Most of you know that it was agricultural curiosity that got me into this subject (why grain-fed cows are less likely to get pregnant than grass-fed cows), coincident with Lannie finding Know the Cause, and regardless of the human implications, I tend to spend a lot of my research time browsing USDA and other agricultural websites in search of more information. Apparently, they feel less of a need to cover it all up than the AMA-FDA-Pharma alliance.

It seems to me that the agricultural community is not only well aware of what fungal toxins can do to the food sources and to those animals who eat them (humans are animals too), but they have known it for a long time and they take it very seriously. So why don’t we humans pay more attention to our diet? Because the Big Money folks tell us not to worry about it and we are only too eager to go along with that as a matter of convenience.

In any case, one such search this week turned up a document entitled Aflatoxins and Other Mycotoxins, put out by the Oklahoma State University Extension Service, which contains a bunch of stuff you folks need to know about. Of course, for every single thing I find, I get 20 more things that need to be researched. In that document, I found a disease of horses called ELEM (Equine Leucoencephalomalacia), so of course I had to chase that one down. Could eating moldy corn stalks or moldy hay be the reason Shadow died last week? I’m still not sure.

All of you animal owners need to read this issue, especially if you have horses or other livestock, but even those of you who don’t have animals might want to scan this issue and note the places I have highlighted in blue because they apply to you as a human. My comments regarding their text will be in green.

Here are some sections copied from that OSU document (no need to bore you with all of it).

Current Report, CR-2195

National Corn Handbook NCH-52

Aflatoxins and Other Mycotoxins

H.E. Duncan and W.M. Hagler, Jr.

North Carolina State University

Reviewers: J.L. Crawford, University of Georgia; B.J. Jacobsen, University of Illinois;

B. Doupnik, University of Nebraska; R.K. Jones, Texas A&M University;

G.A. Payne, North Carolina State University

Mycotoxins, toxic metabolic by-products of fungi, have received increased attention during the past decade. In recent years, aflatoxins B1, B2, G1 and G2 (a group of closely-related mycotoxins produced by the fungus Aspergillus flavus) have been given considerable attention in corn. …

In 1960, aflatoxins literally exploded onto the scene when over 100,000 turkeys died after consuming contaminated peanut meal. Hepatomas in trout hatcheries, later traced to contaminated cotton seed meal, was almost simultaneously found to be due to aflatoxins in the western United States, as was turkey X disease in England. Through the work of several scientists in many disciplines, it was discovered that aflatoxins could be produced by two fungi, Aspergillus flavus and Aspergillus parasiticus. For many years, it was thought that aflatoxins were produced only in storage. However, surveys done in South Carolina in the early 1970s clearly demonstrated that aflatoxins could also be produced prior to harvest. Evidence of pre-harvest contamination of corn with aflatoxins caused additional concerns with regard to potential control measures.

Aspergillus flavus and the closely-related species A. parasiticus are widely distributed in nature. Temperatures ranging from 80 °F to 100 °F and a relative humidity of 85% (18% moisture in the grain) are optimum for A. flavus growth and aflatoxin production. Growth of the fungus is poor at temperatures below 55 °F, but slow growth will occur and low amounts of aflatoxins may be produced under favorable moisture conditions at the lower range of temperatures. Moisture levels in corn below 12 to 13% inhibit growth of the fungus at any temperature.

A. flavus has been reported to occur in most agricultural soils of the south. The fungus occurs on many types of organic material in various stages of decomposition including forages, cereal grains, food, and feed products. All isolates of the fungus do not produce aflatoxins; thus, the mere presence of A. flavus does not mean that aflatoxins will be present in the substrate. The fungus has not been associated with causing a yield reduction in corn. However, it has been associated with causing a reduction in quality. (What that means, folks, is that even though the contaminant was found, the crop was sold for use anyway.)

… based upon surveys done in North Carolina, the percent of the corn samples that contained 100 parts per billion (ppb) or more aflatoxins was as follows: 1976: 8%; 1977: 12%; 1978: 1%; 1979: 4%; 1980: 18%. Other states in the southeast have experienced similar trends. In Alabama, late in 1977, during a five month period, 2,489 corn samples were analyzed for aflatoxin concentration. Of these 2,489 samples, 1,556 (62.5%) exceeded the FDA action-level of 20 PPB aflatoxins. Of the samples exceeding 20 PPB, 924 (59.4%) exceeded 100 PPB. (Note here that previously we had stated that the FDA only permitted 15 ppb, so why the rise to 20 ppb? Is it due to more widespread contamination forcing the acceptability limits higher in order to sell more corn? And 59% of the samples that were over 20 ppb were also over 100 ppb…)

Infection by A. flavus and subsequent production of aflatoxin in corn before harvest have been well documented. Extensive aflatoxin accumulation in the field is more likely in the southern United States than in the corn belt states, but aflatoxin has been found in pre-harvest corn in Iowa, Illinois, Indiana, and Missouri. Jones suggested that high temperatures and high relative humidity favor infection in the field and may account for the greater incidence of aflatoxin in southern regions.

Taubenhaus first reported the occurrence of A. flavus on Texas field corn in 1920. (Obviously this has been a problem for a long time, so why haven’t we heard about it sooner?) He concluded that insect injury to the maturing ear was necessary for infection; however, he never attempted artificial inoculation with the fungus. Since that time, insects have been implicated in transporting inoculum to the developing ear, moving inoculum from silks into the kernel region, and providing wounds for establishment of the fungus in damaged kernels. …

Observations in North Carolina in 1976, 1977, and 1978 revealed a high incidence of A. flavus infection in ears and kernels free of obvious insect damage. Subsequently, a study was undertaken to examine the influence of temperature, humidity, and time of inoculation on the ability of A. flavus to colonize silk tissue and to invade and produce aflatoxin in undamaged kernels. The data obtained in this study showed that A. flavus could colonize silk tissue, invade the corn kernel, and produce aflatoxin in corn grown in the Phytotron (Southeastern Plant Environment Laboratory), greenhouse, and field. Since the plants produced in the Phytotron were free of ear-inhabiting insects, insect feeding does not appear to be necessary for establishment of the fungus or aflatoxin production. Natural outbreaks of aflatoxins in corn, however, are often associated with higher than normal incidences of ear-invading insects…

The results of these studies showed that corn planted in April contained about one-third of the aflatoxins found in corn planted in May (averaged across the varieties, location, and years). Although the results were influenced by location and year, there was a significant association of high aflatoxin levels with delayed harvest. The short-season and mid-season hybrids used in this study contained less aflatoxins than the full-season hybrid. …

Detection

Detection of aflatoxins in corn lots is necessary for regulatory agencies, producers, and the grain buyers for obvious reasons. The detection of aflatoxins is not exact and there are opportunities for error in all of the steps involved. Perhaps the greatest chance for error is in the sampling process, either in the field or from truckload lots. The data obtained in this area indicate that at least a 10 lb. sample should be obtained from the area to be sampled, and the sample should be as representative of the total lot as possible.

Once the main sample has been obtained, a sub-sample must be obtained. This is probably the second greatest source of error. The final analysis for aflatoxin is done on a 50 to 100 gr. sample, which again must be representative of the larger sample. The sub-sampling error can be reduced if the total sample is ground before the sub-sample is obtained. However, in many laboratories neither time nor equipment is available to grind the entire 10 lb. sample. Thus, a sub-sample of the intact kernels is taken before grinding.

Although there is a chance for error in the analytical process, this is the most accurate step in the detection procedure. There are several ways of detecting aflatoxin once the sub-sample has been obtained. Detection methods range from procedures as simple as visual observation of the toxin-producing fungi to complicated chemical analyses of the toxins themselves…

Preventive Measures

• Reduce stress on the corn. Corn exposed to stress, particularly drought stress has a greater risk of contamination with aflatoxins than non-stressed corn. Thus, producers should consider irrigation or other means of reducing drought stress, particularly during the period of pollination.

• Harvest early. Aspergillus flavus is not a good competitor until the moisture content of the grain is at 20% or below. Thus, if the grain can be harvested above this level and dried quickly, there is less chance of aflatoxin contamination.

• Avoid damage during harvest. Aspergillus flavus can spread from infected kernels to other kernels, particularly damaged kernels, under the right environmental conditions. The possibility of this happening can be greatly reduced if the combine is properly adjusted to avoid kernel damage.

• Dry and store corn properly. A. flavus cannot grow in corn with a moisture content less than 12 to 13%. Therefore, if the corn is dried below this level, no additional growth of the fungus or production of aflatoxin will occur if proper storage practices are followed.

• Keep storage and feeding facilities clean. The fungus can survive in residues left in storage and feeding facilities and can rapidly produce aflatoxins under such conditions. Corn and feed residues should be discarded as soon as possible and storage and feeding facilities should be decontaminated. Materials are available for decontamination.

Utilization of Contaminated Corn

The current FDA action level on aflatoxins in corn is 20 parts per billion (PPB). This means that corn that contains more than 20 PPB aflatoxins may be seized if offered for sale in interstate commerce. (Does that mean that if I grow bad corn in my home state and sell it in my home state, it will never be tested and/or seized?) Also, corn that contains more than 20 PPB aflatoxins should not be fed to lactating animals, used in starter rations, or under any circumstances be milled into corn meal or other human food. Decisions to feed aflatoxin-contaminated corn should be based on (1) contamination level, (2) age and species of the livestock to be fed, (3) willingness to risk toxic effects on livestock, and (4) balancing the value of contaminated feed and risk of livestock poisoning against the cost of non-contaminated feedstuffs. (This last line implies, once again, the decision is being made on a financial basis. Also, a table in this document, which I have not reproduced here, suggests livestock should get the same level as humans (=20 ppb) except for beef over 400 pounds in weight being raised for meat (not reproduction). They can be fed as high as 100 ppb. That means, if this guideline is being followed, the meat you buy at the grocery store can have five times the acceptable level for human consumption in it.)

This paragraph precedes that table: An aflatoxin level of zero is recommended. However, the following guidelines are offered to those producers who have decided to risk feeding aflatoxin-contaminated feeds. (then a nice long table that I summarized above)

The questions of a safe contamination level in animal feeds is complex. Safety to one person may not mean the same thing to another since some measure aflatoxin effects in terms of mortality while others measure effects in terms of feed conversions or weight gains. (Money again) The most conservative approach is to realize that we do not know what levels of aflatoxins are completely safe. However, the greater the concentration, the greater the risk involved. If aflatoxins cannot be totally avoided, accept or use as little contaminated corn as possible.

Other Mycotoxins

In the southeastern United States, the word aflatoxin has tended to become synonymous with the word mycotoxin with laymen and many scientists alike. This tendency has led to surprise when farmers have been introduced to mycotoxins other than aflatoxin through contaminated lots of corn or other grain. On the other hand, farmers and scientists outside the southeastern United States have tended to feel that aflatoxin contamination is not a major problem in the mid-western and northern corn belts. Mycotoxins produced by species of Fusaria are considered to be more prevalent in these areas. Interpretation of recent data indicates that there is, as we would expect, considerable overlap among the geographic areas involved and that the mycotoxin “problem” in the United States is due to the growth and production of secondary metabolites by many different species of fungi when suitable conditions exist. By its very nature, mycotoxicology, a relatively recent multidisciplinary field, is complex.

There are many other genera and species of fungi which have been isolated from both grain and other commodities. When these fungi have been tested for their ability to produce toxins in culture in the laboratory, many of the isolates of nearly all the species examined have been toxigenic. That is, cultures of these fungi or extracts of these cultures have been poisonous to test animals in a biological assay. Along these same lines, it has been estimated that there are between 200 and 300 described mycotoxins produced by various fungi. It is easy to see then the potential for mycotoxin problems in grain; however, only a few of these mold metabolites have been definitely proven to cause discrete, characteristic, identifiable, easily diagnosed mycotoxicoses. The “slobber syndrome” caused by the mycotoxin slaframine, which may be found in second cutting red clover infested with the fungus Rhizoctonia leguminicola, is an example of a characteristic and easily diagnosed mycotoxicosis. Slaframine is also an example of a mycotoxin that is produced both in storage and in the field.

The concepts of field and storage fungi have been very useful in assisting laymen and scientists to grasp that production, handling, and storage of grain are biologically dynamic in terms of insect and fungal spoilage of corn. For fungi, the moisture content and temperature of the grain are critical factors governing the length of time a given bin of corn or feed can be safely stored without molding. Both factors are important to the physiology of the fungus and to giving competitive advantages to different groups of fungi. Mycotoxin contamination of grain can arise in the field before harvest or after harvest during handling, storage, feed-making, etc.

There are at least four other important groups of mycotoxins that may occur in corn: 1) the zearalenones and related compounds, 2) the trichothecene toxins, 3) ochratoxins and the Penicillium viridicatum (PV) toxins, and 4) other toxins produced by Aspergillus and Penicillium spp.

Fusarium toxins. In the United States, two major Fusarium mycotoxin groups, zearalenones and trichothecenes, are possibly equal to aflatoxins in importance to agriculture. However, a formal assessment of economic losses due to contamination of corn with Fusarium toxins has not been nearly as well documented as the losses due to aflatoxin contamination. The fungal genus Fusarium is comprised of soil-inhabiting species and includes some important plant pathogens. There were serious infections of mid-western corn in recent years with Fusarium graminearum, which caused stalk and ear rots. When ears are infected, “gib” corn is the result. Most outbreaks of “gib” corn seem to occur in years when wet conditions prevail during the 21 days after pollination and when cool, wet conditions occur at harvest. The mycotoxins produced by Fusarium spp. (trichothecenes and zearalenones) in corn are second only to the aflatoxins in attracting the attention of scientists and farmers. The most familiar trichothecenes include T-2, deoxynivalenol (DON – also called vomitoxin), and diacetoxyscirpenol (DAS), monoacetoxy-scirpenol (MAS), nivalenol, and fusarenone-X. The trichothecenes as a group are strong irritants and have been associated in naturally occurring outbreaks with vomiting, feed refusal, and possibly gastric ulcers when consumed. Zearalenone and zearalenol on the other hand, are Fusarium metabolites possessing estrogenic activity which, when consumed by animals, have been associated with reproductive problems such as abortions, false heat, recycling, reabsorption and mummies, and vulval-uterine prolapse. (Don’t for even one moment think those symptoms are restricted only to livestock!)

There are other biologically active metabolites produced by Fusarium, which are less well known. Moreover, new active metabolites (toxins) of Fusarium are being discovered and characterized. For example, Fusarium moniliforme infection of corn has been strongly linked to a condition in horses called equine leucoencephalomalacia. (see below for more on that one) A portion of the symptoms of this disease can be reproduced by administration of moniliformin, a mycotoxin named after F. moniliforme, but the complete etiology remains unknown.

Ochratoxins and PV Toxins. Ochratoxin, contaminating feed grain in Denmark, is a serious problem to the swine industry there. In fact, in the Balkan countries, there is a disease in humans associated with ochratoxin A in the grain consumed by the population. In the United States, however, outbreaks of ochratoxin A as a contaminant of corn are not well documented. (Not well documented because the AMA/FDA refuses to acknowledge such a thing exists!) One factor limiting research on this mycotoxin is that rapid methods of analysis are not yet available. The PV toxins, xanthomegnin, and viomellein, are produced by Penicillium viridicatum. A lower temperature storage situation seems to favor growth of P. viridicatum and production of the PV toxins. The PV toxins and ochratoxin A are nephrotoxins, that is, the kidney is the target organ for these toxins. Production problems in swine caused by the PV toxins plus small concentrations of ochratoxin A have been particularly well described in Indiana.

Other toxins produced by Aspergillus and Penicillium.

There are several other groups of mycotoxins which may become more important as mycotoxin research continues. These are mainly some of the toxins produced by Aspergillus and Penicillium. Some are produced by only one or a few fungi and some may be produced by several fungi in both genera.

Citrinin is a mycotoxin which has been found as a natural contaminant of corn associated with mycotoxicoses in swine, horses, and poultry. It is a kidney toxin, which can sometimes be found in rather high amounts in corn. Frequency of occurrence and economic impact on agriculture are not well known even though there seem to be several documented cases in the literature.

The tremorgens are toxins, produced mainly by Aspergillus and Penicillium species, possessing activities that give strong central nervous system effects or tremors in test animals. Although tremors are often reported with possible mycotoxicoses in farm animals, there is simply not enough information available to assess their importance to agriculture. Other alkaloids similar to those produced by Claviceps sp., the ergot fungus, are produced by A. flavus. Whether the indole alkaloids or other compounds produced by A. flavus contribute to toxicity to animals is presently unknown.

The A. flavus toxin cyclopiazonic acid (CPA) has been found in corn and peanuts in Georgia leading some researchers to suspect that aflatoxins and CPA are acting in concert when consumed by animals. It has been demonstrated that two or more mycotoxins often act synergistically when consumed together in animal rations.

Equine Leucoencephalomalacia

Dr. W. B. Ley

Equine Leucoencephalomalacia (ELEM) is a sporadic disease of the horse called by many synonyms: blind staggers, foraging disease, corn stalk disease, moldy corn poisoning, fusariotoxicosis, leukoencephalitis and etc. The very early observations of this syndrome linked field outbreaks with the feeding of moldy corn or corn forage. The mold or fungus found to be consistently associated with elaboration of clinical signs of ELEM is Fusarium moniliforme, however the specific mycotoxin(s) produced (and cause of the disease pathology) has yet to be identified.

Fusariotoxicosis is the term used to describe toxin-induced disease associated with feed products or forage contaminated by Fusarium fungi. It is well recognized that all domestic animals and man are susceptible. (If it is so well recognized, how is it that our doctors have never even heard of this stuff?) The toxins produced by the genus of Fusarium are known to include: vomitoxin (deoxynivalenol), tricothecenes (T2 toxin, diacetoxyscirpenol), zearalenone (F2 toxin) and zearalenol. There are most probably other, as yet, unidentified toxins produced as well. Most researchers feel that the toxin(s) produced by Fusarium moniliforme fall within this unknown category.

Fusarium moniliforme is a common field fungus reported to infect many plants including cereal grains, beans and fruits. It has been estimated to be found in 80 to 100% of all the corn harvested in the U. S. The members of the genus Fusarium can infect seed plants and forages in the growth and maturation phases in the field. Moisture content of the grain is critical for Fusarium survival; when greater than 15% moisture content exists within the grain, conditions are good for fungal growth. Fusarium fungi present in grains at harvest will die rapidly at moisture content below 14%, but any residual toxin already produced may remain indefinitely. Temperature requirements for growth generally fall between 20 to 30°C; Fusarium moniliforme grows best between 24 and 30°C. Toxin production however, does not correlate well with optimum growth temperature requirements. Some species produce toxins at a maximum rate when temperatures fall to 0 to 8 °C. The optimum temperature for toxin production by Fusarium moniliforme associated with ELEM is not known. In the United States, where outbreaks have been investigated epidemiologically, there has been an association with feeding of corn exposed to a dry period early in its growth phase and then harvested under wet environmental conditions.

The toxins known to be produced by Fusarium moniliforme are: estrogenic metabolites (zearalenone), a cytotoxin metabolite, fusariocin A, and moniliformin. Other metabolites reportedly produced are malonic acid, benzosanthentrione pigments, fusaric acid, gibberellins, kaurene diterpenoids, and phenolic derivatives. Zearalenone or the F2 toxin has been studied and shown not to be associated with ELEM. Fusariocin A has not undergone extensive toxicity studies in domestic animals including the horse; the primary histopathologic lesion seen in domestic species administered this toxin is acute multifocal myocardial degeneration and necrosis. Fusaric acid is known to produce hypotension of the cardiovascular system in man and laboratory animals. The other toxin(s) and/or metabolites have received little scientific investigation.

During a 15-month period in 1978-1979, 11 herd outbreaks, involving 335 exposed horses were investigated in Illinois. Forty three (43) horses were affected (13% morbidity rate) and 39 died (91% mortality rate). Corn, shelled corn, ground corn stalks and cobs, corn screenings and commercially prepared complete feed containing cracked corn were the feed sources listed in these outbreaks. Some of the corn submitted for analysis from the ELEM cases were visibly affected by mold growth, however mold could not be visibly detected on the majority of the corn samples submitted. Fusarium moniliforme was recovered by culture and specific identification in corn samples from all 11 herd outbreaks. No zearalenone (F2 toxin), trichothecene mycotoxins (T2 toxin), or aflatoxins were detected in any of the corn samples submitted for analysis. These outbreaks followed two seasons of early drought stressed corn that was harvested under extremely wet conditions.

A recent report from Thailand demonstrated an outbreak of sudden illness and associated deaths in horses consuming moldy corn and peanut meal. In this investigation researchers found high levels of aflatoxins (aflatoxin B1) in the livers of affected horses and feed samples collected after the occurrence of the outbreak. Aflatoxins are produced by about 1/3 of the strains of Aspergillus flavus and by Penicillium puberulum. These fungi are frequent contaminants of feeds and foods when stored under conditions of high humidity and temperature. Their almost ubiquitous occurrence makes the detection of their presence and the toxins they produce less than diagnostic unless levels exceed certain thresholds known to cause disease. The toxigenic nature of aflatoxin B1 has been investigated by other researchers in the U.S. and found not to be related to the syndrome of ELEM. The report by the Thailand researchers failed to mention if culturing for Fusarium moniliforme was performed. Considering the nature of aflatoxins and their frequent contamination of stored feeds, it is not difficult to draw a relationship between feed levels, liver levels, and associated hepatic and cerebral disease. Whether or not this relationship is actually valid awaits further research.

In review of the aforementioned investigations, it is difficult to make any clear or well-defined recommendations. The fact that the majority of feed samples from Illinois resulting in culture and identification of Fusarium moniliforme were not visibly moldy, leads us to say that although the corn may not look moldy it still may not be safe. Of course obviously moldy products should be immediately suspect. The feeding of corn screenings was also correlated to a high degree with ELEM production; where possible to identify corn screening as a portion of the prepared or home-mixed feed, it is advised to avoid their use until testing can be performed. Laboratory support in identification of potentially hazardous or suspect feed is limited to: 1) culture and identification of Fusarium moniliforme by personnel well trained in mycology and hyphae identification; 2) aflatoxin analysis as a screening procedure. (In some states, a level of 100 parts per billion, ppb, has been set as a maximum safe level for aflatoxin consumption by nondairy ruminants. The level safe for consumption by horses is unknown.) Since culturing of Fusarium moniliforme from grain associated with ELEM outbreaks has a near 90% positive correlation, it is safe to say that such products should not be fed. The fact that toxin(s) produced may remain indefinitely once contaminating mold or fungi have died and are no longer present lends suspicion even to feed samples tested by culture and found not to contain Fusarium moniliforme. Until further research and clarification of this problem develops some answers to these questions, the horse owner, feed producer, veterinarian and diagnostic laboratory are left in a quandary. The decision to feed or avoid feeding corn-containing rations to the horse in outbreak areas must ultimately be that of the owner and whether or not the economic value of the horse justifies the risk of a corn supplemented diet. (There are other energy supplement alternatives available in the meantime.) With regard to future prediction of potential problems, corn grown in areas affected early by drought and harvested under wet environmental conditions should be immediately suspect and evaluated prior to use as an equine feed additive. Since mold growth requires a minimum moisture content for survival, harvested and stored corn should be dried to a minimum of 13.5%; this will assure the prevention of any fungal growth under long-term storage as long as these conditions are maintained. The unknown presence of mycotoxins(s) produced prior to harvesting and drying for storage remains a problem.

More Moldy Corn Poisoning

By Dr. Bob Mowrey, DVM

For the second time in four years, Equine Leucoencephalomalacia, commonly referred to as ELEM, or Moldy Corn Poisoning, cases have occurred in larger than normal numbers. During the months of December 1981 through January 1982 and December 1984 through January 1985, a notable number of horses have been diagnosed as dying from ELEM.

According to the North Carolina Department of Agriculture Diagnostic Laboratory, 31 horses from 13 eastern counties have been diagnosed as ELEM deaths. It is estimated that as of November 1984, as many as 100 horses may have died from this disease. Within recent weeks, the number of reported ELEM cases has decreased. In previous years ELEM reported cases have decreased or stopped in late January, but sporadic outbreaks have occurred throughout the year. The disease appears to be moisture and temperature related and occurs most often during periods of cool, wet weather.

ELEM is caused by injecting feed containing corn contaminated with a mold known as Fusarium moniliforme which produces a toxin. The toxins develop in corn which is harvested or stored under high moisture conditions, usually during cool weather. Unfortunately, Fusarium moniliforme mold and subsequent toxins can be present without a visible sign of mold growth.

ELEM occurs and progresses to death within a two-to-three day period and is characterized by horses going off feed, partial or total blindness, walking into or attempting to run through fences or walls, lack of appetite, agitation, hyperexcitability when handled, drowsy behavior and seizures which can develop immediately before death. Once signs develop, the disease is incurable. Horses which do survive will no longer be useful due to brain damage.

Currently no tests exist to identify the type or types of toxins being given off by Fusarium moniliforme mold found in contaminated corn. Dr. Cecil Brownie and his colleagues at North Carolina State University are currently working on a project to identify the toxin released from the Fusarium moniliforme mold.

Veterinarians should encourage horsemen to use good feed management practices in efforts to prevent ELEM. The following management practices are recommended:

1. Avoid feeding moldy or suspicious looking grains containing corn. But also remember: even corn that shows no visual signs of mold growth can harbor mold toxins.

2. During periods of excessive moisture, switch from feed containing corn to feed utilizing oats, rolled barley or wheat since these grains do not appear to harbor this (particular) toxin.

3. Feed forages at a rate of at least 50 percent of the total daily diet. Forages should be a major dietary component unless horses are in a high production situation such as lactation, rapid growth (weanlings or yearlings), or heavily worked horses, in which case slightly less than 50 percent of the daily intake should consist of a long stem forage.

4. Avoid purchasing excessive amounts of grain mixes. Grain mixes should be completely fed within a two week period from date of purchase.

5. Attempt to purchase grain mixes with preservatives (mold inhibitors) added. Mold inhibitors will reduce the incidence of mold formation due to high moisture levels.

6. Check feed troughs to determine if feed is remaining in the troughs long enough to develop mold; if so, reduce the amounts fed or clean troughs periodically. Ideally feed should be completely consumed between feeding periods.

7. Check feed storage areas for abnormal moisture levels.

8. Feed at least twice per day with twelve hours between feedings.

9. If your animals show signs of ELEM, discontinue use of their current feed. Change to a ration of oats plus high quality hay and contact your veterinarian immediately.

Grain mixes containing corn that is free of toxins can be fed to horses without danger. (Just try to prove that any such mix even exists without a complete laboratory at your disposal.) Since there is no test to determine the presence of this particular toxin, the safest ration would be a grain mixture containing no corn. Even grain mixtures containing low levels of corn could conceivably contain ELEM toxin levels capable of killing or permanently disabling a horse. Several commercial feed manufacturers are marketing grain mixtures free of corn. The key to the situation is to remember that corn which has been stored properly, whether on the corn producer’s farm, at the feed mill, or in the stable, and maintained at a moisture level lower than 13 percent can be fed.

To that last line, I must ask “How?” How many horse owners do you know who have a humidity-controlled grain storage bin? Those things cost thousands of dollars to buy and quite a bit to maintain. Is your $200 horse worth it? Well, my $3,000 horse just died. I rather doubt it was this particular disease, but I have no doubt that moldy feed (corn and hay stored outside, grain in bins that are not humidity-controlled) contributed to his demise. But if I had known our animals could die from stuff like this, I would have found a way to get them better food and better storage for that food. My feeling is that if you will not take care of your animals as well as you would take care of your own child, then you shouldn’t be allowed to have those animals under your care.

And the parting shot today is: If you noted the lines emphasized in this newsletter, then you also know that all grains are not tested and all grains that are contaminated are not being pulled off the market. If these mycotoxins can kill your horses or cows or sheep or pigs or turkeys, what are they doing to your body?