Acidosis in cattle: a review

Abstract

Acute and chronic acidosis, conditions that follow ingestion of excessive amounts of readily fermented carbohydrate, are prominent production problems for ruminants fed diets rich in concentrate. Often occurring during adaptation to concentrate-rich diets in feedyards, chronic acidosis may continue during the feeding period. With acute acidosis, ruminal acidity and osmolality increase markedly as acids and glucose accumulate; these can damage the ruminal and intestinal wall, decrease blood pH, and cause dehydration that proves fatal. Laminitis, polioencephalomalacia, and liver abscesses often accompany acidosis. Even after animals recover from a bout of acidosis, nutrient absorption may be retarded. With chronic acidosis, feed intake typically is reduced but variable, and performance is depressed, probably due to hypertonicity of digesta. Acidosis control measures include feed additives that inhibit microbial strains that produce lactate, that stimulate activity of lactate-using bacteria or starch-engulfing ruminal protozoa, and that reduce meal size. Inoculation with microbial strains capable of preventing glucose or lactate accumulation or metabolizing lactate at a low pH should help prevent acidosis. Feeding higher amounts of dietary roughage, processing grains less thoroughly, and limiting the quantity of feed should reduce the incidence of acidosis, but these practices often depress performance and economic efficiency. Continued research concerning grain processing, dietary cation-anion balance, narrow-spectrum antibiotics, glucose or lactate utilizing microbes, and feeding management (limit or program feeding) should yield new methods for reducing the incidence of acute and chronic acidosis.