Metabolic Diseases of Feedlot Cattle

– Steven C. Loerch, Department of Animal Sciences, The Ohio State University

There are four main metabolic diseases feedlot operators need to be aware of: polioencephalomalacia (polio), acidosis, rumenitis and bloat. Unlike respiratory diseases, these are not infectious diseases and therefore are not contagious. They do have one thing in common, they occur primarily in cattle fed high grain finishing rations.

Feedlot Polio. This disease is caused by a deficiency of the B vitamin, thiamin. Thiamin is required by the animal for energy metabolism. When it is deficient the brain essentially is starved of energy. In normal situations, rumen microbes synthesize enough of all the B vitamins so that they don’t have to be provided in the feed. However, nationwide, about 1% of feedlot cattle develop polio as a result of thiamin deficiency. The disease is sporadic in that a feedlot may go several years without a case and then have several cases in a single group of cattle. The occurrence of polio is associated with high grain feeding (greater than 85% concentrate in the diet) and usually occurs shortly after switching cattle to their finishing diets. At this time, the rumen microbes are adjusting to the new source of feed and acidosis (low rumen pH) is common. Certain bacteria in the rumen produce thiaminase in this situation which is an enzyme that destroys thiamin and also results in thiamin like compounds which block the action of the true vitamin. Cattle that are affected by polio have normal thiamin production but it is being destroyed before the animal can use it. This causes rapid problems for the animal. Cattle with polio display symptoms of listlessness, incoordination and convulsions. Death occurs rapidly if cattle are not treated. Fortunately, treatment is simple and results in rapid recovery. Afflicted cattle should be given an IV injection of thiamin solution (2 grams for a 700 lb calf) two times per day for two days. They should be pulled from the pen and fed roughage. After recovery they should be slowly readjusted to their finishing diet. Feeding thiamin as a preventative measure is not recommended because it may actually stimulate production of thiaminase and interfering compounds. Supplements that contain niacin and high levels of sulfate should be avoided because they increase thiaminase activity. Methods of reducing acidosis are beneficial in preventing polio; these will be discussed below.

Acidosis. As the name implies, acidosis occurs when the rumen and the blood become acidic. It is caused by two factors; excess acid production in the rumen and decreased buffering of the rumen digesta as a result of decreased saliva flow. Saliva contains large amounts of sodium bicarbonate which is a buffer that neutralizes acids. Acids in the rumen are produced by rumen bacteria during the fermentation of feed. These acids are absorbed and provide the major source of energy to cattle. Two types of acidosis occur; acute acidosis and subacute or chronic acidosis. Acute acidosis is uncommon in well managed cattle. It usually occurs when non-grain adapted cattle accidentally gain access to a large quantity of grain and engorge themselves. This results in a rapid drop in rumen and blood pH (due to excess acid production during fermentation) which often causes sudden death. Subacute acidosis is more common in feedlot cattle and is more costly to the producer. Subacute acidosis occurs when feedlot cattle fed high grain diets are not able to balance acid production with the buffering capabilities of saliva. Cattle normally produce 5 to 10 gallons of saliva daily. Most of this saliva enters the rumen during rumination, the cud chewing process. When finishing diets low in roughage are fed, cattle are not able to regurgitate effectively which greatly reduces rumination, saliva flow and subsequently buffering capacity. The cattle feeder must always walk a tightrope between high acid production and excessive rumen acidity. High grain diets are necessary to maximize performance and economic returns; however, chronic acidosis may cause founder and reduces feed intake, growth and economic return. Our best ally in combating acidosis is the use of ionophores such as Rumensin and Bovatec. These compounds reduce the incidence of acidosis and are largely responsible for our ability to successfully feed diets with little or no roughage. The role of roughage in a feedlot diet is to stimulate rumination which reduces acidosis. However, excessive use of roughage is costly and decreases growth and feed efficiency. The incidence of acidosis can also be reduced by feeding whole corn rather than processed corn and by feeding more than once a day. These practices reduce acid load in the rumen by spreading out the fermentation of starch throughout the day. Good bunk management is also important for hand fed cattle. Empty bunks followed by over feeding the next day often causes acidosis.

Rumenitis. Rumenitis is an inflammation or irritation of the rumen wall. It is caused by long term feeding of high grain diets which results in continuous acidic conditions and lack of physical stimulation or abrasion of the tissue. Feeding some roughage provides a “scratch factor” which helps keep the tissue healthy. This principle is analogous to the recommendation that humans should have adequate fiber in their diets to keep the colon healthy. Like acidosis, a low level of rumenitis is a fact of life when high grain diets are fed. In general, the problem worsens the longer cattle are on their finishing diet. When rumenitis becomes severe, the tissue lining the rumen wall becomes ulcerated and is no longer effective in absorbing nutrients. We see this as cattle that stop growing towards the end of the feeding period. The packer sees it as liver abscesses. When ulcers develop in the rumen wall, bacteria normally present in the rumen pass through to the blood, travel to the liver and cause abscesses. Surprisingly, only cattle with severe liver abscesses have reduced performance. Feeding antibiotics, such as chlortetracycline, reduce the incidence of liver abscesses but do not prevent rumenitis. We are currently doing research to see if “stall out” due to rumenitis can be prevented by adding roughage to the diet late in the finishing period.

Feedlot bloat. One of the results of ruminal fermentation is gas production. In normal situations, cattle are able to belch and relieve this gas that is produced. Feedlot bloat is not caused by increased gas production, but rather, the inability to release gas via the belching process. The use of finely ground feeds promote foaming or frothiness in the rumen. This increases the incidence of bloat because the gasses are trapped in the foam and belching is prevented. High grain diets also encourage the growth of certain rumen bacteria which produce a slimy substance that traps gasses. Acidic conditions in the rumen tend to stabilize the foam. Saliva contains antifoaming agents, but as discussed above, saliva production is greatly reduced on high grain diets. All of these factors contribute to the occurrence of feedlot bloat. If bloating is a problem in your cattle, several steps may be taken. Feeding Rumensin, Bovatec, oxytetracycline, poloxalene (Bloat Guard) and/or long roughage are effective in reducing the incidence of bloat. Death from bloat is believed to be caused by asphyxiation. The rumen becomes so distended that the animal can no longer breathe.

In summary, the diseases discussed above are all associated with feeding high grain diets. The cattle feeder must be able to define the line where the use of these diets maximizes cattle performance and profitability without causing metabolic disorders to the extent that they reduce performance and economic return.