Effects of active dry yeasts on the rumen microbial ecosystem: Past, present and future

Bovine lactic acidosis syndrome is associated with large increases of lactic acid in the rumen, which result from diets that are high in ruminally available carbohydrates, or forage that is low in effective fiber, or both. The syndrome involves two separate anatomical areas, the gastrointestinal tract and body fluids, and is related to the rate and extent of lactic acid production, utilization, and absorption. Clinical manifestations range from loss of appetite to death. Lactic acid accumulates in the rumen when the bacteria that synthesize lactic acid outnumber those that utilize lactic acid. The systemic impact of acidosis may have several physiological implications, including laminitis, a diffuse aseptic inflammation of the laminae (corium). Although a nutritional basis for the disease exists, etiology includes a multitude of interactive factors, such as metabolic and digestive disorders, postpartum stress, and localized trauma, which lead to the release of vasoactive substances that trigger mechanisms that cause degenerative changes in the foot. The severity of laminitis is related to the frequency, intensity, and duration of systemic acidotic insults on the mechanisms responsible for the release of vasoactive substance. The critical link between acidosis and laminitis appears to be associated with a persistent hypoperfusion, which results in ischemia in the digit. Management of acidosis is critical in preventing laminitis. High producing dairy herds attempting to maximize energy intake are continually confronted with subclinical acidosis and laminitis. Management of feeding and husbandry practices can be implemented to reduce incidence of disease.

Subacute ruminal acidosis (SARA) was induced in 3 rumen fistulated Jersey steers by offering them different combinations of wheat-barley pellets and chopped alfalfa hay. Steers were offered 4, 5, and 6 kg/d of pelleted concentrate and 6, 5, and 4 kg/d of chopped alfalfa hay for diets 1, 2, and 3, respectively, during 5-d treatment periods and were fed chopped alfalfa hay between treatment periods. Inducing SARA increased blood concentrations of haptoglobin and serum amyloid-A. Dry matter intake of concentrate and hay decreased from d 1 to 5 in each period. Subacute ruminal acidosis was induced in all steers during d 4 and 5 when concentrate was fed, with ruminal pH remaining below 5.6 for an average of 187 and 174 min/d on these days. Lipopolysaccharide concentration increased significantly during periods of grain feeding compared with times when only hay was fed. Inducing SARA by feeding wheat-barley pellets activated a systemic inflammatory response in the steers.

Ruminant animals depend on cellulolytic ruminal bacteria to digest cellulose, but these bacteria cannot resist the low ruminal pH that modern feeding practices can create. Because the cellulolytic bacteria cannot grow on cellobiose at low pH, pH sensitivity is a general aspect of growth and not just a limitation of the cellulases per se. Acid-resistant ruminal bacteria have evolved the capacity to let their intracellular pH decrease, maintain a small pH gradient across the cell membrane, and prevent an intracellular accumulation of VFA anions. Cellulolytic bacteria cannot grow with a low intracellular pH, and an increase in pH gradient leads to anion toxicity. Prevotella ruminicola cannot digest native cellulose, but it grows at low pH and degrades the cellulose derivative, carboxymethylcellulose. The Prevotella ruminicola carboxymethylcellulase cannot bind to cellulose, but a recombinant enzyme having the Prevotella ruminicola catalytic domain and a binding domain from Thermomonspora fusca was able to bind and had cellulase activity that was at least 10-fold higher. Based on these results, gene reconstruction offers a means of converting Prevotella ruminicola into a ruminal bacterium that can digest cellulose at low pH.