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Understanding the mycotoxin threat is key

For effective solutions, understanding the mycotoxin threat is key. Mycotoxins in feed pose a serious threat to poultry health and performance. However, the level of threat, differences in toxicity and impact on productivity remain less well understood. Let's have a look at mycotoxins in the poultry industry.

With the knowledge that mycotoxins are eating away at poultry operation profits, there has also been a surge in the development and availability of in-feed solutions to the mycotoxin challenge. Although to date most have taken a one-size-fits-all approach that simply adjusts dose rate to bodyweight for each livestock species. This is now changing, however, following the emergence of a strong rationale for mycotoxin solutions that target the specific mycotoxin threat and physiological differences of each individual species. For the poultry industry, for example, the Aspergillus mycotoxin aflatoxin (AFB1) remains the greatest threat, with poultry more susceptible to AFB1 ingestion than any other livestock species.

Prioritising mycotoxin risk

Mycotoxins first came under the spotlight in 1960 when the so-called ‘Turkey X Syndrome’ outbreak was traced to the presence of AFB1 in turkey feed. Since then, many additional mycotoxins have been identified, though AFB1 remains of primary concern to the poultry industry.

The mycotoxins produced by Aspergillus moulds – which includes the ochratoxins (OTA) as well as AFB1 – regularly develop during the storage of feeds and feed ingredients, as well as infecting growing crops. Any time feeds are exposed to moisture, the risk of Aspergillus growth is increased. With many key monogastric feed ingredients produced in regions of the world known to suffer from high humidity, the risk of OTA and AFB1 contamination can be considered to be permanently high.

In addition, commercially-produced poultry in modern production units are routinely exposed to considerable levels of Fusarium mycotoxins due to the heavy reliance on cereal grains within monogastric feeds. In a survey of poultry diets from across Europe, the Middle East and Russia carried out by Micron Bio-Systems between 2014 and 2015, 96-97% of samples contained deoxynivalenol (DON), fumonisin (FUM) and zearalenone (ZON), with DON in particular found at extremely high levels that averaged over 900ppb (Figure 1).

Although no AFB1 or OTA were found in these particular samples, the risk may be higher in other regions of the world.

Species-specific mycotoxin threat

The relative level of toxicity, as well as potential exposure, varies substantially between different livestock species, and is one of the main drivers of new developments to tailor mycotoxin solutions to each species individually. In pigs, for example, the greatest risk to health and performance comes from the Fusarium mycotoxins FUM and ZON, plus the trichothecenes DON and T2 toxin (also produced by Fusarium moulds).

Such differences are already recognised by key regulatory authorities. In the EU, for example, the maximum permitted limit for FUM in poultry is 20ppm and there is no specific limit for ZON, whereas in pig feed the limits for FUM and ZON are set at 5ppm and 0.1ppm, respectively.

Differences also extend to the importance of the various negative effects of mycotoxin ingestion on health and performance. Table 1 outlines the main organs affected by each of the key mycotoxins, and although similar at a cellular level, the impact on production can differ widely.

Despite its lower relative toxicity, ingestion of ZON is of critical importance to breeder and layer units since it is an oestrogen mimic that can reduce fertility and egg production. The effect of DON, FUM and T2 toxin on immune function is also potentially damaging during the breeder stage of the production cycle, due to the impact on the breeder and the potential to cause immune dysfunction in progeny, with knock-on effects such as increased abnormalities and reduced body weight.

Growth performance impact on poultry

Other symptoms of the Fusarium mycotoxins include increased embryonic mortality and diarrhoea, plus reduced hatchability, feed intakes and body weight gain.

It means that although poultry are typically considered to be relatively resistant to the Fusarium mycotoxins, the potential threat should not be overlooked.

Even low levels of DON and T2 toxin, for example, are known to damage the lining of the small intestine and reduce nutrient absorption. This has the potential to negatively affect feed conversion efficiency, feed intakes and liveweight gain.

There is even some evidence to suggest that certain mycotoxins can predispose poultry to other diseases, such as Clostridium perfringens-induced necrotic enteritis and coccidiosis, leading to reduced growth rates, poorer feed conversion and higher mortality.

However, it is the Aspergillus mycotoxins that remain the top priority. AFB1 is a carcinogenic compound that is known to affect gene regulation and metabolism at the cellular level – symptoms include liver damage, development of fatty liver, immune suppression and reduced growth rates – whilst OTA is associated with renal dysfunction and kidney damage, and is reported to affect weight gain, feed intakes and immune function. Both can cause increased mortality where levels of exposure are high.

Mycotoxin remediation strategies

It should be no surprise, therefore that the use of in-feed mycotoxin deactivators and binders to protect bird health and productivity has increased markedly in recent years. The most common approach is to use clay minerals or yeast cell walls to bind with the mycotoxins, though efficacy varies depending on the mycotoxin and is typically more effective against AFB1 and less so against Fusarium mycotoxins.

The ability to maintain efficacy within the pH range typically found in the bird’s gastro-intestinal tract (pH 3-7) is also critical to success, and can vary considerably between different binders (Figure 2).

An additional strategy, particularly for non-polar mycotoxins, is to remove or modify a particular functional site on the surface of the mycotoxin. This transformation can render the mycotoxin harmless, or expose the binding site of the molecule to mineral binding agents, and is typically achieved using specific enzyme combinations and micro-organisms.

Finally, degradation is the application of multiple transformations to ensure that any mycotoxin fragments remaining after transformation – even if bound to a mineral binder – do not retain any toxic effect. For poultry producers, the strategy of transformation and degradation is critical, since it is the most effective in eliminating the effects of DON, which is one of the most prevalent mycotoxins in poultry feeds.

Targeted poultry solutions

The most effective approach is typically a combination of all three strategies. It’s also now clear that to maximise efficacy those strategies need to be correctly prioritised to match the specific needs of poultry, in terms of both exposure and vulnerability.

The recent development of species-specific in-feed mycotoxin solutions such as Ultrasorb P therefore represents a major advance in mycotoxin remediation, and is already leading the way towards potential customised, bespoke solutions based on individual farm mycotoxin profiles. Although reliant on effective and timely testing of feed samples for actual mycotoxin loading, the potential benefits from such a flexible, yet highly targeted, approach are likely to generate considerable interest in years to come.


Source: World Poultry magazine, Volume 32.1 (2016)

Liz Norton, Micron Bio-Systems

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