Mechanisms of appearance of ruminal acidosis and consequences on physiopathology and performances

Abstract

Whereas its acute form is now rare, ruminal acidosis is increasing in intensive production systems in its latent form, more discrete butaffecting a significant number of animals with negative financial impacts. Acute ruminal acidosis results from the accidental overconsumptionof highly fermentable carbohydrates. Their fermentation conducts to a strong drop in ruminal pH (values lower than 5) relatedto lactate accumulation and to the decrease in the diversity of the microbial ecosystem (protozoa, bacteria) to the profit of a lactateproducing,acido-tolerant bacterial population. Latent acidosis occurs more especially during feed transitions towards diets with highenergy density, and is a status of a more or less frequent or transitory imbalance. The pH fall, near to lower physiological values (meanpH between 5 and 6.25), is not related to lactate accumulation, but to that of volatile fatty acids. The acetate proportion decreases in relationto the fall of cellulolytic activity. For a moderated pH fall, the protozoa population increases and fermentations are directed towardsbutyrate. For lower pH, the protozoa population decreases, compensated for by an increase in amylolytic bacteria, with a propionic fermentativepattern. These ruminal events can have physio-pathological consequences in the digestive area (inhibition of ruminal motricity, diarrhoea, lesions of the ruminal wall...), by metabolic disorders or by infectious and locomotor complications. The negative consequenceson performances are effective but very difficult to quantify. Indeed, acidotic diets are rich in concentrates and result in high intakeand performances. Acidotic status could involve transitory decreases and irregularity in intake and productions.