Hazard Identification Report For Seafood 2011

Hazards Affecting Australian
Seafood
Part 1:
Priority Listing of Issues and Risk
Ranking of Hazards Affecting
Australian Seafood
John Sumner
May 2011
Table of Contents
BACKGROUND.............................................................................................................................2
TERMS OF REFERENCE ................................................................................................................2
STRUCTURE OF THE REPORT .......................................................................................................3
TOR 1: MASTER LIST OF POTENTIAL ISSUES ..............................................................................3
TOR 2: DEVELOP CRITERIA FOR EXCLUDING ISSUES THAT ARE NOT TECHNICAL OR
ABLE TO BE PROGRESSED BY TECHNICAL WORK ..............................................................4
TOR 3: SEPARATE TECHNICAL TRADE ISSUES FROM FOOD SAFETY ISSUES INTO TWO
LISTS TO BE RANKED INDEPENDENTLY ............................................................................4
TOR 4 AND TOR 5: ....................................................................................................................5

DEVELOP HAZARD SHEETS FOR THE FOOD SAFETY ISSUES AND SUMMARY
SHEETS GIVING BRIEF BACKGROUND ON THE TECHNICAL TRADE ISSUES .........................5
UNDERTAKE A QUALITATIVE RISK RANKING FOR THE FOOD SAFETY ISSUES ....................5
HAZARD SHEET: CADMIUM.........................................................................................................7
HAZARD SHEET: ARSENIC.........................................................................................................10
HAZARD SHEET: MERCURY ......................................................................................................13
HAZARD SHEET: ALLERGENS ....................................................................................................15
HAZARD SHEET: CIGUATERA ....................................................................................................17
HAZARD SHEET: PARASITES IN SEAFOOD .................................................................................19
ISSUES SHEET: PRODUCT TESTING ............................................................................................22
ISSUES SHEET: POTENTIAL REGULATION OF CYCLIC IMINES IN SHELLFISH ..............................25
ISSUES SHEET: NOROVIRUS TRADE ISSUES (HONG KONG AND SINGAPORE).............................27
ISSUES SHEET: MONITORING INDICATORS OF FAECAL POLLUTION IN BIVALVE
MOLLUSCS ....................................................................................................................30
ISSUES SHEET: VIBRIOS IN AUSTRALIAN BIVALVES ..................................................................32
TOR 6: CREATE CRITERIA AND SCORE OR RANK TECHNICAL TRADE ISSUES ON BASIS
OF CONSEQUENCE AND LIKELIHOOD ..............................................................................34
TOR 7: PRESENT FINDINGS TO A STAKEHOLDER MEETING (WITH SAFEFISH

PARTNERSHIP MEMBERS) AND GIVE PARTNERSHIP MEMBERS INPUT INTO THE
FINAL RANKINGS ...........................................................................................................38
This report is commercial-in-confidence. No part of it may be copied, distributed, or divulged to any agency or
person without the express permission of the authors.
1
Background
SafeFish is a partnership of seafood experts that has been formed to assist the industry to
resolve technical trade impediments, especially in relation to issues associated with food
safety and hygiene. Partnership members of SafeFish include the Australian Quarantine
Inspection Service (AQIS), Food Standards Australia New Zealand (FSANZ), the Australian
Seafood Cooperative Research Centre, Codex Australia, the Seafood Access Forum and
Seafood Services Australia (SSA).
The purpose of SafeFish is to:
• Provide rapid technical response to maintain free and fair access to key markets
• Ensure the safety and hygiene of seafood.
A number of potential food safety and market access issues have been raised by the SafeFish
partnership members and by the Seafood Access Forum. SafeFish seeks to provide technical
support to clarify these issues and to rank them on the basis of various factors such as
severity and likelihood as applied to:
• Seafood captured or grown in Australian waters
• Imported seafood
Terms of Reference
1. Collate master list of current issues and associated data
2. Develop criteria for excluding issues that are not technical, or able to be progressed by
technical work
3. Separate technical trade issues from food safety issues into two lists to be ranked
independently
4. Develop hazard sheets for the food safety issues and summary sheets giving brief
background on the technical trade issues
5. For the food safety issues undertake a qualitative risk ranking and, where data permit, a
semi-quantitative ranking using Risk Ranger
6. Create criteria and score or rank technical trade issues on basis of consequence and
likelihood
7. Provide a concise report describing tasks undertaken and recommendations on which
issues should be addressed in the next one to five years and present findings to a
stakeholder meeting (with SafeFish partnership members) and give partnership
members input into the final rankings
8. Finalise report
2
Structure of the Report
This report is presented in two parts. Part 1 is a response to each TOR and Part 2 contains
background information supporting responses to each TOR as appendices.
Part 2, Section A contains two appendices: Appendix 1: Food poisonings in Australia due to
seafood and Appendix 2: Recalls of seafood in Australia. Part 2, Section B contains detailed
listings of food poisonings associated with consumption of seafood in Tables B1-B4.
Hazard sheets are presented in full in Section C following the Background Tables. Key
information from each hazard sheet is used in summary form where appropriate in TORs 4-6
(Part 1).
TOR 1: Master List of Potential Issues

Issues identified by the Seafood Access Forum and the SafeFish partners are:
1. Parasites in seafood
2. Norovirus trade issues (Hong Kong and Singapore)
3. Arsenic in seafood
4. EU MRL Cadmium in prawns (and crustacean)
5. Review of testing requirements for imported seafood
6. Ciguatoxins
7. Seafood allergens
8. Potential regulation of cyclic imines (e.g. pinnatoxins) in shellfish
9. Faecal pollution indicators
10. Shellfish market access into the US
11. Biosecurity
12. Export regulations: Unloading in foreign ports
13. Environmental trade barriers: Ecolabelling
14. Export trade data
15. Product testing issues
16. Mercury advisory
17. EU IUU legislation
18. XyRex Prawnfresh usage
19. Vibrios in Australian bivalve molluscs
A number of sources have been interrogated to inform on food safety hazards in seafood in
the Australian context:
• National Risk Validation Project (NRVP)
• OzFoodNet food poisoning data
• FSANZ recalls
• AQIS sampling program for imported seafoods
The collated data for these identified hazards are presented in Part 2, Section A, Tables A1-4,
the source data for which is contained in Part 2, Section B, Background Tables B1-B4.
3
TOR 2: Develop criteria for excluding issues that are not
technical or able to be progressed by technical work
In ascribing an issue to a ‘technical’ or ‘not technical and unable to be progressed by
technical work’ category, the following criteria have been used.
Technical
The issue is a hazard which is considered to present a food safety risk and can be progressed
by technical work which, in the present document, may comprise a status report, hazard
sheet, or a qualitative risk assessment e.g. arsenic in seafood.
Non-technical
The issue is not a food safety hazard per se, but rather a regulatory position which requires
resolution between controlling authorities and/or industry bodies e.g. improving the
timeliness of updating trade data.
TOR 3: Separate technical trade issues from food safety

issues into two lists to be ranked independently
Based on the criteria set out in TOR 2 the segregation of hazards and issues is presented in
Tables 1 and 2.
Table 1: Potential hazards in seafood consumed in Australia and in Australian export seafood
Biological Hazards
Parasites in seafood
Chemical Hazards
Arsenic in seafood
EU MRL Cadmium in prawns (and crustaceans)
Ciguatoxins
Seafood allergens
Mercury advisory
4
Table 2: Issues of a regulatory nature
Issue Suggested Progression

Review of testing requirements for imported seafood See issues sheet provided
Shellfish market access into the US See issues sheet provided
Norovirus trade issues (Hong Kong and Singapore) See issues sheet provided
Potential regulation of cyclic imines in shellfish See issues sheet provided
Faecal pollution indicators See issues sheet provided
Product testing issues See issues sheet provided
Vibrios in Australian bivalves See issues sheet provided
Biosecurity Consult industry & AQIS

Export regulations: Unloading in foreign ports Consult industry & AQIS
Environmental trade barriers: Ecolabelling Consult industry & C/wealth
Export trade data Consult industry & AQIS
EU IUU legislation Consult AQIS & EU
XyRex Prawnfresh usage Consult AQIS & Japanese author
TOR 4 and TOR 5:

Develop hazard sheets for the food safety issues and
summary sheets giving brief background on the technical
trade issues
Undertake a qualitative risk ranking for the food safety
issues
Summaries for each of the six regulatory issues and six hazards identified under TOR 2 are
presented in these TORs. With each hazard sheet is presented a qualitative risk assessment.
Complete hazard sheets for the additional hazards that were identified through other data
sources are presented in Part 2.
Qualitative Risk Assessment Tool

A qualitative framework for the rating of risk has been used based on premises published by
the International Commission on Microbiological Specifications of Foods (ICMSF, 2002)
and by Food Science Australia (2000). The ICMSF formulated descriptors for severity of
illnesses caused by various pathogens, which was used in conjunction with a matrix of factors
assembled by FSA (2000) to describe risk profiles of plant products.
Taken together, the present qualitative matrix is based on criteria for:
5
Severity
The severity of the identified hazards was classified according to the International
Commission of the Microbiological Specifications of Food (ICMSF 2002) with level of
severity defined 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.
Occurrence of illness
This is classified as low, medium or high based on the hazard’s involvement as recorded in
public health statistics.
Growth
An indication is given of whether growth of the pathogen in the product is required to cause
disease. In general, microbiological hazards need to grow in the product or be present at high
numbers before there is a significant risk of disease.
In the case of chemicals such as heavy metals where chronic exposure is needed over a
protracted period, for the purposes of the qualitative risk assessment, the situation is
considered analogous to that of growth.
Production, processing or handling of food

The production, processing or handling of the food may increase, decrease or not affect the
concentration of the hazard.
Consumer terminal step

This element considers whether a consumer terminal step, such as cooking, is applied to the
product. Cooking by the consumer will, for most biological hazards, reduce the subsequent
risk of disease.
Epidemiology
Consideration is given as to whether the hazard-commodity combination has been recorded
as a cause of food poisoning.
References
Food Science Australia. 2000. Final Report – Scoping study on the risk of plant products.
SafeFood NSW, Homebush, NSW, Australia.
ICMSF. 2002. Microorganisms in Foods: 7 Microbiological testing in food safety
management. New York, NY, United States of America: Kluwer Academic/Plenum
Publishers.
6
Hazard Sheet: Cadmium
Hazard
In 1972, the Joint FAO/WHO Expert Committee on Food Additives and Contaminants
(JECFA) established a Provisional Tolerable Weekly Intake (PTWI) for cadmium of 400-
500 µg per person, approximately 7-8 µg/kg per body weight per week (bw/w) and 60-70 µg
per day for a 60 kg person.
In 1993, JECFA advised a PTWI of 7 µg/kg bw/w, a level confirmed in 1995 by the
European Commission and reconfirmed by JECFA in 2003.
Currently the European Food Safety Authority (EFSA) has a TWI of 2.5 µg/kg bw, this after
considering a JECFA proposal for a provisional tolerable monthly intake (PTMI) of 25 µg/kg
bw (not radically different from their previous PTWI of 7µg/kg bw).
Cadmium can enter cells and bind with ligands; it is not easily cleared by the body and has a
long residence time (half-life 10-30 years) in organs such as liver, kidney and the intestine.
Cadmium has been associated with disorders of the kidneys, bones and nervous system, and
is also identified as a carcinogen.
The EU set maximum levels (MLs) for foodstuffs, including seafood, based on the results of
a dietary exposure assessment and the opinions of JECFA, as noted above (Table 1). Full
details of the scientific underpinning is contained in a risk assessment carried out by EFSA
(EFSA. 2009).
Table 1: Maximum levels for cadmium in seafood (EFSA, 2009)
Product ML
(mg/kg)
Muscle meat of fish, excluding species listed below 0.05
Bonito (Sarda sarda) 0.10
Common two-banded sea bream (Diplodus vulgaris)
Eel (Anguilla anguilla)
Grey mullet (Mugil labrosus labrosus)
Horse mackerel or scad (Trachurus spp)
Louvar or luvar (Luvarus imperialis)
Mackerel (Scomber spp)
Sardine (Sardina pilchardus)
Sardinops (Sardinops spp)
Tuna (Thunnus spp, Euthynnus spp, Katsuwonus pelamis)
Wedge sole (Dicologoglossa cuneata)
Muscle meat of bullet tuna (Auxis spp) 0.20
Muscle meat of anchovy (Engraulis spp) 0.30
Swordfish (Xiphias gladius)
Crustaceans, excluding brown meat of crab and excluding head and thorax meat 0.50
of lobster and similar large crustaceans (Nephropidae and Palinuridae)
Bivalve molluscs 1.0
Cephalopods (without viscera) 1.0
7
Issue
The issue in the Australian context is that, within a lot of production of prawns, a proportion
may contain cadmium in excess of the European Union ML (0.5 mg/kg).
Over the period 2001-2011 the EU, via its Rapid Alert system, has rejected 133 consignments
of crustaceans, of which 45 were prawns and the remainder crab, on the basis of the ML.
Among the rejections were 39 consignments of Australian frozen prawns with cadmium
levels up to 2 mg/kg, reflecting the bioaccumulation of the metal by prawns in certain
Australian waters.
Current Status
In 2007, the Australian government made a submission to the European Commission to
review the ML for crustaceans citing, as evidence for its deletion that:
• The Codex Alimentarius Commission had set no ML for cadmium in crustaceans, on
the basis that crustaceans represent a minor exposure to cadmium.
• While median levels for prawns in Australia’s export trade were 0.11 mg/kg, the
distribution is highly skewed and a proportion can not meet the ML criterion at the 95th
percentile (e.g. 5%).
• Australian prawns do not contribute significantly to the cadmium ingested by European
consumers.
The status of the submission is not known.
It is noted that all 39 rejections were during the period 2004-2007 and the fact that there have
been no further rejections of prawns from any European country may indicate that:
1 The EU has ceased testing prawns
2 Only prawns from low-risk waters in Australia and other countries are being exported
3 Exports from Australia to EU have been curtailed.
Data do not exist to comment on possibilities 1 and 2 (above). However, ABARE data
provide clear evidence that exports to the EU have diminished over the period 2005-06 until
2008-09 (Table 2).
Table 2: Exports of prawns from Australia to the EU (2005-2009)
2005-06 2006-07 2007-08 2008-09

Export volume (t) to EU 2,666 1,316 548 340
Total exports (t) 8,744 6,376 4,916 4,797
Proportion (%) exported to EU 30.5 20.6 11.2 7.1
Value ($,000) 39,205 17,825 7,537 3,600
Total exports ($,000) 133,923 93,563 68,624 82,180
Proportion (%) exported to EU 34.4 19.1 11.0 4.4
8
ABARE data, as presented in Table 2, indicate the scale of the reduction in prawn exports to
the EU. Whereas in 2005-06 2,666 t of prawn exports entered the EU, by 2008-09 the volume
was 340 t, the more than 2,000 t diminution contributing greatly to an overall reduction in
total exports over the same period of >4,000 t.
It is noted that, while there was some appreciation of the Australian dollar against some
currencies e.g. USD and Yen, no such appreciation occurred against the Euro during the
period cited in Table 1.
Qualitative Risk Assessment

Product/hazard Cadmium in Prawns
Severity IA
Occurrence of illness Low
Chronic exposure required to cause illness? Yes
Impact of processing, handling None
Consumer terminal step? None
Epidemiological link? None
Assessed risk Low
Going Forward
There seems prima facie evidence that the EU maximum Limit for cadmium in crustacea has
had, and continues to have, a significant effect on the prawn industry in general, and the
export prawn sector in particular.
It should be determined whether exports of other crustaceans to Europe (lobsters, crabs) are
similarly affected.
Engaging the EU in risk-based dialogue on ingestion of cadmium from Australian exports
should be referred to AQIS as a high priority.
References
EFSA. 2009. Scientific opinion: Cadmium in food. Scientific opinion of the panel on
contaminants in the food chain. EFSA Journal 908:1-39.
9
Hazard Sheet: Arsenic
Hazard
A provisional maximum tolerable daily intake of 2 µg/kg body weight (b.w.) for inorganic
arsenic was set by the JECFA in 1983 and confirmed as a provisional tolerable weekly intake
(PTWI) of 15 µg/kg b.w. in 1989. The JECFA noted that organic forms of arsenic present in
seafoods needed different consideration from the inorganic arsenic, based on the low toxicity
and rapid metabolism of organoarsenicals.
Both Codex (CAC, 1995) and EFSA (Anon. 2009) note that arsenic in seafoods is mainly the
non-toxic forms Arsenobetaine and Arsenosugars, both of which are metabolic products of
marine algae and are accumulated by herbivorous species, especially filter feeders.
Exposure to arsenic in its inorganic forms (trivalent arsenite and pentavalent arsenate) has a
number of effects, the most important being bladder cancer.
Neither Codex, EFSA nor the New Zealand FSA has a standard for arsenic in seafood,
though the latter has for imported Hijiki seaweed.
Issue
The Food Standards Code contains a Maximum Limit for arsenic in seafood based on a
determination that seafood, particularly molluscan shellfish, contributes significantly to
dietary exposure to arsenic.
Commodity ML (mg/kg)
Crustacea 2
Fish 2
Molluscs 1
Several conflicting statements contained in ANZFA (1999b) are of relevance, particularly in

those sections highlighted in bold type:
1 ‘The main seafoods contributing to inorganic arsenic dietary exposure (>5%) from food
alone were prawns (52%) and marine fish (14%). Although other seafood such as crabs,
mussels and oysters are significant sources of inorganic arsenic per kilogram of food,
the relatively small consumption levels of these foods means they do not make a
significant contribution to mean inorganic arsenic dietary exposure for the whole
population (ANZFA 1999b).’
2 ‘Dietary exposure estimates for high consumers of single food commodity groups
indicate that high fish consumers could receive up to 4 per cent of the PTDI for
inorganic arsenic, and that high consumers of molluscs and crustacea could receive up
to 6 per cent and 18 per cent of the PTDI for inorganic arsenic respectively, assuming
that the inorganic content of seafood is 6 per cent of the total arsenic content and
assuming that these consumers eat molluscs and crustacea every day over a
lifetime (ANZFA 1999b).’
10
Current Status
The assertion is that the ML is too low for molluscan shellfish.

Product/hazard Arsenic in Molluscs
Severity IA
Chronic exposure required to cause illness? Yes
Epidemiological link? None
Assessed risk Low
Going Forward
It appears that FSANZ encountered difficulty in estimating inorganic arsenic because:
Inorganic arsenic analyses are more expensive than total arsenic analyses. To make the best
use of the available funds for analytical testing, total arsenic, rather than inorganic arsenic,
is determined in most cases (20th ATDS).
An assumption on the proportion of total arsenic which was inorganic was made. However,
as FSANZ state: There is no accepted ratio that can be used for all foods to convert the total
arsenic content to inorganic arsenic. For this reason and to enable comparison of the results
with the tolerable limit for inorganic arsenic, it was assumed that all arsenic detected in each
food was in the form of the more toxic inorganic arsenic. This is a significant overestimate
because not all arsenic is present as inorganic arsenic. This is demonstrated by the presence
of total arsenic at levels above the LOR in all of the seafood samples while inorganic arsenic
was not present above the LOR in any of the seafood samples (20th ATDS).
It is recommended that a re-appraisal of the ML for arsenic in seafood be made.
The Australian Seafood CRC is in the process of recruiting a new postdoctoral scientist in the
area of seafood toxicology. This specialist resource may be able to be utilised to progress
work in this area, via an expert solicitation.
The study should follow the process undertaken by Borak and Hosgood (2007) in assessing
the implications of consumption of arsenic in seafoods. These authors state that:
• Inorganic arsenic, the cause of illness in humans subject to chronic exposure, generally
comprises 0.1% and almost always <3% of total arsenic in seafood; organic arsenic
compounds comprise the vast bulk of total arsenic in seafood.
• Organic arsenic compounds found in seafood are mainly arsenobetaine and
arsenosugars and are non-toxic.
• A margin of exposure of 1,000-10,000-times exists between carcinogenic doses used in
rodent studies and those expected after consumption of large quantities of seafood.
11
The authors conclude: The general absence of arsenic toxicity reported in humans and other
mammals after consumption of large amounts of seafood (Andrewes et al. 2004) lends
weight-of-evidence support to its lack of acute toxicity.
References
Andrewes, P., Demarini, D. Funasaka, K. Wallace, K. Lai, V. Sun, H. Cullen, W. and
Kitchin, K. 2004. Do arsenosugars pose a risk to human health? Environmental Science and
Technology 38:4140-4148.
Scientific opinion on Arsenic in food. 2010. EFSA panel on contaminants in the food chain.
EFSA Journal 7(10):1351.
ANZFA. 1999. P158 the review of metal contaminants in food.
Borak, J. and Hosgood, H. 2007. Seafood arsenic: Implications for human risk assessment.
Regulatory Toxicology and Pharmacology 47:204-212.
Codex Alimentarius Commission. 1995. Codex general standard for contaminants and toxins
in food and feed. Codex Standard 193-1995.
FSANZ. 2002. The 20th Australian total diet survey. Canberra, ACT 2610.
12
Hazard Sheet: Mercury
Hazard
Based on an acute mercury food poisoning that occurred in Japan during the 1950s, it is
known that high levels of dietary mercury in seafood cause measurable deficits in the 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 but, in aquatic environments, bacteria can convert inorganic
mercury to Methyl mercury which is readily absorbed by the human body. Methyl mercury is
accumulated in aquatic food chains, so all fish contain small amounts of Methyl mercury in
their muscle tissue. Predatory fish or mammals such as whales at the top of the food web
have the largest amounts.
Mercury levels in most commercially-harvested oceanic fish in Australia are <0.5 mg/kg
Methyl mercury, 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 Methyl
mercury occurs via seafood (predominantly 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 (FDA, 1994; National Academy of
Sciences, 2000).
Issue
FSANZ have issued an advisory which allows adults, including pregnant women, to eat 2-3
serves (300-450 g) per week of low-mercury species (almost all fish except shark, swordfish,
billfish and marlin).
By contrast, the NZ Food Safety Authority (http://www.foodsmart.govt.nz/whats-in-our-
food/chemicals-nutrients-additives-toxins/specific-foods/mercury-in-fish/) recommends that
pregnant women eat seafood:
• Without restriction – a range of named finfish, shellfish and squid
• 3-4 serves/week – wide range of finfish and lobster
• 1 serve every 1-2 weeks – shark, marlin, swordfish, bluefin tuna
The amended advice by FSANZ and NZFSA accords with recent findings that consuming
<340 g seafood/week may have a detrimental effect on foetal development (Hibbeln et al.
2007).
By following the revised FSANZ advice of ‘2-3 serves’ consumers may consider it prudent to
defer to two, rather than three serves, an intake which has been shown to be detrimental
(Hibbeln et al. 2007).
13
Product/hazard Mercury in Seafood
Severity IA
Growth in product required to cause illness? Yes
Epidemiological link? None*
Assessed risk Low
* The Minamata poisoning notwithstanding
Current Status
There appears to be a general move towards allowing increased intake of seafoods, based on
risk:benefit considerations e.g. US FDA, Hibbeln et al. (2007).
Going Forward
Given the NZ FSA stance on consumption of seafood it is requested that FSANZ review their
current advice, with a view to aligning with the NZ approach.
It is noted that Thompson and Lee (2009) state: NZFSA has recently agreed with FSANZ that
both agencies should investigate removing fish monitored for mercury from New Zealand and
Australia’s respective ‘risk lists’ as exposure from mercury in fish would be better managed
by an education programme such as NZFSA’s advisory information for pregnant women.
The process may be facilitated by data from the CRC’s compositional seafood profiles to
assess the mercury content of Australian species of fish and categorise them in categories
similar to the NZFSA.
References
FDA. 1994. Mercury In Fish: Cause For Concern? FDA Consumer Magazine 28(7).
Hibbeln, J. 1998. ‘Fish consumption and major depression’. Lancet 352: 1213.
National Academy of Sciences. 2000. Toxicological effects of mercury. The National
Academy of Sciences, USA.
Thompson, B. and Lee, L. 2009. Mercury content in imported fin fish. Institute of
Environmental Science and Research Ltd. Christchurch, NZ.
14
Hazard sheet: Allergens
Issue
Allergens represent a hazard to susceptible consumers and in seafood comprise two
categories: naturally-occurring allergens and allergens added during processing.
The allergic reaction can vary in intensity from vomiting/nausea to anaphylactic shock and
subsequent collapse.
Naturally-Occurring Allergens
Consumers generally are allergic to one type of seafood e.g. crustaceans or bivalve molluscs
or finfish, and are able to eat other types with safety.
For vulnerable consumers allergic reactions may occur without seafood being ingested, e.g.
via aerosols from seafood being cooked.
Consumers avoid contact with seafood causing the allergy by identifying it during purchase
or when ordering food in a restaurant.
Because the quantity of allergen required to cause a reaction may be very small there is the
possibility of inadvertent transfer during handling and marketing of seafoods. For example,
there is opportunity for cross contact to occur when categories are mixed in a container being
delivered to a wholesaler.
It is unlikely that fish markets, wholesalers and processors identify allergens as hazards
reasonably likely to occur in the food safety plan.
Going Forward
A review commissioned by Sydney Fish Market found an absence of evidence that cross-
contact between seafood categories is a hazard reasonably likely to occur during handling at
the market (Murphy, 2011).
The same report recommended that further work be done on seafood handling, distribution
and processing using the VITAL (Voluntary Incidental Trace Allergen Labelling) grid to
assess the impact of allergen cross contact (http://www.allergenbureau.net/vital/).
Allergens Added During Processing

Allergens may be added during value-adding operations such as crumbing or battering of
seafood. If the allergen is not declared the product must be recalled, and typical examples are
presented in Table 1.
15
Table 1: Recalls of seafood due to presence of allergens (FSANZ 1999-2011)
Year Product Format Hazard Country of origin*

2005 Whiting Frozen, crumbed Allergens (casein) Vietnam
2010 Fish Frozen, battered Allergen (dairy)
2011 Fish Frozen, crumbed Allergen (peanuts)
2011 Calamari Frozen Allergen (peanuts)
2011 Dory Frozen, crumbed Allergen (peanuts)
* Where known
Control of allergens at the plant level is by identifying allergens present in premixes used for
coatings and ensuring that the label reflects the presence of an allergen.
Inadvertent addition of an allergen is prevented by good manufacturing practices such as
cleaning equipment and food contact surfaces between batches.
The above information should be included in the company’s food safety plan.
References
Murphy, R. 2011. Sydney Fish Market – allergen risk review. Rural Development Services,
Hobart, Tasmania.
16
Hazard Sheet: Ciguatera
Hazard
Ciguatera poisoning is caused by eating subtropical and tropical reef fish which have
accumulated naturally-occurring toxins produced by marine algae. The toxins are known to
originate from dinoflagellates (predominantly Gambierdiscus toxicus), common to ciguatera-
endemic regions in tropical waters. These toxins produce a range of gastrointestinal,
neurological and cardiovascular symptoms which can persist for many weeks and may be re-
triggered by dietary changes or exposure to low levels of toxin, months or years after initial
exposure. Ciguatera poisoning is usually self-limiting with a low incidence of death.
Issue
According to data assembled by the National Risk Validation Project and OzFoodNet, over
the period 1988-2010 there were 101 outbreaks of ciguatera food poisoning in Australia
involving more than 597 consumers (Part 2, Table A1), with mackerels and coral trout the
most-frequently implicated species (Part 2, Table A4). By far the majority of food poisoning
incidents occurred in Queensland (Part 2, Table B4).
The issue is that ciguatera food poisoning is Australia’s most frequent cause of illness due to
consumption of seafood, with no reduction over the period 2001-2010 (OzFoodNet data)
compared with 1988-2001 (NRVP data).

Product/hazard Ciguatera in Seafood
Severity III
Occurrence of illness High
Growth in product required to cause illness? No
Epidemiological link? Yes
Assessed risk Medium
Going Forward
In general, ciguatera poisoning is sporadic, typically involves fewer than five people and may
be misdiagnosed by medical staff.
It results from consumption of fish caught recreationally and commercially and the quantum
from each sector is not known.
Current risk reduction strategies include limits on the size and/or type of certain fish species
and restrictions on fishing in known toxic areas. Red bass, chinaman fish and paddletail have
been regarded as unsuitable for sale in Queensland for 20 years due to their likely toxicity
(Lehane, 1999). Other than in Queensland and Northern Territory recreational fishermen are
unlikely to catch affected fish.
17
In subtropical and tropical regions professional fishermen are aware of areas to avoid which
helps reduce the hazard to consumers. Size restrictions are potentially effective since larger
fish may be more frequently toxic than small fish but the practice of filleting into portions for
on-board packing and freezing makes this impossible to monitor as a CCP.
While some fish markets claim to not sell potentially poisonous fish such as reef fish,
anecdotal evidence suggests that due to inconsistent naming, potentially ciguatoxic species
may be sold. It is recommended that SafeFish and Sydney Fish Market undertake a
benchmarking study on levels of ciguatoxin on species linked with ciguatera.
The feasibility should be considered whereby a wholesaler/distributor/marketer requires the
supplying vessel to verify that the catch has been taken from ‘safe’ waters. This could be
done by supplying a GPS log for each trip, analogous to supplying a temperature:time log for
fish vulnerable to histamine formation.
This information could become a CCP in the HACCP plan of fishers and
wholesalers/distributors/marketers. Widespread adoption of the Fish Names Standard would
also assist.
References
Lehane, L. 1999. Ciguatera Fish Poisoning. A Review in a Risk-Assessment Framework.
National office of Animal and Plant Health, Agriculture, Fisheries and Forestry Australia.
National Risk Validation Project. 2002. Food Science Australia and Minter Ellison.
OzFoodNet Annual reports 2000-2010.
18
Hazard Sheet: Parasites in Seafood
Hazard
The consumption of raw seafood as sashimi (pieces of raw fish) and sushi (pieces of raw fish
or cooked prawns with rice and other ingredients) are popular foods in Australia. The
ingestion of raw fish carries with it a number of risks of foodborne infection, including the
risk of parasitic worms that can cause gastrointestinal disease in humans.
Among parasites associated with seafood are helminths (parasitic worms) and include
nematodes (roundworms), cestodes (tapeworms) and trematodes (flat worms, or flukes). Of
most concern are:
• Nematodes: Anisakis simplex
• Cestodes: Diphyllobothrium
• Trematodes: Clonorchis sinensis
Helminth parasites are sensitive to freezing and to relatively mild heating (i.e. normal
cooking temperatures). Consequently, those parasites associated with seafood are generally
passed to consumers via raw, minimally processed or inadequately cooked chilled products,
the latter particularly associated with socio-cultural and behavioural factors (Adams et al.
1997).
A wide range of seafood products have been implicated in human infection (FDA, 1999):
• Ceviche (fish and spices marinated in lime juice; Latin America)
• Lomi lomi (salmon marinated in lemon juice, onions and tomato; Hawaii)
• Poisson cru (fish marinated in citrus juice, onions, tomatoes and coconut milk)
• Salmon roe
• Ako poki (Japanese and Hawaiian cephalopod dish)
• Sashimi (pieces of raw fish; Japan)
• Sushi (pieces of raw fish with rice and other ingredients; Japan)
• Green herring (lightly brined herring; Netherlands)
• Scandinavian gravlax
• Drunken crabs (crabs marinated in wine and peppers; China)
• Cold-smoked fish and undercooked grilled fish
Comprehensive lists of parasites that have been reported in Australian fish are presented in
Beumer et al. (1982), Lester and Sewell (1989), Doupe et al. (2003) and Shamsi et al. (2010).
Data on prevalence of helminths in Australian species are presented in Part 2 of this report.
Current Status
There is one published record of anisakid infection in Australia (Shamsa and Butcher, 2011)
in which a 41-year-old Australian woman of Tongan descent consumed raw mackerel.
In 2010, EFSA published a scientific opinion on risk assessment of parasites in fishery
products and concluded that, while wild-caught fish can never be guaranteed not to have
helminth parasites, the likelihood in farmed fish is much lower.
19
Of relevance in a listing of farmed fish, a number of species were identified which are both
consumed in Australia, and exported in a chilled format, making them potential sources of
infection. These species include Atlantic salmon, Pacific salmon, rainbow trout and tuna, to
which should be added the farmed species Australian Kingfish (Seriola lalandi) and
Mulloway (Argyrosomas hololepidotus).
In a survey of five South Australian species, Shamsi et al. (2010) did not detect anisakid
larvae in ten samples of wild caught S. lalandi.

Product/hazard Parasites in Seafood Consumed Raw
Severity II
Occurrence of illness One case reported in Australia
Growth in product required to cause illness? No
Impact of processing, handling Freezing inactivates parasite
Consumer terminal step? No
Epidemiological link? Not in Australia
Assessed risk Low
Going Forward
There has been activity recently where importers of Australian farmed species are being
directed to a European Union directive (E.C. 853/2004) which, in Annex III, Section III,
Chapter III, Paragraph D states:
D. REQUIREMENTS CONCERNING PARASITES
1. The following fishery products must be frozen at a temperature of not more than -20 °C in
all parts of the product for not less than 24 hours; this treatment must be applied to the raw
product or the finished product:
(a) fishery products to be consumed raw or almost raw;
(b) fishery products from the following species, if they are to undergo a cold smoking
process in which the internal temperature of the fishery product is not more than 60 °C:
(i) herring;
(ii) mackerel;
(iii) sprat;
(iv) (wild) Atlantic and Pacific salmon;
and
(c) marinated and/or salted fishery products, if the processing is insufficient to destroy
nematode larvae.
2. Food business operators need not carry out the treatment required under paragraph 1 if:
(a) epidemiological data are available indicating that the fishing grounds of origin do not
present a health hazard with regard to the presence of parasites; and
20
(b) the competent authority so authorises.
3. A document from the manufacturer, stating the type of process they have undergone, must
accompany fishery products referred to in paragraph 1 when placed on the market, except
when supplied to the final consumer.
The reporting of the first case of anisakidosis in Australia, together with the position adopted
by European countries prompts some investigation of parasites in seafoods.
This is an issue which requires a watching brief to monitor whether rigorous application of
the EU directive is having a deleterious impact on Australian trade.
References
Adams, A.M., Murrell, K.D. and Cross, J.H. (1997). Contamination of animal products:
prevention and risks for public health. Revue Scientifique et Technique Office International
des Epizooties, 16:652-660.
Beumer, J.P., Ashburner, L.D., Burbury, M.E., Jette, E. and Latham, D.J. (1982). A Checklist
of the parasites of Fishes from Australia and its Adjacent Antarctic Territories.
Commonwealth Agriculture Bureaux, Slough, England. 100 pp.
Doupe, R. Lymbery, A. Wong, S. and Hobbs, R. 2003. Larval anisakid infections of some
tropical fish species from north-west Australia. Journal of Helminthology 77:363-365.
EFSA Panel on Biological Hazards (BIOHAZ); Scientific Opinion on risk assessment of
parasites in fishery products. EFSA Journal 2010; 8(4):1543. [91 pp.].
doi:10.2903/j.efsa.2010.1543. Available online: www.efsa.europa.eu
FDA. (1999). Bad Bug Book (Foodborne Pathogenic Microorganisms and Natural Toxins..
Downloaded from: http://vm.cfsan.fda.gov/~mow/intro.html
Lester, R.J.G. and Sewell, K.B. (1989). Checklist of parasites from Heron Island, Great
Barrier Reef. Australian Journal of Zoology, 37: 101-128.
Shamsi, S. Eisenbarth, A. Saptarshi, S. Beveridge, I. and Gasser, R. 2010. Occurrence and
abundance of anisakid nematode larvae in five species of fish from southern Australian
waters. Parasitology Research.
Shamsi, S. and Butcher, A. 2011. First report of anisakidosis in Australia. Medical Journal of
Australia 194:199-200.
21
Issues Sheet: Product Testing
Two issues are identified by SafeFish partners:
Issue 1: Biotoxin Testing of Bivalves

No biotoxin testing facility in Australia is accredited to diagnose marine biotoxins currently
important in domestic and international trade. Around 30% of all diagnostic tests of
Australian seafood (wildcatch and aquaculture) are undertaken in New Zealand by the
Cawthron Institute.
Current Status
A recent report by Ridge Partners to the Seafood CRC recommends that a National Marine
Biotoxin Centre be set up in Sydney; such a venture will allow all biotoxin testing to be done
in Australia.
Issue 2: US Equivalence of Bivalve Testing

South Australian shellfish harvesters wish to export live product (oysters and mussels) to the
USA, but this is impeded by the lack of a Memorandum of Understanding (MoU) between
governments.
Current Status
In 2009, an audit of intending exporters was undertaken by SARDI in conjunction with
Dorothy-Jean & Associates Ltd to advise on changes required to be able to meet USA
requirements.
The report found that:
1 The SASQAP (SA Quality Assurance Program) is of a suitable status to advance an
application to the USFDA for market access for whole, live shellfish.
2 The South Australian shellfish growing area would meet the general requirements for
the USA National Shellfish Sanitation Program (NSSP) with some minor adaptations.
3 There are some hurdles that will need to be addressed to reach a successful MOU.
The recommendations were that:
1) AQIS must be advised of the industry request for market access of live bivalve
molluscan shellfish to the USA. AQIS will be the primary Competent Authority and
will play a central role in the Memorandum of Understanding arrangements with the
USDFDA.
2) As there are multiple agencies involved in the administration of the South Australian
shellfish quality assurance programme there will need to be good co-operation between
the different agencies. There will also need to be evidence of written memoranda of
22
agreement with the agencies which share the programme responsibilities.
3) AQIS will likely need to provide to the USFDA a ‘side by side’ review of the
Australian and USA shellfish food safety legislation.
4) A Central File will need to be established by AQIS that holds all the required
programme records.
5) There needs to be training and appointment of a Shellfish Standardisation Officer for
Australia who will then inspect any processing plants to be used for export of shellfish
to the USA.
6) All premises used for processing shellfish must be listed on the Interstate Certified
Shellfish Shippers List and this list must be maintained by AQIS.
7) Any laboratory used to support the shellfish programme will need to comply with the
requirements of the NSSP manual and be supervised by a designated Laboratory
Evaluation Officer. (Note the scope of this audit did not include Laboratory
compliance).
8) South Australia currently uses a microbiological method for faecal coliforms in
seawater that has not yet been approved by the NSSP. Equivalency will need to be
negotiated with the USFDA.
9) Management plans for conditionally approved areas must be very specific in defining
who, what and when environmental parameters are monitored to officially open and
close a conditionally managed harvest area.
10) PIRSA shall record any polyculture activities at a growing area (more than one species
on the farm). This information may be required for individual species management
criteria.
11) The NSSP programme has specific patrol requirements. A Risk Management Plan for
surveillance must be drafted for the growing areas exporting to the USA to justify the
current surveillance programme (See Chapter VIII, Section B of the NSSP MO).
12) All harvesting vessels must have adequate toilet and hand sanitizing facilities on board.
13) On licensing harvest operators some public health information must be provided to
them on the hazards with harvesting shellfish from closed areas and on the significance
of discharging human sewage overboard.
14) Tagging of product for product from harvest area to dealer must be in compliance with
Chapter VIII .02 F of the NSSP. Note that bulk tagging is acceptable provided that there
is also a transaction record provided to the dealer.
15) There are specific HACCP and sanitation records required by the NSSP. These include
mandatory CCPs, adequate training and weekly sign off on records. The NSSP is
prescriptive in its sanitation requirements, for example wash hand basins must be
supplied with hot water greater than 43 degrees Celsius. The Shellfish Standardization
Officer will need to review the premises, process operation and records to assess full
compliance with these requirements.
16) There will be specific requirements for labelling, temperature control storage and
shipping conditions to the USA. However, it was not possible at this time to review
likely compliance with these requirements. AQIS will need to verify these before
certifying product for export.
23
17) This audit focused on the USA food safety requirements for live bivalve molluscan
shellfish. However, it should be noted that there may also be USA biosecurity
requirements for the entry of live animals. This will need to be referred to AQIS for
consideration.
Going Forward
This centres on the feasibility of AQIS incorporating the necessary work into their program to
complete a MoU with USA. This will provide the potential for all Australian shellfish
harvesters and processors to export to the market. Consideration could be given to SafeFish
technical support to assist AQIS to reignite the MoU.
24
Issues Sheet: Potential Regulation of Cyclic Imines in
Shellfish
Issue
Cyclic imines (CIs) comprise a family of marine biotoxins made up of spirolides,
gymnodimines, pinnatoxins and pteriatoxins. The toxins cause neurotoxic symptoms in mice.
The issue in Australia concerns pinnatoxins and devolves around the fact that:
• A dinoflagellate capable of synthesising pinnatoxins has been confirmed in Australian
and New Zealand oyster-growing waters
• Pinnatoxins were detected in oysters in South Australia in 2007, leading to a protracted
closure of the fishery
• Acute toxicity of pinnatoxins has been demonstrated in mouse tests
• The possibility that the European Commission may impose a regulatory limit for CIs.
Current Status
In 2010, the European Food Safety Authority (EFSA) produced a scientific opinion on cyclic
imines which declared, in summary, that:
• There have been no reports linking pinnatoxins to poisoning events in humans. Note,
however that pinnatoxins were linked with consumption of razorshells in China at a
workshop in South Australia (Rhodes et al. 2010).
• No country has a regulatory limit for CIs in shellfish.
• The acute toxicity of CIs has been established.
• No long-term studies exist to allow the establishment of a tolerable daily intake (TDI).
• No conclusions could be drawn on risk to consumers following consumption of
pinnatoxins.
• Further method development is required for detection of CIs.
• More information is needed on occurrence of CIs in shellfish.
Going Forward
It is noted that the program for the 8th International Conference on Molluscan Shellfish Safety
in June 2011 has a paper by Hess: First report of pinnatoxin in mussels and a novel
dinoflagellate, Vulcanodinium rugosum, from France.
This report may provide EFSA with impetus to revisit the regulation of pinnatoxins and it is
recommended that a watching brief be maintained.
References
EFSA Panel on Contaminants in the Food Chain (CONTAM); Scientific Opinion on marine
biotoxins in shellfish – Cyclic imines (spirolides, gymnodimines, pinnatoxins and
25
pteriatoxins). EFSA Journal 2010; 8(6):1628. [39 pp.]. doi:10.2903/j.efsa.2010.1628.
available online: www.efsa.europa.eu
Rhodes, L. Smith, K. Munday, R. Selwood, A. McNabb, P. Molenaar, S. Adamson, J.
Wilkinson, C. and Hallegraeff, G. 2010. A new benthic dinoflagellate identified as the
causative organism of pinnatoxins in South Australian and New Zealand oysters. Presentation
to Shellfish Safety and Trade Workshop (Port Lincoln, October, 2010).
26
Issues Sheet: Norovirus Trade Issues (Hong Kong and
Singapore)
Issue
For some years, Hong Kong has been concerned about illness caused by consumption of raw
bivalve molluscs. In 2000-2002 Cheng et al. surveyed oysters imported from 11 countries
and found norovirus in 10.7% of the 507 samples investigated.
In September and October 2006, Hong Kong authorities identified oysters imported from
Chile as the probable cause of an outbreak of norovirus.
In Hong Kong, the Centre for Food Safety:
• Requires that suppliers provide a health certificate issued by the controlling authority of
the country of origin certifying the food is fit for human consumption
• Began testing imported shellfish for norovirus nucleic acid.
Health certification provided by AQIS for exporting bivalve molluscs to Hong Kong should
certify that:
• The bivalve molluscs were collected or harvested from sanitary waters, which have not
been polluted; or the molluscs have been cleansed by relaying in clean water for (state
number) days or the molluscs have been cleansed in the approved shellfish purification
plant at (address of plant).
• The molluscs were packed under hygienic conditions.
• The molluscs do not contain any substance or substances, including biotoxins,
contaminants like pesticides, trace metals, etc. in such amount as to be poisonous,
harmful or injurious to health.
• The molluscs are fit for human consumption and can be sold as food for human
consumption in (state country of origin).
In Singapore the Agri-Food and Veterinary Authority (AVA) issued a circular to importers
New requirement of pre-export norovirus testing for frozen oysters exported to Singapore to
the effect that, from July 1, 2007, the competent relevant government authority of the
exporting countries will certify in the health certificate that the consignment of frozen oysters
has been tested and found free of norovirus.
Current Status
It is stated that consignments to Singapore and Hong Kong are held because of the presence
of norovirus nucleic acid in consignments of oysters.
There is uncertainty whether the analysis is capable of determining whether the product under
investigation constitutes a public health risk. The methodology does not allow the
quantification of norovirus particles capable of infecting a consumer, merely identifies the
presence of nucleic acid.
There are a number of current positions being developed on viral contamination of bivalves
which are likely to:
• Extend the context from a Hong Kong/Singapore position to a global one
27
• Intensify current difficulties with methodologies surrounding opening and closing of
harvest areas because of viral build-up in bivalves
These developments include, in chronological order during 2010:
1 Codex have published draft guidelines at Step 3 in which inter alia, the testing of
bivalves for norovirus and HAV should be undertaken as a prerequisite for opening the
harvesting area.
2 The Biohaz panel of the EFSA has decided to initiate a self-tasking issue with the
purpose to provide up-to-date information on the present knowledge on the occurrence
and control of food- and water-borne viruses. EFSA requests the BIOHAZ Panel by
31/12/2011:
- To carry out a review of the available information in the scientific literature with
regards to the biology, epidemiology also including ecological aspects, diagnosis
and public health importance of food- and waterborne viruses. Where possible the
review will cover primary production, food harvesting, food processing, and
storage/retail until consumption. Data needs to support a risk assessment will also
be identified.
- To identify possible control options and their anticipated impact to reduce the
number of food- and water-borne viral human infections.
- To discuss the scientific reasons for and against the establishment of food safety
criteria for viruses for certain food categories (e.g. fresh produce, bivalve molluscs
etc).
3 The Food Safety Authority of Ireland has requested EFSA to provide an opinion on:
- Use of real-time PCR as a means of detecting and quantifying norovirus in oysters
- A safe limit for norovirus genogroups GI and GII in oysters as determined by real-
time PCR (e.g. copy number per gram)
- Treatment regimes that can be relied upon to reduce norovirus counts in oysters
Going Forward
Over recent years, the development of reverse transcriptase polymerase chain reaction
methods (RT-PCR) and nucleotide sequencing methods allows detection and identification of
viruses in faecal specimens and in shellfish.
Noroviruses can be quantified by determining the amount of norovirus RNA extracted from
the shellfish sample and expressing the result as RT-PCR copies per gram. In NZ, for
example, the technique has been used to monitor norovirus in shellfish harvested near an
ocean sewage outfall; prevalence was 89.2% and concentration ranged to >10,000 norovirus
RT-PCR units/g of shellfish (Greening et al. 2009).
A review of management options related to the detection of foodborne viruses in shellfish,
currently being undertaken by McLeod and Kiermeier, raises the possibility of an acceptable
level of norovirus particles in shellfish.
When completed, this review may be useful in determining whether methodology currently
used by Hong Kong and Singapore is rejecting consignments of imported frozen oysters with
concentrations which will not cause infection.
28
Based on the actions being undertaken by EFSA and by Codex it seems likely that testing of
shellfish for viruses (NoV and HAV) may become a legislated reality in the short to medium
term.
These developments prompt the strong recommendation that significant effort be expended
on the development of methods that better reflect the infectivity of the virus. To this end, it is
noted that there is a proposal for a collaborative project involving Australian and New
Zealand scientists to improve the management of the risk of human enteric viruses in
shellfish at harvest.
References
Cheng PK, Wong DK, Chung TW et al. (2005) Norovirus contamination found in oysters
worldwide. Journal of Medical Virology; 76(4): 593-7.
Greening, G. Lake, R. Hudson, A and Cressey, P. 2009. Risk profile: Norovirus in molluscs
(raw). Institute of Environmental Science & Research Limited Christchurch Science Centre,
NZ
29
Issues Sheet: Monitoring Indicators of Faecal Pollution in
Bivalve Molluscs
Issue
At the Annual General Meeting of the Australian Shellfish Quality Assurance Advisory
Committee (ASQAAC) a paper by Ogburn and White (2009) was discussed. The paper stated
that in the NSW oyster industry:
• Indicators of faecal pollution are monitored both in growing waters and in muscle meat.
• An analysis of data from sites in three estuaries (Manning River, Port Stephens and
Hawkesbury River) over the period 2000-2005 indicated that testing waters for faecal
indicators correlated well with rainfall, salinity and temperature while that for testing
muscle did not.
• It might be possible to maintain public health standards while minimising unnecessary
disruptions and costs in the trade of fresh oysters.
Current Status
Two independent reviews were commissioned of the Ogburn-White paper by the NSW Food
Authority.
A review by Dorothy-Jean & Associates Ltd, while in general agreement with the main
findings of the paper, states that:
• Microbiological testing is an adjunct to the primacy of the sanitary survey.
• Neither testing water for faecal coliforms nor muscle for E. coli is a reliable indicator of
the major hazard of public health significance – viruses.
• A result for faecal coliforms/100 mL in growing waters is not directly comparable with
one for E. coli/100 g in muscle.
• It may be desirable to monitor both waters and muscle to allow export to the USA and
European markets, respectively.
A review by Brenda Hay of AquaBio Consultants Ltd while canvassing points already
covered in the review, above, raises a number of aspects about the design of the study, the
interpretation of its results and the conclusions reached by the authors.
Going Forward
Given the breadth and depth of generally unfavourable comments raised in the Hay review it
is important that Ogburn and White receive the opportunity to a rebuttal.
The process of review and rebuttal might be expedited by allowing authors and reviewers to
present their views to the ASQAAC.
Taken together, the exercise would inform controlling authorities on whether they should
emulate the conservative approach taken by the NSW Food Authority, a regulatory approach
perhaps understandable given the public health problems associated with oysters in the State
(Table 1).
30
Table 1: Selected outbreaks of viral illness linked with oyster consumption
Year Origin Agent Cases Reference

1978 Georges River Norovirus >2000 Kraa 1990a,b; Kraa 1995
1989 Georges River Norovirus 370-412 Kraa 1990a,b; Kraa 1995
1990 Georges River Norovirus 461-752* Kraa 1990a,b; Kraa 1995
1996 Terranora Norovirus 97 Stafford et al. 1997; Dalton
1997
1997 Wallis Lake HAV 467 Conaty et al. 2000
* Includes 18 cases from Darwin (Ruben et al. 1992)
References
Conaty, S. Bird, P. Bell, G. 2000. Hepatitis A in New South Wales, Australia from
consumption of oysters: the first reported outbreak. Epidemiology and Infection 124:121-130.
Dalton, C. 1997. An outbreak of Norwalk virus gastroenteritis following consumption of
oysters. Communicable Disease Intelligence 21:321-322.
Kraa, E. 1990a. Oyster related food poisoning. NSW Public Health Bulletin 1:11.
Kraa, E. 1990b. Food poisoning outbreak, Sydney. Communicable Disease Intelligence 14:7-
9.
Kraa, E. 1995. Surveillance and epidemiology of foodborne illness in NSW, Australia. Food
Australia 47:418-423.
Ogburn, D. and White, I. 2009. Evaluation of fecal pollution indicators in an oyster quality
assurance program: application of epidemiological methods. Journal of Shellfish Research
28:263-271.
Ruben, A. Ralston, A. Merianos, A et al. 1992. Investigations of an outbreak of food
poisoning in Darwin. Communicable Disease Intelligence 16:278-279.
Stafford, R., Strain, D., Heymer, M., Smith, C., Trent, M. and Beard, J. 1997. An outbreak of
Norwalk virus gastroenteritis following consumption of oysters. Communicable Disease
Intelligence 21:317-320.
31
Issues Sheet: Vibrios in Australian bivalves
Issue
In 2001, a joint FAO-WHO panel assessed risk under the general heading Vibrios in
Seafoods. The panel was convened in the wake of large outbreaks following consumption of
oysters in the USA in the late 1990s. The FAO-WHO panel adopted a wide-ranging approach
which aligned with the brief Vibrios in seafoods and published as FAO reports:
• Risk assessment of V. vulnificus in raw oysters (2005)
• Risk assessment of choleragenic V. cholerae 01 and 0139 in warm water shrimp in
international trade (2005)
• Risk assessment of V. parahaemolyticus in raw oysters (in press)
Members of the FAO-WHO panel were also part of a USA panel working on Quantitative
risk assessment on the public health impact of pathogenic Vibrio parahaemolyticus in raw
oysters, published in 2005 (Anon. 2005). As a result, the USA model was used by the FAO-
WHO panel as a default model. However, when data were obtained from various countries,
particularly Australia and New Zealand, it was found that the USA greatly overestimated
estimated cases oyster-borne illness caused by V. parahaemolyticus, overestimates which
were corrected in the final draft.
Current Status
Recently, Codex has considered using the FAO-WHO models to provide estimates on
whether implementing microbiological criteria for vibrios in bivalves might reduce illness.
To this end the 42nd session of Codex Committee on Food Hygiene noted that:
Following the request of the 41st session of the Committee to address a number of issues
relating to predictive risk models and testing methodology for Vibrio parahaemolyticus and
Vibrio vulnificus in seafoods, it was noted that JEMRA had implemented an Expert Meeting
to address these issues in September 2010. Direct replies to the requests of the Committee
were provided in CX/FH 10/42/3 and the Representative highlighted the need for further
guidance from the Committee on the next steps to be taken.
With regard to the future work on Vibrio spp. in seafood, the Delegation of Japan highlighted
the importance of continuing with this work but considered that the next step should focus on
methodology and data collection. This approach was supported by several other Delegations.
In noting these recommendations, the Representative of FAO stated that there was potential
to use existing frameworks such as those provided by the Global Foodborne Infections
Network (GFN) 4 to facilitate this work. However, this would be a resource intensive activity,
which would require support and resources from member countries as well as FAO and
WHO, particularly those countries with a high level of expertise in this area. In addition, it
was noted that some of the proposed aspects such as method validation were outside the remit
of FAO and WHO and so could not be addressed as proposed. In light of these discussions,
the Committee recommended that FAO and WHO continue with this work in the following
manner:
Step 1: Provide recommendations on a range of test methods for quantifying V.
parahaemolyticus (total and pathogenic (e.g. tdh+, trh+)) and V. vulnificus in seawater and
bivalves and facilitate performance evaluation of the proposed methodologies;
32
Step 2: Develop data collection strategies (that would facilitate the collection of data) by
countries to support the modification/development of models with a broader scope than those
which currently exist;
Step 3: Encourage the collection of data in different regions, in different bivalve species and
for geographically diverse strains of pathogenic V. parahaemolyticus and V. vulnificus
according to the data collection strategy and using recommended test methods; and
Step 4: To modify/develop risk assessment models that could be used to address a range of
risk management questions in a number of different regions and products, when adequate
data becomes available.
At issue is that use of the FAO-WHO models may not describe correctly the microbiological
status of Australian oysters, particularly via the marketing chain.
Going Forward
It is important to be part of the Codex proposals captured under Steps 1-4 (above). In
particular, there is a data gap on prevalence of V. parahemolyticus, in general, and of
toxigenic strains in particular.
It is proposed that SafeFish both remain in contact with CCFH and undertake benchmarking
studies on Australian bivalves, focusing on V. parahemolyticus and V. vulnificus.
References
Anonymous. 2005. Quantitative Risk Assessment on the Public Health Impact of Pathogenic
Vibrio parahaemolyticus In Raw Oysters. Center for Food safety and Applied Nutrition Food
and Drug Administration; US Department of Health and Human Services, Washington, USA.
Drafting group. Risk assessment of Vibrio vulnificus in raw oysters. FAO/WHO
Microbiological risk assessment series 8 (2005).
Drafting group. Risk assessment of choleragenic Vibrio cholerae O1 and O139 in warm-
water shrimp in international trade. FAO/WHO Microbiological risk assessment series 9
(2005).
Drafting group. Risk assessment of V. parahaemolyticus in raw oysters (in press).
33
TOR 6: Create criteria and score or rank technical trade
issues on basis of consequence and likelihood
Ordering the twelve technical trade issues from 1-12 based on ‘criteria and score or rank’
proved difficult.
Criteria considered, and rejected, included:
• Financial impact
Against this criterion was that a small sector would always be at the end of a long queue
e.g. establishing an MoU for a handful of SA bivalve companies.
• Ability of the responsible agency to undertake work in a timely fashion
However, because several issues are within the purview of FSANZ and AQIS, agencies
which have established work programs and might not have the resources to respond in a
timely manner.
• Immediacy – ‘picking winners’
While at first sight attractive, for every winner there are losers and without objective
criteria, this was not considered suitable for prioritising purposes.
Ultimately it was decided to not fulfil the black letter requirements of the TOR, but rather to
set out a framework by which each issue could be progressed. In adopting this approach it
was necessary to ignore ratings previously assigned in favour of a de novo approach.
Perceived advantages of this approach include:
• Every issue has an equal chance of being progressed – no sector need be left behind
• Key agencies such as FSANZ and AQIS, while having active engagement, would be
spared the onerous tasks of organising and progressing resolution of each issue
• Where appropriate, industry e.g. SSA and ASQAAC would lead resolution of a specific
issue
• Research agencies would lead projects in which expert solicitation or laboratory
research were required
Accordingly, issues are arranged under three broad headings:
• Area 1: Heavy metals in Australian Seafoods
• Area 2: Watching Brief
• Area 3: Market Access
Area 1: Heavy Metals in Australian Seafoods

The three issues within this area can be assessed by one technical panel, which will prepare
technical material suitable for the activating agency to consider.
34
Mercury
Requirement Review advice re consumption to align with NZ advice
How achieved Advice from expert panel
Technical input Data from CRC survey will allow segmenting of species
Exposure assessment required
Lead organisation SafeFish
Activating agency FSANZ
Arsenic
Requirement Review ML for molluscs
Technical input Need work on inorganic:organic arsenic in bivalves.
Exposure assessment required
Activating agency FSANZ
Cadmium
Requirement Provide evidence for AQIS to consider
Technical input Data from CRC survey
Activating agency AQIS
Area 2: Watching Brief

Allergens
Requirement Impact of allergens in seafoods
How achieved Attention to literature and electronic food safety sites such as FS Net
and UTas Food Safety Centre (Seafood News for Today).
SSA subscribes to VITAL (Voluntary Incidental Trace Allergen
Labelling) grid.
Technical input Brief report six-monthly or as necessary
Lead organisation Seafood Services Australia
Activating agency Seafood Services Australia
Potential regulation of cyclic imines (e.g. pinnatoxins) in shellfish

Requirement Remain apprised of positions taken by EFSA
How achieved Attention to EFSA website
Technical input Update report as necessary
Activating agency SafeFish
35
Faecal pollution indicators
Requirement Resolution of issues raised in publication by Ogburn and White
How achieved Expert solicitation and workshop
Technical input Material prepared by lead speakers
Lead organisation ASQAAC
Activating agency State regulators via ASQAP
Parasites
Requirement Knowledge of distribution of parasites in Australian seafoods
How achieved Keep up to date with Australian and international literature
Technical input Safefish literature review and annual report
Area 3: Market access

Shellfish to USA
Requirement Address all issues identified in gap audit to enable an MoU with US
FDA for export of live bivalves to be regenerated
How achieved Industry assist AQIS to prepare all background materials required for
MoU
SafeFish recommends SAF prioritise as number one issue
Technical input Materials to service all recommendations identified in gap audit
Lead organisation Seafood Access Forum
Activating agency AQIS
Ciguatoxin
Requirement Reduction in number of ciguatera poisonings
How achieved Validate a risk management system
Technical input SSA investigate epidemiology (OzFoodNet data)
SafeFish and Sydney Fish Market undertake survey of market fish
susceptible to accretion of ciguatoxin
Virus in bivalves
Requirement Reducing burden of illness from viruses in bivalves
How achieved Advice for risk managers
Technical input Specific guidance on estimating the impact of pollution sources
Activating agency State Shellfish Quality Assurance programs (SQAPs)
36
Product testing
Requirement Resolution on need for an Australian laboratory for testing bivalves
How achieved ASQAAC to schedule process for resolution
Technical input Report by Ridge Partners
Lead organisation ASQAAC
Activating agency ASQAAC
Review of import testing

Requirement Review of import testing
How achieved Expert panel to consider risk basis for import testing
Technical input Confirm scientific underpinning for ‘Risk’ category
Lead organisation FSANZ
Activating agency FSANZ and AQIS
Vibrios in bivalve molluscs

Requirement Assessment of vibrios in bivalve molluscs in Australia
How achieved Laboratory program on V. parahaemolyticus and V. vulnificus in
bivalves
Technical input National temporal survey of vibrios in bivalves to validate the FAO-
WHO models intended to be used to inform risk management options
for different countries.
Activating agency State Shellfish Quality Assurance programs (SQAPs)
37
TOR 7: Present findings to a stakeholder meeting (with
SafeFish partnership members) and give partnership
members input into the final rankings
Conduct of the meeting
A draft report covering TORs 1-6 was distributed to stakeholders prior to a meeting held on
June 3, 2011 in Canberra; attendees are listed in Table 1.
Table 1: Attendees at SafeFish food safety meeting (Canberra, June 3, 2011)
Cath McLeod SARDI Food Safety

Duncan Lash MAF New Zealand
Anthony Zammit NSW Food Authority
Mark Boulter Sydney Fish Market
Ann Backhouse Codex Australia
Lynda Feazey AQIS
John Dawson Oyster grower, NSW
Natalie Dowsett SARDI Food Safety
Dean Merrilees AQIS
Colin Freeman Pristine Oysters, Coffin Bay and others
Mark Schipp AQIS
Jayne Gallagher Seafood CRC
Mark Tamplin University Tasmania
Tom Ross University Tasmania
Ted Loveday Seafood Services Australia
Ewan Colquhoun Ridge Partners
Ben Daughtry FSANZ
Beatrice Dias-Wanigasekera FSANZ
Alison Turnbull DHHS Tasmania
Paw Dalgaard Technical University of Denmark
Steve Hathaway MAF New Zealand
Dean Lisson Abalone Council Australia Ltd
John Sumner M&S Food Consultants Pty Ltd
Andrew Pointon SARDI
The meeting considered the draft report and incorporated amendments into the final report.
38
Recommendations for future work
A number of issues were proposed for the future SafeFish program.
Australia’s delegate to the 31st session of the Codex Committee on Fish and Fishery Products
(Tromso, 2011) proposed that SafeFish schedule work on:
1. Screening of methods for biotoxins
2. Draft standard for fresh/live and frozen abalone
3. Public health significance of histamine in fish and fishery products
4. Food additives
In addition, a watching brief was recommended on the:
1. FAO report on Salmonella in bivalves
2. Review of the draft standard for smoked fish and draft code of practice for fish and
fishery products
3. Review of the draft standard for quick frozen scallop adductor meat, including an
expanded scope to add scallop with roe-on.
Details are provided in the delegate’s report to SafeFish.
The Seafood CRC recommended that a risk assessment be undertaken on the effect of
sulphite in canned abalone and prawns, with a focus on the Chinese market.
Representatives of the NZ Food Safety Authority (NZFSA) commented that parallel research
was being carried out in Australia and NZ, and suggested that there were synergies to be
obtained from cooperation between the NZFSA and the SafeFish scientific work program.
There was general agreement that synergies should be pursued.
The proposed work (above) is additional to the list of issues for SafeFish as lead agency re.
follow-up work and/or keeping a watching brief:
• Heavy metals
• Cyclic imines/parasites
• Parasites
• Ciguatoxin
• Viruses in bivalves
• Vibrios in bivalves
Given the number and scope of projects directed to SafeFish, consideration will need to be
given to resource allocation to permit this list of projects to progress.
39
Hazards Affecting Australian
Seafood
Part 2:
Supporting Information
John Sumner
May 2011
Table of Contents
SECTION A: APPENDICES ............................................................................................................ 2
Appendix 1: Food Poisonings in Australia due to Seafood (1988-2010) .............................. 2
Appendix 2: Recall of Seafood in Australia (1999-2011) ..................................................... 4
SECTION B: BACKGROUND TABLES ............................................................................................ 5
Background Data: Outbreaks of Food Poisoning Attributed to Seafood ............................... 5
SECTION C: HAZARD SHEETS .................................................................................................... 15
Norovirus and Hepatitis A ................................................................................................... 15
Mercury in Finfish ............................................................................................................... 25
Parasites in Raw Fish ........................................................................................................... 31
Ciguatoxins .......................................................................................................................... 41
1
Section A: Appendices
Appendix 1: Food Poisonings in Australia due to Seafood (1988-
2010)
There are two databases which provide information on illness associated with consumption of
seafood. Food Science Australia and Minter Ellison Consulting published the National Risk
Validation Project (NRVP) in 2002, which assembles an exhaustive database of food
poisonings in Australia over the period1988-2001. In 2001, OzFoodNet began collating data
on food poisoning outbreaks on a state-by-state basis.
In Table A1 are presented NRVP and OzFoodNet data on 209 outbreaks of food poisoning
following consumption of oysters over the 23-year period 1988-2010. During the period,
more than 3200 individuals became sufficiently ill to enter the medical system and become
registered cases, of whom seven died.
Table A1: Hazards associated with seafoods implicated in food poisonings 1988-2010
NRVP data (1988-2001) OzFoodNet data (2001-2010)

Hazard Outbreaks Cases (deaths) Outbreaks Cases
Ciguatera 36 >314 65 >283
Histamine 11 54 27 94
Shellfish poison 3 117 0 -
Waxy esters 1 >14 7 >84
Viruses 16 1864 (1) 7 135
Salmonella 0 - 5 60
S. aureus 0 - 1 3
Vibrio spp 8 8 (6) 1 3
L. monocytogenes 1 3 0 0
Unknown 0 - 20 151
Total 76 2374 133 >812
There were striking differences in major causes of illness during both periods:
• Viral illness fell significantly and while oysters from NSW waters were responsible for
illness during 1988-2001, imported shellfish (predominantly frozen oysters) caused
most of the illnesses in 2001-2010.
• There were no illnesses due to shellfish poisons during the second period.
• More outbreaks and illnesses occurred due to consumption of fish containing waxy
esters in 2001-2010.
• The reduction in oyster-associated illness reflects the implementation of shellfish
quality assurance programs by all states.
• Ciguatera and histamine poisoning remained important causes of illness during both
periods, with Queensland being responsible for most cases of the former (Table A2).
• By far the largest number of outbreaks occurred from consumption of fish containing
ciguatoxin; species are listed in Table A3.
2
• Histamine poisonings were second most numerous and though some obviously
stemmed from imported products, a number were probably caused by temperature
abuse of product caught domestically.
• The third most numerous category is ‘Unknown’ which accounted for 20 outbreaks, of
which nine were associated with bivalve shellfish (suspect norovirus), one with tuna
(suspect histamine) and one with Spanish mackerel (suspect ciguatera).
• Although imported bivalves appear to be responsible for some norovirus outbreaks it is
possible some are of domestic origin.
• Waxy esters from Escolar and Rudderfish have also caused outbreaks.
• While there have been no illnesses associated with L. monocytogenes, salmon smoked
domestically has been recalled.
Table A2: State of origin of seafoods associated with outbreaks 2001-10 (after OzFoodNet)
State Number of outbreaks

Queensland 64
New South Wales 36
Victoria 16
Northern Territory 5
Western Australia 4
ACT 5
Tasmania 2
South Australia 1
Total 133
Table A3: Species associated with ciguatera outbreaks (after OzFoodNet)
Species Number of outbreaks

Mackerel 22
Coral trout 10
Kingfish 7
Barracuda 3
Other 23
Total 65
A full listing of hazards and outbreak settings is presented in Tables B1-B4.
3
Appendix 2: Recall of Seafood in Australia (1999-2011)
In Table A4 are presented recalls of seafood over the period 1998-2011. Of the 28 recalls, the
country of origin was recorded for eleven, eight of which were Asian. It is probable, based on
the product and/or format, that most of the remainder were imported e.g. P. monodon and
P. vannamei are likely imports as are Tilapia and anchovy.
Table A4: Recalls of seafood listed by FSANZ (1999-2011)
Year Product Format Hazard Country

of origin*
1998 Trevally May be puffer fish
1999 Mussels Smoked L. monocytogenes
1999 Penaeus monodon Cooked peeled V. cholerae Thailand
2000 Queenfish Fillets Ciguatera
2001 Mackerel Dried Histamine Philippines
2002 Crab Frozen, salted Chemical contamination China
2003 Mackerel Salted Histamine Thailand
2004 Salmon Smoked L. monocytogenes Denmark
2004 Mackerel Fillets in oil Histamine
2004 Penaeus monodon Cooked S. Infants
2005 Whiting Frozen, crumbed Allergens (casein) Vietnam
2005 Mackerel Fillets Ciguatera
2005 Anchovy Canned Histamine Greece
2005 Penaeus vannamei Cooked Microbial contamination
2006 Clams Canned Under processing China
2007 Herring Marinated Glass Sweden
2007 Penaeus monodon Cooked Metal
2007 Prawns Raw, peeled Labelling (states cooked)
2008 Tuna Frozen steaks Histamine Indonesia
2009 Anchovy Frozen Histamine
2010 Fish Frozen, battered Allergen (dairy)
2010 Tuna salad Chilled L. monocytogenes
2010 Tilapia Frozen, fillets Chemical (antibiotics) Vietnam
2011 Fish Frozen, crumbed Allergen (peanuts)
2011 Trout Smoked L. monocytogenes
2011 Calamari Frozen Allergen (peanuts)
2011 Dory Frozen, crumbed Allergen (peanuts)
2011 Salmon Smoked L. monocytogenes
* Where known
4
Section B: Background Tables
Background Data: Outbreaks of Food Poisoning Attributed to Seafood
Table B1: Outbreaks of food poisoning due to consumption of oysters (after NRVP, 2001)
Food Pathogen Cases Year Reference

Business (deaths)
Caterer Norovirus >32 1990 NSW Health
Caterer Norovirus? >19 1990 NSW Health
Caterer Norovirus 30 1990 NSW Health
Caterer Norovirus 18 1992 Ruben et al. 1992
Caterer Norovirus, V. parahaemolyticus >148 1990 NSW Health
Community V. vulnificus 1 1989 NSW Health
Community V. vulnificus (1) 1991 NSW Health
Manufacturer L. monocytogenes 3 1991 Mitchell, 1991; Misrachi et al.1991.
Community V. parahaemolyticus 1(1) 1992 Kraa, 1995
Community V. vulnificus (1) 1990 McAnulty, 1990
Community Virus >461 1990 Lees, 2000; Kraa, 1995
Community Norovirus >370 1989 Kraa, 1995
Community Hepatitis A 467 (1) 1997 Anonymous, 1997; SafeFood NSW, 2001; Conaty et al. 2000
Community Norwalk-like viruses 97 1996 NSW Health
Eating est. Norovirus >18 1990 NSW Health
Eating est. V. vulnificus (1) 1988 NSW Health
Eating est. V. vulnificus (1) 1990 NSW Health
Manufacturer V. parahaemolyticus (1) 1992 NSW Health
Retail V. vulnificus 1 1989 NSW Health
This report is commercial-in-confidence. No part of it may be copied, distributed, or divulged to any agency or person without the express permission of the authors.
5
Table B2: Outbreaks of food poisoning due to consumption of seafood contaminated with toxins (after NRVP, 2001)
Food Business Product Toxin Cases (deaths) Year Reference

Community Spanish mackerel Ciguatoxin 63 1987 Capra, 1997
Caterer Coral trout Ciguatoxin 8 1991 Lehane, 1999
Private residence Coral reef fish Ciguatoxin 1 1991
Retail Coral trout Ciguatoxin 2 1991 Merianos et al. 1991
Retail Spanish mackerel Ciguatoxin 43 1994 Kraa et al., 1994; Kraa, & Campbell, 1994
Private residence Coral trout Ciguatoxin 4 1995 Fenner et al. 1997
Private residence Coral trout Ciguatoxin 4 1995 Anonymous, 1995
Retail Spanish mackerel Ciguatoxin 15 1995 Harvey, 1995
Retail Rock cod Ciguatoxin 2 1996 DOH
Community Coral trout Ciguatoxin 6 1997 Karalis et al. 2000
Community Coral trout Ciguatoxin 10 1997 Karalis et al. 2000
Community Coral cod Ciguatoxin 20 1997 Lucas, et al. 1997
Eating estab. Maori Wrasse Ciguatoxin 18 1997 Ng & Gregory, 2000; Andrews et al. 1998
Retail Fish Ciguatoxin 8 1997 DOH
Retail Coral trout Ciguatoxin 6 1997 Karalis et al. 2000
Private residence Spotted cod Ciguatoxin 12 1998 Karalis et al. 2000
Private residence Barracuda Ciguatoxin 7 1998 Williams & Dentith, 1998
Retail Cod Ciguatoxin 3 1998 DOH
Retail Spotted cod Ciguatoxin 10 1998 Karalis et al. 2000
Retail Ciguatoxin 3 1998 Kirk et al. 1999
Retail Ciguatoxin 5 1998 Kirk et al. 1999
Private residence Mackerel Ciguatoxin 2 1999 Queensland Health
Private residence Queenfish Ciguatoxin 7 1999 Queensland Health
Private residence Spanish mackerel Ciguatoxin 4 1999 Anonymous, 1999
Eating estab. Cod Ciguatoxin 3 2000 Queensland Health
Eating estab. Sweetlip Ciguatoxin 2 2000 Queensland Health
Private residence Black trevally Ciguatoxin ? 2000 OzFoodNet
Private residence Coronation trout Ciguatoxin 9 2000 Queensland Health
6
Food Business Product Toxin Cases (deaths) Year Reference
Private residence Spotted mackerel Ciguatoxin ? 2000 OzFoodNet
Private residence Queenfish Ciguatoxin ? 2000 OzFoodNet
Private residence Black kingfish Ciguatoxin ? 2000 OzFoodNet
Private residence Coral trout or cod Ciguatoxin ? 2000 OzFoodNet
Retail Coral trout Ciguatoxin 4 2000 Queensland Health
Caterer Spanish mackerel Ciguatoxin 14 2001 Queensland Health
Retail Coral trout Ciguatoxin 17 2001 Anonymous, 2001
Retail Spotted mackerel Ciguatoxin 2 2001 Queensland Health
Community Pipis DSP 59 1997 DOH
Pipis DSP 56 1997 Quaine et al. 1997
Shellfish PSP 2 2000 Anonymous, 2000
Eating estab. Flake Marine toxin 2 2000 Queensland Health
Eating estab. Pilchards Scombrotoxin >6 1995 Ross & Sanderson, 2000
Resort Tuna Scombrotoxin 4 1995 DOH
Retail Marlin Scombrotoxin 2 1997 Ross & Sanderson, 2000
Wholesaler Thai fish cakes Scombrotoxin 9 1998 Kirk et al. 1999
Wholesaler Risotto Scombrotoxin 3 1998 Kirk et al. 1999
Wholesaler Tuna Scombrotoxin 6 1998 Kirk et al. 1999
Eating estab. Grenadier Scombrotoxin 5 1999 Klessa & Csizmadia, 2000
Eating estab. Pasta with tuna Scombrotoxin ? 1999 OzFoodNet
Supermarket Tuna Scombrotoxin 4 1999 DOH
Eating estab. Mahi Mahi Scombrotoxin 4 2001 Queensland Health
Mobile canteen Rudderfish or Caster oil Wax esters 9 2001 DOH
fish
Eating estab. Rudderfish (Butterfish) Wax esters >14 1999 Kirk et al. 2000
7
Table B3: Food poisoning outbreaks due to the consumption of prawns in Australia 1990-2010 (after OzFoodNet)
Source Hazard Country Cases (deaths) Year Reference

Retail V. parahaemolyticus Indonesia. 27 1990 NSW Health
Caterer V. parahaemolyticus Indonesia 100 (1) 1990 NSW Health; Kraa, 1995
Importer V. parahaemolyticus Indonesia >50 1992 Kraa, 1995
Eating est. S. Typhi Thailand 4 1995-1996 NSW Health
Eating est. Hepatitis A Burma 23 1997 NSW Health
Eating est. Hepatitis A Burma 17 1997 Anonymous, 1997
Eating est. V. cholerae non 01, non 139* Not known 10 1999 OzFoodNet
Eating est. Hepatitis A Not known 2 2003 OzFoodNet
Eating est. Unknown Not known 2 2009 OzFoodNet
* Red claw crayfish
Table B4: Food poisoning outbreaks due to the consumption of seafood in Australia 1990-2010 (after OzFoodNet)
Year State Setting Hazard Cases Product

2005 NSW Primary produce Ciguatera 10 Barracuda
2003 QLD Home Ciguatera 5 Barracuda (Sphyraena spp.)
2005 NSW Primary produce Ciguatera 5 Black kingfish
2005 NSW Primary produce Ciguatera 2 Black trevally
2003 QLD Home Ciguatera 2 Cod fish heads
2003 QLD Home Ciguatera 7 Coral trout
2005 Vic Primary produce Ciguatera 5 Fijian snapper
2003 QLD Home Ciguatera 3 Fish
2003 QLD Home Ciguatera 3 Fish head soup - Red Emperor
2003 QLD Home Ciguatera 4 Unknown
2003 QLD Home Ciguatera 3 Giant trevally
2002 Qld Home Ciguatera 5 Grunter bream
2009 QLD Primary produce Ciguatera 2 King snapper
2005 NSW Primary produce Ciguatera 4 Mackerel
8
2003 QLD Home Ciguatera 3 Mackerel
2009 QLD Primary produce Ciguatera 2 Reef cod
2005 NSW Primary produce Ciguatera 17 Spanish mackerel
2005 NSW Primary produce Ciguatera 2 Spanish mackerel
2003 QLD Restaurant Ciguatera 15 Spanish mackerel
2002 Qld Takeaway Ciguatera Unknown Spanish mackerel
2002 Qld Home Ciguatera 2 Striped perch
2005 NSW Primary produce Ciguatera 2 Trevally
2005 NSW Primary produce Ciguatera 2 Yellowtail kingfish
2005 NSW Primary produce Ciguatera 8 Yellowtail kingfish
2008 QLD Primary produce Ciguatera 4 Yellow king - Samson fish
2006 QLD Primary produce Ciguatera 4 Black kingfish
2008 QLD Primary produce Ciguatera 6 Black kingfish
2006 QLD Primary produce Ciguatera 2 Cod
2008 QLD Primary produce Ciguatera 3 Cod
2006 Vic Primary produce Ciguatera 2 Coral perch or coral trout
2010 Qld Primary produce Ciguatera 2 Coral trout
2010 QLD Primary produce Ciguatera 6 Fish curry
2010 Qld Primary produce Ciguatera 4 Fish head soup
2010 QLD Private residence Ciguatera 4 Mackerel soup
2008 QLD Primary produce Ciguatera 6 Red throat emperor/ reef snapper
2006 NT Primary produce Ciguatera 14 Slate sweetlips
2006 QLD Primary produce Ciguatera 4 Spanish mackerel
2010 Qld Primary produce Ciguatera 2 Spanish mackerel
2006 QLD Primary produce Ciguatera 2 Trevally
2008 QLD Primary produce Ciguatera 2 Yellowtail kingfish
2001 QLD Home Ciguatera 3 Barracuda (Sphyraena jello)
2001 Vic Home Ciguatera 16 Coral trout
9
2001 QLD Home Ciguatera 14 Spanish mackerel
2001 QLD Home Ciguatera 9 Spanish mackerel
2002 NSW Home Ciguatera Unknown Spanish mackerel
2001 QLD Home Ciguatera 2 Spotted mackerel
2007 QLD Primary produce Ciguatera 3 Coral trout
2004 QLD Restaurant Ciguatera 4 Coral trout
2004 QLD Private residence Ciguatera 2 Fish species unknown
2004 QLD Private residence Ciguatera 2 Golden spotted trevally fish
2004 QLD Private residence Ciguatera 4 Grey mackerel
2004 QLD Takeaway Ciguatera 4 Grey mackerel
2007 QLD Primary produce Ciguatera 2 Mackerel
2007 NT Primary produce Ciguatera 2 Reef cod
2004 QLD Contaminated primary produce Ciguatera 5 Spanish mackerel/golden trevally
2004 QLD Private residence Ciguatera 3 Trevally
2003 Vic Restaurant Escolar 3 Escolar
2003 QLD Restaurant Escolar 20 Escolar
2001 Hunter Conference/ function Escolar esters 20 Escolar
2009 QLD Primary produce Fish wax ester 27 Escolar/rudderfish
2004 Vic Commercial caterer Suspected 9 'Butterfish' (rudderfish)
2001 Vic Restaurant Wax ester 5 Butterfish
2009 ACT Contaminated primary produce Waxy esters Escolar
2007 QLD Private residence Histamine 2 Imported Indonesian tuna
2007 Vic Restaurant Histamine 2 Mahi Mahi
2007 NT Commercial manufactured food Histamine 2 Tinned tuna
10
2007 Vic Restaurant Histamine 2 Tuna
2007 NSW Private residence Histamine 3 Tuna kebab steaks
2007 QLD Private residence Histamine 4 Tuna kebabs
2007 NSW Restaurant Histamine 2 Tuna steak
2010 Vic Private residence Histamine 4 Tuna
2001 QLD Restaurant Histamine 4 Mahi Mahi
2003 QLD Restaurant Histamine 3 Dolphin Fish
2003 Vic Restaurant Histamine 22 Escolar
2005 Vic Primary produce Histamine 2 Fish
2003 NSW Home Histamine 2 Sardine
2009 NSW Restaurant Histamine 2 Tinned anchovies imported from Morocco
2009 QLD Other Histamine 6 Tuna
2005 Vic Restaurant Histamine 2 Tuna
2003 QLD Home Histamine 2 Tuna patties
2005 NSW Private residence Histamine 4 Tuna steak
2009 ACT Private residence Histamine 2 Tuna steak
2005 NSW Restaurant Histamine 2 Yellowfin tuna
2005 Tas Restaurant Histamine 2 Yellowfin tuna
2006 QLD Private residence Histamine 2 Blue fin tuna steaks
2006 Vic Restaurant Histamine 2 Kingfish
2008 NSW Bakery Histamine 1 Canned tuna
2006 NSW Restaurant Histamine 2 Tuna steaks
2006 NSW Restaurant Histamine 6 Yellowtail kingfish fillets
2010 NSW Restaurant Histamine 5 Mahi-mahi fish fillets
2003 WA Restaurant Norovirus 35 Japanese IQF oysters
2003 NT Restaurant Norovirus 48 Japanese IQF oysters
2004 NSW Primary produce Norovirus 24 Oysters
2004 QLD Contaminated primary produce Norovirus 4 Oysters (frozen)
2004 QLD Contaminated primary produce Norovirus 2 Oysters (frozen)
2004 WA Commercial caterer Norovirus 19 Prawns and cold meats
11
2001 Vic Community S. Mississippi 6 Suspected oysters
2004 QLD Restaurant Salmonella 13 Sushi rolls
2006 NSW Commercially manufactured Salmonella 6 Tuna and salmon sushi rolls
2004 ACT Restaurant Salmonella 12 Ling
2007 WA Takeaway Salmonella 23 Sushi and Katsudon (made with eggs)
2003 ACT Home Unknown 3 Fish
2002 NSW Takeaway Unknown 2 Fish
2007 NSW Takeaway Unknown 2 Grilled tuna
2003 WA Caterer Unknown 17 Japanese IQF oysters
2008 NSW Private residence Unknown 3 Mussels - fresh
2008 NSW Private residence Unknown 2 Mussels - fresh
2007 NSW Restaurant Unknown 19 Oysters
2004 NT Contaminated primary produce Unknown 5 Oysters (frozen)
2007 Tas Other Unknown 19 Oysters, suspected
2009 QLD Takeaway Unknown 2 Prawn roll
2004 Vic Contaminated primary produce Unknown 7 Redfin
2007 NSW Restaurant Unknown 4 Seafood platter
2007 SA Commercial caterer Unknown 12 Sushi
2006 NSW Private residence Unknown 4 Suspect Nile perch
2006 NSW Private residence Unknown 6 Suspect oysters
2004 ACT Restaurant Unknown 16 Suspected calamari
2005 Vic Restaurant Unknown 11 Suspected Spanish mackerel
2009 NSW Fair/festival/mobile service Unknown 3 Unknown, possibly prawns or calamari
2006 QLD Takeaway S. aureus 3 Sushi roll
2006 NSW Private residence Vibrio 3 Whitebait
12
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59:81-116.
Lucas, R.E., Lewis, R.J. and Taylor, J.M. (1997) Pacific ciguatoxin-1 associated with a large
common-source outbreak of ciguatera in east Arnhem Land, Australia. Natural Toxins,
5(4):136-140.
McAnulty, J. (1990) Vibrio warning. NSW Public Health Bulletin, 1(6):12-13,18.
Merianos, A., Burrows, J. and Patel, M. (1991) Ciguatera in Darwin following a meal of coral
trout. Communicable Disease Intelligence, 15(21):386-387.
Misrachi, A., Watson, A.J. and Coleman, D. (1991) Listeria in smoked mussels in Tasmania.
Communicable Disease Intelligence, 15(23):427.
Mitchell, D.L. (1991) A case cluster of Listeriosis in Tasmania. Communicable Disease
Intelligence 15(23):427.
Ng. S. and Gregory, J. 2000. Outbreak of ciguatera fish poisoning in Victoria. Communicable
Diseases Intelligence, 24:344-346.
Quaine, J., Kraa, E., Holloway, J., White, K., McCarthy, R., Delpech, V., Trent, M. and
McAnulty, J. (1997) Outbreak of gastroenteritis linked to eating pipis. NSW Public Health
Bulletin, 8(11-12):103-104.
Ross, T. and Sanderson, K. (2000) A risk assessment of selected seafoods in NSW. SafeFood
NSW.
Ruben, A., Ralston, A., Merianos, A. and Patel, M. (1992) An investigation of an outbreak of
food poisoning in Darwin. Communicable Disease Intelligence, 16(18):378-379.
SafeFood New South Wales (2001) Proposed food production (Seafood Safety Scheme)
regulation 2001. Regulatory impact statement. Sydney.
Williams, W. and Dentith, H. (1998) Report on ciguatera poisoning, Groote Eylandt, October
1998. The Northern Territory Disease Control Bulletin, 5(4):5-6.
14
Section C: Hazard Sheets
Norovirus and Hepatitis A
Hazard Identification
Shellfish have been associated with foodborne viral infection throughout the world. In 1991
in Shanghai, almost 300,000 people contracted hepatitis and nine died after consuming
cockles contaminated with Hepatitis A virus (Tang et al., 1991). In the USA in the period
1992-99, there have been 12 documented outbreaks of viral poisoning following consumption
of shellfish (mainly oysters) involving 1473 persons (Smith de Waal, et al., 2000).
In the period 1990-2000, Australian oysters were implicated more frequently in outbreaks
than other shellfish (Table C1) whereas, in the period 2001-2010 viral illness fell
significantly, with imported shellfish (predominantly frozen oysters) causing most of the
illnesses.
Table C1: Outbreaks of food poisoning due to consumption of oysters (after NRVP, 2001)
Setting Pathogen Cases (deaths) Year Reference

Caterer Norovirus? >19 1990 NSW Health
Caterer Norovirus 30 1990 NSW Health
Caterer Norovirus 18 1992 Ruben et al. 1992
Community Virus >461 1990 Lees, 2000; Kraa, 1995
Community Norovirus >370 1989 Kraa, 1995
Community Hepatitis A 467 (1) 1997 Anonymous, 1997; SafeFood
NSW, 2001; Conaty et al. 2000
Community Norovirus 97 1996 NSW Health
Eating est. Norovirus >18 1990 NSW Health
Viruses most commonly associated with these outbreaks are Norovirus (NoV) and
Hepatitis A (HAV). The former typically cause mild, self-limiting diarrhoea while HAV
infection can be severe.
Exposure Assessment
Cooking may inactivate virus particles in shellfish, but is often ineffective particularly
because very mild cooking procedures are employed. The degree of virus inactivation varies
with cooking method and type of virus and is unlikely to render safe a highly contaminated
15
product. However, at a low level of contamination in the product, cooking could reduce virus
levels to ≤ 1 plaque forming units (pfu) per serving, so cooked product will be excluded from
the exposure assessment. The Ministry of Agriculture, Fisheries and Food of the United
Kingdom recommend that to inactivate viruses, the internal temperature of molluscs be
maintained at 90°C for more than 1.5 minutes before consumption (Huss et al. 2000).
Perhaps >90% of oysters are eaten raw or only lightly cooked, leading to an estimate that
approximately 30 million servings of uncooked, or effectively uncooked, oysters are
consumed. Thus, the contribution of cooking to the reduction of risk from oysters in Australia
is negligible.
There are no published data on the level or frequency of viral contamination in shellfish
produced in Australian systems. American data indicate that up to 20% of shellfish from
clean growing waters may be contaminated with viruses (Mosley, 1967; Goldfield, 1976;
Gerba and Goyal, 1978; DeLeon and Gerba, 1990; Sobsey et al., 1991). If this figure is
applied to Australia then approximately six million servings of oysters could be contaminated
with viruses while, with a contamination rate of 1%, some 300,000 servings could be
contaminated.
All immunologically unprotected individuals (i.e. those without serological immunity) are
susceptible to infection with human enteric viruses. There is no indication in the literature
that immunocompromised individuals are at greater risk of infection from enteric viruses than
are immunocompetent individuals.
Hazard Characterisation
Enteric viruses can be introduced into aquatic environments through contamination with
sewage. They may persist longer than enteric bacteria in marine environments and can
accumulate 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 (Jackson
and Ogburn, 1996) 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. Even where control systems are in place (e.g. USA) outbreaks
continue to occur. In general, the incidence of seafood-borne viral food poisoning in
Australia is low, suggesting that control strategies are effective. Australian outbreaks have
been associated with failures or non-implementation of control strategies.
Viral hazards associated with consumption of seafood were the topic of a number of reviews
(Mosley, 1967; Goldfield, 1976; Gerba and Goyal, 1978; Richards, 1985; CDC, 1990;
DeLeon and Gerba, 1990; Sobsey et al., 1991; Fleet et al., 2000; Lees, 2000), the latter two
presenting up-to-date reviews of viral contamination of Australian oysters.
In summary, the main conclusions of these reviews are that:
• Viruses causing disease in fish are not pathogenic to humans.
• Food contaminated with human waste containing viruses that are infective via the
faecal-oral route is a cause of foodborne disease.
• Seafood can be contaminated with enteric viruses through exposure to raw or treated
sewage and during processing and preparation by contaminated water supplies and
infected food handlers.
16
• Finfish and crustaceans are not usually associated with the spread of viral foodborne
disease unless contaminated by food handlers.
• Consumption of both raw and cooked molluscan bivalves (shellfish) is a well
documented cause of viral foodborne disease.
• Virus particles can remain detectable for several months under certain conditions in
seawater and in food.
• Shellfish depuration techniques do not totally eliminate viral particles.
• Infectious doses are presumed to be low e.g. 10-100 virus particles.
• Human enteric viruses do not replicate in seafood products so that time and temperature
of storage/handling are not risk factors.
• Viruses are resistant to moderate heat and pH conditions.
Norovirus
These are non-enveloped RNA viruses classified in the Caliciviridae. Caliciviruses display a
Star of David surface structure when viewed by negative stain electron microscopy and at the
genetic level have their capsid open reading frame fused to and contiguous with the non
structural proteins. The group is described collectively as Small Round Structured Viruses
(SRSV) and contains the Norovirus which is named after places where the outbreaks
occurred e.g. Norwalk and Snow Mountain.
Illness Caused
Symptoms include nausea, vomiting, diarrhoea, fever and abdominal pain with an incubation
period of 1-4 days, usually followed by recovery without complications. Human NLV cause
epidemic gastroenteritis amongst all age groups (Caul, 1996a; Caul, 1996b; Clarke and
Lambden, 1997) and may be the most significant cause of infectious intestinal disease. Attack
rates for SRSV seafood-associated gastroenteritis in outbreaks are relatively high; Kirkland et
al. (1996) reported 56% (27/48) in one outbreak and Linco and Grohmann (1980) reported
89% (25/28) in another.
Unique Host Susceptibility Factors

SRSVs are a major cause of foodborne gastroenteritis especially linked to the consumption of
sewage-contaminated shellfish. It has been estimated that 20-25% of UK, 67% of Japanese
and 39% of USA outbreaks, were food associated (Caul, 1996b). In those incidents in the UK
and Japan, shellfish were identified as the major source.
Human caliciviruses are primarily a paediatric infection, and there is little evidence that they
cause foodborne illness. Seroprevalance studies suggest that childhood infection gives rise to
life-long immunity. Up to 90% of children and adults have specific antibodies to human
caliciviruses which may explain why consumption of contaminated shellfish by adults rarely
causes disease (Caul, 1996b).
17
Hepatitis A virus (HAV)
This virus is classified within the Hepatovirus genus of the Picornaviridae family. HAV has
a single molecule of RNA surrounded by a small (27nm diameter), non-enveloped, protein
capsid.
Hepatitis A is usually a mild illness characterised by sudden onset of fever, malaise, nausea,
anorexia and abdominal discomfort, followed by jaundice, perhaps up to four weeks after
exposure. The infectious dose is unknown but presumably is similar to other RNA
enteroviruses (10-100 virus particles). HAV is excreted in faeces of infected people and can
infect susceptible individuals when they consume contaminated water or foods. Water,
shellfish, and salads are the most frequent sources. Contamination of foods by infected
workers in food processing plants and restaurants is common. The virus has not been isolated
from any food directly associated with an outbreak. Because of the long incubation period,
the suspected food is often no longer available for analysis (Sobsey et al., 1991; FDA, 1999).
Shellfish have been associated worldwide with a large number of hepatitis outbreaks (Tang et
al., 1991; Xu et al., 1992; Leoni et al., 1998).
Illness Caused
The incubation period for Hepatitis A, which varies from 2-6 weeks (mean 4 weeks), is
dependent upon the number of infectious particles consumed. Infection with very few
particles results in longer incubation periods. The period of communicability extends from
early in the incubation period to about a week after the development of jaundice. The greatest
danger of spreading the disease to others occurs during the middle of the incubation period,
well before the first presentation of symptoms. Many infections with HAV do not result in
clinical disease, especially in children. When disease does occur, it is usually mild and
recovery is complete in one to two weeks. Occasionally, the symptoms are severe and
convalescence can take several months. Patients suffer from feeling chronically tired 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, usually occurring in the elderly (Sobsey et al., 1991;
FDA, 1999).
Unique Host Susceptibility Factors

All people who ingest the virus and are immunologically unprotected are susceptible to
infection (Sobsey et al., 1991; FDA, 1999). Hepatitis A infection in children is normally
subclinical, while in adults overt hepatitis develops in the majority of individuals (Hollinger
and Ticehurst, 1990). Infection results in long-term immunity as older individuals are more
likely to have HAV antibodies than younger individuals. In one study of 245 blood donors,
57% of those aged 30-49 years were antibody positive, compared with only 30% of those
aged 18-29 years. Immunity appears to be protective as repeat attacks are rare (Boyd and
Marr, 1980). Other host factors affecting the severity of hepatitis infection are poorly
characterised. Immune impairment is less significant than for other foodborne pathogens.
Existing liver damage (e.g. cirrhosis) may be significant (Cliver, 1989).
18
Table C2: Variability in reported incidence of viruses in seafood
Food (% positive) Viruses detected Reference

Shellfish (21%) HAV, EV* Apaire Marchais et al. (1995)
Oysters (50%) RV (17-246/100g) Boher et al. (1995)
EV (124-200/100g)
Oysters (58%) EV Chung et al. (1996)
Mussel & cockle (73%) HAV Crance et al. (1995)
Oysters (20%), mussels (0/15) RV Hafliger et al. (1997)
Cockles & mussels 67% HAV Le Guyader et al. (1993)
Cockles & mussels EV (22%), HAV (14%) Le Guyader et al. (1994)
RV (20%)
Cockles EV (89%), HAV (84%) Le Guyader et al. (1995)
* (HAV = Hepatitis A; EV = enteroviruses; RV = rotavirus)
Norovirus and HAV have been linked to shellfish-associated gastroenteritis in Australia

(Cross et al., 1979; Kraa, 1990a,b; Bird and Kraa, 1995; Dalton, 1997; Grohmann, 1997;
Murphy, et al., 1979 and Stafford et al., 1997). The first outbreak occurred in 1977 when
oysters harvested from Georges River in Sydney and frozen on the half-shell caused
problems in the UK. Product conformed with the microbiological standard of <2.3 E. coli/g
and no bacterial pathogens were isolated at levels which would cause gastroenteritis. The
oysters had been harvested during rainfall events when the E. coli count had exceeded the
standard, though freezing may have killed E. coli but not viruses. Oysters from Georges
River were also implicated in an outbreak of gastroenteritis involving more than 2000
consumers in 1978 and though NoV was isolated from patients, it was not isolated from
oysters.
These incidents resulted in changes to oyster regulation in NSW with the mandating of
depuration for all oysters before sale (Ayres, 1991). However, in 1984, NoV was implicated
in an outbreak of gastroenteritis in Tamworth, NSW (Kraa, 1990a) and also in 1996, when
oysters harvested from estuarine waters in northern NSW and depurated were implicated in
an outbreak of gastroenteritis involving 96 people. The virus was isolated from one sample of
oysters but not from faecal samples.
The first case of HAV from shellfish in Australia was attributed to incompletely cooked
mussels from contaminated waters in Victoria with seven out of the 10 consumers who ate
the mussels developing symptoms of Hepatitis A (Locarnini and Gust, 1978).
The largest outbreak of Hepatitis A in Australia occurred during 1996-97 following
consumption of oysters from the Wallis Lake region of Australia (CDI, 1997) when almost
500 people were affected and one died. Oysters from the area tested positive for HAV (by
PCR) and also for enterovirus and adenovirus, but not NoV. The E. coli level was <2.3/g and
the oysters had passed through a depuration process. However, a coronial enquiry established
several point sources of faecal contamination into growing areas and the question of
bacteriological criteria for oysters was again questioned (Wilcox, 1999).
Seafood-associated viral gastroenteritis has been reported following the consumption of
seafood that passed microbiological criteria (Chalmers and McMillan, 1995). Shellfish
associated with outbreaks in Australia, however, have generally failed to comply with
microbiological standards indicating faecal contamination prior to harvest (Cross et al., 1979;
19
Bird and Kraa, 1995). In an American risk assessment of viral contamination of shellfish an
average level of viruses of 10 pfu/100g was determined from beds considered to be
‘uncontaminated’. This corresponds to an exposure of 6-24 pfu in a serving (60-240 g) of
shellfish (Rose and Sobsey, 1993).
Due to the high infectivity and low infectious dose of these viruses there is potential for
secondary cases of infection spread via the faecal-oral route. In a clam-associated Hepatitis A
outbreak in Italy there was a secondary attack rate of 7.9% (Leoni et al., 1998).
The infectious dose of human enteric viruses is not known but is presumed to be of the order
of 10-100 particles (FDA, 1999). For HAV, higher doses of virus have been reported to cause
more severe disease.
Growth and Survival

While enteric viruses do not replicate in seafood products, they remain detectable for long
periods of time. Several studies have demonstrated no, or very little, reduction in virus
numbers during prolonged (up to 28 days) storage at refrigeration temperatures (5-8°C). In
the 1978 incident of Norovirus in NSW oysters the agent survived several months freezing on
the half shell. Thus if enteric viruses are present in shellfish at the time of harvest, it is likely
that they will persist until purchased (Sobsey et al., 1991). The effect of these conditions on
their infectivity is unknown.
Heat Treatment
Shellfish are consumed in various forms ranging from raw to thoroughly cooked. When
cooked, heat treatments are usually minimal because excessive heating results in
unacceptable organoleptic changes. Enteric viruses in shellfish may survive heat processes
including stewing, frying, baking, and steaming (Sobsey et al., 1991) and HAV was
recovered from experimentally contaminated mussels steamed for five minutes after the
shells opened (Abad et al., 1997). Epidemiological data also attests to the heat resistance of
enteric viruses. In outbreaks associated with Norovirus-contaminated oysters, persons who
reported eating only thoroughly cooked oysters (grilled, stewed, fried (McDonnell et al.,
1997) or steamed (Kirkland et al., 1996) were as likely to become ill as those who ate raw
oysters. Several outbreaks have been associated with cooked ready-to-eat molluscs (Little et
al., 1997). The outbreak cases cited above suggest that cooking is unlikely to render a highly
contaminated product safe for consumption unless it is so intensive that the sensory aspects of
the product are impaired.
In the United Kingdom, the Ministry of Agriculture recommended an internal meat
temperature of 90°C for 1.5 minutes for commercial cooking, parameters which have been
adopted by the European Community (Anon., 1993). It is likely that home and restaurant
cooking is only partially effective as a control measure, offering more protection with smaller
species e.g. mussels compared with larger species such as oysters.
Depuration Efficacy
The ability of depuration to eliminate microbial pathogens in shellfish was reviewed by
Jackson and Ogburn (1996). In general the efficacy of depuration depends on the physiology
of the oyster (or other mollusc), the pathogen load initially present, the management of the
20
depuration operation, and other factors. Several studies report failure to remove all viruses
(Apaire Marchais et al., 1995; Boher et al., 1995; Abad et al., 1997). In one study, for
example, although depuration for 48 h gave a 95% reduction of bacteria it only gave a 7%
reduction of Norovirus titres (Schwab et al., 1998). Variables affecting the efficacy of
depuration for oysters include the level of contamination, the health of the animals, the
management of the depuration process etc (Jackson and Ogburn, 1996).
Among the conclusions of Jackson and Ogburn (1996) was that depuration is satisfactory for
removal of moderate contamination with bacterial pathogens, but that continued food
poisoning outbreaks in Australia, despite mandatory depuration, indicates that the process is
not sufficient to ensure the safety of shellfish product. In particular, they point to strong
evidence that viral agents often persist in shellfish both in growing areas and after depuration
for periods long after bacterial indicators of faecal contamination can no longer be detected.
In particular, experimental studies have shown the long persistence of Hepatitis A virus in
oysters.
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Intelligence, 21:317-320.
Tang, Y.W., Wang, J.X., Xu, Z.Y., Guo, Y.F., Qian, W.H. and Xu. J.X. (1991). A
serologically confirmed, case-control study, of a large outbreak of hepatitis A in China,
associated with consumption of clams. Epidemiology and Infection, 107(3):651-7.
Wilcox, J. (1999) Ryan vs. Great Lakes Council FCA 177 (5 March, 1999). NSW District
registry, Federal Court of Australia.
Xu, Z.Y., Li, Z.H. Wang, J.X. Xiao, Z.P. and Dong. D.X. (1992). Ecology and prevention of
a shellfish-associated hepatitis A epidemic in Shanghai, China. Vaccine, 10(Suppl 1):S67-68.
24
Mercury in Finfish
Hazard identification
Based on an acute mercury food poisoning that occurred in Japan during the 1950s, it is
known that high levels of dietary mercury in seafood cause measurable deficits in the 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 but, in aquatic environments, bacteria can convert inorganic
mercury to methylmercury which is readily absorbed by the human body. Methylmercury is
accumulated in aquatic food chains, so all fish contain small amounts in their muscle tissue.
Predatory fish or mammals such as whales at the top of the food web have the largest
amounts.
Mercury levels in most commercially harvested oceanic fish in Australia are <0.5 mg/kg
methylmercury, 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
methylmercury occurs via seafood (predominantly 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 (FDA, 1994; National
Academy of Sciences, 2000).
Exposure Assessment
In Australia there is significant production of species associated with elevated levels of
mercury. Predatory fish are associated with elevated levels of mercury and are defined in the
Food Standards Code as: Gemfish, billfish (including marlin), southern bluefin tuna,
barramundi, ling, orange roughy, rays and all species of shark.
Over the past two decades there have been several surveys of Australian finfish (Table C3),
all of which have found that most seafood contains low levels of mercury (Health
Commission, 1978; Working Group on Mercury in Fish, 1979; WA Food Monitoring
Program, 1993; Bureau of Resource Sciences, 1997a and 1997b; White, 1999).
However, these surveys have also established that sharks, particularly warm water sharks
(Carcharinus) and large game fish, such as swordfish and marlin, have mercury levels much
higher than the maximum recommended level of 1 mg/kg (Food Standards Code).
Interestingly, although tuna is a large predatory fish it generally has mercury levels
<0.5 mg/kg.
In a NSW survey, 3/26 shark samples and 3/8 swordfish samples exceeded the 1 mg/kg limit
(White, 1999). The maximum level of mercury found in shark and swordfish in this survey
was 2.3 mg/kg and 1.65 mg/kg, respectively. Several other recent surveys have found fish
with mercury levels above 1 mg/kg. The 1989-1993 NSW health survey found that nearly 3%
of 1,095 fish samples, all shark and swordfish, exceeded the standard.
In the USA, the Food and Drug Administration have also published mercury content ranges
for orange roughy (0.42-0.71 mg/kg), swordfish (0.26-3.22 mg/kg) and marlin (0.10-
0.92 mg/kg) (FDA, 1994).
25
Table C3: Mercury levels in predatory fish in Australia
Mean mercury (mg/kg) Number of samples in parentheses

Health Working Group WA Food White, 1999
Com., 1978 on Mercury in Monitoring
Fish, 1979 Program, 1993
Gemfish - 0.68 (148) - -
Tuna, Skipjack - 0.15 (20) - -
Tuna, Southern - 0.22 (219) - -
Bluefin
Tuna, Yellow Fin - 0.38 (20) - -
Swordfish 1.98 - - 0.98 (8)
Marlin, Black - 7.27 (42) - 0.57 (3)
Shark - - - -
Angel - 0.36 (36) - -
Blacktip Whaler - 1.48 (8) 0.41 (14) -
Blue Pointer - 1.93 (2) 0.83 (2) -
Blue Whaler - 0.41 (2) - -
Bronze Whaler - 0.72 (159) 0.52 (33) -
Carpet - 1.02 (76) 0.69 (12) -
Gummy - 0.44 (507) 0.29 (4) -
‘Shark’ - - - 0.48 (26)
The tissue concentration of mercury in its organic form, methylmercury, is poorly regulated
by vertebrate and invertebrate fish. Inorganic mercury can be methylated by biological
(predominantly microbiological) processes in the aquatic environment. Methylmercury
accumulates in the food chain, with the highest concentrations found in predatory fish. More
than 95% of the total mercury content in edible fish tissue is in the form of methylmercury.
Most regulatory bodies have adopted this level as the maximum permissible limit in large
predatory fish destined for human consumption.
Farmed vertebrate fish are likely to be safer than their counter-parts caught in the wild.
Methylmercury is predominantly taken up from food, and in marine aquaculture systems as
well as other systems, fish are generally fed formulated diets. As feeds will, or should, have
low mercury content, the harvested fish will likewise have low tissue concentrations of
mercury. Moreover, mercury accumulates in fish during their lifetime and tissue
concentrations are greater in older and larger fish. Since farmed fish are usually harvested
young, they would be expected to have low tissue concentrations even if their feed contained
mercury (FAO/NACA/WHO, 1999).
Illness caused
Methylmercury is rapidly absorbed from the gut and enters the brain of adults and foetuses,
where it accumulates and is converted to inorganic mercury. Methylmercury is highly toxic
and has adverse effects over the lifetime of an individual. The most severe effects were seen
26
following two methylmercury incidents in Iraq (contaminated grain) and Japan (contaminated
seafood) and included mental retardation, cerebral palsy, deafness, blindness and dysarthia in
individuals who were exposed in utero and sensory and motor impairment in exposed adults.
More recently, chronic, low-dose prenatal exposure to methylmercury from maternal
consumption of fish has become associated with impaired performance in neurobiological
tests which measure attention, language, memory and fine-motor function.
There is also evidence that exposure to methylmercury can affect the cardiovascular system
(blood pressure regulation, variable heart rate and heart disease).
The developing foetus is particularly susceptible to the toxic effects of mercury. The first
trimester of pregnancy appears to be the critical period of exposure. Since dietary practices
immediately before pregnancy will have a direct bearing on foetal exposure during the first
trimester, women of child-bearing age who might become pregnant are at risk from mercury
exposure. Australian Bureau of Statistics data indicate that around 200,000 women are
pregnant any given time in Australia. Of these, one third (in the first trimester) are at greater
risk, or perhaps more correctly their foetuses are at greater risk. Thus, a group around 60,000
are at increased risk at any given time.
Unless otherwise acknowledged the following material on the hazard of methylmercury
exposure and current studies is drawn from (Kjellstrom et al., 1986, 1989; Davidson et al.,
1998; Johnson, 1998; Levin, 1998; Mahaffey, 1998; Myers, 1998).
Nearly all the human exposure to methylmercury occurs via fish consumption. Richardson,
(1995) states that there are two primary exceptions: accidental releases, usually in industrial
processes and usually for short periods, and mercury used in tooth filling amalgams.
Methylmercury obtained from the diet typically resides in the human body for several weeks.
To date, mercury health risk estimates have primarily relied on data from a 1970 acute
poisoning incident in Iraq that involved severe, rapid exposure from consumption of
contaminated grain, and caused some deaths.
Those data are the basis for the current United States EPA Reference Dose (RfD) which is
defined as an estimate of a daily exposure to the human population (including sensitive
subpopulations) that is likely to be without a risk of adverse effects when experienced over a
lifetime. The US EPA reference dose for methylmercury is 0.1 µg/kg body weight/day and
includes a safety factor of ten. The health standard for mercury in Australia is the reference
acceptable exposure value established by the Joint FAO/WHO Expert Committee on Food
Additives (JEFCA). This committee established a provisional tolerable weekly intake (pTWI)
for methylmercury of 5 µg/kg body weight/week (White, 1999).
The only documented account of mercury poisoning involving seafoods occurred in people
living around Minamata Bay in Japan during the 1950s. In all, there were more than 700
cases of poisoning and 46 deaths. Finfish and shellfish harvested from the area had mercury
levels up to 29 mg/kg and were eaten at least daily by most people to give an estimated
average methylmercury intake of 0.3 mg/day (Coultate, 1992). For a Japanese woman
weighing 50 kg this equates to 6 µg/kg body weight/day, or 42 µg/kg body weight/week,
more than eight times the pTWI and 90 times the RfD.
Scientific studies are currently being conducted to clarify what levels of mercury in children
can produce adverse outcomes. Three studies of children exposed to mercury via fish
consumption were being undertaken: the Seychelle Islands in the Indian Ocean, the Faroe
Islands in the North Atlantic Ocean and New Zealand populations, all having diets that are
highly dependent on marine life. The Seychellois usually eat fish twice a day with an average
27
mercury content of fish consumed of 0.3 mg/kg which is similar to the majority of fish
consumed in Australia.
The National Academy of Sciences expert panel found that children in the Seychelles study
had no significant mercury effect (NAS, 2000). By contrast, the Faroe and NZ studies
indicated that children who were exposed prenatally to the highest mercury levels had slight
abnormalities in development at age seven. The NAS panel has recommended the retention of
the EPA’s RfD of 0.1 µg/kg body weight/day.
Advice to consumers
FSANZ have issued an advisory which allows adults, including pregnant women, to eat 2-3
serves (300-450 g) per week of low-mercury species (almost all fish except shark, swordfish,
billfish and marlin).
By contrast the NZ Food Safety Authority (www.foodsmart.govt.nz/whats-in-our-
food/chemicals-nutrients-additives-toxins/specific-foods/mercury-in-fish) recommends
pregnant women to eat seafood:
• Without restriction – a range of named finfish, shellfish and squid
• 3-4 serves/week – wide range of finfish and lobster
• 1 serve every 1-2 weeks – shark, marlin, swordfish, bluefin tuna
The amended advice by FSANZ and NZFSA accords with recent findings that consuming
<340 g seafood/week may have a detrimental effect on foetal development (Hibbeln et al.
2007).
By following the revised FSANZ advice of ‘2-3 serves’ consumers may consider it prudent to
defer to two, rather than three serves, an intake which has been shown to be detrimental
(Hibbeln et al. 2007). While advice on avoiding particular species is appropriate, by
specifying serves and quantities FSANZ may unwittingly be prompting consumers to limit
seafood intake.
Given the NZ FSA stance on consumption of seafood it is recommended that FSANZ review
their current advice, with a view to aligning with the NZ approach.
It is noted that Thompson and Lee (2009) state: NZFSA has recently agreed with FSANZ that
both agencies should investigate removing fish monitored for mercury from New Zealand
and Australia’s respective ‘risk lists’ as exposure from mercury in fish would be better
managed by an education programme such as NZFSA’s advisory information for pregnant
women.
References
ABARE (2000) Australian Fisheries Statistics. Commonwealth of Australia, Canberra.
Anonymous (1976). Mercury in fish. Medical Journal of Australia, 2:327-328.
Bureau of Resource Sciences (1997a). Report on the National Residue Survey 1995 Results,
Bureau of Resource Sciences.
Bureau of Resource Sciences (1997b). Report on the National Residue Survey 1996 Results,
Bureau of Resource Sciences.
28
Coultate, T.P. (1992). Food: the chemistry of its components. Royal Society of Chemistry,
Cambridge, UK.
Davidson, P.W., Myers G.J., Cox, C. Axtell, C., Shamlaye, C., Sloane-Reeves, J.,
Cernichiari, E., Needham, L., Choi, A., Wang, Y., Berlin, M. and Clarkson, T.W. (1998).
Effects of prenatal and postnatal methylmercury exposure from fish consumption on
neurodevelopment. Journal of the American Medical Association, 280:701-707.
FAO/NACA/WHO (1999) Food safety issues associated with products from aquaculture:
report of a joint FAO/NACA/WHO study group. WHO technical report series: 883. Joint
FAO/NACA/WHO Study Group on Food Safety Issues Associated with Products from
Aquaculture (1997: Bangkok, Thailand).
FDA (1994) Mercury In Fish: Cause For Concern? FDA Consumer Magazine. 28(7).
Healy. M. (2001) ANZFA issues advisory statement on mercury in fish for pregnant women.
Canberra, January 18, 2001.
Hibbeln, J. (1998) Fish consumption and major depression. Lancet, 352: 1213.
Johnson, B.L. (1998) Testimony of Barry L. Johnson, Ph.D., Assistant Surgeon General
Assistant Administrator, Agency for Toxic Substances and Disease Registry Public Health
Service, U.S. Department of Health and Human Services Before the Subcommittee on
Clean Air, Wetlands, Private Property, and Nuclear Safety Committee on Environment
and Public Works United States Senate October 1, 1998. Downloaded on: September 2
1999 from <http://www.senate.gov/~epw/105th/joh_10-1.htm>.
Kjellstrom, T.P., Kennedy, P., Wallis, S. and Mantell, C. (1986) Physical and mental
development of children with prenatal exposure to mercury from fish. Stage 1: preliminary
tests at age 4. National Swedish Environmental Protection Board Report 3080. Solna,
Sweden.
Kjellstrom, T.P., Kennedy, P., Wallis, S., Stewart, A., Friberg, L., Lind, B., Wutherspoon, T.
and Mantell, C. (1986) Physical and mental development of children with prenatal
exposure to mercury from fish. Stage 2: interviews and psychological tests at age 6.
National Swedish Environmental Protection Board Report 3642. Solna, Sweden.
Levin, L. (1998) Statement of Leonard Levin, Ph.D. EPRI Palo Alto, California to U.S.
Senate Subcommittee on Clear Air, Wetlands, Private Property, and Nuclear Safety
Committee on Environment and Public Works, Washington, D.C. October 1, 1998.
Downloaded on: September 2 1999 from <http://www.senate.gov/~epw/105th/lev_10-
1.htm>.
Mahaffey, K. (1998) Methyl mercury exposure and neurotoxicity (Editorial). Journal of the
American Medical Association, 280(8):737-738.
Myers, G. (1998) Statement by the University of Rochester Research Team Studying the
Effects of Methylmercury Read Before the Senate Subcommittee on Clean Air, Wetlands,
Private Property and Nuclear Safety, Committee on Environment and Public Works
October 1, 1998. <http://www.senate.gov/~epw/105th/mye_10-1.htm>.
National Academy of Sciences. (2000) Toxicological effects of mercury. The National
Academy of Sciences, USA.
Richardson, G.M. (1995) Assessment of mercury exposure and risks from dental amalgam.
Medical Devices Bureau, Environmental Health Directorate, Health Canada.
29
Thompson, B. and Lee, L. (2009) Mercury content in imported fin fish. Institute of
Environmental Science and Research Ltd. Christchurch, NZ.
Western Australian Food Monitoring Program. (1993) Mercury in Shark. Department of
Minerals and Energy Western Australia and Health Department of Western Australia.
White, K. (1999) Metal Contamination of Major NSW Fish Species Available for Human
Consumption. NSW Health.
30
Parasites in Raw Fish
Sashimi (pieces of raw fish) and sushi (pieces of raw fish or cooked prawns with rice and
other ingredients) are increasingly popular foods in Australia. The ingestion of raw fish
carries with it a number of risks of foodborne infection, including the risk of parasitic worms
that can cause disease in humans.
Among parasites associated with fish and seafoods, most of those known to cause disease in
humans are helminths (parasitic worms) and include nematodes (roundworms), cestodes
(tapeworms) and trematodes (flat worms, or flukes). Over 50 species of helminths from
fishes, crabs, snails and other molluscs are known to cause human illness. Of most concern
are:
• Nematodes Anisakis simplex, Pseudoterranova decipiens, Eustrongylides and
Gnathostoma
• Cestodes Diphyllobothrium
• Trematodes Clonorchis sinensis, Opisthorchis, Heterophyes, Metagonimus,
Nanophyetes salminicola and Paragonimus
The helminth parasites are sensitive to freezing and to relatively mild heating (i.e. normal
cooking temperatures). Consequently, those parasites associated with seafood are generally
passed to man by consumption of raw, minimally processed or inadequately cooked chilled
products which are mostly associated with socio-cultural and behavioural factors, particularly
the consumption of raw or undercooked seafood (Adams et al., 1997).
A wide range of seafood products have been implicated in human infection (FDA, 1999):
• Ceviche (fish and spices marinated in lime juice; Latin America)
• Lomi lomi (salmon marinated in lemon juice, onions and tomato; Hawaii)
• Poisson cru (fish marinated in citrus juice, onions, tomatoes and coconut milk)
• Salmon roe
• Ako poki (Japanese and Hawaiian cephalod dish)
• Sashimi (pieces of raw fish; Japan)
• Sushi (pieces of raw fish with rice and other ingredients; Japan)
• Green herring (lightly brined herring; Netherlands)
• Scandinavian gravlax
• Drunken crabs (crabs marinated in wine and peppers; China)
• Cold-smoked fish and undercooked grilled fish
Exposure Assessment
Volumes of Product
Parasites are killed by freezing in a time and temperature-dependent manner. It is, therefore,
assumed that only products that are not, and have not been, frozen will pose a risk to
consumers.
31
There is one published record of anisakid infection in Australian consumers (Shamsa and
Butcher, 2011) in which a 41-year-old Australian woman of Tongan descent consumed raw
mackerel.
Sushi/sashimi: Consumption Frequency and Demographics

Ruello (1999) researched consumption of sushi in Sydney during Spring 1998 and Summer
1999 finding that 19% of Sydney residents consumed seafoods and that the average serve size
was 377 g. Of those consumers, only 1-2% reported consuming sushi. Thus, it is estimated
that in Sydney (population 3,500,000) of the order of 10,000 sushi meals are consumed per
week. Of the sushi consumed out-of-home 41% was at restaurants and 33% from a fast
food/take away outlet. There was a strong indication that sushi was consumed by those with
higher household incomes ($60-80,000 p.a.) and with a tendency towards younger consumers
(<40 years old). The ‘in-home’ consumption survey indicated no sushi consumption.
Intuitively, it seems most unlikely that only 10,000 raw fish portions are eaten each week in
Sydney, with the figure expected to be an order of magnitude higher. Scaling from Sydney to
a national consuming public with similar demographic to that of the Sydney survey leads to
total servings between 1.5 and 15 million servings/ annum. One possible estimate of
consumption pattern is that very few (1%) Australians consume raw fish on a monthly basis.
Comprehensive lists of parasites that have been reported in Australian fish are presented in
Beumer et al. (1982), Lester and Sewell (1989), Doupe et al. (2003) and Shamsi et al. (2010).
Nematodes (roundworms) and Cestodes (tapeworms)

Infection with Anisakis simplex has been documented in many species of fish, rockfish,
herring, cod, halibut, mackerel, wild-caught salmon, yellowfin and skipjack tuna and squid
from many regions of the world. The rates of infection are often high with 10-90% of
samples carrying the parasite (Bouree et al., 1997) and multiple larvae in each fish are also
commonly recorded. Where species and geographical differences exist, it is often due to the
feeding habits of the fish, their size and age (older and larger fish typically contain more
parasites) and whether definitive hosts (e.g. marine mammals) and intermediate hosts are
present to complete the life cycle of the parasite. Due to the need for a mammalian host to
complete the parasite’s life cycle, correlations between the presence and density of marine
mammals and level of contamination of fish have been demonstrated. Pereira-Bueno (1992)
discusses some aspects of the distribution and epidemiology of human anisakiasis.
In relation to risks due to Australian species, Humphrey (1995) reports that A. simplex has
been isolated from flathead (Platycephalus speculator) and anisakids have also been
recovered from other flatheads, mackerel (Scomberomorus spp.), mackerel tuna (Euthynnus
alleteratus), striped trumpeter and farmed salmonids from Tasmania. (Ross, 2000) It is not
known, however, whether the strains isolated are pathogenic to humans.
In Tasmania, the incidence of anisakids in wild caught stripey trumpeter and farmed Atlantic
salmon (included in Humphrey, 1995) was 91% (39/43) of samples of striped trumpeter and
1/60 farmed Atlantic salmon. At that time striped trumpeter were being used and promoted
for raw fish dishes, as were Atlantic salmon and Jack mackerel (Mure and Mure, 1993).
Lester and Sewell (1989) reported the incidence of parasites in fish from Heron Island.
Anisakis larvae were found in the organs or viscera of six species of fish including blue
grenadier, gemfish, Jack mackerel and orange roughy. Beumer et al. (1982) provide a list of
parasites of fishes in Australian waters.
32
In 2010, EFSA published a scientific opinion on risk assessment of parasites in fishery
products and concluded that, while wild-caught fish can never be guaranteed not to have
helminth parasites, the likelihood in farmed fish is much lower.
Of relevance in a listing of farmed fish, a number of species were identified which are both
consumed in Australia and exported in a chilled format, making them potential sources of
infection. These species include Atlantic salmon, Pacific salmon, rainbow trout and tuna, to
which should be added the farmed species Australian Kingfish (Seriola lalandi) and
Mulloway (Argyrosomas hololepidotus).
In a survey of five South Australian species, Shamsi et al. (2010) did not detect anisakid
larvae in ten samples of wild caught S. lalandi.
Infections of A. simplex have been reported in New Zealand (Goldsmid and Speare, 1997)
and specifically in New Zealand teleost fishes (Hurst, 1984).
Anisakiasis is a relatively common infection in Japan, largely because fish is often eaten raw,
lightly cooked or pickled. Infection is also relatively common in northern Europe where
cured fish, such as pickled herring, are part of the diet. Deardorff and Overstreet (1991)
report that in Japan, the annual incidence of anisakiasis is >1000 cases/annum.
In contrast, the number in the US, where raw fish is not currently a major part of the cuisine,
is negligible; anisakiasis is not mentioned in a review of the role of seafood in foodborne
diseases in the USA (Lipp and Rose 1997). Although the frequency of infection in Europe is
apparently lower than in Asian countries, the number of reported cases has been increasing in
recent years, particularly in France (Audicana et al., 1995). A retrospective study in France
during January 1985-September 1987 by 32 laboratories specialising in parasitology (Hubert
et al., 1989) confirmed 21 cases of anisakiasis involving several fish species.
The Netherlands was one of the nations recognised to have endemic Aniskiasis. Nonetheless,
in the period 1955 (first identified) and 1968 (before control measures were introduced), only
161 cases were reported ~10-15 cases per annum. After the introduction of control measures
(freezing and gutting on board) the incidence has decreased to virtually nil (Hayunga, 1997).
FDA (1999) reports that ~10 cases per year are reported in the USA, but consider that many
cases go unreported.
Table C4: Guidelines for tolerable levels of parasites in fish (FDA, 1999)
Product Guideline
Tullibies, ciscoes, inconnus, chubs 50 cysts per 45.45 kg (100 lb)
and whitefish
Blue fin and other freshwater herring 60 cysts per 100 fish, if 20% of the fish examined
averaging 1 lb or less are infested
Blue fin and other freshwater herring 60 cysts per 45.45 kg (100 lb), if 20% of the fish
averaging >1 lb examined are infested
Rose fish (red fish and ocean perch) 3% of fillets examined contain one or more
copepods accompanied by pus pockets
At this time, there are no published records of anisakid infections in Australian consumers,
nor do there appear to be any unreported cases (Ross, 2000). Despite the widespread
33
incidence of anisakid larvae in wild fish populations and market fish, there are several reports
(Deardorff and Kent, 1989; Angot and Brasseur, 1993; Ross, 2000) indicating that farmed
Atlantic and other salmon do not develop infections. Similarly, for cod, Hemmingsen et al.
(1993) showed that the accumulation of parasites ceased when wild caught Atlantic cod
(Gadus morhua) were caged and fed artificial diets. This was believed to result from
interruption of the parasite life cycle by the feeding of fish with artificial feed thereby
preventing infection of the fish by intermediate hosts. Infections of mariculture species by
nematodes has not been confirmed (Durborow, 1999).
Diphyllobothrium spp. have been reported to be present in Australian fish (Humphrey, 1995)
but there is little detail of the parasite species or species of fish affected. Goldsmid and
Speare (1997) indicate that D. latum is endemic in North and South America and in parts of
Europe, particularly Finland.
Trematodes (flatworms)
Fish-borne trematode disease is highly endemic in southeast China but also in other parts of
Asia. Clonorchis sinensis affects an estimated 7,000,000 people worldwide. It is the most
common parasite in Hong Kong where 30-60% of the population are believed to be infected.
Opisthorchiasis (O. viverrini) is a major cause of death in northeast Thailand and it is
estimated that 7,000,000 are infected in that country. The infection is also very common in
Laos (Durborow, 1999).
Imported cases may occur in other parts of the world. Shipments of imported dried or pickled
fish are considered a likely source. Additionally, chilled freshwater fish from endemic areas
are flown daily into the United States (Benenson, 1995).
Fish hosts of the liver fluke include silver carp (Hypothalamicthys molitrix) and the grass
carp (Ctenophargyndon idellus) both of which are aquaculture species (Durborow, 1999).
Unless otherwise acknowledged, the following is drawn from FDA (1999), FAO (1999),
Hayunga, (1997) and Deardorff and Overstreet (1991). Adams et al. (1997) also reviewed
helminthic infections acquired from fish and shellfish including risk mitigation and
preventive measures. For ease of reading, the hazard characterisation is presented separately
for each of the three groups of parasites considered.
Of the parasites, the Anisakidae are the most important and will be given the most attention.
The means of controlling Anisakids are equally relevant to other seafood-borne parasites.
Nematodes (rounds worms)

Among the nematodes those of most concern are Anisakis, Capillaria, Gnasthostoma and
Pseudoterranova, the infective cysts of which are found predominantly in the liver, belly
cavity and flesh of marine fish. Of these organisms, A. simplex causes the greatest numbers of
illnesses which tend to be more severe than those caused by other helminths. Nonetheless,
occurrence is considered rare as the infective stage of the parasite is killed by cooking (e.g.
60°C for one minute) or freezing (e.g. -20°C for 24 h).
34
Anisakis simplex is commonly called the ‘herring worm’. Its final hosts are dolphins,
porpoises and sperm whales. The larval (worm-like) stage in fish and squid is usually 18-
36 mm long, 0.24-0.69 mm wide and pinkish to whitish in colour i.e. it is visible, when
exposed, to the naked eye. Anisakiasis, the human illness caused by A. simplex, is associated
with eating raw fish such as sushi, sashimi, lomi lomi, ceviche, Dutch green herring,
marinated fish and cold-smoked fish or undercooked fish (Ward et al., 1997).
Pseudoterranova decipiens, commonly called codworm or sealworm, is another important
parasitic nematode. The usual final hosts of Pseudoterranova are grey seals, harbour seals,
sea lions and walruses. The larval stage in fish are 5-58 mm long, 0.3-1.2 mm wide and
yellowish, brownish or reddish in colour. These nematodes are related to A. simplex and the
disease associated with infections is also termed anisakiasis. They are also transmitted to
humans through raw or undercooked fish (Ward et al., 1997).
Several forms of illness are recognised. A non-invasive form (more usually associated with
P. decipiens) involves a tingling sensation in the throat when worms are released from
ingested seafood and migrate up the oesophagus, typically to be spat out. The invasive form
usually associated with A. simplex occurs when the organism penetrates the mucosa or sub-
mucosa of the stomach or small intestine resulting in gastric pain, vomiting, and diarrhoea
about 12 hours after ingestion. The chronic form can mimic gastric ulcer, appendicitis,
enteritis, or gastric carcinoma. Endoscopic identification and removal of the worm is the most
reliable treatment. Juvenile larvae have also been mistaken for, and linked with, cancerous
cells in the host.
Most infections are reported from Japan and the Netherlands but numbers in other countries
are increasing. This has generally been attributed to changing dietary habits, whether in
established or migrant populations; although Oshima (1987) maintains that the apparent
increase (since 1972) is due to better diagnosis of infections.
A third form of illness - an allergic response to A. simplex antigens - has been recognised
more recently (Audicana et al., 1997). While freezing and cooking may kill A. simplex it may
not protect consumers against reactions to ingested A. simplex antigens. Reactions to the
allergens, and an association of chronic A. simplex infections with some gastric cancers, are
increasingly being recognised as discrete, long term, disease syndromes (Daschner et al.,
1998).
Gnathostoma infections are associated with consumption of inadequately cooked or
marinated freshwater fish. As such they are unlikely to be spread by sushi and sashimi.
Nonetheless, G. spinigerum is endemic in Australia and is the only species recorded to have
caused illness in Australia. It is also found in Asia. Larvae can also penetrate the skin during
handling. Nausea, abdominal pain, and vomiting usually develop 24-48 hours after eating.
Infection can also involve the eye or cause subcutaneous swelling (Goldsmid and Speare,
1997). The larvae migrate and may invade the central nervous system (CNS) resulting in
meningitis or neuropathy. As with anisakiasis chemical treatment is ineffective and surgical
removal of the larvae is required.
Capillaria phillipensis is observed mainly in Thailand and the Philippines and causes
enteropathy and malabsorption (Goldsmid and Speare, 1997). It utilises many species of
freshwater fishes as intermediate host, but its life cycle is incompletely understood.
Disease is usually caused by the direct effects of the presence of the parasite in the host tissue
due to mechanical or biochemical damage to cells, tissues or organs of the host or
competition for space and nutrients. In the case of helminthic infections, clinical disease in
35
the host is usually dependent on the worm load, which is in turn dependent on the infecting
dose. An exception to this rule is Capillaria phillipensis a fish-borne parasite (Goldsmid and
Speare, 1997).
In Japan, achlorhydria or hypochlorhydria was found in at least 50% of cases and may be a
predisposing factor. In the allergic form of sickness, prior exposure is required to cause
sensitisation, though some of the allergens cross react with other organisms (Benenson,
1995). Interestingly, there is some evidence that the Japanese custom of drinking sake wine
with raw fish may reduce the risk of establishment of an infection (Durborow, 1999).
As discussed above, factors affecting the dose include the degree of processing (duration and
severity of heating, freezing, brining) and the age and size of the fish. The handling of the
fish immediately post-harvest has also been implicated as a risk factor. Migration of the
parasites from the viscera to the muscle tissue after catch has been demonstrated and most
parasites in fish are found initially in the intestinal or belly flap regions. Rapid freezing, or
evisceration, can reduce the likelihood or migration to the edible portions of the fish.
Person to person transmission does not occur. Apparently there is universal susceptibility
(Benenson, 1995). Anisakid larvae are generally presumed to be killed by freezing and
cooking (Angot and Brasseur, 1993). Accordingly only those products that have never been
frozen and which are eaten raw or lightly cooked or lightly preserved pose a hazard. A survey
by Adams et al. (1994) of sushi and sashimi in restaurants and retail shops in Seattle, USA,
supported this assumption. All juveniles found in sushi were dead, most likely the result of
using previously frozen fish. The larvae are generally killed after freezing and holding at -
20°C for 24 hours though Bier (1976) found that the larvae of some types may survive for as
long as 52 h at -20°C. Marques et al. (1995) studied ten fishes from the Brazilian Coast and
isolated approximately 48 anisakid larvae of the genera Contracaecum, Phocanema and
Anisakis. Twenty five fishes were held chilled or frozen, and larval survival determined; 98%
of the Contracaecum larvae survived storage at 0° for five days and 96.4% survived storage
at -18°C for 24 h. FDA regulations for the elimination of nematodes in fish by freezing are
either seven days at -20°C or 15 h at -35°C. It should be noted that microbial inactivation is a
stochastic process. That is, a constant proportion of organisms will be inactivated during any
given interval under lethal conditions. Thus, the time required to inactivate all the pathogens
or parasites will depend on the number of them initially present.
Additional details of the survival of nematodes under conditions relevant to seafood handling
and processing are provided in ICMSF (1996).
Anisakis larvae survival was studied in brines by Karl et al. (1994). Traditional German and
Danish procedures for pickling herring require at least five and six weeks respectively to
eliminate viable larvae. A reduction in the salt phase from 9% to 4.3% w/w, without change
in the acetic acid concentration, resulted in the nematode survival time increasing from 35
days to more than 119 days. Hayunga (1997) states that cold smoking and most methods of
brining fish are not reliable preventative methods.
Gnathostoma larvae can be killed by cooking or immersing in strong vinegar for >5 h.
Immersion in lime juice or chilling at 4°C for >1 month were not completely lethal. The salt
tolerance of Gyrodactylus salaris is poor, and it begins to die at salt concentrations >7.5 g/kg,
with normal seawater causing rapid inactivation (Soleng and Bakke, 1997). Similar results
were found for Gyrodactylus derjavini by Buchman (1997).
36
Trematodes (flat worms, flukes)
Fish-borne flatworm (trematode) infections are a public health problem in about 20 nations,
particularly in south-east Asia, where freshwater fish are intermediate hosts. In terms of
human infection the most important species are from the genera Clonorchis and Opistorchis
(liver flukes), Paragonimus (lung flukes) and to a lesser extent Heterophyes and
Echinochasmus (intestinal flukes). Freshwater fish are the intermediate hosts in the life cycle
of Clonorchis and Opistorchis and freshwater crustaceans in the case of Paragonimus.
Reservoir hosts of Clonorchis sinensis are wild and domestic mammals. Metacercariae (the
infective stage) have also been found in crayfishes. Metacercariae encyst in fish gills, fins,
muscles or under the skin. Adult worms (1.2-2.4 cm long and 0.3-0.5 cm wide) reside in the
bile duct. Pancreatitis may also occur, and an association with choleangiocarcinoma has also
been reported.
Infection by Paragonimus westermani (human lung fluke) can occur through eating raw or
improperly cooked freshwater crabs or crayfish. It is common in Asia and to a lesser extent in
Africa and India, and is reported throughout SE Asia/Micronesia, and South Pacific islands.
Important hosts include freshwater and brackish-water crabs of the genera Eriocheir,
Potamon and Sundathelphusa and the crayfish Procambrus.
When eaten by the definitive host the metacercariae of C. sinensis encyst in the duodenum,
migrate into the bile duct and grow to adulthood. Symptoms may be slight or absent in light
infections, the symptoms resulting from local irritation of the bile ducts by the flukes. Loss of
appetite, diarrhoea and abdominal pressure are early symptoms of infection, which may take
up to 30 days to become apparent. Rarely jaundice may result in enlargement and tenderness
of the liver, and progressive ascites and oedema followed by cirrhosis. The organisms may
live in human host for 25-30 years. Diarrhoea, epigastric pain, and anorexia are common
manifestations of acute disease. Adult worms can produce localised tissue damage that may
interfere with bile function, leading to secondary bacterial infection. It is usually a mild
disease, and often asymptomatic, but is a significant risk factor for the development of
cholangiocarcinoma.
Susceptibility appears to be universal. Direct person to person transmission does not occur
(Benenson, 1995). Severity of symptoms is related to the intensity and duration of infection -
infections with as many as 500-1000 worms have been reported.
Freezing at -20°C or below for seven days, or -35°C for about 20 h, will kill infective stages
of these parasites. Fan (1998) reported that metacercariae of C. sinensis remained viable and
infective after 10-18 days storage at -12°C, as did those stored for 3-7 days at -20°C. Those
kept in a heavily salted fish at 26°C for 5-7 days also remained viable and infective. While
pickling does not kill the parasite, boiling for a few minutes does. Infections can also be
acquired from crab/crayfish juices.
Cestodes (tape worms)

Cestodes are tapeworms with segmented bodies and a structure that allows them to attach to
the intestinal wall of their hosts. The species of most concern is Diphyllobothrium latum, the
broad tapeworm. Its distribution is worldwide and D. latum parasitises a variety of fish-eating
mammals of the northern latitudes. A similar species is found in the southern latitudes and is
associated with seal hosts. Cases have been reported from around the world including
Australia. It is the largest human tapeworm, growing up to 9 m, but infections may be mild or
asymptomatic.
37
Fish are intermediate hosts and infective larvae may be found in trout, whitefish, pike and
salmon. Cestode larvae found in fish range from a few millimeters to several centimeters in
length and are white or grey in colour. Diphyllobothrium tapeworms primarily infect
freshwater fish, but salmon and related fish can also carry the parasite. Diphyllobothrium
tapeworms are usually found unencysted and coiled in musculature or encysted in viscera.
Infection is related to dietary and culinary practices. As with the nematodes, human
infections are linked with consumption of raw or minimally processed fish. Freezing and
cooking temperatures lethal for anisakids will kill the infective stage of D. latum.
Common symptoms are nausea, abdominal pain, diarrhoea and weakness, but it may also
cause pernicious anaemia and vitamin B12 deficiency if the worm attaches to the jejunum.
D. denderiticum and Ligula intestinalis (tapeworms of fish eating birds) and D. pacificum
(tapeworm of seals) have also been found in humans. The infection is usually mild, or even
asymptomatic and often of long duration. Massive infections may be associated with
diarrhoea and obstruction of the intestinal tract, because the mature worm may be up to 10 m
long in the human host.
People are universally susceptible and there appears to be no induction of immunity
(Benenson, 1995). FDA (1999) suggests that people of Scandinavian heritage may be
genetically more susceptible. In such cases a severe anaemia may develop because of the
tapeworm's great requirement for and absorption of Vitamin B12. Victims may harbour more
than one worm. As indicated above, the presence of more than one worm can amplify the
symptoms of infection.
Acanthocephala (spiny headed worms).

These burrowing worms are widespread in nature and infect, as secondary hosts, amphipod
crustaceans, freshwater and marine fish (paratenic hosts) and other, non-aquatic species. They
are intestinal parasites and may cause an inflammatory response at the site of proboscis
attachment, although usually there are no clinical signs. Wild aquatic birds (such as ducks,
swans and geese), dogs and their relatives, pigs and Central and South American monkeys are
the definitive hosts. These worms are considered to pose little risk to humans because they
are relatively scarce in fish eaten by man, and because the worms are usually localised in the
viscera of fish and thus less likely to be eaten.
Similarly, most reviews completely discount the potential for protozoan infections from
consumption of fish. The recent review of Durborow (1999) mentions the potential for
aquaculture species to lead to infection with Cryptosporidium sp., Enterocytozoan sp. or
Giardia lamblia, but indicates that there is currently no evidence of the role of fish in the
transfer of these diseases.
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463-477 in M.P. Doyle, L.R. Beuchat and T.J. Montville (Eds.) Food Microbiology:
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Karl, H., Roepstorff, A., Huss, H.H. and Bloemsa. B. (1994) Survival of Anisakis larvae in
marinated herring fillets. International Journal of Food Science and Technology, 29:661–
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(chilling and freezing) on survival of anisakid nematode larvae in Trichiuris lepturus (L.).
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40
Ciguatoxins
Each year, a number of Australians develop an illness known as ciguatera poisoning after
eating certain species of fish. The illness, characterised by gastrointestinal, neurological and
cardiovascular symptoms, may be acute and long-term. This assessment acknowledges the
reviews by Lehane (1999) and Lehane and Lewis (2000).
Ciguatera poisoning is caused by eating subtropical and tropical reef fish which have
accumulated naturally-occurring toxins produced by marine algae. The toxins are known to
originate from several dinoflagellate algae species (predominantly Gambierdiscus toxicus)
that are common to ciguatera-endemic regions in tropical waters. These toxins produce a
range of gastrointestinal, neurological and cardiovascular symptoms which can persist for
many weeks and may be re-triggered by dietary changes or exposure to low levels of toxin,
months or years after initial exposure. Ciguatera poisoning is usually self-limiting with a low
incidence of death.
Exposure Assessment
Because of the distribution of Gambierdiscus most ciguatoxic fish are caught in Queensland
and Northern Territory waters, with some coming from northern Western Australia (Port
Hedland to Bunbury). A list of fish involved in outbreaks in Queensland during the period
1965-1984 (Table C5) compiled by Gillespie et al. (1986) indicates the species involved and
relative frequency. By far the most numerous cause of ciguatera is mackerels in the genus
Scomberomorus, particularly the Spanish mackerel (S. commerson). In Tables A1, A3 and B2
are listed details of ciguatera outbreaks in the period 1998-2010 using data from the National
Risk Validation Project (1998-2001) and OzFoodNet annual data (2000-2010)
41
Table C5: Cases of ciguatoxin illness in Queensland 1965-1984 (after Gillespie et al., 1986)
Scientific Name (common name) Number Number of

of cases outbreaks
Scomberomorus commerson (Spanish mackerel) 226 30
Scomberomorus spp (mackerels, species unknown) 161 62
Sphyraena jello (barracuda) 29 13
Plectropomus spp (coral trout) 27 18
Epinephelus fuscoguttatas (flowery cod & other epinephalids) 27 14
Lutjanus sebae (red emperor) and Lutjanus bohar (red bass) 16 9
Scomberoides commersonnianus (giant dart) 8 3
Lethrinus nebulosa (yellow sweetlip) 4 1
Seriola lalande (yellowtail kingfish and other seriolids) 6 1
Caranx sp (trevally, species unknown) 4 2
Cephalopholis miniatus (coral cod) 3 2
Chelinus trilobatus (maori wrasse) 3 3
Choerodon venustus (venus tusk fish) 2 1
Trachinotus sp (dart) 1 1
Paracesio pedlryi (southern fuselier) 1 1
Lates calcarifer (barramundi) 1 1
Other and unknown 14 16
Despite Spanish mackerel being most frequently implicated, Gillespie et al. (1986) stated that
red bass (Lutjanus bohar), chinamen fish (Symphorus nematophorus) and paddletail
(Lutjanus gibbus) were recognised as high risk species in Queensland and were not accepted
for sale (at that time) by the Queensland Fish Board. The same authors added that, despite its
well-known toxicity, red bass was commonly eaten by Queensland fishers with apparently
few cases of ciguatoxin poisoning. In addition to the list compiled by Gillespie et al. (1986),
Lehane (1999) adds parrot fish (Scarus spp), grunter bream (Pomadsys sp) and moray eel
(Lycodontis or Gymnothorax javanicus) to the list of potentially ciguatoxic species.
It is important to review the scientific and common names listed by Gillespie et al. (1986)
and Lehane (1999) for their current correctness according to the Australian Seafood
Handbook (Yearsley et al., 1999). Names not listed in the Handbook are Lutjamus gibbus,
paddlefish, Epinephalus fuscoguttatus, Paracesio pedlryi and southern fusilier. Changed
names include Lethrinus nebulosa (now Diagramma or Plectorhynchus sp) and altered
specific epithets include Cephalopholis miniatus (C. cyanostigma) and Cheilinus trilobatus
(C. undulatus). Such information is not of mere semantic moment. Ross (2000) reports
anecdotal evidence of a ciguatoxicosis in NSW attributed to ‘queenfish’ which, while not
considered a potentially ciguatoxic species by some, was identified by the Handbook as
Scomberoides commersonnianus, a species regularly implicated in ciguatera poisonings.
Prevalence of intoxication
Estimates of the number of ciguatera cases worldwide are, variously, 20,000 (Durburow,
1999), 50,000 (Benenson, 1995) and 10-50,00 (Lehane, 1999).
In Australia, ciguatera fish poisoning usually occurs as sporadic isolated cases (Fenner et al.,
1997; Lucas et al., 1997), although at least two larger outbreaks (>30 cases) have been
reported (Hallegraeff, 1998). One hundred and sixty-six confirmed outbreaks affecting 479
people were reported in Australia between 1976 and 1984 (Glaziou and Legrand, 1994). In
42
Queensland, several thousand cases were notified to authorities over a 10-year period (Ting et
al., 1998) with an estimated 1.8-2.5% of the population in that state affected (Glaziou and
Legrand, 1994; Lehane, 1999). The average incidence in Queensland (1985-1990) was 1.6
cases/100,000, although in coastal Queensland the annual prevalence was estimated at
33/100,000 (Capra and Cameron, 1988).
Ross (2000) cites a personal communication from Voetsch who collated 41 cases of ciguatera
poisoning in NSW for the period 1996-1998, noting also that the list was not comprehensive.
Due to under-reporting of this often mild illness, these data represent the minimum
prevalence in NSW. There have also been several large outbreaks in Sydney at restaurants. In
1987, 63 people became ill after eating Spanish mackerel (Scomberomorus commerson)
which had been caught in Hervey Bay, Queensland. Another mass poisoning occurred in
1994 in which 43 people were affected after eating Spanish mackerel from Queensland (Kraa,
1994: Capra, 1997). In Darwin, three people were affected after consuming locally-purchased
coral trout (Merianos et al., 1991) and there was an outbreak in Brisbane in 1995 involving
15 people who ate Spanish mackerel caught east of Fraser Island (Harvey, 1995). In Victoria
in 1997 there were 30 cases of ciguatera after a 16.2kg live Maori Wrasse was consumed at a
banquet at an Asian restaurant (Ng and Gregory, 2000).
Seriola dumerili, known in Australia as amberjack and a common component of the catch in
WA and Queensland, was associated with 21% (17/81) of ciguatera fish poisoning outbreaks
in Hawaii between 1975 and 1981. All commercially harvested S. dumerili caught in Hawaii
between 1979 and 1981 were tested with an immunoassay for ciguatoxin (detection limit
1 ng/mL). Fifteen percent (824/5,529) gave borderline or positive results, as did 17%
(269/1,585) of fish weighing 9 kg or more (Katz et al., 1993). Serological test kits for the
detection of ciguatoxin are now available commercially (e.g. Cigua-Check Fish Poison Test
Kit Oceanit Test Systems, Inc., http://www.cigua.com), but little reliable data on the
incidence of ciguatoxin in Australian fish have been published (Ting et al., 1998). Mackerel
and barracuda from mid to northeastern Australian waters have been reported to be frequently
ciguatoxic (Price and Tom, 1999).
When herbivorous fish are eaten by carnivorous fish, dinoflagellate toxin is converted to the
more potent ciguatoxin (Durborow, 1999). These toxins accumulate through the food chain,
from small fish grazing on algae on coral reefs into the organs of larger top-order predators.
Toxin is concentrated in the head, liver and viscera of fish (Ting et al., 1998), but levels are
lower in the muscle, the part more usually eaten. The occurrence of toxic fish is sporadic and
not all fish of a given species or from a given locality will be toxic (Benenson, 1995). If fish
cease ingesting the dinoflagellate the toxin will slowly be purged from the fish. There is one
report of ciguatera poisoning associated with consumption of jellyfish (Zlotnick et al., 1995)
and breast milk (Lehane, 1999).
Ciguatoxicosis in humans usually involves a combination of gastrointestinal, neurological,
and cardiovascular disorders. Initial signs of poisoning occur within six hours of consumption
and include perioral numbness and tingling (paresthesia) which may spread to the
extremities, nausea, vomiting and diarrhoea. Neurological signs include intensified
paresthesia, arthralgia, myalgia, headache, temperature sensory reversal and acute sensitivity
to temperature extremes, vertigo and muscular weakness to the point of prostration.
Cardiovascular signs include arrhythmia, bradycardia or tachycardia, and reduced blood
pressure.
43
Ciguatera poisoning is usually self-limiting and signs of poisoning often subside within
several days of onset. However, in severe cases the neurological symptoms persist from
weeks to months and in rare cases, for several years. Sometimes, recovered patients
experience recurrence of neurological symptoms months to years after recovery. There is a
low incidence of death resulting from respiratory and cardiovascular failure. Clinical testing
procedures are not presently available for the diagnosis of ciguatera in humans, which is
based entirely on symptoms and recent dietary history. The disease has only recently become
known to the general medical community and may be under-reported because of the
generally non-fatal nature and short duration of the disease.
All humans are believed to be susceptible to ciguatera toxins. Populations in
tropical/subtropical regions are most likely to be affected because of the relatively higher
frequency of exposure to toxic fishes. Repeated ciguatoxin exposures are associated with
more severe illness (Glaziou and Martin, 1993; Katz et al., 1993).
Infectious Dose/Dose Response

The ciguatoxins are lipid-soluble toxins. These are relatively inert molecules, and remain
toxic after cooking and exposure to mild acidic and basic conditions. Ciguatoxin (CTX)-1 is
the major toxin (on the basis of both quantity and total toxicity) present in fish, except for
certain herbivorous species which accumulate mostly gambiertoxins and less polar
ciguatoxins. CTX-1 typically contributes ~90% of total lethality. On the basis of available
outbreak data, Lehane (1999) estimated the minimum toxic dose to be ~50 ng in an adult of
50 kg weight (i.e. ~1 ng/kg body weight). In one well-documented incident, six U.S. soldiers
became ill after eating fish containing approximately 20 ng ciguatoxin/g flesh. They all
presented with nausea, vomiting, watery diarrhoea and abdominal cramps 5-8 h after
consumption and some also had numbness in the extremities or perioral region, bradycardia
and scalp paresthesia (Poli et al., 1997).
Several studies have demonstrated that increased toxin dose is equated with increased
severity of cardiovascular effects in animals and humans (Katz et al., 1993). However,
Arcilaherrera et al. (1998) found no association between the amount of toxic fish ingested
and the latency period or the severity and duration of the symptoms in a study of 10 incidents.
It is well recognised that ciguatoxin displays a cumulative exposure phenomenon, with
repeated exposure resulting in more severe and prolonged symptoms.
Critical Control Points and/or Management Options

There are few control strategies available to eliminate the risk of exposure to ciguatera
affected fish. Current risk reduction strategies include limits on the size and/or type of certain
fish species and restrictions on fishing in known toxic areas. Red bass, chinaman fish and
paddletail have been regarded as unsuitable for sale in Queensland for 20 years due to their
likely toxicity (Lehane, 1999).
Ciguatera poisoning is regularly reported in Queensland which may reflect the impact of
recreational fishing. In the US it has been reported that approximately 80% of cases are due
to recreational fishers who are unfamiliar with the types of fish that are commonly ciguatoxic
(Kuenster, 1991. Other than in Queensland and the Northern Territory, recreational fishermen
are unlikely to catch affected fish.
44
In subtropical and tropical regions professional fishermen are aware of areas to avoid which
helps reduce the hazard to consumers. Size restrictions are potentially effective since larger
fish may be more frequently toxic than small fish but the practice of filleting into portions for
on-board packing and freezing makes this impossible to monitor as a CCP.
While some fish markets claim to not sell potentially poisonous fish such as reef fish,
anecdotal evidence suggests that due to inconsistent naming of fish, potentially ciguatoxic
species may be sold.
In the USA, current passive control measures include posting warning signs and the issue of
pamphlets advising about the hazards of particular species. An active control system
involving development of a reliable and inexpensive test for ciguateric fish, regulating fishing
of suspected species, testing these fish either on board fishing vessels or at dock site, and
educating consumers, commercial and sports fishers and health professionals has been
recommended (Ahmed, 1991; Miller, 1991). Recent developments in diagnostic kits for
ciguatera toxin have seen the commercial release of several immunological assays. Increased
testing for ciguatera toxin using such kits would help define the magnitude of the problem.
Their use may be economically viable with high value fish (e.g. coral trout) as a routine
screening test.
Introduction of a system that would allow trace-back of fish to the area where they were
caught (e.g. tagging) would help define problem areas. However, such a system is dependent
on the reporting/diagnosis of ciguatera poisoning incidents. Currently ciguatera poisoning
incidents are under reported because cases are rarely fatal, typically involve few (< 5) people,
are sporadic and are easily misdiagnosed by medical staff (Todd, 1995; Lehane, 1999).
Adoption of a trace back system would need to be backed up with an educational campaign
for clinicians and public health workers to increase their awareness of ciguatera poisoning.
References
ABARE (2000) Australian Fisheries Statistics. Commonwealth of Australia, Canberra.
Arcilaherrera, H., Castellonavarrete, A., Mendozaayora, J., Monterocervantes, J.,
Gonzalezfranco, M.F. and Britovillanueva, W.O. (1998) Ten cases of ciguatera fish
poisoning in Yucatan. Revista de Investigacion Clinica, 50:149-152.
Benenson, A.S. (Ed). (1995) Control of the Communicable Diseases of Man 16th Edition.
American Public Health Association, Washington, pp. 577.
Capra, M.F. (1997) Ciguatera. pp. 573 - 582 in Foodborne Microorganisms of Public Health
Significance (A.D. Hocking, G.Arnold, I. Jenson, K. Newton and P. Sutherland, Eds.).
Australian Institute of Food Science and Technology Inc., NSW Branch Food Microbiology
Group, North Sydney, Australia.
Capra, M.F. and Cameron, J. (1988) Ciguatera poisoning: pharmacology and pathology. Final
report, FIRTA grant 83/41. Commonwealth Department of Primary Industry, Canberra.
Durburow, R.M. (1999) Health and safety concerns in fisheries and aquaculture.
Occupational Medicine:State of the Art Reviews, 14:373-406.
Fenner, P.J., Lewis, R.J., Williamson, J.A. and Williams, M.L. (1997). A Queensland family
with ciguatera after eating coral trout. The Medical Journal of Australia, 166:473-475.
45
Gillespie, N.C., Lewis, R.J., Pearn, J.H., Bourke, A.T.C., Holmes, M.J., Bourke, J.B. and
Shields, W.J. (1986) Ciguatera in Australia. Occurrence, clinical features, pathophysiology
and management. The Medical Journal of Australia, 145:584-590.
Glaziou, P., and Legrand, A.M. (1994) The epidemiology of ciguatera fish poisoning.
Toxicon, 32:863-873.
Hallegraeff, G. M. (1998) Algal toxins in Australian And New Zealand seafood products:
review of their occurrence, analytical detection and public health implications. Report for the
Australia New Zealand Food Authority (ANZFA).
Harvey, N.P. (1995) Ciguatera fish poisoning outbreak in Brisbane. Communicable Diseases
Intelligence, 19: 666-668.
Katz, A. R., Terrellperica, S. and Sasaki, D.M. (1993) Ciguatera on Kauai - investigation of
factors associated with severity of illness. American Journal of Tropical Medicine &
Hygiene, 49:448-454.
Kraa, E. (1994) Ciguatera outbreak, NSW, 1994. New South Wales Public Health Bulletin,
5(6):69.
Lehane, L. (1999) Ciguatera Fish Poisoning. A Review in a Risk-Assessment Framework.
National office of Animal and Plant Health, Agriculture, Fisheries and Forestry Australia.
Lehane, L. and Lewis, R.J. (2000) Ciguatera: the risk remains. International Journal of Food
Microbiology, 61:91-125.
Lucas, R.E., Lewis, R.J. and Taylor. J.M. (1997) Pacific ciguatoxin-1 associated with a large
common-source outbreak of ciguatera in east Arnhem Land, Australia. Natural Toxins,
5:136-40.
Merianos, A., Burrows, J. and Patel, M. (1991) Ciguatera in Darwin following a meal of coral
trout. Communicable Diseases Intelligence, 15:386-387.
National Risk Validation Project (2002) Food Science Australia and Minter Ellison.
Ng, S. and Gregory, J. (2000) An outbreak of ciguatera fish poisoning in Victoria.
Communicable Diseases Intelligence, 24:344-346.
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Poli, M. A., Lewis, R.J., Dickey, R.W., Musser, S.M., Buckner, C.A. and Carpenter, L.G.
(1997) Identification of Caribbean ciguatoxins as the cause of an outbreak of fish poisoning
among US soldiers in Haiti. Toxicon, 35:733-741.
Price, R. J., and Tom, P. (1999) Compendium of Fish and Fishery Product Processes,
Hazards and Controls. Downloaded on: September 3 1999 from
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Ross, T. (2000). Risk assessment of ciguatera poisoning in NSW. Safe Food NSW, Sydney.
Ting, J.Y.S., Brown, A.F.T. and Pearn, J.H. (1998) Ciguatera poisoning - an example of a
public health challenge. Australian and New Zealand Journal of Public Health, 22:140-142.
Yearsley, G.K., Last, P.R. and Ward, R.D. (1999). Australian Seafood Handbook, CSIRO
Marine Research, Australia.
Zlotnick, B.A., Hintz, S., Park, D.L. and Auerbach, P.S. (1995) Ciguatera poisoning after
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46

Hazard Identification Report For Seafood 2011

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Hazards Affecting Australian

TOR 4 AND TOR 5: ....................................................................................................................5

TOR 7: PRESENT FINDINGS TO A STAKEHOLDER MEETING (WITH SAFEFISH

TOR 1: Master List of Potential Issues

TOR 3: Separate technical trade issues from food safety

Issue Suggested Progression

Biosecurity Consult industry & AQIS

TOR 4 and TOR 5:

Qualitative Risk Assessment Tool

Production, processing or handling of food

Consumer terminal step

Table 1: Maximum levels for cadmium in seafood (EFSA, 2009)

Table 2: Exports of prawns from Australia to the EU (2005-2009)

2005-06 2006-07 2007-08 2008-09

Qualitative Risk Assessment

Several conflicting statements contained in ANZFA (1999b) are of relevance, particularly in

Qualitative Risk Assessment

Allergens Added During Processing

Year Product Format Hazard Country of origin*

Qualitative Risk Assessment

Qualitative Risk Assessment

Issue 1: Biotoxin Testing of Bivalves

Issue 2: US Equivalence of Bivalve Testing

Year Origin Agent Cases Reference

Area 1: Heavy Metals in Australian Seafoods

Area 2: Watching Brief

Potential regulation of cyclic imines (e.g. pinnatoxins) in shellfish

Area 3: Market access

Review of import testing

Vibrios in bivalve molluscs

Table 1: Attendees at SafeFish food safety meeting (Canberra, June 3, 2011)

Cath McLeod SARDI Food Safety

NRVP data (1988-2001) OzFoodNet data (2001-2010)

State Number of outbreaks

Table A3: Species associated with ciguatera outbreaks (after OzFoodNet)

Species Number of outbreaks

A full listing of hazards and outbreak settings is presented in Tables B1-B4.

Table A4: Recalls of seafood listed by FSANZ (1999-2011)

Year Product Format Hazard Country

Food Pathogen Cases Year Reference

Food Business Product Toxin Cases (deaths) Year Reference

Source Hazard Country Cases (deaths) Year Reference

Year State Setting Hazard Cases Product

Setting Pathogen Cases (deaths) Year Reference

Unique Host Susceptibility Factors

Unique Host Susceptibility Factors

Food (% positive) Viruses detected Reference

Norovirus and HAV have been linked to shellfish-associated gastroenteritis in Australia

Growth and Survival

Mean mercury (mg/kg) Number of samples in parentheses

Sushi/sashimi: Consumption Frequency and Demographics

Nematodes (roundworms) and Cestodes (tapeworms)

Nematodes (rounds worms)

Cestodes (tape worms)

Acanthocephala (spiny headed worms).

Scientific Name (common name) Number Number of

Infectious Dose/Dose Response

Critical Control Points and/or Management Options

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