Clinical findings in 10 horses diagnosed with monorchidism following exploratory laparotomy or standing laparoscopic surgery

Monorchidism describes the complete absence of one testis and is rare in horses. This study reports the clinical findings in 10 horses diagnosed as monorchids by standing laparoscopy or exploratory laparotomy. Hospital records for all horses undergoing cryptorchidectomy (2000–2016) in four centres were reviewed from which horses diagnosed with monorchidism were identified. Surgery was by either standing flank laparoscopy or an inguinal exploration and subsequent exploratory laparotomy under general anaesthesia. Ten horses were diagnosed as monorchids, five by laparoscopy (one bilateral laparoscopy) and five by laparotomy. Nine horses had a normally descended scrotal testicle, which was also removed at surgery. The right testicle was absent in three horses, and the left testicle was absent in seven horses. Anatomical findings were recorded in each case; the vaginal process was present in all horses, ductus deferens and epididymis were present in 80% of horses and the ligament of the tail of the epididymis and testicular vessels were present in 50% of horses. Laparoscopy allowed easy identification of spermatic structures enabling a prompt diagnosis of monorchidism. In conclusion, when monorchidism occurs, most other associated spermatic structures are likely to be present. A diagnosis of true monorchidism is reliant on hormonal testing and absence of testicular tissue on histopathology and so some of these horses may strictly be somewhere on the spectrum of testicular degeneration. This information is particularly useful in the surgical situation when it is not clear whether the testicle is present or not.     

Tick paralysis in dogs and cats in Australia: treatment and prevention deliverables from 100 years of research

This review of tick paralysis caused by Ixodes holocyclus in Australia addresses the question: What are the key discoveries that have enabled effective treatment and prevention of tick paralysis in dogs and cats? Critical examination of 100 years of literature reveals that arguably only three achievements have advanced treatment and prevention of tick paralysis in animals. First, the most significant treatment advance was the commercial availability of tick antiserum in the 1930s. Hyperimmune serum currently remains the only specific anti-paralysis tick therapy available to veterinarians in Australia. Second, advances in veterinary critical care have increased survival rates of the most severely affected dogs and cats. Critical care advancements have been enabled through specialised veterinary hospitals that can provide appropriate care 24 h a day, and advanced training of veterinarians, veterinary nurses and technicians. Third, perhaps that biggest advance of all in the last 100 years of research has been the commercial availability of the isooxazoline class of acaricidal preventatives in Australia specifically for I. holocyclus. This highly effective class of preventatives offers long duration of action, low cost, spot-on or oral formulations and a low rate of adverse reactions. Animal owners and veterinarians now have the most useful tool of all – a reliable preventative. This review reveals the key events in research over the last 100 years and the tortuous pathway to delivering better treatment and preventative options for this enigmatic Australian parasite.     

Phosphorylation by p38 MAPK as an alternative pathway for GSK3beta inactivation

Glycogen synthase kinase 3beta (GSK3beta) is involved in metabolism, neurodegeneration, and cancer. Inhibition of GSK3beta activity is the primary mechanism that regulates this widely expressed active kinase. Although the protein kinase Akt inhibits GSK3beta by phosphorylation at the N terminus, preventing Akt-mediated phosphorylation does not affect the cell-survival pathway activated through the GSK3beta substrate beta-catenin. Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin. p38 MAPK-mediated phosphorylation of GSK3beta occurs primarily in the brain and thymocytes. Activation of beta-catenin-mediated signaling through GSK3beta inhibition provides a potential mechanism for p38 MAPK-mediated survival in specific tissues.     

The toxicity of Castanospermum australe seeds for cattle

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.     

Does blood contamination of urine compromise interpretation of the urine protein to creatinine ratio in dogs?

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.     

Soil sensitised generation of singlet oxygen in the photodegradation of bioresmethrin

The ability of soil samples of pH 4·2, 5·5 and 7·2 to generate gaseous singlet oxygen was investigated using a separated-surface-sensitised reactor. It was found that the soil samples can act as sensitisers for the production of singlet oxygen in a similar fashion to the well known sensitisers chlorophyll and Rose Bengal. The reaction of singlet oxygen so produced with the pyrethroid insecticide, bioresmethrin, has been investigated.     

The effect of different combinations of local anaesthesia,sedative and non-steroidal anti-inflammatory drugs on daily growth rates of dairy calves after disbudding

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.     

Effect of sodium molybdate supplementation on high concentrations of Cu in liver of yearling bulls

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.