Mycotoxins and mycotoxicosis in livestock production

8/20/2019 Mycotoxins and mycotoxicosis in livestock production

1/6

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

38 | Milling and Grain

F


2/6

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

August 2015 | 39

F

Be prepared for the EU recommendationComplete range of test kits for the analysis of T-2 & HT-2 in food & feed

R-Biopharm Rhône Ltd. • Block 10 Todd Campus, West of Scotland Science Park, Acre Road, Glasgow • Scotland G20 0XA • www.r-biopharm.com

R-Biopharm Rhône Ltd.

•

ELISA For quantitative screening· RIDASCREEN® T-2 / HT-2 Toxin (Art. No. 3505) · RIDASCREEN® T-2 Toxin (Art. No. 3501) · RIDASCREEN®FAST T-2 Toxin (Art. No. R5302)

• Lateral FlowFor rapid quantitative on-site results

· RIDA®QUICK T-2 / HT-2 RQS (Art. No. R5304)

• Immunoaffinity Columns For clean-up prior to HPLC or LC-MS/MS · EASI-EXTRACT® T-2 & HT-2 (Art. No. P43) · DZT MS-PREP® (Art. No. P73)

• Standards &Reference Materials

New


3/6

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


F


4/6

Nothing escapesRomer Labs.

FIND OUT MORE ABOUT ROMER LABSTESTING SOLUTIONS AND CONTACT:

Romer Labs Diagnostic GmbH

Technopark 1, 3430 Tulln, Austria

Tel: +43 2272 61533 10

Email: [email protected]

www.romerlabs.com

AgraS trip®

WA TE X no w

G IPSA appro ved


5/6

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


F


6/6

VIGAN Engineering s.a. Rue de l’Industrie, 16 • 1400 Nivelles (Belgium)Tél.: +32 67 89 50 41 • Fax : +32 67 89 50 60 • www.vigan.com • [email protected]

A win-win solutionbetween customer expertise and VIGAN know-how

Pneumatic or MechanicalShip Loaders & Unloaders

Port Equipment - Turnkey Projects

NIV: up to 800 tons/hour Average efficiency 75%-80%

A l l

t y p e

s of g r a

i n

Documents

Mycotoxins and mycotoxicosis in livestock production