Marine Dinoflagellate-Associated Human Poisoning 33.5 Toxigenic Dinoflagellate-Associated Human Poisoning 801
Part F | 33.5
Sources
People can become ill after ingesting filter-feeding
bivalve shellfish (e.g., oysters, mussels, clams) that concentrate the toxin and are subsequently consumed by
predators, including humans.
Prevalence
The largest documented outbreak of NSP occurred
in New Zealand in 1992–1993 with over 180 cases
reported over a period of several weeks. Green mussel, cockles, and oysters were implicated in the New
Zealand clusters [33.93–98]. Scattered reports of cases
have occurred in Florida in recent years with two
cases in 1995, three in 1996, two in 2001, and four
in 2005 [33.99, 100]. Many reports of NSP involve
a single case or small case series [33.101–104] with
few large outbreaks recorded. The largest and best
documented outbreak in the USA occurred in North
Carolina, 48 documented cases. It began in October
1987 when a Karenia brevis bloom became entrained in
the Gulf Stream off eastern Florida and was transported
up the eastern seaboard [33.105].
Range
NSP causes health problems around the Gulf of Mexico and the Atlantic coast of the southern USA, The
Caribbean, and New Zealand.
Causative Dinoflagellates
and Poisonous Ingredients (Toxins)
The classic causative dinoflagellate Gymnodinium
breve (Ptychodiscus brevis) is found in the Caribbean
and the Gulf of Mexico, although similar species occur throughout the world. The Gymnodinium breve is
relatively fragile and easily breaks open, releasing the
endotoxins. It produces two types of lipid soluble toxins: hemolytic and neurotoxic. The neurotoxic toxins
are known as brevetoxins. The major brevetoxin produced is PbTx-2; lesser amounts of PbTx-1, PbTx-3,
and hemolytic components are produced. The massive
fish kills are due to neurotoxin exposure, with a possible contribution of the hemolytic fraction. They disturb
neuromuscular transmission. After being inhaled as
aerosol they cause bronchial spasms. This may be manifested as an asthma crisis, rhinitis, sneezing, cough, or
burning eyes after walking on the beach while a strong
breeze splashes up water (with the toxin). With the inhalation of the aerosolized red tide toxins (especially
the brevetoxins) from the sea spray, respiratory irritation and possibly other health effects have been reported
in both humans and other mammals.
Action Mechanism
Brevetoxins act by disrupting the flow of Na
C ions in
nerve cells. They bind to sites near the voltage gated
sodium channels, allowing an unchecked flow of Na
C
ions into or out of the cell. This disruption of ion flow
within nerve cells is responsible for the neurological
effects associated with NSP. Incidentally, brevetoxins
have nearly the opposite effect to STXs, which bind to a
different site and effectively block Na
C ions from passing through the sodium channel (NIEHS 2000).
Lethal Dose
The pathogenic dose for humans is in the order of
4272 mouse units. In human cases of NSP, the brevetoxin concentrations present in contaminated clams
have been reported to be 3018 g (78120 g mg
1 ).
Regulatory Tolerances by FDA
The FDA tolerances are 0:8 ppm brevetoxin-2 equivalent (20 mouse units/100 g) in clams, mussels and
oysters. In the USA, legislation has been set by the
FDA; the current regulatory limit is 800 g brevetoxin2 (PbTx-2) equivalents kg
1 shellfish [33.102]. At the
time of writing, the European Food Safety Authority
(EFSA) had not published a scientific opinion on NSPtype toxins.
Incubation Period
The time to onset is anywhere from 15 min to 12 h
(mean time of 3 h).
Symptoms
Symptoms begin 13 h after eating the contaminated
shellfish and include numbness, tingling in the mouth,
arms and legs, incoordination, and gastrointestinal upset. As with ciguatera poisoning, some patients report temperature reversal. In addition, formation of
toxic aerosols by wave action can produce respiratory asthma-like symptoms. They are similar to
ciguatoxins in that they are sodium channel openers that cause neuroexcitatory effects. This results
in neurological complaints such as paresthesia, temperature reversal, and ataxia, as well as GI symptoms such as nausea, abdominal pain, and diarrhoea.
Symptoms are generally mild and self-limited. NSP
presents itself as a milder gastroenteritis with neurologic symptoms compared with PSP. The symptoms
of NSP include nausea, tingling and numbness of
the perioral area, loss of motor control, and severe
muscular pain [33.106, 107]. Paresthesia is foremost
here.
Part F | 33.5
Sources
People can become ill after ingesting filter-feeding
bivalve shellfish (e.g., oysters, mussels, clams) that concentrate the toxin and are subsequently consumed by
predators, including humans.
Prevalence
The largest documented outbreak of NSP occurred
in New Zealand in 1992–1993 with over 180 cases
reported over a period of several weeks. Green mussel, cockles, and oysters were implicated in the New
Zealand clusters [33.93–98]. Scattered reports of cases
have occurred in Florida in recent years with two
cases in 1995, three in 1996, two in 2001, and four
in 2005 [33.99, 100]. Many reports of NSP involve
a single case or small case series [33.101–104] with
few large outbreaks recorded. The largest and best
documented outbreak in the USA occurred in North
Carolina, 48 documented cases. It began in October
1987 when a Karenia brevis bloom became entrained in
the Gulf Stream off eastern Florida and was transported
up the eastern seaboard [33.105].
Range
NSP causes health problems around the Gulf of Mexico and the Atlantic coast of the southern USA, The
Caribbean, and New Zealand.
Causative Dinoflagellates
and Poisonous Ingredients (Toxins)
The classic causative dinoflagellate Gymnodinium
breve (Ptychodiscus brevis) is found in the Caribbean
and the Gulf of Mexico, although similar species occur throughout the world. The Gymnodinium breve is
relatively fragile and easily breaks open, releasing the
endotoxins. It produces two types of lipid soluble toxins: hemolytic and neurotoxic. The neurotoxic toxins
are known as brevetoxins. The major brevetoxin produced is PbTx-2; lesser amounts of PbTx-1, PbTx-3,
and hemolytic components are produced. The massive
fish kills are due to neurotoxin exposure, with a possible contribution of the hemolytic fraction. They disturb
neuromuscular transmission. After being inhaled as
aerosol they cause bronchial spasms. This may be manifested as an asthma crisis, rhinitis, sneezing, cough, or
burning eyes after walking on the beach while a strong
breeze splashes up water (with the toxin). With the inhalation of the aerosolized red tide toxins (especially
the brevetoxins) from the sea spray, respiratory irritation and possibly other health effects have been reported
in both humans and other mammals.
Action Mechanism
Brevetoxins act by disrupting the flow of Na
C ions in
nerve cells. They bind to sites near the voltage gated
sodium channels, allowing an unchecked flow of Na
C
ions into or out of the cell. This disruption of ion flow
within nerve cells is responsible for the neurological
effects associated with NSP. Incidentally, brevetoxins
have nearly the opposite effect to STXs, which bind to a
different site and effectively block Na
C ions from passing through the sodium channel (NIEHS 2000).
Lethal Dose
The pathogenic dose for humans is in the order of
4272 mouse units. In human cases of NSP, the brevetoxin concentrations present in contaminated clams
have been reported to be 3018 g (78120 g mg
1 ).
Regulatory Tolerances by FDA
The FDA tolerances are 0:8 ppm brevetoxin-2 equivalent (20 mouse units/100 g) in clams, mussels and
oysters. In the USA, legislation has been set by the
FDA; the current regulatory limit is 800 g brevetoxin2 (PbTx-2) equivalents kg
1 shellfish [33.102]. At the
time of writing, the European Food Safety Authority
(EFSA) had not published a scientific opinion on NSPtype toxins.
Incubation Period
The time to onset is anywhere from 15 min to 12 h
(mean time of 3 h).
Symptoms
Symptoms begin 13 h after eating the contaminated
shellfish and include numbness, tingling in the mouth,
arms and legs, incoordination, and gastrointestinal upset. As with ciguatera poisoning, some patients report temperature reversal. In addition, formation of
toxic aerosols by wave action can produce respiratory asthma-like symptoms. They are similar to
ciguatoxins in that they are sodium channel openers that cause neuroexcitatory effects. This results
in neurological complaints such as paresthesia, temperature reversal, and ataxia, as well as GI symptoms such as nausea, abdominal pain, and diarrhoea.
Symptoms are generally mild and self-limited. NSP
presents itself as a milder gastroenteritis with neurologic symptoms compared with PSP. The symptoms
of NSP include nausea, tingling and numbness of
the perioral area, loss of motor control, and severe
muscular pain [33.106, 107]. Paresthesia is foremost
here.