d‐Lactic Acidosis in Calves as a Consequence of Experimentally Induced Ruminal Acidosis

Abstract

In order to test the hypothesis that ruminal drinking in calves can lead to D-lactic metabolic acidosis, ruminal acidosis was induced in nine calves by intraruminal application of untreated whole milk via a stomach tube. The amount of the daily force-fed liquid was 3 x 1 l. The experimental design called for an end of intraruminal applications if two or more of the following signs were observed: severe depression, estimated degree of dehydration >10%, absence of sucking reflex, lack of appetite for two consecutive feedings, severe metabolic acidosis with calculated Actual Base Excess (ABE) <-15 mmol/l. The procedure was scheduled to be discontinued on the 17th day of experiment. The onset of ruminal acidification occurred rapidly, and mean pH value fell from 6.70 (+/-0.48) to 4.90 (+/-0.38) after the first application. The following days the pH values varied between 4 and 5. Rumen acidity was characterized biochemically by a significant increase in both isomers of lactic acid. The effects of the intraruminal administration on the calves were detrimental; eight of nine calves showed an acute disease process. According to the pre-established clinical standard, seven of nine calves were removed from the intraruminal feeding schedule. All but one of the calves developed severe systemic acidosis. The increase in anion gap demonstrated the net acid load. In all the calves D-lactate levels were found to show a significant and rapid increase. On the contrary, L-lactate never deviated from physiological levels. These observations confirm that, in young calves as in adult cattle, ruminal acidosis may lead to a clinically manifested D-lactic metabolic acidosis.

Rumen chemical and bacterial changes during stepwise adaptation to a high-concentrate diet in goats

“…This change was coupled with a sharp reduction of feed intake and severe depression, which are two symptoms of acidosis observed in previous reports (Nocek, 1997;Gentile et al, 2004). Thus, in this study, it was observed that feeding on concentrate proportions of around 30% is most suitable for the goats to perform normal rumen function.…”

“…Thus, in this study, it was observed that feeding on concentrate proportions of around 30% is most suitable for the goats to perform normal rumen function. It is generally regarded that decreased ruminal pH during subacute acidosis is associated with VFA accumulation (Burrin and Britton, 1986;Goad et al, 1998), while acute acidosis is associated with lactic acid accumulation (Harmon et al, 1985;Gentile et al, 2004). In this study, as the concentrate level increased to 50% (diet III), total VFA concentration initially continued to gradually increase while lactic acid concentration remained relatively stable.…”

“…However, after feeding diet IV, ruminal pH decreased to 5.3 on day 2 and it was maintained at about 4.7 on day 3. At the same time, goats started to reduce their feed intake on day 2 and refused to take any feed on day 3, indicating the occurrence of metabolic acidosis (Owens et al, 1998;Gentile et al, 2004). Ruminal lactic acid concentration was stable and maintained in a range of 2.71 to 3.63 mmol/l during the initial three feeding periods, but increased significantly 1 day after feeding diet IV, with a peak of 10.6 mmol/l on day 2 of feeding diet IV and then decreased (Table 2).…”

Estimation of milk leakage into the rumen of milk-fed calves through an indirect and repeatable method

“…In veal calves that received large amounts of milk, individual values may account for more than 25% of intake in subclinical cases (Suárez et al, 2007;Berends et al, 2012), which induces reduced growth performances and ruminal and metabolic acidosis in clinical cases (Gentile et al, 2004;Herrli-Gygi et al, 2006). Identification of clinical ruminal drinkers can be achieved through the occurrence of reduced appetite and clay-like feces (Breukink et al, 1988) but the latter indicators do not give any information regarding the amount of milk that enters the rumen.…”

“…It is therefore commonly accepted that digestive processes in milk-fed calves resemble those in true monogastric animals. Nonetheless, even in calves that are not clinically identified as ruminal drinkers, considerable amounts of milk replacer may enter the rumen (called 'ruminal milk'; up to 25% of milk intake, Suárez et al, 2007), which may induce ruminal and metabolic acidosis in a clinical case (Gentile et al, 2004;Herrli-Gygi et al, 2008). Owing to fermentation of nutrients from milk replacer in the rumen, ruminal drinking will decrease nutrient availability and the efficiency of nutrient utilization for protein and fat retention (Armstrong, 1969;Herrli-Gygi et al, 2006), hence reducing growth performance in calves.…”