Introduction
In ruminant nutrition, mycotoxin risk management has historically been relegated to the background under the premise that the rumen microbiota acts as an efficient barrier against these contaminants (Bandyk, 2024). Unlike monogastrics, ruminants are assumed to possess evolutionary resilience thanks to the ability of rumen protozoa and bacteria to hydrolyse and deactivate toxic molecules prior to intestinal absorption (Upadhaya et al., 2010; Bandyk, 2024). However, the intensification of modern production systems has radically transformed this scenario, exposing the biological limitations of this «natural protection» (Falkauskas et al., 2024; Hartinger et al., 2022).
The current reality of the dairy and meat industry faces a dual challenge. On the one hand, the ruminant diet, composed of a complex mixture of forages, silages and concentrates, presents a risk of polycontamination by multiple families of fungi (Fusarium, Aspergillus, Penicillium) that is rarely found in simple diets (Gallo et al., 2015; Falkauskas et al., 2024). On the other hand, the metabolic pressure to achieve high productive yields forces the use of diets rich in starch and fermentable carbohydrates. These diets predispose cattle to Subacute Ruminal Acidosis (SARA), a condition that drastically alters rumen pH and, consequently, inhibits the fermentative and detoxifying capacity of the microbiota (Debevere et al., 2020).
Recent studies show that rumen detoxification is not a guaranteed or static process; it is highly variable and dependent on the stability of the rumen ecosystem (Hartinger et al., 2022). Even more alarming is the evidence that certain metabolic processes in the rumen do not detoxify, but rather bioactivate compounds, transforming mycotoxins such as zearalenone (ZEN) into metabolites with an estrogenic potency much higher than the original molecule (Bandyk, 2024; Falkauskas et al., 2024). This technical article examines the mechanisms by which the rumen barrier fails, the impact of mycotoxin-induced dysbiosis, and why relying solely on microbial degradation is an insufficient strategy to ensure herd health and productivity.
The myth of total ruminant immunity
Ruminants are generally considered less susceptible to mycotoxins than monogastric because rumen microorganisms (bacteria and fungi) act as a first line of defense, transforming certain toxins into less harmful metabolites prior to absorption (Bandyk, 2024; Debevere et al., 2020; Gallo et al., 2024). For example, it has been documented that the rumen microbiota can degrade ochratoxin A (OTA) to ochratoxin alpha (OTα), a compound with lower toxicity, and de-epoxidize trichothecenes such as deoxynivalenol (DON) (Guerre, 2020; Mobashar et al., 2010; Gallo et al., 2024).
However, this «shielding» capacity is not absolute. Recent studies indicate that systemic exposure to multiple mycotoxins is routine in cattle, and that the historical assumption of safety has led to underestimation of the real risks in milk and meat production (Bandyk, 2024). Rumen detoxification has clear boundaries defined by the chemical stability of the toxin, the rate of feed passage, and the health of the rumen ecosystem.
1. Resistance to degradation
Not all mycotoxins are efficiently degraded. Fumonisins (FBs), for example, are poorly metabolized in the rumen and resist microbial action, maintaining their toxic potential in the posterior intestinal tract (Bandyk, 2024; Hartinger et al., 2022). Similarly, certain metabolites such as mycophenolic acid show almost zero disappearance in rumen fluids in vitro, suggesting that they remain intact and bioavailable (Debevere et al., 2020).
2. Bioactivation
In some cases, rumen metabolism transforms a mycotoxin into a more potent metabolite, a process known as bioactivation or toxification. The most critical case is that of zearalenone (ZEN). The rumen microbiota converts ZEN mainly to α-zearalenol (α-ZEL) and, to a lesser extent, to β-zearalenol. α-ZEL is significantly more estrogenic than the original molecule, exacerbating reproductive problems rather than mitigating them (Bandyk, 2024; Falkauskas et al., 2024; Gallo et al., 2015; Hartinger et al., 2022).
3. Overload and pass rate
In high-production systems, the ruminant becomes a fast-flowing metabolic unit that compromises biological detoxification. Accelerated passage kinetics is not just a change in velocity; it is an alteration of rumen retention time, which is the limiting factor for bacteria and protozoa to hydrolyze complex molecules such as deoxynivalenol (DON) or other mycotoxins. When the animal consumes massive levels of dry matter to avoid Negative Energy Balance (BEN), the contact time between toxins and microbial enzymes becomes insufficient, transforming the rumen from a protective filter into a simple transit conduit to the small intestine. This scenario is aggravated in situations of Subacute Ruminal Acidosis (SARA), where low pH (< 6.0) not only inhibits detoxifying microbes, but also increases the bioavailability and absorption of toxins such as aflatoxin B1 and ochratoxin A, allowing them to enter the bloodstream more easily (Bandyk, 2024; Debevere et al., 2020).
The Critical Impact of Subacute Ruminal Acidosis (SARA)
Considering that pH is the regulatory axis of microbial activity, the incidence of Subacute Ruminal Acidosis (SARA) derived from modern starch-rich diets, is positioned as the determining factor in the collapse of detoxification, acting as a catalyst that dismantles the rumen barrier by three key mechanisms (Debevere et al., 2020; EFSA, 2022).
- Inhibition of the detoxifying microbiota: The ability of microbes to degrade toxins decreases dramatically under low pH conditions (<6.0 or <5.8). In vitro studies have shown that the disappearance of mycotoxins such as DON, nivalenol, and enniatin B is significantly reduced under conditions of acidosis (Debevere et al., 2020; Falkauskas et al., 2024).
- Rumen dysbiosis: Acidosis alters the composition of the microbiota, reducing the population of protozoa (which play a central role in the degradation of toxins such as OTA) and beneficial bacteria, while favoring bacteria that do not have detoxifying capacity (Gallo et al., 2024; EFSA, 2022; Bandyk, 2024).
- Increased bioavailability: It has been observed that a low rumen pH, induced by high-starch diets, can increase the bioavailability of certain toxins such as aflatoxin B1 and ochratoxin A, enhancing their systemic absorption (Gallo et al., 2024).
Oxidative stress
Mycotoxin damage in high-demand animals does not end with absorption; it becomes a biochemical attack by generating oxidative stress. At the cellular level, toxins such as Fumonisins (FBs) and deoxynivalenol (DON) act as catalysts for redox imbalance that trigger a cascade of free radicals, which attack the mitochondria and cell membranes of the rumen and intestinal epithelium. This process of lipid peroxidation destroys tight junctions, resulting in a leaky gut that allows the translocation of pathogens and toxins into the liver (Lin et al., 2022).
Direct effects of mycotoxins on the rumen
Beyond being degraded, mycotoxins can attack the rumen microbiota itself, creating a vicious circle that reduces digestive efficiency.
Many mycotoxins possess antimicrobial properties that disrupt fermentation. Exposure to DON or FBs has been shown to reduce volatile fatty acid (VFA) production and microbial protein synthesis, affecting the digestibility of fiber and organic matter (Hartinger et al., 2022; Dong et al., 2023; Wang et al., 2026). On the other hand, sequencing studies have revealed that exposure to ZEN or FBs reduces the abundance of key bacterial families such as Lachnospiraceae and Prevotellaceae, essential for rumen health (Hartinger et al., 2022). In addition, DON can affect signaling molecules (quorum sensing), interfering with bacterial communication necessary for adaptation and efficient fermentation (Wang et al., 2026).
Emerging mycotoxins and co-contamination
The traditional approach has focused on a few regulated mycotoxins (AFB1, DON, ZEN). However, silage and forages often contain a «mixture» of toxins, including so-called emerging mycotoxins (enniatins, beauvericin, tenuazonic acid, etc.) (Bandyk, 2024; Reisinger et al., 2019). Analysis of corn silage samples in Europe revealed that more than 87% contained five or more mycotoxins simultaneously (Reisinger et al., 2019). These emerging toxins are not regulated, and their degradation in the rumen is often incomplete (as in the case of enniatin B under conditions of acidosis) (Debevere et al; Bandyk, 2024). The interaction between multiple toxins can generate synergistic effects that exceed the animal’s detoxification capacity (Falkauskas et al., 2024).
Conclusion
Rumen detoxification is not a guarantee of safety. It is a variable biological process that is easily compromised by factors common in intensive production, such as high feed intake, diets rich in concentrates, and the prevalence of SARA. In addition, the conversion of toxins such as zearalenone (ZEN) into more potent metabolites turns the rumen into a site of bioactivation rather than detoxification.
Therefore, relying solely on rumen capacity is insufficient. It is necessary to implement comprehensive strategies that include the use of sequestering agents, capable of acting where the rumen fails, thus protecting the health, fertility and performance of the herd.
