Investigations on the association of D-lactate blood concentrations with the outcome of therapy of acidosis, and with posture and demeanour in young calves with diarrhoea

The objective of this prospective study was to elucidate whether amounts of bicarbonate needed for correction of acidosis and normalization of clinical signs are influenced by blood D-lactate concentrations in calves with diarrhoea. In 73 calves up to 3 weeks old with acute diarrhoea and base excess values below -10 mmol/l correction of acidosis was carried out within 3.5-h by intravenous administration of an amount of sodium bicarbonate which was calculated using the formula: HCO (mmol) = body mass (kg) x base deficit (mmol/l) x 0.6 (l/kg). Clinical signs, venous base excess, and plasma D-lactate concentrations were monitored immediately following admission, following correction of acidosis at 4 h and 24 h after admission. The base excess and plasma D-lactate concentrations throughout the study were -17.8 +/- 4.0, -0.4 +/- 0.4, -3.0 +/- 5.5 mmol/l (base excess), and 10.0 +/- 4.9, 9.8 +/- 4.8, 5.4 +/- 3.4 mmol/l (D-lactate) for the three times of examination. Metabolic acidosis was not corrected in more than half of the calves (n = 43) by the calculated amount of bicarbonate, whereas the risk of failure to correct acidosis increases with D-lactate concentrations. The study shows that calves with elevated D-lactate concentrations do not need additional specific therapy, as D-lactate concentrations regularly fall following correction of acidosis and restitution of body fluid volume, for reasons that remain unclear. However, calves with distinct changes in posture and demeanour need higher doses of bicarbonate than calculated with the factor of 0.6 in the formula mentioned above probably because of D-hyperlactataemia.     

Influence of D-lactate on metabolic acidosis and on prognosis in neonatal calves with diarrhoea

Three hundred bucket-fed diarrhoeic calves up to the age of 21 days were used to investigate the degree in which D-lactic acid contributes to metabolic acidosis in bucket-fed calves with naturally acquired neonatal diarrhoea. Fifty-five percent of all diarrhoeic calves had serum D-lactate concentrations higher than 3 mmol/l. Mean (+/-SD) D-lactate values were 5.7 mmol/l (+/-5.3, median: 4.1 mmol/l). D-lactate values were distributed over the entire range of detected values from 0 to 17.8 mmol/l in calves with base excess of -10 to -25 mmol/l. Serum D-lactate concentration was higher in patients with ruminal acidosis (6.6 +/- 5.2 mmol/l; median: 5.9 mmol/l) than in those with physiological rumen pH (5.3 +/- 5.4 mmol/l; median: 3.7 mmol/l). There was no evidence of a correlation (r = 0.051) between the serum levels of D-lactate and creatinine (as an indicator of dehydration). D-lactate was correlated significantly with both base excess (r = -0.685) and anion gap (r = 0.647). The proportion of cured patients was not significantly different between the groups with elevated (>3 mmol/l) and normal serum D-lactate concentrations. This study shows that hyper-D-lactataemia occurs frequently in diarrhoeic calves, has no impact on prognosis but may contribute to the clinical picture associated with metabolic acidosis in these animals.     

The prevalence and clinical relevance of hyperkalaemia in calves with neonatal diarrhoea

One hundred and twenty-four calves with neonatal diarrhoea were investigated in order to assess the prevalence of hyperkalaemia and the associated clinical signs. Hyperkalaemia (potassium concentration >5.8 mmol/L) was recognized in 42 (34%) calves and was more closely associated with dehydration than with decreases in base excess or venous blood pH. In 75 calves with normal blood concentrations of D-lactate (i.e. ?3.96 mmol/L), K concentrations were moderately correlated with base excess values (r = ?0.48, P < 0.001). In contrast, no significant correlation was observed in 49 calves with elevated D-lactate. Only three hyperkalaemic calves had bradycardia and a weak positive correlation was found between heart rate and K concentrations (r = 0.22, P = 0.014). Ten of the 124 calves had cardiac arrhythmia and of these seven had hyperkalaemia indicating that cardiac arrhythmia had a low sensitivity (17%) but a high specificity (96%) as a predictor of hyperkalaemia.In a subset of 34 calves with base excess values ??5 mmol/L and D-lactate concentrations <5 mmol/L (of which 22 had hyperkalaemia), changes in posture/ability to stand could be mainly explained by elevations of K concentrations (P < 0.001) and to a lesser extent by increases in L-lactate concentrations (P = 0.024). Skeletal muscle weakness due to hyperkalaemia alongside hypovolaemia may produce a clinical picture that is similar to that in calves with marked D-lactic acidosis. However, since reductions in the strength of the palpebral reflex are closely correlated with D-lactate concentrations, a prompt palpebral reflex can assist the clinical prediction of hyperkalaemia in calves presenting with a distinct impairment in their ability to stand (specificity 99%, sensitivity 29%).     

D-Lactic acidosis in calves

Metabolic acidosis has long been known as a frequent and potentially severe complication of neonatal calf diarrhoea. It has also been described in 'acidosis-without-dehydration' syndrome in calves and was suspected to occur during ruminal drinking. Clinical signs of central nervous impairment, particularly changes in behaviour and posture, progressing to coma and recumbency, were originally attributed to this metabolic disturbance. The loss of bicarbonate in the faeces was regarded as the main cause of acidosis in this context. During the past decade, however, evidence has accumulated that d-lactic acidosis is a more common occurrence in calves with neonatal diarrhoea. The most probable source of D-lactataemia is bacterial fermentation of undigested substrate that reaches the large intestine due to damage to small intestinal mucosal epithelium. Recent research has shown that most of the clinical signs that were formerly attributed to acidosis were in fact due to elevated blood levels of D-lactate. The aim of this review is to provide a current overview of d-lactic acidosis.     

Anion gap correlates with serum D- and DL-lactate concentration in diarrheic neonatal calves

The objective of this study was to investigate the relationship between serum D- and L-lactate concentrations, and anion gap (AG) in neonatal calves. The association of AG with lactic acidosis in diarrheic calves has only been investigated by measurement of L-lactate in calves with experimentally induced diarrhea. D-lactate has recently been reported to be present in high concentrations in the serum of some diarrheic neonatal calves. The contribution of this acid to AG is not reported. The relationship between AG and L- and D-lactate concentrations was examined in 24 healthy calves and 52 calves with naturally occurring infectious diarrhea with metabolic acidosis. AG was calculated as [Na+ + K+] - [Cl- + HCO3-]. D- and L-lactate were quantified using high-performance liquid chromatography. There was no correlation between L-lactate and AG, contrary to previous reports in the literature. Moderate correlations between D-lactate concentration and AG (r = .74, P < .0001), and between DL-lactate and AG (r = .77), P < .0001) were detected. No differences existed due to the age or sex of the calf. This study indicates that AG provides information on the nature of acidosis in the diarrheic, neonatal calf and reinforces the importance of investigating clinical, in addition to experimental, populations.     

The aetiology of generalized alopecia in young calves

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.     

Investigations of D-lactate metabolism and the clinical signs of D-lactataemia in calves

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.     

Serum concentrations of tumor necrosis factor-alpha in neonatal calves with presumed septicemia

This study was performed to determine the concentrations of tumor necrosis factor (TNF) in the serum of neonatal calves with presumed sepsis and determine the correlation between serum concentrations of TNF and the severity and outcome of disease. Thirty-five sick calves < 30 days old that suffered from enteritis, respiratory disease, or both were considered suitable for inclusion in this study by satisfying clinical and laboratory criteria suggestive of septicemia. At admission, blood samples were collected from all calves to determine the prevalence of high concentrations of TNF. The clinical course and outcome of disease then were recorded. Of the 35 calves with presumed sepsis, 10 had high serum TNF concentrations. Scleral injection, weak or absent suckling reflex, sternal or lateral recumbency, unresponsive or comatose state, and death rate of calves with high serum TNF concentration were greater than those values for calves without high serum TNF concentration. Calves with high serum TNF concentration had significantly lower mean IgG (P < .001), globulin (P < .0001), and calcium (P < .0001) concentrations; greater serum creatinine concentrations (P < .0001); and > or = 2+ toxic changes in neutrophils than did calves without high serum TNF concentrations. Mean values for packed cell volume, band neutrophil count, and venous Pco2 were significantly (P < .007) higher in the group of calves with high serum TNF concentration. Results of this study indicate that serum TNF concentration is correlated with clinical criteria of sepsis in neonatal calves. A close association was apparent between disease severity and serum TNF concentrations in this group of calves with presumed septicemia.     

D-lactate production and excretion in diarrheic calves

The origin of D-lactate, the most important acid contributing to metabolic acidosis in the diarrheic calf, is unknown. We hypothesized that because D-lactate is produced only by microbes, gastrointestinal fermentation is the source. The objective of this study was to determine whether D-lactate production occurs in the rumen, colon, or both, and to measure D- and L-lactate concentrations in urine. Fecal, rumen, blood, and urine samples were obtained from 16 diarrheic and 11 healthy calves. Serum electrolyte concentrations were measured in both groups, and blood gas analyses were performed for diarrheic calves. All samples were analyzed for D- and L-lactate by high performance liquid chromatography (HPLC). Diarrheic calves were generally hyperkalemic with high serum anion gap, depressed serum bicarbonate, and low blood pH. L-lactate was markedly higher in rumen contents (22.7 mmol/ L [median]) and feces (8.6 mmol/L) of diarrheic calves than healthy calves (0.5 mmol/L and 5.1 mmol/L, respectively), but not different in serum or urine. Rumen, fecal, serum, and urine D-lactate concentrations were all significantly higher (P < .05) in diarrheic calves (17.0, 25.4, 13.9, and 19.2 mmol/L, respectively) than in healthy calves (0.5, 9.1, 1.4, and 0.5 mmol/L, respectively). Higher D-lactate concentrations in the rumen and feces of diarrheic calves suggests these sites as the source of D-lactate in blood and urine.     

Lactobacillus GG does not affect D-lactic acidosis in diarrheic calves, in a clinical setting

D-lactate, produced by gastrointestinal fermentation, is a major contributor to metabolic acidosis in diarrheic calves. Lactobacillus rhamnosus GG survives gastrointestinal transit in the neonatal calf and does not produce D-lactate. To determine whether this probiotic reduces gastrointestinal D-lactate production or severity of diarrhea or both, 48 calves (mean, 11 days old; range, 2-30 days) admitted to the clinic for treatment of diarrhea were randomly allocated to 2 groups. The experimental group was given Lactobacillus rhamnosus GG (1 x 10(11) cfu/d) PO, dissolved in milk or oral electrolyte solution, in addition to clinic treatment protocols; the other group served as a control. Serum and fecal samples were obtained at admission and at 24 and 48 hours after initial administration of Lactobacillus rhamnosus GG. All samples were analyzed for D- and L-lactate by using high-pressure liquid chromatography. Feces were also analyzed for pathogens, Lactobacillus rhamnosus GG recovery, and dry matter. D-lactic acidemia (>3 mmol/L) was present in 37/48 calves at admission. Lactobacillus rhamnosus GG was recovered in the feces of 13 experimental calves and 0 control calves 24 hours after administration. No difference in serum or fecal D- or L-lactate between the groups was detected at any time point. After therapy, D-lactic acidosis was absent at 48 hours in all but 1 calf. No relation between fecal pathogen (viral, bacterial, or protozoal) and degree of D-lactic acidosis was observed. The reduction in mortality and greater fecal dry matter in Lactobacillus rhamnosus GG-treated calves was not statistically significant.     

Comparison of two oral electrolyte solutions for the treatment of dehydrated calves with experimentally-induced diarrhoea

We compared the ability of two oral electrolyte solutions to resuscitate calves with experimentally induced diarrhoea and dehydration. Sucrose solution, furosemide, spironolactone, and hydrochlorothiazide were administered to 18 male Holstein-Friesian calves to induce diarrhoea and dehydration. Clinical changes after 24 h included severe diarrhoea, moderate dehydration (8-10% body weight), azotemia, and clinical depression. Calves were then randomly assigned to one of three treatment groups (milk replacer, 2 L every 12 h; hyperosmotic oral electrolyte solution, 2 L every 12 h; iso-osmotic oral electrolyte solution, 1.5 L every 6 to 12 h) and followed for an additional 48 h.Compared to feeding milk replacer, the hyperosmotic solution significantly (P< 0.05) improved hydration status, increased body weight, maintained urine production, decreased the degree of clinical depression and prevented development of metabolic acidosis, although serum glucose concentration was decreased at 24 h and 48 h. The hyperosmotic solution produced a similar resuscitative response to the iso-osmotic solution, but maintained higher serum glucose concentrations and lower serum beta-OH butyrate and non-esterified fatty-acid concentrations, indicating that the hyperosmotic solution provided greater nutritional support. The hyperosmotic solution rehydrated calves faster and more effectively than feeding equivalent volumes of milk replacer and can, therefore, be recommended as part of the initial treatment of dehydrated calves with diarrhoea.     

D-Lactic acidosis in calves as a consequence of experimentally induced ruminal acidosis

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.     

The alkalinizing effects of metabolizable bases in the healthy calf.

The alkalinizing effect of citrate, acetate, propionate, gluconate, L and DL-lactate were compared in healthy neonatal calves. The calves were infused for a 3.5 hour period with 150 mmol/L solutions of the sodium salts of the various bases. Blood pH, base excess, and metabolite concentrations were measured and the responses compared with sodium bicarbonate and sodium chloride infusion. D-gluconate and D-lactate had poor alkalinizing abilities and accumulated in blood during infusion suggesting that they are poorly metabolized by the calf. Acetate, L-lactate and propionate had alkalinizing effects similar to bicarbonate, although those of acetate had a slightly better alkalinizing effect than L-lactate. Acetate was more effectively metabolized because blood acetate concentrations were lower than L-lactate concentrations. There was a tendency for a small improvement in metabolism of acetate and lactate with age. Sodium citrate infusion produced signs of hypocalcemia, presumably because it removed ionized calcium from the circulation. D-gluconate, D-lactate and citrate are unsuitable for use as alkalinizing agents in intravenous fluids. Propionate, acetate and L-lactate are all good alkalinizing agents in healthy calves but will not be as effective in situations where tissue metabolism is impaired.     

Acid-base disorders in milk-fed calves with chronic indigestion.

Acid-base disorders were investigated in 50 calves with chronic indigestion and metabolic acidosis. In the calves that were unable to stand up, the acidosis was significantly more severe than in the calves that could stand up. The anion gap and four different components of the base excess were calculated by the method described by Fencl. The anion gap was high in more than half of the calves, and it was significantly associated with the base excess due to unidentified anions. However, in seven of the calves, the excess of unidentified anions would not have been detected without the calculations, which made it possible to measure the effect of sodium, chloride, plasma protein and unidentified anions on the acid-base balance. Twenty-four of the calves had a combination of hyperchloraemic and high anion gap metabolic acidosis. Changes in sodium and plasma protein concentrations had a minor impact on the calves' acid-base status.     

Experimentally induced systemic hyperchloremic acidosis in calves

Background: Among the various metabolic disturbances occurring in calves affected by neonatal diarrhea or ruminal acidosis, acidemia constitutes an important condition requiring specific therapy. Although various attempts have been made to estimate the degree of metabolic acidosis on the basis of clinical signs alone, some doubts have been raised regarding the accuracy and predictive value of the clinical variables suggested. HYPOTHESIS: The induction of metabolic acidosis in healthy calves via the infusion of hydrochloric acid (HCl) will lead to a clinical picture similar to that seen in neonatal calves with diarrhea or ruminal acidosis. ANIMALS: The study was carried out on 15 Holstein male calves between 5 and 19 days of age. METHODS: Hyperchloremic metabolic acidosis was induced over a period of 80 minutes by an IV infusion of 4,000 mL of 0.9% NaCl solution containing 400 mM HCl. RESULTS: Acidemia occurred rapidly and increased constantly up to a maximum value, which was reached in all calves by the end of the administration and amounted to a 22.4 mM/L mean base deficit (range from 17.0 to 33.1 mM/L). Despite the relatively severe acute acid-base imbalance during the entire observation period, no calves showed any clinical signs or depressed appetite. CONCLUSIONS AND CLINICAL IMPORTANCE: Factors other than a disturbance of the acid-base balance should be considered to be primarily responsible for the clinical picture in calves affected by diarrhea or ruminal acidosis.     

Role of Cryptosporidium parvum as a pathogen in neonatal diarrhoea complex in suckling and dairy calves in France.

This study was carried out to find the importance of Cryptosporidium parvum in diarrhoea of neonatal calves in two types of breeding - suckling and dairy calves - in France. Different agents causing neonatal diarrhoea, E. coli, rotavirus, coronavirus, Salmonella and Cryptosporidium were systematically researched in faeces. 1. Suckling calves: In 40 livestock farms selected for diarrhoea, 311 calves 4 to 10 days old which had diarrhoea for less than 24h or no diarrhoea, were included in the study. A prophylaxis of neonatal diarrhoea had been carried out in 21 of the 40 livestock farms. On D0 (inclusion day), the mean age was 6 days, 82% presented a good initial general condition and 76.2% had a good appetite; 48.6% were diarrhoeic but 91.3% presented no sign of dehydration. Only 6.1% were infected by E. coli K99, 14.3% by rotavirus, 6.8% by coronavirus, 0.3% by Salmonella but 50% excreted C. parvum oocysts. This later percentage increases up to 84% and 86% by D3 and D7, respectively . We note that 16% of the 4-day-old calves on D0 are excreting oocysts and this percentage increases as a function of the age of the calf on D0 to reach 90% to 95% by the age of 8 days. 10 out of 12 dead calves excreted C. parvum oocysts. From D0 to D14 the other pathogen agents show a relative or a decreasing stability. 2. Dairy calves: 382 calves which had diarrhoea for less than 24 h or no diarrhoea, aged 8 to 15 days coming from six industrial livestock farms were included in the study. On D0, 99% of the calves presented a good initial general condition, 99.7% had a good appetite and no calf was dehydrated. At this date (D0), 16.8% of the calves excreted cryptosporidia. This percentage increases up to 23% and 51.8% on D3 and D8, respectively, then decreases to 31.9% on D14. The pressure of the other pathogenicagents remains relatively stable, excepted for rotavirus on D7 (from 9.9% on D0 to 27.2% on D7, then 12.6% on D14) which does not explain the concomitantpeak in diarrhoea because the infection by rotavirus on D7 is more frequent in non-diarrhoeic calves than in diarrhoeic calves. Our results show that Cryptosporidium prevalence is higher in suckling than in dairy calves and C. parvum constitutes actually in both cases the major aetiological agent of neonatal diarrhoea.     

Changes in the profile of liver enzymes in newborn calves induced by experimental,subclinical acidosis in pregnant cows and osmotic diarrhoea

Experimental, subclinical acidosis was induced by oral administration of sacharose during the last 2 months of pregnancy in 15 cows. Seven cows and their newborn calves were used as a control group. The liver enzyme activities in the serum and the blood acid-base status were determined in the 15 calves from the cows in the experimental group. Mannitol was administered orally to 8 calves from the experimental group to induce osmotic diarrhoea. It was concluded that subclinical acidosis in pregnant cows alters the biochemical liver profile of their newborn calves, affecting the aspartate aminotransferase, alanine transaminase, beta glucuronidase, glutamate dehydrogenase and bilirubin activities in the serum, which are associated with oedematous changes to the hepatocytes. Diarrhoea was accompanied by an increase in the alkaline phosphatase and gammaglutamyl transferase activities and a decrease in the total protein concentration in the serum. These changes were apparently related to the numerous necrotic foci in the liver and the proliferation of the Kuppfer cells. It would appear from these results that the liver damage in the newborn calves was associated with the subclinical, metabolic acidosis in their dams and that osmotic diarrhoea occurring in the neonatal period additionally impaired the liver function.Abbreviations ALP alkaline phosphatase - ALT alanine transaminase - AST aspartate aminotransferase - GR betaglucuronidase - bw body weight - ELISA enzyme-linked immunosorbent assay - GD glutamate dehydrogenase - GGT gammaglutamyl transferase - IU international unit     

Effects of hypertonic sodium bicarbonate solution on electrolyte concentrations and enzyme activities in newborn calves with respiratory and metabolic acidosis

OBJECTIVE: To determine concentrations of electrolytes, total bilirubin, urea, creatinine, and hemoglobin; activities of some enzymes; and Hct and number of leukocytes and erythrocytes of newborn calves in relation to the degree of acidosis and treatment with a hypertonic sodium bicarbonate (NaHCO(3)) solution. ANIMALS: 20 acidotic newborn calves with a blood pH < 7.2 and 22 newborn control calves with a blood pH > or = 7.2. PROCEDURES: Approximately 10 minutes after birth, acidotic calves were treated by IV administration of 5% NaHCO(3) solution. The amount of hypertonic solution infused was dependent on the severity of the acidosis. RESULTS: Treatment resulted in a significant increase in the mean +/- SEM base excess from -8.4 +/- 1.2 mmol/L immediately after birth to 0.3 +/- 1.1 mmol/L 120 minutes later. During the same period, sodium concentration significantly increased from 145.3 +/- 0.8 mmol/L to 147.8 +/- 0.7 mmol/L. Mean chloride concentration before NaHCO(3) administration was significantly lower in the acidotic calves (99.6 +/- 1.1 mmol/L) than in the control calves (104.1 +/- 0.9 mmol/L). Calcium concentration in acidotic calves decreased significantly from before to after treatment. Concentrations of potassium, magnesium, and inorganic phosphorus were not affected by treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of hypertonic NaHCO(3) solution to acidotic neonatal calves did not have any adverse effects on plasma concentrations of several commonly measured electrolytes or enzyme activities. The treatment volume used was smaller, compared with that for an isotonic solution, which makes it more practical for use in field settings.     

Clinical efficacy of intravenous hypertonic saline solution or hypertonic bicarbonate solution in the treatment of inappetent calves with neonatal diarrhea

BACKGROUND: The clinical efficacy of IV administered hypertonic saline solution and hypertonic bicarbonate solution (HBS) in the treatment of inappetent diarrheic calves has not been compared yet. HYPOTHESIS: HBS is more advantageous than hypertonic saline in the treatment of calves with severe metabolic acidosis. ANIMALS: Twenty-eight dehydrated, inappetent calves with neonatal diarrhea. METHODS: In 2 consecutive clinical studies, calves were initially treated with saline (5.85%; 5 mL/kg body weight [BW] over 4 minutes; study I: N = 16) or bicarbonate solution (8.4%; 10 mL/kg BW over 8 minutes; study II: N = 12), respectively, followed by oral administration of 3 L isotonic electrolyte solution 5 minutes after injection. Clinical and laboratory variables were monitored for 72 hours. RESULTS: Treatment failed in 6 calves of study I and in 1 calf of study II as indicated by a deterioration of the general condition. All treatment failures had more severe metabolic acidosis compared with successfully treated calves before treatment. In the latter, rehydration was completed within 18 hours after injection; metabolic acidosis was corrected within 24 hours (study I) and 6 hours (study II) after injection. CONCLUSIONS AND CLINICAL IMPORTANCE: Diarrheic calves with slight metabolic acidosis (base excess [BE] >-10 mM) can be treated successfully with hypertonic saline. HBS is appropriate in calves without respiratory problems with more severe metabolic acidosis (BE up to -20 mM). Intensive care of the calves is required to ensure a sufficient oral fluid intake after the initial IV treatment.     

Studies on rotavirus infection and diarrhoea in young calves.

The occurrence of diarrhoea in calves was monitored during the first three weeks of life. Calves fed amounts of colostrum sufficient to produce serum Ig levels in excess of 30 mg per ml did not develop diarrhoea, whereas calves fed less colostrum did. Rotaviruses and mycoplasma-like particles were observed in the faeces of calves with and without diarrhoea. The epidemiology of rotavirus infection in calves is discussed.