Why rumen degradation doesn’t protect cattle from mycotoxins

In Brief:

• Rumen degradation of mycotoxins is not always beneficial for the animal.
• The metabolites resulting from the aflatoxins and zearalenone degradation are more toxic than the original compounds.
• Mycotoxins can cause major problems related to productivity, health and fertility.

If you are an animal nutritionist or vet from the old days, you probably heard that ruminants are the least affected by mycotoxins. It used to be assumed that cattle are protected from mycotoxins due to the microbial degradation that could take place in the rumen. However, research and field experience increasingly show that this belief is not true, and could lead to more problems than the original mycotoxin contamination. 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.

Degradation in the rumen does not always equate to detoxification

Decades of research now show that cows are susceptible to a host of detrimental effects including impaired immune function, reduced feed efficiency, and compromised reproductive performance.

Mycotoxin degradation can backfire

While the rumen contains microbial populations that can degrade certain mycotoxins, the degradation is not always beneficial to the animal. Therefore, it is better not to talk about mycotoxins generically, rather by mycotoxin group because the capacity to be degraded and its result, vary molecule by molecule.

Table 1 gives a summary of  the main mycotoxins found on cattle farms, and how much it is broken down in the rumen (middle column, degradation in the rumen) , or not (right column, no degradation in the rumen), meaning that it goes straight to the intestine where most mycotoxins will cause major damage. The use of color indicates to which degree, the degradation happens:

• Red: degradation results in a more toxic compound, so it’s a potentiation of the toxicity
• Yellow: a partial degradation may happen but it’s very variable and depending on the circumstances
• Green: degradation goes as desired, leading to a reduction of the toxicity
• Orange: none to very little degradation takes place

What happens to each mycotoxin?

Table 1. Ruminal degradation of mycotoxins

Alfatoxin is the most carcinogenic compound found in nature. When consumed by cows, it can be transferred to milk, endangering consumers. Aflatoxins can be degraded in the rumen, but they are degraded into Aflatoxicol which is even more toxic to the cow than the original mycotoxin. So this degradation leads to a potentiation of its toxicity.

Zearalenone (ZEN) can be degraded to α-Zearalenol (α-ZEL) and β-Zearalenol (β-ZEL), but mostly to the earlier, up to a 50%. α-ZEL is 60 times more estrogenic than zearalenone, so the impact after passing through the rumen is potentiated. The remaining 50% is not broken down in the rumen and passes to the intestines as zearalenone.

Tricothecenes (such as deoxynivalenol (DON) and nivalenol (NIV)) are partially degraded in the rumen. However, degradation is very inconsistent with a range of 1-85%. This degradation depends on several factors but the two most relevants are:

• Ruminal pH: you need the right microbial populations to degrade the trichothecenes and lower pH’s, associated to high starch in diets, reduces the rate of this degradation
• Passage rate: This degradation also requires time, especially if the rate of degradation is reduced due to low pH. High yielding cows require high dry matter intakes, thus they experience very high passage rates, leaving short time for this degradation, particularly in smaller feed particles that escape the room in first hours.

Fumonisin (FUM) passes through the rumen and into the intestines completely unchanged. There is no degradation of fumonisin in the rumen.

Little is known about the emerging mycotoxin, Enniantin B. Research suggests that while some degradation takes place, most of the mycotoxin passes through to the intestines.

Ochratoxin A is one of the few positive examples where rumen degradation does take place and the metabolite is not harmful to the animal.

Mycotoxins impair health and immune status

While mycotoxins are often discussed in the context of productivity losses, seldomly, a dive between the origins of the productivity losses is made. 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. 75% of the body’s immune cells are found in the intestine. 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 is compromised.

75% of the body’s immune cells are found in the intestine so gut health and immunity are closely linked

How much contamination is needed to cause intestinal epithelium damage or death?

Intestinal damage, where 25% of intestinal cells are killed off, begins at very low levels; 138 ppb NIV or 172 ppb DON, for bovines.

 “Even at one tenth of the normal levels of silage contamination, you are already in the region of these levels”.

This means it is more than likely that the intestine is under some level of stress most of the time.  Deoxynivalenol (DON) and  Nivalenol (NIV) are often co-occurring, and when you put them together, the result is worse than the sum of the individual mycotoxins (Reisinger et al., 2019).

Recent trials in swine (the same cell 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.

E. coli is always present in the gut. Mycotoxins compromise the tight junctions as well as the ability of the gut lining to defend itself from colonization. Figure 2 shows contaminated (left) and non-contaminated (right) images of gut lining taken from pigs after 6 days of exposure to FUM.

Figure 2. Microscopic images of pig gut lining taken from an animal in the control group (right) and an animal exposed to fumonisin (FB1) for 6 days (left)

The contaminated image (left) 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 absorption capability. In the bottom left of the picture, you can see some E. coli colonizing units have managed to pass through the intestinal barrier.

In the image of gut lining tissue from an animal in the control group, 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 clearly show how E. coli can always be in the environment but all 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.

Mycotoxin degradation is not always helpful

As awareness of the problems associated with mycotoxin contamination in ruminants increases, we are better able to 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 also seen that even very low levels of contamination are enough to harm gut health, immunity, productivity and fertility in cattle herds. Effective mycotoxin management should start with accurate diagnosis and detoxification using Mycofix® before other feed additives are used to boost performance.