mycotoxins and mycotoxicosis in livestock production
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Mycotoxicosis refers to the
different diseases caused
by exposure to different
mycotoxins, and it has a
high occurrence in livestock
production.
Mycotoxins are fungal
secondary metabolites, toxic
to humans and animals,
produced by certain species of fungus.
The growth capacity of these fungi depends on several
environmental factors such as moisture, temperature and
availability of energy and nitrogen sources.
Likewise, the production of mycotoxins depends on specic
environmental factors, and the presence of mycotoxigenic fungi
does not imply a presence of mycotoxins and vice versa, since
mycotoxins present great stability and can be present in feedstuffseven after the deterioration of the producing fungus.
Cereal and cereal by-products, corn grains and corn silage
are thought to be the most exposed ingredients to mold and
mycotoxin contamination, depending on various factors such as
grain handling, processing and storage conditions.
Mechanically damaged grain seeds are more prone to mold
contamination than intact ones. Storage facilities with high
moisture content (above 13 – 15 percent) and high temperatures
(above 25–27ºC) facilitate mold growth and contamination ofgrain.
Depending on the feed contamination level, exposure,
environmental factors, mycotoxin, fungal species and animal
species involved, the clinical symptoms may differ.
However, mycotoxins rarely occur at concentrations high
enough to cause clinical symptoms: mycotoxins are more
frequently present in animal feed at low concentrations,
producing subclinical symptoms over a long period of time,
which are more difcult to diagnose and are of greater economic
importance (Marquardt, 1996; Bryden, 2004).
It is important to emphasize that mycotoxicosis are often owed
to the action of several mycotoxins ingested by the animals.
Indeed, different mycotoxins can occur simultaneously in
feedstuffs, since some mycotoxigenic fungi are known to
produce different kinds of mycotoxins, and feed raw materials
are commonly contaminated with different fungi species at a
time (Bottalico, 1998; Sweeney et al., 1998). In addition, a large
number of studies have shown toxicological interactions between
different mycotoxins, ranging from synergistic to antagonistic
interactions (Grenier et al., 2011; Mallmann et al., 2011).
Therefore, it is important to test for an array of mycotoxins and
not for a single one in order to analyze feed quality and risks.
Major mycotoxins in animal feed
There are over 300 mycotoxins discovered, but the mainmycotoxins classes of concern in animal and human health are
produced mostly by species of genus Aspergillus, Fusarium and
Penicillium. In the European Union context, only a few of these
mycotoxins (aatoxins, fumonisins, deoxynivalenol, zearalenone
and ochratoxin A) are subjected to legal regulations setting
Mycotoxins and mycotoxicosis inlivestock productionby Francisco J. Martínez and Fernando Aguado, Export Department, Nufoer SL, Madrid, Spain
Cereal and cereal by-products, corn grains and corn
silage are thought to be the most exposed ingredients
to mould and mycotoxin contamination. This article by
Francisco Martinex and Fernando Aguado at Nufoer
SL in Spain looks at the major mycotoxins and why it is
important to test for an array and not for a single one
in order to analyse feed quality and risks
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maximum levels or guidance values for the major mycotoxins in
different feedstuffs for different animal species.
Aatoxins
Aatoxins are a group of mycotoxins produced by two
ubiquitous species of Aspergillus. They primarily occur in crops
produced in tropical and subtropical regions. Peanut cake, palm
kernel, copra and corn gluten meal are considered to be the
primal source of aatoxin exposure (EFSA, 2004a).
Toxigenic Aspergillus avus produces aatoxins B1 and B2,
while toxigenic Aspergillus parasiticus produces aatoxins B1,
B2, G1 and G2 (Cotty et al., 1994). Among those, aatoxin
B1 (AFB1) is considered to be the most prevalent and toxic
compound for animals and humans (EFSA, 2004a).
Aatoxins are liposoluble compounds, and therefore are easily
absorbed in the digestive tract. AFB1 metabolism has been
thoroughly studied.
It is known to be metabolized in the liver, resulting in ve
main metabolites, some of them with mutagenic, carcinogenic
and teratogenic effects, and with the capacity of diminishing
protein production (WHO, 1983; Nibbelink, 1986). Aatoxin
M1 (AFM1), one of AFB1 metabolites, is excreted throughmilk in signicant concentrations, and it is thought to have an
hepatotoxic and carcinogenic effects in humans (Henry et al.,
2001).
Furthermore, AFB1 metabolites can also be found in muscular
tissues of different livestock species (and therefore found in meat
intended for human consumption) (Trucksess et al., 1983) and in
eggs of laying hens (Herzallah, 2013).
In pigs, acute symptoms appear right after consumption of
highly contaminated feed and the animals show depression,
anorexia, jaundice, hemorrhages, ataxia, diarrhea and death;
Chronic intoxications result in long term economic losses because
of drops in daily weight gain, feed intake, worsening in feed
conversion ratio, etc.
Occasionally, animals can present scaly skin or purple coloring,
lethargy and depression (Diekman et al., 1992; Radostits et al.,
2000; Mallmann et al., 2011).
Susceptibility to aatoxins varies among poultry species and
breeds, being ducklings and turkeys the most susceptible species,
followed by quails and pheasants, and nally chickens, which
appear to be the most resistant species (Leeson et al., 1995).
Symptoms vary from decreased feed intake and weight loss to
a drop in hatch-ability and fertility, egg production and weight
(Leeson et al., 1995; Pandey et al., 2007, Herzallah, 2013).
Chronic intoxication in ruminants results in weight loss,
abortions, abnormal estrus cycle, decreased milk production,
mastitis, diarrhea and respiratory disorders (Cassel et al., 1988;
Guthrie, 1979).
Fumonisins
Fumonisins are a group of mycotoxins mainly produced by
fungi of the genus Fusarium. Among them, the most importanttoxins are those belonging to the B group (fumonisins B1, B2
and B3) (Cawood et al., 1991); being fumonisin B1 (FB1) the
most toxic and frequent one (EFSA, 2005). They are toxic to
both animals and humans and they are framed in the group 2B of
carcinogenic substances (IARC, 1993).
Although fumonisins are almost exclusively found in corn, they
can still be found in other crops (Bullerman et al., 1994). Corn
and corn by-products are extensively used in animal nutrition.
Corn grain, for instance, because of its high energy content, is
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one of the main components used in monogastric diets and cattle
concentrates.
Moreover, corn silage is frequently used in cattle nutrition,
and may represent up to 80 % of the daily ration. Corn by-
products such as corn oil, corn gluten or corn germ meal are also
frequently used in animal nutrition. Since fumonisins are stable
in high temperatures and resist fermentation, they can be found in
processed feedstuffs.
Fumonisins chemically resemble sphinganine and sphingosine,
responsible for the synthesis of sphingolipids, structural
compounds of cell membranes and are present in different tissues,
especially in the nervous system. These mycotoxins are able to
disrupt the metabolism of sphingolipids, causing alterations in
cell growth and differentiation, apoptosis and necrosis (Merrill et
al., 1996; Norred et al., 1998).
The toxins are eliminated mainly through feces, but a certain
amount can be eliminated through eggs and milk in laying hens
and dairy cattle respectively when high doses of fumonisins are
consumed.
Swine and horses are the most sensitive species to fumonisins,
especially to FB1; while poultry and ruminants are apparently
more resistant. Chronic intoxication in pigs is characterized
by low feed intake and weight gain, hepatic encephalopathy
syndrome, hyperplastic oesophagitis, gastric ulceration and heart
and pulmonary arteries hypertrophy (Casteel et al., 1994; Smith
et al., 1999; Gumprecht et al., 2001).
In poultry, symptoms range from a decrease in feed intake and
weight gain (Javed et al., 1993) to a decrease in egg production
and mortality increase (Prathapkumar et al., 1997).
Dairy cows show a decreased feed intake and milk production
(Richard et al., 1996; Diaz et al., 2000).
Ochratoxins
Ochratoxins are a group of secondary metabolites produced by
species of Penicillium and Aspergillus. There are seven known
ochratoxins. Among them, ochratoxin A (OTA) is the most
important mycotoxin, because of its toxicological signicance,
carry-over capacity into human food, frequent presence in
contaminated feedstuffs, stability against cooking and fermenting
processes and possible signicance as human carcinogen
(classied as an IARC group 2B carcinogen in 1993). OTA is
mostly found in barley, wheat and rye (Cabañes et al., 2010).
In ruminants, OTA is metabolized into a less toxic compound
by the ruminal microora. Once OTA reaches the bloodstream, itbinds to serum proteins, especially to albumin, conferring OTA an
elevated half-life in blood serum, and therefore can be found in
blood-based products, such as bloodpudding or additives made of
pig-blood or pig-plasma. Residual concentrations can be found in
liver, muscle and fat tissues, eggs and milk (Suzuki et al., 1977;
Galtier et al., 1981; WHO/FAO, 2001; EFSA, 2004c; Völkel et
al., 2011).
OTA inhibits protein synthesis by competition with the amino
acid phenylalanine, and also promotes cell oxidation (WHO/
FAO, 2001; Marin et al., 2009). Furthermore, OTA is thought to
be involved in the occurrence of Balkan Endemic Nephropathy
in humans (Vrabcheva et al., 2004), though there might be other
environmental agents required to develop the disease (Abouzied
et al., 2002).
The pig is one the most sensitive species to OTA. The
mycotoxin primarily affects kidneys (Krogh, et al., 1979), sperm
production and quality reduction in boars (Biro et al., 2003).
Intoxicated animals develop polydipsia, up to four times the
normal water intake, and polyuria as a consequence. These signs
can be accompanied by diarrhea, bloody urine, decreased feed
consumption, decreased feed efciency and decreased weight
gain (Szczech et al., 1973; Krogh et al., 1979; Cook et al., 1986).
Poultry species seem to be less sensitive than pigs to the effects
of OTA, mostly showing altered performance: reduced feed
consumption, feed conversion, weight gain and egg production
(Duarte et al., 2011).
Zearalenone
Zearalenone (ZEA) is a mycotoxin produced by different
species of the Fusarium genus (Bennett et al., 2003), and
almost always co-occurs with other Fusarium toxins such as
deoxynivalenol (DON). ZEA is particularly found in corn grains
cultivated in temperate and warm regions, but it can also be
found in other cereal crops such as wheat, barley or rice, and
occasionally in sorghum and soy beans (EFSA, 2004b; Zinedine
et al., 2005). ZEA resists high temperatures, and shows good
stability during storage and processing, and therefore it can be
found in processed feed and food.
As a detoxifying mechanism, plants are able to chemically
modify ZEA and DON via acetylation, glucosidation and
sulfation (Berthiller et al., 2005). The resulting metabolites,
which have been found to be toxic to animals, are often
undetectable with standard laboratory techniques. To fail to detect
them could lead to an underestimation of the toxic potential of
feeds (Vendl et al., 2009). It has been reported that gut microbiota
is able to hydrolyze those “masked” mycotoxins and release their
native forms (ZEA and DON) (Gareis et al., 1990; Gareis, 1994;
Berthiller et al., 2011).
ZEA is an estrogenic compound that binds competitively
estrogen receptors in different tissues (especially uterus, mammary
gland and liver) and generates estrogen-like responses. ZEA is
metabolized mainly in the liver, resulting in two major metabolites,
both also possessing binding afnity to estrogen receptors. Because
of its estrogenic activity, ZEA affects females over males and
young animals (particularly young females) over adults.
Pigs seem to be most susceptible to ZEA (Diekman et al., 1992),
showing hyperemia, edematous swelling of the vulva, increase
of uterine, ovarian and mammary gland size, and occasionally
vaginal or rectal prolapse (Etienne et al., 1981; Haschek et al.,
1986). ZEA also have teratogenic effects in piglets and affects
embryonic survival (D’Mello et al., 1999). In males, ZEA induces
a reduction of the weight of testes and sperm quality (Mirocha et
al., 1977).
Poultry species are less susceptible to ZEA, and adverse effectsare only observed at very high doses of the mycotoxin that are
unusual in eld conditions.
Cattle seem to be more resistant to the estrogenic effects of
ZEA because of the ruminal degradation of the mycotoxin
(Kiessling et al., 1984).
Cereal and cerealby-products, corn
grains and cornsilage are thought tobe the most exposed
ingredients to moldand mycotoxin
contamination
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Trichothecenes
Trichothecenes are a group of chemically related compounds
produced by a wide number of fungi and are classied
into four different chemical groups: Types A, B, C and D
(McCormick et al., 2011). However, those of concern in
livestock production are those produced by Fusarium species,
and include Type A and Type B toxins. Type A toxins include
in turn T2-toxin and its metabolite HT-2 toxin, and Type B
toxins include DON.
DON, T2-toxin and HT-2 toxin usually occur with other
Fusarium mycotoxins such as ZEA and fumonisins, in warmer
climates. T2 toxin and HT-2 toxin concentrations in wheat, rye
and oats were found to be highly correlated (Gottschalk et al.,
2009; Edwards, 2009). Among trichothecenes, DON is the most
frequently occurring toxin, but is about 100 times less toxic than
T2-toxin. T2 and HT-2 toxins are signicantly bound to the outer
hull of cereal grains; therefore by-products for the feed industry
obtained through de-hulling may contain greater concentrations
of those two toxins.
Trichothecenes inhibit protein synthesis, interact with
proteins and cause oxidative stress by generating free
radicals (McCormick et al., 2011). T2 toxin also inducescell apoptosis in the digestive tract (Li et al., 1997). Pigs
are very sensitive to DON while poultry species seem to be
more resistant to its effects. In pigs, exposure to these toxins
causes immunosuppression, vomiting, diarrhea, gastric and
intestinal hemorrhage, dermatitis, feed refusal, weight loss
and lower milk production, among other problems (Mallmann
et al., 2011). Vomiting has been observed at high doses of
DON in feed, making this toxin to be commonly known as
“vomitoxin”.
Broilers and laying hens appear to be less sensitive to
the mycotoxin. At low dietary concentrations in chicken,
DON causes a reduction in feed consumption, and at high
concentrations, weight loss, immunosuppression, and decreased
intestinal nutrient absorption (Prelusky et al., 1986; He et al.,
1992; Rotter et al., 1996; Awad et al., 2008). Ruminants are more
resistant to DON, which is attributed to its metabolism by rumen
bacteria (Seeling et al., 2006).
Animal products do not contribute in a signicant way to
human exposure to DON (EFSA, 2004b). Since no human
diseases due to carry-over have been reported, DON’s importance
remains primarily economic because of its decrease of animal
productivity (Völkel et al., 2011).
Pigs are among the most affected animals towards the effects
of the T2-toxin. Dietary exposure to the toxin resulted in reduced
feed intake which led to reduced weight gain, in most cases
without affecting feed conversion rate (Harvey et al., 1994;
Rafai et al., 1995). Lesions caused by ingestion of T2-toxin are
observed mainly in the upper digestive tract, mainly ulcerations
and hemorrhages (Weaver et al., 1978). High concentrations of
the toxin in feed can induce diarrhea and perineal lesions due to
the contact with residual toxins in faeces (Mallmann et al., 2011).
Effects of T2-toxin on reproductive performance in sows have
been reported (Glavits et al., 1983).
In poultry, acute intoxication leads to nervous symptomatology:
hyperpnoea, lethargy, loss of balance and head dropping appeared
after a few minutes and disappeared quickly. Soon after, digestive
problems follow, characterized by repeated deglutition, diarrhea,feed refusal and hemorrhages in the digestive system (Grevet,
2004). Chronic intoxication is characterized by alterations in
production and reproduction performance, skin and mucosa
lesions, and immune system alterations in different poultry
species.
Though ruminants are more resistant to trichothecenes because
of the toxin metabolism in the rumen, T2 intoxication in cattle
causes feed refusal, gastroenteritis and gastrointestinal lesions
(Petrie et al., 1977; Weaver et al., 1980), intestinal hemorrhages
(Petrie et al., 1977), ruminal ulcers and even death (Pier et al.,
1980). Decreased feed consumption, decreased milk production
and alterations in the estrous cycle were the observed effects in
dairy cattle (Kegl et al., 1991).
Because of the metabolism and biotransformation of T2 toxin,
it is though that its accumulation in animal tissue is prevented.
However, it has been shown that transfer to milk is possible
(Völkel et al., 2011).
Mycotoxicosis prevention
There is no effective treatment of the intoxication once the
clinical signs appear and in some cases, even if the animal
recovers from the intoxication, its performance will remain
low. It is then important to highlight the necessity of preventing
mycotoxicosis, either by preventing mold contamination and
mycotoxin formation or by eliminating mycotoxins in feedstuffs.
Though preventing the formation of mycotoxins in the feed is the
best measure to avoid mycotoxicosis, it is not always an easy oravailable strategy. And, as aforesaid, even if the mycotoxigenic
fungi are eliminated from feed, some mycotoxins show
great stability and can remain in feedstuffs. Thus, mycotoxin
elimination measures in feed should be a secure way to prevent
mycotoxicosis in animals.
Different methods for mycotoxin elimination in animal
feed have been described, ranging from inclusion of natural
compounds (such as organic acids) to physical methods (X-ray
or UV light), microbiological methods (enzymes produced
by microorganisms) and chemical methods (oxidant agents or
mycotoxin adsorbents among others). Among all these methods
for mycotoxin elimination in animal feed, the most implemented
is the addition of natural clays, because of its low cost, simple
application and the absence of adverse effects in animals. Those
clays adsorb mycotoxins that may be present in the feed and
prevent them to be absorbed (Van Kessel et al., 2010).
Our solution
Knowing the risks inherent to the presence of mycotoxins in
animal feed and its repercussions in animal health and livestock
production, NUFOER’s main concern has been to develop a
product able to prevent and to counteract the impact of these
fungal toxins while remaining affordable. Assuring the quality of
the ingredients used, and excluding any drug or pharmaceutical
compound, we developed a series of mycotoxin binders which we
brought together under the brand NUFOTOX.
Our binders’ product line range from basic mycotoxin binder
(NUFOTOX) 100 percent made of natural clay (Hydrated
Sodium Calcium Aluminum Silicate, HSCAS) to a most
advanced binder (NUFOTOX ADVANCE), adding different
ingredients such as organic acids, enzymes, plant extracts, yeast
extracts or biopolymers, depending on the toxin binder required.
How so “depending on the toxin binder required”?
There are many different molds and mycotoxins that
contaminate animal feed, some more complex than others,
and affecting the animal differently. On this basis it becomes
necessary to implement the binding activity of the HSCAS,control mold contamination levels, and sometimes, even help
the animals’ recovery from the intoxication. Each of NUFOER’s
toxin binders is designed differently in order to fulll those
different aims.
References available upon request
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