Why rumen degradation doesn’t provide complete protection to cattle from mycotoxins

In Brief:

Natural protection via rumen degradation of mycotoxins is highly variable across different mycotoxins and influenced by factors such as ruminal pH and passage rate.
The metabolites resulting from the degradation of zearalenone and aflatoxin B1 can be more toxic than the original compounds, so rumen degradation of mycotoxins is not always beneficial for the animal.
Mycotoxins can cause major problems related to productivity, health and fertility in cattle.

If you are a nutritionist or veterinarian who has been in the industry for some time, you probably have heard that ruminants are the animals least affected by mycotoxins. It used to be assumed that cattle are protected from mycotoxins by natural microbial degradation that could take place in the rumen. However, decades of research and field experience increasingly show that cows are susceptible to a host of detrimental effects from mycotoxins including impaired immune function, reduced feed efficiency, and compromised reproductive performance.

Degradation in the rumen does not always equate to detoxification. In fact, in some cases, the resulting metabolites are more harmful than the original compounds.

This article focuses on the fate of mycotoxins in the rumen and summarizes the implications on productivity, health and fertility in the herd.

Mycotoxin degradation is variable

While the rumen contains microbial populations that can degrade certain mycotoxins, the degradation is highly variable and not always beneficial to the animal. Many factors influence the potential for natural microbial degradation of mycotoxins to occur including diet composition, ruminal pH, and passage rate (Debevere et al., 2020; Hartinger et al., 2023). Therefore, it is best to talk about these effects by mycotoxin group rather than as mycotoxins as a whole since the capacity to be degraded and its result varies molecule by molecule.

Table 1 provides a summary of some of the main mycotoxins found in cattle diets, and how much the respective mycotoxin is reportedly broken down in the rumen and the resulting metabolites of that degradation process. Any remaining intact mycotoxin is left to pass into the intestines where most mycotoxins can cause major damage. The use of colors in the table indicates to which degree the degradation occurs:

Red: degradation results in an equally toxic or more toxic compound, so it’s a potentiation of the toxicity (i.e., not a detoxification step but rather potential amplification of toxicity occurs in the rumen)
Yellow: a partial degradation may occur but it’s highly variable and depends on a variety of factors
Orange: none to very little degradation takes place
Green: degradation goes as desired, leading to a reduction in toxicity

What happens to each mycotoxin?

Table 1. Ruminal degradation of mycotoxins

Roughly half of Zearalenone (ZEN) is degraded into α-Zearalenol (α-ZOL) and β-Zearalenol (β-ZOL) in the rumen with the resulting proportion of these two metabolites being highly variable and influenced by dietary factors and conditions in the rumen. α-ZOL is reportedly anywhere from 3 to 60 times more estrogenic than zearalenone, so the impact after passing through the rumen is amplified. The remaining toxin that is not broken down in the rumen passes into the intestines as zearalenone.
Aflatoxin B1 (AfB1) is the most carcinogenic compound found in nature. When consumed by cows, it can be transferred into milk as Aflatoxin M1, which becomes a human health concern. Aflatoxin B1 can be degraded in the rumen, but conversion into Aflatoxicol does not provide complete protection for a couple of reasons. First of all, Aflatoxicol is carcinogenic and genotoxic, so it can still have detrimental effects on the animal. Additionally, Aflatoxicol can be re-oxidized back into the parent toxin AfB1 in post-ruminal tissues, essentially canceling out the degradation that occurred in the rumen. Generally, less than half of AfB1 is expected to be degraded in the rumen.
Tricothecenes (such as deoxynivalenol (DON) and nivalenol (NIV)) are partially degraded in the rumen. The good news is that the resultant metabolites are less toxic than the original forms. The bad news is that degradation is very inconsistent and can range from as little as 1% up to 85% clearance. This degradation depends on several factors but the two most relevant are:

Ruminal pH: the right microbial populations are needed to degrade trichothecenes. Lower ruminal pH values which are typically associated with higher starch diets have been shown to reduce the rate of degradation.
Passage rate: Degradation requires time, especially if the efficacy of degradation is reduced due to low pH. High yielding cows have high dry matter intakes; thus, they experience very high passage rates, leaving less time for this degradation to occur. This is particularly true in smaller feed particles that escape the rumen in the first hours following consumption.

Fumonisins (FUM) reportedly pass through the rumen and into the intestines completely unchanged. There is little to no degradation of fumonisin in the rumen.
Little is known about many of the emerging mycotoxins like Enniatin B. Research suggests that while some degradation takes place of this specific metabolite, most of Enniatin B passes through to the intestines where it can exert its toxic effects.
Ochratoxin A is one of the few positive examples where rumen degradation does take place and the resulting metabolite is not harmful to the animal. However, like all ruminal degradation, factors like rumen pH and passage rate may affect this natural protective mechanism.

Mycotoxins impair health and immune status

While mycotoxins are often discussed in the context of productivity losses, their impact on gut integrity and immune function is equally—if not more—critical. The gastrointestinal tract is not just a site of nutrient absorption; it is the body’s largest immune organ. When mycotoxins compromise gut health, they also undermine the immune system’s ability to defend against pathogens, leading to cascading effects on animal health, performance, and resilience.

The intestine is responsible for the absorption of nutrients, and it is the most important immune organ in the body as over 70% of the body’s immune cells are found along the intestinal tract. Any compromise to intestinal function will also compromise the immune system.

Intestinal tissue is very sensitive to mycotoxins. Even at low levels of contamination, immunity can be compromised since gut health and immunity are so closely linked.

How much contamination is needed to cause damage in the gut?

Intestinal damage begins at very low concentrations in bovine intestinal epithelial cells. As little as 138 ppb nivalenol (NIV) or 172 ppb deoxynivalenol (DON) was shown to reduce cellular metabolic activity by 25% using an in vitro calf small intestinal epithelial cell model (Reisinger et al., 2019). This means it is more than likely that the intestine is under some level of stress most of the time. Deoxynivalenol and NIV are often co-occurring, and when you put them together, the result is worse than the sum of the individual mycotoxins.

Recent trials in swine (the same cellular mechanisms apply for all animals) show that at much lower contamination levels, intestinal cell function is lost. The first function to go is nutrient transport because it requires energy.

Additionally, mycotoxins compromise the tight junctions as well as the ability of the gut lining to defend itself from bacterial colonization. Escherichia coli is a bacterial pathogen that is almost always present in the gut. Figure 2 shows contaminated (left) and non-contaminated (right) images of gut lining taken from pigs after 6 days of exposure to fumonisins (FUM).

Figure 1. Microscopic images of pig gut lining taken from an animal in the control group (right) and an animal exposed to fumonisin B1 (FB1) for 6 days (left).

The contaminated image (left, FB1 treated) shows a lot of E. coli contamination on the lining of the gut (black dots) and fusion of some villi which reduces the surface area of the gut and therefore limits its nutrient absorption capacity. In the bottom left of the picture, you can see some E. coli have managed to cross the intestinal barrier due to the damage in the gut that was induced following mycotoxin exposure.

In the image of gut lining tissue from an animal in the control group (right, Control), you can see much less colonization of the gut surface, no loss of surface area with distinct villi, and no colonizing units having crossed the gut barrier. These images show how E. coli can be in the environment, but all that is needed for it to cause harm is an opening in the epithelium which can be mediated by mycotoxin contamination, in this case by FUM, but according to Reisinger et al. (2019) also possibly by DON and NIV.

Unfortunately, mycotoxin degradation is limited and unreliable

As awareness of the problems associated with mycotoxin contamination in ruminants increases, we will continue to investigate and better understand the mechanisms at play. We now know that simply relying on the rumen to degrade mycotoxins is not enough and could in fact make problems worse.

We have seen that very low levels of contamination are enough to harm gut health, immunity, productivity and fertility in cattle herds. So, cattle are in fact susceptible to the detrimental effects of mycotoxins despite some natural microbial degradation which may occur in the rumen.

References

Debevere S., Cools A., De Baere S., Haesaert G., Rychlik M., Croubels S., Fievez V. In vitro rumen simulations show a reduced disappearance of deoxynivalenol, nivalenol and enniatin B at conditions of rumen acidosis and lower microbial activity. Toxins. 2020; 12:101. https://pmc.ncbi.nlm.nih.gov/articles/PMC7076776/

Gruber‑Dorninger C., Faas J., Doupovec B., Aleschko M., Stoiber C., Höbartner-Gußl A., Schöndorfer K., Killinger M., Zebeli Q., Schatzmayr, D. Metabolism of zearalenone in the rumen of dairy cows with and without application of a zearalenone‑degrading enzyme. Toxins. 2021; 13(2): 84. https://doi.org/10.3390/toxins13020084

Hartinger T., Kröger I., Neubauer V., Faas J., Doupovec B., Schatzmayr D., Zebeli Q. Zearalenone and its emerging metabolites promptly affect the rumen microbiota in Holstein cows fed a forage‑rich diet. Toxins. 2023; 15(3): 185. https://doi.org/10.3390/toxins15030185

Reisinger N., Schürer-Waldheim S., Mayer E., Debevere S., Antonissen G., Sulyok M., Nagl V. Mycotoxin occurrence in maize silage-A neglected risk for bovine gut health? Toxins. 2019;11(10):577. https://pubmed.ncbi.nlm.nih.gov/31590302/