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"Poisonous" does not mean deadly. Some manifestations of toxicity are subtle. The dose, as always, determines if a plant is safe source of nutrients or a toxic hazard.


Some mycotoxins directly inhibit the growth of microorganisms. The term Mycotoxin literally means poison from a fungi. Mycotoxins are substances produced from fungal secondary metabolic processes, which impair animal health thereby causing great economic losses of livestock through disease. They are usually named on the basis of the fungus that produces them. For instance, "Aflatoxin" uses the A for Asperigillus and fla for the species flavus along with the word toxin.

There are three major genera of fungi that produce mycotoxins: Aspergilius, Fusarium and Penicilium. Mycotoxin-producing fungi grow on a wide spectrum of feeds that include cereal grains, groundnuts, beans and peas. They can invade the food supply at any time during production, processing, transport or storage. These organisms are aerobic and can both be pathogenic to plants or saprophytic with them. Several factors influence the degree of fungal growth in plants or plant products and the production levels of mycotoxins: Substrate characteristics, climate, physical interference and stress (Price et al 1993). Ambient temperature (12-47 C) and moisture levels of about >70% are optimal for proper fungal development and mycotoxin production. Other factors that might contribute to the growth of mycotoxin-producing fungi are insect and mechanical damage which destroy some of the plant's physical barriers thereby allowing fungal colonization. Poor fertilization and drought can also cause some levels of stress in the plant which weakens the plant's natural defenses. Since fungal growth is often associated with a particular climatic event such as a drought, outbreaks characteristically occur during seasonal weather.

Mycotoxins affect specific tissues or organs depending on the particular toxin involved. Some affect the nervous system, some cause liver and kidney damage, and others even cause vomiting in some species. Clinical syndromes in farm animals range from acute death to chronic disease, from reproductive deficiencies to just an overall debilitation. In general, mycotoxins are specifically associated with a particular feed, are not transmissible from organism to organism (except when special circumstances are considered like milk production for later human consumption), and are usually not responsive to any kind of direct treatment.

Some ruminant diseases proven to be directly related to mycotoxin consumption are: facial eczema in New Zealand's sheep, salivation factor in cattle, death of cattle from T-2 toxin, Stachybotryotoxicosis in Eastern Europe's sheep and goats, Lupinosis in sheep in South Africa, and maltoryzine poisoning in cattle (Allcroft 1969).

Among the most common mycotoxins implicated as health problems for ruminants are aflatoxins, zearalenone, trichotechenes and ochratoxins.

An example of a well known mycotoxin is aflatoxin. Aflatoxins are produced by both Aspergillus flavus and Aspergillus parasiticus and often cause liver damage and cancer, decreased milk production and immune suppression. The pedriatic members of the species are usually more susceptible to the effects of aflatoxins, which may be expressed as gastrointestinal disturbances, anemia, reduced feed consumption and overall retarded growth and development. Lactating mothers excrete less than 5% of ingested mycotoxins in the milk thereby directly affecting the nursing animal.

Since their discovery in the early 1960's, aflatoxins (B B G G ) have been a significant problem in the feed industry. A. flavus outbreaks can occur in the field during pre harvest or on crops in storage at a substrate moisture content of 14% and a temperature of 25-40 C. Some signs of aflatoxin production in ruminants include reduction in feed intake, weight loss and rapid death. Early detection signs of mycotoxicoses include moldy feed and feed refusal, however, aflatoxins are often present in feeds that appear to be normal. Death losses can occur without a diagnosis of an infectious disease. In any case, the diagnosis of mycotoxicosis is very difficult. This is due in part to the time lapse between exposure to the toxin, development of symptoms in the animal, and the observation of concrete clinical signs. Mycotoxin intoxications are not dramatically obvious, and as in any field investigation, a detailed clinical history should first be obtained (Spainhour and Posey 1992). It is important to pay close attention to changes in the feeding regimen such as the opening of a new feed bunker or change in the feed supplier. Mycotoxicosis can also occur even if the feed supply remains constant due to the presence of "hot spots", a focus of intense fungal growth in stored feeds. One of the main problems with "hot spots" is that after they are consumed by the animal there is no evidence of their existence and therefore proper diagnosis is further hindered. Field samples should always include feed, biopsy specimens and necropsy material as supportive evidence. Direct evidence of mycotoxicosis include the isolation and proper identification of a specific mycotoxin in both the feed and tissue or body fluid from the affected animal.

The equipment required to diagnose mycotoxicosis are only located at a local diagnostic laboratory, however, a readily available assay technique is often utilized to rapidly prescreen feed samples.

Proper identification of an aflatoxin problem comes not only from a positive analysis of aflatoxins in feed and animal tissue but also from milk samples of lactating animals. When analyzing stored feeds, a representative sample of the lot must be carefully taken to ensure reliable analytical data (Dickens and Whitaker 1986). Most samples of grains and feeds can be analyzed by the method known as CB method. In short, the representative samples are ground and mixed before sub samples are extracted with chloroform. A portion of the extract is then placed on a column of silica gel, and the lipids and pigment are eluted from the column. After the mycotoxins are properly eluted, they can be analyzed by TLC, HPLC or gas-chromatography-mass spectrometry (Richard et al., 1993). Milk and other dairy products are analyzed by the official method for International Union of Pure and Applied Chemistry, Association of Official Analytical Chemists, and the International Dairy Federation (Stubblefield 1986). Animal tissue is analyzed from the official AOAC method (Helrich 1990).

Adult cattle are much more resistant to aflatoxins than calves, but some investigations have indicated that lactating cows show a significant reduction in milk yield within a few days of eating aflatoxin contaminated feeds. Some indicators of aflatoxin poisoning in calves were poor feed utilization and a rapid rise in serum alkaline phosphatase activity (Lynch 1979). in several experiment, calves given aflatoxin-contaminated feed showed increased enzyme activity as early as one week after consuming the contaminated feed. The susceptibility of ruminants to aflatoxins poisoning depends on species, age, form of toxin, and specific nutritional status of the animal at the moment. Aflatoxins are both teratogenic and carcinogenic; the liver being the primary target organ in most species. The specific observed hepatic changes in calves with aflatoxin poisoning are bile duct proliferation, loss of hepatic glycogen, fatty infiltration, fibroblastic proliferation, and perivascular edema (Lynch 1979). At the cellular level, aflatoxins carcinogenic effects include degranulation of endoplasmic membranes. Membrane-ribosome sites are fully occupied and destroyed. Hepatic changes at the cellular level include loss of ribosomes from the endoplasmic reticulum, loss of nuclear chromatin material, and altered nuclear shapes.

The trichothecenes produced by Fusarium species on the other hand, are a group of tetracyclic 12,13-epoxytrichothecene skeleton mycotoxins. As a group, they cause a variety of symptoms in the animal that include hemorrhage throughout the digestive tract, depression of blood regeneration processes, and changes in the reproductive system. Signs of intoxication with this mycotoxin include weight loss, reduced feed consumption and utilization, vomiting, diarrhea, abortion and death. Diacetoxyscirpenol, T-2 toxin and deoxinivalenol (DON, vomitoxin) are three of the most important groups that have been detected in agricultural crops and products. Deoxivalenol (DON) is found in all major commodity grain crops in the United States. The two cereal grains most often contaminated with DON are corn and wheat. Although different assays for DON have been developed for these substrates, the newest technology for DON assays is the ELISA screening procedure (Richard et al. 1993). This can be used to evaluate DON levels for both practical and research purposes.

Studies have demonstrated, however, that in general ruminants are much more resistant to DON poisoning than non-ruminants. In vitro procedures utilizing rumen fluids have shown that toxins such as deoxinivalenol can be degraded by the rumen microflora (Hobson 1988). Pure cultures of certain rumen bacteria were capable of degrading T-2 toxin to HT-2 toxin, T-2 triol and in some cases, neosolianol (Westlake et al. 1987). These data support the theory that the rumen microflora is directly responsible for conferring a degree of mycotoxin resistance in the ruminant. Further studies by Westlake et al. utilized four different strains of Butyvibrio fibrisolvens to determine the extent of mycotoxin breakdown and the specific growth rate of this microorganism in the presence of several mycotoxins.

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