Rumen Acidosis

This fact sheet was updated on 11/20/2020. 

Other names: Grain overload, Corn toxicity, Lactic acidosis, Carbohydrate engorgement

Cause

Rumen acidosis occurs in wild or domestic ruminants (deer, elk, moose, cattle, sheep etc.) when they ingest large quantities of readily digestible and highly fermentable carbohydrates such as grain. Corn, wheat, and barley are most commonly responsible for rumen acidosis, though apples, bread, carrots, and sugar beets can also cause this disease. 

Significance

Rumen acidosis is most commonly seen in wild deer, elk, and moose in late winter, but can occur at any time of the year, when they suddenly ingest large quantities of these foods which are not the usual diet. Though it can result in rapid death, it does not currently have a significant impact on wild ruminant populations. However, in restored or endangered populations it can be a serious source of mortality. Its affect on local populations may be underestimated because of the inability to quantify the animals that survive with shortened life spans because of the effects of this disease.

Species Affected

Rumen acidosis can occur in any wild or domestic ruminant. This disease is most commonly observed in deer, elk, moose, and domestic cattle. Bison seem less susceptible but can also suffer from grain overload. 

Distribution

This disease can occur anywhere in the world where wild or domestic ruminants are suddenly introduced to large quantities of carbohydrates.

Transmission

Rumen acidosis is not a transmissible disease.

Clinical Signs

The severity of disease depends on the type and amount of grain consumed, the animal’s nutritional state and the physical condition as well as previous exposure of the animal to these foodstuffs. Ingestion of large quantities of carbohydrates disrupts the normal rumen flora required for digestion, resulting in excessive acid production and reduced rumen motility. The ingesta then becomes trapped and causes fluid to move into the rumen resulting in dehydration of the animal. The increased acid damages the rumen lining preventing absorption of nutrients and allowing the acid to enter the blood stream. Harmful fungi and bacteria can then also become blood borne.

Within 24 to 48 hours of ingesting large quantities of carbohydrates, an animal will stop eating and may be staggering, unable to rise, or standing quietly. Affected animals often have an enlarged rumen and diarrhea. The most severely affected will die within 24 to 72 hours. Since death is sudden, animals are usually in good body condition.

Diagnosis

Rumen acidosis can usually be diagnosed when ruminants in good body condition are found dead with large quantities of grain in their stomachs. At necropsy, dark red erosions in the lining of the abomasum (4th chamber) may also be present. Laboratory analysis of the rumen microflora can be used to support the diagnosis. The pH of the rumen begins to rise after death, so normal values at necropsy do not rule out the disease.

Treatment

There is no treatment for rumen acidosis in wild ruminants because they are typically found dead. There is also no treatment for those who survived but have a permanently damaged rumen lining.

Management

Supplemental feeding of wild ruminants is often the cause of rumen acidosis. Restrictions on supplemental feeding may help prevent the occurrence of this disease. Hunters should be discouraged from using bait and farmers should make sure wild ruminants do not have access to grain stores.