As a result, high numbers of mycotoxins could already be present in the ingredients before they are received in feed mills or farms. Mould can also grow during feed processing especially when the temperature and humidity in the feed is increased during mixing. Finally, mould growth and mycotoxin production can also occur at the farm level from improperly cleaned silos, transport systems and feeders. The production of mycotoxins is enhanced by factors such as the moisture of the substrate (10 to 20%), the relative humidity (≥ 70%), the temperature (0 to 50°C, depending on the fungus species) and the availability of oxygen (Kanora and Maes, 2009). The most important role of feed mills is to keep the levels of mycotoxins as low as possible while multi-mycotoxin contamination should be also avoided. Most of the mycotoxins occur concurrently and a commodity usually contains more than one mycotoxin at the same time.

Test the raw ingredients

The best practical way to control mycotoxin levels is to use rapid test kit systems for the analysis of mycotoxins in raw ingredients which are not yet in silos. Different rapid test kit systems are validated for different mycotoxins and commodities and offer a very quick and effective way of raw material screening before they enter the feed mill. Once the levels are known, every feed mill can estimate the quality of its raw ingredients in terms of mycotoxin contamination and can effectively and more precisely (dosage adjustment) apply mycotoxin deactivator during feed production.

Test the finished feed

Another strategy of mycotoxin risk management is to test for the presence of mycotoxins in finished feeds. This method has some advantages and disadvantages. The most important advantage is that as every raw ingredient can bring its own mycotoxins into the finished feed and by only testing some raw ingredients by rapid test kits, some important raw ingredients whose inclusion is not high (5-10%) and which can still cause significant contamination of finished feed can be missed.

Since the 1960’s, many analytical methods have been developed for the testing of mycotoxins in human food and animal feeds due to the concern of toxicity for human health. Among them, the methods of thin-layer-chromatography (TLC), enzyme-linked immunosorbent assay (ELISA) and immunosensor-based methods have been widely used for rapid screening, while high-performance liquid chromatography (HPLC) with fluorescence detection (FD) and mass spectrometry detection (MS) have been used as confirmatory and reference. Accredited laboratory service is required for this step. The most important disadvantage is that analysis of finished feed takes quite a long time such that the tested feed is likely to have been fed to the animals by the time the results from the analysis are known.

Use mould inhibitors

Storage mycotoxin contamination (ochratoxins, aflatoxins) can be prevented by keeping temperature and moisture content in silos low whilst grain is regularly aerated. In case perfect storage conditions cannot be guaranteed, use of mould inhibitor is highly recommended.

Recognize typical symptoms in swine

Mycotoxins may cause various toxic effects or mycotoxicosis. Symptoms caused by mycotoxin contamination depend not only on the level and type of mycotoxin, but also on several factors such as animal species, sex, environment, nutritional and health status and other toxic entities. However, mycotoxin contamination is not transmissible between animals and contaminated feed is the likely cause. Diagnosis of mycotoxicosis is often very difficult because the effects of mycotoxins in animals are diverse, varying from specific to unspecific symptoms like immune suppression, diarrhoea, haemorrhages or reduced performance.

The most frequently concurrently occurring non-specific symptoms of mycotoxin contamination in fattening pigs and piglets is decreased feed intake or feed refusal – very typical for deoxynivalenol (DON) contamination and diarrhoea. It isknown that DON is capable of compromising several intestinal barrier functions, including a decreased surface area available for nutrient absorption and potentiation of intestinal inflammation. Both feed refusal and diarrhoea might contribute to decreased daily weight gains and low FCR in growing pigs.

Zearalenone is the mycotoxin most detrimental to swine and somewhat to ruminants with serious effects on the breeding stock. Young gilts and piglets are the most sensitive. Toxicity results in the reddening and swelling of the vulva, increased size of mammary tissue, straining with subsequent rectal and vaginal prolapse, as well as pseudo-pregnancy and false heat. The piglets of affected sows may experience depressed piglet growth in utero, early embryonic mortality and born with splayed legs. Fertility problems surface at 100 to 200 ppb. Zearalenone also produces swelling of the prepuce in boars.

The splay leg syndrome is the major congenital cause of lameness in suckling piglets. It is characterized by a temporarily impaired functionality of the hind leg muscles immediately after birth, resulting in inability to stand and walk (Papatsiros, 2012). Aetiology and pathogenesis of splay leg syndrome is complex and remain still poorly understood. Infectious factors might also be involved in the etiology. Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) causes late term reproductive failure in sows, which is characterised by increased number of stillbirths, weak, light weight and splay-legged piglets (Papatsiros et al., 2006). Exposure of piglets to another Fusarium mycotoxin – fumonisin B1 (FB1) increased the risk for PRRSV disease (Bane et al., 1992). Various management and genetic factors have been connected with the etiology of splay leg syndrome, such as farrowing induction, low birth weight, short gestation lengths, slippery floors and breeds (e.g., Large White and Landrace pigs) (Ward, 1978). In addition, nutrition can play a role to pathogenesis, as choline or methionine deficiency in sow diets are correlated with the presence of slay leg syndrome. Some researchers supported that one cause of splay leg was a deficiency of choline and methionine in the diet of the sow which are essential for normal myelin production (Kornegay and Meacham, 1973). In contrast, the addition of 3g choline and 5g methionine to the sows’ daily ration feed had no effect on the occurrence of splay leg (Dobson, 1971). Finally, nutrition is also involved in the etiological factors especially the zearalenone toxicity. The contamination of feed in sows with more than 4 ppm zearalenone can result in an increase in the number of piglets born with splay leg (Kanora and Maes, 2009).

Apply mycotoxin deactivator

The final possible step in mycotoxin management is the application of a mycotoxin deactivator. These products work strictly in vivo and will not counteract or mask mycotoxin in stored feed or raw ingredients. It is highly recommended to apply effective mycotoxin deactivator which offers an opportunity to significantly improve animal health, performance, productivity and profit impaired by mycotoxins. Depending on the target performance different mycotoxins can be more or less problematic. Therefore, using different products for different animal groups become a rational trend.

References

Bane D.P., Neumann E.J., Hall W.F., Harlin K.S., Slife, R.L.N. 1992. Relationship between fumonisin contamination of feed and mystery swine disease-a case-control study. Mycopathologia; 117, 121–124.

Dobson, K.J. 1971. Failure of choline and methionine to prevent splay leg in piglets. Austral. Vet. J., 47: 587-590. PMID: 5137938.

Kanora A. and Maes D. 2009. The role of mycotoxins in pig reproduction: a review. Veterinarni Medicina, 54, 2009 (12): 565–576.

Kornegay E.T. and Meacham T.N. 1973. Evaluation of supplemental choline for reproducing sows housed in total confinement on concrete on in dirt lots. J. Anim. Sci.37:506-509.

Papatsiros V. 2012. The splay leg syndrome in piglets: A Review. American Journal of Animal and Veterinary Sciences 7 (2): 80-83.

Ward, P. 1978. The Oxford companion to Spanish literature. 1st Edn., Clarendon Press, Oxford, pp: 629.