Ciguatoxin: A seafood toxin that is acquired by eating fish that have consumed toxic single-celled marine

organisms called dinoflagellates or fish that have consumed other fish that have become toxic. When
someone eats these fish, they suffer seafood poisoning. Food poisoning from ciguatoxin is called
ciguatera.
Ciguatera can cause gastrointestinal, neuromuscular symptoms and respiratory problems. The
gastrointestinal problems include abdominal pain, diarrhea, nausea and vomiting. The
neuromuscular problems may include tingling around the lips, abnormal or impaired skin sensations,
hot-to-cold reversal, vertigo, lack of muscle coordination, weakness and numbness, muscle pain,
and itching. There may be respiratory paralysis. Ciguatera symptom strike shortly after eating tainted
fish. Symptoms may recur up to 6 months. Death is uncommon, but is known.
Fish with ciguatoxin come from the southeastern United States, Bahamian, and Caribbean regions,
Hawaii, and subtropical and tropical areas worldwide including the central Pacific and northern
Australia. Barracuda, amberjack, horse-eye jack, black jack, other large species of jack, king mackerel,
large groupers, and snappers are particularly likely to contain ciguatoxin. Many other species of large
fish-eating fish may also contain ciguatoxin.
Ciguatoxins
Are a class of toxic polycyclic polyethers found in fish that cause ciguatera. There are several different
chemicals in this class. "CTX" is often used as an abbreviation. Ciguatoxins are lipid-soluble cyclic
polyethers structurally similar to brevetoxins. Several variants occur; however, the most common and
potent is ciguatoxin-1 (Figure 38.11). Although water-soluble toxins, such as maitotoxin, coexist
with ciguatoxinsin G. toxicus, and can be isolated from digestive tracts of herbivorous fish, the
concentrations in muscle tissues are so low that they are deemed unlikely to be a major cause of
toxicosis in people who eat fish.
Ciguatoxins act as agonists at receptors on voltage-gated sodium channels of neuromuscular junctions,
sensory neuron membranes, and other excitable cells. Both cholinergic and α-andrenergic receptors are
affected by ciguatoxins. Like brevetoxins, they act on site 5 of the alpha subunit of the sodium channel
receptor to increase excitability and prolong refractory periods of sensory and motor nerves. The result
of high-affinity interaction of ciguatoxins for such sodium channels is the opposite effect of tetrodotoxin
or saxitoxin, which block sodium channels. In vitro, ciguatoxin induces contraction of the ileum and
exerts a positive inotropic effect on guinea pig cardiac muscle.
Mycotoxins are secondary metabolites produced by microfungi that are capable of causing disease and
death in humans and other animals. Because of their pharmacological activity, some mycotoxins or
mycotoxin derivatives have found use as antibiotics, growth promotants, and other kinds of drugs; still
others have been implicated as chemical warfare agents. This review focuses on the most important
ones associated with human and veterinary diseases, including aflatoxin, citrinin, ergot akaloids,
fumonisins, ochratoxin A, patulin, trichothecenes, and zearalenone.
Fungi are major plant and insect pathogens, but they are not nearly as important as agents of disease in
vertebrates, i.e., the number of medically important fungi is relatively low. Frank growth of fungi on
animal hosts produces the diseases collectively called mycoses, while dietary, respiratory, dermal, and
other exposures to toxic fungal metabolites produce the diseases collectively called mycotoxicoses.
Mycotoxins are a group of naturally occurring chemicals produced by certain molds. They can grow on a
variety of different crops and foodstuffs including cereals, nuts, spices, dried fruits, apple juice and
coffee, often under warm and humid conditions.
The mycotoxins of most concern from a food safety perspective include the aflatoxins (B1, B2, G1, G2
and M1), ochratoxin A, patulin and toxins produced by Fusarium moulds, including fumonisins (B1, B2
and B3), trichothecenes (principally nivalenol, deoxynivalenol, T-2 and HT-2 toxin) and zearalenone.
Mycotoxins can cause a variety of adverse health effects in humans. Aflatoxins, including aflatoxin B1
are the most toxic and have been shown to be genotoxic i.e. can damage DNA and cause cancer in animal
species. There is also evidence that they can cause liver cancer in humans. Other mycotoxins have a range
of other health effects including kidney damage, gastrointestinal disturbances, reproductive disorders or
suppression of the immune system. For most mycotoxins, a tolerable daily intake (TDI) has been
established, which estimates the quantity of mycotoxin which someone can be exposed to daily over a
lifetime without it posing a significant risk to health.
In order to protect consumer safety, rules and strict legislative limits for aflatoxins, ochratoxin A, patulin
and Fusarium toxins in certain foodstuffs are set out in European Commission legislation. The legislation
applies to the specified foods whether they are imported into the UK or produced in the UK. In addition,
there are a number of special import conditions currently in place for some foods from certain third
countries where the risk from aflatoxin contamination is increased, which further improves consumer
protection.
The Agency has produced several pieces of guidance and advice to industry including farmers to advise
them on the agronomic and storage practices to help to reduce the contamination of cereals with
mycotoxins and therefore the likelihood of exceeding the current European legal limits.
Scombrotoxin formation as a result of time/temperature abuse of certain species of fish can cause
consumer illness. The illness is most closely linked to the development of histamine in these fish. In most
cases histamine levels in illness-causing fish have been above 200 ppm, often above 500 ppm. There are
indications that decomposition can result in the production of other toxins (e.g. biogenic amines, such as
putrescine and cadaverine) that have the potential to cause illness, even in the absence of histamine
formation. Such illnesses have been reported in a number of fish species. FDA has also received a
number of consumer complaints concerning illnesses that are associated with the consumption of
decomposed shrimp (FDA, 2001a; FDA, 2001b). Scombroid poisonings have primarily been associated
with the consumption of tuna, mahi mahi, and bluefish. However, Table #3-1 lists a number of species
that are also capable of developing elevated levels of histamine when temperature abused.
The kinds of bacteria that are associated with histamine development are commonly present in the salt
water environment. They naturally exist on the gills and in the gut of live, salt water fish, with no harm
to the fish. Upon death, the defense mechanisms of the fish no longer inhibit bacterial growth, and
histamine-forming bacteria start to grow and produce histamine. Evisceration and removal of the gills in
a sanitary manner may reduce, but not eliminate, the number of histamine-forming bacteria. However,
when done under insanitary conditions, these steps may accelerate the process of histamine
development in the edible portions of the fish by spreading the bacteria to the flesh of the fish. With
some harvesting practices, such as long lining, death can occur before the fish is removed from the
water. Under the worst conditions histamine formation can already be underway before the fish is
landed on the vessel. This condition can be aggravated when the fish is allowed to remain on the line for
a period of time after death, a situation that in certain tuna species may cause its internal temperature
to increase to a more favorable growth range for the enzymeforming bacteria.
Histamine or scombrotoxin is a foodborne toxin that is associated with the consumption of fish,
particularly species belonging to the Scombridae and Scomberesocidae families (scombroid
fish), such as mackerel and tunas.
Paralytic shellfish poisoning (PSP) is a serious illness caused by
eating shellfishcontaminated with dinoflagellate algae that produce harmful toxins. Some of
thesetoxins are 1,000 times more potent than cyanide, and toxin levels contained in a
single shellfish can be fatal to humans.

Shellfish poisoning includes four (4) syndromes that share some common features and are
primarily associated with bivalve molluscs(such
as mussels, clams, oysters and scallops.)[1] These shellfish are filter feeders and, therefore,
accumulate toxins produced by microscopic algae, such
as cyanobacteria, diatoms and dinoflagellates.

The syndromes are:

 Amnesic shellfish poisoning (ASP)

 Diarrheal shellfish poisoning (DSP)
 Neurotoxic shellfish poisoning (NSP)
 Paralytic shellfish poisoning (PSP)
Shellfish poisoning is a general term used to indicate poisoning that occurs when
shellfish (mainly oysters, clams, scallops or mussels) are eaten by humans. Shellfish
are usually associated with saltwater habitats, but some species inhabit freshwater.
Both freshwater and saltwater shellfish may cause poisoning. Because the symptoms of
shellfish poisoning are somewhat similar and patients often did not know exactly what
type of shellfish they ate, the tendency of the medical community was to simply lump
the symptoms together and diagnose "shellfish poisoning" for any shellfish-related
problem. However, more recent clinical studies have separated the group of shellfish
poisonings into four groups:

1. Amnesic shellfish poisoning (ASP)

2. Diarrheal shellfish poisoning (DSP)
3. Neurotoxic shellfish poisoning (NSP)
4. Paralytic shellfish poisoning (PSP)

These groups are based on the specific toxins or chemicals that poison humans; they
cause specific and nonspecific symptoms. The toxins can accumulate in many different
types of shellfish (see above) because the shellfish are filter-feeders and consume
marine diatoms and algae that may contain the chemicals. If shellfish consume high
levels of the foods that produce the poisons, the shellfish then contain high levels of
poison that can be absorbed by humans when they eat the shellfish. In addition,
shellfish may concentrate other things such as bacterial and viral pathogens while filter-
feeding and transfer these pathogens to people when the shellfish are eaten. These
problems are discussed in other articles (for example, Vibrio infections). The goal of this
article is to acquaint the reader with shellfish poisoning.