What are mycotoxins?

The word mycotoxin stems from the Greek word "mykes", meaning
mould, and "toxicum" meaning poison. Human cases of ergotism or St.
Anthony's Fire have been described in Europe since the Middle Ages and
are now known to be caused by alkaloids produced in rye by the
mould Claviceps purpurea. In 1960, an outbreak of Turkey X disease in
England and the subsequent discovery of the aflatoxins stimulated great
interest in the field of mycotoxin research (Bullerman, 1979). Since then
many more mycotoxins, such as trichothecenes, zearalenone, ochratoxins
and fumonisins have been discovered.
Mycotoxins are toxic secondary metabolites produced by fungi
growing on crops in the field, during handling and in storage. They enter
the animal production system via feed (concentrate, silage or forage) or via
bedding. Mycotoxins negatively affect animal performance, animal health
and product quality. Thus mycotoxin control is crucial for production
economics, animal welfare, product quality and food safety reasons.
Mycotoxins are chemically different representing a variety of
chemical families and range in molecular weight from about 200 to 500 kD.
There are hundreds of known mycotoxins, but few have been extensively
researched and fewer still have good methods of available analysis.
Mycotoxins vary greatly in their severity.
Mycotoxins exert their effects through four primary mechanisms:
 Intake reduction or feed refusal
 Alteration in nutrient content of feed in terms of nutrient
absorption and metabolism
 Effects on the endocrine and exocrine systems
 Suppression of the immune system
These effects often lead to rather unspecific symptoms, which can
also be caused by many other factors making if difficult to properly
diagnose mycotoxin problems. General symptoms (reduced performance,
impaired immunity) are seen when dealing with moderate mycotoxin levels,
while symptoms caused by higher mycotoxin levels are often more specific.
Further complications in mycotoxicosis diagnoses can be caused by
secondary symptoms resulting from opportunistic disease related to the
suppression of the immune system following mycotoxin exposure.
In order to effectively identify mycotoxicosis, experience with
mycotoxin-affected animals is important. This experience, combined with
adequate feed and tissue analyses, provide the basis for the most accurate
diagnosis of mycotoxicosis.
Moulds grow by producing long filaments called hyphae, which are
important for the survival and dispersal of fungi. The hyphal network is
responsible for cementing kernels together, which in stored grain or feed
can result in clumps of grain that cannot be separated. Grain-mould fungi
also produce spores (conidia) capable of aerial dispersal in the field as well
as within a grain storage bin. It is usually masses of these spores that give
the mould a characteristic colour. Spores can lay dormant for months or
years until the proper conditions for fungal development are available.

Fungal growth
Fungal species are often divided into two groups: 
 Field fungi
 Storage fungi
Field fungi are those that invade the seeds while the crop is still in
the field and require high moisture conditions (20-21%). These include
species of Fusarium, Alternaria, Clodosporium, Diplodia, Gibberella and
Helminthosporium.
Storage fungi (also called storage moulds) are those that invade
grains or seeds during storage. They need less moisture than field fungi
(13-18%) and usually do not present any serious problem before harvest.
Storage fungi include species of Aspergillus and Penicillium. 
While the field/storage terminology is generally used to indicate the
differences in temperature and moisture required by various fungi, the
proper conditions for the growth of a specific organism can occur in either
the field or storage bin. Ideal conditions for fungal growth depend on the
species, but normally moulds require high temperature and moisture.
Mycotoxins are produced as secondary metabolites. Under field
conditions, stress and subsequently reduced vigour often predispose plants
to infestation and colonisation by toxigenic fungi. In stored grain, toxigenic
fungal infection and mycotoxin production result from a complex interaction
between moisture, temperature, substrate, oxygen (O 2) and carbon dioxide
(CO2) concentration, fungal abundance and insect presence. Insects can
influence a differentiation of fungal species, that is a specific insect
determines the presence of a specific fungal species.
Mycotoxins can be found in forage. On one side plants can modify
the concentration of mycotoxins due to different enzymatic systems. On the
other side, it seems that they can move substances from the site of
production to the hull and the stem and then to the leaves.
In general, most fungi need at least 1-2% oxygen and usually grow
at temperatures between 20 and 30°C. It is important to note that if the
grain is at high temperature at harvest, it can maintain that high
temperature for several days or weeks after harvest unless the storage
facility has cooling capabilities. Normally, in storage conditions fungi grow
at 13-18% moisture. However, in case of grains with high levels of oil (e.g.
peanuts) fungal growth occurs at moisture contents as low as 7%. 

Overview of mycotoxins
Under the appropriate conditions, fungi proliferate, grow colonies
and mycotoxin levels become high. As conditions for fungal growth vary
greatly between field and storage, different fungal populations may be
present, resulting in cocktails of mycotoxins being produced. This must be
taken into consideration when conducting an appropriate risk assessment
and implementing preventative measures.

Factors affecting mycotoxin formation in the field

As temperature and moisture levels are key factors for fungal growth
and subsequent mycotoxin production, the climate plays a key role in the
occurrence of mycotoxins. Crop surveys show large variations in
contamination levels from one year to another due to varying climatic
conditions. However, in addition to climatic conditions, agronomic practices
also have a pronounced effect on mycotoxin formation as they affect the
presence of fugal spores in the field as well as fungal growth. Three key
agronomic factors have been shown to affect mycotoxin presence and
concentration significantly:
 Crop presence and rotation: Monocultures or planting of
closely related crops one after the other will enhance the risk of mycotoxin
formation, as spores will transfer to the subsequent crop and thus allow
fungal growth to establish quickly and strongly.
 Soil cultivation: Ploughing harvest residues will reduce spore
contamination of the subsequent crop and thus reduce fungal infestation
and mycotoxin formation. No-till systems will enhance the risk.
 Crop and crop variety: Crop varieties that are more resistant
to fungal foliar diseases reduce fungal infection and thus mycotoxin
formation of the crop.
Mycotoxins are generally very stable and will persist during storage
as they are independent of storage conditions. As no efficient
decontamination procedures are available today, most of the mycotoxins
that are present at the time of harvest in a crop will reach the final animal
diet during feed consumption.

Mycotoxins in pig production

Mycotoxins are compounds produced in grain by specific moulds or
fungi as secondary metabolites that may or may not be toxic to man or
animal. Fungal infestation and subsequent mycotoxin production can occur
during plant growth, maturity, harvesting, storage, and processing of grains,
and is influenced primarily by moisture level, temperature, and availability
of oxygen. In addition, grain that is damaged, immature, drought stricken or
otherwise stressed is more susceptible to mould growth.
Moulds may reduce the nutrient content and quality of the grain, but
the toxic effects of metabolites are generally of primary concern. Scientists
have identified 300 to 400 mycotoxins to date, but only a few have been
shown to cause significant, detrimental health and performance problems
in pigs fed mycotoxin-contaminated plant based feedstuffs. These include
aflatoxin, deoxynivalenol, zearalenone, fumonisin, ochratoxin, ergot, and T-
2 toxin.
 It is important to remember that the presence of moulds in grains
does not automatically indicate mycotoxin presence. Aspergillus,
Penicillium, Claviceps, and Fusarium fungi have been identified as
producing the mycotoxins most detrimental to pigs.
The symptoms exhibited and the degree with which pigs are
affected by mycotoxin toxicity is largely affected by the kind of mycotoxin
involved and its concentration in feed, but also by the age and phase of
production of the pig. Young pigs and breeding pigs are generally the most
susceptible to mycotoxins.
The development of novel feeding and housing systems has added
a new dimension to mycotoxin control in pigs. Mycotoxin exposure can
occur in both dry and wet feeding systems, especially the latter, with long
distribution lines that are hard to clear. High welfare systems using straw
bedding pose an additional risk and this is especially pertinent to the group-
housing of sows. Mycotoxins suppress immune function in pigs and this
may eventually decrease resistance to infectious diseases, re-activate
chronic infections and/or reduce vaccine and therapeutic efficiency.
Common symptoms associated with mycotoxicosis include:
 Reduced feed intake
 Poorer growth rate
 Decreased feed conversion efficiency
 Increased incidence of disease
 Reduced immunity
 Vomiting
 Rectal / vaginal prolapse
 Sudden death
 Pale / weak pigs
 Bloody faeces
 Reduced sow productivity
 Abortion
 Increased foetal re-absorption = return to oestrus
 Inconsistency of sow body condition
 Delayed puberty in gilts and boars
 Reduced libido
 Poorer semen quality = reduced fertility
 Higher incidence of liver and/or kidney disease

Liquid Feeding
Liquid or wet feeding systems can present a significant challenge to
the pig industry with respect to mycotoxins. It is important to employ strict
hygiene procedures to minimise the presence of mycotoxins within the
mixer tanks, feed lines and troughs. Although regular cleaning should be
performed, it should be noted that mycotoxins are extremely resilient and
can survive in the biofilms of feed lines and equipment for significant
periods. It is also important not to recycle the waste water after the system
is cleaned as this serves to re-introduce mycotoxins into the system.

Aflatoxins
Aflatoxins are produced mainly by Aspergillus flavus and Aspergillus
parasitium. They are of concern in warm and humid climatic conditions.
Although aflatoxins are not considered to be a major problem in cold or
more temperate regions, caution must be exercised in colder climates
when using feedstuffs imported from warm and humid countries.
There is a variety of aflatoxins (B 1, B 2, G 1, G 2, M 1, M 2)
produced byAspergillus flavus. Relative to the temperature, Aspergillus
flavus easily produces aflatoxins at about 25°C, and under 10°C the toxin
production has never been demonstrated. Grain moisture levels of 22% to
26% provide ideal conditions for producing aflatoxins in a variety of grains,
including corn, wheat, barley, and oats.
Aflatoxins have been shown to be carcinogenic, and therefore there
are concerns about the mycotoxin entering the human food chain. For pigs,
they are the most acutely toxic of all mycotoxins, causing extensive liver
pathology. There is also concern about residues of aflatoxin and
metabolites in food, because of the well-documented carcinogenic nature
of these compounds. Therefore, many countries have set upper limits for
aflatoxins in feeds (See regulations page on this site for more details).
Grains containing aflatoxin levels in excess of 20 ppb cannot be used for
human consumption and animal feeds, and should not be fed to young
animals.
At low levels (20 - 200 ppb), aflatoxin decreases performance and
well-being. Feed intake is commonly reduced, resulting in depressed
growth rate, while immune function is suppressed. At high levels (1000 ppb
+), death may occur.

Clinical effects:
These include reduced growth rate and feed efficiency and, at
extreme levels, liver damage, such as fatty changes, lobular necrosis, with
an increase in basophilic cells at the periphery of the lobule and bile duct.
In extreme chronic cases cirrhosis and death may occur.
Indicators of liver damage are elevated serum activities of gamma-
glutamyltransferase (GGT) and alkaline phosphatase, as well as elevated
levels of serum albumin and total protein.
Feeding diets contaminated with aflatoxin may exacerbate vitamin A
and vitamin E deficiency in pigs, as well as reduce the immune function.
This renders the animal more susceptible to any concurrent disease, such
as PRRS, PWMS, viral influenza and mycoplasma pneumonia and
secondary infections are common.
 Although low concentrations of aflatoxins are tolerated, the
combined adverse effects of aflatoxin on hepatic metabolism, protein
synthesis and immune status reduce swine reproductive efficiency.
Increasing the level of aflatoxin B2 to 800 microgram/kg of feed resulted in
fewer piglets born alive and weaned [Smith, T.K., Diaz, G. and Swamy,
H.V.L.N. (2005). Recent Advances in understanding mycotoxicoses in
swine. In:'Manipulating Pig Production X. Proceedings of the Tenth
Biennial Conference of the Australian Pig Swine Association (APSA)'.
Edited by J.E. Paterson; pp 236-247. APSA, Werribee, Australia.]. Indeed,
the effects of different aflatoxins on swine reproduction seem to be
cumulative:
Clinical signs of aflatoxin toxicosis include:
 Reduced feed intake
 Reduced growth rate
 Poor feed conversion efficiency
 Lower sow reproductive performance
 Reduced lipid digestion
 Altered kidney function

Liver damage:
 elevated y-glutamyltransferase
 elevated serum alkaline phosphatase
 reduced serum albumin and total protein concentration
 Reduced serum retinol and tocophenol concentration
 Vitamin A and E deficiency
 Reduced immuno competence = more susceptible to disease.

Intervention levels
It is proposed that 50 ppb should be the intervention level to prevent
the adverse effects of aflatoxins on pig performance. This takes account of
the possible cumulative or synergistic effects of other mycotoxins that may
affect immuno-competence and ensure minimal residue in pork, which may
affect the healthiness and safety of pork products.

Ochratoxin
Ochratoxin A is the most important of the ochratoxins which are
produced by several species of Aspergillus (ochraceus) and Penicillum
(verrucosum). Citrinine and oxalic acid are also produced by those moulds.
Ochratoxins are ubiquitous in both tropical and temperate climates and are
commonly found on oats, barley, wheat and maize. These moulds are
capable of producing ochratoxin A (or more simply, "ochratoxin") at levels
up to 10 parts-per-million (ppm). Such levels are rarely encountered, but
ochratoxin is hazardous to pigs at much lower levels, typically 0.2 ppm
(Krogh, 1991).
Ochratoxin introduced into the feed of monogastric livestock
contaminates organs, fat, muscle tissue, and blood. If ingested over a long
enough period of time by pigs, this mycotoxin can contaminate most of the
edible tissues, and can produce enough kidney damage to result in carcass
condemnation. Acute ochratoxicosis (concentrations greater than 5 ppm in
the diet) is characterised by nephropathy (impaired kidney function),
enteritis fatty liver, necrosis of the lymph nodes, immunosuppression along
with a variety of other pathological conditions. In acute cases, death may
occur due to acute renal failure. Interest in this mycotoxin has focused on
the carcinogenic nature of the compound as it can accumulate in the meat
of animals, leading to human health issues. Indeed, the Danish swine
industry uses ochratoxin levels in kidneys as an indicator to measure the
potentially harmful residue in pork products. Clinical signs and post-mortem
findings are indicative of ochratoxicosis which can be confirmed by
identifying the toxin in the feed or in the kidney at slaughter.
Pigs are quite susceptible to contamination owing to a rather long
serum half-life of 72-120 hr. Recent surveys have detected ochratoxins as
a natural contaminant of pig blood in Canada, and in many European
countries, including Germany, Norway, Poland, Sweden, and former
Yugoslavia. In addition, ochratoxin has been found in swine kidneys in the
USA, Austria, Belgium, Denmark, Finland, Germany, Poland, Switzerland,
Britain, and former Yugoslavia.
Ochratoxin residues in animal products are transmissible to
consumers, and some national governments have taken stringent
measures to allay consumer fears regarding their pork products. In Europe,
for example, in 1997 maximum tolerances of 5 parts-per-billion (ppb) for
ochratoxin were set for all foods, and Germany is presently enforcing its
own 3 ppb limit. In Denmark, an entire swine carcass is considered
contaminated, and is condemned, if 25 µg/mL ochratoxin is detected in the
blood.

Clinical effects:
The main symptoms of ochratoxin poisoning include reduced growth
rate and feed efficiency. Liver damage may occur, but the main effect is on
the kidneys, resulting in interstitial fibrosis. Increased water intake
(polydypsia), and hence increased urine output (polyuria) is a feature of this
syndrome. In young growing pigs perirenal oedema may occur, with
general stiffness. Gastric ulceration is also a consistent finding. Semen
quality in boars is reduced affecting fertilisation rate and hence overall
reproductive performance.
Clinical signs of ochratoxin poisoning include:
 Reduced performance (feed intake, growth rate, feed
conversion efficiency)
  Pale and enlarged kidneys = tubular degeneration, interstitial
fibrosis
 Impaired renal function = hyperproteinaemia, azotemia
 Kidney failure = mortality
 Increased water intake (polydypsia) and urinary output
(polyuria)
 Suppression of cellular immunity = greater susceptibility to
infection
 Reduced boar semen quality = reduced fertilisation rate =
reproductive performance
 Oedema in piglets = stiff arched back, impaired gait
 Gastric ulcerations

Intervention level
Dietary ochratoxin levels in pig feeds should not exceed 50 ppb.
Residues in pork products present a human health hazard, but at these
levels, the problems will be minimal. In combination with other mycotoxins,
ochratoxins can suppress immunocompetence in pigs.

Zearalenone
Zearalenone (F2) is produced by a strain of Fusarium
gramearum and proliferates under hot, humid conditions in a variety of
feedstuffs, but especially maize. It is an oestrogenic toxin and hence affects
reproduction. Rectal and vaginal prolapses are also common symptoms in
grow-finish animals.
Zearalenone is absorbed from the ration and is detected in the
plasma for 5 days after the last administration either as Zearalenone or ?-
Zearalenone. It is excreted in urine bound to glucuronic acid, as well as in
faeces and influences reproductive function and reduces the activity of 3-
alpha-hydroxysteroiddehydrogenase.
Zearalenone contamination may occur with DON with Gibberella ear
rot in corn or scabby wheat, but is more likely to occur during storage of the
grain rather than in the field.
Prepubertal gilts are most susceptible to contamination. Gilts and
sows exhibit vulval reddening and swelling, while vaginal and rectal
prolapses may also occur with zearalenone consumption. Irregular
oestrous cycles and reduced litter sizes are also commonly observed.
When fed 60-90 ppm zearalenone for the first 15 days post-mating, embryo
development is stopped . Not only is the litter lost, but females often won't
return to oestrus for several months.

Clinical effects/signs
 The most striking clinical feature is the swollen, red vulva of gilts and
sows. Reproductive performance is also affected and the consumption of
zearalenone-contaminated feedstuffs results in the birth of small litters, as
well as stillborn, splay-legged and weak piglets. Piglet birth weight is also
variable, as blood flow within the uterus may be impaired. Semen quality is
boars may also be affected. Clinical effects are listed below:

Intervention level
Like DON, zearalenone has been found in masked forms, which
complicates analysis. The proposed action/intervention level for
Zearalenone is 200 ppb.

Fumonisin
Fumonisins are produced mainly by Fusarium moniliform. Their
chemical structure enables them to inhibit lipid synthesis. Historically pigs
have been considered not as sensitive to Fumonisins as other species
such as horses, but recently fumonisins have been identified as a
mycotoxin of concern to pig production.
Fumonisins can be found in corn-producing areas. Types B1, B2,
and B3 are the most abundant fumonisins found, with B1 accounting for
approximately 75 percent of total fumonisin content.
Unacceptably high levels of fumonisins can cause excessive fluid to
leak into lung tissue causing pulmonary oedema. They also affect the liver,
resulting in jaundice and orange-yellow coloured lesions, evident at post
mortem examination. The presence of fumonisins can be easily detected
by the ratio of sphingamine to sphingosine in the liver, pancreas and
adrenal glands. This is used as a biomarker to indicate fumonisin
poisoning. It can also be used as a marker to indicate the presence of other
mycotoxins.
Clinical effects/signs
At toxic levels, pig performance is reduced and pulmonary oedema
is evident. Foetal damage may occur and immunocompetence is reduced
 Reduced performance
 Foetal damage
 Acute respiratory failure
 Pulmonary oedema
 Cyanosis (blue colour) of skin
 Jaundice
 Increased tissue sphingamine: sphingosine ratio (biomarker)
 Reduced immune competence = increased susceptibility to
infection = reduced vaccination response.

Intervention level:
 A threshold level of 200 ppb is proposed for fumonisin, as immune-
suppression effects are observed at this level. Residues in pork products
are not as hazardous as those of other mycotoxins.

Trichothecenes (T-2 toxin, Diaceptoxyscirpenol (DAS),

Deoxynivalenol (DON), HT-2 toxin etc.)
Trichothecenes are a group of toxins produced by several Fusarium
fungi, notably Fusarium graminearum and Fusarium sporotrichioides. The
most important structural features causing the biological activities of the
Trichothecenes are the 12, 13-epoxy ring, the presence of hydroxyl or
acetyl groups and the structure and position of the side-chains.
Trichothecenes are typical field toxins. They are produced on crops
and enter the feed via contaminated ingredients. Trichothecenes are
proven tissue irritants with the major observation associated with their
ingestion being oral lesions, dermatitis and intestinal irritation.
The major physiological response to trichothecenes mycotoxins is
loss of appetite, thus earning them the name, feed refusal toxin.
Trichothecenes are strong immune suppressive mycotoxins affecting
cellular immune response by directly affecting bone marrow, spleen,
lymphoid tissues, thymus and intestinal mucosa, where actively dividing
cells are damaged.

Vomitoxin (Deoxynivalenol or DON)

Deoxynivalenol (DON) is commonly known as vomitoxin. This
mycotoxin is produced by Fusarium graminearum that often occurs on corn
(Gibberella ear rot), wheat and barley (Head scab). The mould usually
develops during cool damp weather, resulting in a white or reddish fungus.
Levels above 1 ppm may reduce feed intake and subsequent rate of
weight gain. Concentrations above 5 ppm result in feed refusal and above
10 ppm may result in weight loss and vomiting. When contaminated feed is
replaced with clean, uncontaminated feed, pigs will generally resume
consuming feed with no other visual apparent signs.
Vomitoxin:
 Affects the gastro-intestinal tract (for example lesions)
 Levels of 1-2 ppm cause a reduction in feed intake and, as a
result, rate of gain
 As levels increase above 5 ppm, feed intake depression may
become severe
 Levels of 10-20 ppm cause vomiting and complete feed refusal,
resulting in reduced body weight gain or body weight loss
 Pigs will initially consume sufficient amounts of the ration to
induce vomiting, but will voluntarily reduce intake to stop vomiting
 Sows are more tolerant than young pigs
 Low levels can suppress the immune system
 T-2 Toxin
 More potent but less common than vomitoxin
 More likely to be produced during long periods of cool wet
weather
 1 ppm or greater causes vomiting and decreased feed intake
and growth rates
 Levels of 16-20 ppm cause complete feed refusal.

Clinical effects/signs
DON or vomitoxins are the most common toxins and have a major
effect on pigs. The large family of compounds is generally implicated when
there is feed refusal, vomiting and lesions of the gastro-intestinal tract in
pigs. The health of pigs is also affected due to the immuno-suppressive
effects of the mycotoxins. Liver weight is increased, whereas hepatic
protein synthesis is reduced. Brain serotonin concentration and activity may
also be increased.
Several studies have shown that at 3-5 mg/DON/kg feed, appetite in
pigs is greatly depressed, resulting in reduced pig performance. This has
considerable consequences for the lactating sow, since reduced appetite
influences milk yield and piglet growth rate and leads to greater weight loss
and poorer body condition at weaning. This lengthens the wean-oestrus
interval and affects subsequent reproductive performance. 

Intervention level
Because of the decline in appetite and performance, as well as the
immuno-suppressive effects, it is recommended that action be taken if the
concentration of DON in animal feed is >0.2 ppm. 

Ergot Toxins
These are produced from the ergot fungus Claviceps
purpurea which affects wheat, oats, ryegrass and other grains by entering
the seed and developing into a dark elongated body called a sclerotum.
This contains toxic alkaloids, one of which is ergometrine. This reduces the
size of the blood vessels and restricts the blood supply, particularly to the
mammary gland and body extremities.

Clinical effects/signs
Levels above 1 g of sclerotum per kg of feed produce clinical signs
of ergot poisoning. Typical symptoms include: poor growth rates, increased
respiratory rate and general depression. Newborn piglets are small and
weak, with a low survival rate. Blood flow to the mammary gland is
restricted and this causes agalactia in lactating sows. Lameness may also
be evident due to necrosis and sloughing of the hooves. Tail and ear
necrosis is common, eventually leading to gangrene.

Synergy of mycotoxins
The toxic responses and clinical symptoms observed when more
than one mycotoxin is present in feed are complex and diverse. The
combined negative effects on productivity and health of mycotoxins appear
greater than the sum of their individual effects.
The worldwide trading of feedstuffs may have contributed to the
proliferation of mycotoxins and increasing incidence of mycotoxicosis.
Mixing of different feed ingredients from different parts of the world
increases the risk that the feed will contain mixtures of different mycotoxins.
Synergies between mycotoxins may increase the severity of the attack. In
addition, the threshold level at which symptoms occur may be lower.
Indeed, it has also been shown that feedstuff contaminated naturally with
mycotoxins produces higher toxicity than equivalent amounts of purified
toxins. For example, Fusaric acid, the most common of
the Fusarium mycotoxins, increases the toxicity of DON in piglets.
In general, animal responses are more affected by a combination of
mycotoxins than by the individual mycotoxin and the response could be
described as either cumulative or synergistic, depending on the specific
combination of mycotoxins. It may well be that the severity of the symptom
is dependent upon the different sensitivities to the combination of
mycotoxins rather than to the differing effects on brain neurochemistry.
The toxicity thresholds vary between classes of pigs and their health
status. Individual mycotoxins seldom occur in isolation and there are
additive or synergistic interactions which markedly decrease the threshold
levels at which toxicity occurs. Consequently, there are no safe levels of
mycotoxins.

Non-feed sources of mycotoxins

It is generally assumed that feed-borne mycotoxins are the sole
source of contamination. Housing of pigs on straw is common in many
countries because of its perceived benefits to animal welfare and
environmental concerns. The consumption of straw is considerable and has
been estimated to be between 10 and 15% of total feed intake in weaned
pigs, and even higher in sows. If the straw is contaminated with
mycotoxins, then pigs on straw bedding may be at risk of increased
mycotoxin ingestion. In a recent Australian study [Moore, D.D. (2005).
Mycotoxins in straw used in deep-litter pig housing. In: 'Manipulating Pig
Production X. Proceedings of the Tenth Biennial Conference of the
Australian Pig Swine Association (APSA)'. Edited by J.E. Paterson; p 251.
APSA, Werribee, Australia], over 80% of straw samples examined were
positive for mycotoxins. Indeed, in one study, adding a mycotoxin
sequestering agent to the diet of pigs kept on straw bedding, improved
growth rate. This highlights the potential risk that straw and other material
used for bedding poses to pigs and the urgent need for appropriate
preventative action.

On-farm tests for mycotoxins

Pigs can be used to test for the presence of mycotoxins on the farm,
please see below for details;
Zearalenone
 Feed 4-6 week old gilts suspect feed for 7-10 days and
compare the redness and size of their vulvas with same aged gilts fed
clean feed
 A slight redness and swelling after 1 week indicates approx 1
ppm zearalenone
 Considerable swelling and redness after 3-4 days indicates 5
ppm or more
Vomitoxin
 Feed 4-6 week old piglets (for feeder operations use 35 kg pigs)
suspect feed for 1 week
 Compare feed intake and growth rate with same aged pigs fed
clean feed
 Levels of 1-2 ppm vomitoxin cause a slight decrease in feed
intake and growth rate which may be difficult to detect
 At 3-5 ppm, reduced feed intake will be apparent
 Levels of 10 ppm cause dramatic decreases in feed intake,
vomiting within 1 day of feeding and slow growth rate
T-2 toxin causes decreases in feed intake at 1 ppm.
As pigs eating T-2 and vomitoxin respond the same way, a lab test
is necessary to show if one or both are present in grain or feed.

Sampling and testing for mycotoxins

If clinical signs of mycotoxicosis are observed, it is important to
properly collect a grain or feed sample and send it to a laboratory to
determine the presence and level of the suspected mycotoxin(s). Sampling
accounts for 80 - 90% of the error associated with measuring mycotoxins in
grain or feed. Analytical tests for mould spore counts are of little or no
value.
Random samples (10 to 30) should be collected from several
locations within a batch of grain or feed and combined thoroughly to
provide a composite sample for submission. Using a grain probe at several
evenly distributed locations will provide the most representative sample.
Samples can also be collected periodically from grain being augured
which can also be an effective form of sampling. Paper bags should be
used to transport sample(s), since plastic bags retain moisture, and
therefore can promote additional fungal growth.
Contact the laboratory for specific sampling requirements prior to
submission.
It is important to remember that based on the uncertainties
associated with any mycotoxin test procedure, it is difficult to determine the
true concentration of a bulk lot.
Mycotoxins are difficult to measure for a number of reasons:
 Many different mycotoxins can be present simultaneously,
making analysis difficult and expensive. Under commercial conditions
analyses is normally limited to a couple of indicator mycotoxins.
 Sampling of bulk feeds is difficult. Mycotoxins are present in
'hot' spots and are not evenly distributed throughout the feed. Therefore
strict sampling procedures should be followed with many samples taken
from a particular batch to get a realistic reading.
 Latest research has identified complexes of mycotoxins and
their metabolites for which there is no accurate analysis method.

Feeding Strategies
As the risk of mycotoxicosis is very difficult to predict or evaluate,
prevention strategies should be initiated when assessing even a low risk
situation. Prevention strategies must primarily aim at minimising mycotoxin
formation in the field and during storage.
A significant reduction in mycotoxin formation can be achieved by
good agronomic practices, for example: 
 Selection of crop varieties that are more resistant to fungal foliar
diseases
 Ploughing up harvest residues
 Avoiding no-till soil management practices
 Proper crop rotation
 Avoiding monoculture
 During storage of dry feed ingredients, mycotoxin formation can be
successfully controlled by monitoring the moisture content of the feed. If the
moisture content is below 12%, moulds become metabolically inactive, and
the risk of mycotoxin formation is strongly reduced. To avoid mycotoxin
formation be aware of the following: 
 Moisture content below 12%
 Relative humidity below 60%
 Storage temperature below 20 °C
 Clean grain, avoid broken kernels
 Control insects and rodents
 Avoid stress (frost, heat, pH changes)
The incorporation of technical mould inhibitors such as Moldzap
(Alltech Inc, USA) further enhances stability of feed and ingredients during
storage. 

Mycotoxin adsorbents and binders

As we know mycotoxins are usually found in combinations in
complete animal feeds. A broad substrate binding capacity will ensure at
least some fraction of all the mycotoxins will be rendered non-bioavailable
and the bioavailable mycotoxins will be below the threshold of biological
activity. Broad substrate binding capacity of a binding agent will also
minimise the potential for toxicological synergy between mycotoxins.
Speciality feed additives, known as mycotoxin adsorbents or binding
agents are the most common approach to prevent and treat mycotoxicosis
in animals. It is believed that the agents bind to the mycotoxin preventing
them from being absorbed. The mycotoxins and the binding agent are
excreted in the manure.
The effective level of dietary inclusion for mycotoxin adsorbents will
depend on the mycotoxin binding capacity of the adsorbent and the degree
of contamination of the feed in question. A high binding capacity will
minimise the level of inclusion and minimise the reduction in nutrient
density caused by the feeding of the adsorbent. High levels of inclusion of
adsorbents can also alter the physical properties of the feed which might
impair feed processing such as pellet formation, in addition to altering the
actual diet specification.
Mycotoxin binding is achieved through both:
 Physical adsorption
 Relatively weak bonding involving van der Waals interactions
and hydrogen bonding
 Chemical Adsorption:
 (Chemisorption) is a stronger interaction which involves ionic or
covalent bonding.
An effective binder or sequestering agent is one that prevents or
limits mycotoxin absorption from the gastro-intestinal tract of the animal. In
addition, they should be free from impurities and odours. Be aware that not
all are equally effective. Many can impair nutrient utilisation and are mainly
marketed, based on in-vitro data only.
There are two types of mycotoxin adsorbent/binder:
 Inorganic binders
 Organic adsorbents
Inorganic binders
Inorganic mycotoxin binders are silica based polymers. Examples
could include:
 zeolites
 bentonites
 bleaching clays from the refining of canola oil
 hydrated sodium calcium aluminosilicates (HSCAS)
 diatomaceous earth
 numerous clays
They can be grouped into two categories: Phyllosilicates and
Tectosilicates:
Phyllosilicates: bentonites/montmorillonites
 Phyllosilicates are characterised by alternating layers of
tetrahedral silicon and octahedral aluminium coordinated with
montmorillonite oxygen atoms
 Isomorphous substitution leads to a net negative charge which
must be satisfied by the presence of inorganic cations (Na, Ca, Mg, K)
 Applications: Adsorbents for heavy metals, suspension-
stabilising agents in coatings, bonding agents for foundry sands and
washes, binder in pelletisation processes, desiccants in feed products.
Tectosilicates: zeolites
 Tectoalumosilicates of alkali and alkaline earth cations that
have an infinite three-dimensional cage-like structure
 Isomorphous substitution leads to a net negative charge which
is satisfied by the presence of inorganic cations (Na, Ca, Mg, K)
 Applications: Adsorbents for ammonia, heavy metals,
radioactive cesium and mycotoxins.
Such materials are often inexpensive and easy to handle. These
products are traditionally mixed with compound feed at a mill or mixed on
farm for home mixers. Costs are cheap but require a high inclusion rate in
animals. Most either only adsorb specific mycotoxins, bind minerals and
vitamins, cause other health complications or due to the high inclusion rate
required, are too expensive for industrial applications. However they are
also non-biodegradable and can present disposal problems when fed at
high levels of dietary inclusion.
The amount of organic acids in clays is often very small. Does the
small amount of organic acid(s) really work in inhibiting moulds? The
answer is NO; and it can actually do more harm than good: The small
amount of acids quite often has no effect. Worst of all, if the acids do work,
due to such small amounts, they are not enough to kill the mould. Instead,
the acids change the pH of the environment and bring pH stress to the
moulds. The pH stress can actually stimulates the moulds to produce
MORE mycotoxins. (REMEMBER, mycotoxins are the secondary
metabolites from moulds produced due to stress from environmental
factors, such as pH).

Organic Adsorbents
Organic mycotoxin adsorbents are carbon based polymers.
Examples could include: 
 fibrous plant sources such as:
 oat hulls
 wheat bran
 alfalfa fibre
 extracts of yeast cell wall
 cellulose
 hemi-cellulose
 pectin
Such materials are biodegradable but can, in some cases, also be
vectors of mycotoxin contamination. Benefits of yeast cell wall are low
inclusion, high surface area and certainly no toxic contaminants.
The efficacy of glucomannan-containing yeast products as
mycotoxin adsorbents in feeds has been investigated globally with several
studies with all animals. Research conducted in France at the National
Institute for Agricultural Research (INRA) identified four Saccharomyes
cerevisiae yeast strains that differed greatly in their glucan/mannan ratio. It
was found that large differences existed in adsorptive capacity between the
yeast strains with the amount of mycotoxin adsorbed strongly related to the
beta-D-glucan content. This research confirms earlier work carried out in
Alltech which led to the selection of a yeast strain high in insoluble beta-D-
glucan content for the design and production of glucomannan-containing
yeast product. (A. Yiannikouris et al., 2004) Advanced molecular
techniques were used to elucidate the spatial conformation and molecular
sites of interaction between zearalenone and glucomannan-containing
yeast product. Molecular modelling was used to locate the interaction sites.
Both hydrogen bonds and van der Waal's stacking interactions were
identified as key interactions between mycotoxins and glucomannan-
containing yeast product (Figure A).
 
Figure A
 Mycotoxin adsorbents offer an attractive short-term solution to the
challenge of mycotoxin-contaminated animal feeds. The only complete
solution to the mycotoxin challenge will be the long-term goal of eliminating
mycotoxins from the food and feed chains through improved quality control
based on better analytical techniques coupled with genetic advances in
plant resistance to fungal infestation.
If you are considering adding a mycotoxin adsorbent to your feed
you need to look for the following:
 Proven efficacy in vivo as well as in vitro
 Low effective inclusion rate
 Stable over a wide pH range (This is necessary so that the
mycotoxin stays attached to the adsorbent throughout the gut and is
excreted.)
 High affinity to adsorb low concentrations of mycotoxins
 High capacity to adsorb high concentrations of mycotoxins
 Ability to act rapidly before the mycotoxin can be absorbed into
the blood stream.
Above all when you are considering using a mycotoxin adsorbent
you need to be confident that the product has been proven to work in the
animal in a commercial situation. It is extremely important that any in
vitro results be supported by in vivo experiments relevant to the species
being fed.