NATURALLY OCCURRING
FISH AND SHELLFISH
POISONING
1
High risk groups
•
Consumers of raw molluscan shellfish
•
Consumers of recreational fishery products
•
Consumers of subsistence fishery products
2
Various types of naturally occurring fish
and shellfish poisoning:
•
Diarrhetic shellfish poisoning ( DSP )
•
Ciguatera poisoning
•
Scombroid poisoning
•
Paralytic shellfish poisoning ( PSP )
•
Neurotoxic shellfish poisoning ( NSP )
•
Puffer fish poisoning
•
Amnesic shellfish poisoning ( ASP )
3
Diarrhetic Shellfish Poisoning (DSP)
•
caused by ingestion of mussels, scallops or clams
that have been feeding on the dinoflagellate
Dinophysis fortii or D. acuminata and other species
of Dinophysis and possibly Prorocentrum sp.
•
common in Japan and has become a problem in
Europe
4
Symptoms
•
Diarrhea
•
Nausea
•
Vomiting
•
Abdominal pain
•
Onset of symptoms occurs from 30 minutes to a
few hours after eating toxic shellfish, and the
duration is usually short with a maximum of a few
days in severe cases
•
The disease is not life threatening
5
•
At least five toxins have been isolated from
dinoflagellates and shellfish.
•
Okadaic acid is most commonly encountered in
Europe where D. acuminata is the usual agent.
•
Mixtures of okadaic acid, dinophysistoxins and
pectenotoxins are detected in cases in Japan,
usually involving D. fortii ( Yasumoto and
Murata, 1990 ).
•
There is a mouse assay for the toxins.
6
Ciguatera poisoning
•
Clinical syndrome caused by eating the flesh of
toxic fish caught in tropical reef and island
waters
•
Toxin originates in a microscopic dinoflagellate
alga, Gambierdiscus toxicus that grows on reefs
(Bangnis et al., 1980)
•
Other benthic algae have also been implicated
•
Fish eating the algae become toxic, and the
effect is magnified through the food chain so
that the large, predatory fish become the most
toxic
7
•
occurrence of toxic fish - localized
•
>400 species of fish have been implicated in
ciguatera poisoning
• fish most commonly implicated:
• Amberjack
• Snapper
• Grouper
• Barracuda
• Goatfish
• Reef fish belonging to the family
Carangidae
8
Groupers (Kossa)



Reef dwelling
Usually not
poisonous
Ciguatoxic in
some countries
9
Snappers (Atissa)



Reef dwelling
Ciguatoxic in
some countries
Non poisonous in
Sri Lanka
10
Barracuda (Jeelava)




Common on reefs
Large predators
Can be aggressive
Reported to be
ciguatoxic in some
parts of the world
11
•
The disease affects both the gastro-intestinal and
neurological systems
•
Gastro-intestinal symptoms:
• Diarrhea
• Nausea
• Vomiting
• Abdominal pain
•
Appear 3-5 hours after ingestion of the fish and are
of short duration
•
Neurological symptoms begin 12-18 hours after
consumption of the fish and may be moderate to
severe
•
Commonly last for 1 - 82 days but may persist for
several months.
12
•
In rare cases, symptoms may last for years, and get
worse in association with fish consumption or
possibly alcohol.
Symptoms typically include:
• hot-cold inversion (hot coffee taste cold, ice cream
tastes hot)
• muscular aches
• tingling and numbness of lips. tongue and perioral
region
• metallic taste
• dryness of mouth
• anxiety
• extreme physical weakness
• dizziness, chills, sweating, dilated pupils, blurred
vision and temporary blindness
• paralysis and death may occur in a few extreme
13
cases
•
Several toxic compounds have been isolated from
ciguatoxic fish and from Gambierdiscus.
•
The principal toxin called “ciguatoxin” is a small,
lipid-soluble polyether with a molecular weight of
1,112 (Schueuer et. al., 1967).
•
This toxin has been purified and its structure
determined (Murata et. al., 1990).
•
Ciguatoxin ( CTX ) has a molecular formula of
C60H88O19 and is a brevitoxin-type ether, about 100
times more potent than tetrodotoxin.
•
Ciguatoxin opens voltage-dependent sodium
channels in cell membranes (Bidard, 1984), and
studies in vitro of tissue preparations suggest that
the toxin causes a nerve conduction block after
initial neural stimulation.
14
15
•
Another lipid-soluble neurotoxin from ciguateric
fish is called “scaritoxin”.
•
The pharmacological action is close to that of
ciguatoxin, and they may be related compounds.
•
Another toxin found, called “maitotoxin”, is a
water-soluble toxin that may interfere with or
modify calcium movement or calcium
conductance in tissues.
16
•
In the USA, the reported incidence of ciguatera is
about 15 - 20 outbreaks per year, involving 50 100 cases.
•
For the majority of US consumers, the disease
can be contracted only from fish imported from
endemic areas.
•
For the residents in endemic areas, safety
depends on abstinence from eating reef fish.
•
The Amberjack (Seriola dumerii Kahala ) is not
sold commercially in Hawaii because of the known
high incidence of ciguatoxic fish of this species.
17
•
Control options are limited by the impossibility of
detecting toxic fish by organoleptic inspection.
•
At present, the only ciguatera screening
programme in existence is that employed by the
Tokyo Central Wholesale Fish Market in Japan.
•
Muscle extracts are prepared and tested on cats
and mice for evidence of ciguatoxicity. This is a
lengthy and expensive screening technique.
18
•
A radioimmunoassay (RIA ) was developed by
Hokama and co-workers in Hawaii ( Hokama et.
al., 1977 ) and then modified to a simpler enzyme
immunoassay (Hokama 1985).
•
The method has been further simplified to a “stick”
test that has been used to screen fish landed in
Hawaii and holds promise as a practical basis for
control (Hokama et. al., 1989b).
•
The stick test measures ciguatoxin and polyether
compounds, including okadaic acid.
•
This whole area needs further research,
particularly because of the concern over falsepositive results from the stick test.
19
•
Research is needed into methods for predicting
the development of ciguateric conditions in reef
fishing
areas,
perhaps
by
assessing
Gambierdiscus or other toxigenic microorganism
populations and somehow closing such areas to
fishing when the risk is high.
•
The risk of contracting ciguatera poisoning are
low for most consumers in the mainland United
States. Risks are much higher in Hawaii, other
Pacific islands, Puerto Rico and the Virgin
Islands. There are moderate risks in areas such
as Miami.
20
Paralytic shellfish poisoning (PSP)
•
Results from ingesting bivalve molluscs (mussels,
clams, oysters, scallops) which have consumed
toxigenic dinoflagellates (Halstead and Schantz,
1984; Schantz, 1973).
•
Toxins are assimilated and temporarily stored by
the shellfish.
•
Outbreaks occur mostly when these shellfish are
gathered and eaten by recreational collectors from
closed areas.
•
In the USA, during 1978-1986, 12 outbreaks
involving 134 people with one death were
21
recorded.
•
PSP is potentially life threatening because the
toxins involved are among the most poisonous
known.
•
Symptoms are neurological and normally appear
within an hour of eating toxic shellfish. They
include:
• Tingling
• Numbness
• burning sensation of the lips and fingertips
• Ataxia
• Giddiness
• Staggering
• Drowsiness
• Dry throat and skin
• Incoherence
• Rash and fever
22
•
In severe cases, respiratory paralysis occurs,
which can cause death during the first 24 hours.
•
No antidote is known.
•
Immunity is not conferred and multiple incidence
can occur.
•
The cause of PSP is a complex of toxins known
as saxitoxins, including saxitoxin, neotoxin and
gonyautoxins.
•
In the USA, the toxic dinoflagellates of importance
are Gonyaulax catenella and G. tamarensis.
23
•
The saxotoxins are neurotoxins which act by
blocking the flow of sodium (Na+) ions through the
sodium channels of the nerves.
•
The lethal dose for humans is 1 - 4 mg expressed
as saxitoxin equivalents (Schantz, 1986)
•
FDA action limit is 80g of toxin per 100g of
shellfish tissue.
•
The classic method for analysis of saxitoxins is by
mouse bioassay.
24
•
The chemical analytical methods which have used
include column separation, thin-layer
chromatography, and fluorescence assays, either
directly or after separation by high performance
liquid chromatography (HPLC).
•
Recently, immunoassay methods have been
developed and reported (Sullivan and Iwaoka,
1983).
•
These involve rabbit serum antibody preparations
and monoclonal antibodies, and both
radioimmunoassays and enzyme-linked
immunoabsorbant assays ( ELISA ) have been used
(Chu and Fan, 1985). So far, these methods are not
acceptable for regulatory use.
25
•
The occurrence of blooms of toxic dinoflagellates
are not predictable.
•
When these blooms occur, shellfish become
toxic and remain toxic for several weeks after the
bloom subsides.
•
Protection of the consumer is achieved by
closure of shellfish harvesting in affected areas.
•
Warnings are issued through the media, posted
on public beaches and a surveillance system is
carried out.
•
Commercial producers are required to submit
samples for testing.
26
27
Neurotoxic shellfish poisoning
Neurotoxic shellfish poisoning (NSP)
•
Also known as brevetoxic shelling poisoning
(BSP)
•
Caused by ingesting shellfish which have fed on
the red tide organism, Gymnodinium breve.
•
The red tides can be observed as a red
colouration of the seawater, and the organisms
can be seen under the microscope.
•
Irritant aerosols, produced by wind and wave
action, cause respiratory distress. If there is
more than 5,000 G. breve cells per litre of
seawater, a ban on shellfish harvesting is
imposed.
Surveillance and closure systems
have been found to be effective.
28
Neurotoxic shellfish poisoning
Symptoms include:
•
•
•
•
•
Tingling
Numbness of the lips, tongue, throat and perioral
area
Muscular aches
Gastrointestinal upset
Dizziness
•
The symptoms appear to be due to two
brevetoxins produced by G. breve that bind to
nerve cells (Baden et. al.,1984).
•
The intoxication is usually not fatal. There is no
antidote.
29
Fish Kills due to Harmful Algal Blooms
toxic dinoflagellate
Gymnodinium breve
30
Algal blooms
31
Puffer fish poisoning
•
Results from the ingestion of the flesh of certain
species of fish belonging to the family
Tetraodontidae.
•
The toxin involved is called tetrodotoxin.
•
The toxicity of poisonous puffers fluctuates
greatly.
•
It has recently been shown that certain common
marine vibrios can produce a form of the toxin,
and because they occur as part of the microflora
of puffer fish, may be implicated in toxicity
development (Narita et. al., 1987).
32
•
There are 20 - 100 deaths from puffer fish (fugu)
poisoning each year.
•
The symptoms are similar to those described for
paralytic shellfish poisoning.
•
Tetradotoxin also blocks sodium channels.
•
No antidote has been identified.
•
The lethal dose for humans is 1 - 4 mg of
tetradotoxin.
33
Boxfishes and pufferfishes (Peththaya)



Reef and sand
dwelling
Most have
poison
Should not be
eaten
34
Amnesic Shellfish Poisoning (ASP)
Amnesic Shellfish Poisoning (ASP)
•
The severe symptoms of this poisoning are
caused by domoic acid.
•
The toxin is present in some varieties of the
diatom, Nitzchia pungens and accumulated in
mussels and clams.
Symptoms include:
• Vomiting
• Abdominal cramps
• Diarrhea
• Disorientation and memory loss ( Perl et. al.,
1988; Teitelbaum et al., 1990 ).
• Short term memory loss is the most common
symptom.
35
Amnesic Shellfish Poisoning (ASP)
•
Autopsies on three fatalities showed necrosis of
the hippocampus.
•
The poisoning has a particularly severe effect
among older people.
•
Canadian authorities now enforce closure of beds
when levels of 20 g /g are detected in the tissues
of mussels and clams (Gilgan et. al., 1989).
36
Butterflyfish (Panawa)



Reef dwelling
Sometimes in
bottom set net or
trawl net catches
Should not be used
as a food fish
37
Surgeonfish (Dhetta)


Reef
dwelling
Has a mild
poison in
spines
38
Squirrelfish and soldierfish
(Balalmaruwa)


Reef
dwelling
Has a mild
poison in
spines
39
Scorpionfish (Ginimaha, Gonmaha)



Reef
dwelling
Highly
venomous
Should not
be eaten
40
Rays and skates (Maduwa)


Reef and
sand
dwelling
Almost all
have a
poison gland
and sting
41
Moray eels (Galgulla)



Reef dwelling
Non poisonous
Eaten in some
countries, not
in Sri Lanka
42
Angelfish (Nambah)



Reef dwelling
Sometimes in
bottom set or
trawl net catches
Should not be
used as a food
fish
43