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Silage Acids Play Minor Role in Ruminal Acidosis


Silage Acids Play Minor Role in Ruminal Acidosis

By Bill Mahanna

I recently spent two weeks working in New Zealand interacting with nutritionists, veterinarians and dairy producers and discovered that, besides the use of pasture-based systems, the other interesting difference between New Zealand and North American dairy farming is New Zealand's perspective on acidosis.

For much of lactation, cows in New Zealand consume very lush pastures that provide minimal effective fiber. I saw pictures of the rumen mat in fistulated cows - which were consuming upward of 115 kg of as-fed pasture per day — and it appeared more like a "slurry" than the raft-matrix to which North American nutritionists are accustomed (Bryan McKay, personal communication).

Yet, for these 35-42% neutral detergent fiber grasses, even with less than a 12-hour rumen retention time, with rumen pH hovering at or slightly below 5.5 and with frequent observations of manure scores of one to two (loose manure), problems with reduced intakes and milkfat depression do not seem to exist (Eric Kolver, personal communication).

This could be the result of several factors, including: (1) the unintentional selection for a modified rumen microbial population, (2) differing consumption patterns among pastured cows, (3) rapid solid and liquid dilution turnover rates caused by consuming such high-moisture diets and/or (4) less consumption of feeds high in linoleic acid.

Many New Zealand dairy producers are beginning to incorporate more grass and corn silage in their farming systems to supplement occurrences of lower-quality pasture, to extend lactations as pastures wane or to enhance body condition before the dry period.

The increased use of silages raised the concern among dairy producers as to the effect of silage fermentation acids on feed intake and ruminal acidosis. I thought this discussion might also be of interest to North American nutritionists.

Silage Acid Production

Lactic acid is a 10-fold stronger acid than other silage (or rumen) volatile fatty acids. Lactic acid is produced by both silage bacterial species (Lactobacillus and Streptococcus) and rumen organisms (Selenomonas ruminantium, Streptococcus bovis and Megasphaera elsdenii). Lactic acid can lose a proton from the acidic group when in solution to produce the lactate ion.

There are two distinct isomeric forms of lactic acid: D-lactic acid and L-lactic acid. Both forms are produced by microorganisms in silage and in the rumen.

At a neutral pH, the L-isomer is produced, but the percentage of the D-isomer increases as the pH drops. At a pH of 6.0, the D-isomer constitutes around 20% of the total, while when the pH is less than 5.0 and lactate concentrations are above 100 millimoles, the D-isomer may account for 50% of the total. The enzyme L-lactate dehydrogenase used in oxidation of L-lactate is widely distributed in the cytosol of all host animal tissues. D-lactate must pass the mitochondrial membrane before it can be oxidized by the D-2-hydroxy-acid dehydrogenase enzyme. Thus, D-lactate acid produced during acidosis is more slowly degraded and is considered more toxic (Dawson and Allison, 1988).

A high level of silage lactic acid, per se, does not appear to be the primary causative agent in reducing intakes in high-silage-based diets.

A Pennsylvania State University study (Clancy et al., 1976) showed that infusing alfalfa silage extract into fistulated wethers depressed voluntary intakes. However, the researchers could account for only about 40% of the effect when they infused “synthetic” silage juice containing the same amount of volatile fatty acids, lactic acid, soluble carbohydrate, ammonia, nitrite and nitrate. The researchers concluded that other factors such as protein degradation products like amines may have contributed to the silage intake depression.

Depressed intake has long been associated with silages high in ammonia, amides and amine compounds (such as histamine), which are end products of silage protein degradation that occurs during fermentation.

If fermentation is extended, these protein degradation products typically increase in concentration similar to acid concentrations. Ammonia nitrogen (expressed as a percentage of total nitrogen) of less than 5% typically indicates high-quality silage.

A summary of silage studies (Erdman, 1993) indicated that a practical range of silage pH of 4.5-7.0 resulted in minimal intake depression in silage, and in studies where silage composition was related to intake, increasing lactic acid content usually was associated with improved silage intake.

Furthermore, Cornell research (Van Soest, 1982) has shown that many silages low in dry matter and high in pH can also be associated with lowered intakes.

Contribution of silage acids from 20 lb. of corn silage dry matter (DM.)

Rumen Acid Production

Classical rumen “lactic acidosis” is caused by the accumulation of acid in the rumen and bloodstream.

Lactic acid has long been considered the primary culprit in acidosis, especially the more slowly absorbed D-lactate isomer. However, the term “D-lactic acidosis” is too confining to describe acidosis because the problems associated with acidosis (reduced intakes, malabsorption, liver abscesses and founder) are due to the cumulative effects of all organic acids produced in the rumen (Britton and Stock, 1989).

From a gross physiological perspective, lactic acid production increases osmotic pressure within the rumen so that fluid is drawn into the rumen from the circulatory system, thus contributing to rumen hypertonicity. Furthermore, an intestinal osmotic gradient is also established that draws fluids into the intestines and contributes to profuse diarrhea. The rumen pH drop also elicits rumen stasis typified by reduced rumen contractions. Some of the lactate — mainly D-lactate because of its slower metabolism — becomes absorbed into the circulation and contributes to a depression in blood pH (Wass et al., 1986).

Lactic acid concentrations are typically not present in large amounts in rumen fluid due to being metabolized within 10-20 minutes. This is why feedyards use “step-up rations” to increase the concentration of lactic-acid metabolizing microbes as a transition to all-grain finishing rations.

Lactic acidosis in dairy cattle is caused by a combination of both low fiber and abrupt dietary changes. If fiber is gradually removed, the cow is remarkably adaptable to metabolizing lactic acid as fast as it is produced (D.R. Mertens, personal communication).

When cows are fed diets high in forage, starch is scarce, and the growth rate of S. bovis is restricted by the availability of a suitable energy source. At slow growth rates: (1) intracellular fructose diphosphate (FDP) concentrations are low and (2) lactate dehydrogenase (LDH) is not activated. Biochemically, this means that little lactate is produced. In the absence of lactate, rumen fluids remain well buffered, intracellular pH remains near neutral and pyruvate formate lyase (PFL) favors the energetically efficient production of formate and acetate by S. bovis (Russell and Hino, 1985).

However, when the supply of carbohydrate substrate is abundant, the rates of acid production by the normal rumen microbes increase. At the same time, some species begin to produce more lactic acid, and some ethanol begins to accumulate. The production of these metabolites can be related to increases in the growth rate of several groups of rumen bacteria (Dawson and Allison, 1988).

When large amounts of starch (grain) are added to the ration, S. bovis grows faster than other species of rumen bacteria. As their growth rate increases, intracellular FDP and pyruvate concentrations increase, and these intermediates activate LDH. Triose phosphate concentrations may also increase, and this would inhibit PFL.

The net effect is a switch from acetate and formate production to “lactate” production. This allows for microbial survival, but interestingly enough, it is not as efficient a pathway for the organism. This pathway produces only two adenosine triphosphates for growth, whereas the switch to a more efficient fermentation at normal rumen pH results in the production of four adenosine triphosphates for growth (Russell and Hino, 1985).

Rumen microflora can produce as many as 160 moles of total fermentation acids per day (Russell, 2002). The Table compares ruminal acid production to the moles of fermentation acids contributed by a relatively high level (20 lb. of dry matter per day) of corn silage consumption.

The Bottom Line

The total acid (notably lactic acid) contribution from reasonably well-fermented silage is only a small fraction of the total acid load produced by rumen organisms.

While poorly fermented silages can cause intake depression (primarily due to protein degradation end products) or refusals (clostridial fermentation), it is unlikely that silage acids play a major role in either lactic acidosis or subacute ruminal acidosis.


Britton, R., and R. Stock. 1989. Acidosis: A continual problem in cattle fed high grain diets. Proceedings of the 1989 Cornell Nutrition Conference. Oct. 24-26. p. 8-15.

Clancy, M.J., P.J. Wangsness and B.R. Baumgardt. 1976. Effect of conservation method on digestibility, nitrogen balance and intake of alfalfa. J. Dairy Science 60:572.

Dawson, K.A., and M.J. Allsion. 1988. The Rumen Microbial Ecosystem. P.N. Hobson (ed.). Elsevier Applied Science, New York, N.Y. p. 445-447.

Erdman, R. 1993. Silage fermentation characteristics affecting feed intake. Silage production from seed to animal. Proceedings of the National Silage Production Conference, Syracuse, N.Y. Feb. 23-25. p. 210-219.

Russell, J.B. 2002. Rumen Microbiology & Its Role in Ruminant Nutrition: A Textbook. Cornell University, Ithaca, N.Y. p. 9.

Russell, J.B., and T. Hino. 1985. Regulation of lactate production in Streptococcus bovis: A spiraling effect that contributes to rumen acidosis. J. Dairy Science. 68:1712-1721.

Van Soest, P.J. 1982. Nutritional Ecology of the Ruminant. O & B Books, Corvallis, Ore. p. 147-148.

Wass, W.M., J.R. Thompson, E.W. Moss, J.P. Kunesh, P.G. Eness and L.S. Thompson. 1986. In: J.L. Howard (ed.). Current Veterinary Therapy #2. Elsevier Inc., New York, N.Y. p. 716-718.

This article was originally published in the June 2011 Feedstuffs issue and is reproduced with their permission.