Nutrition Impacts Feedlot Health, Part 4: Finishing Phase

By: Dr. Jeremy Martin and Dr. Dan Larson, Great Plains Livestock Consulting, Inc.

Nutritional management of calves in utero through receiving and effects of nutrition on health in the feedlot have been the focus of the previous articles in this series. Once the receiving period is over and the cattle are well-started on feed, we tend to experience fewer health challenges as an industry.

From this point on though, a high percentage of pulls are either related to feeding management or nutrition in some way. Nutritional disorders that impact cattle during the finishing phase can have serious consequences in terms of performance and conversion; three of the more common issues are acidosis, liver abscesses, and polioencephalomalacia (PEM). The three are distinct but interrelated conditions.

The goal of feedyards and their nutritionists for finishing cattle is generally to achieve maximum performance and feed conversion while minimizing digestive disorders. In ruminant animals adjusted to high starch rations, we can expect cattle to experience acidosis of varying degrees at some point during the feeding period.

In general, acidosis is simply low rumen pH due to an imbalance between volatile fatty acid (VFA) production in the rumen and the ability of cattle to absorb and utilize VFAs. Since cattle convert energy in feeds to VFAs in the rumen, VFA production increases as cattle are stepped up to rations with more grain and less roughage, or due to increasing intakes. Managing the risk of acidosis is the very reason for the step-up process.

Since acidosis is a continuum of rumen pH, rather than a disease, it can be classified as acute or subacute. Acute acidosis occurs when rumen pH drops below 5.2 and produces noticeable symptoms including reduced intake, cattle panting in an effort to maintain acid-base balance in the blood, bloat, loose stools that contain bubbles and a white appearance when dried, and pen deads.

Unseen results of acute acidosis include founder which becomes apparent 45-60 days further into the feeding period, damage to the gut lining which reduces ability of cattle to absorb nutrients, and liver abscesses. All of these result in reduced feed efficiency and performance at the least. Additionally, there is a link between acidosis and polioencephalomalacia (PEM) – more on that later. University of Nebraska-Lincoln data also associate risk of PEM with reduced roughage levels in the ration. In 2002, Loneragan and associates showed a 70% increased risk for acute interstitial pneumonia (AIP) in pens with at least one digestive death.

Subacute acidosis is generally diagnosed in research scenarios as rumen pH 5.2-5.6, but practical observation is more difficult. Although intakes and performance suffer, it is often masked by the fact that it is an individual response in a pen setting. Intake patterns of cattle experiencing subacute acidosis are more erratic, but within a pen those individual patterns are not necessarily discernible.

Behaviors that may be noticeable are cattle eating dirt, kicking at their bellies, loose stools, or more erratic pen intakes. During the feeding period, individual cattle likely experience subacute acidosis to varying degrees (Erickson et al., 2003), and this experience helps train them to avoid acidosis in the future. Therefore, while subacute acidosis does have a cost in terms of cattle performance and efficiency, it is essential to training cattle to avoid the more serious consequences of acute acidosis. Under ideal management, individual subacute acidosis bouts do not result in whole pens displaying erratic or depressed intakes.

Managing risk of digestive disorders is in the details, because finish rations have the potential to create acidosis and that is unlikely to change. Cattle are creatures of habit, and the less change they experience in feeding times, feedstuffs, weather, handling, etc. the better in terms of avoiding acidosis.

Often when incidence of bloat increases in feedlots, it can be linked to variations in processes or environmental variables. To avoid problems, do not step cattle up onto a higher energy ration during a change in weather, particularly if barometric pressure is changing significantly.

In terms of ration formulation, preventing extreme peaks in VFA production involves several steps. Roughage inclusion provides a buffer for the rumen and maintains gut health to help prevent digestive disorders, and risk of acidosis generally decreases as roughage levels increase.

However, maintaining enough forage in the ration to prevent all digestives is counterproductive to feed efficiency. Focus on managing roughage sources so they do not vary widely and are not prone to picking up moisture from the environment, and ensure ration mixing is adequate to distribute roughage evenly in the bunk. Energy sources ferment at different rates in the rumen, so utilizing multiple energy sources with different rates of fermentation helps alleviate high acid load in the rumen and minimize risk of digestive deads. This may include combinations of different grains, different processing methods of grains, and inclusion of byproduct feedstuffs.

The majority of cattle on feed receive an ionophore as a tool to improve feed efficiency. Research clearly demonstrates the ability of the ionophore Rumensin to increase average rumen pH, reduce the amount of time cattle experience acidotic conditions in the rumen, and stabilize intake patterns (Fanning et al., 1999 UNL Beef Reports). While managing roughage, feeding multiple energy sources, and supplementing Rumensin alleviate risk, it remains critical that bunk management and consistency of process are priorities for a feedlot to avoid acute and subacute acidosis.

Liver abscesses are a consequence of acidosis that deserve special mention because they not only affect feedlot performance but are detrimental to carcass value. When acidotic episodes occur, the rumen wall that is damaged can become susceptible to Fusobacterium necrophorum and Actinomyces pyogenes (the primary bacteria involved in liver abscesses although others are often involved as well) colonization. This allows bacteria access to the bloodstream and thus they can travel to the liver.

The resulting colonization of liver tissue produces abscesses that not only contribute to reduced feed efficiency but also potentially to reduced dressing percentage due to adhesions and thus negatively impacts margins at both the feedlot and packer level. Tylan is the most widely used antimicrobial feed additive which is approved for reducing the incidence of liver abscesses. Liver abscesses not only cost the industry money, but they are evidence that the effects of acidosis in feedlot cattle can persist through the entire feeding period and beyond, so cattle do not necessarily recover from bunk management and feeding management mistakes once intakes are corrected.

Another disease of finishing cattle that is nutritionally induced is polioencephalomalacia (PEM), which is a noninfectious disease of cattle characterized by reduced feed intake, impaired vision, muscle tremors, and incoordination. Affected animals will press their head against inanimate objects, grind their teeth, groan, and display convulsions and recumbency.

There are two forms of the disease: the acute form sporadically seen in feedlot cattle where affected animals are extensively affected, and the subacute form occasionally seen in animals on pasture. The incidence of the disease is low; however, the death rate can be high (90%) in the acute case with death occurring in about 50% of the affected animals within a few days of the disease. In the subacute form, mortality is about 50%. Animals with the subacute form may recover completely or may have a lower lifetime average daily gain.

There are two primary causes of PEM in cattle, a thiamin deficiency and excess dietary sulfur intake. The excess sulfur can come from either the feed or the water. Thiamin is integral to energy metabolism. The brain, due to its high demand for energy, is especially sensitive to a thiamin deficiency. Thus, a thiamin deficiency does not specifically target the brain but is rather seen in a neurological aspect first. Thiamin is supplied by two chief means in a ruminant: microbial production and from feedstuffs. However, processed or long-term stored feedstuffs have lower thiamin content, making ruminal microbial production more important.

The principal problem associated with thiamin is thiamin destruction in the rumen. An increase in the amount of thiaminase may occur when dietary concentrates are increased too rapidly. This change ostensibly causes the amount of thiamin to fall rapidly. Apparently, the sudden increase in rumen acidity releases the enzyme. Therefore, acidosis is clearly linked to PEM. Certain species of mold also produce high amounts of thiaminase and can lead to increased destruction of thiamin in the rumen.

Excessive sulfur intake, as a consequence of high sulfur in either the feed and/or the drinking water of cattle, can also lead to the destruction of thiamin in the rumen. When excess sulfur is consumed, rumen microbes produce excess hydrogen sulfide gas. This condition is exacerbated by low pH, otherwise defined as acidosis. The hydrosulfides stay in the rumen fluid phase and hydrogen sulfide gas accumulates in the rumen gas cap. The hydrogen sulfide is absorbed across the rumen wall into the bloodstream. This elevated level of sulfide in the blood interferes with energy production, similar to a thiamin deficiency.

Although sulfur has recently received substantial criticism for causing PEM, acidosis and other issues not discussed here such as cobalt deficiency and amprolium represent a significant portion of PEM cases. In addition, the disease must be differentiated from similar conditions such as lead poisoning, (grass) tetany, water deprivation, antifreeze ingestion, or a vitamin A deficiency.

A number of plant species, including the bracken fern, produce a thiaminase and can cause similar symptoms if ingested. There are also a number of infectious diseases that can cause neurological symptoms similar to PEM. Rabies can cause similar symptoms and is common in feedlots with a raccoon or skunk problem. Thrombotic meningoencephalitis can also present very similar symptoms and is caused by a Haemophilus somnus infection. Vaccination for this disease is difficult and can be prevalent in many feedlots.

A substantial coccidiosis infection may result in a disorder known as nervous coccidiosis, presenting similar symptoms as those seen in PEM cases. Listeriosis also presents similar symptoms to PEM. Listeriosis is caused by a bacterium harbored in the intestinal tract of cattle and also found in poorly fermented silages. A large rodent population will help spread listeriosis. Making high quality silages is the best preventative for listeriosis. A number of clostridial diseases, including tetanus and enterotoxemia, can also cause neurological symptoms similar to PEM. Cases of PEM are likely a combination of subacute or acute acidosis, coupled with a high sulfur diet, which is why thiamin administration is often a successful treatment. However, be certain to differentiate PEM from other infectious and noninfectious diseases.

If cattle are appropriately transitioned to a high-concentrate diet and bunks are managed correctly, acidosis related issues including bloat and PEM should be rare. Most cattle will experience subacute acidosis during the feeding period and we know liver abscesses will occur at some level. However, care should be taken in ration formulation to test roughage sources and high sulfur feedstuffs and to adjust diets accordingly. With appropriate vigilance and diligence, including a systematic daily approach to reading bunks, calling feed, and evaluating cattle, we can limit the effects of these nutritional disorders during the finishing phase.