Dynamic exophthalmos and lateral strabismus in a dog caused by masticatory muscle myositis.

CASE DESCRIPTION: A 5.5-year-old neutered male mixed-breed dog was presented for evaluation of a 5-month history of deviation of the right globe upon opening the mouth and a 1-month history of conjunctivitis in the same eye. Clinical findings, diagnostic imaging results, treatment and follow-up are described. CLINICAL FINDINGS: When the mouth was opened, the right globe deviated rostrally and laterally. There was no pain or resistance to opening the mouth, or resistance to retropulsion of the globe. No other abnormalities were observed. Computed tomography was performed, revealing a contrast-enhancing region associated with the right masseter muscle impinging into the right orbit; this was more pronounced with the mouth open. Cytology revealed a small number of mildly to moderately atypical mesenchymal cells. Histopathology was consistent with polyphasic myositis, with a predominance of lymphocytes and plasma cells. No infectious agents were identified. Serum antibody titers for Toxoplasma gondii and Neospora caninum were negative. Serum titers for 2 M antibody were positive at 1:500, consistent with a diagnosis of masticatory muscle myositis. TREATMENT AND OUTCOME: Therapy with prednisone was initiated. During a follow-up period of 5 months, there was no recurrence of clinical signs, and the dose of prednisone was reduced by 25%. CLINICAL SIGNIFICANCE: To the authors' knowledge, this is the first reported case of masticatory muscle myositis causing dynamic exophthalmos and strabismus in a dog.

Mucopolysaccharidosis type VI in a juvenile miniature schnauzer dog with concurrent hypertriglyceridemia, necrotizing pancreatitis, and diabetic ketoacidosis.

A 7-month-old, neutered male miniature schnauzer dog with a history of cryptorchidism and umbilical hernia was referred for diabetic ketoacidosis. Clinical evaluation revealed stunted growth, skeletal abnormalities, hypertriglyceridemia, diabetic ketoacidosis, and acute necrotizing pancreatitis. Further testing was diagnostic for mucopolysaccharidosis type VI causing the stunted growth and skeletal deformities, but no connection between mucopolysaccharidosis type VI, hypertriglyceridemia, and pancreatic diseases was found.

Mucopolysaccharidose de type VI chez un jeune chien Schnauzer miniature atteint d'hypertriglycéridémie, de pancréatite nécrosante et d'acidocétose diabétique concomitantes. Un chien Schnauzer miniature castré âgé de 7 mois avec une anamnèse de cryptorchidie et d'hernie ombilicale a été référé pour une acidocétose diabétique. L'évaluation clinique a révélé une croissance arrêtée, des anomalies squelettiques, l'hypertriglycéridemie, l'acidocétose diabétique et une pancréatite nécrosante aiguë. Des tests supplémentaires ont permis de diagnostiquer une mucopolysaccharidose de type VI causant une croissance arrêtée et des difformités squelettiques, mais aucun lien avec la mucopolysaccharidose de type VI, l'hypertriglycéridémie et les maladies pancréatiques n'a été trouvé.(Traduit par Isabelle Vallières).

Partial cytogenetic response with toceranib and prednisone treatment in a young dog with chronic monocytic leukemia.

Treatment of chronic monocytic leukemia (CMoL) in dogs has traditionally consisted of hydroxyurea. The use of tyrosine kinase inhibitors has been proposed as a treatment option for dogs with CMoL but has never been reported. We report a case of CMoL in a young dog that achieved clinical remission with treatment with the tyrosine kinase inhibitor toceranib and prednisone.

A retrospective evaluation of coral snake envenomation in dogs and cats: 20 cases (1996-2011).

OBJECTIVE: To describe the clinical signs, treatment, and outcomes of dogs and cats following envenomation by the eastern coral snake and to report our clinical experience with the use of Coralmyn. DESIGN: Retrospective study (1996-2011). SETTING: University teaching hospital. ANIMALS: Sixteen dogs and 4 cats with eastern coral snake envenomation. MEASUREMENTS AND MAIN RESULTS: Medical records meeting the study inclusion criteria were reviewed and evaluated for signalment, date and time of the snake encounter, elapsed time between encounter and hospital examination, initial physical examination findings, antivenom type, length of hospitalization, and outcome. Initial physical examination findings included: quiet mentation, tetraparesis, ptyalism, tachypnea, abdominal breathing, shallow breathing, decreased to absent gag reflex, ataxia, muscle fasciculations, and decreased spinal reflexes. Laboratory findings in dogs included proteinuria, bilirubinuria, hemeproteinuria, increased aspartate aminotransferase activity, increased alanine aminotransferase activity, and hemolysis. Four dogs and 2 cats received Coralmyn and 4 dogs received North American Coral Snake Antivenom. Adverse reaction to antivenom was suspected in 1 dog that received North American Coral Snake Antivenom. Eight of 11 envenomated dogs survived with a median length of hospitalization of 4.5 days. Two of 3 envenomated cats survived with a median length of hospitalization of 4 days. Two dogs were euthanized, 1 dog suffered acute respiratory arrest, and 1 cat developed tachycardia that progressed to pulseless electrical activity. Five dogs and 1 cat in the encounter group survived to discharge. CONCLUSIONS: Diagnosis of eastern coral snake envenomation is likely in the dog that has concomitant lower motor neuron neuropathy, bulbar palsy, and hemolysis. Early diagnosis is crucial as antivenom administration can reduce morbidity. Prognosis is considered good with 71% of the envenomated patients in this study surviving to discharge. Supportive care that may include ventilator assistance and antivenom administration are the mainstays of therapy.