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.     

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.     

Significance of respiratory compensation in acidosis in calves

The respiratory component PvCO2 of acid-base-status was observed in n = 36 calves (age: x +/- s = 8.7 +/- 5.0 d) with neonatal diarrhea and an acidosis (venous blood-pH: < 7.30; x +/- s = 7.08 +/- 0.15). In n = 10 (28%) calves with a severe metabolic acidosis (pH: x +/- s = 7.03 +/- 0.12; BE: x +/- s = -22.1 +/- 5.3 mmol/l) the PvCO2 was decreased < 5.3 kPa (x +/- s = 4.5 +/- 0.5 kPa) and showed a distinct respiratory compensation. A PvCO2 between 5.3-6.7 kPa (x +/- s = 6.0 +/- 0.4 kPa) was observed in n = 16 (44%) acidotic calves (pH: x +/- s = 7.11 +/- 0.13; BE: x +/- s = -15.2 +/- 7.4 mmol/l). These n = 26 (72%) calves showed a simple metabolic acidosis which is well known for calves with neonatal diarrhea. The remaining n = 10 (28%) calves showed an increase of the PvCO2 > 6.7 kPa (x +/- s = 8.0 +/- 1.5 kPa). These animals had a mixed respiratory-metabolic acidosis (pH: x +/- s = 7.08 +/- 0.20; BE: x +/- s = -13.9 +/- 10.3 mmol/l), as the decrease of the pH could not be determined by the decreased metabolic component HCO3- of acid-base-status alone. Calves which died during hospitalization and calves with a PvCO2 > 6.7 kPa tended to be younger and showed partially significant lower values for the parameters of oxygen-supply PvO2 and SvO2. Lactate was significantly higher in dying calves but not in calves with a mixed acidosis which on the other hand were more dehydrated. The functional capacity of respiratory compensation of acidotic disorders in the calves studied promised to be almost the same as in dog and man. One reason for the failure of respiratory compensation in some calves could be a more severe hypovolemia. With the use of "venous hypoxemia" (decrease PvO2 and decrease SvO2) the detection of tissue hypoxia was easier than with lactate concentration.     

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.     

Ruminal lactic acidosis in sheep and goats.

The clinical findings in 37 sheep and goats with acute ruminal lactic acidosis included a disturbed general condition characterised by anorexia, apathy, teeth grinding and muscle twitching, ruminal stasis, and the excretion of soupy or watery faeces. The ruminal fluid of affected animals was milky, had a sour odour and a low pH. There was a predominance of Gram-positive bacteria in smears of ruminal fluid. In comparison with 10 control animals, the rumen fluid of 23 sheep with ruminal lactic acidosis had higher lactic acid and lower volatile fatty acid concentrations. In addition, the affected animals often had haemoconcentration and metabolic acidosis. Treatment included single or repeated transfer of ruminal fluid from healthy cows and, depending on the severity, the administration of antacids, yeast and chlortetracycline, and the intravenous infusion of isotonic sodium chloride and 5 per cent sodium bicarbonate solutions. Of the 37 treated sheep and goats, four died within 24 hours, and three others were euthanased after one, two and three days because their condition rapidly deteriorated. Thirty animals were discharged one to nine days after treatment. Twenty-nine of them (78.4 per cent) recovered completely but one was euthanased later.     

Response to monensin in cattle during subacute acidosis

A steer metabolism study was conducted to measure changes in ruminal and blood components in response to monensin level following an abrupt switch from forage to a concentrate diet. Six ruminal-cannulated crossbred steers (373 kg) were fed either 0, 150 or 300 mg monensin per head daily in a replicated 3 X 3 Latin-square design. In all treatments, ruminal pH declined to a low of 5.4 to 5.6 12 h post-feeding, suggesting steers experienced subacute acidosis. Also in the first 12 h post-feeding, all treatments exhibited nearly a twofold increase in total ruminal volatile fatty acid (VFA) concentrations, while peak ruminal lactate concentrations ranged from .86 to 1.50 mM. During the entire 48-h period, there were no significant treatment differences in blood pH, HCO3- or ruminal lactate, although there was a trend of higher ruminal and blood lactate associated with increased level of monensin supplementation. Feeding higher levels of monensin resulted in higher pH and propionate with lower acetate and butyrate concentrations. Increasing the level of monensin fed resulted in reduced (P less than .01) total ruminal VFA concentrations. Ruminal pH was more highly correlated to total ruminal VFA concentrations (r = -.69, P less than .01) than lactate concentrations (r = -.14, P less than .10). Results from this study indicate the significance of total ruminal organic acid concentration rather than ruminal lactate concentration during subacute acidosis. Monensin maintained a higher ruminal pH by reducing concentrations of VFA.     

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.     

Ruminal lactic acidosis: relationship of forestomach motility to nondissociated volatile fatty acids levels

Ruminal lactic acidosis was produced in 9 overnight fasted rumen-fistulated sheep by placing ground wheat (40 g/kg of body weight) into the rumen. Ruminal stasis occurred within 8 hours of grain engorgement in 6 sheep (early stasis group) and between 10 and 12 hours in the remaining 3 sheep (late stasis group). The initial impairment to forestomach motility was a decrease in the mean frequency of reticulo-ruminal contractions which occurred within 4 hours of the intraruminal placement of wheat in the early stasis group and within 6 hours in the late stasis group. Since blood pH, carbon dioxide pressure, and serum bicarbonate were all normal, systemic acidosis was not a contributing factor to this decrease in contraction frequency. The concentrations of total nondissociated volatile fatty acids (VFA; acetic, propionic, and butyric acid) in ruminal fluid, however, were significantly increased, being 13.60 mM/L (mean, pH 4.92) in the early stasis group and 15.77 mM/L (pH 4.80) in the late stasis group. Free DL-lactic acid in ruminal fluids was 6.37 +/- 6.1 mM/L (mean +/- SD) in the early stasis group and 9.72 +/- 4.2 mM/L in the late stasis group. A reduction in contraction amplitude was observed within 6 hours of grain engorgement in the early stasis group and within 8 hours in the late stasis group. At these times, the concentrations of nondissociated VFA were 10.19 mM/L (pH 4.46) in the early stasis group and 10.52 mM/L (pH 4.62) in the late stasis group. The ruminal values of free DL-lactic acid were 13.93 mM/L in the early stasis group and 16.14 mM/L in the late stasis group.(ABSTRACT TRUNCATED AT 250 WORDS)     

D-lactic acid interferes with the effects of platelet activating factor on bovine neutrophils

D-lactic acidosis occurs in ruminants, such as cattle, with acute ruminal acidosis caused by ingestion of excessive amounts of highly fermentable carbohydrates. Affected animals show clinical signs similar to those of septic shock, as well as acute laminitis and liver abscesses. It has been proposed that the inflammatory response and susceptibility to infection could both be caused by the inhibition of phagocytic mechanisms. To determine the effects of d-lactic acid on bovine neutrophil functions, we pretreated cells with different concentrations of D-lactic acid and measured intracellular pH using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM) and calcium flux using FLUO-3 AM-loaded neutrophils. Reactive oxygen species (ROS) production was measured using a luminol chemiluminescence assay, and MMP-9/gelatinase-B granule release was measured by zymography. CD11b and CD62L/l-selectin expression, changes in cell shape, superoxide anion production, phagocytosis of Escherichia coli-Texas red bioparticles, and apoptosis were all measured using flow cytometry. Our results demonstrated that D-lactic acid reduced ROS production, CD11b upregulation and MMP-9 release in bovine neutrophils treated with 100 nM platelet-activating factor (PAF). D-lactic acid induced MMP-9 release and, at higher concentrations, upregulated CD11b expression, decrease L-selectin expression, and induces late apoptosis. We concluded that D-lactic acid can interfere with neutrophil functions induced by PAF, leading to reduced innate immune responses during bacterial infections. Moreover, the increase of MMP-9 release and CD11b expression induced by 10mM D-lactic acid could promote an nonspecific neutrophil-dependent inflammatory reaction in cattle with acute ruminal acidosis.     

Effect of virginiamycin on ruminal fermentation in cattle during adaptation to a high concentrate diet and during an induced acidosis.

The objective of Exp. 1 was to compare the effects of virginiamycin (VM; 0, 175, or 250 mg x animal(-1) x d(-1)) and monensin/tylosin (MT; 250/ 90 mg x animal(-1) x d(-1)) on ruminal fermentation products and microbial populations in cattle during adaptation to an all-concentrate diet. Four ruminally cannulated, Holstein steers were used in a 4x4 Williams square design with 21-d periods. Steers were stepped up to an all-concentrate diet fed at 2.5% of BW once daily. Ruminal pH, protozoal counts, and NH3-N and VFA concentrations generally were unaffected by VM or MT. Mean counts of Lactobacillus and Streptococcus bovis were lower (P<.05) for VM-treated compared with control or MT-treated steers. Both VM and MT prevented the increase in Fusobacterium necrophorum counts associated with increasing intake of the high-concentrate diet observed in the control. The objective of Exp. 2 was to compare the effects of VM and MT on ruminal pH, L(+) lactate and VFA concentrations, and F. necrophorum numbers during carbohydrate overload. Six ruminally cannulated Holstein steers were assigned randomly to either the control, VM (175 mg/d), or MT (250 + 90 mg/d) treatments. Acidosis was induced with intraruminal administration of a slurry of ground corn and corn starch. The VM and MT premixes were added directly to the slurry before administration. Carbohydrate challenge induced acute ruminal acidosis (pH was 4.36 and L (+) lactate was 19.4 mM) in controls by 36 h. Compared with the controls, steers receiving VM or MT had higher (P<.05) ruminal pH, and the VM group had a lower (P<.05) L (+) lactate concentration. Fusobacterium necrophorum numbers initially increased in VM- and MT-administered steers. In the control steers, F. necrophorum was undetectable by 36 h. Virginiamycin seemed to control the growth of ruminal lactic acid-producing bacteria and, therefore, has the potential to moderate ruminal fermentation in situations that could lead to rapid production of lactic acid.     

Oxidative response of neutrophils to platelet-activating factor is altered during acute ruminal acidosis induced by oligofructose in heifers

Reactive oxygen species (ROS) production is one of the main mechanisms used to kill microbes during innate immune response. D-lactic acid, which is augmented during acute ruminal acidosis, reduces platelet activating factor (PAF)-induced ROS production and L-selectin shedding in bovine neutrophils in vitro. This study was conducted to investigate whether acute ruminal acidosis induced by acute oligofructose overload in heifers interferes with ROS production and L-selectin shedding in blood neutrophils. Blood neutrophils and plasma were obtained by jugular venipuncture, while ruminal samples were collected using rumenocentesis. Lactic acid from plasma and ruminal samples was measured by HPLC. PAF-induced ROS production and L-selectin shedding were measured in vitro in bovine neutrophils by a luminol chemiluminescence assay and flow cytometry, respectively. A significant increase in ruminal and plasma lactic acid was recorded in these animals. Specifically, a decrease in PAF-induced ROS production was observed 8 h after oligofructose overload, and this was sustained until 48 h post oligofructose overload. A reduction in PAF-induced L-selectin shedding was observed at 16 h and 32 h post oligofructose overload. Overall, the results indicated that neutrophil PAF responses were altered in heifers with ruminal acidosis, suggesting a potential dysfunction of the innate immune response.     

Experimentally induced lactic acidosis in the goat

Lactic acidosis was produced experimentally twice in each of 4 adult, female goats, by giving sucrose orally at the rate of 18 g/kg bodyweight. Changes in pH, osmolality, lactic acid concentration, and other constituents in ruminal fluid, plasma and blood were monitored over a period of 48 h. Also changes in urinary pH and sediment were examined. To ameliorate the metabolic disturbance, calcium hydroxide and bicarbonate treatment was employed after the 24 h samples had been collected and their acid-base status determined. A feature of the disturbance in the goats was that a metabolic alkalosis preceded the onset of lactic acidosis.     

The role of endotoxins in induced ruminal acidosis in calves.

Experimentally induced ruminal acidosis was carried out in 4 calves to investigate the possibility of resorption of endotoxins from Gram negative bacteria originating from the gastro-intestinal tract. The ruminal acidosis was induced by overfeeding of oats and the effect was evaluated by clinical and blood biochemical changes. Blood samples were collected every 2 h for 60 h before and after experimental feeding. The animals showed signs of ruminal acidosis and also the clinical and blood biochemical changes were similar to those seen after experimental endotoxaemia. However, although being less dramatic the changes in many relevant parameters such as an increase in prostaglandin F metabolite levels, body temperature, endotoxins and a decrease in iron indicate that an endotoxaemic state had occurred. The results of the present study show that ruminal acidosis/stasis is linked to resorption of endotoxins from the gastro-intestinal tract causing endotoxaemia/endotoxicosis.     

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.     

A retrospective study of the relationship between clinical signs and severity of acidosis in diarrheic calves

A retrospective study of 123 calves under two months of age with signs of diarrhea was performed to investigate the relationships among the calf's demeanor, dehydration, rectal temperature, and base deficit. The severity of dehydration, hypothermia, and metabolic acidosis were associated with level of depression. Clinical signs and age of calf could be used to predict the severity of acidosis. Acidosis was more severe in calves over eight days of age and also increased in severity with the degree of depression. The most severe metabolic acidosis was seen in calves over eight days of age presented in sternal or lateral recumbency; the base deficit in these groups was 16.3 ± 8.3 (means ± 1SD) and 20.3 ± 10.1 mmol/L respectively, and on average these calves require 2.4 and 3.0 L respectively of 1.3% sodium bicarbonate solution to correct the acidosis.     

Impact of lactic acid fermentation in the large intestine on acute lactic acidosis in cattle

Microbial and fermentation changes in the ingesta of the large intestine and their influence on the pathogenesis of acute lactic acidosis were studied in 4 cows fitted with permanent cannulas in the ileum and cecum. Feed mixture containing 65% of maize was infused into the cecum for several days in amounts of 2 and 4 kg per day. The daily amount was divided in 8 equal portions and given with 3 l of warm physiologic saline solution. During the period of ad libitum feeding of hay, the pH values in cecal digesta were 7.4 to 7.6 and the amount of total volatile fatty acids 40-60 mmol/kg with high molar percentage (87-90 mol%) of acetic acid. As to lactic acid only the L(+) lactic isomer was found in a concentration of about 0.4 mmol/kg. Infusion of low amounts of starch induced mild lactic acid fermentation in the cecum associated with a pronounced increase in the concentration of L(+) and D (-) lactic acid to peak levels of 80 +/- 10 mmol/kg and 7 +/- 1 mmol/kg, respectively. Lactic acid fermentation ceased within 2 to 3 days indicating that the gut microflora had adapted to the starch infusion. Slight decreases of blood pH and bicarbonates in blood as well as a moderate increase of netto acid-base excretion in urine indicated mild changes of acid-base balance, but clinically no pathological symptoms were observed. Higher amounts of infused starch caused pronounced lactic acid production in the large intestine which persisted throughout the experiment. Peak L(+) and D(-) lactic acid concentration in cecal digesta reached on the average 137 +/- 16 mmol/kg and 45 +/- 7 mmol/kg respectively. Significant decreases of blood pH values from 7.41 +/- 0.02 to 7.18 +/- 0.08 (P < 0.001), actual bicarbonate from 28.2 +/- 3.2 to 11.0 +/- 2.6 mmol/l (P < 0.001) and base excess from 3.9 +/- 3.6 to -15.2 +/- 3.8 mmol/l (P < 0.001) were observed. D (-) lactic acid concentration in blood increased to 3.2 +/- 0.4 mmol/l, but L(+) lactic acid values remained unchanged under 1 mmol/l. Clear clinical symptoms of indigestion and intoxication characterized by severe inappetence, ruminal stasis and general weakness were also observed. Typical clinical symptoms of disease as well as blood and urine changes in acid-base balance indicated that lactic acid fermentation in the large intestine contributes considerably to the pathogenesis of acute ruminant lactic acidosis.     

Chronic indigestion in milk-fed calves]

Calves with chronic indigestion have disturbed general attitude and condition, decreased appetite, loss of hair, clay-like faeces and ruminal and metabolic acidosis. Possible causes include dysfunction of the oesophageal-groove reflex, reflux of abomasal contents into the rumen and abnormal ruminal motility. The anion gap may be increased or within normal limits. Metabolic acidosis is significantly more severe in calves that are unable to stand than in calves that can stand. Treatment of chronic indigestion consists primarily of intravenous administration of sodium bicarbonate, transfaunation of the rumen and oral administration of electrolyte solutions.     

Effects of induced subacute ruminal acidosis on milk fat content and milk fatty acid profile

Two lactating dairy cows fitted with a rumen cannula received successively diets containing 0%, 20%, 34% and again 0% of wheat on a dry matter basis. After 5, 10 and 11 days, ruminal pH was measured between 8:00 and 16:00 hours, and milk was analysed for fat content and fatty acid profile. Diets with 20% and 34% wheat induced a marginal and a severe subacute ruminal acidosis respectively. After 11 days, diets with wheat strongly reduced the milk yield and milk fat content, increased the proportions of C8:0 to C13:0 even- or odd-chain fatty acids, C18:2 n-6 and C18:3 n-3 fatty acids but decreased the proportions of C18:0 and cis-9 C18:1 fatty acids. Wheat also increased the proportions of trans-5 to trans-10 C18:1, the latter exhibiting a 10-fold increase with 34% of wheat compared with value during the initial 0% wheat period. There was also an increase of trans-10, cis-12 C18:2 fatty acid and a decrease of trans-11 to trans-16 C18:1 fatty acids. The evolution during adaptation or after return to a 0% wheat diet was rapid for pH but much slower for the fatty acid profile. The mean ruminal pH was closely related to milk fat content, the proportion of odd-chain fatty acids (linear relationship) and the ratio of trans-10 C18:1/trans-11 C18:1 (nonlinear relationship). Such changes in fatty acid profile suggested a possible use for non-invasive diagnosis of subacute ruminal acidosis.     

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.     

Comparison between pre- and postnatal acid-base status of calves and their perinatal mortality

The acid-base status of 58 calves (all in normal anterior presentation) was determined from venous blood samples before the onset of traction and immediately after vaginal delivery. Calves were assigned to one of three groups according to their blood pH value: group 1 - normal, pH greater than 7.2; group 2 - acidotic, pH 7.2 to 7.0; group 3 - severely acidotic, pH less than 7.0. Before the onset of traction (i.e. during the 30 minutes following the appearance and rupture of the membranes), 43 calves (74.1%) had normal acid-base values, 14 (24.1%) had slight acidosis, and only 1 (1.7%) had severe acidosis. At birth the three groups of calves showed the following distribution: 23 (39.7%) were normal, 29 (50%) had slight acidosis, and 6 (10.3%) had severe acidosis. Seven calves (12.1%) died during birth or within 48 hours after birth; 2 were normal shortly before birth, 4 were acidotic shortly before birth, and 1 was severely acidotic even before the onset of traction. Traction was significantly longer for cows that delivered severely acidotic calves compared to cows in the other two groups.