Spotted black snake (Pseudechis guttatus) envenomation in a maned wolf (Chrysocyon brachyurus).

Envenomation by a spotted black snake (Pseudechis guttatus), following multiple bites on the buccal mucosa of a captive maned wolf (Chrysocyon brachyurus), caused the animal's collapse, hemolysis, rhabdomyolysis, local tissue necrosis, hepatic and renal failure, and subsequent death. The wolf died despite intensive supportive care including antivenom administration, fluid support, and a blood transfusion. Gross necropsy findings included myocardial and intestinal hemorrhage, pulmonary congestion, hepatomegaly, and splenomegaly. Microscopic examination of formalin-fixed tissues demonstrated pulmonary and abdominal visceral hemorrhage, acute nephrosis with casts, multifocal hepatic necrosis, and splenic congestion.     

Intramyocardial haematoma causing right ventricular outflow obstruction after brown snake (Pseudonaja species) envenomation in a dog

A 15-month-old, male neutered Staffordshire Bull Terrier cross was presented to its referring veterinarian collapsed and agonal. He was immediately intubated, manually ventilated, and treatment commenced for presumptive snake envenomation with two vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial). The dog was transferred to a referral hospital intubated. Additional diagnostics performed following arrival at the referral hospital included a urine snake venom detection kit test, which was positive for brown snake immunotype. Three additional vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial) were administered until the dog was extubated and able to stand. Venom-induced consumptive coagulopathy (VICC) was diagnosed based on prolonged clotting times and scleral haemorrhage. Paroxysms of right ventricular outflow tract (RVOT) origin ventricular arrhythmias were treated with lignocaine and sotalol. Four days after presentation, a new-grade IV/VI systolic heart murmur was auscultated, prompting an echocardiogram. An anechoic and compartmentalised mass measuring 43 mm × 19 mm was visualized within the right ventricular wall at the RVOT, immediately adjacent to the pulmonic valve. The mass was causing a RVOT obstruction. Its appearance was suggestive of an intramyocardial haematoma, most likely secondary to VICC. The dog remained cardiovascularly stable, and treatment consisted of supportive care. Recheck echocardiograms at 2 and 7 weeks after discharge revealed progressive improvement of the intramyocardial mass and resolution of the associated heart murmur. Although intramyocardial haematomas are rare, it should be considered as a differential in dogs that develop a newly diagnosed heart murmur and/or cardiac arrhythmia following brown snake envenomation.     

Some toxicity thresholds for the clinical effects of common tiger snake (Notechis scutatus) envenomation in the dog

SUMMARY Common tiger snake (Notechis scutatus) venom was administered experimentally to dogs at doses from 0.25 lethal dose (LD) to 20 LD. Haemolysis and increased creatine kinase values occurred rapidly after injection of sublethal (subparalytic) doses, but the clotting time of blood was extended and blood became incoagulable only when dogs were dosed with 10 LD or more of venom. Haemolysis, although of a low threshold of toxicity, was not severe and should not greatly affect the lethality of the venom. Coagulopathy is a sign that the dog has been lethally envenomed and will need to be given antivenom if skeletal muscle paralysis is to be overcome.     

Vine snake (Thelotornis capensis) bite in a dog

A vine snake bite in a dog is reported. There was continued minor bleeding from the assumed nose bite site for 4 days. Currently manufactured snakebite antivenom is not effective against vine snake bites and treatment is supportive.     

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.     

Acute intrinsic renal failure and blood coagulation disorders after a snakebite in a dog

Acute intrinsic renal failure was diagnosed in a two-year-old, male, German shepherd dog following a Vipera aspis bite. Clinical signs included depression, hypersalivation, vomiting, tachypnoea, abdominal pain, splenomegaly, oliguria with haematuria and haemolysed serum. Leucocytosis with a shift to the left, thrombocytopenia, prolonged coagulation times (activated partial thromboplastin time, prothrombin time and thrombin time), hypofibrinogenaemia, azotaemia and hyposthenuria were the most prominent laboratory abnormalities. Histopathological evaluation of the kidneys showed a discrete glomerular hypercellularity, mesangial lysis and renal tubules filled with many hyaline casts and some necrotic cells.     

Toxoplasmosis in a red-bellied woodpecker (Melanerpes carolinus)

A red-bellied woodpecker (Melanerpes carolinus), clinically exhibiting intermittent seizures, was examined by the Southeastern Cooperative Wildlife Disease Study. Microscopically, the woodpecker had protozoal meningoencephalitis. Toxoplasma gondii was identified by immunohistochemistry and polymerase chain reaction. Sequence analysis of the SAG2 locus disclosed that the T gondii detected was the Type III genotype. This is apparently the first report of clinical neural toxoplasmosis in any species in the order Piciformes.     

Tumoral calcinosis in a dog with chronic renal failure

A 2-year-old male German shepherd dog in poor bodily condition was evaluated for thoracic limb lameness due to a large, firm mass medial to the left cranial scapula. Radiography revealed several large cauliflower-like mineralized masses in the craniomedial left scapula musculature, pectoral region and bilaterally in the biceps tendon sheaths. Urinalysis, haematology and serum biochemistry showed that the dog was severely anaemic, hyperphosphataemic and in chronic renal failure. The dog was euthanased and a full post mortem performed. A diagnosis of chronic renal failure with secondary hyperparathyroidism was confirmed. The mineralised masses were grossly and histopathologically consistent with a diagnosis of tumoral calcinosis. Tumoral calcinosis associated with chronic renal failure that does not involve the foot pads is rarely seen.     

Acute renal failure following Bull ant mass envenomation in two dogs

Acute renal failure was diagnosed in a German Short Haired Pointer bitch and a Kelpie cross-bred dog following envenomation by Bull ants. Both dogs had been tethered over a Bull ant nest and had experienced mass envenomation. There was local reaction at the envenomation sites and each dog had experienced vomiting that was poorly controlled by symptomatic therapy. Intensive treatment of renal failure was successful in the German Short Haired Pointer and the bitch remains well 19 months after envenomation. The Kelpie cross-bred deteriorated despite intensive treatment and was euthanased 36 hours after presentation. Necropsy examination revealed haemorrhage and necrosis of the small intestine and myocardium, bilateral nephrosis with tubular necrosis, and patchy haemorrhage of the lung alveoli, pancreas and adrenal cortices. Electron microscopy revealed necrosis of the small intestine and hydropic swelling of proximal renal tubules with necrosis of medullary tubules.     

Hemodialysis of a dog with acute renal failure

A dog with oliguric acute renal failure presumed to have been caused by ethylene glycol ingestion was treated by hemodialysis for 1 month. Hemodialysis was effective in controlling azotemia, hyperphosphatemia, and hyperkalemia when performed on a daily or alternate-day basis. The major complications during treatment were infection and severe weight loss. Serial renal biopsies disclosed a progression from initial acute tubular necrosis to severe diffuse interstitial fibrosis and mononuclear cell inflammation. Infection, cachexia, development of end-stage renal lesions, and terminal hyperkalemia contributed to the eventual death of the dog.     

Gentamicin-associated acute renal failure in the dog

Gentamicin-associated acute renal failure was diagnosed in 10 dogs. The disease was characterized by a poor prognosis and lengthy hospitalization. Hypoalbuminemia, disorders of potassium homeostasis, proteinuria, hematuria, and cylindruria were common during therapy for renal failure. Fever and dehydration were the most commonly identified potential predisposing factors.     

Elapid snake envenomation in dogs in New South Wales: a review

Elapid snake envenomation in dogs is a commonly occurring yet poorly described clinical entity. Twelve species of dangerously venomous elapid snakes are found in New South Wales that are capable of causing disease in dogs. Geographical distribution of these species varies, as does their venom composition and systemic envenomation syndromes produced in target species. Elapid venom may be divided into the components of prothrombin activating enzymes, lipases and peptidic neurotoxins. Each species of elapid snake may possess venom components that fit any or all of these classifications. The action of these venom components may result in neurotoxic (pre-synaptic and post-synaptic), haemotoxic (red-cell destruction and coagulation disturbance), cardiovascular, myotoxic and secondary nephrotoxic effects. Marked variability may occur in venom composition between and within snake species, resulting in varying toxicity between species and also potentially unreliable clinical syndromes following envenomation. The existence of certain components consistently within the venom of each snake species allows the broad definition of basic pathological processes and clinicopathological changes resulting from snake species-specific envenomation and these are discussed. Diagnosis of snake envenomation is unreliable if based on clinical signs alone and the use of these signs in conjunction with history, physical examination and laboratory investigation, including snake venom detection kits, is recommended. Treatment of systemic envenomation should be undertaken with initial effective first aid and subsequent administration of snake species-specific antivenom.     

Hemodialysis in a dog with acute renal failure from currant toxicity

A 3 1/2-year-old Labrador retriever being presented for acute onset vomiting and lethargy was diagnosed with acute renal failure (ARF). The dog had ingested dried currants, a type of raisin. Hemodialysis was successfully performed to treat the ARE Raisin toxicity can cause ARF and warrants early recognition and aggressive treatment.