Serological evidence of exposure of healthy dogs to Leptospira in Sydney, New South Wales, Australia.

In 2017, highly fatal canine leptospirosis emerged in Sydney, Australia. Based on results of microscopic agglutination testing (MAT), serovar Copenhageni appeared to be the most common causative serovar. Prior to this, no clinical cases had been reported since 1976. In a serosurvey of healthy dogs in Australian shelters in 2004, 2.4% of 431 New South Wales dogs had serological evidence of exposure to Copenhageni, the most prevalent serovar. The aim of this study was to estimate the current prevalence of Leptospira exposure and associated serovars in healthy Sydney dogs, previously unvaccinated against Leptospira. Serum samples from 411 healthy dogs in leptospirosis hotspots and neighbouring suburbs were collected before vaccination. MAT for 23 serovars was performed at the WHO Leptospirosis Reference Laboratory in Queensland, Australia. The overall seroprevalence was 4.1% (17/411) with low titres (1/50-1/200) detected. Eleven dogs were from known leptospirosis hotspots. Eight dogs were known to hunt rodents. One dog had been in contact with a leptospirosis positive dog 1 year prior. Serovar Topaz was the most prevalent serovar (n = 5) followed by serovars Australis (n = 4), Copenhageni (n = 4), Djasiman (n = 2), Cynopteri (n = 1), Javanica (n = 1), Medanensis (n = 1), and Pomona (n = 1). In conclusion, serological evidence of exposure of dogs in Sydney to Leptospira is low, but apparently has increased since 2004. Positive titres to serovars not previously reported to cause disease in dogs could be due to low virulence of those serovars or cross-reactivity with other serovars.

Effectiveness of aspirin vs. clopidogrel in dogs with immune mediated haemolytic anaemia evaluated by serial thromboelastography and platelet mapping.

Most dogs with immune mediated haemolytic anaemia (IMHA) are hypercoagulable, as measured by thromboelastography (TEG). Thromboelastography-platelet mapping (TEG-PM) has been used to assess platelet function in human patients treated with aspirin or clopidogrel. The aim of this study was to compare platelet thromboxane A2-receptor inhibition (TXA2-RI) and platelet adenosine diphosphate (ADP)-receptor inhibition (ADP-RI) as measured by TEG-PM in dogs with primary IMHA receiving aspirin or clopidogrel to determine if TEG-PM might be useful to monitor treatment. Eighteen client-owned dogs with IMHA were enroled in a prospective double blinded study. Dogs were randomised to receive aspirin or clopidogrel in addition to standard therapy. Thromboelastography was measured before, and 1 and 4 days after commencing treatment. Thromboelastography-PM was performed on days 1 and 4. Non-responders were defined as < 50 % platelet thromboxane A2-receptor inhibition (TXA2-RI) in the aspirin group and < 50 % platelet adenosine diphosphate (ADP)-receptor inhibition (ADP-RI) in the clopidogrel group, on day 4. Mean platelet TXA2-RI and platelet ADP-RI were not significantly different between groups at any timepoint (P > 0.05). The overall mean percentage inhibition of TXA2-receptor was 25 % (aspirin 33 %, clopidogrel 15 %), and of ADP-receptor was 82 % (aspirin 83 %, clopidogrel 80 %). On day 4, 6/9 dogs (66 %) in the aspirin group and 2/8 dogs (25 %) in the clopidogrel group were non-responders (P = 0.086). Two dogs defined as responders based on TEG-PM developed thromboembolism. Overall, there was no significant difference in efficacy between aspirin and clopidogrel based on measurement of receptor inhibition using TEG-PM (P > 0.05), and routine TEG was not reliable for monitoring treatment response in dogs with IMHA. In some dogs, there was a discrepancy between TEG-PM results and clinical response. Further investigation of TEG-PM use in dogs, including its usefulness to monitor treatment response and adjust treatment in individual dogs and any effect of anaemia, is warranted.

Emerging leptospirosis in urban Sydney dogs: a case series (2017-2020).

Canine leptospirosis has not been reported in the Sydney dog population since 1976. However, between 2017 and 2020, leptospirosis was confirmed in 17 dogs, five of which were known to hunt rodents. Dogs infected between 2017 and 2019 lived within a 3 km radius in the Inner City of Sydney (n = 11). In 2020, cases emerged across a broader area of Sydney; Inner City (n = 1), Inner West (n = 3), Lower North Shore (n = 1) and Upper North Shore (n = 1). The disease was characterised by severe hepatorenal involvement resulting in an unusually high case fatality rate (88%). In conjunction with supportive clinical signs, diagnosis was confirmed by real-time PCR on whole blood (n = 1), kidney (n = 1), urine (n = 4), whole blood and urine (n = 9) or by seroconversion (n = 3). Antibody titres determined by Microscopic Agglutination Test (MAT) to Leptospira serovars were measured in 12 dogs: seven were positive for serovar Copenhageni, one was positive for serovar Hardjo, three were negative for all serovars, likely due to insufficient time for seroconversion before death and one had a low positive titre (1/50) for serovars Australis and Robinsoni. This sudden emergence of a highly fatal disease in pet dogs in Sydney has led to the introduction of Leptospira vaccination protocols for dogs living in inner Sydney using a monovalent vaccine containing serovar Copenhageni. The success of this vaccination program will require ongoing research to understand the emergence of leptospirosis in this region and the serovars involved.

Intravenous vitamin K1 normalises prothrombin time in 1 hour in dogs with anticoagulant rodenticide toxicosis.

Four dogs with anticoagulant rodenticide toxicosis were treated with intravenous vitamin K1 in lieu of plasma transfusion due to client cost constraints. Two dogs experienced a suspected anaphylactoid reaction, necessitating cessation of the treatment in one dog. Prothrombin time was rechecked 1 h after treatment in the remaining three dogs and all results were within the normal reference range. All four dogs were discharged from hospital within 48 h of presentation. Intravenous vitamin K1 rapidly reverses the coagulopathic state in dogs with anticoagulant rodenticide toxicosis. It is a viable alternative therapy to plasma transfusion if circumstances preclude its use; however, patients must be monitored for anaphylactoid reactions.

Effect of trilostane on hormone and serum electrolyte concentrations in dogs with pituitary-dependent hyperadrenocorticism.

BACKGROUND: The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary-dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and ionized calcium concentrations, and plasma renin activity over a 24-hour period after administration of trilostane to dogs with well-controlled PDH. ANIMALS: Nine dogs (mean age 9.3 ± 0.67 years, mean weight 31.9 ± 6.4 kg) with confirmed PDH. METHODS: Prospective study. Thirty days after the first administration of trilostane, blood samples were taken at -30, 0 (baseline), 15, 30, 60, and 90 minutes, and 2, 3, 4, 6, 8, 12, 16, 20, and 24 hours after administration of trilostane and plasma concentration of cortisol, endogenous ACTH, aldosterone, sodium, potassium, ionized calcium, and renin activity were determined. RESULTS: Cortisol concentrations decreased significantly (P < .001) 2-4 hours after trilostane administration. From baseline, there was a significant (P < .001) increase in endogenous ACTH concentrations between hours 3-12, a significant increase (P < .001) in aldosterone concentration between hours 16-20, and a significant (P < .001) increase in renin activity between hours 6-20. Potassium concentration decreased significantly (P < .05) between hours 0.5-2. CONCLUSION AND CLINICAL IMPORTANCE: Treatment with trilostane did not cause clinically relevant alterations in plasma aldosterone and potassium concentration. Results suggest that in dogs with PDH, the optimal time point for an ACTH-stimulation test to be performed is 2-4 hours after trilostane dosing. Future studies are necessary to establish interpretation criteria for a 2- to 4-hour postpill ACTH-stimulation test.