Mycotoxins in
dairy cattle

Do mycotoxins affect the health of dairy cows? Is it possible for them to reach the milk that they produce?

María Rodríguez-Blanco, Sonia Marín, Vicente Sanchis, Antonio J. Ramos

Unidad de Micología Aplicada, Departamento de Tecnología de Alimentos, ETSEA-Universitat de Lleida, UTPV-XaRTA, Agrotecnio, Spain.

antonio.ramos@udl.cat

Mycotoxins are low molecular weight secondary metabolites produced by certain genera of filamentous fungi under environmental conditions that are favourable for their synthesis (Bennett and Klich 2003).

Contamination of raw materials used for the formulation of feed with mycotoxins is a worldwide problem that causes significant economic losses.

Furthermore, the intake of contaminated feed may lead to acute or chronic intoxication in the animals and may also contribute to its consumption by humans, due to the possible transfer of these compounds to animal products such as milk, meat or eggs (Fink-Gremmels 2008a; Pinotti et al. 2016).

The main mycotoxins that can be found contaminating feed and feed materials are aflatoxins (AFs), deoxynivalenol (DON), fumonisins (FBs), ochratoxin A (OTA), T-2 toxin and zearalenone (ZEN).

Toxic effects of mycotoxins in dairy cows

Ruminants are considered to be relatively resistant to mycotoxins, as ruminal microorganisms are able to degrade these compounds to less toxic, or even biologically inactive, compounds at normal exposure levels (Fink-Gremmels 2008b).

However, it should be noted that the rumen’s degradation capacity can become saturated or affected by changes in the diet or as a result of metabolic diseases (Fink-Gremmels 2008b). Therefore, consumption of feed contaminated with these compounds can affect the health status of dairy cows.

Some of the negative effects caused by mycotoxins in cattle are listed in Table 1.

Table 1. Main toxic effects in dairy cows derived from the consumption of feed contaminated with AFs, FBs, ZEN and DON.

Mycotoxins in feed for dairy cattle

Dairy cows need fiber, proteins, water, vitamins and minerals as fundamental nutrients in daily diets. Furthermore, it is necessary to include a sufficient amount of forage in their feed to maintain a functional ruminal microbiota. In addition, high amounts of energy-rich components are needed, as they are essential to achieve high milk production and maintain the animal’s weight (Gonçalves et al. 2015).

The great variety and variability of ingredients used in diets increases the risk of exposure to a wide range of different mycotoxins.

Among the materials included in the formulation of dairy rations, energy-rich components represent the main potential source of mycotoxins.

  • AFs, FBs, OTA, trichothecenes, and ergot alkaloids have been found contaminating some of these components such as cereals, soybeans, peanuts, or cottonseed.
  • Fodder is the second source of mycotoxins, and preserved feeds such as silage, hay and straw are the third (Fink-Gremmels, 2008a).

Silage is an important part of the diet of dairy cows, as it usually represents a high percentage of the final ration. These materials can be contaminated in the field, in postharvest stages, as well as during storage.

Aspergillus, Fusarium, Alternaria and Penicillium sare some of the filamentous fungi frequently found contaminating silage, so mycotoxins such as AFs, FBs, ZEN, trichothecenes, mycophenolic acid and roquefortine C can be detected in this raw material (Storm et al. 2008; Driehuis et al. 2008; Schmidt et al. 2015).

Mycotoxin carry-over to milk

In addition to the direct effects on animal health, one of the main problems associated with the presence of mycotoxins in animal feed is their possible carry-over to products derived from animals, such as milk.

When dairy cows consume feed contaminated with aflatoxin B1 (AFB1), a part is broken down in the rumen to aflatoxicol, and another part reaches the liver where it is metabolized by liver enzymes through hydroxylation, hydration, demethylation and epoxidation.

The hydroxylation of AFB1 results in aflatoxin M1 (AFM1) and some of this compound is eventually excreted through the milk (Dhanasekaran et al. 2011).

AFM1 is detected in milk approximately 6 hours after consumption of the contaminated feed. Peaks of toxin can be detected 24 and 48 hours later if the intake of the feed continues and it disappears almost completely 72 hours after the withdrawal of the contaminated feed (Rodrigues 2014).

The transfer rate from AFB1 in feed to AFM1in milk can vary from 1-2% in low yielding cows to 6% in high yielding cows (Britzi et al. 2013; Rodríguez-Blanco et al. 2019).

Monitoring AFM1in milk has increased, especially since this toxin was classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer (IARC) (IARC, 2012).

To minimize the exposure of AFM1, in humans, different countries have established regulations for maximum allowed concentrations of  AFM1 in milk.

The European Commission and the Codex Alimentarius Commission (EC 2006; Codex Alimentarius 2001) established a limit of:

  • 50 ng/kg AFM1 in raw milk, heat-treated milk and milk for dairy product fabrication.
  • 25 ng/kg AFM1 in infant milk and follow-on milk.

In other countries such as the United States, the maximum limit is:

  • 500 ng/kg toxin in raw milk.
  • 25 ng/kg in baby milk products.
  • The maximum limits of AFB1 established in feed for dairy animals (5 µg/kg) are aimed at reducing the presence of AFM1 in milk due to the transfer from feed to milk.

AS FOR THE TRANSFER OF OTHER TOXINS TO MILK, FEWER STUDIES HAVE BEEN CARRIED OUT

The European Food Safety Authority (EFSA) reported that the carry-over of FBs to milk is limited and does not contribute significantly to total human exposure (EFSA 2005).

Similarly, as regards to ZEN, EFSA reported that the carry-over rate of this toxin to milk is very low (EFSA 2004).

POn the other hand, several studies have shown that DON is transformed to de-epoxy-deoxynivalenol (DOM1) in the rumen (Coté et al. 1986; Seeling et al. 2006; Keese et al. 2008) and that the part that is not metabolized is excreted in the milk at a very low rate (Prelusky et al. 1984).

Reduction of mycotoxin contamination

Despite the limits for mycotoxins established in different countries to reduce the level of exposure to these compounds, their presence in food and feed is usually unavoidable.

Mycotoxin contamination can occur at any point in the feed production chain, so strategies have been developed to prevent its occurrence as well as to eliminate them from contaminated products. However, they are very stable compounds and difficult to remove.

The implementation of good agricultural practices, good manufacturing practices, good hygiene practices and good storage practices is essential to reduce mycotoxin contamination.

The problem of mycotoxins in feed can be addressed from a preventive point of view, by avoiding postharvest mycotoxin production in crops, by controlling feed storage conditions, or once the contamination of the products has occurred, by applying different technological strategies.

Physical treatments

Some of the physical treatments that have been tested are thermal inactivation or the application of UV light (CAST 2003).

Chemical treatments

Among the chemical methods, treatments with acid/base solutions or the use of additives have been successfully employed (CAST 2003).

Although it should be noted that the use of chemical methods of mycotoxin detoxification is prohibited in the EU.

Biological treatments

Moreover, biological methods based on the detoxifying action of microorganisms, such as yeasts, moulds, bacteria and algae, may represent in the future a more suitable alternative for the elimination of mycotoxins (EU 2018; EFSA 2013)

Another strategy, widely used in the field of animal nutrition, consists of adding adsorbent compounds to the feed, which bind to the toxins during its transit through the gastrointestinal tract, reducing its absorption, promoting its excretion or modifying its mechanism of action.

Its use has already been authorized by the EU (EC, 2009).

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