Dr. Richard Bowen, Professor, Department of Biomedical Sciences, Colorado State University (Previously published online with Colorado State University, VIVO Pathophysiology)

The rumen encases a complex ecosystem containing numerous species of bacteria and protozoa that collectively provide the capacity for efficient fermentation of carbohydrates. Among the major products of such fermentation are volatile fatty acids and lactic acid. Wild ruminants and those raised on pasture consume a diet rich in grasses of one sort or another that consist mostly of cellulose. Cellulose is a molecule that might be called a “slowly fermentable carbohydrate”. In contrast, grains such as wheat, barley, and corn are considered “highly fermentable carbohydrates”, meaning that they can be very rapidly fermented to generate – you guessed it – large quantities of volatile fatty acids and lactic acid. Ruminal acidosis results from consumption of a unaccustomed quantity of highly fermentable carbohydrate, almost always well described as grain overload.

Ruminal acidosis is most commonly a disease of dairy and feedlot cattle, and occasionally sheep in feedlots. All of these animals are typically fed large quantities of grain, because such a diet promotes production of milk and enhances growth. The key point is that animals and their ruminal microbes must be adapted over time to a high grain diet, rather than being acutely changed to such feed, otherwise acidosis commonly ensues. In some cases, animals develop acute acidosis “accidentally”, when, for example, they escape from their pen and get into a store of grain.

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