Most Common Mycotoxins
Deoxynivalenol (DON, vomitoxin)
Deoxynivalenol is a Group-B trichothecene produced by several species of Fusarium. It tends to occur in fairly high quantities under natural conditions; it is, however, less toxic than T-2 toxin to most species. In species affected, feed consumption is reduced, daily gain is reduced, somatic cell counts are elevated, milk production is lowered, reproductive performance is affected, loose and inconsistent manure (considerable cow-to-cow variation), and immune response is dysfunctional.
Swine may exhibit feed refusal as DON levels rise. Primary antibody response is generally okay but secondary response (e.g., response to a booster vaccine or second challenge) is reduced.
In dairy cows, milk production has been shown to begin declining around 300 ppb DON and milk fat can be depressed. A survey of 100 Dairy Farms conducted by North Carolina State University showed a relative milk production loss of over 3 lbs. per day at DON levels of 500 ppb. While there is evidence for some deactivation of DON by rumen microbes, there is also evidence to show that enteric (gut) microbes can convert the deactivation product back to the parent DON molecule.
Beef cattle and sheep are generally more resistant to DON than other ruminants.
Poultry are generally refractive to DON; significant amounts (at the ppm level) are required to produce DON-related effects. DON is more water soluble than other trichothecenes; research shows little uptake in tissues or residues in milk and relatively rapid clearance rates once the toxin is withdrawn.
However, in all species, DON is a primary feed marker for presence of both known and unknown mycotoxins. As DON levels rise, problems also rise in production species, even though not necessarily caused by this mycotoxin per se. As such, regardless of species, feed or ingredients testing positive for DON should be considered as potentially injurious on the production farm.
T-2 Toxin (T-2)
Occurs in various commodities (e.g., corn, milo, soymeal, wheat midds, etc.) as T-2 or HT-2 toxin produced by various species of the genus Fusarium. They are within the Group-A trichothecenes which include diacetoxyscirpenol (DAS) but not deoxynivalenol (DON, vomitoxin) which is a Group-B trichothecene. T-2 is a dermal irritant and produces characteristic lesions in the oral cavity of some species (e.g., chicken). It is also a potent inhibitor of protein synthesis when absorbed from the intestine. Toxicity derives from the presence of an epoxide ring (oxygen between carbon #12 and #13). Problems common to T-2 toxin, in addition to dermal lesions mentioned before, are gastroenteritis, intestinal hemorrhage, some feed refusal (in the cow, pig), immunosuppression (including reduced immunoglobulins, complement proteins, white blood cells, and neutrophils), and the more general symptoms seen with other mycotoxicoses including reduced weight gain, poor feed conversion, morbidity and mortality. T-2 toxin can induce loose stools due to irritation of the gut lining. In pure T-2 toxin studies, several ppm may be required to produce overt disease. However, an additional factor is the interaction capacity of T-2 with other mycotoxins. Where high levels in swine rations may be toxicologically self-limiting because swine exhibit feed refusal so readily, species, such as the chicken, which do not show tendency to feed refusal, or ruminants, which are only slightly affected in that way, are sensitive to levels on the order of ppb. Because of the biochemical site of interference with protein synthesis, T-2 at very small levels may interact synergistically with other toxic agents to produce significant disease states. This is particularly significant for the cow whose complex ration (forages + concentrates + pasture) places a very large diversity of mycotoxins before the animal daily. Risk of adverse interactions, is, therefore, great. As a general rule of thumb, total time of exposure also is a determinant of ultimate toxicity. For example, in an acute dosing situation, 800 ppm to 1 ppm may be required over two weeks or less to result in oral lesions, but 500 ppb or less over 4-5 weeks will also produce significant oral lesions in broiler chickens. In poultry feed levels of 250 ppb or higher should trigger producer action. For dairy, and under chronic exposure, 75 ppb should be cause for concern.
Zearalenone (Zea)
Zearalenone is a toxic metabolite produced by several species of the genus Fusarium, notably F. graminearum. While commonly found in corn and wheat, it occurs frequently in oats, rye, sorghum, barley, etc. Fusarium spp. Generally are less able to flourish in ensiled commodities, the major exception being that they will do well on cut surfaces or entrapped air pockets within the post-harvest silage. However, given their prevalence in pre-harvest crops, silage is only rarely absent such toxins. Zea is structurally related to cholesterol and estrogen; in the animal it acts as an estrogen thus causing irregularities in the reproductive physiology. Poultry are typically not affected severely by this toxin except in breeder situations.
Swine are very sensitive with abortion, vulvovaginitis, and vaginal prolapse being common occurrences in both sows and prepubertal gilts.
In dairy cattle, rumen microflora degrades an estimated 90% of ingested zearlanone (presuming normal, healthy rumen microflora); however, the end product is ?lpha-zearalenol which is considered to be as much as 4 times more estrogenic than the parent compound. Thus, reproductive failures should always be expected, which include a) decreased embryo survival and hypertrophy of the genitalia in pre-pubertal females; b) decreased LH and progesterone affecting the uterus, feminization of males, and infertility; and c) vaginitis, abortions, and mammary gland enlargement in virgin heifers. Low fertility herds typically are found to have higher blood and urinary levels of Zea metabolites. Also, straw, but not alfalfa, is not degraded well in the rumen in the presence of Zea plus DON. Other feedstuffs may suffer similar effects that are related to the adverse action of Zea on some rumen microorganisms. Dairy herd problems are reported at levels of 300-400 ppb (sole toxin). In swine, expect effects related to hyper-estrogenism at levels of 75 - 150 ppb.
Fumonisin
Fumonisins are a family of toxins produced by Fusarium verticillioides (formerly F. moniliforme) and F. proliferatum. The latter is one of the most commonly isolated fungi from corn throughout the world. While most toxicology studies focus on Fumonisin B1, other forms (e.g. B2), have been shown to have substantial toxicity and act very much like the B1 form. Fumonsins seem to be of relatively low toxicity (by laboratory trials); conversely, the fungi produce very high levels of these under natural conditions. Fumonisins are very water soluble and have a chemical structure very similar to sphingosine (a lipid with a variety of physiological functions and closely related to integrity of neural tissues). Its toxicity is, in large part, a result of the substitution of fumonisin for sphingosine in biological reactions in the animal’s body. When these substitutions occur, the function or molecular structure fails. In some animals, low dose chronic feeding has resulted in a large variety of clinical symptoms such as torsion of the colon, skin hemorrhages, wasting, mild jaundice, and upon necropsy, hepatosis, ulcerations of stomach and colon, and necrosis in the colon.
Amongst production species, poultry are the most tolerant with estimated field levels of 1-4 ppm causing problems in broilers and turkeys. Weight loss, poor feed conversion, enlargement of liver and gizzard, and reduction of serum cholesterol, albumin, and calcium. Kidney damage is likely in cattle and sheep.
Dairy cows fed 100 ppm pre- and post-parturition had lowered feed consumption and milk production (research trial). As a rule, toxin doses at 10 to 100 times less than research levels will produce similar conditions in commercial settings, suggesting dairy cows are at risk at 100-1,000 ppb dietary fumonisin.
Horses at 5 ppm succumb to leukoencephalomalacia, a fatal, necrotic brain disease, while swine fed 10 ppm develop pulmonary edema. Knowledge of specific interaction capacities is not well known yet with this family of mycotoxins.
Aflatoxin(s) – AF
Occur in various agricultural commodities (e.g., corn, milo, soymeal, almond hulls, wheat midds, etc.) in one or more of four different chemicals – AFB1> AFG1>AFB2>AFG2 (in order of presumptive toxicity) produced by Aspergillus flavus or A. parasiticus. Antibody-based tests generally determine only AFB1. AF is absorbed in the intestine and transported to the liver where it is metabolized to several chemically related end-products. Two of these are the primary toxic form; they bind to DNA and protein, interrupting protein synthesis (includes enzymes and structural proteins) in the animal leading to multiple adverse conditions. Among common problems are damage to the liver with resulting impairment of normal metabolism in the animal, damage to the endocrine system which may lead to problems with reproduction, depression of humoral (antibody) and cell-mediated immune functions as well as interference with mucosal immunity in the GI tract increasing sensitivity to pathogens, lowering of digestive and absorptive capacity in the gut (malabsorption syndrome), and losses in body weight gain, feed efficiency, and production milk, meat, eggs, etc. Aflatoxin is well known to interact negatively with other mycotoxins present in the ration to produce substantially worse problems in the animal than can be predicted. One liver metabolite, AFM1, is excreted in the milk. It is almost as toxic as the parent molecule, AFB1, and, thus, is regulated by FDA. Consumption of AF by dairy cows at levels below 10ppb is generally without consequence except to the extent interactions may occur. Cows consuming 20 ppb will have milk AFM1 approaching the violative level (0.5 ppb AFM1), and those exposed to 25 ppb or more are at significant risk of having their milk condemned for AF contamination.
