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.

Background This report describes 17 cases of red‐bellied black snake envenomation (RBBS; Pseudechis porphyriacus) in dogs in south‐eastern Queensland. Patients were prospectively enrolled for the treatment with a new tiger‐brown snake antivenom 8000 units, (TBAV; Padula Serums Pty Ltd, VIC, Australia). Case Report Clinical diagnosis of RBBS envenomation was made by either snake venom detection kit, snake identification using scale counting, or owner observed dog‐snake interaction in patients with clinical signs of envenomation. An RBBS venom antigen sandwich ELISA was used to retrospectively quantify venom levels in frozen serum and urine. Mechanical ventilation was required in 11% (2/17) patients, whole blood transfusion in 12% (2/17), tissue swelling at the bite site occurred in 53% (9/17) and facial palsy in 12% (2/17). One dog was euthanised, and overall, 94% (16/17) survived to hospital discharge. Clinicopathological changes pre‐TBAV included variable haemolysis, increased CK, pigmenturia and mildly prolonged active clotting time with a median of 134 s (n = 13, range 91–206 s). Haematological profiles post envenomation revealed anaemia (6/6) and spherocytosis (5/5), which resolved without the use of corticosteroids. Pre‐TBAV, median RBBS venom antigen concentration was 22.6 ng/mL (n = 15, range 2–128) in serum and 58 ng/mL (range 1–452) in urine; RBBS venom antigen was undetectable in serum post‐TBAV in all patients. Conclusion Some RBBS envenomed dogs required, critical care including mechanical ventilation, blood transfusion, additional antivenom and prolonged hospitalisation. TBAV was effective with excellent prognosis despite stated specificity for tiger and brown snake.

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Introduction Most cases of red-bellied black snake (RBBS) envenomation in dogs respond favourably to treatment comprising of tiger-brown snake antivenom (TBAV), intravenous fluid therapy, analgesia and, if indicated, mechanical ventilation and/or blood transfusion. However, there remains a subset of patients who develop fatal complications despite intensive treatment and risk factors for these occurring remain unknown. Here we present a retrospective crosssectional survey of 91 canine and feline RBBS envenomation cases.Methods Cases seen between June 2010 and June 2020 were retrieved from the databases of seven practices in South East and coastal Queensland. From the canine case population, logistic regression analysis was performed to assess the impact of potential risk factors at presentation on the likelihood of death. A final multivariable model was developed using a manual backwards elimination approach based on overall likelihood ratio tests and Wald chi-square P-values for each variable. Where model convergence failed due to quasicomplete separation, Firth's penalised maximum likelihood method was implemented. Such separation may occur when an outcome is completely predicted by an explanatory variable in one group. ResultsOf the 88 canine cases, 7 died (8.0%), all after prognosis-based euthanasia. Of the three feline cases, one died after unsuccessful resuscitation following cardiopulmonary arrest. Compared to survivors, dogs that died were older, exhibited pigmenturia, received antivenom later and had a higher total plasma protein (TPP), activated clotting time (ACT) and lower packed cell volume (PCV) at presentation.

Case report This case report describes the clinical signs and case management of a 1‐year‐old neutered male Siberian Husky that accidentally ingested 635 mg/kg of oral acetazolamide (a carbonic anhydrase inhibitor). The dog presented with severe tachypnoea due to the development of hyperchloraemic metabolic acidosis and associated hypokalaemia that persisted for 7 days. Clinical and biochemical changes resolved with intravenous and subsequent oral supplementation of sodium bicarbonate and potassium. Complete recovery occurred within 9 days of presentation. Conclusion To the authors' knowledge, this is the first case that reports overdosage of an oral carbonic anhydrase inhibitor in a dog and subsequent recovery with adequate supplementation and supportive care.