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In calves with diarrhoea, systemic acidosis and hyper-L- and D-lactatemia constitute the most important metabolic consequences. Recent studies indicate, however, that clinical signs are determined more by the extent of D-lactate accumulation than by the metabolic acidosis. We summarize the results of different trials in which the single effects of metabolic acidosis, hyper-L-lactatemia, and hyper-D-lactatemia on the clinical condition were studied. 1st trial: induction of metabolic acidosis: 15 Holstein calves received 4.0 l of a 0.1M HCl solution i.v. over a period of 80 minutes (50 ml/min). The procedure managed to provoke a relatively severe metabolic acidosis, that reached a ABE mean value of -22.4 mmol/l (range -17.0 to -33.1 mmol/l). Despite the acidemia during the entire observation period no calves showed any clinical repercussions. 2nd trial: induction of hyper-L-lactatemia: 5 Holstein calves received 400 ml of a 25% L-lactate solution: 100 ml as i.v. bolus (1 min.), and 300 ml via an i.v. infusion over 35 minutes. The experimental procedure provoked a severe hyper-L-lactatemia that reached a peak mean value of 25.0 mmol/l at the end of the infusion (range 18.8 to 38.3 mmol/l). No clinical signs accompanied the hyper-L-lactatemia. Signs of metabolic alkalosis were observed. 3rd trial: induction of hyper-D-lactatemia: 5 Holstein calves received 100 ml of a 25% D-lactate solution via an i.v. bolus (1 minute). A clear increase of the D-lactatemia was observed right from the first control after the administration. At this time the mean value was 16.4 mmol/l (range 13.8 to 18.7 mmol/l). Afterwards the D-lactatemia tended slowly to recover its pre-trial value. Between eight and 40 minutes after the injection all calves showed the following clinical signs: impairment of the palpebral reflex, somnolence, staggering, prolonged periods of motionless, standing with unphysiological postures, lowered and sometimes waving head, and drooping ears. Calves lay down often and for longer, and had to be helped to rise. No impairment of the sucking reflex was observed. After four hours all calves appeared clinically normal. No deviation of the acid-base balance was observed. Conclusions The results of the summarized studies show that with the exception of any impairment of the sucking reflex, all the signs once attributed to metabolic acidosis can be reproduced by inducing hyper-D-lactatemia without acidosis.

Between September, 2010, and August, 2011, a series of cases of jaundice of unknown origin in young calves was detected in a number of farms in Southern Germany. This paper describes the syndrome on the basis of 57 cases, and the approach taken to discover the cause.The clinical course of the disease is described in 19 patients. Using a case definition (calves aged 1-3 weeks, total serum bilirubin20 µmol/l and/or serum glutamate dehydrogenase [GLDH] activity50U/l and/or autopsy findings with striking liver pathology [jaundice, liver dystrophy, cirrhosis]), 36 farms were included in an epidemiological survey. In a feeding trial, two batches of a dietary supplement feed, previously used in diseased calves on farms, were fed at the dosage recommendations of the manufacturer to four clinically healthy calves over 5days. Four other calves served as controls. The calves were clinically monitored daily, and blood samples were investigated using clinical chemistry and haematology.Clinical examination revealed behavioural alterations (weakness, tonic-clonic seizures and bawling just before death), recumbency, jaundice and discolouration of faeces. In less severe cases without clinical signs, there was an increase in serum bilirubin concentration and/or GLDH activity. In the epidemiological survey of affected farms, the feeding of a diet supplement feed was registered in 54 of 57 cases. The feeding of two batches of that diet supplement feed to four clinically healthy calves resulted in a significant (p0.05) increase in bilirubin and lactate concentrations, as well as the GLDH activity in serum, but without serious impairment of the general condition, whereas in control calves, no comparable changes were observed.The results of the epidemiological survey and the feeding trial suggest a causal involvement of a dietary supplement feed. The toxic principle is unknown.Knowledge of the clinical picture and the probable feed-related context is important to detect this disease early. The suspected dietary supplement feed has been taken off the market, but with other products similar problems may arise.

The objective of this study was to test for correlations between alopecia and ruminal drinking in young calves. 331 calves up to an age of 31 days were tested for evidence of generalized hair loss daily during their stay in the clinic. Incidence of diarrhoea and the results of ruminal fluid and blood analysis were compared between the groups with and without alopecia. Calves with alopecia showed a significantly higher incidence of diarrhoea and of ruminal acidosis persisting for at least 24 hours. Blood analysis revealed significant differences in degree of acidosis, in concentrations of D-lactate, urea, and creatinine in serum as well as in the activities of glutathione peroxidase, aspartate amino transferase, and creatine kinase. Alopecia in calves is correlated to longer periods of diseases, which are known to be accompanied by the production of D-lactate in the gastrointestinal tract, such as diarrhoea and ruminal drinking. The question, whether alopecia is due to formation of toxic substances or to deficiency of essential substances can not be answered.

In contrast to the situation in adult cattle there are high concentrations of sodium and low concentrations of potassium in the faeces of suckling calves. It was investigated in this study in which stage of the development of the ruminant these changes in electrolyte levels occur, and whether there are changes in electrolyte levels in urine as well. Samples of faeces and urine from healthy calves were examined fortnightly starting with the 5th day after birth. There was a distinct decrease in sodium concentration in faecal water within the first three weeks of life, i.e. without any relation to the intake of solid feed. However, the levels of sodium, potassium and chloride in urine samples and of potassium in faecal water increased with the development of rumination. The concentration of chloride in faeces was on a low level during the whole period of investigation.

The study involved 50 hospitalized calves (four weeks to five months old) suffering from diarrhoea and hyponatraemia (blood sodium concentration below 130 mmol/l). Starting from the day of admission blood, urine, and faecal samples were taken each morning and sodium and potassium concentrations were measured. In addition, blood and urine samples were taken in the evenings, if electrolytes had been given orally during the day. The obtained values from urine samples were compared with the plasma concentrations in order to check for inadequate renal excretion of electrolytes. Consistency of the faeces and visible blood admixture were the main criteria in the evaluation of electrolyte concentration in the 317 samples of faecal water. With one exception no inadequate renal losses of sodium were observed. Sodium and potassium concentrations in faecal water showed a distinct negative correlation. As the consistency of faeces grew increasingly normal, electrolyte contents of faeces approached those reported for adult cattle, i.e. potassium levels rose and sodium levels decreased. Visible blood admixtures had no significant effect on the sodium and potassium concentrations in the faeces. A distinct relationship between electrolyte contents in faecal water and the consistency of the faeces was found. There were highly significant differences in electrolyte concentrations between faeces of watery (Na: 82 +/- 21 mmol/l; K: 23 +/- 12 mmol/l) and soupy (Na: 54 +/- 26 mmol/l; K: 42 +/- 19 mmol/l) consistency (mean +/- standard deviation). By contrast, soupy and pulpy faeces just showed a slight or no difference in electrolyte concentrations. Only faeces of watery consistency contained approximately as much sodium as observed in neonatal calf diarrhoea. These results show that the pronounced hyponatraemia in older calves can hardly be attributed to loss of sodium via faeces and urine. The following possible causes are proposed: (a) older calves usually have access to water (therefore there is more gradual dehydration or no dehydration at all); (b) oral electrolyte solutions are seldom administered.

The usefulness of the dry-chemistry blood analyzer, SPOTCHEM SP-4410, for analysis of bovine blood chemistry was studied in a veterinary clinic. The control serum Precipath-U, Boehringer-Mannheim, was used to measure precision within each run and between days. The coefficients of variation (CV) ranged between 1.54% and 4.86%, with the exception of albumin and creatine phosphokinase showing a CV of 6.3% and 10.03% for between-day precision. For methodological comparison bovine serum samples were assayed with both the SPOTCHEM SP-4410 and the automated blood analyzer HITACHI 705, which served as a wet-chemistry reference system. The following analytes were measured: glucose, urea, creatinine, total protein, albumin, total bilirubin and the enzymes AST, CPK and gamma-GT. For hemoglobin, which was measured in heparinized whole blood, the CO oximeter 855, CIBA-CORNING, was used as a reference system. The comparative analysis showed very good correlation in eight of ten parameters and their correlation coefficients (r) ranged between 0.962 and 0.998. Only the correlation coefficients of the analysis of total bilirubin (r = 0.903) and albumin (r = 0.771) were less satisfactory. The recovery test was carried out with the two parameters glucose and blood urea. The recovery of glucose was 93.7% and of urea 98.8%. The SPOTCHEM SP-4410 is easy to use and proved to be reliable and accurate, and therefore it seems to be useful for analysis of bovine blood samples.

Five clinically healthy calves received an intravenous injection of 25 g sodium D-lactate (223 mmol) in 100 ml sterile water and five control calves were given the same volume of 0·9 per cent sodium chloride. Two clinical examiners who were blinded to the status (test or control) of the calves observed that between eight and 40 minutes after the injections the calves that had received sodium-D-lactate could be distinguished with certainty from the control calves on the basis of their clinical signs, for example, an impaired palpebral reflex, somnolence and a staggering gait. One-compartment and two-compartment analyses of the changes in the plasma concentration of D-lactate, and its renal clearance, indicated that the calves metabolised considerable amounts of D-lactate.

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 3x1 liter. 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 out of the nine calves showed an acute disease process. According to the pre-established clinical standard, seven out of the 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.