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Fusarium verticillioides | Photo: BIOMIN

Mycotoxins definition

Mycotoxins are toxic secondary metabolic products of molds present on almost all agricultural commodities worldwide.

Unlike primary metabolites (sugars, amino acids and other substances), secondary metabolites are not essential in the normal metabolic function of the fungus.15 Other known secondary metabolites are phytotoxins and antibiotics.

Michele Muccio (Regional Product Manager APAC, BIOMIN) provides the definition of a mycotoxin and how mycotoxins can harm farm animals.

Currently there are around 400 mycotoxins reported. These compounds occur under natural conditions in feed as well as in food. Some of the most common mycotoxins include: aflatoxins, trichothecenes, fumonisins, zearalenone, ochratoxin and ergot alkaloids.10 Mycotoxins are produced by different strains of fungi and each strain can produce more than one mycotoxin. The major classes of these mycotoxin-producing fungi are listed below.

Each plant can be affected by more than one fungus and each fungus can produce more than one mycotoxin. Consequently, there is a high probability that many mycotoxins are present in one feed ingredient, thus increasing the chances of interaction between mycotoxins and the occurrence of synergistic effects, which are of great concern in livestock health and productivity. Synergistic effects occur when the combined effects of two mycotoxins (even at low levels) are greater than the individual effects of each toxin alone. Simple additive effects can also occur with the combined effects of two mycotoxins being equal to the sum of the effects of each toxin on its own.10, 14, 19

Mycotoxins are invisible, tasteless, chemically stable and resistant to temperature and storage. They are resistant the normal feed manufacturing processes.

Mycotoxin producing fungi can be divided into two groups.13, 25

  • Field fungi (such as Fusarium sp.) typically produce mycotoxins in the field (“pre-harvest”)
  • Storage fungi (such as Aspergillus and Penicillium sp.) typically occur after harvest (“post-harvest”)

However, in special cases like under unusually hot or dry conditions Aspergillus and Penicillium species can also affect crops during the growing season. On the other hand, field fungi can continue growing and produce mycotoxins during transport and storage.7

Mycotoxins cause economic losses at all levels of food and feed production, including crop and animal production, processing and distribution.6, 21, 26 According to the FAO (Food and Agriculture Organization) around 50% of the world’s crop harvests may be contaminated with mycotoxins.11

Major classes of mycotoxin producing fungi and mycotoxins


A. flavus
A. parasiticus
A. nomius
A. pseudotamarii
(B1, B2, G1, G2)
A. ochraceusOchratoxin
(Ochratoxin A)
A. clavatus
A. terreus
A. flavus
A. versicolor
Cyclopiazonic acid


C. purpurea
C. fusiformis
C. paspali
C. africana

Penitrem A

Ergot alkaloids:
Clavines (Argroclavine)
Lysergic acids
Lysergic acid amides


F. verticillioides
(syn. F. moniliforme)
F. proliferatum
Fumonisin (B1, B2, B3)
Fusaric acid
F. graminearum
F. avenaceum
F. culmorum

Type A Trichothecenes:

T-2 toxin, HT-2 toxin,

F. poae
F. equiseti
F. crookwellense
F. acuminatum
F. sambucinum
F. sporotrichioides

Type B Trichothecenes:


F. graminearum
F. culmorum
F. sporotrichioides


P. verrucosum
P. viridicatum
(Ochratoxin A)
P. citrinum
P. verrucosum
P. roquefortiRoquefortine C
PR toxin
Penitrem A
P. cyclopium
P. camemberti
Cyclopiazonic acid (CPA)
Penitrem A
P. expansum
P. claviforme
P. roquefortii


N. coenophialum

Tall fescue toxins:

Ergot alkaloids,
Lolines, Peramine

N. lolii

Ryegrass toxins:

Lolitrems, Peramine,
Ergot alkaloids
(e.g. Ergovaline)


P. chartarum

Undetected Mycotoxins

Mycotoxins can occur despite negative analytical results due to two main reasons. Firstly, they are often located in so-called “hot-spots” (Figure 1) and therefore they might stay undetected depending on sampling procedures.1, 18, 22

Secondly, masked mycotoxins could occur in feed. Masked mycotoxins are product of a specific biochemical reaction where mycotoxins can be bound to certain molecules including e.g. glycosides, glucuronides, fatty acid esters and proteins. Due to the biochemical modification, these masked mycotoxins are not detectable with conventional analytical methods, i.e. when using a conventional testing method samples may show up as having no (or low) contamination whereas, in reality, there is a mycotoxin risk present.3, 5, 16 The mycotoxin-molecule bond may be cleaved in the gastrointestinal tract of the animal and the mycotoxin is released (figure 2).4, 8


Figure 1. In every lot there are particular areas where fungi grow intensively. This might be due to variations in humidity and presence of other factors such as air pockets. In these hot spots the load of mycotoxins can be much higher compared to the rest of the lot, hence in order to obtain a representative sample proper mixing should be done.
Figure 2. Scheme of mycotoxin conjugate formation in plants and mycotoxin release in the mammalian digestive tract.

Mycotoxin Toxicity

Mycotoxins differ in their structure, which explains the great variation of symptoms.9, 13, 23 Toxicity of mycotoxins can be acute and chronic. In acute cases, the effects of the toxin will appear after a short exposure time (seconds, minutes or hours). Usually, acute toxicity is the result of exposure to high doses and is characterized by the presence of easily recognizable severe symptoms.9, 17 Chronic toxicity is characterized by weaker symptoms that might only occur after an initial period of exposure. Chronic toxicity can occur with long-term exposure to low doses of mycotoxins. A chronic effect of some mycotoxins is the induction of cancer, especially of the liver (e.g. aflatoxin). The major acute and chronic effects of mycotoxins are listed in table 1.17

Table 1. Major acute and chronic effects of mycotoxins

Acute effect Chronic effects
Deterioration of liver and kidney functionLiver cancer
Jaundice (yellow skin)Chronic hepatitis
EmesisSlow developing jaundice
AnorexiaHepatomegalite (abnormal size of liver)
Ascites (fluid in the peritoneal cavity)Liver cirrhosis
Gastrointestinal hemorrhage (bleeding)Immune suppression

Toxic effects of mycotoxins can be reversible and irreversible. Reversible effects include minor damages that can heal such as skin irritation. Irreversible effects involve permanent damage to health. One example, is vasoconstriction, (blood vessel constriction) caused by ergot alkaloids, leading to necrosis of extremities (e.g. toes, ears or tail).13, 17

The main toxic effects of mycotoxins are carcinogenicity, genotoxicity, nephrotoxicity, hepatotoxicity, estrogenicity, reproductive and digestive disorders, immunosuppression and dermal effects.6, 10, 13, 17 

There are several factors which influence symptoms:13

  • Type of mycotoxins consumed, intake level and duration of exposure
  • Animal species, sex, breed, age, general health, immune status
  • Farm management: hygiene, temperature, production density
  • Possible synergism between mycotoxins simultaneously present in feeds 

Primary toxic effects of mycotoxins are summarized in table 2.17

Table 2. Primary mechanism of action of main mycotoxin groups

Mycotoxins are capable of direct-target toxicity towards certain organs such as the liver, nervous system, kidney, skin, cardiovascular, reproductive and immune systems. Non-direct-target effects include carcinogenicity, teratogenicity and mutagenesis.6, 10, 13, 17

Mycotoxins are absorbed through the gastro-intestinal tract (GIT), the lungs, the skin and other organs like the eyes.17 In the GIT, mycotoxins can be absorbed in the mouth and esophagus (minimal absorption), in the stomach and in the small intestine. In the stomach, absorption is generally correlated with the fraction of non-dissociated contaminants like weak acids.17 The small intestine, is where the maximal absorption takes place. A fraction of mycotoxins can also be absorbed in the colon.9, 10, 17

In the lungs, mycotoxins that are generally carried by dust are absorbed in the alveoli (i.e. ochratoxin A).17

Once in the body, mycotoxins can be distributed through different pathways. Some mycotoxins can bind to plasma proteins and be transported into the blood plasma (e.g. ochratoxin A).17, 20, 23 Mycotoxins can also be lipophilic and accumulate in the fat tissues. Lipophilic compounds can easily penetrate the blood-brain barrier and the placental barrier.6, 13, 17 The half-life elimination time, or the time required to reduce the initial plasma concentration of the toxin, can be very long in the case of chronic exposure (ochratoxin A half-life elimination time in humans is longer than 560 hours.9, 17

Mycotoxins can be partially excreted through several pathways. Usually polar and hydrophilic substances are excreted via the kidneys with the urine. Accumulation of mycotoxins in kidneys has been observed and can produce toxic effects (i.e. ochratoxin A).17

Compounds that are characterized by high molecular weight are usually excreted via the bile. Other pathways of excretion include transfer to milk (aflatoxin B1) and elimination through sweat and saliva. Unabsorbed mycotoxins may be excreted in feces but could still have had an effect on the gut wall during passage.17

MycotoxinPrimary mechanism of action
AflatoxinBinds to guanine (DNA-adduct) after metabolic activation in the liver
TrichothecenesInhibition of protein synthesis
ZearalenoneBinds to mammalian estrogen receptor
OchratoxinsBlocks protein synthesis
Ergot alkaloidsBinding to adrenergic, dopaminergic and serotonin receptors
FumonisinsInhibit ceramide synthase (sphingolipid biosynthesis)
  1. Andersson, M. G., Reiter, E. V., Lindqvist, P. -., Razzazi-Fazeli, E., & Häggblom, P. (2011). Comparison of manual and automatic sampling for monitoring ochratoxin A in barley grain. Food Additives and Contaminants - Part A Chemistry, Analysis, Control, Exposure and Risk Assessment, 28(8), 1066-1075.
  2. 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
  3. Berthiller, F., Dall'Asta, C., Schuhmacher, R., Lemmens, M., Adam, G., & Krska, A. R. (2005). Masked mycotoxins: Determination of a deoxynivalenol glucoside in artificially and naturally contaminated wheat by liquid chromatography-tandem mass spectrometry. Journal of Agricultural and Food Chemistry, 53(9), 3421-3425.
  4. Berthiller, F., Krska, R., Domig, K. J., Kneifel, W., Juge, N., Schuhmacher, R., & Adam, G. (2011). Hydrolytic fate of deoxynivalenol-3-glucoside during digestion. Toxicology Letters, 206(3), 264-267.
  5. Berthiller, F., Schuhmacher, R., Adam, G., & Krska, R. (2009). Formation, determination and significance of masked and other conjugated mycotoxins. Analytical and Bioanalytical Chemistry, 395(5), 1243-1252.
  6. Bryden, W. L. (2012). Food and feed, mycotoxins and the perpetual pentagram in a changing animal production environment. Animal Production Science, 52(7), 383-397.
  7. Dawlal, P., Barros, E., & Marais, G. J. (2012). Evaluation of maize cultivars for their susceptibility towards mycotoxigenic fungi under storage conditions. Journal of Stored Products Research, 48, 114-119.
  8. Gareis, M., Bauer, J., Thiem, J., Plank, G., Grabley, S., & Gedek, B. (1990). Cleavage of zearalenone-glycoside, a "masked" mycotoxin, during digestion in swine. Journal of Veterinary Medicine, Series B, 37(3), 236-240.
  9. Grenier B., & Applegate T.J., (2013). Modulation of Intestinal Function Following Mycotoxin Ingestion: Meta-Analysis of Published Experiments in Animals. Toxins, 5(2), 396-430
  10. Grenier, B., & Oswald, I. P. (2011). Mycotoxin co-contamination of food and feed: Meta-analysis of publications describing toxicological interactions. World Mycotoxin Journal, 4(3), 285-313.
  11. http://www.fao.org/docrep/U3550t/u3550t0e.htm
  12. Huff, W. E., & Doerr, J. A. (1981). Synergism between aflatoxin and ochratoxin A in broiler chickens. Poultry Science, 60(3), 550-555.
  13. Krska R. (2016) Introduction to the mycotoxin issue. Mycotoxin Summer Academy – IFA Tulln
  14. Kubena, L. F., Edrington, T. S., Harvey, R. B., Buckley, S. A., Phillips, T. D., Rottinghaus, G. E., & Casper, H. H. (1997). Individual and combined effects of fumonisin B1 present in Fusarium moniliforme culture material and T-2 toxin or deoxynivalenol in broiler chicks. Poultry Science, 76(9), 1239-1247.
  15. Labuda R. Taxonomy of Toxigenic Fungi. Mycotoxin Summer Academy – IFA Tulln
  16. Lancova, K., Hajslova, J., Poustka, J., Krplova, A., Zachariasova, M., Dostalek, P., & Sachambula, L. (2008). Transfer of Fusarium mycotoxins and 'masked' deoxynivalenol (deoxynivalenol-3-glucoside) from field barley through malt to beer. Food Additives and Contaminants - Part A Chemistry, Analysis, Control, Exposure and Risk Assessment, 25(6), 732-744.
  17. Lemmens M., (2016). Mycotoxin Summer Academy – Module 1. IFA Tulln
  18. Miraglia, M., De Santis, B., Minardi, V., Debegnach, F., & Brera, C. (2005). The role of sampling in mycotoxin contamination: an holistic view. Food Additives and Contaminants, 22(SUPPL. 1), 31-36.
  19. Pinton P., & Oswald I.P., (2014). Effects of Deoxynivalenol and Other Type B Trichothecenes on the intestine: A Review. Toxins (6) 1615-1643
  20. Richard, J. L. (2007). Some major mycotoxins and their mycotoxicoses-an overview. International Journal of Food Microbiology, 119(1-2), 3-10.
  21. Robens, J., & Cardwell, K. (2003). The costs of mycotoxin management to the USA: Management of aflatoxins in the United States. Journal of Toxicology - Toxin Reviews, 22(2-3), 139-152.
  22. Shephard, G. S., Berthiller, F., Burdaspal, P. A., Crews, C., Jonker, M. A., Krska, R., Lattanzio, V. M. T., MacDonald, S., Malone, R. J., Maragos, C. & Sabino, M. (2012). Developments in mycotoxin analysis: An update for 2010-2011. World Mycotoxin Journal, 6(1), 3-30.
  23. Speijers, G. J. A., & Speijers, M. H. M. (2004). Combined toxic effects of mycotoxins. Toxicology Letters, 153(1), 91-98.
  24. 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.
  25. Weidenbörner, M. (2007) Mycotoxins in Feedstuffs, Springer-Verlag, New York.
  26. Wu, F. (2007). Measuring the economic impacts of Fusarium toxins in animal feeds. Animal Feed Science and Technology, 137(3-4), 363-374.
  27. http://www.ars.usda.gov/is/graphics/photos/jul00/k8931-2.htm

Mycotoxin formation/fungal growth

Fungal colonization and growth and/or mycotoxin production are generally influenced by a variety of factors.

Therefore, it is not possible to describe a single set of conditions that are favorable for fungal growth and mycotoxin production. The most important conditions are temperature and water activity (available water content to a mold in a substrate). Generally, the optimal temperature for mycotoxin production by many molds range between 20 to 30°C.

The most important factors can be categorized in three groups:

  • plant and environmental factors, including substrate characteristics (e.g. composition, pH, water activity, oxygen content)
  • possible competitive actions (e.g. associated growth of other fungi or microbes)
  • climatic conditions (e.g. temperature, atmospheric humidity)

Generally, in warm (tropical and subtropical) regions aflatoxins are of major concern, while fusariotoxins, such as zearalenone or trichothecenes mainly occur in more moderate climatic regions.2, 5

Furthermore, stress factors such as drought, poor fertilization, high crop densities, weed competition, insect or mechanical damage can weaken the plant’s natural defenses and promote colonization by mycotoxin-producing fungi as well as toxin-formation.

The optimum production conditions vary according to substrate, mycotoxin type, temperature and humidity. The Figures 1 to 7 outline the available data about temperature for fungal growth and mycotoxins formation as well as water activity (aw) for fungal growth and mycotoxins formation of the main fungi, which produce mycotoxins, as these parameters mainly influence mycotoxin production.1, 4, 6, 7, 8, 9, 10, 11 But even small changes in aw-values or temperatures can already lead to large changes in the optimum growth rate of the fungi and mycotoxins, that is why the values in the Figures 1, 2, 4 and 5 should be seen as indicator and not as the only, single optimal domain.

Interaction between water activity (aw) and temperature on fungal growth and mycotoxin formation

Interactions between certain aw-values and certain temperatures on the growth of F. verticillioides strains and production of mycotoxins were outlined in the study of Medina et al. (2013).4 The study showed that with an aw of 0.995 the optimum growth rate of F. verticillioides was between 20 and 25 °C, but when the aw-value changed to 0.98 the optimum growing temperature shifted between 30 and 35 °C (Figure 3).4 Opposite conclusions could be outlined for the mycotoxin production. In fact, the optimal temperature and aw for FB1 production were 20°C and an aw of 0.98-0.995. From this it can be concluded that the optimal conditions for production of certain mycotoxins are not the same as for their growth.

Figure 1: Minimum, optimum and maximum temperature range in °C for fungal growth.
Figure 2: Minimum, optimum and maximum water activity (aw) for fungal growth.
Figure 3: Effect of temperature and water activity (aw) on the growth rate of a strain of F. verticillioides. Means of five replicates per treatment (Medina et al., 2013).

Figure 4: Minimumoptimum and maximum temperature range in °C  for mycotoxins formation.
Figure 5: Minimumoptimum and maximum water activity (aw) for mycotoxins formation.
Figure 6: The effect of (a) water activity (aw) and (b) temperature on the fumonisin B1 production by a strain of F. verticillioides. Bars indicate standard error of the means (Medina et al., 2013).

Figure 7a: The effect of water activity (aw) on the fumonisin B2 production by a strain of F. verticillioides. Bars indicate standard error of the means (Medina et al., 2013).
Figure 7b: The effect of temperature on the fumonisin B2 production by a strain of F. verticillioides. Bars indicate standard error of the means (Medina et al., 2013).

  1. HUSSEIN, H. S. & BRASEL, J. M. 2001. Toxicity, metabolism, and impact of mycotoxins on humans and animals. Toxicology, 167, 101-134.
  2. MAGAN, N., MEDINA, A. & ALDRED, D. 2011. Possible climate-change effects on mycotoxin contamination of food crops pre- and postharvest. Plant Pathology, 60, 150-163.
  3. MARTH, E. H. 1992. Mycotoxin: Production and control. Food Laboratory News, 35-51.
  4. MEDINA, A., SCHMIDT-HEYDT, M., CÁRDENAS-CHÁVEZ, D. L., PARRA, R., GEISEN, R. & MAGAN, N. 2013. Integrating toxin gene expression, growth and fumonisin B1 and B2 production by a strain of Fusarium verticillioides under different environmental factors. Journal of the Royal Society Interface, 10.
  5. PATERSON, R. R. M. & LIMA, N. 2011. Further mycotoxin effects from climate change. Food Research International, 44, 2555-2566.
  6. POPOVSKI, S. & CELAR, F. A. 2013. The impact of environmental factors on the infection of cereals with Fusarium species and mycotoxin production - A review. Acta Agriculturae Slovenica, 101, 105-116.
  7. RAMOS, A. J., LABERNIA, N., MARÍN, S., SANCHIS, V. & MAGAN, N. 1998. Effect of water activity and temperature on growth and ochratoxin production by three strains of Aspergillus ochraceus on a barley extract medium and on barley grains. International Journal of Food Microbiology, 44, 133-140.
  8. RIBEIRO, J. M., CAVAGLIERI, L. R., FRAGA, M. E., DIREITO, G. M., DALCERO, A. M. & ROSA, C. A. 2006. Influence of water activity, temperature and time on mycotoxins production on barley rootlets. Lett Appl Microbiol, 42, 179-84.
  9. RICHARD, J. L. & PAYNE, G. A. 2003. Mycotoxins in plant, animal, and human systems. Council for Agricultural Science and Technology, Task Force Report No. 139.
  10. SANCHIS, V. 2004. Environmental conditions affecting mycotoxins. In: Magan N. and Olsen M. (Eds.), Mycotoxins in food. CRC Press, Boca Raton Bosten New York, Washington, DC, 174-189.
  11. SWEENEY, M. J. & DOBSON, A. D. W. 1998. Mycotoxin production by Aspergillus, Fusarium and Penicillium species. International Journal of Food Microbiology, 43, 141-158.