Subacute Ruminal Acidosis (SARA): a Review

Abstract

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.U.S.

Effects of rumen-escape starch and coarseness of ingredients in pelleted concentrates on performance and rumen wall characteristics of rosé veal calves

“…The growth rate was at a high performance level for this type of production and comparable to values seen in previous studies (Therkildsen et al, 1998;Jørgensen et al, 2007). Although several studies observed a better FCE when barleyand wheat-based concentrates were compared with sorghum and corn based (Kleen et al, 2003;Bengochea et al, 2005;Castillo et al, 2009) this was not the case in the present study. The actual batch of grain, its processing, degree of grinding and its proportion of the concentrate mixture are likely causes of the different outcome of these results.…”

“…This is in agreement with our previous finding (Jørgensen et al, 2007) that despite a significant difference in LA status between two groups of concentrate-fed young bulls there was no significant differences in rumen wall and papillae characteristics at slaughter. Furthermore, despite a high starch level (Kleen et al, 2003) and a low roughage intake (Kreikemeier et al, 1990) on the one side, and bloat (Ramsey et al, 2002), ruminal acidosis (Galyean and Rivera, 2003), pathological rumen wall characteristics (Scanlan and Hathcock, 1983) and LA (Jørgensen et al, 2007) on the other side are somewhat linked (Smith, 1944;Jensen et al, 1954;Tamate et al, 1973), this is not a straight forward relation. However, when a more intensive grain feeding was compared with a less intensive feeding it caused a higher incidence of post mortem evaluated ruminal lesions and also a higher incidence of LA (Smith, 1944;Jensen et al, 1954;Tamate et al, 1973).…”

Total mixed ration pellets for light fattening lambs: effects on animal health

“…Thus, in response to acidosis, the rate of metabolism and proliferation of stratified squamous epithelium increase dramatically, resulting in premature transition of cells into the keratinous layer, a condition known as parakeratosis (Kleen et al, 2003;Steele et al, 2011;Plaizier et al, 2012). All animals that received any type of concentrate had a darker colour than those fed on alfalfa.…”

“…Albeit all values observed in this experiment were within the normal range, Alfalfa lambs had significantly higher blood pH values than the rest of the animals by mid-fattening period, but these differences were not maintained until the end of the period. This perhaps could be related to increased keratinisation of ruminal mucosa or its development in the final stages of the fattening period, which may reduce acid absorption from the rumen (Krehbiel et al, 1995;Kleen et al, 2003). Therefore, the development of parakeratosis as a result of a chemical injury, such as that caused by acidosis, may protect the animals against a continuous drop in blood pH.…”

Changes in milk performance and hepatic metabolism in mid-lactating dairy goats after being fed a high concentrate diet for 10 weeks

“…As a consequence, the ruminant microbial ecology and systemic metabolic state will change because of the rapid fermentation and subsequent excessive organic acids accumulation, and such animals are likely to suffer metabolic disorders such as acidosis, fatty liver, laminitis and even systemic inflammation (Alegre et al, 1988;Kleen et al, 2003;Plaizier et al, 2008;Dong et al, 2011;Tao et al, 2014). Our previous studies also showed that long-term feeding of a 65% high concentrate (HC) diet to lactating dairy goats led to subacute ruminal acidosis (SARA) and disruptions of mucosal barrier in the hindgut (Dong et al, 2013;Tao et al, 2014).…”