Mycotoxin occurrence in silage.
When it comes to managing mycotoxins in silage, prevention is always better than cure. However, treating this problem has limitations and there are several risk factors that can hamper your silage-making efforts.
From a ruminant point of view, grain and roughage, being the two main sources of animal nutrition, are always potential harbourers of mycotoxins. Silage is a key component in ruminant rations, especially in terms of quantity as it is a high-moisture roughage storage form and when not done correctly tends to support mould growth. Silage is therefore an important potential contributor to mycotoxin contamination of rations.
Moreover, maize silage combines the grain and roughage components, as a large quantity of the toxins that can potentially form in-field on grain can, among others, also end up in the silage.
A distinction must be made between field-derived and silage-derived mycotoxins. Field-derived mycotoxins that end up in your bunker are beyond your control. The presence of these mycotoxin producing moulds in the field depends on several factors, including climate, season, region, cultivar and the crop cultivated on the same field the previous season.
However, mycotoxin formation in silage is dependent on the producer’s management framework, because a lack of management combined with incorrect inputs afford these potentially dangerous moulds the opportunity to proliferate. Hence, it is preventable.
Deterioration and formation
The good news is that well-preserved silage that is fully anaerobic renders some toxins inactive, allowing them to deteriorate over time – they detoxify, as it were. Unfortunately, some species do survive this storage period of silage and play a negative role in ruminant nutrition.
It is worth noting that not all environments are conducive to mycotoxin formation. Mycotoxins are mould’s defense mechanism against its environment. During the aerobic growth of mould (when it is even visible to the naked eye), it is often not actively forming toxins; however, toxins are formed in the layer directly beneath this visible mould, where it has been activated by the remaining oxygen but is not actively multiplying.
Let’s take the silage bunker’s top layer for example – the spoilt, mould-ridden part of the top layer, which is typically removed first, is only the first layer of the problem. The silage directly underneath this visible spoilt layer can in some cases contain extremely high levels of mycotoxins, but because it is usually not discarded, it is fed to animals without the producer being aware of it.
Is removing the oxygen as quickly as possible enough to prevent mould growth and therefore mycotoxin formation in silage? Unfortunately, the answer is ‘no’; however, there are some misconceptions regarding this process. The oxygen removal rate is indeed an aspect of silage-making that prevents mould. This relates to the time oxygen is still available in the silage, potentially leading to microbial growth, including that of mould.
Most silage is eventually rendered anaerobic, but the last of the oxygen not removed by mechanical processes such as compaction can still serve as fuel for aerobic spoilage organisms, giving them a chance to multiply before entering dormancy in a preserved, anaerobic environment. If the rate of oxygen removal was slow, these spoilage organisms would have increased in number and when the silage is eventually opened for feed-out, they will have a major negative impact.
This problem typically presents itself when having to manage the silage bunker face. The number of oxygen-activated spoilage organisms is directly proportional to aerobic instability and subsequent deterioration of and losses occurring on the silage face.
Negative effects
Finally, some mycotoxins, when ingested, lead to major problems and suppress rumen function. Intake is the main driver of efficient livestock production and anything that suppresses intake will have a negative effect on production. This also pertains to impaired rumen function, as it causes substandard feed conversion and reduced immunity. Prevention therefore remains the preferred strategy.
