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PHOTO: KATERYNA KON


of fungal invasion under field conditions at the pre-harvest stage is a remaining challenge. Intensified plant production, plant genetics and cultivation methods including minimum tillage (to prevent soil erosion) are known factors that increased the vulnerability of cultivars to fungal invasion and subsequently increased the mycotoxin burden. The use of antifungal agents is restricted to certain times of plant growth and hampered by weather conditions, the structure of (leafy) plants and the risk to induce resistance to common antifungal agents. Soil management, crop rotation and lower seeding density are known to reduce fungal invasion. Moreover, optimising harvest times and cleaning of small grains after harvest are known strategies to reduce the mycotoxins burden of feed materials prior to processing. The most prominent factor driving fungal invasion and mycotoxin contamination, however, is the global climate change. Increasing temperature and draught, but also heavy local rainfall and flooding, are considered as unchangeable threats to plant health and subsequently fungal invasion and mycotoxin contamination.


Masked mycotoxins and multiple exposure scenarios The term masked mycotoxins had been coined following the observation that in controlled feeding experiments naturally contaminated diets seem to show higher adversity in animals than experimental diets prepared with crystalline, purified mycotoxins. The initial explanation of this phenomenon was that precursors of the known mycotoxin under consideration and the fact that fungal species often produce more than one toxin using different synthetic pathways. In the last decade, and with the advancement of analytical methods, it appeared that most of such masked mycotoxins are plant-derived con- jugates of known mycotoxins, mainly with one or more glu- cose molecule, as first described for deoxynivalenol (DON). Further analytical testing indicated that indeed in naturally contaminated materials, many Fusarium toxins occur in differ- ent forms (so-called modified mycotoxins) originating from plant metabolism of fungal toxins. The currently known struc- tures and the calculation of total diet contamination and tox- ic equivalent factors is summarised for various Fusarium tox- ins in recent EFSA Opinions addressing among others deoxynivalenol, zearalenone, and HT2/T-2 Toxin.


Animal exposure and primary and secondary health effects Adverse effects of mycotoxins in animals depend on diet composition, total mycotoxin intake and duration of mycotoxin exposure in the life-cycle of an animal. In the initial phase of mycotoxin research, interest focussed on acute clinical intoxications characterised by significant and visible organ damage resulting in the classification of hepatotoxic, nephrotoxic or teratogenic mycotoxins. Soon it


18 ▶ MYCOTOXINS | NOVEMBER 2021


became evident that many mycotoxins exhibit also immunomodulatory or immunosuppressive effects, cause cellular oxidative stress, and affect the reproductive system. In recognition of these detrimental effects of mycotoxins, in many countries feed quality programs based on (national) statutory limits were established to prevent significant adversity on animal health and well-being. The statutory limits are generally based on the toxicological (dose- response) assessment of a single mycotoxin. In real life, however, animals are given a mixed diet, containing mycotoxins from different sources. Subsequently, with feed quality programmes in place, the interest focusses now on the assessment of real-life exposure scenarios for mycotoxins in (farm-) animal populations under current animal feeding regimes.


Mycotoxins in pigs and poultry With the first investigations demonstrating that Fusarium mycotoxins (deoxynivalenol, nivalenol, fumonisins and others like patulin) affect intestinal integrity even at low feed concentrations thereby inducing gut leakage, a new phase in mycotoxin research emerged. Gut leakage cam facilitate the translocation of pathogens, endotoxins and other (bacterial) antigens form the intestinal lumen into the submucosal tissue, and ultimately into the blood stream. As the intestinal tract is also the largest immune organ of the body, an impaired intestinal barrier initiates a cascade of events resulting in a chronic inflammatory syndrome. Indeed, further research demonstrated that Fusarium toxins like deoxynivalenol (which is often used as a model compound) affect almost all functional components of the intestinal system, including changes in the microbiome, the production


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