RUMINANT NUTRITION SYMPOSIUM: Productivity, digestion, and health responses to hindgut acidosis in ruminants1

Abstract

Microbial fermentation of carbohydrates in the hindgut of dairy cattle is responsible for 5 to 10% of total-tract carbohydrate digestion. When dietary, animal, or environmental factors contribute to abnormal, excessive flow of fermentable carbohydrates from the small intestine, hindgut acidosis can occur. Hindgut acidosis is characterized by increased rates of production of short-chain fatty acids including lactic acid, decreased digesta pH, and damage to gut epithelium as evidenced by the appearance of mucin casts in feces. Hindgut acidosis is more likely to occur in high-producing animals fed diets with relatively greater proportions of grains and lesser proportions of forage. In these animals, ruminal acidosis and poor selective retention of fermentable carbohydrates by the rumen will increase carbohydrate flow to the hindgut. In more severe situations, hindgut acidosis is characterized by an inflammatory response; the resulting breach of the barrier between animal and digesta may contribute to laminitis and other disorders. In a research setting, effects of increased hindgut fermentation have been evaluated using pulse-dose or continuous abomasal infusions of varying amounts of fermentable carbohydrates. Continuous small-dose abomasal infusions of 1 kg/d of pectin or fructans into lactating cows resulted in decreased diet digestibility and decreased milk fat percentage without affecting fecal pH or VFA concentrations. The decreased diet digestibility likely resulted from increased bulk in the digestive tract or from increased digesta passage rate, reducing exposure of the digesta to intestinal enzymes and epithelial absorptive surfaces. The same mechanism is proposed to explain the decreased milk fat percentage because only milk concentrations of long-chain fatty acids were decreased. Pulse-dose abomasal fructan infusions (1 g/kg of BW) into steers resulted in watery feces, decreased fecal pH, and increased fecal VFA concentrations, without causing an inflammatory response. Daily 12-h abomasal infusions of a large dose of starch (~4 kg/d) have also induced hindgut acidosis as indicated by decreased fecal pH and watery feces. On the farm, watery or foamy feces or presence of mucin casts in feces may indicate hindgut acidosis. In summary, hindgut acidosis occurs because of relatively high rates of large intestinal fermentation, likely due to digestive dysfunction in other parts of the gut. A better understanding of the relationship of this disorder to other animal health disorders is needed.

Genome sequencing of rumen bacteria and archaea and its application to methane mitigation strategies

“…However, much remains to understand how microbes have an impact on the remainder of the ruminant digestive tract. For example, hindgut fermentation in ruminants typically provides 5% to 10% of dietary energy and is responsible for 6% to 14% of CH 4 output (Gressley et al, 2011). The role hindgut microbes have to play in ruminant nutrition remains largely unstudied and may present researchers with new avenues for CH 4 reduction not previously considered.…”

Rumen microorganisms and fermentation

“…For amylolytic bacteria (table 1), starch is an important component of the diet of cattle and high milk-producing cows which are fed with concentrates containing major proportions of grains. Although these diets for ruminants have been effective as a fermentable energy source, they are also associated with metabolic disorders such as acidosis (Gressley et al 2011), low-fat milk syndrome and liver abscesses (Owens et al 1998).…”

Respuesta productiva de corderos en engorda a la suplementación con extractos de taninos

“…Se ha sugerido que dietas conteniendo alrededor de 80 % de maíz, como las ofrecidas en el presente estudio, inducen un pH intestinal ácido (Gressley et al, 2011;Fredin et al, 2014), y por lo tanto, favorecen la formación de complejos tanino-proteína. También se ha informado, que cuando existe la presencia de taninos en el alimento, en cantidades suficientes, estos pueden formar complejos con las enzimas digestivas (Mandal y Ghosh, 2010), así como con las proteínas de membrana de las células del epitelio intestinal, interfiriendo en la digestión y absorción de nutrientes (Cowan, 1999;Sharma et al, 2009;Barbehenn y Constabel, 2011).…”