SnakeMap: four years of experience with a national small animal snake envenomation registry.

SnakeMap is a national cloud-based, veterinary snakebite registry. It was designed to prospectively collect data of the clinical circumstances and temporospatial information on cases of snake envenomation in dogs and cats. We herein introduce the project and summarise the data from the first 4 years of SnakeMap. The registry is a veterinary community-based online database allowing case entry from veterinary hospitals across Australia. Registry data comprise hospital characteristics, patient characteristics, envenoming snake type, treatment and outcome variables, including time and geolocation of the snake bite. We present summative information on select key variables from the SnakeMap registry (1 July 2015 to 30 June 2019). Twenty-eight hospitals from 6 states/territories entered 624 cases into the registry, including 419 dogs (67%) and 205 cats (33%). Bite time was available in 216 animals of which 90 (42%) were reported to be bitten in the 3 hours between 03:00 pm and 05:59 pm; median bite to presentation interval was 60 (interquartile range [IQR] 30, 211) minutes in dogs and 95 (IQR 41, 238) minutes in cats. Bites occurred in the owner's yard in 356 dogs (85%) and 53 cats (26%). A snake venom detection kit was used in 172 cases (28%) and antivenom was administered in 523 cases (85%). Most animals (n = 534, 88%) survived to discharge (median hospitalisation of 25 [IQR 16, 62] hours). SnakeMap effectively collects relevant clinical data from dogs and cats with presumed snake bite and provides locally specific information on the epidemiology of snake envenomation in small animals.

Tiger snake (Notechis scutatus) envenomation in a horse.

BACKGROUND: A 7-year-old Thoroughbred gelding presented with muscle fasciculation, reluctance to move, profuse sweating, tachycardia, tachypnoea and a localised, unilateral swelling on the muzzle. History and physical examination were suggestive of snake envenomation. METHODS: A sandwich ELISA for the detection of snake venom was performed on serum and urine samples. RESULT: The test performed on urine confirmed a diagnosis of tiger snake envenomation. CONCLUSION: The response to treatment with antivenom and supportive medical therapy was excellent.

Aplysia gigantea toxicosis in 72 dogs in Western Australia.

OBJECTIVES: This study aimed to: (1) confirm a temporal association between exposure to the sea hare Aplysia gigantea and the development of a neurotoxicosis in dogs and (2) further characterise the clinical signs, treatment and outcomes in dogs with this suspected toxicosis. METHODS: The medical records from four veterinary practices within the Geraldton region of Western Australia were searched for dogs that had been exposed to A. gigantea and subsequently presented to a veterinarian during the period of January 2001 to March 2011. Signalment, exposure history, clinical signs, treatment and outcome were recorded. RESULTS: In total, 72 dogs met the inclusion criteria. Clinical signs included ptyalism, emesis, ataxia, hyperaesthesia, tremors, muscle fasciculations, seizures, nystagmus and respiratory distress; 30 dogs did not have abnormal clinical signs at presentation; 69 dogs were presented during January to April. Treatment included gastrointestinal and dermal decontamination, and supportive management of seizures, tremors and muscle fasciculations. Of the 72 dogs, 65 survived to discharge, 4 died and 3 were euthanased. Information from subsequent examinations was available for 57 dogs and no long-term complications were reported. CONCLUSIONS: Exposure to A. gigantea was temporally associated with the development of neuroexcitatory clinical signs in dogs. Gastrointestinal and respiratory signs also occurred in some dogs. Dogs with suspected toxicosis were presented mostly in the months of January to April. The proportion of dogs that died or were euthanased because of worsening clinical signs was approximately 10%.

Histopathological analysis and in situ localisation of Australian tiger snake venom in two clinically envenomed domestic animals.

OBJECTIVE: To assess histopathological changes in clinically envenomed tiger snake patients and identify tissue specific localisation of venom toxins using immunohistochemistry. SAMPLES: One feline and one canine patient admitted to the Murdoch Pet Emergency Centre (MPEC), Murdoch University with tiger snake (Notechis sp.) envenoming. Both patients died as a result of envenomation. Non-envenomed tissue was also collected and used for comparison. METHODOLOGY: Biopsy samples (heart, lung, kidney andskeletal muscle tissue) were retrieved 1-2 h post death and processed for histopathological examination using Haemotoxylin and Eosin, Martius Scarlet Blue and Periodic Acid Schiff staining. Tissues were examined by light microscopy and tissue sections subjected to immunohistochemical staining using in-house generated monoclonal and polyclonal antibodies against Notechis venoms. RESULTS: Venom-induced pathological changes were observed in the lungs, kidneys and muscle tissue of both patients. Evidence, not previously noted, of procoagulant venom effects were apparent, with formed thrombi in the heart, lungs (small fibrillar aggregates and larger, discrete thrombi) and kidneys. Immunohistochemical assays revealed venom present in the pulmonary tissue, in and around the glomerular capsule and surrounding tubules in renal tissue and scattered throughout the Gastrocnemius muscle tissue. CONCLUSION: This work has shown pathological evidence of procoagulant venom activity supporting previous suggestions that an initial thrombotic state occurs in envenomed patients. We have shown that venom toxins are able to be localised to specific tissues, in this case, venom was detected in the lung, kidney and muscle tissues of clinically envenomed animals. Future work will examine specific toxin localisation using monoclonal antibodies and identify if antivenom molecules are able to reach their target tissues.

Prospective determination of the specificity of a commercial snake venom detection kit in urine samples from dogs and cats.

OBJECTIVE: To determine the specificity of a snake venom detection kit in urine samples from dogs and cats presenting to a referral centre for diseases unrelated to snake envenomation. DESIGN: Urine was collected from 50 dog and 25 cats presented for investigation and treatment of diseases unrelated to snake envenomation. Urine was collected as a voided sample, by cystocentesis or by catheterisation, and routine urinanalysis was performed. Snake venom testing was performed within 2 h of collection using a commercially available snake venom detection kit, which was observed continuously during the 10-min colour reaction phase for evidence of a visible colour indicating a positive test. RESULTS: No false-positive reactions occurred in any sample analysed. CONCLUSION: The snake venom detection kit appears to have 100% specificity for using urine as a test sample.

Toxicity in three dogs from accidental oral administration of a topical endectocide containing moxidectin and imidacloprid.

Three dogs were presented with a history of oral administration of a topical endectocide containing imidacloprid and moxidectin. They were diagnosed with imidacloprid and moxidectin intoxication, having ingested doses ranging from 7.5 to 1.4 mg/kg of imidacloprid and 1.9 to 2.8 mg/kg of moxidectin. The three dogs were affected to different degrees of severity, but all displayed signs of ataxia, generalised muscle tremors, paresis, hypersalivation and disorientation. Temporary blindness occurred in two cases. The three dogs were tested for the presence of the multi-drug resistance 1 gene deletion, which can cause an increased sensitivity to the toxic effects of moxidectin, and were found to be negative. Treatment included gastrointestinal decontamination, intravenous fluid therapy and benzodiazepines to control muscle tremors. All three dogs made a complete recovery within 48 h of ingestion.

Activated coagulation times in normal cats and dogs using MAX-ACT tubes.

OBJECTIVE: To establish reference values for activated coagulation time (ACT) in normal cats and dogs, by visual assessment of clot formation using the MAX-ACT(TM) tube. SUBJECTS: We recruited 43 cats and 50 dogs for the study; 11 cats and 4 dogs were excluded from the statistical analysis because of abnormalities on clinical examination or laboratory testing including anaemia, prolonged prothrombin time (PT) or activated partial thromboplastin time (APTT), or insufficient plasma volume for comprehensive laboratory coagulation testing. PROCEDURE: Blood samples were collected via direct venipuncture for MAX-ACT, packed cell volume/total solids, manual platelet estimation and PT/APTT measurement. Blood (0.5 mL) was mixed gently in the MAX-ACT tube at 37 degrees C for 30 s, then assessed for clot formation every 5 to 10 s by tipping the tube gently on its side and monitoring for magnet movement. The endpoint was defined as the magnet lodging in the clot. The technique was tested with 10 dogs by collecting two blood samples from the same needle insertion and running a MAX-ACT on each simultaneously. RESULTS: In normal cats the mean MAX-ACT was 66 s (range 55-85 s). In normal dogs the mean was 71 s (range 55-80 s). There was no statistical difference between the first and second samples collected from the same needle insertion. CONCLUSIONS: and Clinical Relevance In both cats and dogs, a MAX-ACT result >85 s should be considered abnormal and further coagulation testing should be performed. Additionally, failure to discard the first few drops of the sample does not appear to significantly affect results.

Extradural haematoma secondary to brown snake (Pseudonaja species) envenomation.

A 4-year-old Siberian Husky dog was treated with brown snake antivenom by his regular veterinarian after a witnessed episode of brown snake envenomation. The dog was discharged 5 hours post presentation despite an ongoing coagulopathy. The dog was presented to the emergency centre 2 hours later because the owner believed the dog to be in pain. Initial examination revealed an ambulatory but neurologically normal patient with thoracolumbar pain and laboratory evidence of a coagulopathy. Despite correction of the coagulopathy, the signs progressed to bilateral hind limb paresis after approximately 3 hours of hospitalisation, and continued to deteriorate over the next 56 hours to loss of deep pain perception in the right hind limb. Computed tomography imaging identified the presence of an extradural haematoma which was subsequently removed via a hemilaminectomy. Surgical decompression was successful in treating the spinal compression and the dog recovered with minimal complications. To our knowledge this is the first report of extradural haematoma secondary to coagulopathy induced by brown snake envenomation.

Four cases of snake envenomation responsive to death adder antivenom.

Death adder envenomation is rare in humans and there is only one brief report previously in dogs. This paper details three cases of canine common death adder (Acanthophis antarcticus) envenomation and one case of bardick (Echiopsis curta) envenomation which were responsive to death adder antivenom. The available literature on death adder envenomations is also reviewed. The main clinical sign in the four dogs was severe lower motor neuron paralysis. There was no clinical evidence of coagulopathy or myopathy. Use of a snake venom detection kit was essential for selection of appropriate antivenom. Death adder and bardick envenomation in dogs potentially has a good prognosis if sufficient antivenom is administered and intensive supportive care is available.

Influence of oral antioxidants on ultraviolet radiation-induced skin damage in humans.

Ultraviolet radiation (UVR) causes a range of acute and chronic adverse cutaneous effects, in addition to some beneficial effects. In present times, the skin is generally exposed to higher levels of UVR, such that inherent defence mechanisms become overwhelmed. Complications, notably skin malignancies, show a serious rise in incidence. Since many effects of UVR are mediated through generation of reactive oxygen species, antioxidant supplementation provides a strategy to combat their excess generation, and hence reduce the clinical consequences. Human supplementation studies examining the potential of a range of oral agents to protect against UVR-induced skin effects show mixed results; further studies should examine whether certain subgroups of the population may show augmented benefit.