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FISH DISEASES CAUSED BY TOXINS
 BY KIRAN AFTAB KHOKHAR
 FISHERIES AND AQUACULTURE LAB
 WHAT ARE TOXINS?
 A toxin is a poisonous substance produced within living cells or
organisms. The term was first used by organic chemist Ludwig
Brieger , derived from the word toxic.
 Toxins can be small molecules, peptides or proteins that are capable of
causing disease on contact with or absorption by body tissues
interacting with biological macromolecules such as enzymes or cellular
receptors and typically capable of inducing antibody formation.
 Toxins vary greatly in their toxicity, ranging from usually minor (such
as a bee sting) to almost immediately deadly(such as botulinum toxin).
TYPES OF TOXINS AFFECTING FISH
TOXINS
ALGAL TOXINS
CYANOTOXINS
EUGLENOPHYCIN
MYCOTOXINS
AFLATOXINS
F2 TOXINS
ALGAL TOXINS
 Algal toxins are organic molecules that are produced by a variety of algae
in marine, brackish and fresh waters, as well as on wet soils during their
life cycle.
 These are released from the cell into the surrounding water.
 The production of algal toxins is normally associated with algal blooms.
 These can cause problems in the freshwater affecting both vertebrates (fish)
and invertebrates (shellfish). Such problems include:
 off-flavor
 indirect toxicity through changes in water quality
 or direct toxicity.
ALGAL TOXINS
 Algal toxins are a problem in aquaculture when they are produced in
sufficient quantities, with sufficient potency, to kill cultured organisms,
decrease feeding and growth rates, or adversely affect the quality of the
product.
 Some species of algae, especially members of the Cyanophytae produce
toxins in the water that can cause mortality even in low concentration.
 This toxicosis occurs mostly in ponds where excess organic and chemical
fertilizers are used.
 It is assumed that in natural waters toxins of a cyanobacterial alga,
Cylindropermopsis raciborski cause poisoning of both the flora and fauna,
including fish.
ALGAL TOXINS
 Severe blooms of even non-toxic algae can be disastrous, because
blooms deplete the oxygen in the shallow waters of many aquaculture
systems.
 The two most important algal toxins affecting freshwater fish are:
1. Cyanotoxins
2. Euglenophycin
 CYANOTOXINS
 Cyanotoxins are naturally produced by cyanobacteria also known as
blue green algae.
 Cyanobacteria are structurally and physiologically like other gram-
negative bacteria, but they conduct photosynthesis like plants in aquatic
systems.
 These can rapidly overtake an aquaculture pond and contribute to
unstable conditions.
 Cyanobacteria blooms can decrease fish production and kill fish
because of oxygen depletion.
 These can also cause off-flavor and unpleasant odor in fish.
 CYANOTOXINS
 Die - offs of cyanobacteria are well known to cause
environmental hypoxia.
 A die - off appears as a change in the water’s color from
green or green - brown to light brown.
 The water often smells because of cyanobacterial
decomposition.
 The problem is most common in ponds receiving large
additions of feed or fertilizer.
TYPES OF CYANOTOXINS
CYANOTOXINS
NEUROTOXINS HEPATOTOXINS
NEUROTOXINS
 Neurotoxins are organic molecules that can attack the nervous systems
of vertebrates and invertebrates.
 Neurotoxins produced by Anabaena spp., Oscillatoria spp. and
Aphanizomenon blooms have been responsible for animal poisonings
around the world.
 Three primary types of neurotoxins have been identified:
1. anatoxin-a, an alkaloid (blocks post-synaptic depolarization)
2. anatoxin-a(s) blocks acetylcholinesterase (similar to organophosphate
pesticides)
3. saxitoxins (act like carbamate pesticides by blocking sodium channels).
 CLINICAL SIGNS
 Neurotoxins usually have acute effects in
vertebrates, with rapid paralysis of the
peripheral skeletal and respiratory muscles.
 Other symptoms include loss of coordination,
twitching, irregular gill movement, tremors,
altered swimming, and convulsions before
death by respiratory arrest.
 HEPATOTOXINS
 Hepatotoxins are produced by many genera of cyanobacteria and have been
implicated in the deaths of fish.
 These toxins target the liver by binding the organic anion transport system in
hepatocyte cell membranes.
 Microcystins are the toxins produced in fresh waters by species of Microcystis,
Anabaena.
 CLINICAL SIGNS
 Symptoms of poisoning in fish include flared gills because of difficulty breathing and
weakness or inability to swim.
 All fish may be killed within 24 hours of exposure. At necropsy, severe lesions may
be observed in liver tissues.
 OFF-FLAVOUR OR MUDDY TASTE
 The muddy taste in trout (and other fish) comes from chemical
compounds called “geosmin and 2 – methyl-isoborneol’’.
 There are two primary producers of geosmin. These are the blue-
green alga or cyanobacteria (e.g. Oscillatoria, Anabaena) and the
Streptomyces, a Gram-positive type of Actinobacteria.
 The chemical is released by the bacteria when they die. It is a
bicyclic alcohol with the chemical formula C12H22O.
 2 – methyl-isoborneol is an organic molecule produced by
cyanobacteria along with geosmin.
 OFF-FLAVOUR OR MUDDY TASTE
 The algae and bacteria release the geosmin into the water.
 As a trout breaths, it acquires geosmin through the gills where it is
transferred into the bloodstream of the trout and then deposited
into the skin and dark muscle tissue.
 The chemicals impart an undesirable flavor to the fillet, preventing
fish from being harvested until the compounds leave the fish.
 Off-flavor commonly occurs during autumn and summer when
stocking densities are high, organic loading is also high and the
water is warm.
 DIAGNOSIS
 To confirm the problem, a diagnostician will need fresh
samples of the water containing the suspected cyanobacteria .
 A sample of both sick and dead fish will also be needed, along
with information on fish behavior and any other symptoms
observed.
 Young fish are generally more sensitive than older fish.
 The diagnostician may look for lesions on fish livers.
 Muddy tasting fish often smells.
 TREATMENT AND CONTROL
 The chemicals associated with the muddy taste can be metabolized by
fish.
 Placing affected fish in uncontaminated water for a period of time will
resolve the problem (depuration).
 Depuration of 2-methylisoborneol and geosmin will occur in channel
catfish from 96 to 150 h after removal of the fish from exposure to the
chemicals.
 In ponds, algicides (e.g. copper) can inhibit many harmful algae, but
extreme care must be taken to avoid oxygen depletion.
 TREATMENT AND CONTROL
 The only effective one that is environmentally and toxicologically safe is
sodium carbonate.
 Copper sulphate has been used to control algal growth, but toxic levels of
copper and the impact on waters receiving aquaculture effluents are concerns.
Treatment with copper can also cause release of toxin from dying algae.
 Treating with potassium permanganate instead of copper has been found to
result in less mortality in some cases.
 With any algicidal treatment, bloom recurrence may occur. Cyanobacteria are
significantly inhibited at 5 – 10 ppt salinity.
 Relatively small volumes of water (e.g., for aquaria) can be disinfected and
detoxified using ozonation and activated carbon filtration before adding or use.
 TREATMENT AND CONTROL
 Non-chemical treatments include:
1. physical mixing and aeration,
2. increasing flow rate or flushing to decrease hydraulic
retention time,
3. decreasing or altering nutrient content and composition.
 Some of these options may not be viable at all sites and in
all situations.
EUGLENOPHYCIN
 Euglena sanguinea produces euglenophycin, a toxin that exhibits not
only ichthyotoxic but also herbicidal and anticancer activity.
 Based on behavioral changes in exposed fish, it was suggested that this
toxin functions as a neurotoxin which has a chemical structure similar to
that of fire ant venom.
 Euglena bloom can be common in very nutrient-rich waters like stock
ponds and sewage lagoons.
 Water with Euglena blooms may appear bright pea green in color. The
species of Euglena that caused the fish kill can turn red during daylight
hours, thereby causing a sort of freshwater "red tide."
 SYMPTOMS
 The typical progression of symptoms from exposure to Euglena toxin
begins with the fish going off feed for no apparent reason.
 Within 24 hours of cessation of feeding, the fish swim at or near the
surface in an agitated or disorientated state, often with the dorsal fin
extending out of the water or swimming on their sides and even upside
down.
 If steps are not taken immediately after observing this state, within 24
hours the fish will be dead.
 Field observation of dead fish indicated rapid onset of mortality with
reddening of gill tissue.
 SYMPTOMS
 A bloom of euglena sanguinea was fatal to juvenile channel catfish
within 2 hours of exposure (Zimba et al.,2004).
 Several other fish species have been observed susceptible to it
including, sheep head, striped bass, blue tilapia and Nile Tilapia.
 DIAGNOSIS
 Microscopic examination of a water sample can confirm the
presence of Euglena.
 TREATMENT AND CONTROL
 The toxin is water soluble, non-protein, heat stable (30 °C for 10
minutes), freezing stable (-80 °C for 60 days), and labile to
oxidation.
 Euglenoid should be sensitive to several of the algicides available.
 If a toxic Euglena bloom occurs, try to minimize mixing of the
water because mixing will disburse the bloom throughout the pond.
 TREATMENT AND CONTROL
 Aerate only if needed to save the fish from acute oxygen depletion.
 A research showed that potassium permanganate applied at a rate of
2.5 times the permanganate demand of the pond apparently detoxified
the toxin and eliminated the source.
MYCOTOXINS
 Mycotoxins are toxic chemicals produced by certain species of
molds usually belonging to the Aspergillus, Penicillium or Fusarium
genera.
 When fish feeds are improperly stored, they may decay and become
moldy, producing toxins which are dangerous for fish.
 Feeding fish with unsuitable, poor or bad quality feeds is the reason
for most of the losses of fish in pond culture.
 Its direct effect is the development of inflammation in the intestine,
which can appear as general inflammation or as the loss of appetite
due to catarrhal changes in the epithelium.
MYCOTOXINS
 Two most important types of mycotoxins affecting fish include:
1. Aflatoxins
2. F2 toxins
 AFLATOXINS
 Aspergillus flavus is the mold that produces aflatoxin.
 It causes aflatoxicosis in the fish eating contaminated feed.
 The fungus is most problematic during hot, droughty summers,
especially when developing corn kernels are damaged by insects.
AFLATOXINS
 Aflatoxins in feeds or feed ingredients are usually a mixture of four
aflatoxins with only slightly different chemical structures.
 The most prevalent and most toxic to animals is AFB1. The other forms
are AFB2, AFG1 and AFG2 and collectively said to be “total aflatoxins’’.
 While rainbow trout are very sensitive to the presence of aflatoxin in their
diets, with as little as 0.4 ppb dietary aflatoxin producing hepatocellular
carcinoma (HCC) in 14 percent of trout over a period of 15 months.
 Warmwater fish do not appear to be as sensitive to dietary aflatoxin.
 Both channel catfish and tilapia appear to be much less vulnerable to
aflatoxin than rainbow trout.
 CLINICAL SIGNS
 Aflatoxins are both potent hepatotoxins and carcinogens. Trout are
extremely sensitive to aflatoxins, associated with moldy feeds, and
develop hepatomas when contaminated feed is fed for several months.
F2 TOXINS
 also known as Zearalenone (ZEN) and RAL.
 is a potent estrogenic metabolite produced by Fusarium graminerum
, a fungal plant pathogen which causes fusarium head blight, a
devastating disease on wheat, corn and barley.
 It enters fish body through contaminated feed.
 CLINICAL SIGNS
 F2 toxin of Fusarium graminearum is harmful to the genital organs. By feeding
moldy corn significantly drops sperm production.
 DIAGNOSIS
 Presumptive diagnosis of food-borne toxins is based on compatible clinical signs,
combined with evidence of an inadequate diet.
 When the moisture level is higher than 12 percent, mold can grow in fish feeds
and possibly produce mycotoxins.
 Stored feed that is found to be moldy should be tested for the presence of
mycotoxins before it is fed to fish. There are many simple test kits available for
commonly found mycotoxins.
 DIAGNOSIS
 Tests usually provide a yes or no answer as to the presence of the mycotoxin of
interest, rather than its concentration in the feed.
 Commercial or state testing laboratories can test for the presence of mycotoxins in
aquaculture feeds. These services usually provide information about the mycotoxins
present and their concentrations.
 TREATMENT AND CONTROL
 There are adsorbents that bind foodborne mycotoxins to prevent them from being
absorbed by fish after consumption. These binders fall into two main classes:
1. hydrated sodium calcium aluminosilicate (HSCAS) clays
2. modified fractions of the single-cell yeast organism Saccharomyces cerevisiae, or
common bakers’ yeast.
 TREATMENT AND CONTROL
 The clays seem to work well with aflatoxins,
but are less effective with other mycotoxins.
 The yeast preparations appear to be effective
on a broader range of mycotoxins. Neither
type of binder has been extensively evaluated
in fish feeds.
 A research showed that heat chemically
transforms aflatoxin into aflatoxin breakdown
products during feed manufacturing.
 Diseased fish cannot be treated.
fish diseases caused by toxins

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fish diseases caused by toxins

  • 1. FISH DISEASES CAUSED BY TOXINS  BY KIRAN AFTAB KHOKHAR  FISHERIES AND AQUACULTURE LAB
  • 2.  WHAT ARE TOXINS?  A toxin is a poisonous substance produced within living cells or organisms. The term was first used by organic chemist Ludwig Brieger , derived from the word toxic.  Toxins can be small molecules, peptides or proteins that are capable of causing disease on contact with or absorption by body tissues interacting with biological macromolecules such as enzymes or cellular receptors and typically capable of inducing antibody formation.  Toxins vary greatly in their toxicity, ranging from usually minor (such as a bee sting) to almost immediately deadly(such as botulinum toxin).
  • 3. TYPES OF TOXINS AFFECTING FISH TOXINS ALGAL TOXINS CYANOTOXINS EUGLENOPHYCIN MYCOTOXINS AFLATOXINS F2 TOXINS
  • 4. ALGAL TOXINS  Algal toxins are organic molecules that are produced by a variety of algae in marine, brackish and fresh waters, as well as on wet soils during their life cycle.  These are released from the cell into the surrounding water.  The production of algal toxins is normally associated with algal blooms.  These can cause problems in the freshwater affecting both vertebrates (fish) and invertebrates (shellfish). Such problems include:  off-flavor  indirect toxicity through changes in water quality  or direct toxicity.
  • 5. ALGAL TOXINS  Algal toxins are a problem in aquaculture when they are produced in sufficient quantities, with sufficient potency, to kill cultured organisms, decrease feeding and growth rates, or adversely affect the quality of the product.  Some species of algae, especially members of the Cyanophytae produce toxins in the water that can cause mortality even in low concentration.  This toxicosis occurs mostly in ponds where excess organic and chemical fertilizers are used.  It is assumed that in natural waters toxins of a cyanobacterial alga, Cylindropermopsis raciborski cause poisoning of both the flora and fauna, including fish.
  • 6. ALGAL TOXINS  Severe blooms of even non-toxic algae can be disastrous, because blooms deplete the oxygen in the shallow waters of many aquaculture systems.  The two most important algal toxins affecting freshwater fish are: 1. Cyanotoxins 2. Euglenophycin
  • 7.  CYANOTOXINS  Cyanotoxins are naturally produced by cyanobacteria also known as blue green algae.  Cyanobacteria are structurally and physiologically like other gram- negative bacteria, but they conduct photosynthesis like plants in aquatic systems.  These can rapidly overtake an aquaculture pond and contribute to unstable conditions.  Cyanobacteria blooms can decrease fish production and kill fish because of oxygen depletion.  These can also cause off-flavor and unpleasant odor in fish.
  • 8.  CYANOTOXINS  Die - offs of cyanobacteria are well known to cause environmental hypoxia.  A die - off appears as a change in the water’s color from green or green - brown to light brown.  The water often smells because of cyanobacterial decomposition.  The problem is most common in ponds receiving large additions of feed or fertilizer.
  • 10. NEUROTOXINS  Neurotoxins are organic molecules that can attack the nervous systems of vertebrates and invertebrates.  Neurotoxins produced by Anabaena spp., Oscillatoria spp. and Aphanizomenon blooms have been responsible for animal poisonings around the world.  Three primary types of neurotoxins have been identified: 1. anatoxin-a, an alkaloid (blocks post-synaptic depolarization) 2. anatoxin-a(s) blocks acetylcholinesterase (similar to organophosphate pesticides) 3. saxitoxins (act like carbamate pesticides by blocking sodium channels).
  • 11.  CLINICAL SIGNS  Neurotoxins usually have acute effects in vertebrates, with rapid paralysis of the peripheral skeletal and respiratory muscles.  Other symptoms include loss of coordination, twitching, irregular gill movement, tremors, altered swimming, and convulsions before death by respiratory arrest.
  • 12.  HEPATOTOXINS  Hepatotoxins are produced by many genera of cyanobacteria and have been implicated in the deaths of fish.  These toxins target the liver by binding the organic anion transport system in hepatocyte cell membranes.  Microcystins are the toxins produced in fresh waters by species of Microcystis, Anabaena.  CLINICAL SIGNS  Symptoms of poisoning in fish include flared gills because of difficulty breathing and weakness or inability to swim.  All fish may be killed within 24 hours of exposure. At necropsy, severe lesions may be observed in liver tissues.
  • 13.  OFF-FLAVOUR OR MUDDY TASTE  The muddy taste in trout (and other fish) comes from chemical compounds called “geosmin and 2 – methyl-isoborneol’’.  There are two primary producers of geosmin. These are the blue- green alga or cyanobacteria (e.g. Oscillatoria, Anabaena) and the Streptomyces, a Gram-positive type of Actinobacteria.  The chemical is released by the bacteria when they die. It is a bicyclic alcohol with the chemical formula C12H22O.  2 – methyl-isoborneol is an organic molecule produced by cyanobacteria along with geosmin.
  • 14.  OFF-FLAVOUR OR MUDDY TASTE  The algae and bacteria release the geosmin into the water.  As a trout breaths, it acquires geosmin through the gills where it is transferred into the bloodstream of the trout and then deposited into the skin and dark muscle tissue.  The chemicals impart an undesirable flavor to the fillet, preventing fish from being harvested until the compounds leave the fish.  Off-flavor commonly occurs during autumn and summer when stocking densities are high, organic loading is also high and the water is warm.
  • 15.  DIAGNOSIS  To confirm the problem, a diagnostician will need fresh samples of the water containing the suspected cyanobacteria .  A sample of both sick and dead fish will also be needed, along with information on fish behavior and any other symptoms observed.  Young fish are generally more sensitive than older fish.  The diagnostician may look for lesions on fish livers.  Muddy tasting fish often smells.
  • 16.  TREATMENT AND CONTROL  The chemicals associated with the muddy taste can be metabolized by fish.  Placing affected fish in uncontaminated water for a period of time will resolve the problem (depuration).  Depuration of 2-methylisoborneol and geosmin will occur in channel catfish from 96 to 150 h after removal of the fish from exposure to the chemicals.  In ponds, algicides (e.g. copper) can inhibit many harmful algae, but extreme care must be taken to avoid oxygen depletion.
  • 17.  TREATMENT AND CONTROL  The only effective one that is environmentally and toxicologically safe is sodium carbonate.  Copper sulphate has been used to control algal growth, but toxic levels of copper and the impact on waters receiving aquaculture effluents are concerns. Treatment with copper can also cause release of toxin from dying algae.  Treating with potassium permanganate instead of copper has been found to result in less mortality in some cases.  With any algicidal treatment, bloom recurrence may occur. Cyanobacteria are significantly inhibited at 5 – 10 ppt salinity.  Relatively small volumes of water (e.g., for aquaria) can be disinfected and detoxified using ozonation and activated carbon filtration before adding or use.
  • 18.  TREATMENT AND CONTROL  Non-chemical treatments include: 1. physical mixing and aeration, 2. increasing flow rate or flushing to decrease hydraulic retention time, 3. decreasing or altering nutrient content and composition.  Some of these options may not be viable at all sites and in all situations.
  • 19. EUGLENOPHYCIN  Euglena sanguinea produces euglenophycin, a toxin that exhibits not only ichthyotoxic but also herbicidal and anticancer activity.  Based on behavioral changes in exposed fish, it was suggested that this toxin functions as a neurotoxin which has a chemical structure similar to that of fire ant venom.  Euglena bloom can be common in very nutrient-rich waters like stock ponds and sewage lagoons.  Water with Euglena blooms may appear bright pea green in color. The species of Euglena that caused the fish kill can turn red during daylight hours, thereby causing a sort of freshwater "red tide."
  • 20.  SYMPTOMS  The typical progression of symptoms from exposure to Euglena toxin begins with the fish going off feed for no apparent reason.  Within 24 hours of cessation of feeding, the fish swim at or near the surface in an agitated or disorientated state, often with the dorsal fin extending out of the water or swimming on their sides and even upside down.  If steps are not taken immediately after observing this state, within 24 hours the fish will be dead.  Field observation of dead fish indicated rapid onset of mortality with reddening of gill tissue.
  • 21.  SYMPTOMS  A bloom of euglena sanguinea was fatal to juvenile channel catfish within 2 hours of exposure (Zimba et al.,2004).  Several other fish species have been observed susceptible to it including, sheep head, striped bass, blue tilapia and Nile Tilapia.
  • 22.  DIAGNOSIS  Microscopic examination of a water sample can confirm the presence of Euglena.  TREATMENT AND CONTROL  The toxin is water soluble, non-protein, heat stable (30 °C for 10 minutes), freezing stable (-80 °C for 60 days), and labile to oxidation.  Euglenoid should be sensitive to several of the algicides available.  If a toxic Euglena bloom occurs, try to minimize mixing of the water because mixing will disburse the bloom throughout the pond.
  • 23.  TREATMENT AND CONTROL  Aerate only if needed to save the fish from acute oxygen depletion.  A research showed that potassium permanganate applied at a rate of 2.5 times the permanganate demand of the pond apparently detoxified the toxin and eliminated the source.
  • 24. MYCOTOXINS  Mycotoxins are toxic chemicals produced by certain species of molds usually belonging to the Aspergillus, Penicillium or Fusarium genera.  When fish feeds are improperly stored, they may decay and become moldy, producing toxins which are dangerous for fish.  Feeding fish with unsuitable, poor or bad quality feeds is the reason for most of the losses of fish in pond culture.  Its direct effect is the development of inflammation in the intestine, which can appear as general inflammation or as the loss of appetite due to catarrhal changes in the epithelium.
  • 25. MYCOTOXINS  Two most important types of mycotoxins affecting fish include: 1. Aflatoxins 2. F2 toxins  AFLATOXINS  Aspergillus flavus is the mold that produces aflatoxin.  It causes aflatoxicosis in the fish eating contaminated feed.  The fungus is most problematic during hot, droughty summers, especially when developing corn kernels are damaged by insects.
  • 26. AFLATOXINS  Aflatoxins in feeds or feed ingredients are usually a mixture of four aflatoxins with only slightly different chemical structures.  The most prevalent and most toxic to animals is AFB1. The other forms are AFB2, AFG1 and AFG2 and collectively said to be “total aflatoxins’’.  While rainbow trout are very sensitive to the presence of aflatoxin in their diets, with as little as 0.4 ppb dietary aflatoxin producing hepatocellular carcinoma (HCC) in 14 percent of trout over a period of 15 months.  Warmwater fish do not appear to be as sensitive to dietary aflatoxin.  Both channel catfish and tilapia appear to be much less vulnerable to aflatoxin than rainbow trout.
  • 27.  CLINICAL SIGNS  Aflatoxins are both potent hepatotoxins and carcinogens. Trout are extremely sensitive to aflatoxins, associated with moldy feeds, and develop hepatomas when contaminated feed is fed for several months. F2 TOXINS  also known as Zearalenone (ZEN) and RAL.  is a potent estrogenic metabolite produced by Fusarium graminerum , a fungal plant pathogen which causes fusarium head blight, a devastating disease on wheat, corn and barley.  It enters fish body through contaminated feed.
  • 28.  CLINICAL SIGNS  F2 toxin of Fusarium graminearum is harmful to the genital organs. By feeding moldy corn significantly drops sperm production.  DIAGNOSIS  Presumptive diagnosis of food-borne toxins is based on compatible clinical signs, combined with evidence of an inadequate diet.  When the moisture level is higher than 12 percent, mold can grow in fish feeds and possibly produce mycotoxins.  Stored feed that is found to be moldy should be tested for the presence of mycotoxins before it is fed to fish. There are many simple test kits available for commonly found mycotoxins.
  • 29.  DIAGNOSIS  Tests usually provide a yes or no answer as to the presence of the mycotoxin of interest, rather than its concentration in the feed.  Commercial or state testing laboratories can test for the presence of mycotoxins in aquaculture feeds. These services usually provide information about the mycotoxins present and their concentrations.  TREATMENT AND CONTROL  There are adsorbents that bind foodborne mycotoxins to prevent them from being absorbed by fish after consumption. These binders fall into two main classes: 1. hydrated sodium calcium aluminosilicate (HSCAS) clays 2. modified fractions of the single-cell yeast organism Saccharomyces cerevisiae, or common bakers’ yeast.
  • 30.  TREATMENT AND CONTROL  The clays seem to work well with aflatoxins, but are less effective with other mycotoxins.  The yeast preparations appear to be effective on a broader range of mycotoxins. Neither type of binder has been extensively evaluated in fish feeds.  A research showed that heat chemically transforms aflatoxin into aflatoxin breakdown products during feed manufacturing.  Diseased fish cannot be treated.