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Mycotoxins: a Serious Threat to the Breeder Flock

16 November 2012


The effects of the various mycotoxins on breeders and their progeny are outlined here by Biomin.

The occurrence of mycotoxins is ubiquitous, which is why it represents a worldwide problem for the animal industry. Even with the use of prevention techniques in the field or during storage, it is actually impossible to avoid mycotoxins completely in agricultural commodities.

Thanks to modern analytical methods and growing interest in this field of research, more than 400 different mycotoxins have currently been identified. The toxicity of different mycotoxins brings serious risks to humans and animals. Mycotoxicoses are animal or human diseases caused by mycotoxin ingestion, inhalation or skin-contact. In animals, these range from immunosuppression and performance effects to hepatotoxic, nephrotoxic, neurotoxic, dermal, carcinogenic, reproductive, teratogenic and gastro-intestinal effects depending on animal-, environmental- and toxin-related factors.

The effects of mycotoxins in poultry depend upon the age, physiological state and nutritional status of the birds at time of exposure. Unfortunately, mycotoxins often occur in low concentrations that are difficult to detect, interactions between individual mycotoxins are not well characterised and unidentified mycotoxins may be causing sub-optimal performance. Nowadays, the poultry industry gives a lot of importance to cost management at all the steps of production.

In broilers, the production of hatching eggs or Day-Old Chick (DOC) does not represent a high proportion of the overall cost of production per kg of bird slaughtered. Nevertheless, the performance of broiler breeder is looked at with a lot of attention, and the number of saleable chicks per hen is always focused on. The quality of DOC and especially its influence on the improvement of their performance is a bit neglected. In general, the way that parental nutrition impacts the subsequent broiler and layer performance is poorly studied: most of the time, egg fertility and hatchability are more emphasised.

Difficult Diagnosis

It is not easy to detect or diagnose problems related to mycotoxins as their effects in poultry are diverse, varying from immunosuppression to death in severe cases, depending on toxin-related (type of mycotoxin consumed, level and duration of intake), animal-related (species, sex, age, breed, general health, immune status, nutritional standing) and environmental (farm management, hygiene, temperature) factors.

In the field, birds are exposed to a wide range of mycotoxins and are subject to a broad variety of stressing factors. They may be in poor health conditions, fragile immune and antioxidant status as well as subjected to problematic management practices. All these factors contribute a great deal to the final susceptibility of animals in the presence of mycotoxins. So, it is not surprising if birds exhibit mycotoxicoses even at apparent 'low levels' of mycotoxins present in the feed.

Invisible Losses - Subclinical Effects

Acute mycotoxicoses outbreaks are rare events in modern poultry production. However, low mycotoxin doses, which very often are not detected, are responsible for reduced efficiency of production and increased susceptibility to infectious diseases. Nonetheless, a more likely scenario is to find mycotoxins at lower levels interacting with other stressors leading to subclinical losses in performance, increases in incidence of disease and reduced reproductive performance.

To the poultry producer, these subclinical losses are of greater economic importance than losses from acute effects, but again, even more difficult to diagnose.

Clinical Effects of Mycotoxins in Poultry

Poultry are farm animals sensitive to mycotoxins as they suffer several toxic effects. Broiler chickens are more resistant to aflatoxins than other poultry like ducks, geese or turkeys.

Predominately, aflatoxins are the most immune suppressive, carcinogenic and hepatotoxic. Aflatoxins decrease feed intake, decrease daily weight gain leading to decreased slaughtering weight and egg production. Aflatoxins impair health of breeding birds and may cause inhomogeneous flocks and can cause decreased hatchability of eggs.

Type A trichothecenes (T­2 toxin, HT­2 toxin, diacetoxyscripenol) are of major concern to poultry industries and cause economic losses in productivity. They are highly toxic for poultry, especially for chickens, because they have very low LD50 values (2mg per kg for diacetoxyscirpenol and 4mg per kg for T­2 toxin). T­2 toxin, particularly, reduces feed intake, body weight, egg production and causes oral and gizzard lesions.

Young chicks and turkey poults are highly sensitive to ochratoxins. These nephrotoxins can suppress feed intake, growth, egg production and additionally causes poor egg shell quality.

Fumonisins are associated with spiking mortality in poultry. Signs of dietary fumonisin are decreased body weight and average daily weight gain as well as increased gizzard weights.

In comparison to other species like pigs, poultry are less affected by zearalenone (ZON) and also appear to be less sensitive to type B trichothecenes such as deoxynivalenol (DON). However, ZON can have negative effects on both fertility and hatch of fertile eggs.

Ergot alkaloids may induce neurotoxic effects as reduced feed intake while birds are reluctant to move and may be suffering by respiratory difficulties. Birds affected by ergot alkaloids have lower performance including poor growth and decreased egg production. Most obvious pathological changes are gangrenous lesions on toes, beaks and claws.

Table 1. Effects of mycotoxins during the critical periods in the life of breeders
Key stages   Effects of mycotoxins
Critical period 1
(0-6 weeks)
Massive intestinal development Reduced feed intake (Brake et al., 2006) and inhibition of protein synthesis reducing structural growth
  Development of the active immune system Immunosuppression (Sakhatsky & Trufanova, 2000; Harvey, 1991)
Increased risks and more difficult therapies to infection (Harvey, 1984)
  Start of the vaccination programme Reduced vaccine efficacy leading to lower titre levels (Yegani et al., 2006)
Reduced coccidiostat efficacy (Varga & Vanyi, 1992)
Critical period 2
(14/15-18/20 weeks)
Testis development Zearalenone shown to reduce testis growth (Chi et al., 1980; Maryarmma et al., 1992)
Cysts in testes (Brake et al., 1999)
  Ovary development Cysts in ovaries (Speers et al., 1970)
Early maturity
  Calcium metabolism Interference in vitamin D metabolism reducing calcium transport (Ellisalde et al., 1994; Verma, 2006; Devegowda & Ravikiran, 2009)
Critical period 3
(19/20-35/40 weeks)
Early laying period Haemorrhagic ovaries
Reduced egg production (Chowdhury & Smith, 2004; Yegani et al., 2006)
Reduced egg quality (Hoerr 2003; Oliviera et al., 2004)
Cessation of egg production (Palyusik & Koplik-Kováks, 1975)
  Mating stress Immune suppression leading to increased infections
  Growth Reduced feed intake limiting nutrient availability thereby reducing egg production and growth

Carry-over of Mycotoxins

Scientific reports mention that feeding diets contaminated with mycotoxins (DON, ZON) increased the percentage of non-viable germs, increased early and late embryonic mortality associated with reduced eggshell thickness. Fusarium toxins in naturally contaminated oats increased embryonic developmental anomalies and delayed ossification. Moreover, it was reported that hatchability was reduced due to embryonic mortality, being confirmed the teratogenicity of OTA. Aflatoxin accumulates in the genitals of chickens, turkeys and ducks, resulting in a transfer to the egg (albumen and yolk) as well as to their offspring (yolk sac and liver). When high T-2 toxin doses get into the egg, the eggs will appear infertile.

At lower toxin contamination embryonic development will start but the embryo will die at a later stage of development, presenting blood-spots. Alternatively, the fully developed embryo may fail to hatch due to its reduced vitality, or may die after hatching. All in all, the result of the mycotoxin transference into the egg and offspring is impaired fertility and hatchability which leads to less DOCs per breeder hen.


As poultry may be confronted by such a huge number of different mycotoxins it is a must to apply an efficient and successful mycotoxins risk management. Mycofix® product line represents a complex solution for the successful mycotoxin risk management.

The biotransformation agents may become the technology of choice, as enzymatic reaction offers a specific, irreversible and very efficient way of detoxification that leaves neither toxic residues nor undesirable by-products.

The elimination of adsorbable mycotoxins, such as aflatoxins and ergot alkaloids, can be achieved through adsorption while selected plant and algae extracts that counteract effects of non-degradable mycotoxins complete the picture for the successful control of mycotoxins.

November 2012

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