Factor IX deficiency in an Alaskan Malamute

Factor IX deficiency, consistent with hemophilia B, was detected in a 6-month old male Alaskan Malamute with a 2-week history of persistent oozing from an oral wound. Laboratory studies disclosed an intrinsic coagulation defect. Hemophilia A was initially suspected. Further evaluation demonstrated normal factor VIII activity and factor VIII-related antigen, but factor IX activity was only 1.3% of normal.     

Renal failure and hyperparathyroidism in an Alaskan Malamute pup

In a 5-month-old male Alaskan Malamute, clinicopathologic and radiographic findings supported a diagnosis of renal failure and hyperparathyroidism. At necropsy, the parathyroid glands were enlarged and the kidneys were shrunken and irregular. The histopathologic findings were consistent with the diagnosis of logic findings were consistent with the diagnosis of terminal renal failure and hyperparathyroidism. Based on the history, a heritable disorder was suspected.     

Subacute necrotising encephalopathy in an Alaskan husky

A 29-month-old female Alaskan husky was presented recumbent, tetraparetic and in a state of dementia, with blindness and cranial nerve deficits. The dog's progress was followed for over two months, as the signs resolved to an non-progressive mild hypermetria with slight proprioceptive ataxia, a diminished menace response and inability to prehend food. Magnetic resonance imaging (MRI) revealed bilateral cavitation extending from the thalamus to the medulla, with less pronounced degenerative lesions in the caudate nucleus, putamen and claustrum. Cerebrospinal fluid lactate and pyruvate concentrations were in their normal ranges. Necropsy and histological examination confirmed the MRI findings as well as neuronal degeneration of the cerebellar cortex in the vermis and degenerative changes in the neocortex at the depths of the cerebral sulci. In view of the similarity of lesions to subacute necrotising encephalomyelopathy, known as Leigh's disease in humans, a tentative diagnosis of a mitochondrial encephalopathy was made.     

Combined surgical and radiotherapy treatment of a mandibular ameloblastic carcinoma in a pony

A 9‐year‐old Welsh Section D gelding was referred to an equine hospital for evaluation and computed tomographic (CT) imaging of a left mandibular swelling. An expansile mass, found within the left mandible at the level of the caudal 2 cheek teeth, was surgically debulked and histology of the lesion identified it as an ameloblastic carcinoma. Radiotherapy using 4 fractions of 800 cGy, 7 days apart, was subsequently undertaken. The pony made excellent clinical progression following treatment. Repeat CT imaging at 7.5 and 19.5 months post surgery showed no apparent recurrence of the lesion and marked improvement in the remodelling of the mandible. In conclusion, radiotherapy in conjunction with surgical debulking appears to have been successful in treating an ameloblastic carcinoma in this pony and could be considered for similar tumours in other cases.     

Hereditary encephalomyelopathy and polyneuropathy in an Alaskan husky

An Alaskan husky puppy was examined for a neurologic disease which began at six weeks of age with generalised paresis that progressed resulting in recumbency by 18 weeks. Thoracic limbs primarily exhibited lower motor neuron signs that included distal muscle atrophy and persistent elbow and carpal flexion that resisted manual extension. Pelvic limb signs primarily exhibited upper motor neuron and general proprioceptive deficits, but also included lower motor neuron signs. Abnormal vocalisation suggested a laryngeal paresis. Histopathologic lesions included a diffuse axonopathy and secondary demyelination in the nerves of the limbs and larynx and a similar bilaterally symmetrical degeneration in the spinal cord white matter suggestive of a dying back axonopathy. In addition, a degenerative process was present in nuclei in the brain stem and cerebellum. Recognition of this disease through clinical and pathologic examination in other related Alaskan Huskies suggested an autosomal recessive inherited disorder.     

Surgical treatment of a mandibular ameloblastic carcinoma with metastases to the mandibular lymph nodes in a pony

A 4-year-old Connemara filly was presented with a rapidly growing oral mass on the right rostrolateral mandible and a right mandibular lymphadenopathy. Radiographs of the rostral mandible revealed a lytic, infiltrative mass consistent with soft tissue and mineralised material, and displacement of tooth 403. A biopsy showed characteristic histopathological features of an ameloblastic carcinoma. Subsequent FNA of the right abnormally firm and enlarged mandibular lymph node confirmed the metastatic spread. Computed tomography of the head was performed for surgical planning, including sentinel lymph node mapping to rule out other lymph node involvement. An aggressive lesion, consistent with soft tissue of the rostral right mandible was identified with intralesional contrast injection showing drainage of contrast within the right mandibular lymph nodes (Sentinel node). Based on the infiltrative and destructive nature reported in ameloblastic carcinoma in humans, a rostral mandibulectomy was performed, along with complete mandibular lymphadenectomy. The horse recovered uneventfully from surgery. In the early post-operative period marked lymphoedema of the ventral mandibular region was observed, which resolved 4–5 days post-operatively. Optimal cosmesis was maintained post-operatively, and no recurrence has been observed to date – 12 months post-surgery.     

Endometrial Adenocarcinoma and Mucometra in a 6-year-old Alaska Malamute Dog

A 6-year-old female Alaska Malamute dog was presented for evaluation of abdominal enlargement referred by a local veterinarian. On the history, the owner complained of chronic abdominal enlargement initiated more than 4 months ago, reduced appetite, occasional vomiting and general dullness. He also complained of greenish mucous intermittent vaginal discharge starting 10 days ago. The bitch was chronically treated with medroxiprogesterone acetate. A laparatomy was performed and fluid in the abdomen was found and aspirated during the surgery. Also a very fluid-filled distended uterus and a mass in the distal part of the left uterine horn were found. The mass was encapsulated by the omentum, but areas of necrosis and calcification were identified. Histopathological diagnosis was endometrial adenocarcinoma.     

Maxillary bone epithelial cyst in an adult miniature schnauzer

Maxillary bone epithelial cyst is rare in dogs. A 5-year-old, spayed female miniature schnauzer developed a swelling below the nasal canthus of left eye. Plain radiograph demonstrated a 1.5 cm diameter of radiolucent lesion on the maxillary bone anteroventral to the eye, and contrast dacryocystorhinography confirmed an obstructed nasolarcrimal duct. The swelling showed poor response to antibiotic treatment but responded well to oral prednisolone. Exploratory surgery revealed a cyst-like structure filled with brown serous fluid. Histopathological examination of the removed cyst revealed a double cuboidal epithelial cyst. The dog recovered rapidly after surgery, and the swelling had not recurred for a 36-month follow-up. It is the first case of periorbital bone epithelial cyst reported in an adult miniature schnauzer.     

Surgical management of ameloblastic fibroma in the cat

A 14-month-old spayed female domestic short-haired cat was presented for evaluation of a rostral mandibular mass diagnosed from biopsy as an ameloblastic fibroma. Radiographs of the mandible demonstrated marked osteolysis and cortical expansion. A rostral mandibulectomy was performed extending from the caudal edge of the second premolar on the right side to the caudal edge of the canine tooth on the left side. Histological evaluation of the excised mass confirmed the diagnosis of ameloblastic fibroma. Follow-up evaluation at eight months revealed normal oral function with the exception of occasional saliva soiling of the chin. The owner was satisfied with the cosmetic result.     

Idiopathic Polyneuropathy in Alaskan Malamutes

Clinical and morphologic features of a progressive polyneuropathy in young mature Alaskan Malamutes are described. Clinical signs included progressive paraparesis, synchronous pelvic limb gait, exercise intolerance, hyperesthesia, hypore-flexia, muscle atrophy, and tetraplegia. Electromyographic testing revealed diffuse fibrillation potentials and positive sharp waves in limb muscles, especially in muscles below the elbow and stifle. Pathologic findings in skeletal muscles and peripheral nerves included neurogenic muscle atrophy, focal or diffuse loss of myelinated nerve fibers, myelinoaxonal necrosis, and variable demyelination or remyelination.
Ultrastructural changes included axonal degeneration, presence of numerous Büngner bands, and denervated Schwann cell subunits. The nature and distribution of abnormal electrophysiologic and pathologic findings were suggestive of a distal sensorimotor polyneuropathy, which we have termed idiopathic polyneuropathy of Alaskan Malamutes to distinguish this condition from hereditary polyneuropathy of Norwegian Alaskan Malamutes, last described in 1982.