Degrading mycotoxins – effects on a pig’s gut
The fight against mycotoxin occurrence in swine feed has a new dimension with the introduction of a fumonisin degrading enzyme in recent years. How does this enzyme contribute to pig health on the intestinal level?
Fumonisins are a group of mycotoxins mainly produced by Fusarium verticillioides and F. proliferatum. As these toxins mainly occur in (corn) maize, they represent a serious threat to swine production. The occurrence of fumonisins is ubiquitous and not limited to a specific climate. Recent Biomin Mycotoxin Survey data (Jan-Dec 2014) shows that 73% of all 1,071 corn samples analysed tested positive for fumonisin contamination, reaching a maximum level of 154,000 ppb fumonisins (in South East Asia, Table 1) with an average of positives of 2,914 ppb.
In Central European countries, where 76 corn samples were analysed, 46% tested positive for fumonisins with an average contamination of 454 ppb. 2,650 ppb was the maximum concentration found. The highest contamination levels are normally found in tropical and sub-tropical regions. In Southern European countries, 94% of corn samples tested positive for fumonisins, with an average contamination of 3,275 ppb and a maximum of 56,948 ppb. High contamination levels were also found in South America (average 3,171 ppb, maximum 52,438 ppb) and South East Asia (average 3,389 ppb, maximum 130,246 ppb).
Mechanism of action
Fumonisins disrupt sphingolipid metabolism and block the synthesis of complex sphingolipids, which are important components of nerves, muscles and membranes. As a consequence, free sphingoid bases (sphinganine and sphingosine) that are toxic to most cells accumulate in tissues leading to oxidative damage and lipid peroxidation, cell damage and apoptosis. Based on this, the sphinganine-sphingosine ratio (Sa/So) in serum is used as a biomarker for fumonisin exposure, an increase indicating a major disruption in the sphingolipid metabolism. Swine, besides horses and rabbits, is the species most affected by fumonisins. The main effects in swine are listed in Table 2.
Fumonisin counteraction
Preventive measures counteracting mycotoxins during growth of the grain as well as during harvesting or storage can only reduce the risk of mycotoxin contamination. Successful detoxification procedures after harvest are essential. The most effective way to counteract fumonisins is via enzymatic biotransformation, the highly specific and irreversible conversion of mycotoxins into non-toxic metabolites. The recently developed purified fumonisin esterase fumD (commercially available as FUMzyme), converts fumonisins into non-toxic hydrolysed FB1 (HFB1). Scientific studies demonstrate that HFB1 does not cause intestinal or hepatic toxicity in the sensitive pig model and does not induce major changes in the sphingolipid metabolism. This suggests that the conversion to HFB1 could be a good strategy to reduce FB1 exposure.
The efficacy of the aforementioned fumonisin degrading enzyme (FDE) in piglet diets contaminated with fumonisins was investigated further in in vivo experiments. A group of 18 four-week old, weaned, castrated male pigs (Piétrain x Duroc x Large White) were assigned to three treatment groups:
- a control group with no inclusion of fumonisins and FDE;
- a group with fumonisin contamination (6 ppm); and
- a group with 6 ppm fumonisins and the FDE (0.1%).
Fumonisins are well known to induce pulmonary oedema at high doses in pigs. In the present experiment, low doses of fumonisins (6 ppm FUM) induced lesions in the lung, especially depletion of bronchiole-associated lymphoid tissue and vascular disorders. These microscopic alterations resulted in a higher score in comparison to the control group. Occurrence and extent of these lesions were strongly diminished after addition of the FDE (Figure 1).
In the jejunum of animals fed fumonisin contaminated diets without FDE, histopathological analysis revealed the occurrence of many lesions, mostly villi flattening and fusion of villi. Inclusion of the FDE markedly decreased the occurrence and extent of lesions (Figure 2).
The enterocyte proliferation assessed through the number of mitosis was totally restored when FDE was added to the contaminated diet. A reduction of enterocyte proliferation in the presence of FDE was also observed in the control group (Figure 3).
Ingestion of fumonisins disrupts the sphingolipid metabolism by inhibiting the ceramide synthase, leading to an increased sphinganine/sphingosine (Sa/So) ratio in plasma. Fumonisins in the diet led to a significant increase of the Sa/So ratio in plasma. By the addition of the FDE, this remarkable increase in the Sa/So ratio was no longer observed (Figure 4).
Counteragent
Results of the study indicate that fumonisins represent a major risk to animal health and performance. Inclusion of an effective counteragent in the diets of pigs is crucial to help the animal to face fumonisin-induced impairment of the immune response and reduce intestinal disorders (inflammation and malabsorption) due to fumonisins.
Article featured in Pig Progress 31.2 2015.
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