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Rumen bacteria rob cattle of nutrients.

The discovery--and thwarting--of three previously unknown microorganisms in the rumen of cattle could lead to a dramatic decrease in the amount of dietary protein wasted by ruminant animals, says one of the researchers who discovered the bacteria.

ARS microbiologist James B. Russell worked in the late 1980's with graduate students Guangliong Chen and Herbert J. Strobel to identify the microorganisms. Russell is based at the agency's U.S. Plant, Soil, and Nutrition Laboratory at Ithaca, New York.

According to Russell, the three microorganisms are collectively responsible for wasting up to 25 percent of the protein in cattle diets--a loss of as much as $5 billion annually to cattle producers.

Fortunately, Russell, Chen, and Strobel also identified a possible solution: ionophores, a class of antibiotics approved in 1976 by the Food and Drug Administration as additives to feed for beef cattle and dairy heifers. Ionophores have not yet been approved for use in lactating dairy cattle.

All three of the bacteria are vulnerable to ionophores such as monensin, a feed additive marketed under the trade name Rumensin.

"The bacteria have no outer membrane to protect themselves from these antibiotics," explains Russell.

When monensin is fed to beef cattle in feedlots, the result is generally an 8 percent improvement in growth efficiency, but the benefit could be twice as great in grazing animals, says Russell.

"The difference in improvement between feedlot and grazing cattle is probably related to protein utilization in the rumen," he says. "Grazing animals are often deficient in protein, even though their protein intake appears to be adequate."

Russell describes the rumen, largest of the four stomach compartments of ruminants, as "a mysterious black box." The activity of microorganisms living there has complicated animal nutritionists' attempts to produce for cattle the same sort of fine-tuned diets that exist for poultry and swine.

"In the ruminant, the microorganisms get first crack at the feed," Russell points out. "Then the animal gets what's left in terms of fermentation products."

Russell hastens to point out that simply wiping out all ruminal microorganisms with antibiotics is not the answer, since ruminant animals need the microorganisms and vice versa.

"Without ruminal microorganisms, cattle would not be able to digest cellulose, the material that makes up the bulk of plant cell walls," he notes.

"Mammals do not make enzymes that break down cellulose. But rumen bacteria can degrade this material, enabling cattle to derive nourishment from eating grass."

Of course, the nation's 100 million cattle eat more than just grass. They also consume about $60 billion worth of feed each year; since high-producing ruminants are usually fed large amounts of feed grains and protein supplements.

But when ruminants consume protein, it is often wastefully degraded to ammonia by ruminal microorganisms. As the protein breaks down, large amounts of ammonia can accumulate in the rumen.

When this occurs, ammonia is absorbed across the rumen wall and is converted to urea by the liver and kidney, to be excreted in urine. This waste is often less severe for the feedlot animal on a cereal grain diet.

Russell explains, "Rumen microorganisms need nitrogen to grow, and they can use the ammonia as a nitrogen source. Larger numbers of microorganisms in the rumen can use greater amounts of this ammonia and cut down on the waste.

"Since most microorganisms need carbohydrates as an energy source to grow, the starch in cereal grains nourishes the microorganism population and allows it to increase, in turn increasing the ammonia utilization."

Feeding the animals starch to boost their microbial population is not always possible, Russell adds.

"If the cattle are grazing on lush pastures, it may not be feasible for the producer to feed them grain as well," he points out. "So grazing animals often lose more protein than is lost by cattle in the feedlot.

"That's why I believe stopping this protein loss would result in an even greater improvement in feed efficiency for grazing animals than it has for feedlot animals."

Naming the Culprits

For many years, researchers were uncertain as to which ruminal microorganisms were responsible for the rapid rate of ammonia production in the rumen.

By the late 1950's, Marvin P. Bryant, an ARS scientist at Beltsville, Maryland, and his colleagues had isolated the main ruminal bacteria responsible for the various phases of digestion.

In the early 1960's, Bryant studied the capacity of these bacteria to produce ammonia from protein, and noted that only a few species produced any ammonia.

Based on these results, Bryant concluded that Bacteroides ruminicola was usually the most important ammonia-producing bacterium in the rumen of mature cattle.

But when Russell conducted his own experiments at Ithaca in the early 1980's, he found the ability of B. ruminicola to produce ammonia simply couldn't account for the amount of ammonia accumulation taking place.. Russell suspected that ruminal protozoa--large, one-celled organisms--might be responsible for the unexplained ammonia output. However, subsequent experiments indicated the protozoa were less adept than the bacteria at ammonia production.

"By the mid-1980's, it had become apparent that the most active ammonia-producing microorganisms had not yet been isolated from the rumen," recalls Russell.

Then in 1987, Russell, Chen, and Strobel isolated a ruminal bacterium that had a 20-fold greater capacity than B. ruminicola to produce ammonia.

The following year, Chen and Russell identified two more bacteria with similar capacities for ammonia production.

Because the newly isolated bacteria could not be classified by traditional techniques of bacterial taxonomy, Russell asked Bruce Paster of the Forsyth Dental Center at Boston, Massachusetts, to join the investigation. Together, the Ithaca scientists and Paster identified the bacteria through a relatively new technique: RNA sequencing.

"In the 1970' s, it had been determined that bacteria could be genetically classified according to subtle differences in the RNA sequences of their ribosomes, which are particles of RNA and protein found inside cells," Russell explains.

RNA sequencing indicated the first bacterium was closely related to Peptostreptococcus anaerobius, an organism that had been isolated previously from human clinical specimens, periodontal infections, and feces.

Another of the bacteria proved to be Clostridium sticklandii, previously found in soil, San Francisco Bay black mud, and in the feces of a person in Uganda.

The third bacterium, however, did not resemble any bacterial species that had ever been classified. Russell and Paster have proposed the naming of a new bacterial species, Clostridium aminophilum.

Once the culprits had been identified, a strategy for counteraction was not long in coming.

In tests at the Ithaca lab, cattle were fed monensin, the most widely used ionophore. C.M.J. Yang, a nutritionist working with Russell at Ithaca, reported a 50-percent decrease in the steady concentration of ammonia in the rumen of those animals, a 50-percent decrease in the ability of mixed ruminal bacteria to produce ammonia in vitro, and a 10-fold reduction in the numbers of the newly isolated bacteria.

"Based on these results, it appears that the newly isolated ruminal bacteria produce as much as half of the excess ammonia in the rumen," Russell says.

"We're continuing our search for other ways of inhibiting these bacteria, to decrease the wasteful degradation of protein in the rumen."--By Sandy Miller Hays, ARS

James B. Russell is affiliated with the USDA-ARS U.S. Daby Forage Research at Madison, Wisconsin, and is based at the U.S. Plant, Soil and Nutrition Laboratory, Tower Road, Ithaca, NY 14853.. Phone (607) 255-4508, fax number (607) 255-3904.
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Author:Hays, Sandy Miller
Publication:Agricultural Research
Date:May 1, 1993
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