During subacute ruminal acidosis (SARA) rumen pH is depressed for several hours per day due to accumulation of volatile fatty acids and insufficient rumen buffering. Surveys suggested an incidence of SARA of between 19% and 26% in early and mid-lactation dairy cows. Causes of SARA include feeding excessive amounts of non-structural carbohydrates and highly fermentable forages, and insufficient dietary coarse fiber. Consequences of SARA include feed intake depression, reduced fiber digestion, milk fat depression, diarrhea, laminitis, liver abscesses, increased production of bacterial endotoxin and inflammation characterized by increases in acute phase proteins. The increase in endotoxin is similar among methods for SARA induction, but depends on the diet fed before induction. Increases in acute phase proteins vary among methods of SARA induction, even when the methods result in similar rumen pH depressions. This suggests that the inflammatory response might not be solely due to bacterial endotoxin in the rumen.

Subacute ruminal acidosis in dairy cows: the physiological causes, incidence and consequences.

A grain-based subacute ruminal acidosis challenge causes translocation of lipopolysaccharide and triggers inflammation.

Subacute Ruminal Acidosis Induces Ruminal Lipopolysaccharide Endotoxin Release and Triggers an Inflammatory Response

Highly fermentable diets are rapidly converted to organic acids [i.e., short-chain fatty acids (SCFA) and lactic acid] within the rumen. The resulting release of protons can constitute a challenge to the ruminal ecosystem and animal health. Health disturbances, resulting from acidogenic diets, are classified as subacute and acute acidosis based on the degree of ruminal pH depression. Although increased acid production is a nutritionally desired effect of increased concentrate feeding, the accumulation of protons in the rumen is not. Consequently, mechanisms of proton removal and their quantitative importance are of major interest. Saliva buffers (i.e., bicarbonate, phosphate) have long been identified as important mechanisms for ruminal proton removal. An even larger proportion of protons appears to be removed from the rumen by SCFA absorption across the ruminal epithelium, making efficiency of SCFA absorption a key determinant for the individual susceptibility to subacute ruminal acidosis. Proceeding initially from a model of exclusively diffusional absorption of fermentation acids, several protein-dependent mechanisms have been discovered over the last 2 decades. Although the molecular identity of these proteins is mostly uncertain, apical acetate absorption is mediated, to a major degree, via acetate-bicarbonate exchange in addition to another nitrate-sensitive, bicarbonate-independent transport mechanism and lipophilic diffusion. Propionate and butyrate also show partially bicarbonate-dependent transport modes. Basolateral efflux of SCFA and their metabolites has to be mediated primarily by proteins and probably involves the monocarboxylate transporter (MCT1) and anion channels. Although the ruminal epithelium removes a large fraction of protons from the rumen, it also recycles protons to the rumen via apical sodium-proton exchanger, NHE. The latter is stimulated by ruminal SCFA absorption and salivary Na(+) secretion and protects epithelial integrity. Finally, SCFA absorption also accelerates urea transport into the rumen, which via ammonium recycling, may remove protons from rumen to the blood. Ammonium absorption into the blood is also stimulated by luminal SCFA. It is suggested that the interacting transport processes for SCFA, urea, and ammonia represent evolutionary adaptations of ruminants to actively coordinate energy fermentation, protein assimilation, and pH regulation in the rumen.

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RUMINANT NUTRITION SYMPOSIUM: Role of fermentation acid absorption in the regulation of ruminal pH

Sub-acute ruminal acidosis (SARA) has become an increasing problem in well-managed, high yielding dairy herds and the monitoring of groups of cows for signs of the condition is now crucial. Rumenocentesis may be ethically questionable but the technique remains the most reliable means of diagnosing SARA. Continuous measurement of ruminal pH may however be possible in the future. Parameters reflecting the metabolic acidosis caused by SARA are also promising tools, and measurement of milk fat content may be useful in individual mid-lactation cows although it is less valuable for bulk tank milk samples. The prevention of SARA includes the establishment of feeding and management guidelines seeking to minimize rumen acidotic load. Regular monitoring may facilitate early recognition of the condition and limit economic losses. Some degree of SARA may however be inevitable and presents a challenge to the dairy industry as consumers become increasingly concerned about the welfare of production animals.

The monitoring, prevention and treatment of sub-acute ruminal acidosis (SARA): a review.

Subacute ruminal acidosis (SARA) is likely to arise when an easily palatable, high-energy diet meets a ruminal environment not adapted to this type of substrate. Increase of short-chained fatty acids (SCFA) will occur. Eventually, this may result in a transient nadir of ruminal pH below 5.5. Two situations are likely to represent the risk of SARA. First, fresh lactating cows are confronted with a diet considerably differing from that in the dry-period. A diet change carried out too rapidly or without proper transition management will put the animals at risk. Secondly, further in lactation, inaccurate calculation of dry-matter-intake (DMI) leading to wrong roughage/concentrate ratio, an inadequate content of structure within the diet or mistakes in preparing of total mixed rations may produce SARA. The consequences of SARA are diverse and complex. Laminitis is regularly connected to SARA and the negative impact of organic acids on the ruminal wall may lead to parakeratosis enabling translocation of pathogens into the bloodstream provoking inflammation and abscessation throughout the ruminant body. Moreover, milk-fat depression (MFD) can be related to SARA. In order to achieve a proper diagnosis, SARA has to be understood as a herd-management problem. A screening of the herd for SARA by means of a rumenocentesis, performed on a sample-group, preferably 12 individuals, may reveal the presence of SARA. The herd screening should include the risk group suspected, preferably. The prevention of SARA applies to the principles of ruminant feeding. Careful transition management from the dry to the lactation period and control of fibre-content and ration quality should be more yielding than the use of buffers or antibiotic drugs.

Subacute ruminal acidosis (SARA): a review.

The pH value of the abomasal contents in adult cattle is normally constant and has a value of 2. Abomasal contents with pH values of 5.5 and higher could give rise to bacterial fermentation with subsequent gas production. The accumulation of gas is thought to form a key event in the pathogenesis of abomasal displacement. The aim of the present study was to determine the pH values of abomasal contents of dairy cows in the first 3 weeks after calving. The pH of the abomasal contents was, over several days. higher than the pH value of the abomasal juice in mid-lactation cows. The highest pH values were measured on day 14 after calving, thereafter the pH declined. Possible explanations for the rise in the pH value of the abomasal contents are discussed.

J. P. T. M. Noordhuizen

Papers

Subacute ruminal acidosis (SARA): a review.

Studies on the pH value of abomasal contents in dairy cows during the first 3 weeks after calving.