most common algal species incriminated in paralytic
shellfish poisoning are Gonyaulax catenella and
G. tamarensis. The blooms of the toxic dinoflagel-
lates are quite sporadic, so shellfish are hazardous
only at certain times. Most shellfish clear the toxins
from their system within a few weeks after the end of
a dinoflagellate bloom, but some shellfish species,
especially the Alaskan butter clam, appear to retain
the toxins for long periods. The toxins involved in
paralytic shellfish poisoning are known as saxitoxins.
These are neurotoxins that act by blocking the pas-
sage of sodium ions into the nerve cells, an essential
process in nerve transmission. The symptoms of para-
lytic shellfish poisoning include a tingling sensation
and numbness of the lips, tongue, and fingertips,
followed by numbness in the legs, arms, and neck
with general muscular incoordination. Respiratory
distress and muscular paralysis often occur. Death
from respiratory failure can occur within 2–12 h
depending on the dose. If the victim survives 24 h,
the prognosis for a full recovery is good. No antidote
exists for paralytic shellfish poisoning.
0016 Pufferfish poisoning occurs more rarely because
pufferfish are not frequently consumed except in
Japan and China. About 30 species are found world-
wide, but most are not poisonous. The most poison-
ous species occur along the coasts of Japan and
China. The most choice, edible species belonging to
the genus Fugu are the most poisonous and the most
commonly consumed. The toxin in pufferfish accu-
mulates in the ovaries, liver, intestine, skin, and roe
(egg sac), so a carefully cleaned and eviscerated puf-
ferfish may be safe to eat. Pufferfish likely become
toxic through the ingestion of toxic dinoflagellate
algae, although the food-chain relationships have
not been completely elucidated. The toxin involved
in pufferfish poisoning is a potent neurotoxin called
tetrodotoxin, which also acts by blocking the sodium
channel in nerve cells. The symptoms resemble those
of paralytic shellfish poisoning. Death can result if a
sufficient dose of tetrodotoxin is ingested.
0017 Mycotoxins Mycotoxins are produced by a wide
variety of molds that can grow on a wide variety of
foods. The toxicity of many of the mycotoxins has
been recognized by observing domestic animals fed
moldy animal feeds. Their effects on humans are not
so clearly established, although they are potentially
hazardous to humans as well. (See Mycotoxins: Toxi-
cology.)
0018 Historically, ergotism was the first mycotoxin-as-
sociated illness recognized in humans. Claviceps
purpurea is the responsible mold, which infects the
heads of rye and sometimes wheat, barley, and oats.
The shriveled, purplish grain kernel contains the
mycotoxin. Ergotism is caused by a group of toxins
known collectively as the ergot alkaloids and can be
manifested in two forms: gangrenous ergotism and
convulsive ergotism. In the former, also known as
St. Anthony’s fire, a burning sensation in the feet
and hands is followed by a progressive restriction of
blood flow to the hands and feet. This results in
gangrene, which can lead to the loss of limbs. Con-
vulsive ergotism involves hallucinations leading to
convulsive seizures and sometimes death. No out-
breaks of ergotism have been recorded since the
early 1950s.
0019Aspergillus molds are known to produce several
types of mycotoxins, most notably the aflatoxins
and ochratoxin. The aflatoxins are produced primar-
ily by Aspergillus flavus and A. parasiticus and often
contaminate moldy peanuts and corn. Feeding of
aflatoxin-contaminated grains or oilseeds to dairy
cows can result in aflatoxin contamination of milk.
The aflatoxins are potent carcinogens, especially
affecting the liver. The role of aflatoxins in human
carcinogenesis remains uncertain, but they are among
the most potent animal carcinogens known. (See
Aflatoxins.) Ochratoxin is produced primarily by A.
ochraceus, which can contaminate cereals, peanuts,
and tree nuts. Ochratoxin affects both the livers and
kidneys of domestic animals, with the effects on the
kidney being particularly damaging. The toxicity of
ochratoxin to humans is unknown.
0020Fusarium molds produce a number of different
mycotoxins, including the trichothecenes, fumoni-
sins, and zearalenone. The trichothecenes are known
to cause human illness and can be found as contam-
inants of grains primarily. Alimentary toxic aleukia
(ATA) was observed in the former Soviet Union,
owing to consumption of grains containing trichothe-
cenes. ATA has four stages. In the first stage, a person
experiences a burning sensation in the mouth and
throat, which proceeds down the esophagus to the
stomach. This is followed by diarrhea, nausea, and
vomiting, occurring 1–3 days later and ceasing after
about 9 days. The second stage occurs from about 2
weeks to 2 months and involves bone-marrow de-
struction, leukemia, agranulocytosis, anemia, and
loss of platelets. At the end of this stage, small hem-
orrhages may occur on the skin. The third stage of
ATA lasts from 5 to 20 days and involves total loss of
bone marrow with necrotic angina, sepsis, total
agranulocytosis, and moderate fever. The hemor-
rhages become larger, and necrotic lesions appear on
the skin. Bronchial pneumonia appears, along with
abscesses and hemorrhages in the lungs. The fourth
stage is death, with the mortality rate approaching
80% and dependent on the dose and frequency of
exposure to the trichothecenes.
5816 TOXINS IN FOODS – NATURALLY OCCURRING