Fumonisins (FUMs) are mycotoxins produced by Fusarium proliferatum and F. verticilloides.6, 9 These mycotoxins occur worldwide and are predominant contaminants of maize and maize by-products.6 This group of mycotoxins mainly consist of fumonisin B1 (FB1), FB2 and FB3, with FB1 being the most toxic.1, 9 It is unknown what the exact conditions that trigger FUM production are, but drought stress followed by warm, wet weather during flowering seem to be relevant.4, 6 Insect damage to plant plays a role as well, allowing fusarium to penetrate the ear and the kernels. Fusarium is mainly a field fungus and can be present on soil and on the plants seeds.1, 5, 6, 7 This fungus is capable of penetrating the stylar canal of intact kernels, therefore even those kernels that look completely fine from the outside may be infected by fusarium on the inside.4 FUMs are quite stable mycotoxins and resist several decontamination and manipulation processes being able to reach final products intended for human consumption like corn flakes.5


FUMs disrupt the metabolism of sphingolipids (important components of cellular membranes and neural tubes) through the inhibition of the enzyme ceramide synthase.1, 5, 6, 9, 10 These mycotoxins are generally poorly absorbed by the gastrointestinal tract, hence intestinal cells are exposed to their toxic effects for longer periods of time and this can result in their damaging.3, 5, 6, 9 FUMs are cancer promoters and possible carcinogens to humans (group 2B, IARC 2002). These mycotoxins are hepatotoxic, nephrotoxic and immunosuppressive.6, 9, 10 FUMs cause alteration of the intestinal barrier function and undergo synergistic effects with other mycotoxins like DON, contributing to the disruption of the intestinal barrier and favoring the translocation of other toxic entities and pathogens.1, 3, 6, 9, 10 Other adverse effects of FUMs are cardiotoxicity, decreased feed consumption, dyspnea, weakness, cyanosis and neural tube defects (NTDs).8 Known animal diseases caused by FUMs are the porcine pulmonary edema (PPE) and the equine leukoencephalomalacia (ELEM).1, 6, 7, 9, 10 Horses, followed by pigs are the animals that are affected the most by FUMs. Poultry was considered generally more resistant to FUMs although this position has been recently revised due to recent studies where the synergistic interactions between FUM and deoxynivalenol (DON) have been demonstrated to play a relevant role in the presence of a challenge with pathogens.6


Regulation in feed materials are available in both the EU and USA (tables 1 and 2).2, 11

European Union

Table 1. EU legislation regarding FUM in feed material.2
European Union
Products intended for animal feed Guidance value in mg/kg (ppm) relative to a feedingstuff with a moisture content of 12%
maize and maize products 60
Complementary and complete feedingstuffs for: pigs, horses (Equidae), rabbits and pet animals 5
fish 10
poultry, calves (<4 months), lambs and kids 20
adult ruminants (>4 months) and mink 50


Table 2. FDA legislation regarding FUM in feed material.11
Corn and corn by-products intended for: Total FUM (FB1+FB2+FB3)
Equids and rabbits5 ppm
(no more than 20% of diet)**
Swine and catfish20 ppm
(no more than 50% of diet)**
Breeding ruminants, breeding poultry and breeding mink*30 ppm
(no more than 50% of diet)**
Ruminants > 3 months old being raised for slaughter and mink being raised for pelt production60 ppm
(no more than 50% of diet)**
Poultry being raised for slaughter100 ppm
(no more than 50% of diet)**
All other species or classes of livestock and pet animals10 ppm
(no more than 50% of diet)**

* Includes lactating dairy cattle and hens laying eggs for human consumption
Dry weight basis

  1. Antonissen G., Martel A., pasman F., Ducatelle R., Verbrugghe E., Vandenbrouke V., Shaoji L., Haesebrouck F., Van Immerseel F., Croubels S. (2014). The Impact of Fusarium Mycotoxins on Human and Animal Host Susceptibility to Infectious Diseases. Toxins (6) 430-452
  2. Commission regulation (EC) No 1881/2006. Communities, The commission of the European (2006).
  3. Dilkin P., Zorzete P., Mallmann C.A., Gomes J.D.F, Utiyama C.E., Oetting L.L., Corrểa B. (2003). Toxicological effects of chronic low doses of aflatoxin B1 and fumonisin B1-containing Fusarium moniliforme culure material in weaned piglets. Food and Chemical Toxicology (41) 1345-1353.
  4. Duncan K.E.; Howard R.J. (2009). Biology of Maize Kernel Infection by Fusarium verticillioides. Molecular Plant-Microbe interactions 23, 1 (2010) 6-16
  5. Escrivà L., Font G., Maynes L. (2015). In vivo toxicity studies of fusarium mycotoxins in the last decase: A review. Food and Chemical Toxicology (78) 185-206.
  6. Grenier B., Schwartz-Zimermann H.E., Caha S., Moll W.D., Schatzmayr G., Applegate T.J. (2015). Dose-dependednt Effects on Sphingoid Base and Cytokines in Chickens Fed Diets Prepared with Fusarium Verticilloides Culture Material Containing Fumonisins. Toxins (7) 1253-1272.
  7. Krska R., Nährer K., Richard J. L., Rodrigues I., Schuhmacher R., Slate A. B., Whitaker T. B., (2012). Guide to Mycotoxins featuring Mycotoxin Risk Management in Animal Production. BIOMIN edition 2012
  8. Marin S., Ramos A.J., Cano-Sancho G., Sanchis V., (2013). Mycotoxins: Occurrence, toxicology, and exposure assessment. Food and Chemical Toxicology (60) 218-237
  9. Masching S., Naehrer K., Schwartz-Zimermann H.E., Sặrặndam M., Schaumberger S., Dohnal I., Schatzmayr D. (2016). Gastrointestinal Degradation of Fumonisin B1 by Carboxylesterase FumD Prevents Fumonisins induced Alteration of Sphingolipid Metabolism in Turkey and Swine. Toxins (8) 84.
  10. Voss K.A., Smith G.W., Haschek W.M. (2007). Fumonisins: Toxicokinetics, mechanism of action and toxicity. Animal Feed Science and Technology (137) 299-325.
  11. Opens external link in new windowhttp://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/ChemicalContaminantsMetalsNaturalToxinsPesticides/ucm109231.htm