Fusarium mycotoxins like fumonisin affect several systems when consumed by animals, leading to reduced feed intake and efficiency, lameness and liver damage. Understanding the effects of these mycotoxins on cattle is key to maintaining animal health and productivity.

Mycotoxins are secondary metabolites of molds and fungi that infect plants. More than 500 mycotoxins have been identified, and most animal feedstuffs are likely to be contaminated with multiple mycotoxins. Each mycotoxin has specific, differing effects on animals consuming the contaminated feed. 

The Fusarium species are the predominant molds that contaminate crops. Ranging from white to pink or red in color, these molds are associated with wet conditions and moderate temperatures, especially following insect damage. They occur worldwide, largely in corn. Fusariums produce several mycotoxins, including fumonisin, deoxynivalenol (aka vomitoxin) and zearalenone, with higher concentrations in stalks and cobs than in the grain.

While cattle are generally resistant to many of the negative effects of mycotoxins, thanks to the degradation of the compounds by rumen microbes, high levels in feeds can have significant impacts. Fumonisin, despite not being significantly degraded in the rumen, is also not well absorbed. The majority of fumonisins consumed by cattle are passed out in the feces. However, in large enough quantities, fumonisins overwhelm the gut and cause significant issues. The presence of fumonisin in feed reduces palatability, slowing intake. Cattle may stand off the bunk with high levels of fumonisin contamination.  Calves without fully developed rumens and animals in stressful situations, such as weaning or transportation, have increased sensitivity to fumonisin because of reduced rumen fermentation and weakened immune function.

The gastrointestinal tract is impaired when cattle are fed mycotoxins. Gut epithelial cells need protection from direct interaction with microbes and the gut environment. Specialized cells in the epithelium provide this protection. Examples are goblet cells, which produce mucus-coating epithelial cells to lubricate and protect them from gut contents. Intestinal cells also have specialized structures to form tight junctions, limiting the passage of molecules between cells. These mechanisms and others work in concert to prevent pathogen colonization and systemic access by toxins and pathogens.

Although fumonisin is poorly absorbed and metabolized by cattle, it disturbs the gastrointestinal tract. Rumen motility can be slowed, resulting in increased exposure of the intestinal epithelium to fumonisin and other mycotoxins. Even low amounts of mycotoxins impair intestinal health and immune function, resulting in altered host pathogen interactions and increased susceptibility to disease. Gastrointestinal epithelial cells are damaged by fumonisin, reducing mucin layer thickness, tight junction strength and cell proliferation, ultimately increasing the opportunity for pathogen invasion.

Analyses of tissues from cattle fed Fusarium in high doses indicate that of the fumonisin absorbed, the majority is retained in the liver, with lesser amounts in muscle and the kidneys. This accumulation is concerning, as fumonisin is toxic to the liver and kidneys, causing apoptosis, followed by proliferation of regenerative cells in the affected tissues. Fumonisin also reduces liver antioxidant levels, lessening defense mechanisms. This leads to liver lesions and elevated enzymes indicative of liver damage.

Sphingolipids protect cells from environmental damage by forming a stable, chemically resistant layer on the cell membrane. Fumonisins disrupt cell signaling by inhibiting ceramide synthase, interrupting sphingolipid synthesis and metabolism. Also, the decreased concentrations of important sphingolipids play a role in the altered morphology of the affected cells. This inhibition results in a buildup of compounds that are cytotoxic, reducing cellular stability and protection, leading to cell death. 

Calves consuming fumonisin have decreased immune function. Sphingolipid metabolism in immune cells is involved in signaling, which controls lymphocyte development, differentiation, activation and proliferation. Lymphocyte development is impaired when cattle are fed fumonisins. These white blood cells are important in maintaining a strong antigen response. Consumption of Fusarium-contaminated feeds can increase susceptibility to diseases and reduce vaccine efficacy.

Unfortunately, once mycotoxins are formed in the plant, there is no commercial method to remove them from contaminated feeds. Harvesting and storage of contaminated crops at low moisture (less than 15 percent), along with separation of highly contaminated feeds, is important to reduce the risk of mold growth and mycotoxin production in uncontaminated grain. 

While the European Commission has determined that adult cattle can tolerate fumonisins up to 50 parts per million (ppm) in diets, the U.S. Food and Drug Administration guidance document for fumonisin recommends a maximum concentration in the diet of feedlot cattle of 30 ppm, 15 ppm for breeding stock and 10 ppm for calves.  Furthermore, contaminated corn or corn byproducts should contribute no more than 50 percent of the diet. It is crucial to check the fumonisin level in the complete diet, as fumonisin is three times more concentrated in corn byproducts such as distillers grains and corn gluten feed, and 10 times more concentrated in corn screenings.

If contaminated feeds must be used to feed cattle, elevators may blend corn to reduce the fumonisin concentration to acceptable levels. As fumonisin is associated with reduced feed consumption, there is a concern that even low levels of fumonisin can interact with other mycotoxins, reducing the growth of calves and the weight gain of feedlot cattle. Fumonisin contamination can be especially detrimental to newly received cattle and calves, preventing them from getting off to a healthy start.