The determination of a fecal D‐lactate threshold in neonatal ruminants with diarrhea

Abstract

We have documented D‐lactic acidosis secondary to diarrhea in neonatal calves and lambs. The acidosis only appears after sufficiently high levels of D‐lactate are produced by microbial action in the gut. Measurements of serum and fecal lactate led to a determination of a fecal threshold for D‐lactate systemic absorption from the gut in neonatal ruminants. Jugular blood and feces were collected from 27 diarrheic and 4 healthy lambs, and 19 diarrheic and 4 healthy calves. Blood was analysed for pH, bicarbonate concentration (HCO3−), base excess (BE), hemoglobin (Hb), Na+, K+, Ca2+, Cl−, anion gap, and glucose. Serum, feces, and urine were analyzed for lactate enantiomers. A range of mild to severe diarrhea, as well as metabolic acidosis was observed with a corresponding wide range of D‐lactate concentrations in both serum (< 0.05‐24.0 mmol/L) and feces (< 0.05‐31.0 mmol/L). The fecal D‐lactate threshold was determined statistically using biphasic (break‐point) regression analysis (serum vs fecal D‐lactate). This fecal threshold concentration for absorption of D‐lactate was 10.2 and 8.8 mmol/L in lambs (n=31) and calves (n=23), respectively. These similar values in different species support a lumen D‐lactate threshold (~10 mmol/L) for monocarboxylic (i.e. lactate) transporters and uptake into the mucosal cells and then blood circulation. Therefore, controlling the amount of D‐lactate produced by gut bacteria, and hence lowering levels below threshold, may be key in preventing the metabolic acidosis common in enteritis.