Copper deficiency in sheep: An assessment of the relationship between concentrations of copper in serum and plasma

AIM: To assess the relationship between concentrations of copper in serum and plasma in sheep.

METHODS: Concentrations of Cu were measured in paired serum and heparinised plasma samples collected from 110 sheep in nine flocks. Linear regression was used to evaluate whether flock or gender had a significant effect on the association between concentrations of Cu in serum and plasma. The individual results for concentrations of Cu in serum were then compared with those from plasma, using correlation and limits of agreement plotting.

RESULTS: Concentrations of Cu in serum ranged from 7.3 to 22 (mean 14.0) µmol/L, while concentrations in plasma ranged from 9 to 27 (mean 16.3) µmol/L. On average, concentrations of Cu in serum were 2.3 µmol/L lower than in plasma. Over the range of values seen in this study, concentrations of Cu in plasma and serum were significantly correlated (r=0.89), and mean concentrations in serum were 87% of those in plasma. There was no effect of flock or gender on the relationship between concentrations of Cu in serum and plasma. Despite the significant correlation, there was marked variability between individual samples in the proportion of Cu that was lost during clotting, with the 95% limits of agreement for serum Cu ranging from 70 to 104% of the plasma concentration.

CONCLUSIONS: As in cattle, the individual variability in the loss of Cu during clotting in sheep is too great for concentration of Cu in serum to be used as a substitute for that in plasma.

CLINICAL RELEVANCE: When assessing the blood Cu pool as part of the diagnosis of Cu-responsive disease in sheep, the concentration of Cu in plasma should be measured in preference to that of serum. We suggest that a range of 4.5 to 9 µmol/L in plasma be used to define marginal Cu status in sheep.     

Pre-hospital low-volume resuscitation with hemoglobin-glutamer-200 (Hb-200) in a canine hemorrhagic shock model

The Bowen Technique is a unique hands‐on therapy developed by Tom Bowen of Australia in the 1950s–60s and adapted for use in animals by Carol Bennett in 1997. It consists of a specific sequence of gentle, precise rolling moves done with thumb and fingers over muscle and tendon edges, across the direction of tension. A short waiting period follows each set of moves. Definitive mechanism(s) of action remains to be identified; however, autonomic nervous system modulation (heart rate variability studies) has been documented in humans. The technique has also been reported effective for back, hip, neck, and shoulder pain in human studies. Five geriatric dogs (13–16 years old) of various breeds were presented in a case series at a small animal clinic for primary complaints of stiffness, poor ambulation, and difficulty lying down/getting up. Four had hindlimb proprioceptive deficits; three had arthritic changes to coxofemoral joints and/or lumbar spine; three showed active indicators of pain (chronic pacing/panting; irritability; social withdrawal). All were on NSAID and/or nutritional therapy with unsatisfactory results. One dog had acupuncture weekly for over 1 year but no longer tolerated the needles. Treatment consisted of Animal Bowen at weekly or biweekly intervals. Three dogs were pain scored [0–10; average starting score 6.7 ± 0.6 (mean ± S.D.); range 6–7] by owner before and after treatment. All five dogs showed significant positive changes in attitude, and four had notable improvement in ease of ambulation, after the first treatment. Improvement was progressive over treatment course. Average post‐treatment score was 2.3 ± 2.1 (0, 3, 4); average pain score reduction was 4.3 ± 1.5 (range 3–6) after two to six treatments for the three dogs scored. One dog had complete resolution of hindlimb lameness of 5 years duration after three sessions. Animal Bowen, used alone or in conjunction with standard analgesics and other treatments, can be an effective therapy for chronic musculoskeletal conditions in dogs.     

Nephrogenic diabetes insipidus in a 14-year-old gelding

Abstract

CASE HISTORY: A 14-year-old Cleveland Bay cross gelding was presented with severe urinary incontinence that had been present for 1 year, and chronic polydipsia and polyuria over 4 years. Water intake had been recorded as 240 L over a 24-hour period.

CLINICAL FINDINGS: The horse had marked urinary incontinence and polyuria and polydipsia. The urine was markedly hyposthenuric, but no abnormalities on urinalysis were detected. There were no other abnormal clinical or neurological signs. Haematological and serum biochemical examinations showed no abnormalities and ultrasonographic and endoscopic examination of the urinary tract did not reveal any abnormalities. The horse underwent a modified water deprivation test and failed to concentrate its urine after 5 days. 1-desamino-8-d-arginine vasopressin (DDAVP) was administered I/V but the urine remained isosthenuric with a specific gravity of 1.010.

DIAGNOSIS: Nephrogenic diabetes insipidus. A definitive cause of the urinary incontinence was not found but overflow incontinence was considered a possibility.

CLINICAL RELEVENCE: Despite being a rare condition in the horse diabetes insipidus should be considered in cases of severe polydipsia and polyuria in mature horses.     

动物疫苗及其合理使用（一）

疫苗接种是预防动物传染病发生的重要举措。依据免疫学理论,疫苗作为抗原,通过激发动物机体免疫系统,产生特异的体液免疫和细胞免疫,从而获得针对某种疾病的特异性免疫。疫苗一般分为细菌疫苗、病毒疫苗和类毒素疫苗等。用于防病治病的各种疫苗、菌苗又是特殊的生物药品,与普通化学药品具有完全不同的成分、功能和特性,疫苗中含有多种蛋白质（除细菌或病毒外,有的还含有保护剂、鸡胚尿囊液或细胞培养液）,它们均适合许多病原体的生长,有些制品还是活的微生物,一旦污染后果不堪设想。疫苗在保存、运输和使用时有其特别要求。如果方法不当,不但会使活性物质失活,起不到免疫防病作用;而且还可能适得其反,引发动物新的疾病,造成重大损失。     

Alpaca plant poisonings: nitrate–nitrite and possible cyanide

Nitrate–nitrite poisoning killed four adult alpacas and induced the abortion of a full-term fetus after access to oaten hay ( Avena sativa ) containing 3.2% KNO₃ equivalent in dry matter. Necropsy findings were cyanosis, dark-coloured blood, and pulmonary congestion and oedema. Aqueous humour from two adults contained 25 mg NO₃/L and that from the fetus contained 10 mg NO₃/L. Cyanide poisoning possibly killed two adult wether alpacas that ate a garden-cultivated variety of Osteospermum ecklonis (South African daisy, bietou) with a cyanide potential of 6800 mg HCN/kg dry matter.     

Epidemic of blindness in kangaroos - evidence of a viral aetiology

OBJECTIVE: To determine the cause of an epidemic of blindness in kangaroos. DESIGN AND PROCEDURES: Laboratory examinations were made of eyes and brains of a large number of kangaroos using serological, virological, histopathological, electron microscopical, immunohistochemical methods, and PCR with cDNA sequencing. In addition, potential insect viral vectors identified during the disease outbreak were examined for specific viral genomic sequences. SAMPLE POPULATION: For histopathological analysis, 55 apparently blind and 18 apparently normal wild kangaroos and wallabies were obtained from New South Wales, Victoria, South Australia, and Western Australia. A total of 437 wild kangaroos and wallabies (including 23 animals with apparent blindness) were examined serologically. RESULTS: Orbiviruses of the Wallal and Warrego serogroups were isolated from kangaroos affected with blindness in a major epidemic in south-eastern Australia in 1994 and 1995 and extending to Western Australia in 1995/96. Histopathological examinations showed severe degeneration and inflammation in the eyes, and mild inflammation in the brains. In affected retinas, Wallal virus antigen was detected by immunohistochemical analysis and orbiviruses were seen in electron microscopy. There was serological variation in the newly isolated Wallal virus from archival Wallal virus that had been isolated in northern Australia. There were also variations of up to 20% in genotype sequence from the reference archival virus. Polymerase chain reactions showed that Wallal virus was present during the epidemic in three species of midges, Culicoides austropalpalis, C dycei and C marksi. Wallal virus nucleic acid was also detected by PCR in a paraffin-embedded retina taken from a blind kangaroo in 1975. CONCLUSION: Wallal virus and perhaps also Warrego virus are the cause of the outbreak of blindness in kangaroos. Other viruses may also be involved, but the evidence in this paper indicates a variant of Wallal virus, an orbivirus transmitted by midges, has the strongest aetiological association, and immunohistochemical analysis implicates it as the most damaging factor in the affected eyes.