A neurological presentation caused by brain metastases in a dog with interventricular septal hemangiosarcoma.

BACKGROUND: Brain metastases are well known for disseminated hemangiosarcoma involving the right atrium/auricle. CASE REPORT: An 8-year-old male Australian Shepherd Dog presented with a 3-day history of circling to the left. A neurological examination revealed obtunded mentation, right hemi-inattention, bilateral strabismus towards the left side and absent physiological nystagmus. In addition, the dog had muffled heart sounds on auscultation and exercise-induced weakness. Laboratory findings included hypercoagulability and marked elevation in the C-reactive protein concentration. Electrocardiography detected a sinus rhythm with right bundle-branch block and ventricular bigeminy. Echocardiography revealed an extensive interventricular septal mass. Due to the grave prognosis, the owners elected for euthanasia, and a complete necropsy was performed. The main pathological findings were an interventricular septal and left ventricular hemangiosarcoma, with metastases in the brain, lungs, spleen and adrenal glands. No evidence of tumour infiltration was found in the right atrium. CONCLUSION: To the authors' knowledge, this is the first report of neurological signs due to confirmed brain metastases in a dog with interventricular septal hemangiosarcoma. Although the right atrium is the main location for cardiac hemangiosarcoma, the interventricular septum should be evaluated in all cases.

Obstructive shock caused by right atrial thrombosis secondary to malignant pheochromocytoma in a dog.

BACKGROUND: Obstructive shock can be caused by any lesion leading to extraluminal compression or intraluminal occlusion of the cardiac chambers or major vessels. CASE REPORT: A 12-year-old, male castrated, Border Collie cross dog presented to a veterinary teaching hospital for collapse. A physical examination revealed severe vasoconstrictive shock and abdominal distension. Abnormalities on blood tests were consistent with systemic hypoperfusion. Cardiac underfilling, hepatomegaly with distended vasculature and ascites were identified by focused ultrasonography, raising suspicion of obstructive shock. This was supported by the radiographic findings of microcardia and a distended caudal vena cava (CVC). There was transient response to fluid therapy for blood volume expansion. Repeat focused ultrasonography during rapid intravenous fluid administration identified a right intra-atrial mass, assessed as likely to be causing obstruction of venous return. The dog was humanely euthanased given the guarded prognosis. At postmortem evaluation, a malignant pheochromocytoma in the left adrenal gland with tumour thrombus extending to the tricuspid valve through the CVC was found. The extensive thrombus caused the obstructive shock in this case. Metastasis in a peripheral lymph node and neoplastic emboli in the heart and lungs were also visible at the histopathological evaluation. CONCLUSION: To the best of authors' knowledge, this is the first report of severe obstructive shock secondary to extension of caval tumour thrombus into the right atrium in a dog with malignant pheochromocytoma. Tumour thrombus from a malignant pheochromocytoma should be included as a differential diagnosis of obstructive shock, with or without a visible right intra-atrial mass, in dogs. Serial focused ultrasonography during intravenous fluid administration can aid diagnosis.

Long-term neurologic and cardiac correction by intrathecal gene therapy in Pompe disease.

Pompe disease is a lysosomal storage disorder caused by acid-α-glucosidase (GAA) deficiency, leading to glycogen storage. The disease manifests as a fatal cardiomyopathy in infantile form. Enzyme replacement therapy (ERT) has recently prolonged the lifespan of these patients, revealing a new natural history. The neurologic phenotype and the persistence of selective muscular weakness in some patients could be attributed to the central nervous system (CNS) storage uncorrected by ERT. GAA-KO 6neo/6neo mice were treated with a single intrathecal administration of adeno-associated recombinant vector (AAV) mediated gene transfer of human GAA at 1 month and their neurologic, neuromuscular, and cardiac function was assessed for 1 year. We demonstrate a significant functional neurologic correction in treated animals from 4 months onward, a neuromuscular improvement from 9 months onward, and a correction of the hypertrophic cardiomyopathy at 12 months. The regions most affected by the disease i.e. the brainstem, spinal cord, and the left cardiac ventricular wall all show enzymatic, biochemical and histological correction. Muscle glycogen storage is not affected by the treatment, thus suggesting that the restoration of muscle functionality is directly related to the CNS correction. This unprecedented global and long-term CNS and cardiac cure offer new perspectives for the management of patients.

Necrotizing Meningoencephalitis in a Captive Black and White Ruffed Lemur (Varecia variegata variegata) Caused by Acanthamoeba T4 Genotype.

A mature male, black and white ruffed lemur (Varecia variegata variegata) died in a zoological garden after a 4-day history of lethargy and non-responsive convulsions. Necropsy and histopathological examinations revealed acute necrotizing and haemorrhagic meningoencephalitis with intralesional amoebas confirmed by immunohistochemistry. Acanthamoeba T4 genotype was identified as the causative agent of the brain lesion, based on amplification and sequencing of 18S ribosomal RNA genes. The presence of free-living amoebas in water and mud from the lemur's environment was investigated by morphological and molecular analyses. The two predominant genera, representing 80% of isolated amoebas, were Naegleria spp. and Acanthamoeba spp. All Acanthamoeba isolates belonged to the T4 genotype. To the author's knowledge, this is the first report of a meningoencephalitis due to Acanthamoeba T4 genotype in Lemuridae with concurrent analysis of pathological tissues and environment.