growth of L. monocytogenes when other conditions are near optimum
* Growth can occur in a variety of foods at normally encountered refrigeration temperatures
Survival in food L. monocytogenes is quite hardy and resists the deleterious effects of
freezing, drying and heat remarkably well for a bacterium that does not
form spores
Survival in environment Listeria have been isolated from a wide variety of habitats, including soil,
silage, sewage, and food-processing environments. Wet surfaces in food-
processing plants often harbour listeriae and this, combined with the ability
of listeriae to grow at low temperatures, is reflected in their occurrence in
refrigerators and on chilling units. Owing to the prevalence of
L. monocytogenes in raw materials and its ability to multiply in the
environment of many food-processing, traditional cleaning and disinfection
methods, equipment design and management practices may be inadequate
or even impair the control of L. monocytogenes

Controls The prevention of human listeriosis begins at the farm and continues
through processing to the selection and handling of food by the consumer.
A complete diet that is free of L. monocytogenes is impossible to obtain.
However, the application of farm-to-consumer controls can reduce the risk
of foodborne listeriosis
On farm:
♦ Silage should be rapidly acidified to pH <4.0 to prevent the
development of high numbers of L. monocytogenes. This is particularly
important for use on dairy farms where milk could be used for raw
milk cheeses
In processing:
♦ Minimise the growth of L. monocytogenes in raw materials, particularly
before and during the processing of raw foods
♦ Where possible use listericidal processes to assure the destruction of
L. monocytogenes
♦ Minimise the risk of recontamination of RTE foods that are further
processed after receiving a listericidal treatment through
environmental controls and GMP
Storage:
♦ Storage at 5°C or below will retard, but not prevent, multiplication in
many food products
Retail:
♦ Separate raw food of animal origin from RTE foods
♦ Use an effective method, at appropriate intervals, of disinfecting slicing
equipment and display cases
♦ Maintain proper storage and display temperatures and monitor “use
by” and best before dates
Consumers:
♦ The risk of foodborne listeriosis is much greater among persons with
reduced immunity (eg pregnant women, persons with malignant
disease or AIDS) and patients with certain underlying illnesses (eg
heart disease, diabetes, renal disease). These groups should follow
published advice on the selection and handling of foods to reduce the
risk of listeriosis

Vibrio parahaemolyticus
Pathogenic and non-pathogenic forms of Vibrio parahaemolyticus can be isolated
from marine and estuarine environments and from fish and shellfish dwelling in these
environments.
Gastroenteritis is the most common clinical syndrome caused by
V. parahaemolyticus. The infectious dose for healthy individuals, recorded in
outbreaks, is about 105 to 109 viable cells and results in an acute illness, following a
short incubation period of between 4-30 hours. The major symptoms include
diarrhoea which can be bloody, abdominal pain, nausea, and vomiting. Usually
gastroenteric infections remain in the gut and are self limiting however, a death due
to V. parahaemolyticus following the consumption of oysters was reported in NSW in
1992 (Desmarchelier, 2003). The infectious dose may be markedly lowered by the
coincident consumption of antacids (FDA, 1992)
Associated foods
Infections with this organism have been associated with the consumption of raw,
improperly cooked, or cooked and recontaminated fish and shellfish. A correlation
exists between the probability of infection and the warmer months of the year.
Improper refrigeration of seafood contaminated with this organism will allow its
proliferation, which increases the probability of infection.
A pandemic strain of V. parahaemolyticus O3:K6 has caused epidemics in Southeast
Asia and North America since 1995. In Australia, sporadic cases occasionally occur
and these often have a recent history of overseas travel (Desmarchelier, 2003).
Serotype O3:K6 and its serovariants are undergoing global spread (Balakrish Nair et
al, 2007). The organism could arrive in Australia in ballast water, imported seafood
or carried by a traveller. International evidence suggests that domestic foodborne
illness could result.
Other Vibrio spp. of concern include Vibrio cholera and Vibrio vulnificus. There is a
risk associated with imported seafood and travellers arriving from countries where
cholera is endemic.
V. vulnificus is found in Australia and there have been rare episodes of foodborne
illness. The controls listed above for V. parahaemolyticus are effective against
V. vulnificus. There is a strong association between V. vulnificus infection and
patients with underlying chronic conditions including liver disease, malignancy and
increased serum iron levels. Avoidance of raw seafood is recommended in these
cases.

Table 55 – Characteristics of Vibrio parahaemolyticus
Optimum Range
Temperature (°C) 37 5-43
pH 7.8-8.6 4.8-11
aw 0.981 0.940-0.996
Salt (%) 3 0.5-10
Survival in food V. parahaemolyticus die when exposed to temperatures below 5-7°C the
rate of mortality is highest between 0-5°C. The organisms are only
moderately sensitive to freezing and will persist in frozen seafoods for
long periods
Survival in environment The number of culturable V. parahaemolyticus in water is directly related
to temperature and the organisms are rarely isolated when water
temperatures are <15°C. The apparent disappearance of vibrios in the
aquatic environment when conditions are suboptimal may be explained
in part by the ability of the organisms to enter a dormant or viable but
non-culturable state. Associations between vibrios and higher organisms
and animals play a significant environmental role for vibrios and may be
protective during adverse conditions
Controls ♦ The primary control measure is to prevent multiplication of the
organism after harvesting and this is most readily achieved by
chilling seafoods to <5°C and holding them under refrigeration.
Since temperatures are maintained in the range 0-5°C in fish
storage and distribution systems this may considerably reduce the
risk. (Note that live bivalve molluscs have differing storage
requirements)
♦ Cooking to an internal temperature of >65°C will effectively destroy
V. parahaemolyticus
♦ Cross-contamination of cooked foods, such as crabs or prawns,
should be avoided by strict separation of raw and cooked products
and by preventing transfer via containers or shared surfaces or by
employees preparing both raw and cooked products

Shigella species
Shigellosis is principally a disease of humans and rarely occurs in animals. Most cases
of shigellosis result from the ingestion of faecally contaminated food or water. The
major contribution to contamination of food is poor personal hygiene of food
handlers.
The illness is caused when virulent Shigella organisms attach to, and penetrate,
epithelial cells of the intestinal mucosa. Some strains produce endotoxin and Shiga
toxin (very much like the verotoxin of E. coli O175:H7). After invasion, they multiply
intracellularly and spread to contiguous cells resulting in tissue destruction.
Symptoms include abdominal pain cramps diarrhoea fever vomiting blood, pus or
mucous in stools and tenesmus. The onset time is from 12 to 50 hours.
Infections are associated with mucosal ulceration, rectal bleeding and drastic
dehydration. The fatality rate may be as high as 10-15% with some strains. Reiter’s
disease, reactive arthritis and haemolytic uremic syndrome are possible sequelae that
have been reported following shigellosis.
Associated foods
A variety of foods have been associated with shigellosis. Faecally contaminated water
and unsanitary handling by food handlers are the most common cause.
Table 56 – Characteristics of Shigella spp.

Minimum Maximum
S. sonnei
Temperature (°C) 6.1 47.1
pH 4.9 9.34
Salt (%) 5.18
S. flexneri
Temperature (°C) 7.9 45.2
pH 5.0 9.19
Salt (%) 3.78
Survival in food Shigellae survive in a wide range of foods
Survival in environment On inanimate surfaces shigellae survive well between -20°C and 37°C
Controls ♦ Contamination can be prevented or minimised by using clean
utensils instead of hands. Control is achieved by good personal
hygiene and hand washing prior to working with food is most
important
♦ Cooked foods should not be touched with the hands
♦ Persons who are ill should be excluded from areas where food is
prepared

Escherichia coli
Escherichia coli is a normal non-pathogenic and useful inhabitant of the bowel. There
are a minority of enterovirulent strains within the species that cause illness ranging
from travellers’ diarrhoea through to a destructive and, not uncommonly, fatal
illness. Enterohaemorrhagic E. coli (EHEC) are associated with “hamburger disease”
in the USA and the Garibaldi outbreak in Australia. EHEC produce potent toxins
known as Shiga toxins which are toxic to cultured Vero cells (thus the abbreviations
STEC and VTEC) and other toxic factors.
The illness caused by EHEC is called haemorrhagic colitis. It is characterised by
severe cramping and diarrhoea which is initially watery but becomes grossly bloody.
Occasionally vomiting occurs. Fever is usually low grade or absent. The illness is
usually self limiting and lasts for an average of eight days.
Some victims, particularly the very young, have developed haemolytic uremic
syndrome (HUS), which is characterised by renal failure and haemolytic anaemia.
From 0-15% of haemorrhagic colitis victims may develop HUS. The illness can lead to
permanent loss of kidney function.
In the elderly, HUS with fever and neurologic symptoms constitute thrombotic
thrombocytopenic purpura. This illness can have a mortality rate in the elderly as
high as 50% (FDA, 1992).
Associated foods
Undercooked or raw hamburger mince has been implicated in many of the
documented US EHEC outbreaks. However, E. coli O157:H7 outbreaks have
implicated alfalfa sprouts, unpasteurised fruit juices, dry-cured salami, lettuce, game
meat and cheese curds. Raw milk was the vehicle in a school outbreak in Canada
(FDA, 1992). Other EHEC strains include O111 and O26.
Humans are believed to be the major, if not the only, source for most of the
enterovirulent E. coli that cause human illness. Infected food handlers can
contaminate food. Humans may also be carriers of EHEC strains. However, the major
reservoirs of a number of important EHEC strains that infect humans are the
intestinal tract of ruminants such as cattle and sheep (Desmarchelier & Fegan,
2003).

Table 57 – Characteristics of pathogenic Escherichia coli
Temperature (°C) ~ 7-8 35-40 ~ 44-46
pH 4.4 6-7 9.0
aw 0.95 0.995
Survival in food Pathogenic E. coli generally survive well in refrigerated and foods and in
frozen ground beef. EHEC may survive for long periods in fermented or
acid foods
Survival in environment E. coli is capable of growth in food and on inadequately cleaned surfaces
associated with food processing. It can also become established in food
processing plants (Desmarchelier & Fegan, 2003). Pathogenic E. coli have
no unique resistance to chlorine
Controls ♦ Protect vegetable crops from manures and untreated sewage effluent
♦ Rapidly cool carcases after slaughtering and processing
♦ Use safe food handling techniques and proper personal hygiene to
avoid contamination of RTE foods
♦ Properly heat foods to kill pathogens and hold food at appropriate
temperatures
♦ Do not use un-chlorinated water for cleaning food-processing
equipment or food contact surfaces
♦ Avoid raw and partially cooked meats and unpasteurised milk

Foodborne botulism is a severe type of food poisoning caused by ingestion of foods
containing the potent neurotoxin formed during the growth of the organism. As little
as 30 ng of neurotoxin is sufficient to cause illness and even death. The toxin is heat
labile and can be destroyed if heated at 80°C for 10 minutes or longer. The incidence
of illness is low but is of considerable concern because of its high mortality rate if not
treated immediately and properly. Limiting the pathogen’s growth in foods is
important for public health.
Onset of symptoms in foodborne botulism is usually 18 to 36 hours after ingestion of
food containing the toxin, although cases have varied from four hours to eight days.
Early signs of intoxication consist of marked lassitude, weakness and vertigo followed
by double vision and progressive difficulty in speaking and swallowing. Difficulty in
breathing, weakness in other muscles, abdominal distension and constipation may
also be common symptoms.
Foodborne botulism is primarily associated with two physiologically and genetically
distinct obligately anaerobic bacteria, proteolytic C. botulinum and non-proteolytic
C. botulinum. Proteolytic C. botulinum is a mesophile, while non-proteolytic
C. botulinum is a psychrotroph that grows and forms toxin at 3°C. With an ability to
grow at chill temperatures, non-proteolytic C. botulinum is the principal
microbiological safety concern, in relation to spore-forming bacteria, in the
manufacture of chilled foods (Peck et al, 2008).
Associated foods
Any food that is conducive to outgrowth and toxin production, that when processed
allows spore survival and is not subsequently heated before consumption can be
associated with botulism. Almost any type of food that is above pH 4.6 can support
the growth and toxin production by C. botulinum.
Botulism toxin has been isolated in a considerable variety of foods such as canned
corn, peppers/capsicum, green beans, soups, beets, asparagus, mushrooms, ripe
olives, spinach, tuna, chicken and chicken livers and liver pâté, luncheon meats,
ham, sausage, stuffed eggplant, lobster, smoked and salted fish and chopped garlic-
in-oil (FDA, 1992).
Refrigerated processed foods of extended durability (REPFEDS) are of concern as
some strains of C. botulinum grow and form toxin at refrigeration temperatures
(Szabo & Gibson, 2003).
Peck et al (2008) reviewed data from 1307 independent challenge tests. The results
from some of those tests demonstrate that non-proteolytic C. botulinum, if present,
is able to form toxin in certain foods and materials at <10°C within 10 days. At 8°C,
100/514 (19.5%) independent challenge tests were positive for toxin by day 10,
while at 4-7°C only 5/387 (1.3%) tests were positive. The products that were
positive for toxin by day 10 were mainly fish and meat products. One cooked
vegetable food was also positive.

Peck et al (2008) noted that 1010 prepared chilled meals have been produced in the
UK over the last two decades. In that time no reports could be identified of
foodborne botulism associated with correctly stored commercial chilled food. They
attribute the lack of botulism to one or more ‘unquantified controlling factors’ (eg
raw material quality, heats process that damage spores, high hygiene during
manufacture, good chill chain) and note the need for better understanding of the
controlling factors.
Table 58 – Characteristics of Clostridium botulinum

Proteolytic C. botulinum
Temperature (°C) 10 45-50
pH 4.6
aw ~ 0.94
Non-proteolytic C. botulinum
Temperature (°C) 3.3 40-45
pH 5.0
aw ~ 0.97
C. botulinum produces heat resistant spores and grows in the absence of oxygen
Survival in food Spores survive well in foods. Also survive normal cooking temperatures
Survival in environment C. botulinum is ubiquitous and survives well in a wide variety of
environmental conditions
Controls ♦ Retort low acid canned food correctly. Outbreaks are mostly reported
with home canned products and rarely with commercial products
following a formulation change
♦ Ensure all components of high acid foods and acidified foods are below
pH 4.6
♦ Include additional hurdles to Clostridial growth or limit shelf life of
products on RTE chilled foods
adapted from ICMSF (1996); Szabo & Gibson (2003)

Yersinia enterocolitica
Yersiniosis is frequently characterised by such symptoms as gastroenteritis with
diarrhoea and/or vomiting however, fever and abdominal pain are the hallmark
symptoms. Yersinia infections mimic appendicitis and mesenteric lymphadenitis, but
the bacteria may also cause infections of other sites such as wounds, joints and the
urinary tract.
Illness onset is usually 24-48 hours after the ingestion of food or drink. The major
“complication” is the performance of unnecessary appendectomies, since one of the
main symptoms of infections is abdominal pain in the lower right quadrant. Reactive
arthritis occurs in 2-3% of cases bacteraemia and diffuse disease occur rarely (FDA,
1992).
Associated foods
Strains of Yersinia enterocolitica can be found in pork, beef, lamb, oysters, fish and
raw milk, however not all serotypes carry the plasmid encoding the virulence factors
for pathogenicity (Barton & Robins-Brown, 2003). The exact cause of food
contamination is unknown. However, the prevalence of this organism in soil, water
and in animals offers ample opportunities for it to enter the food supply. Pigs are
believed to be the principal reservoir of bioserotypes pathogenic to humans (ICMSF,
1996).
Table 59 – Characteristics of Yersinia enterocolitica

Temperature (°C) - 1.3 25-37 42
pH 4.2 7.2 Growth at 9.6
No Growth at 10
NaCl (%) Growth at 5
No Growth at 7
Survival in food Y. enterocolitica is quite resistant to adverse storage conditions. Since it

capable of multiplying at very low temperatures, refrigerated storage may
not be a reliable means of preventing foodborne illness
Survival in environment The organism survives well in water and soil. The major reservoir is the live
pig
Controls ♦ Reduction in contamination of pig carcases can be achieved by
changes in pig slaughtering procedures (Barton & Robins-Browne,
2003)
♦ Proper handling of raw pork when preparing food in food-service
establishments and the home. Especially separating raw pork from RTE
foods

Enterobacter sakazakii
Enterobacter sakazakii has been associated with neonatal meningitis, necrotising
enterocolitis, bacteraemia and necrotising meningoencephalitis. Reported mortality
rates are high 10-55% for necrotising enterocolitis and 40-80% for meningitis.
Invasive E. sakazakii illness is not a common occurrence in infants. Approximately 60
cases were reported between 1958 and 2008. However, there is concern that it has
been underreported. Studies estimate the annual rate of invasive E. sakazakii to be 1
per 100,000 children under 12 months old and 9.4 per 100,000 in very low birth
weight infants.
Meningitis tends to be associated with near-term infants of normal birth weight
where infection occurred soon after birth. Bacteraemia tends to be associated with
pre-term infants of very low birth weight where infection occurs in the first two
months of life (FSAI, 2007).
E. sakazakii has been isolated from many foods and environmental sources and can
be considered to be ubiquitous. The role of these sources in neonatal infection has
not been determined. However, infection studies provide evidence of the role of
powdered infant formula:
♦ Eight cases cite infant formula as the suspected cause with the source unknown
or not specified in the other 19 cases
♦ In 26 cases where feeding patterns were specified 24 were fed on powdered
infant formula 15 of the formula samples yielded E. sakazakii in 13 of the cases
the clinical and formula strains were indistinguishable.
E. sakazakii has been isolated from infant formula milk powder on many occasions,
although contamination can be considered as low and sporadic.
A number of control measures are emerging:
♦ Tight microbiological specifications on powdered infant formula
♦ The use of recommended procedures for the preparation of formula
♦ Limitations on “hang times” for prepared formula
♦ The use of commercially sterilized ready-to-feed formula in some circumstances.

Parasitic protozoa and worms
Foodborne infections due to parasites have been known since ancient times, and
continue to be of great importance in many regions of the world (ICMSF, 1996).
Some may be confined to tropical regions for climatic reasons. Others are world-wide
in distribution, although they are more often found at a higher level of prevalence, in
such areas as Third World countries, being associated with conditions of poor
sanitation and hygiene.
While some parasitic diseases may be a significant cause of human mortality, most
cause chronic illness and are associated with unbelievably high levels of morbidity,
especially in the developing countries of the world.
Parasites may be involved with food in a number of ways:
♦ The may directly contaminate food or water, mainly through direct or indirect
faecal contamination of the soil or via infected food handlers
♦ They may contaminate invertebrates which are eaten as food or accidently
ingested on salads
♦ They may infect food animals comprising a direct part of their life cycle as an
intermediate host (or as a transfer or transport host where no development
occurs) and which infects the human host when the meat is eaten (Goldsmid et
al, 2003).
Many of the strategies used to control foodborne parasites are commonplace in
Australia. General sanitation levels are high, water quality is good, community
infection rates are low and meat inspection is required. Manure control and effluent
reuse are possible issues.

Viruses
Hepatitis A and viral gastroenteritis are the only viral diseases that have been
regularly shown in recent years to be foodborne. Foodborne viral gastroenteritis is
commonly caused by members of the small, round, structured viruses group, the
best known being the Norwalk and Norwalk-like viruses.
The human body is the only ultimate source of the contamination by the human
enteric viruses discussed here. The viruses are shed in large quantities in the faeces
of infected persons for a period varying from a few days to several weeks.
Contamination of food occurs only through direct (eg food handlers) or indirect (eg
environmental) faecal contamination.
Two general types of food have been dominant amongst reports of viral
contamination: bivalve molluscs harvested from polluted waters and foods prepared
by infected food handlers and not subsequently cooked. Contamination of food by
infected food handlers is attributed to poor personal hygiene.
Bivalve molluscs feed by filtering large volumes of surrounding water in order to trap
suspended particles. Bivalves can contain human enteric viruses and increase their
concentration to a higher level than that in water. Viruses are introduced into
watercourses and coastal waters by the routine discharge of treated and untreated
domestic sewage and by runoff from land during rain. Bivalves are generally eaten
raw or after light cooking that does not inactivate viruses.
Prevention of contamination by food handlers relies on the adoption of appropriate
work practices. Food handlers must not work while suffering from intestinal illness.
Food handlers must practise good personal hygiene and should use food-handling
techniques that prevent the contact between the hands and foods that will not
receive a virucidal treatment.
Control of shellfish-borne viral illness is difficult. The main measure is ensuring that
shellfish growing areas are sufficiently remote from sources of pollution with human
waste to be considered safe. This has reduced the incidence of shellfish-borne illness
but failed to eliminate the transmission of viruses (ICMSF, 1996).
Survival of noroviruses
Based on infectivity in human dose response research studies norovirus is stable and
resistant to heat, acid and solvents. The virus retained infectivity after incubation at
60°C for 30 min. Pasteurisation is not sufficient to eliminate viruses. Resistance is
reported to be greater in foods and shellfish. Steaming of oysters might not
inactivate norovirus (Greening et al, 2003).
Under refrigeration and freezing conditions the virus remains intact (and presumably
viable) for several months, possibly years. Freezing generally does not inactivate
viruses. Norovirus resists gastric acids at pH 3-4. The virus retained infectivity after
exposure to pH 2.7 for 3 hours at room temperature. It is believed to be sensitive to
pH >9.0 but this is unproven.
Norovirus is resistant to drying. Infectious norovirus were detected on environmental
surfaces, including carpets, for up to 12 days after outbreaks in institutions.

Survival of Hepatitis A
Hepatitis A is caused by a nonenveloped RNA picornavirus that infects only primates.
Lack of a lipid envelope confers resistance to bile lysis. The virus is hardy, surviving
on human hands and fomites and requiring temperatures higher than 85°C for
inactivation. Hepatitis A virus survives for extended periods in seawater, fresh water,
wastewater, and soil. The virus is resistant to freezing, detergents, and acids, but it
is inactivated by formalin and chlorine (Brundage & Fitzpatrick, 2006).

Scombroid poisoning
Scombroid poisoning or ‘histamine fish poisoning’ is the most common form of
toxicity caused by the ingestion of fish (Hahn & Capra, 2003). It is caused by the
ingestion of food that contains high levels of histamine and possibly other vasoactive
amines and compounds. Histamine and other amines are formed by the growth of
certain bacteria and the subsequent action of their decarboxylase enzymes on
histadine and other amino acids (FDA, 1992).
Fishery products that have been implicated in Scombroid poisoning include tuna,
mackerel and other fish with dark flesh. However, any food that contains the
appropriate amino acids and is subject to certain bacterial contamination and growth
may lead to scombroid poisoning. For example, Swiss cheese has been implicated
with intoxication.
Neither cooking, canning nor freezing reduces the toxic effect. Common sensory
examination by the consumer cannot ensure the absence or presence of the toxin
(FDA, 1992). Prevention of scombroid poisoning in fish can be achieved by
appropriate post harvest practice. Handle fish hygienically to reduce bacterial
contamination and ice fish to control decomposition.

Ciguatera
Ciguatera poisoning is caused by the consumption of toxic fish from tropical and sub-
tropical marine environments. Ciguatera has a circumtropical distribution, usually in
close association with coral reefs. It is caused by ingestion of small quantities of a
group of closely related, very powerful toxins that occur in the tissues of offending
fish. The toxins are bioaccumulated by fish through dietary exposure prior to
capture.
Toxin and toxin precursors are produced by a dinoflagellate alga named
Gamberierdiscus toxicus. Ciguatoxins enter the human food chain by grazing fish and
then move through the various trophic levels. In Australia ciguatera poisoning in
humans usually occurs after consumption of high level carnivorous fish such as
Spanish mackerel and coral trout.
After ingestion the illness often follows a reasonably predictable pattern. Initial
symptoms usually occur about 6 hours after ingestion and include vomiting,
diarrhoea and abdominal cramps. Neurological symptoms usually begin to appear 12-
18 hours after consumption of toxic fish. Symptoms can include tingling of the lips
and extremities, bone pain, muscle pain, dental pain, convulsions, muscular
paralysis, vertigo, severe headache, short term memory loss, temperature
perceptions reversals, sweating and itching.
The neurological symptoms are prominent and account for the major discomfort of
most victims. In some cases symptoms are evident for months or years (Hahn &
Capra, 2003).
Shellfish poisoning
Microscopic unicellular algae form an important component of the plankton diet of
shellfish such as oysters, mussels and scallops. Some species of dinoflagellates and
diatoms produce potent neurological toxins which can find their way though shellfish
to humans. When humans eat seafood contaminated by these microalgae, they may
suffer gastrointestinal and neurological illnesses.
These include paralytic shellfish poisoning (PSP) which in extreme cases can lead to
death through respiratory paralysis diarrhoetic shellfish poisoning (DSP) which
causes severe gastrointestinal problems and may promote stomach cancers and
amnesic shellfish poisoning (ASP) which can lead to permanent brain damage
including short-term memory loss (FDA, 1992).
Poisonous seafood neither looks or tastes different from uncontaminated seafood.
Cooking and other treatments do not destroy the toxins. If precautions are not taken
with shellfish harvest then public health problems can be considerable. Control
measures include routine monitoring of shellfish harvest areas for levels of toxic
algae and testing shellfish for toxin presence (Hallegraeff, 2003).

Mycotoxins / Aflatoxins
Toxic fungal metabolites, mycotoxins, have been responsible for a number of major
epidemics in man and animals during recent historical times. Historically, the most
important epidemics have been ergotism, which have killed hundreds of thousands of
people in the last millennium; alimentary toxic aleukia, which was responsible for the
death of at least 100,000 Russian people between 1942 and 1948;
stachybotryotoxicosis, which killed tens of thousands of horses in the USSR in the
1930s; and aflatoxicosis, which came to attention when it killed 100,00 young
turkeys in the United Kingdom in 1960 and has caused death and illness in many
other animals, including man (Hocking & Pitt, 2003).
Table 60 – Important Aspergillus, Fusarium and Penicillium species and their

mycotoxins
Toxigenic species Mycotoxins Affected Toxic effects
commodities
Aspergillus flavus Aflatoxins B1, B2 Maize, peanuts, Acute liver damage,
cottonseed, oilseed, carcinogenic, teratogenic,
tree nuts, spices immunosuppressive
Aspergillus parasiticus Aflatoxins B1, B2, Maize, peanuts, Acute liver damage,
G1, G2 cottonseed, oilseed, carcinogenic, teratogenic,
tree nuts immunosuppressive
Hydroxylated metabolites Aflatoxin M1 Milk Carcinogenic
of aflatoxin B
Fusarium verticillioides Fumonisin B1 Maize Carcinogenic
Aspergillus ochraceus, Ochratoxin A Nuts, barley, Kidney damage, teratogenic,
Penicillium verrucosum processed meats, and immunosuppressive
many others
Fusarium graminearum, Zearalenone Maize, wheat Gastrointestinal symptoms
Fusarium culmorum,
Fusarium crookwellense
Fusarium graminearum, Deoxynivalenol Maize, wheat Gastrointestinal symptoms
Fusarium culmorum,
Fusarium crookwellense
Penicillium expansum Patulin Apple, pears Kidney damage, chromosomal
aberration
adapted from Hocking & Pitt (2003)
Aflatoxicosis is poisoning that results from ingestion of aflatoxins in contaminated

food or feed. Aflatoxins are toxic compounds produced by certain strains of the fungi
Aspergillus flavus and Aspergillus parasiticus. Under favourable conditions of
temperature and humidity, these fungi grow on certain foods and feeds, resulting in
the production of aflatoxins. The most pronounced contamination has been
encountered in tree nuts, peanuts and other oilseeds, including corn and cottonseed.
The major aflatoxins of concern are designated B1, B2, G1 and G2. Aflatoxin B1 is
usually prominent and is the most toxic. Aflatoxin M is a major metabolic product of
aflatoxin B1 in animals and is usually secreted in the milk and urine of dairy cattle.

Aflatoxins produce acute necrosis, cirrhosis and carcinoma of the liver in a number of
animal species. In well-developed countries contamination rarely occurs in foods at
levels that cause acute aflatoxicosis in humans. Studies on human toxicity from
ingestion of aflatoxins have focussed on their carcinogenic potential (FDA, 1992).
While it will never be possible to eliminate mycotoxins completely from the food
supply, better cropping, harvesting, storage and processing techniques can minimise
the opportunities for fungi to produce toxic metabolites in food (Hocking & Pitt,
2003).
Gempylotoxin
Purgative properties are reported for fish of the marketing groups escolar
(Lepidocybium flavobrunneum, Ruvettus pretiosus) and rudderfish (Centrolophus
niger and Tubia species). Escolar are commonly sold in the domestic market
mislabelled as 'rudderfish' or 'butterfish'. Studies have found that both escolar and
rudderfish have higher oil composition than most seafood, but it is the high wax
ester content in escolar oil that explains the purgative property. In humans,
indigestible wax esters accumulate in the rectum causing oily diarrhoea (Yohannes et
al, 2002).

References – Appendix 1
AIFST (2008). Hocking, A.D. (Ed.). Foodborne Microorganisms of Public Health Significance.
Australian Institute of Food Science and Technology, Waterloo.
− Barton, M.D. & Robins-Brown, R.M. (2003). Yersinia enterocolitica. (pp. 577-596).
− Bates, J.R. & Bodnaruk, P.W. (2003). Clostridium perfringens. (pp. 479-504).
− Desmarchelier, P.M. (2003). Pathogenic vibrio. (pp. 333-358).
− Desmarchelier, P.M. & Fegan, N. (2003). Enteropathogenic Escherichia coli. (pp. 267-
310).
− Goldsmid, J.M., Speare, R. & Bettiol, S. (2003). The parasitology of foods. (pp. 703-722).
− Hahn, S. & Capra, M.F. (2003). Fishborne illnesses: Scombroid and ciguatera poisoning.
(pp. 689-702).
− Hallegraeff, G.M. (2003). Algal toxins in Australian shellfish. (pp. 675-688).
− Hocking, A.D. & Pitt, J.I. (2003). Mycotoxigenic fungi. (pp. 641-674).
− Jay, S., Davos, D., Dundas, M., Frankish, E., & Lightfoot, D. (2003). Salmonella (pp. 207-
266).
− Jenson, I. & Moir, C.J. (2003). Bacillus cereus and other Bacillus species. (pp. 445–478).
− Sutherland, P.S., Miles, D.W. & Laboyrie, D.S. (2003). Listeria monocytogenes. (pp. 381–
443).
− Szabo, E.A. & Gibson, A.M. (2003). Clostridium botulinum. (pp. 479-504).
− Wallace, R.B. (2003). Campylobacter. (pp. 311-331).
Balakrish Nair, G. et al. (2007). Global Dissemination of Vibrio parahaemolyticus Serotype

O3:K6 and its Serovariants. Clinical Microbiology Reviews, Jan 2007, 39-48. Retrieved 1
September 2008, from http://cmr.asm.org/cgi/content/abstract/20/1/39
Bell, C. & Kyriakides, A. (2002). Salmonella, a practical approach to the organism and its
control in foods. Blackwell Science.
Brundage, S. & Fitzpatrick, A. (2006). Hepatitis A. American Family Physician 73 (12) (web
version). Retrieved 19 December 2008, from
http://www.aafp.org/afp/AFPprinter/20060615/2162.pdf
Davos, D. (2007). Australian Salmonella Reference Centre 2007 Annual Report, Institute of
Medical and Veterinary Science.
EC SCF [European Commission, Scientific Committee on Food] (2002). Risk profile on the
microbiological contamination of fruits and vegetable eaten raw, 29 April 2002. European
Commission Health & Consumer Protection Directorate-General, Scientific Committee on
Food. Retrieved 8 December 2008, from http://ec.europa.eu/food/fs/sc/scf/out125_en.pdf
FDA (1992). The “Bad Bug Book” - Foodborne Pathogenic Microorganisms and Natural Toxins
Handbook US Food and Drug Administration, Center for Food Safety and Nutrition. Originally
published 1992, with periodic updates. Retrieved 25 August 2008 from
http://www.cfsan.fda.gov/~mow/intro.html
Friedman C. R. et al. (2004). Risk Factors for Sporadic Campylobacter Infection in the United
States: A Case-Control Study in FoodNet Sites. Clinical Infectious Diseases 38(3), S285-96.
Retrieved 25 August 2008, from http://origin.cdc.gov/enterics/publications/70_friedmanc.pdf
FSAI [Food Safety Authority of Ireland] (2007). Guidance Note 22: Information Relevant to
the Development of Guidance Material for the Safe Feeding of Reconstituted Powdered Infant
Formula. Retrieved 12 September 2008, from
http://www.fsai.ie/publications/guidance_notes/gn22.pdf

Greening, G., et al (2003) Risk Profile: Norwalk-like Virus in Mollusca (Raw). Institute of
Environmental Science and research Ltd, Christchurch, NZ.
Microorganisms in Foods 5: Microbiological specifications of food pathogens. Roberts, T.A.,
Baird-Parker, A.C. & Tompkin, R.B. (Eds.). Blackie Academic & Professional.
Peck, M.W., Goodburne, K.E., Betts, R.P. & Stringer, S.C. (2008). Assessment of the potential
for growth and neurotoxin formation by non-proteolytic Clostridium botulinum in short shelf-
life commercial foods designed to be stored chilled. Trends in Food Science & Technology
19(4), 207-216.
Yohannes, K. et al. (2002). An outbreak of gastrointestinal illness associated with the
consumption of escolar fish. Communicable Diseases Intelligence, Volume 26(3). Retrieved 11
September 2008, from http://www6.health.gov.au/internet/main/publishing.nsf/Content/cda-
pubs-cdi-2002-cdi2603-htm-cdi2603l.htm

Appendix 2: Australian food
recalls (2004 to 2008)
Table 61 – Recalls of dairy products between 2004 and 2008
Product Reason for recall Was the recall Distribution Year
instigated due
to illness?
1. Ice-cream cake Escherichia coli Not reported WA 2004
pp
2. Custard Possibility of spoilage Not reported National 2004
before expiry date
3. Haloumi Coagulase positive Not reported VIC 2004
staphylococcus
4. Yoghurt Escherichia coli Not reported NSW 2004
5. Custard Microbial spoilage Not reported National 2004
6. Cream Escherichia coli Not reported WA 2004
7. Milk, UHT, flavoured may spoil before expiry n/a National 2005
(variety) date.
8. Cheese, soft Listeria monocytogenes No National 2005
9. Cheese, soft Escherichia coli No WA 2005
10. Bocconcini, soft Listeria monocytogenes No NSW, ACT 2005
11. Cheese, hard Listeria monocytogenes No National 2006
12. Cream Escherichia coli No NSW 2006
13. Cream Escherichia coli No NSW 2006
14. Goats cheese Listeria monocytogenes No National 2006
15. Milk Escherichia coli No NSW, ACT 2006
16. Infant formula mould No National 2007
17. Ricotta mould (Salmonella) No QLD 2007
18. Cheese, hard + Salmonella No National 2007
ingredients
19. Dairy dessert Listeria monocytogenes No NSW 2007
20. Cheese, hard + Escherichia coli No NSW 2007
ingredients
21. Mozzarella, shredded Listeria monocytogenes No VIC 2008
22. Milk, goats, frozen Salmonella Zanzibar No QLD 2008
unpasteurised,
23. Cheese, hard Listeria monocytogenes No National 2008
24. Feta Listeria monocytogenes No National 2008
25. Ice-cream + Listeria monocytogenes No NSW 2008
pp
National includes distribution to three or more states and territories

instigated due
to illness?
ingredients

Table 62 – Recalls of meat products between 2004 and 2008
Product Reason for recall Was the Distribution Year
recall
instigated
due
to illness?
1. Chicken, BBQ, Listeria monocytogenes Not reported WA 2004
shaved
2. Ham, sliced Listeria monocytogenes Not reported NSW 2004
3. Pork, pickled Listeria monocytogenes Not reported NSW 2004
4. Beef, roast, Listeria monocytogenes Not reported NSW 2004
sliced
5. Ham, sliced Listeria monocytogenes Not reported NSW 2004
6. Brawn Listeria monocytogenes Not reported NSW 2004
7. Frankfurts Listeria monocytogenes Not reported National 2004
8. Salami Insufficient salt added during Not reported National 2004
processing that may result in microbial
growth
9. Meat, roast Listeria monocytogenes Not reported National 2004
10. Chicken, breast, Listeria monocytogenes No VIC 2005
sliced
11. Pork pies Escherichia coli No WA 2005
12. Devon Some product not thoroughly cooked. No National 2005
13. Smallgoods Listeria monocytogenes No QLD 2005
(variety), sliced
14. Smallgoods Listeria monocytogenes No National 2005
(variety), sliced
15. Silverside Listeria monocytogenes No VIC, NSW 2006
16. Chicken, whole, Listeria monocytogenes No NSW, ACT 2006
smoked
17. Smallgoods Salmonella Not reported National 2006
18. Lamb, sliced Listeria monocytogenes No National 2006
19. Cacciatore Listeria monocytogenes No NSW 2007
20. Chicken breast, Listeria monocytogenes No National 2007
shaved
21. Prosciutto Listeria monocytogenes No NSW 2007
Ham, slices &
whole legs
22. Smallgoods Salmonella No National 2007
23. Silverside Listeria monocytogenes No National 2007
24. Beef, cooked, Listeria monocytogenes No SA, NT 2007
sliced
25. Ham Listeria monocytogenes No QLD 2007
Silverside, sliced
26. Pastrami Listeria monocytogenes No National 2007

Product Reason for recall Was the Distribution Year
recall
instigated
due
to illness?
27. Cabanossi Listeria monocytogenes No National 2008
smoked
29. Ham, sliced Listeria monocytogenes No National 2008
30. Bacon Listeria monocytogenes No QLD 2008
31. Ham Listeria monocytogenes No National 2008
32. Beef, cooked, Listeria monocytogenes No National 2008
sliced
Pastrami, sliced
sliced

Table 63 – Recalls of plant products between 2004 and 2008
instigated due
to illness?
1. Peppercorns Salmonella Not reported National 2004
2. Mushrooms, in brine Not commercially sterile No National 2005
- Suspected under
processing.
3. Parsley, fresh Listeria monocytogenes, No National 2006
Salmonella
4. Alfalfa Salmonella Oranienburg No WA 2006
5. Alfalfa Salmonella, Listeria No VIC, TAS 2006
6. Sprouts Escherichia coli No National 2007
7. Orange juice Salmonella No NSW, VIC. 2007
Table 64 – Recalls of seafood products between 2004 and 2008

instigated due to
illness?
1. Prawns, cooked & Salmonella Infantis not reported National 2004
peeled
2. Mackerel, in oil Histamine not reported National 2004
3. Salmon, smoked, Listeria Not reported NSW 2004
sliced monocytogenes
4. Prawns, frozen, Microbial No SA, QLD 2005
cooked & peeled contamination
5. Clams, frozen Potential Salmonella No National 2005
contamination
6. Tuna, steaks Histamine Yes SA 2008
7. Tuna, canned Potential pathogenic No National 2008
contamination

Appendix 3: Australian foodborne
illness outbreaks (1995-2008)
The tables on the following pages list foodborne illness outbreaks affecting two or
more people from 1995 to 2008 and attributed to foods that are regulated by the
food safety schemes contained in the Food Regulation 2004, or where those foods
were included as an ingredient in the food implicated in the outbreak.
These tables use the epidemiological data from the following sources:
- Food Science Australia & Minter Ellison Consulting (2002). National Risk Validation
Project. Final Report.
- OzFoodNet Working Group (2002). Enhancing foodborne disease surveillance across
Australia in 2001: the OzFoodNet Working Group. Communicable Diseases Intelligence,
26(3), 375-406.
- OzFoodNet Working Group (2003). Foodborne disease in Australia: incidence,
notifications and outbreaks. Annual report of the OzFoodNet network, 2002.
Communicable Diseases Intelligence, 27(2), 209-243.
- OzFoodNet Working Group (2004). Foodborne disease investigation across Australia:
Annual report of the OzFoodNet network, 2003. Communicable Diseases Intelligence,
28(3), 359-389.
- OzFoodNet Working Group (2005). Reported foodborne illness and gastroenteritis in
Australia: Annual report of the OzFoodNet network, 2004. Communicable Diseases
Intelligence, 29(2), 164-190.
- OzFoodNet Working Group (2006). Burden and causes of foodborne disease in Australia:
Annual report of the OzFoodNet network, 2005. Communicable Diseases Intelligence,
30(3), 278-300.
- OzFoodNet Working Group (2007). Monitoring the Incidence and Causes of Diseases
Potentially Transmitted by Food In Australia: Annual Report of the OzFoodNet network,
2006 Communicable Diseases Intelligence, 31(4), 345-365.
Key for contributing factors (CF)
T1 Improper heating
T2 Improper reheat
Temperature misuse T3 Inadequate storage
T4 Preparation far in advance
T5 Inadequate thawing
C1 Food handler contamination
Inadequate handling C2 Cross contamination
E1 Insufficient hygiene
Inadequate environment E2 Inadequate facilities
R1 Contaminated raw ingredient
Raw material R2 Infected animals
R3 Food from unsafe source
Process P Inadequate process
Assumption made on the basis
a of information available eg implicated microorganism, normal mode of
transmission

Table 65 – Foodborne illness outbreaks attributed to milk, dairy products and dairy products used as an ingredient
State Year Food vehicle Agent Contributing Number Hospitalised Setting prepared
factors (CF) affected (deaths)
SA 1998 Gelato S. Oranienburg C2 102 Manufacturer
43
WA 1998 Unpasteurised milk Campylobacter R3 9 Camp
SA 1999 Unpasteurised milk S. Typhimurium 44 R3 12 Farm
a
VIC 1999 Continental custard cake S. Typhimurium 9 T3 54 Bakery
SA 2000 Unpasteurised milk Campylobacter R3 12 Retail dairy
VIC 2000 Unpasteurised milk Campylobacter R3 25 Camp
ACT 2001 Cheese sticks unknown T3 2 Restaurant
QLD 2001 Unpasteurised pets milk (cow) Cryptosporidiosis 8 3 Community
VIC 2001 Unpasteurised milk Unknown R3 12 0 Camp
VIC 2001 Unpasteurised milk (suspected) Campylobacter 12 0 Camp
WA 2001 Cranachan (dessert) Unknown 50 1 Function
NSW 2002 Cream filled cake S. Typhimurium 135 29 Bakery
VIC 2002 Cream filled cakes/pastries S. Typhimurium U290 10 Bakery
VIC 2002 Cheesecake (suspected) Norovirus 25 Commercial caterer
NSW 2003 Apple strudel Norovirus 67 0 Restaurant
QLD 2003 Cheese Sorbic acid 23 1 Childcare
QLD 2003 Trifle Norovirus 31 0 Restaurant
SA 2003 Unpasteurised milk Campylobacter R3 14 0 Camp
VIC 2003 Unpasteurised milk/animal Campylobacter 13 0 Camp/excursion
contact
43
Unpasteurised cows milk is not currently regulated under the dairy food safety scheme or the Food Standards Code, however FSANZ is reviewing the regulatory requirements relating to
unpasteurised milk as part of Proposal P1007 - Primary Production & Processing Requirements For Raw Milk Products

SA 2004 Creamed cakes S. Typhimurium 108 13 5 Bakery
QLD 2005 Custard filled dumplings S. aureus 2 - Grocery store/delicatessen
SA 2006 Sweet potato and feta cheese S. Typhimurium 9 6 0 Restaurant
salad
NSW 2007 Fruit, meringue and custard tart Unknown 9 Unknown
VIC 2007 Fetta cheese (suspected) Unknown 10 Restaurant
SA 2008 Milk (suspected) Unknown 5 Camp

Table 66 – Foodborne illness outbreaks attributed to meat, meat products and meat products used as an ingredient
ACT 1995 Roast chicken S. Bredeney T1a 3 Takeaway
NSW 1995 Deboned roast pork S. Typhimurium pt 9 T1 C2 22 1 Camp
NSW 1995 Sandwiches Suspected viral T3 C1 17 Commercial caterer
NSW 1995 BBQ chicken Unknown T3 19 Private residence
NSW, ACT, 1995 Meat or chicken S. Bredeney C2 157 23 Takeaway
QLD, VIC
SA 1995 Mettwurst (uncooked) E. coli O:111 E1 P 173 unknown (1) Manufacturer
ACT 1995 Cold chicken, salad, prawns, S. Bredeney U 14 Commercial caterer
custard
QLD 1996 Anglaise sauce S. Heidelberg pt 16 R1 R3 >500 Commercial caterer
a
NSW 1996 Ham sandwiches (suspected) Norwalk-like virus C2 20 4 Commercial caterer
NSW 1996 Chicken soup Suspected viral C1 67 Commercial caterer
VIC 1996 Beef & pork cooked on spit C. perfringens T3 33 Commercial caterer
NSW 1996 Beef, chinese cabbage & sprouts S. Typhimurium 135 C1 C2 E1 17 5 Restaurant
NSW 1997 Chicken or thai-style beef salad C. perfringens T3 C2 171 Commercial caterer
NSW 1997 Cold chicken pieces S. Typhimurium pt 9 T3 C2 E2 78 3 Function
NSW 1997 Meat loaf & gravy Unknown U 8 Institution
NSW 1997 Turkey/pork S. Typhimurium 135 T1 T3 85 2 Institution
SA 1997 Bread rolls with meat filling S. Typhimurium 135 T1a T3a C2a E2a 71 Manufacturer
a
VIC 1997 Beef/lamb curry with rice C. perfringens T3 9 Commercial caterer
VIC 1997 Ham & corned beef S. Anatum C2a Pa 25 Manufacturer
VIC, SA 1997 Sliced corned beef / ham S. Muenchen T3 C2 32 unknown (2) Manufacturer
WA 1997 Roast lamb C. perfringens T3a 12 Commercial caterer
NSW 1998 Ham & potato bake L. monocytogenes (non- T1 T3 32 Commercial caterer
invasive)
SA 1998 Ham S. sonnei biotype g C1 13 Commercial caterer

SA 1998 Spatchcock S. Typhimurium rdnc T1 T2 38 Commercial caterer
ao45
SA 1998 Chicken nuggets S. Typhimurium 12 T1 18 Private residence
SA 1998 Steak roll Unknown U 200 Takeaway
a
TAS 1998 Chicken Suspected viral C1 15 Commercial caterer
VIC 1998 Chicken meal S. Typhimurium 64 T1 32 Restaurant
VIC 1998 Cooked chicken S. Typhimurium 64 T1a T3a C2a 46 Takeaway
NSW 1999 Salami (suspected) Unknown E1 92 Function
NSW 1999 Chicken kebab S. Typhimurium T3 4 Takeaway
QLD 1999 Spit roast pork C. perfringens T1 T3 29 Commercial caterer
QLD 1999 Roast lamb Viral C1 74 Commercial caterer
QLD 1999 Meat pie C. perfringens T3 >2 Manufacturer
QLD 1999 Curried chicken C. perfringens T3 3 Takeaway
VIC 1999 Chicken vol au vents C. perfringens T3 >34 Commercial caterer
VIC 1999 Pancake with meat filling S. Hessarek T1 T3 C2 >11 Commercial caterer
VIC 1999 Chicken briyani S. aureus T3a 35 Private residence
VIC 1999 Stir-fry chicken & vegetable (or C. perfringens T3 16 Private residence
sweet and sour pork)
VIC 1999 Chicken vietnamese dish Unknown T3 >14 Restaurant
VIC 1999 Chicken/beef satay, beef dish S. Virchow 34 T1 C2 32 1 Wholesaler
ACT 2000 Chicken breast Unknown T3 3 Restaurant
ACT 2000 Lamb curry C. perfringens T3 14 Restaurant
ACT 2000 Venison stew Unknown T3 2 Restaurant
NSW 2000 Range of foods especially sliced Norwalk-like virus C1 35 Commercial caterer
smallgoods and antipasto
NSW 2000 Thai beef salad Salmonella spp T3 21 Restaurant
NSW 2000 Beef enchiladas/nachos Unknown C1 3 Restaurant

NSW 2000 Roast beef & roast pork C. perfringens T3 E1 5 Restaurant
NSW 2000 Meat pie & gravy Unknown U 3 Bakery
NT 2000 Chicken-a-la-king C. perfringens T3 56 Commercial caterer
QLD 2000 Burger (suspected) Unknown U 2 1 National franchised fast
food
QLD 2000 Steak salad & chip meal Unknown C2 5 Restaurant
QLD 2000 Chicken meal S. aureus T3 C2 3 1 Takeaway
QLD 2000 Lemon chicken Suspected viral C1a 2 Takeaway
QLD 2000 Chicken Unknown U 4 Takeaway
VIC 2000 Frankfurters S. Typhimurium 9 T1 5 Private residence
VIC 2000 Sucuk S. Typhimurium 170 T1 R3 P 8 Private residence
VIC 2000 Chicken kebabs S. Virchow pt T1 3 Takeaway
34/campylobacter/s.
Typhimurium pt64
ACT 2001 Spit roast meal (suspected) Suspected toxin 22 0 Function
ACT 2001 Spit roast Unknown U 9 Restaurant
ACT 2001 Chicken burger Unknown U 3 Takeaway
NSW 2001 Prawn stuffed chicken breast Unknown C2 9 Commercial caterer
NSW 2001 Honey chicken (suspected) Unknown 10 0 Restaurant
NSW 2001 Roast beef with gravy C. perfringens T3 27 Restaurant
NSW 2001 Chicken pizza S. Typhimurium 126 2 1 Takeaway
NSW 2001 Takeaway chicken (suspected) Unknown 2 0 Takeaway
NSW 2001 Chicken kebab (suspected) Unknown 2 0 Takeaway
NSW 2001 BBQ chicken (suspected) Unknown 3 0 Takeaway

NSW, VIC 2001 Chicken kebab S. Virchow pt 36 var 1 T1 C2 38 Takeaway
QLD 2001 Cajun chicken B. cereus T3a 6 Commercial caterer
QLD 2001 Chicken salad in pita bread S. Bovismorbificans 32 36 6 Community
QLD 2001 Chicken S. Virchow pt 8 2 0 Function
QLD 2001 Duck liver Campylobacter 2 0 Restaurant
QLD 2001 Beef curry C. perfringens 8 0 Restaurant
QLD 2001 Beef curry C. perfringens T3 15 Restaurant
QLD 2001 Chicken kebabs C. jejuni T1 3 0 Takeaway
QLD 2001 Chicken kebabs C. jejuni 3 Takeaway
SA 2001 Chicken S. Typhimurium 126 88 unknown Community
SA 2001 Chicken Salmonella spp. R1 50 Farm
SA 2001 Homemade italian sausages S. Typhimurium 135a 2 0 Private residence
VIC 2001 Soup or roast beef (suspected) Suspected toxin 269 0 Function
VIC 2001 Lamb's fry S. Typhimurium 99 22 2 Hotel
VIC 2001 Potato and bacon soup C. perfringens 9 0 Hotel
(suspected)
VIC 2001 BBQ chicken/meat S. Virchow 34 11 2 Private residence
VIC 2001 Eye fillet meal S. Typhimurium 99 95 1 Restaurant
VIC 2001 Sausages (suspected) Norwalk virus 65 0 Restaurant
VIC 2001 Kebabs (suspected) Unknown (1 positive Salmonella) 3 1 Takeaway
WA 2001 Chicken (suspected) Norwalk virus 56 0 Function
WA 2001 Undercooked turkey (suspected) Unknown 6 0 Restaurant
NSW 2002 Spit roast beef/and or pork C. perfringens 16 Commercial caterer
NSW 2002 Chicken casserole Unknown 3 Commercial caterer
NSW 2002 Chicken S. Virchow 3 Fast food outlet
NSW 2002 Beef dish (suspected) Unknown 4 Restaurant

NSW 2002 Beef curry Unknown 2 Restaurant
NSW 2002 Lamb curry C. perfringens 70 Restaurant
NSW 2002 Bbq chicken Unknown 2 Takeaway
NSW 2002 Pasta (suspected) Unknown 20 Private residence
NSW 2002 Thai salad S. Typhimurium 126 21 Restaurant
NSW 2002 Baked beans/chilli con carne S. Typhimurium 9 132 School
NSW 2002 Kebabs (suspected) Unknown 2 Takeaway
NSW 2002 Pizza Unknown 4 Takeaway
NSW 2002 Pizza Unknown 5 Takeaway
QLD 2002 Chicken C. jejuni 24 Community
QLD 2002 Pizza S. aureus 8 National franchised fast
food
SA 2002 Potato and meat pie C. perfringens 8 Private residence
SA 2002 Sliced ham S. Typhimurium 43 5 Community
VIC 2002 Roast chicken S. Typhimurium 135 19 Private residence
VIC 2002 Home bbq chicken S. Typhimurium 135 6 Private residence
VIC 2002 Pea and ham soup Unknown 10 Restaurant
VIC 2002 Steak or sauce Unknown 5 Restaurant
NSW 2003 Chicken Campylobacter 19 0 Camp/excursion
NSW 2003 Chicken / eggs (suspected) S. Typhimurium 20 2 Community
NSW 2003 Soccerball ham Unknown 1 0 Private residence
NSW 2003 Pork dish Salmonella 4 1 Restaurant
NSW 2003 Chicken S. Typhimurium 3 0 Restaurant
NSW 2003 Pigeon meat S. Typhimurium 61 5 Restaurant
NSW 2003 Chicken S. Typhimurium 12 0 Takeaway
NSW 2003 Pigs ear salad, ducks gizzard S. Typhimurium 20 0 Takeaway

NT 2003 Rice, beef and black bean sauce S. aureus 5 4 Camp/excursion
NT 2003 Quail (suspected) Unknown 10 0 Commercial caterer
NT 2003 Pizza Unknown 18 0 Private residence
NT 2003 Roast turkey (suspected) S. Typhimurium 7 0 Takeaway
QLD 2003 Beef burgundy Unknown 7 0 Restaurant
QLD 2003 Roast pork Salmonella 21 2 Restaurant
VIC 2003 Roast pork S. Typhimurium 20 0 Commercial caterer
VIC 2003 Roast pork S. Typhimurium 12 0 Commercial caterer
VIC 2003 Club sandwiches Unknown 17 0 Commercial caterer
NSW 2004 BBQ meat pizza (suspected) Unknown 5 1 National franchised fast
food
NSW 2004 Roast pork S. Typhimurium 170, 27 1 Other
Rdnc
NSW 2004 Chicken S. Typhimurium 170 13 3 Restaurant
NSW 2004 Cold chicken sandwiches Unknown 7 0 Restaurant
NSW 2004 chicken (suspected) Campylobacter 21 1 Restaurant
NSW 2004 Bacon & ham (suspected) Unknown 12 0 Restaurant
NSW 2004 Chicken (suspected) S. Typhimurium 170 3 1 Takeaway
NSW 2004 Takeaway chicken Unknown 5 0 Takeaway
NSW 2004 Chicken S. Typhimurium 12 141 unknown Unknown
QLD 2004 Meat pizza C. perfringens 6 0 National franchised fast
food
QLD 2004 Chicken kebab Campylobacter 2 0 Takeaway
VIC 2004 Chicken vol au vents Suspected toxin 20 0 Commercial caterer
ACT 2005 Pork bruschetta & duck tart Norovirus 25 1 Commercial caterer
ACT 2005 Chicken salad & chicken pasta Campylobacter 11 1 Restaurant
NSW 2005 Beef casserole Unknown 13 0 Commercial caterer

NSW 2005 Lambs liver S. Typhimurium 197 43 13 Private residence
NSW 2005 Chicken caesar salad burger Unknown 3 2 Restaurant
NSW 2005 Lamb & beef Unknown 5 0 Restaurant
NSW 2005 Chicken Unknown 2 0 Restaurant
NSW 2005 Chicken Unknown 2 0 Restaurant
NSW 2005 Ham pizza Unknown 9 0 Restaurant
NSW 2005 Chicken, rice, coleslaw, potatoes S. Typhimurium 9 4 3 Takeaway
QLD 2005 Chicken kebabs Campylobacter 4 0 Grocery store/delicatessen
QLD 2005 Beef rendang C. perfringens 3 0 Restaurant
QLD 2005 Chicken and lamb guvec C. perfringens 14 0 Restaurant
QLD 2005 Chicken meat S. Typhimurium 170/108 2 1 Takeaway
SA 2005 Marinated chicken roll S. Typhimurium 170/108 9 - Restaurant
VIC 2005 Veal rolls & red curry Unknown 40 0 Commercial caterer
VIC 2005 Chicken vol-au-vents Unknown 29 0 Commercial caterer
VIC 2005 Gravy & pork Unknown 17 0 Commercial caterer
VIC 2005 Pork (suspected) S. Typhimurium 170/108 20 1 Restaurant
NSW 2006 Chicken curry C. perfringens 70 0 Commercial caterer
NSW 2006 Cooked chicken B. cereus 14 0 Commercial caterer
NSW 2006 Pork dish or fried ice-cream S. Typhimurium 170 2 2 Restaurant
(suspected)
NSW 2006 Chicken pizza Unknown 2 0 Restaurant
NSW 2006 Chicken schnitzel in gravy Unknown 3 0 Takeaway
NSW 2006 Chicken/beef burgers with eggs S. Typhimurium 170 4 2 Takeaway
(suspected)
NSW 2006 Roast pork C. perfringens 80 0 Takeaway
NT 2006 Sticky rice balls with chicken S. Oslo 2 0 Private residence
(suspected)

QLD 2006 Chow mien S. Singapore 2 1 Restaurant
QLD 2006 Chicken teriyaki sushi roll Unknown 2 0 Restaurant
QLD 2006 Chicken and lamb guvec C. perfringens 13 0 Restaurant
QLD 2006 Chicken teriyaki sushi rolls S. Typhimurium 135 6 1 Restaurant
(suspected)
QLD 2006 Lamb korma C. perfringens 6 0 Restaurant
QLD 2006 Beef/lamb kebab (suspected) Unknown 4 0 Takeaway
SA 2006 Chicken dish Campylobacter 5 0 Commercial caterer
SA 2006 Ravioli S. Typhimurium 108 23 7 Other
SA 2006 Silverside S. Typhimurium 135 4 0 Private residence
VIC 2006 Salami (non commercial) S. London 5 0 Unknown
WA 2006 Capocollo S. Bovismorbificans 11 15 4 Commercial manufactured
food
NSW 2007 Chicken stir-fry / beef massaman Unknown 9 Restaurant
NSW 2007 Marinated chicken dish, noodle S. Typhimurium 12 7 Restaurant
dish, fried rice (suspected)
NSW 2007 Chicken schnitzel (suspected) Unknown 5 Restaurant
NSW 2007 Fried chicken (suspected) Unknown 4 Takeaway
NSW 2007 Hot dogs Unknown 5 Takeaway
NSW 2007 Beef & chicken kebabs Unknown 4 Takeaway
(suspected)
NSW 2007 Meat kebab Campylobacter 2 Takeaway
NT 2007 Roast pork (suspected) S. Oslo 3 Commercial caterer
QLD 2007 Wurst Unknown 7 Private residence
QLD 2007 Duck pâté S. Typhimurium 135a 8 Restaurant
VIC 2007 Chicken massaman curry S. Typhimurium 9 5 Restaurant
(suspected)

VIC 2007 Meat curry (suspected) Unknown 17 Takeaway
VIC 2007 Roast chicken and/or stuffing Unknown 20 Commercial caterer
NSW 2008 Chicken curry, curry pumpkin, C. perfringens / B. cereus 75 Commercial caterer
rice with lamb, plain rice
NSW 2008 Chicken rissoles (suspected) S. Typhimurium 135 5 Commercial caterer
NSW 2008 Chilli beef dish S. Typhimurium U290 7 Restaurant
NSW 2008 Stir-fry beef Unknown 2 Restaurant
QLD 2008 Chicken Campylobacter 2 Restaurant
QLD 2008 Chicken liver pâté Campylobacter 4 Restaurant
SA 2008 Chicken (suspected) S. Typhimurium 9 3 Private residence
VIC 2008 Chicken & pasta salad and ham S. Typhimurium 170 18 Commercial caterer
VIC 2008 Chicken & pasta salad and ham Campylobacter 4 Commercial caterer
VIC 2008 Chicken curry Unknown 21 Commercial caterer
VIC 2008 Roast pork S. Johannesburg 14 Restaurant

Table 67 – Foodborne illness outbreaks attributed to plant products
SA 1995 Cucumber Campylobacter C2 78 Commercial caterer
NSW 1998 Cold salad Unknown U 26 1 Commercial caterer
NSW 1998 Pasta salad or coleslaw, tossed Unknown T3 C1 E1 E2 29 Commercial caterer
salad
NSW, VIC, 1998 Semi-dried tomatoes with garlic S. Virchow 8 R1 P 85 unknown (1) Manufacturer
QLD, SA in oil
SA, VIC 1999 Orange juice, unpasteurised S. Typhimurium 135a E1 R1 533 Manufacturer
QLD 2000 Vegetables & dips Unknown C2 3 Restaurant
ACT 2001 Salad at BBQ (suspected) Suspected viral 61 0 Function
QLD 2001 Lettuce S. Bovismorbificans 32 C2 E1 36 Takeaway
VIC 2001 Tomato and cucumber salad Campylobacter 50 0 Function
NSW 2003 Salad (suspected) Unknown 24 0 Restaurant
VIC 2003 Cucumbers (suspected) Salmonella 6 0 Community
VIC 2004 Gourmet rolls/red onion S. Typhimurium 12a 28 3 Commercial caterer
NSW 2005 Self serve salad bar Unknown 37 1 Institution
TAS 2005 Salad rolls/sandwiches S. Typhimurium 135 6 0 Bakery
WA 2005 Alfalfa sprouts S. Oranienburg 125 11 Contaminated primary
produce
VIC 2006 Alfalfa sprouts S. Oranienburg 15 2 Contaminated primary
produce
VIC 2006 Bean shoots (suspected) S. Saintpaul 11 1 Restaurant
WA 2006 Rockmelon S. Saintpaul 79 12 Contaminated primary
produce
WA 2006 Paw paw S. Litchfield 17 4 Contaminated primary
produce
NSW 2007 Watermelon (suspected) Unknown 7 Private residence

NSW 2007 Mushroom & cos lettuce Unknown 6 Restaurant
(suspected)
NSW 2007 Fresh fruit juice (suspected) Unknown 6 Takeaway
QLD 2007 Baby corn S. sonnei biotype g 55 Contaminated primary
produce
VIC 2007 Passionfruit coulis (suspected) Unknown 37 Commercial caterer
VIC 2007 Fruit salad Norovirus 18 Commercial caterer
NSW 2008 Fattouch salad Unknown 17 Restaurant

Table 68 – Foodborne illness outbreaks attributed fish and seafood products
NSW 1995 Chargrilled tuna Scombroid poisoning T3 4 Restaurant
NSW 1995/1996 Prawns S. Typhimurium R3 4 Restaurant
QLD 1995 Coral trout Ciguatoxin R1 4 Private residence
QLD 1995 Spanish mackerel steak Ciguatoxin R1 15 1 Retail
WA 1995 Coral trout Ciguatoxin R1 4 Private residence
WA 1995 Pilchards Scombroid poisoning T3 >6 Restaurant
NSW 1996 Rock cod Ciguatoxin R1 2 Private residence
NSW, QLD 1996 Oysters Norwalk-like virus R3 97 Community
NSW 1997 Prawns Hepatitis A T1 R3 23 Restaurant
NSW 1997 Coral trout Ciguatoxin R1 6 Community
NSW 1997 Coral trout Ciguatoxin R1 10 Community
NSW 1997 Pipis Diarrhoetic shellfish toxin R1 59 Community
NSW 1997 Marlin Scombroid poisoning T3 2 Private residence
NSW 1997 Coral trout Ciguatoxin R1 6 Private residence
NSW 1997 Prawns Hepatitis A C1a R3 17 Restaurant
NSW 1997 Fish Ciguatoxin R1 8 3 Retail
NSW 1997 Pipis Diarrhoetic shellfish toxin R1 56 Unknown
NSW, QLD, 1997 Oysters, raw Hepatitis A R3 467 64 (1) Community
WA
NT 1997 Coral cod Ciguatoxin R1 20 4 Community
VIC 1997 Maori wrasse fish Ciguatoxin R1 18 17 Restaurant
NSW 1998 Spotted cod Ciguatoxin R1 12 4 Private residence
NSW 1998 Cod Ciguatoxin R1 3 Private residence
NSW 1998 Spotted cod Ciguatoxin R1 10 3 Private residence
NT 1998 Barracuda Ciguatoxin R1 7 6 Private residence

SA 1998 Scampi Unknown T1 T5 R1 38 Commercial caterer
VIC 1998 Thai fish cakes Scombroid poisoning T3 9 Function
VIC 1998 Fish head soup Ciguatoxin R1 3 Private residence
VIC 1998 Fish head soup Ciguatoxin R1 5 Private residence
a
VIC 1998 Fish B. cereus T3 9 Restaurant
VIC 1998 Seafood risotto Scombroid poisoning T3 3 Restaurant
VIC 1998 Tuna steaks Scombroid poisoning T3 6 Restaurant
NSW 1999 Tuna Scombroid poisoning T3 4 Private residence
NSW 1999 Curried prawns C. perfringens T3 E2 39 1 Restaurant
NT 1999 Grenadier fish fillets Scombroid poisoning T3 5 1 Restaurant
QLD 1999 Mackerel Ciguatoxin R1 2 Private residence
QLD 1999 Leatherskin/queenfish Ciguatoxin R1 7 Private residence
QLD 1999 Red claw crayfish V. cholerae non 01, non C2 10 1 Restaurant
139
VIC 1999 Spanish mackerel Ciguatoxin R1 4 Private residence
VIC 1999 Pasta with tuna and chilli sauce Scombroid poisoning T3 unknown Restaurant
VIC 1999 Rudderfish (butterfish) Wax ester (butterfish R1 >14 Restaurant
diarrhoea)
QLD 1999 Scallops or trout & ham dish, Norwalk-like virus T1a C1a 14 Commercial caterer
mildly cooked prawn dumplings
NSW 2000 Black trevally Ciguatoxin R1 unknown Private residence
QLD 2000 Coronation trout Ciguatoxin R1 9 Private residence
QLD 2000 Spotted mackerel Ciguatoxin R1 unknown Private residence
QLD 2000 Queenfish Ciguatoxin R1 unknown Private residence
QLD 2000 Black kingfish Ciguatoxin R1 unknown Private residence
QLD 2000 Coral trout Ciguatoxin R1 4 Private residence
QLD 2000 Cod Ciguatoxin R1 3 Restaurant

QLD 2000 Crab cakes & sweetlip Ciguatoxin R1 2 2 Restaurant
QLD 2000 Flake Marine toxin R1 2 Takeaway
VIC 2000 Coral trout / coral cod Ciguatoxin R1 unknown Private residence
ACT 2001 Prawns Unknown U 3 Restaurant
NSW 2001 Escolar Escolar wax esters R1 20 0 Function
NSW 2001 Fish curry made using rudderfish Scombroid poisoning & T3 R1 9 7 Takeaway
wax ester
QLD 2001 Spanish mackerel steak Ciguatoxin R1 14 11 Commercial caterer
QLD 2001 Spanish mackerel Ciguatoxin R1 14 11 Private residence
QLD 2001 Spotted mackerel Ciguatoxin R1 2 0 Private residence
QLD 2001 Barracuda Ciguatoxin R1 3 3 Private residence
QLD 2001 Coral trout Ciguatoxin R1 4 0 Private residence
QLD 2001 Spanish mackerel Ciguatoxin R1 9 0 Private residence
QLD 2001 Spotted mackerel Ciguatoxin R1 2 Private residence
QLD 2001 Mahi mahi Scombroid poisoning T3 4 0 Restaurant
QLD 2001 Mahi mahi Scombroid poisoning T3 4 Restaurant
VIC 2001 Suspect oysters S. Mississippi 6 0 Community
VIC 2001 Coral trout Ciguatoxin R1 16 0 Private residence
VIC 2001 Coral trout Ciguatoxin R1 17 Private residence
VIC 2001 Butterfish Wax ester (butterfish R1 5 0 Restaurant
diarrhoea)
NSW 2001 Seafood sauce (suspected) Unknown 6 0 Restaurant
NSW 2002 Seafood vehicle (suspected) Unknown 5 Fast food outlet
NSW 2002 Spanish mackerel Ciguatoxin R1 7 Private residence
NSW 2002 Seafood (suspected) Unknown 3 Restaurant
NSW 2002 Seafood (suspected) Unknown 4 Restaurant
NSW 2002 Fish Unknown 2 Takeaway

NSW 2002 Yum cha Hepatitis A 8 Restaurant
QLD 2002 Striped perch Ciguatoxin R1 2 Private residence
QLD 2002 Brunter bream Ciguatoxin R1 3 Private residence
QLD 2002 Spanish mackerel Ciguatoxin R1 2 Takeaway
VIC 2002 Suspect rudderfish Suspected wax ester R1 10 Restaurant
WA 2002 Oyster shooters Unknown unknown Commercial caterer
WA 2002 Seafood salad Norovirus 60 Restaurant
ACT 2003 Fish Unknown 3 0 Private residence
NSW 2003 Sardines Scombroid poisoning T3 2 2 Private residence
NSW 2003 Prawns Hepatitis A 2 0 Restaurant
NT 2003 Japanese IQF oysters Norovirus R1 48 0 Restaurant
QLD 2003 Mackerel steaks Ciguatoxin R1 3 0 Private residence
QLD 2003 Tuna patties Scombroid poisoning T3 2 0 Private residence
QLD 2003 Fish (Mooloolaba bay) Ciguatoxin R1 3 0 Private residence
QLD 2003 Curried prawn dish C. perfringens 19 0 Private residence
QLD 2003 Cod fish heads Ciguatoxin R1 2 0 Private residence
QLD 2003 Giant trevally fish Ciguatoxin R1 3 0 Private residence
QLD 2003 Barracuda Ciguatoxin R1 5 5 Private residence
QLD 2003 Fish head soup - red emperor Ciguatoxin R1 3 0 Private residence
QLD 2003 Fish species unknown Ciguatoxin R1 4 0 Private residence
QLD 2003 Dolphin fish Scombroid poisoning T3 3 0 Restaurant
QLD 2003 Spanish mackerel Ciguatoxin R1 15 0 Restaurant
QLD 2003 Escolar fish Wax ester (butterfish R1 20 0 Restaurant
diarrhoea)

VIC 2003 Japanese IQF oysters Unknown 17 0 Commercial caterer
VIC 2003 Escolar fish Scombroid poisoning T3 22 0 Restaurant
VIC 2003 Japanese IQF oysters Norovirus R1 35 0 Restaurant
VIC 2003 Escolar fish Wax ester (butterfish R1 3 0 Restaurant
diarrhoea)
ACT 2004 Calamari Seafood (suspected) Unknown 16 0 Restaurant
ACT 2004 Ling fish S. Typhimurium 197 12 2 Restaurant
NSW 2004 Oysters Norovirus R1 24 1 Contaminated primary
produce
NSW 2004 Fish cakes S. Typhimurium u290 3 0 National franchised fast
food
NSW 2004 Chinese style minced fish balls S. Typhimurium u290 3 2 Private residence
NSW 2004 Fried rice, pipis Unknown 7 6 Restaurant
NSW 2004 Crab S. Typhimurium 135 3 2 Restaurant
NT 2004 Oysters (frozen) Unknown 5 0 Contaminated primary
produce
QLD 2004 Oysters (frozen) Norovirus R1 4 0 Contaminated primary
produce
QLD 2004 Spanish mackerel/trevally Ciguatoxin R1 5 unknown Contaminated primary
produce
QLD 2004 Oysters (frozen) Norovirus R1 2 unknown Contaminated primary
produce
QLD 2004 Golden spotted trevally fish Ciguatoxin R1 2 2 Private residence
QLD 2004 Fish species unknown Ciguatoxin R1 2 0 Private residence
QLD 2004 Trevally Ciguatoxin R1 3 0 Private residence
QLD 2004 Grey mackerel Ciguatoxin R1 4 0 Private residence
QLD 2004 Coral trout Ciguatoxin R1 4 1 Restaurant
QLD 2004 Grey mackerel Ciguatoxin R1 4 0 Takeaway

VIC 2004 Butter fish (rudderfish) Suspected toxin R1 9 0 Commercial caterer
VIC 2004 Redfin Unknown 7 3 Contaminated primary
produce
NSW 2005 Tuna steak Scombroid poisoning T3 4 0 Private residence
NT 2005 Vietnamese rice paper rolls S. Typhimurium rdnc 4 1 Private residence
QLD 2005 Mackerel steaks Ciguatoxin R1 4 0 Contaminated primary
produce
QLD 2005 Black trevally Ciguatoxin R1 2 0 Contaminated primary
produce
QLD 2005 Yellowtail kingfish Ciguatoxin R1 2 0 Contaminated primary
produce
QLD 2005 Spanish mackerel Ciguatoxin R1 17 2 Contaminated primary
produce
QLD 2005 Black king fish Ciguatoxin R1 5 0 Contaminated primary
produce
produce
QLD 2005 Trevally Ciguatoxin R1 2 0 Contaminated primary
produce
QLD 2005 Barracuda Ciguatoxin R1 10 0 Contaminated primary
produce
QLD 2005 Yellowtail king fish Ciguatoxin R1 8 0 Contaminated primary
produce
QLD 2005 Prawn soup S. Typhimurium 44 23 22 Private residence
QLD 2005 Yellow fin tuna Scombroid poisoning T3 2 0 Restaurant
QLD 2005 Seafood mornay & rice Unknown 18 0 Restaurant
TAS 2005 Seafood (suspected) Vibrio 2 0 Private residence
TAS 2005 Yellow fin tuna Scombroid poisoning T3 2 0 Restaurant

VIC 2005 Fijian snapper Ciguatoxin R1 5 0 Contaminated primary
produce
VIC 2005 Fish Scombroid poisoning T3 2 0 Contaminated primary
produce
VIC 2005 Seafood platter, baked fish, Unknown 16 0 Restaurant
octopus
VIC 2005 Tuna Scombroid poisoning T3 2 0 Restaurant
VIC 2005 Spanish mackerel seafood Unknown 11 0 Restaurant
(suspected)
NSW 2006 Tuna and salmon sushi rolls S. Typhimurium 170 6 0 Commercial manufactured
food
NSW 2006 Nile perch seafood (suspected) Unknown 4 0 Private residence
NSW 2006 Oysters seafood (suspected) Unknown 6 0 Private residence
NSW 2006 White bait V. cholerae 3 2 Private residence
NSW 2006 Tuna steaks Scombroid poisoning T3 2 1 Restaurant
NSW 2006 Yellowtail kingfish fillets Scombroid poisoning T3 6 6 Restaurant
NT 2006 Slate sweetlips fish Ciguatoxin R1 14 4 Contaminated primary
produce
QLD 2006 Cod fish heads Ciguatoxin R1 2 0 Contaminated primary
produce
QLD 2006 Blue fin tuna Scombroid poisoning T3 2 0 Contaminated primary
produce
QLD 2006 Trevally Ciguatoxin R1 2 0 Contaminated primary
produce
produce
produce

QLD 2006 Black kingfish Ciguatoxin R1 4 0 Contaminated primary
produce
VIC 2006 Coral perch or coral trout Ciguatoxin R1 2 0 Contaminated primary
produce
VIC 2006 Kingfish Scombroid poisoning T3 2 0 Restaurant
NSW 2007 Fish balls B. cereus 32 Commercial caterer
NSW 2007 Tuna kebab steaks Scombroid poisoning T3 3 Delicatessen
NSW 2007 Seafood platter Unknown 4 Restaurant
NSW 2007 Tuna steaks Scombroid poisoning T3 2 Restaurant
NSW 2007 Oysters Norovirus R1 19 Restaurant
NT 2007 Tinned tuna Suspect scombroid T3 2 Commercial manufactured
poisoning food
NT 2007 Reef cod Ciguatoxin R1 2 Contaminated primary
produce
QLD 2007 Mackerel Ciguatoxin R1 2 Contaminated primary
produce
produce
QLD 2007 Coral trout Ciguatoxin R1 3 Contaminated primary
produce
produce
produce
produce
QLD 2007 Spanish mackerel Ciguatoxin R1 2 Contaminated primary
produce
QLD 2007 Tuna Scombroid poisoning T3 2 Private residence

QLD 2007 Tuna kebabs Scombroid poisoning T3 4 Private residence
TAS 2007 Oysters (suspected) Unknown 19 Contaminated primary
produce
VIC 2007 Tuna Scombroid poisoning T3 2 Restaurant
VIC 2007 Mahi mahi Scombroid poisoning T3 2 Restaurant
NSW 2008 Marinated mussels (suspected) Unknown 7 Restaurant
NSW 2008 Rice or salt & pepper prawn Unknown 7 Restaurant
QLD 2008 Black kingfish Ciguatoxin R1 6 Contaminated primary
produce
QLD 2008 Yellowtail kingsfish Ciguatoxin R1 2 Private residence

Table 69 – Foodborne illness outbreaks attributed to foods served to vulnerable persons
NSW 1995 Unknown Suspect S. Infantis T3 C2 39 unknown (3) Aged-care facility
NSW 1995 Unknown Unknown U 64 Aged-care facility
NSW 1996 Eggs flip Salmonella spp. R3 13 1 Aged-care facility
QLD 1996 Sandwiches S. Typhimurium U 52 unknown (1) Hospital
TAS 1996 Chicken with gravy C. perfringens T3 32 Aged-care facility
VIC 1996 Unknown E. coli O157 U 2 Childcare
NSW 1996 Sandwiches & meat salad L. monocytogenes U 5 Hospital
SA 1996 Chicken (cooked) L. monocytogenes o1 C2 5 unknown (1) Hospital
NSW 1997-1999 Fruit salad L. monocytogenes C2 R1 9 unknown (6) Aged-care facility & hospital
NSW 1997 Beef casserole C. perfringens T3 T4 E1 36 Aged-care facility
VIC 1997 Unknown C. perfringens T3 25 unknown (1) Aged-care facility
NSW 1998 Chicken soup Suspect viral U 13 Hospital & MOW
NSW 1998 Unknown Norwalk-like virus U 20 Childcare
VIC 1998 Eggs S. Virchow PT 34 T1a R1 12 Aged-care facility
NSW 1999 Unknown Norwalk virus C1a 25 Aged-care facility
QLD 1999 Unknown Unknown U 8 Childcare
QLD 1999 Unknown Salmonella spp. U 29 Childcare
VIC 1999 Oranges S. Typhimurium 135a R3 unknown Childcare
(4cx+)
QLD 2000 Egg flip S. Heidelberg pt 1 12 6 Aged-care facility
QLD 2000 Chicken nuggets (suspected) Norwalk virus geno 2 T1 24 Childcare
SA 2000 Unknown Cryptosporidiosis U 4 Childcare
SA 2000 Unknown Rotavirus U 12 Childcare
SA 2000 Unknown Rotavirus U 13 Childcare
QLD 2001 Unknown Unknown 19 0 Aged-care facility

QLD 2001 Unknown S. Muenchen 3 0 Aged-care facility
QLD 2001 Unknown Suspect B. cereus T3a C2a E1a 19 Aged-care facility
QLD 2001 Eggs (suspected) S. Heidelberg PT 1 12 6 Aged-care facility
QLD 2001 Eggs flip S. Heidelberg PT 1 E1 R3 12 6 Aged-care facility
SA 2001 Raw eggs S. Typhimurium 135 17 3 Aged-care facility
SA 2001 Rice pudding, potato pie S. Typhimurium 135 18 3 Aged-care facility
VIC 2001 Unknown Campylobacter 49 1 Aged-care facility
QLD 2002 Eggs white dish (suspected) S. Typhimurium 102 12 Aged-care facility
QLD 2002 Eggs sandwiches (suspected) S. Typhimurium 135a 12 0 Childcare
QLD 2002 Eggs sandwiches (suspected S. Typhimurium 135a 16 0 Childcare
VIC 2002 Rice S. aureus 7 Childcare
VIC 2002 Gravy (suspected) C. perfringens 15 Aged-care facility
VIC 2002 Gravy (suspected) C. perfringens 23 Aged-care facility
NSW 2003 Chicken schnitzel Unknown 3 3 Hospital
QLD 2003 Raw eggs (suspected) S. Typhimurium 47 16 Aged-care facility
VIC 2003 Gravy (suspected) C. perfringens 42 DK Aged-care facility
NSW 2004 Beef curry (suspected) Unknown 5 5 Hospital
SA 2004 Unknown S. Typhimurium 126 var 13 0 Aged-care facility
SA 2004 Unknown Listeria 2 2 Hospital
VIC 2004 Unknown C. perfringens 22 1 Aged-care facility
VIC 2004 Unknown Suspected toxin 9 1 Aged-care facility
VIC 2004 BBQ (suspected) Campylobacter 24 2 Aged-care facility
VIC 2004 Drinking water (suspected) Campylobacter 7 0 Aged-care facility
VIC 2004 Unknown Suspected toxin 14 unknown Hospital
VIC 2004 Unknown Suspected toxin 21 unknown Hospital
QLD 2005 Braised steak and gravy C. perfringens 36 0 Aged-care facility

SA 2005 Cold meats Listeria 3 3 Hospital
VIC 2005 Eggs (suspected) S. Enteritidis 26 var 7 2 Aged-care facility
NSW 2006 Undercooked chicken C. jejuni 3 3 Aged-care facility
NSW 2007 Beef sausages (suspected) Unknown 4 Aged-care facility
NSW 2007 Tiramisu & cream, fruit salad, Unknown 6 Aged-care facility
strudel & custard (suspected)
QLD 2007 Unknown S. Kiambu 2 Aged-care facility
SA 2007 Unknown Campylobacter 6 Aged-care facility
VIC 2007 Unknown S. Typhimurium 44 22 Aged-care facility
VIC 2007 Unknown Unknown 17 Aged-care facility
VIC 2007 Unknown Campylobacter 6 Aged-care facility
VIC 2007 Several foods were suspected C. perfringens 30 Aged-care facility
VIC 2007 Unknown Campylobacter 6 Aged-care facility
VIC 2007 Unknown S. Saintpaul 3 Aged-care facility
VIC 2007 Unknown S. Typhimurium 9 4 Hospital
SA 2008 Vitamised foods S. Typhimurium 135 38 Aged-care facility
VIC 2008 Unknown C. perfringens 6 Aged-care facility
WA 2008 Unknown Norovirus 42 Aged-care facility

Table 70 – Foodborne illness outbreaks attributed to eggs, egg products and eggs used as an ingredient
VIC 1996 Mayonnaise S. Typhimurium RDNC R1 36 Café
A015
VIC 1997 Pork rolls S. Typhimurium 9 T1 T3 C2 150 8 Bakery
VIC 1997 Pork rolls S. Typhimurium 1 T1 T3 C2 E1 808 79 Bakery
NSW 1998 Curried eggs (suspected) S. Typhimurium 135 R1 11 Commercial caterer
NSW 1999 Fish & eggs sauce S. Typhimurium R1 16 2 Commercial caterer
NSW 1999 Curried eggs rolls Streptococcus pyogenes C1 72 Institution
Group A B-haemolytic
QLD 1999 Tiramisu S. Typhimurium PT 8 T3 R1 51 Restaurant
QLD 1999 Eggs-based dessert S. Typhimurium PT 8 R1 60 Restaurant
a
QLD 1999 Hollandaise sauce S. Typhimurium 135 T1 17 Restaurant
ACT 2000 Curried eggs or home-made S. Typhimurium PT 9 T3 R1 22 Takeaway
mayonnaise
NSW 2000 Fried ice-cream S. Typhimurium PT 9 C2 E1 41 2 Restaurant
QLD 2000 Eggs sandwich S. Mbandaka T3 C2 27 Manufacturer
WA 2000 Ice-cream dessert S. Typhimurium 135 R1 53 Unknown
NSW 2000 Mango mousse S. Typhimurium PT 9 C1 40 1 Restaurant
SA 2001 Custard tarts S. Typhimurium 126 T3 C2 E1 9 Bakery
SA 2001 Custard tart with strawberries S. Typhimurium 126 9 3 Takeaway
and a jelly glaze
NSW 2001 Chicken, mayonnaise S. Typhimurium 126 17 11 Restaurant
QLD 2001 Eggs S. Montevideo 8 0 Hotel
SA 2001 Tiramisu dessert S. Typhimurium 135a 11 4 Private residence
TAS 2001 Duck eggs whites (suspected) S. Typhimurium 9 6 1 Private residence
WA 2001 Fried ice-cream S. Typhimurium 64 36 4 Restaurant
SA 2001 Mango pudding S. Typhimurium 64 var 28 0 Restaurant

SA 2002 Custard and cream cakes S. Typhimurium 99 22 Bakery
NSW 2002 Deep fried ice-cream S. Typhimurium 9 8 Restaurant
NSW 2002 Vietnamese pork/chicken rolls S. Typhimurium 126 32 Bakery
NSW 2002 Eggs based dressing S. Potsdam 17 Restaurant
NSW 2002 Caesar salad dressing, S. Potsdam 12 0 Restaurant
mayonnaise
QLD 2002 Salmon/eggs/onion/rice patties S. Typhimurium 135a 10 Private residence
QLD 2002 Asparagus egg surprise dish S. Hadar 22 3 0 Restaurant
SA 2002 Caesar salad S. Typhimurium 8 78 Restaurant
VIC 2002 Vietnamese pork rolls S. Typhimurium 135 20 Bakery
VIC 2002 Hedgehog - possibly eggs S. Typhimurium 170 6 Private residence
VIC 2002 Raw egg mayonnaise (suspected) S. Hessarek 3 1 Restaurant
VIC 2002 Caesar salad with raw egg S. Typhimurium 135 4 0 Restaurant
mayonnaise (suspected)
NSW 2003 Mayonnaise S. Typhimurium 41 0 Restaurant
NT 2003 Curried eggs sandwiches Norovirus 11 0 Commercial caterer
QLD 2003 Sauces based on raw eggs S. Typhimurium 18 3 Restaurant
(suspected)
QLD 2003 Mousse (suspected) S. Typhimurium 6 1 Private residence
VIC 2003 Pork rolls S. Typhimurium 213 22 Bakery
VIC 2003 Raw eggs dishes S. Typhimurium 52 4 Restaurant
NSW 2003 Caesar salad Campylobacter 2 1 Restaurant
SA 2003 Cold set cheesecake S. Typhimurium 4 6 1 Community
NSW 2004 Custard S. Typhimurium 135 43 17 Institution
NSW 2004 Tiramisu S. Typhimurium 126 11 3 Private residence
QLD 2004 Custard fruit tarts S. Typhimurium 135a 5 5 Bakery

QLD 2004 Japanese rice balls, omelette, Mixed toxins 16 0 Restaurant
chicken, fish
SA 2004 Home made ice-cream S. Typhimurium 9 4 0 Private residence
SA 2004 Boiled eggs S. Saintpaul 4 0 Private residence
SA 2004 Potato bake, lemon meringue, S. Typhimurium 108 8 0 Private residence
chicken patty
VIC 2004 Sauce - raw eggs (suspected) S. Typhimurium 9 8 1 Café
VIC 2004 Eggs (suspected) S. Typhimurium 126 11 5 Contaminated primary
produce
ACT 2005 Hollandaise sauce S. Hessarek 5 2 Restaurant
NSW 2005 Raw eggs dishes (suspected) S. Typhimurium 9 16 - Restaurant
NSW 2005 Caesar salad dressing S. Typhimurium 44 8 2 Restaurant
NSW 2005 Pork rolls S. Typhimurium 9 21 1 Retail
NSW 2005 Tiramisu S. Typhimurium 44 7 0 Private residence
NT 2005 Vietnamese pork rolls Unknown 5 0 Private residence
QLD 2005 Eggs based filled dumplings S. Typhimurium 197 13 7 Bakery
QLD 2005 Eggs and bacon roll S. Typhimurium 44 3 0 Private residence
TAS 2005 Bakery products S. Typhimurium 135 107 6 Bakery
TAS 2005 Sauces/dressing containing raw S. Typhimurium 135 11 2 Restaurant
eggs
TAS 2005 Mayonnaise & tartare sauce S. Typhimurium 135 77 2 Restaurant
VIC 2005 Pork rolls (suspected) Unknown 6 0 Bakery
VIC 2005 Chocolate mousse S. Typhimurium 9 14 5 Commercial caterer
VIC 2005 Eggs (suspected) S. Typhimurium 126 var 4 5 0 Private residence
VIC 2005 Hollandaise sauce S. Typhimurium 9 13 5 Restaurant
ACT 2006 Free range eggs S. Typhimurium 44 4 1 Contaminated primary
produce

ACT 2006 Free range eggs S. Typhimurium 170 13 0 Contaminated primary
produce
NSW 2006 Pikelets made from whole eggs S. Potsdam 4 0 Childcare
(suspected)
NSW 2006 White chocolate mousse S. Typhimurium 170 47 32 Institution
NSW 2006 Plain hamburger cross S. Montevideo 3 2 Takeaway
contaminated with eggs
NSW 2006 Eggs (suspected) S. Typhimurium 135a 2 1 Takeaway
NSW 2006 Eggs S. Typhimurium 170 4 3 Takeaway
NSW 2006 Chicken/beef hamburger cross S. Typhimurium 170 3 1 Camp/excursion
contaminated with eggs
(suspected)
SA 2006 Eggs through a bakery S. Typhimurium 9 15 1 Bakery
SA 2006 Homemade ice-cream and ice- S. Typhimurium 108 7 0 Private residence
cream topping
SA 2006 Beef burger with bacon & eggs S. Anatum 5 0 Restaurant
VIC 2006 Eggs (suspected) S. Typhimurium 44 43 9 Community
VIC 2006 Milkshake containing raw eggs S. Typhimurium 44 4 4 Private residence
VIC 2006 Hazelnut gateau cake made with S. Typhimurium 44 10 1 Private residence
raw eggs mousse filling
VIC 2007 Chicken foccacia/raw eggs aioli S. Typhimurium 44 16 Restaurant
NSW 2007 Eggnog S. Typhimurium 29 3 Private residence
NSW 2007 Fried ice-cream S. Typhimurium 9 12 Restaurant
NSW 2007 Vietnamese pork & chicken rolls S. Typhimurium 9 294 Takeaway
QLD 2007 Eggs (suspected) S. Typhimurium 197 21 Community
QLD 2007 Eggs (suspected) S. Typhimurium 197 3 Restaurant

TAS 2007 Eggs (suspected) S. Typhimurium 135a 20 Bakery
VIC 2007 Pork rolls S. Typhimurium 44 45 Bakery
VIC 2007 Milkshake includes raw eggs S. Typhimurium 44 4 Private residence
VIC 2007 Trifle - includes raw eggs S. Typhimurium 44 11 Private residence
VIC 2007 Tiramisu - include raw eggs S. Typhimurium 44 10 Private residence
VIC 2007 Chocolate mousse S. Typhimurium 9 8 Private residence
VIC 2007 Caesar salad dressing includes S. Typhimurium 44 15 Restaurant
raw eggs
VIC 2007 Eggs used in a undercooked food S. Typhimurium 44 13 Restaurant
(risottini)
WA 2007 Caesar salad S. Typhimurium U307 75 Restaurant
QLD 2007 Cheesecake S. Typhimurium 135a 7 Bakery
NSW 2008 Custard cake S. Typhimurium 170 17 Private residence
VIC 2008 Continental custard cake Unknown 21 Commercial caterer
NSW 2008 Eggs S. Typhimurium 126/126 var 1 41 Private residence
NSW 2008 Suspect eggs S. Typhimurium 135 4 Private residence
NSW 2008 Raw eggs dressing S. Typhimurium 126/126 var 1 3 Restaurant
TAS 2008 Eggs (suspected) S. Typhimurium 135a 3 Private residence
TAS 2008 Eggs (suspected) S. Typhimurium 135a 78 Restaurant
VIC 2008 Lemon dessert S. Typhimurium 44 12 Private residence
VIC 2008 Eggs (suspected)/custard dessert S. Typhimurium 135a 4 Private residence
VIC 2008 Suspect dessert S. Typhimurium 44 4 Restaurant

NSW Food Authority
6 Avenue of the Americas
Newington NSW 2127
PO Box 6682 Silverwater NSW 1811
Phone 1300 552 406
Fax 02 9647 0026
www.foodauthority.nsw.gov.au

Food Safety Scheme Risk Assessment

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Food Safety Scheme Risk Assessment

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Food Safety Risk

Food Safety Scheme Risk Assessment Page 1 of 214

Meat food safety scheme

Plant products food safety scheme

Seafood safety scheme

Food Safety Scheme Risk Assessment Page 2 of 214

Egg food safety scheme

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Food Safety Scheme Risk Assessment Page 4 of 214

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Dairy food safety scheme

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Meat food safety scheme

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Plant products food safety scheme

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Vulnerable persons food safety scheme

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Egg food safety scheme (draft)

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Overview of risk assessment

Previous risk assessment work

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Table 2 – Microbiological hazards in dairy products

Pathogens Significance in dairy products

adapted from FSANZ (2006)

These hazards were considered significant due to either:

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Agricultural and veterinary chemical hazards

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Table 3 – Consumption of dairy products

Sex Age Proportion of persons Median daily intake per consumer

Female 2-3 98.1 394.3

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Consumption of raw milk

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Table 4 – Summary of foodborne illness outbreaks attributed to dairy products

While there is little corresponding evidence in Australia linking consumption of

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Pathogenic Escherichia coli in raw milk

Salmonella in dairy products

Yersinia enterocolitica in milk

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Bacillus cereus in liquid milk

Clostridium botulinum in dairy products

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Staphylococcus aureus in milk

Listeria monocytogenes in dairy products

Enterobacter sakazakii in infant formula

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Table 5 – NZFSA risk profile outcomes examining hazards in dairy products

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