Mycotoxins are secondary metabolites produced by a wide variety of filamentous fungi, including species from the genera Aspergillus, Fusarium and Penicillium. The fungi typically grow on various feedstuffs, such as grains and cereals. Mycotoxins are invisible, tasteless, chemically stable, and survive high temperatures and many environmental conditions. Most animal feedstuffs are likely to be contaminated with multiple mycotoxins. The growth of moulds and mycotoxin production occurs worldwide, especially in climates with high temperatures and humidity and where grain is harvested with high water content. The Food and Agriculture Organization (FAO) estimates that as much as 25% of the world’s agricultural commodities are contaminated with mycotoxins, leading to significant economic losses.
The most common source of food and feed contamination are mycotoxins produced by the fungi Aspergillus, Penicillium and Fusarium genera. Other mycotoxin-producing fungi include Alternaria, Chaetomium, Cladosporium, Claviceps, Diplodia, Myrothecium, Monascus, Phoma, Phomopsis, Pithomyces, Trichoderma and Stachybotrys.
While Aspergillus and Penicillium species are generally found as contaminants in feed during storage, Fusarium and Alternaria species can produce mycotoxins before harvesting or immediately after. Every plant can be contaminated by more than one fungus, and each fungus can produce more than one mycotoxin. Up until now, approximately 400 secondary metabolites with toxigenic potential produced by more than 100 moulds have been reported.
Aspergillus, Fusarium, Penicillium and Claviceps produce the most extensively studied mycotoxins. Some of the mycotoxins produced by these moulds include aflatoxins, ochratoxins, deoxynivalenol (DON), T-2 toxins, zearalenone, fumonisins, Citrinin and ergot alkaloids. Mycotoxins cause diverse effects on animals, such as carcinogenesis, hepatotoxicity, and neurotoxicity, as well as impaired reproduction, digestive disorders, immunomodulation, and decreased performance.
Multiple factors determine the contamination of agricultural commodities with mycotoxins. Mycotoxin occurrence varies between crops, as fungal species and strains differ in their ability to infest a particular host. It also varies between varieties of the same plant species, as varieties show different levels of susceptibility or resistance to fungal infestation. Furthermore, environmental conditions, such as temperature and humidity, affect the infestation of crop plants with mycotoxigenic fungi and mycotoxin; therefore, climate and weather are strong determinants of mycotoxin contamination. Moreover, agricultural practices, the timing of harvest, and post-harvest handling of crops affect mycotoxin formation.
Crops may be infested with multiple strains of fungi, and most fungal strains produce more than one type of mycotoxin. Therefore, co-contamination of agricultural commodities with multiple mycotoxins is frequently observed. When feed raw materials are mixed, mycotoxin co-contamination becomes even more likely. If mycotoxins co-occur, their combined toxic effect may be much greater than the summed effects of the individual mycotoxins.
Contamination of feed commodities with fungus is commonly seen in every part of the world and it varies from region to region depending upon the environmental conditions like temperature and humidity. Prominent mycotoxins occurring in agricultural commodities, include: aflatoxins (AFLA), ochratoxin A (OTA), zearalenone (ZEN), deoxynivalenol (DON), fumonisins (FUM) and T-toxin (T-2). Some of these mycotoxins have hepatotoxic, nephrotoxic, immunosuppressive, genotoxic, teratogenic, and/or carcinogenic effects in animals. During the last 10 years, incidence of multiple mycotoxins (AFLA, OTA, ZEN, DON and FUM) produced by different fungal species particularly Fusarium and Aspergillus genus have been reported in cereals from different countries. Co-occurrence now gains much attention worldwide owing to its more toxic capacity (synergistic effect) as compared to single mycotoxin. According to studies, more than 50% of mycotoxin contaminated feed samples contained multiple mycotoxins. The co-occurrence of mycotoxins can affect both the production of mycotoxin and the toxicity of the contaminated material. Frequency of mycotoxins produced by Fusarium fungal species containing DON, FUM, ZEN are more frequent and co-occurrence of these mycotoxins can result severe detrimental impacts. The majority of mycotoxins in animal feed are associated with lower performance, poor growth, health and reproductive issues and significant economic impact on livestock production.
It is suggested that ruminants are less susceptible than other animal species to the adverse health effects associated with mycotoxin exposure. This assumption is based on the fact that the rumen flora can convert several mycotoxins into less potent or biologically inactive metabolites. This does not apply, however, to all mycotoxins that contaminate feed materials and during the risk of exposure to more than one mycotoxin or mycotoxin cluster. Mycotoxins can increase the incidence of disease and reduce production efficiency in cattle. Mycotoxins can be the primary agent causing acute health or production problems in a dairy herd, but more likely, mycotoxins are a factor contributing to chronic problems, including a high incidence of disease, poor reproductive performance or suboptimal milk production.
Aflatoxin is produced primarily by Aspergillus flavus and can contaminate corn, wheat, rice, cottonseed, and peanuts. Aflatoxin is a carcinogen and is excreted in milk. Therefore, in the United States, the Food and Drug Administration (FDA) limits aflatoxin to no more than 20 ppb in lactating dairy feeds and 0.5 ppb in milk. A general rule is that milk aflatoxin concentrations will equal about 1.7% of the aflatoxin concentration in the total ration dry matter. Therefore, cows consuming diets containing 30 ppb of aflatoxin will produce milk containing aflatoxin residues just above the FDA action level of 0.5 ppb.
Production and health of dairy herds are affected at aflatoxin levels above 100 ppb, which is three times the amount that produces illegal milk residues. For example, reproductive efficiency declined when lactating dairy cattle in a field situation were consuming 120 ppb of aflatoxin. When cows were switched to an aflatoxin-free diet, milk production increased by over 25%.
Deoxynivalenol is a Fusarium-produced mycotoxin commonly detected in grains such as corn, wheat, barley, and oats. It is sometimes called vomitoxin because it was first associated with vomiting in swine. The impact of DON on dairy cattle is not established, but clinical data show an association between DON contamination of diets and poor performance in dairy herds. For example, results from a Canadian study using 18 first-lactation cows during mid-lactation showed that cows consuming DON-contaminated diets (4 to 5 ppm) produced 13% less fat-corrected milk (P<0.16) than cows consuming clean feed. Beef cattle and sheep have tolerated up to 21 ppm of DON without obvious effects.
Like other mycotoxins, pure DON added to diets does not have as much toxicity as does DON supplied from naturally contaminated feeds. This is thought to result from the interaction of multiple mycotoxins in naturally contaminated feeds. These mycotoxins can interact to cause different or more severe symptoms than expected. For example, it is now known that fusaric acid interacts with DON to cause the vomiting effects earlier attributed to DON alone, which resulted in the use of the trivial name of vomitoxin for DON. It is believed that DON serves as a marker, indicating that feed was exposed to a situation conducive to mould growth and the possible formation of several mycotoxins. A feed positive for DON may contain other mycotoxins; therefore, a dietary level of 300 to 500 ppb DON may indicate a problem feed and warrants attention.
Zearalenone is a Fusarium-produced mycotoxin with a chemical structure similar to estrogen and can produce an estrogenic response in animals. Controlled studies with purified zearalenone at high levels have failed to reproduce the degree of toxicity associated with zearalenone-contaminated feeds in field observations. A controlled study with non-lactating cows fed up to 500 mg of zearalenone (calculated dietary concentrations of about 25 ppm zearalenone) showed no obvious effects except that corpora lutea were smaller in treated cows. In a similar study with heifers receiving 250 mg of zearalenone by gelatin capsule (calculated dietary concentrations of about 25 ppm zearalenone), the conception rate was depressed by about 25%; otherwise, no obvious effects were noted.
Several case reports have related zearalenone to estrogenic responses and severe fertility problems in cattle, including abortions. Symptoms have included vaginitis, vaginal secretions, poor reproductive performance and mammary gland enlargement of virgin heifers. In a field study, diets with about 750 ppb zearalenone and 500 ppb DON resulted in poor consumption, depressed milk production, diarrhea, increased reproductive tract infections, and total reproductive failure. New Zealand workers have measured blood zearalenone and metabolites to estimate zearalenone intake. Dairy herds with low fertility had higher levels of blood “zearalenone.” Individual cows within herds examined by palpation and determined to be cycling had lower blood “zearalenone” levels than cows that were not cycling. The reproductive problems in dairy cattle were associated with dietary zearalenone concentrations of about 400 ppb.
The establishment of a tolerable level of zearalenone for cattle is impossible based on the limited amount of data. As with DON, zearalenone may serve as a marker for toxic feed. Zearalenone above 200 to 300 ppb in the diet may be of concern.
T-2 toxin is a very potent Fusarium-produced mycotoxin that occurs in a low proportion of feed samples (<10%). T-2 is associated with reduced feed consumption, loss in yield, gastroenteritis, intestinal hemorrhage, reduced reproductive performance, and death. T-2 is toxic to intestinal tissue, lymphoid tissues, liver, kidney, spleen and bone marrow and is known to interfere with protein synthesis and suppress immunity. While data with cattle are limited, the effects in laboratory animals are well documented. Cattle deaths have been associated with dietary levels above 500 ppb. Although data in cattle are insufficient to establish a tolerable level of T-2, we recommend avoiding more than 100 ppb of T-2 toxin in the total diet.
Fumonisin B1 is produced by the fungus F. verticillioides and was first isolated in 1988. It causes leukoencephalomalacia in horses, pulmonary edema in swine, and hepatoxicity in rats. Fumonisins are structurally similar to sphingosine, a component of sphingolipids. While FB1 is less toxic to ruminants than swine, it has now been shown to be toxic to sheep, goats, beef cattle, and dairy cattle. Osweiler et al fed 18 young steers, either 15, 31, or 148 ppm of fumonisin in a short-term study (31 days). With the highest feeding level, mild liver lesions were found in two of six calves, and the group had elevated liver enzymes indicative of liver damage. Lymphocyte blastogenesis was significantly impaired at the end of the feeding period in the group having the highest dose.
Dairy cattle (Holsteins and Jerseys) fed diets containing 100 ppm fumonisin for approximately seven days prior to freshening and for seventy days thereafter demonstrated lower milk production (6 kg/cow/day), explained primarily by reduced feed consumption. Increases in serum enzymes concentrations suggested mild liver disease. Because of greater production stress, dairy cattle may be more sensitive to fumonisin than beef cattle. Fumonisin carryover from feed to milk is thought to be negligible.
In 2001, the FDA released a guidance document for fumonisin in human foods and animal feeds. It is recommended that human food products should contain no more than 2 to 4 ppm of total fumonisins. For dairy cattle, the guideline recommends that contaminated corn or corn byproducts be limited to no more than 50% of the diet and that the maximum concentration of total fumonisins in corn and corn byproducts are 30 ppm for lactating and breeding age cattle and no more than 10 ppm for calves. Because fumonisin is associated with reduced feed consumption, there is a concern that low levels of fumonisin interacting with other mycotoxins may reduce milk production.
Many other mycotoxins may affect ruminants, but they are thought to occur less frequently or be less potent. Diacetoxyscirpenol, HT-2 and neosolaniol may occur along with the T-2 toxin and cause similar symptoms. Ochratoxin has been reported to affect cattle, but it is rapidly degraded in the rumen and is thus thought to have little consequence except for pre-ruminants (calves). Tremorgens such as fumigaclavine A and B produced by Aspergillus fumigatus are thought to be common in silages of the southeastern United States and have been shown to be toxic to cattle. Tremorgens can cause anorexia, diarrhea, unthriftiness and irritability. Mycotoxins such as rubratoxin, citrinin, patulin, cyclopiazonic acid, sterigmatocystin, and ergot alkaloids may also be of importance
Recognition of the impact of mycotoxins on animal production has been limited by the difficulty of diagnosis. The symptoms are often nonspecific and the result of a series of effects, making a diagnosis difficult or impossible because of the complex clinical results. The difficulty of diagnosis is increased due to limited research, the occurrence of multiple mycotoxins, non-uniform distribution, interactions with other factors, and problems of sampling and analysis.
Mycotoxins are prevalent in feedstuffs, and many different mycotoxins exist. They affect ruminants in many ways, the most important perhaps being immunosuppression, which can lead to a variety of problems in dairy cattle, including increased transition cow disease (e.g., mastitis, metritis, retained placentas). Diagnosis of a mycotoxicosis is difficult and indirect, but mycotoxins must be considered a potential cause of increased disease and loss of production. While mycotoxins can cause acute toxicity, they are more likely to cause chronic problems of increased disease and decreased milk production. Contamination of milk by aflatoxin can cause substantial economic losses. Management of crops and feeds is essential to reduce mycotoxin contamination. Regular analysis of feed components and silage can help identify potential mycotoxin threats to animals. Good silage management is necessary to avoid further mould growth and prevent mycotoxins production. Regular supplementation with a potent mycotoxin deactivator is the best insurance to prevent mycotoxins from harming cows’ health and productivity.
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