TOXIC

SUBSTANCES
Cells of Alexandrium IN FOOD

Algal
Fungal
Bacterial
 Microbial Toxins in Foods
Aquatic Bio-toxins
- Marine toxins: shellfish & fish
- Freshwater toxins

Myco-toxins (produced by certain fungus)

Bacterial Toxins
- Toxico-infections
- Intoxications
Aquatic Bio-toxins in Seafood
and Fresh Water
Microscopic planktonic algae as a source of food
for lter-feeding bivalve shellsh proliferate
algal bloom.
Marine Toxins: Shellfish
Paralytic Shellsh Poisoning (PSP)

has been known in Europe & America since the 17th century.
Documented in the Philippines, Argentina, Japan,
Mediterranean, the Atlantic coast of Spain, Gulf of California,
Gulf of Mexico, Portugal, and the Northeastern & Western
coastlines of the U.S

PSP-toxin producers:
- Dinoagellates - genera Alexandrium (formerly Gonyaulax)
, Pyrodinium , and Gymnodinium
- Freshwater blue-green algae, such as Aphanizomenon
osaquae saxitoxin and neosaxitoxin
- A red macroalga, Jania sp. gonyautoxins 1-3 (GTX) &
saxitoxin.
Paralytic Shellfish Poisoning mechanism
The mechanism of action of PSP the toxins block
the sodium channels associated with nervous
conduction, affecting the respiratory,
neuromuscular, and cardiovascular systems.
The lethal dose for humans is 1 to 4 mg expressed as
STX (saxitoxin) equivalents.
Symptoms usually observed in humans include tingling
and numbness around the lips and extremities leading
to respiratory paralysis.
Diarrheic Shellsh Poisoning (DSP)

A gastrointestinal disturbance resulting from ingestion

of shellsh (mussels, oysters and or scallops) infested
with dinoagellate toxins

DSP-toxin producers:
D.fortii, D. rotundata, D. tripos, D. acuta, D. noruegica,
& D. acuminata okadaic acid (OA) &/or
dynophysistoxin-1 (DTX-1)
Prorocentrum lima okadaic acid (OA) &
dynophysistoxin-1 (DTX-1)
Diarrheic Shellsh Poisoning (DSP)

Symptoms: incapacitating diarrhea, nausea,

vomiting, abdominal cramps, and chills.
No human fatalities have ever been
reported; however, OA and DTX-1 may be
tumor promoters, producing stomach tumors
and chronic problems in shellsh
consumers.
Amnesic Shellsh Poisoning (ASP)
Understates the severity of the problem, as it is known
that domoic acid (DA), the principal toxin responsible
for ASP, also accumulates in sh and in crab viscera
along the west coast of the U.S, Canada, Europe,
Australia, Japan, New Zealand.

Domoic Acid producers: The diatoms Nitzschia

pungens f. multiseries, Pseudonitzschia australis ( N.
pseudoseriata ), and N. pseudodelicatissima
 Amnesic Shellsh Poisoning (ASP)

Symptoms: vomiting, abdominal cramps, diarrhea,

confusion, disorientation, and memory loss (the most
persistent symptom; can last over a year in several
cases).
Shellsh containing more than 20 g DA/g are
considered unt for human consumption.
Neurotoxic Shellsh Poisoning (NSP)
The Brevetoxins (PbTxs) induce a long-lasting
excitation of the sodium channel. The action site is the
same as that of ciguatoxins.
Symptoms: tingling and numbness of the lips, tongue,
throat and perioral area, muscular aches,
gastrointestinal upset, and dizziness.
No deaths have been reported from this relatively mild
form of poisoning.
 Marine Toxins: Fish
Barracuda

Ciguatera Fish Poisoning (CFP)

A disease associated with the ingestion of sh living in
tropical & subtropical regions contaminated with one/more
polyether toxins of the ciguatoxin (CTX) class.
The illness is now wide- spread in the tropical Caribbean,
subtropical North Atlantic, and the Pacic regions.
The most common species implicated with CFP are the
moray eel, snapper, grouper, Spanish mackerel,
barracuda, parrot sh, surgeon sh, amberjack, and
dolphin sh.
Ciguatera Fish Poisoning (CFP)
The major source of the toxins is a group of benthic
(Gambierdiscus toxicus; Prorocentrum spp. (P. lima, P.
concavum, P. emarginatum, P. mexicanum); Amphidinium
carterae, Ostreopsis spp. (O. ovata, O. siamensis, O.
lenticula, O. heptagona); Thecadinium sp.; and Coolia
monotis) and epiphytic dinoagellates.
CTXs appear to be stored for long periods in sh and
humans.
>175 ciguatera symptoms: gastrointestinal, neurological,
cardiovascular, and general symptoms.
Freshwater Toxins

Cyanobacterial Toxins
All continents except Antarctica have reported toxic
blooms.
There are no known vectors, such as shellsh, that
concentrate toxins of fresh- water cyanobacteria in the
human food chain.
Four classes of this biotoxins: hepatotoxins, neurotoxins,
nonspecic toxins, and lipopolysaccharides.
 The main genera responsible for freshwater toxic blooms
are the cyanobacteria Anabaena & Aphanizomenon
(alkaloid neurotoxins), Oscillatoria, Gloeotrichia,
Nodularia, and Microcystis (i.e.in acute toxicoses are the
hepatotoxins of M. aeruginosa)
Microcystins are monocyclic heptapeptide hepatotoxins
that have been isolated from Microcystis, Anabaena,
Nodularia, Nostoc, and Oscilla toria.
There are several similarities between marine toxins and
freshwater toxins:

1. Both are water-based.

2. Both are produced by microorganisms.
3. While retained within the cells to varying degrees,
both groups are exotoxins.
4. Both groups of toxins are fast-acting neuro- toxins via
the oral route.
5. Certain cyanobacteria toxins have
structural/functional similarities to certain paralytic
shellsh toxins (saxitoxin and neosaxitoxin).
Mycotoxins

Aatoxins
It occurs when aatoxigenic species of Aspergillus sp.
successfully colonize a commodity, grow and nd
conditions appropriate for toxin production.
The three species of Aspergillus that produce
aatoxins are A. avus, A. parasiticus, and A. nomius.
The effect of aatoxins on animals the LD50 ranges
from 0.5 mg/kg for the duck to 60 mg/kg for the mouse.
Aflatoxins

The organ primarily affected is the liver, but

changes can be seen in most organs.
Toxicity types: The carcinogenicity, mutagenicity,
teratogenicity, and acute toxicity of aatoxins.
AF-B1 is the most important in terms of
occurrence and toxicity, and the most potent of
the naturally occurring carcinogens.
Ochratoxin A

A group of related compounds that are produced

by Aspergillus ochraceus and related species, as
well as Penicillium verrucosum, and certain other
Penicillium species.
Ochratoxin A, the main toxic component of the
group, is classied as a chlorine-containing
pentaketide dihydroisocoumarine linked to L- -
phenylalanine.
Toxicity: porcine nephropathy, and also has been
reported to be teratogenic to mice, rats, and
chicken embryos.
Bacterial Toxins

Toxico-infections
Bacillus cereus, a Gram-positive, facultative aerobic,
spore-forming rod produces two types of toxins:
(i) a heat-labile, large molecular weight protein which
produces effects that are similar to those caused by
Clostridium perfringens Diarrhea a toxicoinfection.
(ii) a heat-stable, low molecular weight peptide which
produces a severe emetic (vomiting) reaction B.
cereus emetic intoxication.
 Campylobacter jejuni is recognized as a major
cause of human diarrhea. Implicated vehicles of
transmission are under- cooked chicken,
processed turkey, cake icing, raw clams, and
drinking water.
Symptoms vary from enteritis with abdominal pain
and profuse diarrhea, usually malaise, fever,
vomiting, and, in extreme cases, grossly bloody
stools.
 C. perfringens, a Gram-positive, nonmotile, spore-
forming, anaerobic rod, is a normal inhabitant of the
large intestine of man and animals. Spores of the
organism persist in soil, dust, and foods (raw meat,
poultry, sh, and vegetables) subject to fecal pollution.

Symptoms: nausea, abdominal pain, and acute

diarrhea, and are the result of the uid accumulation
in the intestinal lumen when an enterotoxin is
released in the gut during sporulation of the
consumed cells.
Escherichia coli
Escherichia coli is part of the normal ora of the
intestinal tract of humans and other warm-blooded
animals.
Foodborne diarrheagenic E. coli are grouped into four
categories according to virulence properties, clinical
syndromes, differences in epidemiology, and distinct
O:H serogroups.
They are enterotoxigenic E. coli (ETEC),
enteropathogenic E. coli (EPEC),
enterohemorrhagic E. coli (EHEC), and
enteroinvasive E. coli (EIEC).
Figure. Interaction of various pathogenic E.coli with the epithelial cells of
the gut.
 INTOXICATION
1. Bacillus cereus (emetic) produces a heat-
stable toxin of severe emetic (vomiting) reaction
accompanied by gastric pain between 1 to 6 h after
food ingestion. The illness usually lasts 6 to 24 hrs.

2. Clostridium botulinum : the toxin, a heat-

labile high molecular weight protein produced
during growth of the organism under anaerobic
conditions, is very lethal. Just a few nanograms of
the toxin can cause illness. The toxin can be
destroyed if heated (80C for 10 min).
3. Staphylococcus aureus
The staphylococcal food poisoning
(staphyloenterotoxicosis, staphyloenterotoxemia) is
an intoxication which results from the ingestion of
enterotoxins produced by this pathogen within
various foods.
A toxin dose of less than 1.0 g produces the
symptoms.
Thank You!