Reduction of the prevalence of footrot on New Zealand farms by vaccination

AIM: To compare serum analyses of vitamin B₁₂ and methylmalonic acid (MMA) as indices of cobalt/vitamin B₁₂ deficiency in lambs around weaning.

METHODS: Lambs on five properties, considered to be cobalt- deficient, were supplemented with either cobalt bullets, or short- or long-acting vitamin B₁₂ preparations. Blood samples, and in some cases liver biopsies, and liveweights were obtained at monthly intervals. Serum samples were assayed for vitamin B₁₂ and MMA and liver for vitamin B₁₂ concentrations. Pasture cobalt concentrations were measured on three of the properties.

RESULTS: Pasture cobalt concentrations were generally maintained below 0.07 μg/g dry matter (DM) on the properties sampled. Growth responses to supplementation were observed on only 2/5 properties, despite serum vitamin B12 concentrations being within the currently used ’marginal‘ reference range (336–499 pmol/L) for at least 3 months on all properties and in the deficient reference range (0–335 pmol/L) for at least 2 months on all farms except one. Serum MMA concentrations in supplemented lambs were <2 μmol/L, except in those animals sampled 1 month after receiving treatment with a short-acting vitamin B12 injection. Serum MMA concentrations in unsupplemented animals on properties on which no growth response to supplementation occurred generally reached peak levels of between 4 and 7 μmol/L at the nadir of serum vitamin B12 concentration. When a growth response was observed, differences in weight gain between supplemented and unsupplemented lambs occurred as mean serum MMA concentrations increased from 9 to 14 μmol/L. On one property where supplementation commenced before weaning, normal growth rates were maintained despite serum vitamin B12 concentrations of 140 pmol/L and serum MMA concentrations in excess of 40 μmol/L serum.

CONCLUSIONS: The possibility that current serum vitamin B₁₂ references ranges for diagnosis of cobalt deficiency are set too high and lead to over-diagnosis of responsiveness to cobalt/ vitamin B₁₂ supplementation is discussed. The suggestion is made that serum MMA concentrations in excess of 9–14 μmol/L will provide a more reliable diagnostic test for cobalt deficiency. However, there was sufficient variation between properties in the relationships between cobalt concentrations of pasture and serum vitamin B₁₂ or MMA concentrations to require more rigorous testing of the reliability of using serum MMA concentration for this purpose. The possibility that differences in rumen fermentation and therefore propionate and vitamin B₁₂ production could be involved is discussed. The measurement of serum MMA and vitamin B₁₂ appears to be of little value whilst the lamb is still suckling.

CLINICAL SIGNIFICANCE: Serum MMA concentration may offer advantages over serum vitamin B₁₂ concentrations in the diagnosis of a cobalt/vitamin B₁₂ responsiveness in weaned lambs.     

Changes in serum concentrations of methylmalonic acid and vitamin B12 in cobalt-supplemented ewes and their lambs on two cobalt-deficient properties

AIM: To determine concurrent changes in serum methylmalonic acid (MMA) and vitamin B12 concentrations of ewes and their lambs on cobalt-deficient properties, subsequent to cobalt supplementation. METHODS: Three experiments were carried out on two farms. Groups of ewes (n=25-50) were either supplemented with cobalt bullets during late pregnancy, 23-47 days before the mean lambing date, or left unsupplemented. In two experiments, lambs from within each group were supplemented directly by vitamin B12 injection at 3-weekly intervals from birth, and in the third experiment by injection with micro-encapsulated vitamin B12 at tailing and 3 months later. Pasture samples were obtained for analysis of cobalt content at each sampling time. Blood samples were obtained and liveweight recorded from ewes and lambs at approximately monthly intervals. On one farm (two experiments), liver and milk samples were obtained from ewes and liver samples from lambs. RESULTS: Serum vitamin B12 concentrations in unsupplemented ewes fell below 250 pmol/L during early lactation in all experiments and mean concentrations as low as 100 pmol/L were recorded. MMA concentration was maintained below 2 micromol/L in serum from supplemented ewes but increased to mean concentrations ranging from 7 to 14 micromol/L at the nadir of serum vitamin B12 concentration during peak lactation. A significant liveweight response to supplementation was recorded in ewes on one property, and the vitamin B12 concentration in the ewes' milk and in the livers of their lambs more than doubled. No liveweight-gain response to supplementation was observed in lambs on this property. Mean serum MMA concentrations in lambs ranged from <2 in supplemented, to 19.2 micromol/L in unsupplemented lambs, and the latter had concurrent serum vitamin B12 concentrations of >300 pmol/L. Pasture cobalt concentration was lowest at 0.04-0.09 microg/kg dry matter (DM) on the property on which responses in lambs occurred but considerably higher (>0.09 microg/kg DM) on the property on which responses in ewes occurred. On the second property, serum vitamin B12 concentrations in lambs at tailing were extremely low (100 pmol/L), irrespective of supplementation of dams with cobalt. Mean serum MMA concentration was increased to 20 and 42 micromol/L in lambs from supplemented and non-supplemented ewes, respectively. Weight-gain response to direct supplementation of lambs with vitamin B12 occurred during suckling in the latter, but not the former. Lambs from ewes supplemented with vitamin B12 showed a much bigger increase in serum vitamin B12 concentrations a month after supplementation than did lambs from unsupplemented ewes (+1,400 pmol/L vs + 650 pmol/L). CONCLUSIONS: Serum MMA concentration gave a more precise indication of responsiveness to vitamin B12 or cobalt supplementation than serum vitamin B12 concentrations in ewes and lambs. Neither very low serum vitamin B12 nor elevated MMA concentrations were necessarily indicative of responsiveness to supplementation in suckling lambs, but the latter gave an early indication of impending responsiveness. Supplementation of the ewe with a cobalt bullet appeared to protect the growth performance of the lamb for 90 days and influence the subsequent serum vitamin B12 response in the lamb to vitamin B12 supplementation. CLINICAL SIGNIFICANCE: Supplementing ewes with cobalt bullets in late pregnancy can improve the vitamin B12 status of their lambs, and modify their response to vitamin B12 supplementation.     

White liver disease in goats

Three field cases of ill-thrift, hepatic lipodystrophy and low tissue levels of vitamin B12 in young angora cross goats are reported. The cases meet the criteria for the diagnosis of white liver disease (WLD) described for sheep. The hypothesis that WLD is a metabolic consequence of cobalt/vit B12 deficiency in sheep and goats on a diet rich in propionate is developed, together with possible reasons for its occurrence in these species but not in cattle or red deer.     

The occurrence of Anthrax in New Zealand

A field outbreak of facial eczema occurred during a vitamin B12 response trial in young growing sheep. Pasture cobalt levels were in the low range for sheep <0.08 mg/kg, 1.358 µmol/kg) and mean (of 3) liver vitamin B12 levels in the sheep were low (>100 nmol/kg) during the period in which facial eczema occurred.

Mean serum vitamin B12 levels of the untreated group were low (>185 pmol/1) for the two months (January and February) preceding the period of facial eczema. However, levels showed an approximate 3.5 fold increase in both cobalt supplemented and unsupplemented groups with the onset of facial eczema in March. From February to March the mean serum vitamin B12 and glutamyl transferase (GGT) activity showed parallel increases with a positive correlation (r = 0.73) between log serum vitamin B12 and log serum GGT activity during the period January to July for both groups. This finding suggested that the increase in serum vitamin B12 was due to sporidesmin induced liver damage.

The diagnostic implication is that, in areas where facial eczema is a problem, liver is the sample of choice for determining vitamin B12 status, because sporidesmin toxicity can elevate low serum vitamin B12 levels to diagnostically normal levels.     

Ovine white-liver disease (OWLD). Serum copper and effects of copper and selenium supplementation

Serum copper was generally higher in lambs affected with ovine white-liver disease (OWLD) than in cobalt/vitamin B12 supplemented lambs grazing the same pastures. Although the copper content of the grass was very low on the OWLD pastures, dosing lambs with Cu alone resulted in worsening of the clinical condition and aggravation of clinical pathology. Dosing with selenium had no effect on OWLD. Dosing with a combination of Co, Se and Cu resulted in normal lamb growth and normal laboratory tests. Lambs growing well on other pastures (H) showed elevated serum Cu when they were subclinically B12 deficient.     

Growth response to increasing doses of microencapsulated vitamin B12 and related changes in tissue vitamin B12 concentrations in cobalt-deficient lambs

AIM: To investigate growth response of cobalt deficient lambs to increasing doses of microencapsulated vitamin B12, and to measure associated changes in serum and liver vitamin B12 concentrations over 243 days. METHODS: From a flock grazing pastures that had low cobalt (Co) levels (about 0.06 mg Co/kg dry matter), 4-6-week-old lambs (n=137) were assigned to four groups and received either no treatment or a subcutaneous injection of 3.0, 4.5 or 6.0 mg of microencapsulated vitamin B12 on Day 1. At approximately monthly intervals, all lambs were weighed and blood samples were collected from a selection (n=10) of monitor animals, up to Day 243. Liver biopsies were also carried out on the monitor lambs (n=8) on Days 1, 124 and 215. RESULTS: The vitamin B12-treated lambs grew significantly faster (p<0.001) than untreated animals. Liveweights after 243 days were 28, 45, 45 and 47 kg for the untreated, 3.0, 4.5 and 6.0 mg vitamin B12-treated lambs, respectively. Of the initial group of untreated lambs, 68% had to be removed before the end of the trial because of substantial weight loss, but none of the treated animals were similarly afflicted. Serum vitamin B12 concentrations increased in all vitamin B12-treated lambs, reaching a peak at Day 25, and those of the 4.5 and 6.0 mg vitamin B12-treated lambs remained significantly higher (except at Day 124) than the untreated lambs to Day 187. However, at Day 124, but not Day 215, the liver vitamin B12 concentrations of treated lambs were two to three times higher than those of controls. CONCLUSIONS: The growth rates of Co deficient lambs were markedly improved by injection of 3.0, 4.5 or 6.0 mg of microencapsulated vitamin B12, and liveweights were maintained for at least 243 days. Serum vitamin B12 concentrations were related to this growth response; concentrations of <220 pmol vitamin B12/l were associated with a 95% probability that lambs were Co deficient and would thus respond to Co/vitamin B12 supplementation. Based on these data, the current New Zealand reference criteria for Co deficiency should be reviewed. CLINICAL SIGNIFICANCE: An injection of 3 mg microencapsulated vitamin B12 given to lambs at tailing will treat Co deficiency and will increase and maintain liveweights in a flock for up to 8 months.     

Concurrent changes in serum vitamin B12 and methylmalonic acid during cobalt or vitamin B12 supplementation of lambs while suckling and after weaning on properties in the South Island of New Zealand considered to be cobalt-deficient

AIM: To compare serum analyses of vitamin B12 and methylmalonic acid (MMA) as indices of cobalt/vitamin B12 deficiency in lambs around weaning. METHODS: Lambs on five properties, considered to be cobalt- deficient, were supplemented with either cobalt bullets, or short- or long-acting vitamin B12 preparations. Blood samples, and in some cases liver biopsies, and liveweights were obtained at monthly intervals. Serum samples were assayed for vitamin B12 and MMA and liver for vitamin B12 concentrations. Pasture cobalt concentrations were measured on three of the properties. RESULTS: Pasture cobalt concentrations were generally maintained below 0.07 microg/g dry matter (DM) on the properties sampled. Growth responses to supplementation were observed on only 2/5 properties, despite serum vitamin B12 concentrations being within the currently used 'marginal' reference range (336-499 pmol/L) for at least 3 months on all properties and in the deficient reference range (0-335 pmol/L) for at least 2 months on all farms except one. Serum MMA concentrations in supplemented lambs were <2 micromol/L, except in those animals sampled 1 month after receiving treatment with a short-acting vitamin B12 injection. Serum MMA concentrations in unsupplemented animals on properties on which no growth response to supplementation occurred generally reached peak levels of between 4 and 7 micromol/L at the nadir of serum vitamin B12 concentration. When a growth response was observed, differences in weight gain between supplemented and unsupplemented lambs occurred as mean serum MMA concentrations increased from 9 to 14 micromol/L. On one property where supplementation commenced before weaning, normal growth rates were maintained despite serum vitamin B12 concentrations of 140 pmol/L and serum MMA concentrations in excess of 40 micromol/L serum. CONCLUSIONS: The possibility that current serum vitamin B12 references ranges for diagnosis of cobalt deficiency are set too high and lead to over-diagnosis of responsiveness to cobalt/ vitamin B12 supplementation is discussed. The suggestion is made that serum MMA concentrations in excess of 9-14 micromol/L will provide a more reliable diagnostic test for cobalt deficiency. However, there was sufficient variation between properties in the relationships between cobalt concentrations of pasture and serum vitamin B12 or MMA concentrations to require more rigorous testing of the reliability of using serum MMA concentration for this purpose. The possibility that differences in rumen fermentation and therefore propionate and vitamin B12 production could be involved is discussed. The measurement of serum MMA and vitamin B12 appears to be of little value whilst the lamb is still suckling. CLINICAL SIGNIFICANCE: Serum MMA concentration may offer advantages over serum vitamin B12 concentrations in the diagnosis of a cobalt/vitamin B12 responsiveness in weaned lambs.     

Absence of a weight gain response to Vitamin B12 supplementation in weaned dairy heifers grazing pastures of marginal cobalt content

AIM: To obtain information on serum and liver vitamin B12 and urinary methylmalonic acid concentrations as diagnostic tests to predict a weight gain response to supplementation with vitamin B12 in young dairy cattle when grazing pasture of low cobalt content. Methodology. Forty dairy cattle (12 Friesian, 14 Friesian x Jersey and 14 Jersey) were allocated to two equal sized groups, treated and untreated, based on liveweight. At monthly intervals for 14 months, all animals were weighed, their serum and urine sampled, their liver biopsied and the pasture sampled from the paddocks they were grazing and going to graze. Serum and liver were assayed for vitamin B12 concentrations. For the first 5 months of the trial, urine was assayed for methylmalonic acid concentrations. Both washed and unwashed pasture samples were assayed for cobalt concentrations. RESULTS: No weight gain response occurred vitamin B12 supplementation in young growing cattle grazing pasture with a cobalt concentration of 0.04-0.06 mg/kg DM. For 5 months of the trial, liver vitamin B12 concentrations from untreated calves were in the range 75-220 nmol/kg and serum vitamin B12 concentrations were as low as 72 pmol/1. There was no associated growth response to supplementation. CONCLUSION: Further trials involving young cattle grazing pastures with cobalt concentrations less than 0.04 mg/kg DM are required to reliably determine liver and serum vitamin B12 concentrations at which growth responses to vitamin B12 or cobalt supplementation are likely under New Zealand pastoral grazing conditions.     

Vitamin E,selenium and polyunsaturated fatty acids in clinically normal grower (9–16 week old) pigs and their feed: their relationship to the vitamin E/selenium deficiency (“VESD”) syndrome

Vitamin E, selenium and polyunsaturated fatty acids (PUFAs) were determined in feed used at three piggeries over a four-week period and compared with corresponding concentrations in clinically normal grower pigs at slaughter. Mean values were vitamin E: 59 IU/kg (feed), 6 μmol/kg (liver), 1.7 μmol/1 (serum); and selenium: 310 μg/kg (feed), 5200 nmol/kg (liver), 1700 nmol/1 (blood). Alpha-tocopherol accounted for 80% of the mean vitamin E activity in the feed and over 95% that in the liver and serum. The mean ratio of PUFA to total fatty acid (FA) in the feed (38%) was similar to that in the serum (36%) and liver (39%), but the ratio of peroxidisable PUFA (PPUFA) to FA increased from 1.7% in the feed to 4.2% in the serum and 10.8% in the liver. The ratio of α-tocopherol (mmol) to PPUFA (mol) in the liver varied from 0.16 to 0.48. The relationship of these data to the “VESD” syndrome is discussed in the light of other published data.     

Pathological changes in cobalt-supplemented and non-supplemented twin lambs in relation to blood concentrations of methylmalonic acid and homocysteine.

In a controlled field study of three years' duration we evaluated the effect of cobalt supplementation on pathological changes in cobalt/vitamin B12-deficient Texel twin lambs grazing the same cobalt-deficient pasture. Semi-quantitative evaluation of the histopathology of liver and brain was done on 44 sets of twins. Pathological changes were related to blood concentrations of vitamin B12, methylmalonic acid, and homocysteine. Lesions were mainly confined to the liver and brain. Acute hepatic changes were characterized by steatosis, hepatocytic degeneration, and single cell necrosis. Chronic changes consisted of bile duct proliferation, the presence of ceroid containing macrophages, and fibrosis in the portal triads. Many non-supplemented lambs showed polymicrocavitation and Alzheimer type II reaction in the brain. Polioencephalomalacia was observed in three non-supplemented lambs but was regarded as a secondary lesion. Our results indicate that the main lesions found in cobalt/vitamin B12-deficient lambs are acute and chronic hepatitis. These lesions were associated with low concentrations of vitamin B12 and high concentrations of methylmalonic acid and homocysteine in the blood. The liver lesions were also associated with polymicrocavitation of the brain, probably as morphological evidence of hepatoencephalopathy.     

Investigation into diagnosis and treatment of cobalt deficiency in lambs.

The development of cobalt deficiency was studied in 30 Scottish Blackface lambs grazing pasture on a soil containing 0-17 ppm cobalt. By the end of an eight-week period 50 per cent of lambs were subjectively appraised as showing signs of cobalt deficiency. After a further period lasting four weeks, during which three groups of lambs were studied (one group, least affected by cobalt deficiency, acted as control, the second received a single cobalt bullet and the third received oral doses of 200 mg cobalt chloride at the beginning of the period and three weeks later). Mean urinary formiminoglutamic acid (FIGLU) concentrations were inversely related to serum vitamin B12 concentrations and increased from 0-08 to 0-20 mumole per ml in group 1, and decreased to virtually zero within one week of treatment in groups 2 and 3. The use of serum vitamin B12 and urinary FIGLU concentrations in the diagnosis of cobalt deficiency in sheep are discussed.     

Boluses of controlled release glass for supplementing ruminants with cobalt

Boluses of controlled release glass containing cobalt and weighing approximately either 60 g or 14.5 g were administered to 22 steers and 21 sheep respectively. The steers were housed and slaughtered at intervals between 17 and 145 days after dosing. The boluses released more than 0.85 mg cobalt daily. In both untreated and dosed animals serum and liver vitamin B12 concentrations were at the upper end of the normal range. Two types of glass were administered to sheep. In five wethers one glass released 0.07 mg cobalt per day, and in 16 grazing lambs a second glass released more than 0.15 mg cobalt per day. Fourteen of the boluses were recovered from the lambs up to 276 days after dosing. The concentration of B12 in serum of lambs increased significantly from a mean +/- sd of 1.64 +/- 0.47 to 2.02 +/- 0.04 ng/ml serum and the concentration in liver from 3.84 +/- 0.85 to 4.99 +/- 0.72 micrograms/g dry weight liver.     

The effect of sporidesmin toxicity on ovine serum vitamin B12 levels

A field outbreak of facial eczema occurred during a vitamin B12 response trial in young growing sheep. Pasture cobalt levels were in the low range for sheep (<0.08 mg/kg, 1.358 micromol/kg) and mean (of 3) liver vitamin B12 levels in the sheep were low (<400 nmol/kg) during the period in which facial eczema occurred. Mean serum vitamin B12 levels of the untreated group were low (<485 pmol/l) for the two months (January and February) preceding the period of facial eczema. However, levels showed an approximate 3.5 fold increase in both cobalt supplemented and unsupplemented groups with the onset of facial eczema in March. From February to March the mean serum vitamin B12 and glutamyl transferase (GGT) activity showed parallel increases with a positive correlation (r = 0.73) between log serum vitamin B12 and log serum GGT activity during the period January to July for both groups. This finding suggested that the increase in serum vitamin B12 was due to sporidesmin induced liver damage. The diagnostic implication is that, in areas where facial eczema is a problem, liver is the sample of choice for determining vitamin B12 status. because sporidesmin toxicity can elevate low serum vitamin B12 levels to diagnostically normal levels.     

Dose response effects of long-acting injectable vitamin B12 plus selenium (Se) on the vitamin B12 and Se status of ewes and their lambs

AIM: To determine the effect of increasing doses of long-acting injectable vitamin B12 plus selenium (Se) given pre-mating on the vitamin B12 and Se status of ewes and their lambs from birth to weaning. METHODS: Four groups of 24 Poll Dorset ewes each were injected 4 weeks pre-mating with different doses of a long-acting vitamin B12 + Se product, containing 3 mg vitamin B12 and 12 mg Se per ml. The treatment groups received 5 ml (15 mg vitamin B12 + 60 mg Se), 4 ml (12 mg vitamin B12 + 48 mg Se), 3 ml (9 mg vitamin B12 + 36 mg Se), or no vitamin B12 or Se (control). Twelve of the twin-bearing ewes per group were selected for the study. Efficacy of the product was evaluated from changes in the concentrations of vitamin B12 in serum and liver, and of Se in blood, liver and milk in the ewes during gestation and lactation, and in their lambs from birth to weaning. Pasture samples in paddocks grazed by the ewes and lambs were collected at about 2-monthly intervals from 200-m transects. RESULTS: The flock was Se-deficient, as the mean initial concentration of Se in the blood of ewes was 182 (SE 20.3) nmol/L. Compared with untreated controls, all doses significantly (p < 0.01) increased concentrations of Se in the blood of ewes for at least 300 days. Selenium concentrations in milk were likewise increased throughout lactation, as were those in the blood and liver of lambs. The mean concentration of vitamin B12 in the serum of ewes was initially > 1,000 pmol/L, but this decreased within 28 days to < 460 pmol/L. Treatment with the 5-ml and 4-ml doses raised serum vitamin B12 concentrations of ewes for at least 176 days (p < 0.01), while their lambs had significantly greater concentrations of vitamin B12 in serum and liver for less than 37 days after birth. Tissue concentrations and duration of elevation of both vitamin B12 and Se were proportional to the dose administered. The mean concentrations of Se and cobalt (Co) in the pastures were 32 and 74 microg/kg dry matter (DM), respectively. CONCLUSIONS: Injecting ewes from a Se-deficient flock 4 weeks prior to mating with 48 or 60 mg Se and 12 or 15 mg vitamin B12 increased and maintained the Se status of ewes for at least 300 days, and of their lambs from birth to weaning. The vitamin B12 status of ewes was increased for at least 176 days and that of their lambs for less than 37 days. Due to the proportional nature of the response to increasing dosage, the dose rate of the formulation tested can be adjusted according to the severity of Se and Co deficiency in a flock. CLINICAL SIGNIFICANCE: A single subcutaneous injection of vitamin B12 + Se administered pre-mating to Se-deficient flocks is likely to prevent Se deficiency in ewes and their lambs until weaning, as well as increase the vitamin B12 status of ewes and their lambs until 5 weeks after lambing.     

Effects of vitamin A supplementation in young lambs on performance, serum lipid, and longissimus muscle lipid composition

Forty crossbred wethers (BW = 28.7 kg) were used to evaluate the effects on LM lipid composition of diets containing high and low levels of vitamin A. Four treatments arranged as a 2 x 2 factorial with a completely random design were investigated: backgrounding (BG) and finishing (FN) with no supplemental vitamin A (LL); BG with no supplemental vitamin A and FN with high vitamin A (6,600 IU/kg of diet, as fed) supplementation (LH); BG with high vitamin A supplementation and FN with no vitamin A supplementation (HL); and BG and FN with high vitamin A (HH) supplementation. Diets included cracked corn (62.4%), soybean meal (16.0%), cottonseed hull pellets (14.8%), and supplement (7%), and contained <100 IU of vitamin A/kg (as fed) from carotenes before vitamin A was added. During the BG period (d 1 to 56), feed intake was restricted to achieve 0.22 kg of ADG. During the FN period (d 57 to 112), lambs consumed the same diet ad libitum. Lambs were weighed every 14 d, and blood was sampled every 28 d to evaluate changes in serum fatty acids and vitamin A levels. Lambs were slaughtered after 112 d. Lipid composition was determined for liver and LM. There were no treatment differences (P > 0.05) in feed intake, ADG, or final BW. Carcass weights were not affected by vitamin A treatment (P > 0.20), although backfat thickness tended to be different between HL and LL lambs (0.80 vs. 0.64 cm, respectively; P = 0.08). Carcasses from the HH group had greater (P < 0.05) marbling scores than those from the LL group (514 vs. 459) and had 25.8% more extractable intramuscular lipids (3.88 vs. 3.08% for HH and LL, respectively; P < 0.05); the LH and HL treatments were intermediate. Interestingly, the LL group had the greatest increase in serum fatty acids throughout the experimental period (change of 127 vs. 41 microg/g for LL and HH, respectively; P < 0.01). The degree of saturation of fatty acids was not affected by treatment (P = 0.18) in the serum but was affected in the longissimus thoracis fat. Oleic acid increased and linoleic acid decreased in the longissimus thoracis of HH-treated lambs (P < 0.02). These data suggest that increases in total intramuscular lipids may be achieved with high levels of vitamin A supplementation for 112 d in young lambs.     

Ovine white-liver disease (OWLD). Changes in blood chemistry

Changes in blood chemistry were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), and were compared with values of cobalt/B12 supplemented lambs on the same pastures, as well as clinically healthy, but sometimes B12 deficient, lambs on other pastures (H). In the OWLD group, signs of hepatic damage were seen concurrently with reduction in weight gain, or 1-3 weeks before, and comprised elevation of serum glutamate dehydrogenase (GLDH) and decrease of phospholipid and cholesterol. Drop of plasma glucose and elevation of gamma GT also came in the earlier phase of the disease. All other blood changes developed later, and were partly regarded as reflections of the inappetence or hepatic injury. The changes included a drop in packed cell volume (PCV) and mean corpuscular volume (MCV), elevation of serum iron, and reduction of total serum protein and urea. Generally Co/B12 supplementation prevented hepatic damage and normalized blood values. The clinically healthy H lambs also showed signs of hepatic damage, especially one year when they were B12 deficient, indicating that simple B12 deficiency causes a moderate liver damage as well. For diagnostic purposes, clinical pathology is recommended mainly on a flock basis.     

A review of tissue reference values used to assess the trace element status of farmed red deer (Cervus elaphus)

AIMS: This paper reviews the principles for the establishment of biochemical reference criteria for assessing the trace element status of farmed livestock and summarises data for copper, selenium, vitamin B12 and iodine for farmed red deer. COPPER: Enzootic ataxia and osteochondrosis occur when liver copper concentrations are below 60 micromol/kg fresh tissue, and serum copper concentrations are below 3-4 micromol/l. Growth responses to copper supplementation have been equivocal when blood copper concentrations were 3-4 micromol/l, but were significant when mean blood copper concentrations were 0.9-4.0 micromol/l. No antler growth or bodyweight response to copper supplementation was observed when blood ferroxidase levels averaged 10-23 IU/l (equivalent to serum copper concentrations of 6-13 micromol/l) and liver copper concentrations averaged 98 mumol/kg fresh tissue. These data suggest that 'deficient', 'marginal' and 'adequate' ranges for serum copper concentrations should be 5, 5-8, and 8 micromol/l, respectively, and those for liver copper concentrations should be 60, 60-100, and 100 micromol/kg, respectively. SELENIUM: White muscle disease has been reported in young deer with blood and liver selenium concentrations of 84-140 nmol/l and 240-500 nmol/kg fresh tissue, respectively. No growth-rate response to selenium supplementation occurred in rising 1-year-old deer when blood selenium concentrations were less than 130 nmol/l, the range in which a growth-rate response would be expected in sheep. VITAMIN B12: Vitamin B12 concentrations in deer are frequently below 185 pmol/l without clinical or subclinical effects. No growth response was observed in young deer with vitamin B12 concentrations as low as 75-83 pmol/l. A growth response to cobalt/vitamin B12 supplementation occurs in lambs with serum vitamin B12 concentrations 336 pmol/l. CONCLUSIONS: Data that can be used to establish reference ranges for assessing trace element status in deer are limited. More robust reference values for farmed red deer need to be established through further studies relating biochemical data to health and performance.     

A comparison of vitamin B12 levels in the liver and serum of sheep receiving treatments used to correct cobalt deficiency

The efficacies of four methods, used for the prophylaxis of cobalt deficiency in sheep as measured by the elevation of liver and serum vitamin B12 levels, were compared in marginally deficient sheep over 14 weeks. The methods used were weekly drenches of either cobalt sulphate or cobalt chelate (EDTA) three-weekly injections of hydroxocobalamin, and ruminal cobalt pellets. On the basis of elevated liver and serum vitamin B12 levels, chelated cobalt was shown to be available to rumen microflora for the synthesis of vitamin B12. However, at no stage were liver and serum vitamin B12 levels of sheep receiving the chelate significantly different from those receiving the same amount of cobalt as the sulphate. After five, three-weekly injections of hydroxocabalamin liver vitamin B12 levels were significantly higher (p<0.01) than for the other treatments, with the exception of cobalt sulphate. Cobalt pellets led to an initial rapid and significant rise in serum vitamin B12 when compared with the other treatments. However, at four weeks there was no significant difference between treatment groups for serum vitamin B12. Fourteen weeks after the administration of cobalt pellets, serum and liver.vitamin B12 levels in this group were not significantly different from those of untreated sheep. At this time, three out of 12 sheep had lost their pellets.     

Ovine white-liver disease (OWLD). Trace elements in liver

Trace elements in liver were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), in cobalt/vitamin B12 supplemented lambs on the same pastures as well as clinically healthy, but sometimes subclinical B12 deficient lambs on other pastures (H). Liver Co was marginal to deficient in both OWLD lambs (S lambs) and H lambs. Supplementation with B12 or Co elevated liver Co. Liver copper was significantly lower in OWLD lambs than in the H lambs, and Co/B12 supplementation on pasture generally had no significant effect on the contents. Dosing lambs on OWLD pastures with copper oxide needles (SCuO), however, resulted in high/toxic liver Cu. Dosing with Co, Se and Cu glass boluses resulted in adequate liver Cu, except for 1 lamb with toxic amounts indicating dissolution and absorption of the bolus. OWLD lambs had significantly lower liver molybdenum than H lambs, and Co/B12 supplementation elevated values, while CuO treatment depressed them. Liver zinc, manganese and selenium are also reported.     

A critical evaluation of serum methylmalonic acid and vitamin B12 for the assessment of cobalt deficiency of growing lambs in New Zealand

AIM: To derive reference ranges for serum methylmalonic acid (MMA) for the diagnosis of cobalt/vitamin B12-responsiveness in lambs and critique existing serum vitamin B12 reference ranges. METHODS: Individual animal data from earlier supplementation trials, involving 225 ewes, 106 suckling lambs, 301 lambs during the suckling and post-weaning periods and 414 weaned lambs, for which weight gain to supplementation was observed, were used to derive relationships between serum vitamin B12 and MMA, and liveweight gain. RESULTS: Serum MMA concentrations were rarely elevated above the norm of <2 micromol/L when serum vitamin B12 concentrations were >375 pmol/L, and not elevated into the range where a liveweight response to supplementation occurred (>10 micromol/L) unless serum vitamin B12 concentrations were below 200 pmol/L. Suckling lambs were able to maintain high growth rates despite elevated serum MMA concentrations (>20 micromol/L). CONCLUSIONS: The current reference ranges used in New Zealand for serum vitamin B12 are set conservatively high. Serum MMA concentrations appear to allow better differentiation of a responsive condition than vitamin B12 concentrations. Serum MMA concentrations >13 micromol/L indicate responsiveness to supplementation whilst concentrations <7 micromol/L indicate unresponsiveness. In the range 7-13 micromol/L, variation in response was observed and predictability of response is less certain, but supplementation is advisable. CLINICAL RELEVANCE: The current reference ranges for vitamin B12 responsiveness are conservatively high and lead to over-diagnosis of vitamin B12 deficiency in ill-thriftiness of sheep.