Your Breeder Flock on Mycotoxins

The importance of mycotoxin risk management for breeder flocks is explained by Biomin.
calendar icon 25 November 2011
clock icon 7 minute read

It is a fact that feed represents from 40 to 70 per cent of production costs in poultry production. Even if the amount of feed needed to grow a day-old chick (DOC) into a finished broiler is around 12 times higher than that needed to produce a DOC – and because of that some might say mycotoxins are no real issue in breeders – the fact is that while a broiler takes approximately 40 days to grow, a breeder will be exposed to these toxic substances found in the feed for much longer. And how valuable is a breeder in comparison to a broiler? And what are the consequences of this exposure to the offspring?

All people dealing with animal production will have heard the term mycotoxins, these ubiquitous toxic substances produced by toxigenic moulds (Table 1). Mycotoxins have a great negative impact on the performance and health of the animals ingesting them. When mycotoxins exist in breeder flocks, several aspects must be taken into account which will have a negative impact on the final productivity of the animals. General problems such as decreased feed intake, feed refusal, egg production, egg weight, egg shell quality, hatchability and higher mortality rates are well described in the literature and are known to occur in the presence of mycotoxin contaminated feeds. However, there are some other problems which may exist in a farm in which mycotoxins are (mistakenly) not considered to have an impact.

Table 1. Major mycotoxin-producing fungi and respective mycotoxins produced
Major mycotoxin producing fungi (amongst others) Major mycotoxins produced (amongst others)
A. flavus
A. parasiticus
A. ochraceus
Aflatoxin (B1, B2, G1, G2)
Ochratoxin (Ochratoxin A)
F. verticillioides (syn. F. moniliforme)
F. graminearum
F. pseudograminearum
F. culmorum
F. poae
Fumonisins (B1, B2, B3)
Type-A Trichothecenes:
T-2 toxin, HT-2 toxin, diacetoxyscirpenol
Type-B Trichothecenes:
Nivalenol, deoxynivalenol (DON), fusarenon-X, acetyl-deoxynivalenol

Mouth and Tongue Lesions

Type-A trichothecenes such as T-2 toxin exert an inflammatory response in the mouth that often progresses to necrosis and invasion by normal microbial flora. Lesion can vary from the so-called ‘black tongue’ in which usually the tip of the tongue is necrotised without further inflammation of the oral cavity or oesophagus, to raised, yellow necrotic plaques. In flocks where this condition is observed, it might be worth investing in type-A trichothecene analyses as for differential diagnosis tool.

Toxin Transference into Eggs

Although found at very low levels to, alone, represent a danger to human health, mycotoxins might be other concerns for producers who care about the quality of products they deliver, those being eggs for human consumption or DOC. In the latter case, thoughts must be focused on the viability of the offspring. Scientific reports mention the incidence of chick development abnormalities together with unabsorbed yolk sac and delayed ossification in birds fed DON-contaminated diets, although no signs are detected in the breeders. Also in the case of aflatoxins and their metabolites, studies show evidence of their accumulation in genitals and their transfer to the egg and progeny. Likewise, metabolites of zearalenone and T-2 toxin have also been reported to be transferred into the egg, with the same associated risks. Other evetns that might be connected with the ingestion of mycotoxin-contaminated diets are, for example, the increased incidence of soft-shelled eggs in hens fed diacetoxyscirpenol (DAS), alone or in combination with T-2 toxin.


Another aspect closely related to the transference of mycotoxins into eggs and malabsorption of the yolk sac is actually the immunity of the offspring as the immune system is a key target of several important mycotoxins.

Salmonellosis and candidiasis outbreaks were associated with the outbreak of aflatoxicosis in the 1960s, when aflatoxins were first identified. Moreover, other mycotoxins such as the trichothecenes group are good modulators of the immune system due to their capacity to inhibit protein synthesis. Regardless of the mode of action on how mycotoxins damage the immune system – either by affecting cellular responses or humoral factors – the net result is often the impaired resistance to infectious agents. Proof is provided in numerous papers reporting increased susceptibility to diseases such as pasteurellosis, coccidiosis, Marek’s disease, salmonellosis, infectious bursal disease (IBD), infections by Staphylococcus, Listeria, Mycobacterium and infectious bronchitis, amongst others. Interestingly, other studies report the impact of mycotoxins in poultry antibody titres. Figure 1 shows the decrease of the antibody titres against Newcastle disease, IBD and hydropericardium syndrome in broilers experimentally fed ochratoxin A in comparison with the control group.

Figure 1. Antibody titre response in broilers fed ochratoxin A-contaminated diets

Proper Mycotoxin Risk Management

After the acknowledgment that mycotoxins are a major hindrance to a successful production, mycotoxin risk management is crucial to eliminate the effects of mycotoxins and their toxicity. Binders are commonly referred to as substances used in animal feeds which will adsorb mycotoxins in the gastrointestinal tract, thus impeding them to be absorbed by the animal. However, while binders may be successful in the case of adsorbable mycotoxins, such as aflatoxins, for others, such as zearalenone, trichothecenes, ochratoxins and fumonisins their efficacy is much reduced or even zero.

The use of different strategies combined in one product such as the Mycofix® Product Line has proven to be very successful in vitro, in vivo and under the pressure of commercial production. Together with adsorption, biotransformation enables the conversion of non-adsorbable mycotoxins into non-toxic metabolites by means of microorganisms and their enzymes. Furthermore, bioprotection provides the hepato-protection and the immune support needed when animals are confronted with these toxic substances.

When to Carry out Mycotoxin Risk Management?

Whilst it is true that prevention should be done on a continuous basis since the mycotoxin threat is permanent, there are some critical periods during a breeder production cycle where their risk management should be stricter. These periods refer to those when animals, because of their stage and largely due to the stress that there are subjected to, are mostly sensitive to the hazardous effects of toxins (Figure 2). Young animals (up to eight weeks of age) are the most sensitive against mycotoxins even though their feed intake is low. Later on, the risk is that pullets do not maintain feed intake due to formulation changes, where mycotoxins are a threat. If the necessary laying weight is not reached, the achievement of sexual maturity might be jeopardised. Finally, the last critical period comprises the time from start of laying until after the laying peak, just following the stress of transfer, when animals are under very high production demand and still growing to reach their mature bodyweight.

Figure 2. High-risk periods in breeders when mycotoxin risk management should be stricter

Take Home Message

The management of mycotoxin risk must be done on a preventative basis rather than focusing on treatment. More frequently than not, the money lost with the reduced productivity and irregular results, increased mortality and susceptibility to diseases due to mycotoxins is greater than that invested in prevention. The use of a good mycotoxin risk management tool, such as the Mycofix Product Line, is of utmost importance to guarantee a successful and stable production with fluctuating feed quality in terms of mycotoxin contamination.

Important messages to be highlighted:

  • Regardless of the mode of action on how mycotoxins damage the immune system – either by affecting cellular responses or humoral factors, the net result is oftentimes the impaired resistance to infectious agents.

  • The money lost with the reduced productivity and irregular results, increased mortality and susceptibility to diseases due to mycotoxins is greater than that invested in prevention.

November 2011
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