The Mycotoxin Deoxynivalenol and Dairy
What is deoxynivalenol (DON) and why does it matter for dairy producers & silage farmers?
What is deoxynivalenol (DON) and why does it matter for dairy producers & silage farmers?
If you manage a dairy herd and feed corn silage or haylage, there is a good chance you have encountered deoxynivalenol, or it was in your feed supply at some point. The question is how much, and whether it is enough to cost you.
Deoxynivalenol, also known as DON or vomitoxin in the trade, is a secondary metabolite mycotoxin produced by fungi in the genus Fusarium. Fusarium graminearum is one of the key producers of DON and is also the fungal pathogen behind Gibberella ear rot in corn. During infection and disease progression, DON accumulates in grain and silage before harvest, moves to the silo, continues to change during ensiling, and reaches cows at the feed bunk, where it can cause several issues depending on the dose. The name vomitoxin comes from its effects in monogastric animals, specifically pigs, which are acutely sensitive, but dairy cattle are not totally immune. Because of the ruminant digestive system, they are more tolerant, so the damage is slower, subtler, and more likely to be attributed to something else.
How DON gets into corn silage
As hinted at earlier, the story starts in the crop field, not the silo. Fusarium species like F. graminearum and F. cerealis that produce DON infect corn during silking, when their airborne spores land on silk strands and travel down into the developing ear in conducive conditions. Wet, humid weather in July and August (the pollination window in the upper Midwest) creates ideal conditions for spore infection. These soil-borne spores are found in residue from previous plants, where they overwinter, and usually become airborne through water splashes during rainfall or movement by insects. Once the infection is established on the cob, the fungus colonizes ear tissue and activates biosynthesis genes that produce DON. Researchers believe this is done as a defense against competing microorganisms and plant immune responses.
Similarly, some of these Fusarium species also cause stalk rot in corn, and they can produce mycotoxins alongside it. By the time the combine runs, DON is already present in the chopped material from both infected ears and stalks. Ensiling does not eliminate DON, but research shows that after complete fermentation, the silo is fully anaerobic and the pH has dropped; DON levels remain relatively stable. DON is a stable, heat-resistant, water-soluble molecule that survives anaerobic fermentation largely intact. In fact, during ensiling, its concentrations often increase in the first 30 days after harvest as continued fungal activity and conversion of DON-3-glucoside (DON3G) back to free DON contribute to the total toxin burden.
What DON does to dairy cows
Dairy cattle metabolize DON in the rumen, which provides some protection compared to monogastric animals. Rumen microbes can convert DON to a less toxic form called deepoxy-DON (DOM-1). But this conversion is incomplete and inconsistent, depending on rumen health, feed composition, and total toxin load.
At concentrations seen in commercial silage (typically 1 to 5 ppm in heavily contaminated years) DON has documented effects on:
Feed intake. DON may activate satiety signals in the brain, reducing voluntary dry matter intake. Cows eat less, which reduces milk yield regardless of ration quality.
Rumen microbiology. DON is toxic to rumen bacteria and protozoa, disrupting fiber digestion and volatile fatty acid production. This can reduce energy availability from the ration.
Immune function. DON is an immunosuppressant. Cows exposed to elevated DON are likely to be more susceptible to mastitis, metritis, and other infectious diseases that carry their own production costs.
Liver function. The liver handles DON detoxification. Chronic exposure elevates liver enzyme markers and can compromise overall metabolic capacity in early-lactation cows already under nutritional stress.
Why DON is easy to underestimate
The regulatory threshold for DON in dairy cattle rations in the United States is 5 ppm in the total ration (not in a single ingredient). At this level, effects on intake and production are documented but rarely catastrophic in a single pen of cows. The economics of mycotoxins in dairy are diffuse; about a half-pound of milk per cow per day in a herd of 500 is $40,000 per year, but it looks like normal variation on a monthly milk check.
The more important underestimation problem is analytical. Standard on-farm testing for DON uses lateral flow immunoassay strips or ELISA, which are fast and cheap, but not very accurate and blind to DON3G, one of the plant-conjugated forms of DON that vary in proportion alongside free DON. When those conjugated forms like DON3G make it to the silo, they are hydrolyzed back to free DON, and similar conversion likely occurs in the rumen. A test that only reads free DON can substantially underreport the actual toxin load the cow encounters at digestion.
What the numbers look like in practice
In surveys of upper Midwest corn silage over multiple seasons, DON concentrations above 1 ppm (the level at which subtle effects on dairy cows begin to appear) are common in years with wet silking periods. Concentrations above 3 ppm occur regularly in problematic or highly infested fields, disease hotspots, or mold hotspots in the silo. In outbreak years (2018 was notable in the upper Midwest), concentrations above 10 ppm have been documented.
The variation does not appear to be random. Corn hybrid, fungicide application timing, field drainage, tillage and residue management practices, harvest date, and conducive weather conditions all influence final DON concentration in measurable and manageable ways.
The bottom line for dairy farmers
DON is not a crisis-level toxin in dairy the way it is for pigs, which is precisely why it is underdiagnosed and underpriced. Other mycotoxins produced by Fusarium species, like fumonisin, T-2/HT-2, and zearalenone, also have varying toxicity levels and effects on animals. Therefore, a systematic approach involving broad sampling and LC-MS/MS testing of silage (rather than strip tests), followed by tracking dry matter intake and body condition against known silage lots, and making hybrid selection decisions with Gibberella ear rot risk in mind, would help recover dollars. Producers who don’t consider vomitoxin aren’t protected from it. They are paying for it without knowing the bill.