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81.
82.
AIMS: To determine the effect of contamination of urine with 0–5% blood, varying in haematocrit and protein concentrations, on the urine protein to creatinine ratio (UPC) in dogs, and to determine whether the colour of urine can be used to aid interpretation of UPC results.

METHODS: Urine samples were collected by free catch from 18 dogs, all of which had UPC?<0.2. Venous blood samples were also collected from each dog, and the blood from each dog was added to its own urine to produce serial concentrations of 0.125–5% blood. The colour of each urine sample was recorded by two observers scoring them as either yellow, peach, orange, orange/red or red. Protein and creatinine concentrations were determined, and dipstick analysis and sediment examination was carried out on each sample. Based on colour and dipstick analysis, samples were categorised as either having microscopic, macroscopic or gross haematuria. A linear mixed model was used to examine the effect of blood contamination on UPC.

RESULTS: The uncontaminated urine of all 18 dogs had a UPC?<0.2. Adding blood to the urine samples resulted in an increase in UPC at all contamination concentrations compared to the non-contaminated urine (p<0.001). None of the 54 samples with microscopic haematuria had UPC?>0.5. For 108 samples with macroscopic haematuria the UPC was >0.5 in 21 samples (19.4 (95% CI=13.1–27.9)%), and for 54 samples with gross haematuria 39 (72 (CI=59.1–82.4)%) had a UPC?>0.5. No samples had a UPC?>2.0 unless the blood contamination was 5% and only 3/18 (17%) samples at this blood contamination concentration had a UPC?>2.0.

CONCLUSIONS AND CLINICAL RELEVANCE: This study showed that while blood contamination of ≥0.125% does increase the UPC, if the urine remains yellow (microscopic haematuria), then there is negligible chance that a UPC?>0.5 will be solely due to the added blood. In that scenario, attributing the proteinuria present to the haematuria in the sample would be inappropriate. However blood contamination that results in discolouration of the urine sample from yellow (indicating macroscopic or gross haematuria) could increase the UPC above the abnormal range and would need to be considered as a differential for the proteinuria. Thus knowledge of urine colour, even if limited to simple colour scores (yellow, discoloured, red) could be utilised to aid interpretation of the UPC in samples with haematuria.  相似文献   

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AIM: To assess the effect of sedation and local anaesthesia (LA) at disbudding, and the addition of meloxicam or ketoprofen treatment, on weight gain in dairy calves following disbudding.

METHODS: Friesian-Jersey cross calves, from four dairy farms, were enrolled when 3–6 weeks old. All calves (n=271) were disbudded by veterinary personnel and randomly assigned to six groups: 136 were disbudded without sedation or LA, of which 31 received 20 mg meloxicam S/C and 75 received 150 mg ketoprofen I/M. A further 135 were disbudded with sedation (0.25 mg/kg xylazine I/M) and LA, of which 30 also received meloxicam and 75 received ketoprofen. Calves were weighed 3 days before, and 15 and 30 days after, disbudding (Day 0). Daily weight gain was analysed using mixed models and ANOVA.

RESULTS: Complete results were obtained from 263 calves. From Day ?3 to Day 15, the growth rate of calves disbudded without pain relief (0.53 (95% CI=0.47–0.60) kg/day) was less that of calves disbudded with some form of pain relief (0.65 (95% CI=0.62–0.68) kg/d; p=0.004). There was no difference between the effect of meloxicam or ketoprofen (p=1.00). An interaction between use of sedation and LA and additional non-steroidal anti-inflammatory drugs (NSAID) meant that NSAID treatment did not increase growth rates in calves disbudded with sedation and LA but did increase growth rates for calves disbudded without pain relief (p<0.05). From Day 16 to Day 30 there was no effect of NSAID treatment on growth rate, but calves receiving LA and sedation grew faster (0.74 (95% CI=0.69–0.80) kg/day) than calves disbudded without LA and sedation (0.66 (95% CI=0.61–0.71) kg/day; p=0.018). From Day ?3 to Day 30, calves disbudded with sedation and LA grew faster (0.71 (95%CI=0.64–0.77) kg/day) than calves disbudded without sedation and LA (0.60 (95% CI=0.55–0.65) kg/day; p=0.011). However, addition of NSAID to sedation and LA made no further difference to growth rates (p=0.69).

CONCLUSIONS: Dairy calves disbudded with no pain relief had slower growth rates than calves receiving pain relief. From Day 15 to 30 calves given no pain relief, or NSAID alone, grew more slowly than those receiving sedation and LA at disbudding. The addition of NSAID treatment to sedation and LA did not further increase growth rates.

CLINICAL RELEVANCE: This study adds to the evidence that pain management when disbudding is beneficial for calf productivity as well as calf welfare.  相似文献   
86.
AIM: To determine the impact of sodium molybdate treatment, given weekly, on concentrations of Cu in liver, activity of liver enzymes, and weight gain over 4 weeks, in yearling bulls with elevated concentrations of Cu in liver.

METHODS: The study was carried on two commercial grazing farms in the Otago region of New Zealand in yearling Friesian bulls (n=150 on Farm A and n=49 on Farm B) with mean concentration of Cu in liver >3,000 µmol/kg fresh weight. On Day 0, all animals were weighed and half were systematically allocated to treatment with sodium molybdate (3?mg/kg liveweight on Farm A and 7?mg/kg liveweight on Farm B); the remainder received no treatment (Control). Sodium molybdate was given as a drench weekly for 4 weeks and all animals were weighed again on Day 28. Ten animals on each farm (five from each treatment group) were systematically selected for blood sampling and liver biopsies on Days 0 and 28. Samples were analysed for concentrations of Cu in plasma, vitamin B12 in serum, activities of γ–glutamyl transferase, aspartate aminotransferase and glutamate dehydrogenase in serum, and concentrations of Cu and vitamin B12 in liver. Separate multivariable linear models were used to compare the change in outcome variables between Days 0 and 28 between bulls that had been drenched with sodium molybdate or not.

RESULTS: On Farm A, mean concentrations of Cu in liver on Day 28, as a percentage of concentrations on Day 0, for the control group was 55 (95% CI=40–73)% and for the treatment group was 73 (95% CI=43–111)%. On Farm B, the equivalent mean for the control group was 75 (95% CI=42–131)% and for the treatment group was 85 (95% CI=38–134)%. The multivariable linear models indicated that the changes in concentrations of Cu in liver, activities of liver enzymes and weight gain between Days 0 and 28 did not differ between the bulls treated or not with sodium molybdate (p>0.18).

CONCLUSIONS AND CLINICAL RELEVANCE: Treatment with sodium molybdate in one bolus at weekly intervals for 4 weeks did not affect concentrations of Cu in liver, activity of liver enzymes or weight gain in animals with high concentrations of Cu liver on two farms.  相似文献   
87.
In equids, phenylbutazone at high doses induces gastric disease, primarily in the glandular portion of the stomach. However, the mechanism of nonsteroidal anti‐inflammatory drug (NSAID)‐induced gastric disease in horses has yet to be determined. While phenylbutazone‐associated ulceration is often attributed to a decrease in basal gastric prostaglandins, this has not been demonstrated in the horse. Twelve horses were randomly assigned to treatment (n  = 6; 4.4 mg/kg phenylbutazone PO in 20 ml molasses q 12 hr for 7 days) or placebo (n  = 6; 20 ml molasses PO q 12 hr for 7 days) groups. Before treatment and 3 and 7 days after initiation of treatment, gastroscopy was performed and glandular gastric biopsies were collected and frozen at ?80°C. Glandular disease was assessed on a scale of 0–4. Prostaglandin E2 concentrations in biopsies were measured using a commercially available enzyme‐linked immunosorbent assay. All phenylbutazone‐treated horses developed grade ≥2 glandular disease. Prostaglandin concentrations increased over time (p  = .0017), but there was no effect of treatment (p  = .49). These findings indicate that despite induction of glandular disease grade ≥2, phenylbutazone did not decrease basal glandular gastric prostaglandin E2 concentration.  相似文献   
88.
Objective Describe the presence of arrhythmias in dogs with myxomatous mitral valve disease (MMVD) and the potential association with class of heart failure and left atrial enlargement. Compare the standard electrocardiogram (ECG) with Holter monitoring for assessing heart rate (HR). Experimental procedure The study group of 36 dogs weighing less than 20 kg was divided into MMVD and no clinical signs (preclinical) or MMVD and clinical signs (clinical). A standard echocardiogram, ECG and 24-h Holter recording were obtained in all dogs. Results Minimum and mean Holter HRs were higher in the clinical group than in the preclinical group. Clinical dogs had more ventricular arrhythmias than preclinical dogs. An enlarged left atrium was associated with the presence of more supraventricular arrhythmias. Conclusions Arrhythmias are a common finding in dogs with MMVD and Holter monitoring is a reliable tool for both HR monitoring and diagnosis.  相似文献   
89.
Objective To report the rapid transmission of bovine ephemeral fever ( BEF) virus from north-western New South Wales south to the Victorian border in January 2008 and to present data that suggests an uncommon meteorological event caused this rapid southward dispersal of vectors. Procedure The locations of reported clinical cases, data from sentinel herds and results from a survey of cattle in the southern affected area were examined to delineate the distribution of virus transmission. Synoptic weather charts for January 2008 were examined for meteorological conditions that may have favoured movement of vectors in a southerly direction. Results Cases of BEF and exposure to BEF virus in NSW were confirmed west of the Great Dividing Range, extending from the Queensland border to Finley, on the far North Coast and around the Hunter Valley. A low-pressure system moved south across the state on 18–19 January 2008, preceding the first cases of BEF in the south of NSW by 1–2 days. Conclusion Heavy rainfall in December 2007 provided a suitable environment for vector breeding, resulting in the initiation of and support for continuing BEF virus transmission in north-western NSW. The movement of a low-pressure system south across central western NSW in mid-January 2008 after the commencement of BEF virus transmission in the north-west of the state provided a vehicle for rapid southward movement of infected vectors.  相似文献   
90.
A nasal mass in a Domestic Shorthair cat was causing facial deformity, sneezing and intermittent epistaxis. Biopsy samples obtained previously had been non-diagnostic. Computed tomography images revealed an irregular, contrast-enhancing mass occupying a large portion of the righthand side of the nasal cavity. Previously described criteria for malignancy were not present. A ventral surgical approach combined with temporary, ipsilateral, common carotid arterial occlusion provided excellent access for debulking the lesion and collecting samples for histopathology. A nasal vascular hamartoma was diagnosed and clinical signs resolved postoperatively. This is the first documentation of this abnormality in the cat. Hamartomatous abnormalities should be included on the list of differential diagnoses for feline nasal mass lesions. The prognosis for hamartomatous lesions postoperatively is good, in keeping with their limited propensity for growth after maturity.  相似文献   
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