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Types of Mycotoxins

The most extensively studied mycotoxins are those produced by the moulds Aspergillus, Fusarium, Pennicillium and Claviceps. Some of the key mycotoxins produced by these moulds are aflatoxins, ochratoxins, deoxynivalenol (DON, vomitoxin), T-2/HT-2 toxins, zearalenone, fumoninsins, mycophenolic acid, cyclopiazonic acid and ergot toxins.



Ochratoxins and citrinin can be produced both during field conditions and during storage of feedstuffs and are found in both temperate and tropical regions. Many species can be impacted by these mycotoxins, however, in a correctly functioning rumen ochratoxin  is rapidly degraded so is assumed to be a lesser threat to ruminants.

Clinical signs of ochratoxin/citrinin toxicity may include kidney damage, liver damage and immune suppression. Very high levels of ochratoxin (e.g. 3ppm) can cause increased mortality.

Other Penicillium mycotoxins:

Examples of other Penicillium mycotoxins include mycophenolic acid, penicillic acid and patulin. The production of these mycotoxins typically occurs during commodity storage, although production can also begin in the field.

These mycotoxins have antibiotic properties which could play a role in rumen and intestinal microbial population growth and function. These mycotoxins can also alter internal organ health and suppress immunity.


Not considered to be a particularly potent mycotoxin, Patulin is produced by certain fungal species of Penicillium growing on fruit, including apples, pears and grapes. Fruit by-products stored under conditions that promote bruising and rotting increase the probability of Patulinformation. Contamination with Patulin has also been reported in vegetables, cereal grains and silage.



What is Aflatoxin? Aflatoxins can occur in all regions across the globe as a result of factors such as changing weather patterns and agricultural practices. Warm and dry field conditions that increase drought stress to the plant often promote the production of aflatoxins by Aspergillus molds in the field, whereas high moisture levels and poor storage conditions may promote mycotoxin production during crop storage. Aflatoxins are carcinogenic and commodity contamination is regulated globally.

A primary sign of aflatoxin intake is liver damage. Animals consuming aflatoxins may also have reduced growth performance, intestinal disfunctions, immune suppression, poor reproductive performance and/or poor milk quality. Aflatoxin B1 can convert to aflatoxin M1, which is excreted in milk.

Other Aspergillus mycotoxins:

Other mycotoxins produced by Aspergillus include, but are not limited to, cyclopiazonic acid, gliotoxin and sterigmatocystin. These mycotoxins are typically produced during feedstuff/feed storage but could also be produced when plants are growing in the field.

These mycotoxins can cause liver damage, impact gain and efficiency, poor production, immune suppression, internal haemorrhaging and muscle tremors. Mortality rates may increase due to the presence of these mycotoxins.



Trichothecenes   are common field toxins found in grains and silages. Examples include deoxynivalenol (DON or vomitoxin), nivalenol, T-2/HT-2 toxins and diacetoxyscirpenol (DAS). Susceptibility to trichothecenes varies between mycotoxin type, mycotoxin concentration, animal species/breed and management systems. Swine are often considered to be one of the more sensitive species to DON, while T-2/HT-2 toxins are fairly toxic to most species. Trichothecenes be partially metabolised in the rumen, although their breakdown can be inhibited by acidic rumen conditions.

Clinical signs of trichothecene  toxicity include reduced feed intake, lower weight gains, intestinal haemorrhaging, diarrhoea, an increase in intestinal pathogen occurrence, lost milk production, reproductive failure and even mortality.


Zearalenone often occurs in combination with DON in naturally contaminated cereals or forages. This mycotoxin mimics the activity of hormones (as an oestrogen analogue), which causes the majority of the reproductive-related symptoms seen, especially in pregnant animals. Upon absorption, zearalenone can be metabolised to alpha-zearalenol and, to a lesser extent, to beta-zearalenol. Alpha-zearalenol is about four times more oestrogenic than its parent mycotoxin. Swine are considered most sensitive to zearalenone, although all breeding animals can be impacted. Partial metabolism of zearalenone in the rumen to its breakdown compounds can occur. These metabolites have shown no toxic effects on rumen bacteria, but as alpha-zearalenol is more oestrogenic than its parent mycotoxin, this rumen-mediated transformation actually causes greater toxicity. The rate ofzearalenone transfer into milk is low and is currently through to present no real risk to consumers of dairy products.

Clinical signs of zearalenone toxicity include vaginal reddening and prolapses, abortions, decreased embryo survival, infertility, vaginitis, feminisation of young males and mammary gland enlargement.


Fumonisins occur worldwide in a variety of feedstuffs. In contrast to other mycotoxins, fumonisin B1 (the most prevalent of the fumonisin mycotoxins) is slowly and poorly metabolised in the rumen and gastrointestinal tract causing it to be a mycotoxin of lower toxicity. However, the presence of even common levels of fumonisins can impact intestinal microbial balance and intestinal immunity prior to mycotoxin absorption.

Clinical signs of fumonisin toxicity can include reduced feed intake, lower weight gain, altered gastrointestinal balance, increased diarrhoea, and lost milk production. Swine and horses are particularly sensitive. Following fumonisin consumption, swine may develop porcine pulmonary edema while horses can develop equine leukoencephalomalacia.