Mécanismes d'apparition de l'acidose ruminale latente et conséquences physiopathologiques et zootechniques

Abstract

Whereas its acute form is now rare, ruminal acidosis is increasing in intensive production systems in its latent form, more discrete but affecting a significant number of animals with negative financial impacts. Acute ruminal acidosis results from the accidental overconsumption of highly fermentable carbohydrates. Their fermentation conducts to a strong drop in ruminal pH (values lower than 5) related to lactate accumulation and to the decrease in the diversity of the microbial ecosystem (protozoa, bacteria) to the profit of a lactate-producing, acido-tolerant bacterial population. Latent acidosis occurs more especially during feed transitions towards diets with high energy density, and is a status of a more or less frequent or transitory imbalance. The pH fall, near to lower physiological values (mean pH between 5 and 6.25), is not related to lactate accumulation, but to that of volatile fatty acids. The acetate proportion decreases in relation to the fall of cellulolytic activity. For a moderated pH fall, the protozoa population increases and fermentations are directed towards butyrate. For lower pH, the protozoa population decreases, compensated for by an increase in amylolytic bacteria, with a propionic fermentative pattern. 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 consequences on performances are effective but very difficult to quantify. Indeed, acidotic diets are rich in concentrates and result in high intake and performances. Acidotic status could involve transitory decreases and irregularity in intake and productions.