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Corn toxicity is a general term related to two diseases which can affect white-tailed deer throughout Michigan and elk in the northeastern portion of the state. Both diseases occur acutely and result in the rapid death of animals in good physical condition. These diseases are acidosis (grain overload) and enterotoxemia (overeating disease).
Acidosis occurs when ruminants gain access to large quantities of readily digestible carbohydrates, particularly grain (in Michigan usually corn is involved). Apples, sugarbeets and mangels have been found to cause acidosis in domestic ruminants. Acidosis is characterized by indigestion, rumen stasis, dehydration, diarrhea, toxemia, incoordination, and death.
A change from a natural diet of high fiber woody browse to low fiber high carbohydrate foods initiates the disease. The severity of the illness depends on the type of grain (ground or whole), previous exposure of the animal to the grain, the amount of grain consumed, the animal's nutritional state and physical condition, and the microflora present. Ingestion of toxic amounts of corn are followed within 2 to 6 hours by a change in the microbial population in the rumen. The number of gram-positive bacteria (Streptococcous sp.) increase markedly (replacing the normally abundant gram-negative bacteria), thereby producing large quantities of lactic acid. This results in the rumen pH falling to or below 5, destroying protozoa, cellulolytic organisms, and lactate utilizing organisms, and reducing rumen mobility. Chemical rumenitis and absorption result in lactic acidosis. The lactic acid and lactate build-up cause excessive quantities of fluid to move into the rumen, causing dehydration.
Within 24 hours of grain ingestion animals may be recumbent, staggering, or standing quietly. Death may occur within 24 to 72 hours. The rumen is usually static, diarrhea, and a normal temperature are commonly seen.
Acidosis is diagnosed when deer and elk in good physical condition are found to have died acutely and there are large quantities of corn in the stomachs. The most common lesions observed are black to maroon-colored eroded areas on the lining of the abomasum. These erosions are normally found on the abomasal folds but in severe cases, may be observed anywhere on the lining. Protozoa are absent in ruminal fluid examined microscopically. A gram's stain of the fluid will reveal predominately gram-positive bacteria.
Enterotoxemia occurs when ruminants ingest excessive amounts of high carbohydrate feed, specifically grain (in Michigan usually corn is involved). Deer and elk that rapidly change to a high grain diet increase their starch and carbohydrate intake, providing a medium for the causative organism Clostridium perfringens. Enterotoxemia is characterized by acute indigestion, central nervous system involvement (including convulsions), incoordination, depression, diarrhea, colic, and death.
Clostridium perfringens is a common inhabitant of the lower digestive tract that proliferates when there is an increase in undigested starch and carbohydrate levels (which are normally digested and metabolized higher in the digestive tract). Excessive bacterial growth and the production of lethal amounts of several very potent toxins are released into the intestinal tract and absorbed into the animal's system.
Sudden death of an animal in good physical condition is usually the first clinical sign observed. Death usually occurs within 24 hours of ingestion of grain. Central nervous system involvement may result in circling, rapid eye movement, convulsions, tremors, and pushing of the head against fixed objects. Diarrhea, frothing at the mouth, grinding of the teeth, and generalized weakness may also be seen.
Necropsy findings include an abundance of grain in the stomachs and often-times in the ileum, autolyzed kidneys, a fluid-filled pericardial sac, hemorrhagic and discolored areas on the serosal surface of the intestines, petechial or ecchymotic hemorrhages on the heart (epicardial, myocardial, and endocardial surfaces), on the abdominal musculature, diaphragm and thymus. A moderate catarrhal enteritis is often seen. Confirmation of enterotoxemia is accomplished by either culturing scrapings or tissue from the intestines or by demonstrating the presence of toxin in the small intestinal contents via immunologic testing, mouse assay, or polymerase chain reaction testing.
In deer and elk there is no effective treatment for either of these diseases because of the short duration of the illness and that normally animals are found dead, not sick.
In domestic ruminants, vaccination for protection against enterotoxemia has been effective. Antitoxin and tetracycline therapy has been used in the treatment of enterotoxemia in domestic ruminants. In acute cases it has not been successful. In areas where recreational feeding for viewing purposes is allowed (see the Michigan Hunting Guide or DNR website at www.michigan.dnr.com), deer and elk should be introduced gradually to grains and fruit over a period of three weeks to allow the rumen flora to adjust.
Both of these diseases are a mortality factor usually seen in late winter (but can occur at any time of the year) in deer and elk that have not had access to corn for an extended period of time and suddenly find a source of this grain. This mortality factor does not significantly impact the deer or elk population in the state, only a limited number of individuals in isolated areas. Prohibiting supplemental feeding may prevent these diseases from occurring.
