Physio-pathological aspect of ruminal acidosis

Ruminal acidosis is one of the most common nutritional disorders in domestic ruminants and it usually occurs when ruminants ingest an excessive amount of readily fermented carbohydrates. High intake of such carbohydrates first stimulates growth rates of allruminal microorganisms resulting in an overall increase in the rate of fermentation. This situation leads to a nonphysiological accumulation of total organic acids (volatile fatty acids and lactic acid) in the rumen. Since the production of these acids is not compensated by transport function of the rumen epithelium and by buffer inflow with the saliva the ruminal pH drops. Ruminal pH of 5.6 or below is generally considered the benchmark for ruminal acidosis. Acute ruminal acidosis is a condition that occurs when the ruminal pΗ is approximately less than 5.0, whereas the subacute or chronic acidosis is defined as a ruminal pΗ of approximately 5.0 to 5.6. In acute acidosis, the reason for pH to reach 5.0 or below is related to lactate accumulation and to the decrease in the growth rates of lactic acid fermenting bacteria and protozoa to the profit of a lactic acid producing, acido-tolerant bacterial population. In subacute or chronic ruminal acidosis, the reason for pH to drop below 5.6 is not related to lactate accumulation, but to that of volatile fatty acids. In this form of ruminal acidosis, lactic acid does not accumulate in the rumen lumen because lactic acid fermenting bacteria still active and rapidly metabolize it to volatile fatty acids. These microbial and biochemical changes lead to impairments in the barrier and transport function of the rumen epithelium and to a number of physio-pathological consequences. This review mainly addresses the changes in the rumen lumen and in the rumen wall, as well as impaired physiological mechanisms during the development of ruminal acidosis.