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Aspergillus mold

Mycotoxins in Cattle

Effects and symptoms of mycotoxicoses in cattle

Mycotoxins are toxic substances produced by molds and fungi on plants, in the field, or during storage.  

The BIOMIN Mycotoxin Survey provides regular updates on the occurrence of mycotoxins in the raw commodities and finished feed based on thousands of samples collected from across the globe in addition to regional reports on US corn-based feed ingredients.

    Most affected raw materials pertinent to the livestock industry are:  

    • Corn-based feed ingredients, silages, and by-products 
    • Small grains such as wheat and barley and small grain silages 
    • Grasses and forages and grass-based silages 

      Mycotoxin contamination found in complete feed is often from multiple ingredients, regularly resulting in herd exposure to multiple mycotoxins over the course of their time in production. Due to the wide variety of feedstuffs utilized and complex nature of ruminant diets, ruminants are at an increased risk for broad-spectrum mycotoxin exposure.  

      Overall, mycotoxin risk management is critical to reduce the effects on animal health and performance, which when unaddressed, can lead to significant economic losses for producers. 

      General effects of mycotoxins on livestock

      The presentation of mycotoxicosis is a culmination of factors, including the nature of the mycotoxin exposure (duration, concentration, types of mycotoxins), the environment (management, hygiene, other pathogens, and stressors), and the status of the animal itself (species, life stage, sex). 

      Mycotoxins in general have drastic effects on the gastrointestinal tract, where the mycotoxins make direct contact to the gastrointestinal mucosa. Once mycotoxins are taken up into the blood stream, various internal organs and systems can be impacted.The liver, kidneys, and immune system can also be affected by multiple types of toxins. Clinical presentations involving the respiratory system, nervous system, and integument can be observed depending on the mycotoxins present, while the reproductive system can be impacted through direct and indirect effects depending on degree of challenge.  Overall mycotoxin exposure can culminate in decreased performance and increased sensitivity to pathogens.  

      Typically, ruminants are considered more resistant to mycotoxins than monogastric species due to natural detoxification by rumen microbes. Some natural microbial detoxification is known to occur, but unfortunately, the rumen does not provide complete protection to ruminants. Additionally, many mycotoxins have antimicrobial properties that can influence the rumen environment, reducing toxin metabolism by rumen protozoa and bacteria. Detoxification is also affected by diet composition, low pH, and increased passage rate. Additionally, rumen microorganisms are ineffective at degrading some types of mycotoxins and there is evidence that some mycotoxins are converted into more potent metabolites, amplifying toxicity. 


      These toxins are commonly found in areas where crops are subjected to heat and drought stress, and can be found in sub-optimal storage conditions. Aflatoxins can cause death when administered at high levels, but the greatest impact comes from reduced reproductive and performance capabilities. Aflatoxins suppress the immune system, cause hepatocellular damage and fatty liver syndrome in multiple species, and are highly carcinogenic. Aflatoxins can carry over into both meat and organ tissue, and indeed are a great concern in the dairy industry due to the ability for these toxins to carry over into the milk. Aflatoxin M1 (AfM1) is the metabolite transferred into milk, which is highly regulated, resulting in significant economic losses for producers if present above legal limits. In the United States, the action level set forth by the Food and Drug Administration (FDA) for AfM1 in milk for human consumption is 0.5 parts per billion (ppb). Many dairy processors follow more conservative thresholds when rejecting milk due to AfM1 contamination. 


      Type A-Trichothecenes 

      Type A-Trichothecenes (A-Trich) consist of a group of multiple toxins, the best known of which are T-2 toxin and HT-2 toxin. Type A-Tricothecenes are considered more potent compared to Type B-Trichothecenes (B-Trich) and are more frequently detected in feeds in the US than B-Trich. The A-Trich are so potent that they can cause contact lesions in the oral mucosa in various species as well as have also been associated with ulcers throughout the gastrointestinal tract including the rumen and abomasum. These toxins often contribute to reduced feed intake and poor performance, can cause immune suppression, and have been associated with reproductive effects in both males and females. In ruminants, this category of mycotoxins is more frequently associated with death than most of the other major mycotoxins. 

      Type B-Trichothecenes 

      Deoxynivalenol, acetyldeoxynivalenol, fusarenon X, and nivalenol, are all mycotoxins that are part of the Type B-Trichothecenes family. The most well-known is deoxynivalenol (DON), which is frequently referred to as “vomitoxin” for its ability to induce vomiting in swine. These mycotoxins can cause ruminants to spit out their cud boluses rather than reswallowing like normal. 

      Deoxynivalenol inhibits intestinal nutrient absorption and alters intestinal cell and barrier functions which can contribute to reductions in milk yield, changes in milk composition, and poor growth rates. These mycotoxins significantly affect the immune system, reducing lymphocyte proliferation, macrophage activity, and antibody response to certain vaccinations and influence immunoglobulin levels. Such negative effects on immune function leave animals more susceptible to infection by other pathogens such as bacteria, viruses, and protozoans. 

      Additionally, numerous studies have indicated that DON, by itself or in combination with other mycotoxins, may be a predisposing factor for several diseases. 



      Although commonly thought to require high levels to impact animal health, chronic exposure of fumonisins can have profound impacts to gastrointestinal health, the immune system, and liver and lung function.  

      Low levels of fumonisins can increase the ability of E.coli to bind to enteric cells thus facilitating their crossing over into the blood stream. Chronic exposure to fumonisin B1 (FB1) decreases the proliferation of epithelial intestinal cells. Fumonisins are known to increase the risk and severity of respiratory disease in swine, and likely can do so in other species as well. Fumonisins also impair vaccination response through reducing the level of several specific antibodies and the period of vaccine protection. Fumonisins are an important consideration in mycotoxin risk management programs as they act as predisposing factors for diseases in multiple ways, and amplify the impacts of DON.  


      Despite relatively low levels of acute toxicity, zearalenone (ZEN) can have a significant impact on reproduction performance in ruminants, as well as all species.   

      Negative effects are due to the interaction of ZEN and its metabolites with estrogen receptors. In general, ZEN contaminated feed induces the swelling and reddening of the vulva, false heats, and false pregnancy. Higher levels can result in embryonic death, abortions, and stillbirths. Chronic ZEN exposure can result in atrophic ovaries and vaginal prolapse, as well as interfering with the reproductive development of replacement heifers.  

      Ergot alkaloids  

      Ruminants have a well-known susceptibility to the effects of ergot alkaloids. Ergots can be formed by fungi growing on cereals or by endophytic fungi within tall fescue and other grasses. One of their main effects is vasoconstriction (restricting blood flow), which has an impact on hoof health, heat stress, mastitis, and reproduction. 

      Agalactia (due to interference with the release of prolactin), feed refusal, and consequent weight gain reductions are classical signs of ergot alkaloid intoxication. Other frequently noted symptoms have been observed in the cardiovascular and central nervous system because of increased blood pressure, causing vasoconstriction and strong uterotonic effects, resulting in stillbirths and reduced pregnancy rates. Certain ergots can cause neurologic signs including staggers and tremors. 

      Ochratoxin A  

      Hepatotoxic effects, decreased performance parameters, nephrotoxicity, and necrosis are the major toxic effects caused by ochratoxin A (OTA). This mycotoxin has been shown to suppress cell-mediated immune response in pigs, resulting in reduced macrophage activity and weakened stimulation of lymphocytes. Furthermore, OTA tends to accumulate in kidneys, liver, and muscle tissues, as well as in blood serum and, therefore, it represents a potential hazard in the human food chain. There is evidence that the majority of OTA is degraded in the rumen. However, high feed intake and passage rate as well as other stress factors (e.g., acidotic conditions) may reduce the degradation rate of OTA in the rumen, resulting in an increased passage of toxin into the lower digestive tract and an elevated risk of OTA toxicity. Ochratoxin A toxicity is a greater concern in calves which do not have a functional rumen to potentially provide natural detoxification. 

      Synergistic effects of mycotoxins  

      Toxicological interactions between mycotoxins enhance the toxic effects, even at low levels.  

      Fusarium graminearum and Fusarium culmorum are known to produce several different fusariotoxins, including zearalenone and deoxynivalenol, which are known to interact synergistically. In addition, the analysis of deoxynivalenol often indicates the co-occurrence of other fusariotoxins such as other trichothecenes (T-2 toxin, nivalenol, diacetoxyscirpenol), zearalenone, and fumonisins. 

      Additive (dashed black line) and synergistic (red line) effects in poultry
      Additive (dashed black line) and synergistic (red line) effects in poultry, AFB1 - Aflatoxin B1 ; FB1 - Fumonisin B1 ; DON - Deoxinivalenol; OTA - Ochratoxin A; ZEN - Zearalenone; FA - Fusaric acid; DAS - Diacetoxyscirpenol; CPA - Cyclopiazonic acid; MON - Moniliformin

      Diagnosis of mycotoxicosis  

      Mycotoxicoses are diseases caused by ingestion of mycotoxins, inhalation, or contact with the skin. The effects of mycotoxins in livestock species are diverse, varying from immunosuppression to death in severe cases, depending on various factors including those which are toxin-related (type of mycotoxin consumed, level, and duration of intake), animal-related (animal species, sex, age, breed, general health, immune status, nutritional standing) and environmental (farm management, biosecurity, hygiene, temperature). This complexity often impedes correct attribution of problems caused by mycotoxins. 

      There are multiple diseases in ruminants that are attributed to stress stimuli and are opportunistic infections. Mycotoxins have been shown to be sufficient to induce and exacerbate multiple diseases, and thus preventative health programs for herds need to have a mycotoxin risk management plan in place. 

      Mycotoxin risk management  

      Robust mycotoxin risk management comprises three steps:  

      • Detection  
      • Prevention  
      • Mitigation  

      Reducing animal exposure to mycotoxins in feed is key. Regular analysis of feed components and silage can help to uncover potential threats to animals. Identifying contamination can help to reduce exposure and determine what the best options are for prevention and mitigation. However, a highly contaminated sample does not mean the entire crop is bad and a ‘clean’ sample does not guarantee that all of the feed is mycotoxin-free. 

      Good storage practices, along with proper bin and silage management, are essential to avoid further growth of molds and thereby prevent the production of additional mycotoxins.

      When it comes to counteracting mycotoxins, the livestock industry tends to think of toxin binders or mycotoxin binders first. (Learn the truth about mycotoxin binders).  Regular application of mycotoxin binders is advisable; however, clay mineral binders are not an effective answer to all major mycotoxins. This is especially true when attempting to mitigate trichothecenes since their structures are not suitable for adsorbing by binders. Biotransformation, the use of microbes and enzymes to degrade mycotoxins, is the most effective strategy. This mode of action provides reliable protection against Fusarium mycotoxins by biodegrading mycotoxins into non-toxic metabolites.  

      In addition to biotransformation, a bioprotection strategy is also important. Feed additives are available that contain plant and algae extracts to provide support to the liver and the immune system. 

      • A combination of different strategies can counteract the negative effects of mycotoxins more completely, especially in cases of multi-mycotoxin contamination with the poorly absorbed Fusarium mycotoxins in feedstuffs. 

      Mycofix® is not sold in the United States and Canada.