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ABSTRACT. A large subcutaneous mass at the left cervical site in a 9-year-old male Siberian husky was removed surgically. Histopathologically, the mass was mainly consisted of a proliferation of spindle-shaped neoplastic cells arranging in solid sheath and partially vascular channels containing few blood cells. The tumor cells exhibited highly invasive activity to the surrounding tissues. In a ddition, the tumor cells were immunopositive for Factor VIII-related antigen. On the basis of these findings, the tumor was diagnosed as lymphangiosarcoma. Recurrent mass was noticed 3 weeks after surgery but completely disappeared after the doxorubicin treatment. Neither recurrence nor metastasis was observed for 9 months after the remission.

Background: GM2 gangliosidosis variant 0 (human Sandhoff disease) is a lysosomal storage disorder caused by deficiencies of acid b-hexosaminidase (Hex) A and Hex B because of an abnormality of the b-subunit, a common component in these enzyme molecules, which is coded by the HEXB gene.Objective: To describe the clinical, pathological, biochemical, and magnetic resonance imaging (MRI) findings of Sandhofflike disease identified in a family of Toy Poodles.Animals: Three red-haired Toy Poodles demonstrated clinical signs including motor disorders and tremor starting between 9 and 12 months of age. The animals finally died of neurological deterioration between 18 and 23 months of age. There were some lymphocytes with abnormal cytoplasmic vacuoles detected.Methods: Observational case study.Results: The common MRI finding was diffuse T2-hyperintensity of the subcortical white matter in the cerebrum. Bilateral T2-hyperintensity and T1-hypointensity in the nucleus caudatus, and atrophic findings of the cerebrum and cerebellum, were observed in a dog in the late stage. Histopathologically, swollen neurons with pale to eosinophilic granular materials in the cytoplasm were observed throughout the central nervous system. Biochemically, GM2 ganglioside had accumulated in the brain, and Hex A and Hex B were deficient in the brain and liver. Pedigree analysis demonstrated that the 3 affected dogs were from the same family line.Conclusions and Clinical Importance: The Sandhoff-like disease observed in this family of Toy Poodles is the 2nd occurrence of the canine form of this disease and the 1st report of its identification in a family of dogs.

The authors herein describe the morphologic and immunohistochemical features of normal Merkel cells as well as the clinicopathologic findings of Merkel cell carcinoma in cats. Merkel cells were characterized as vacuolated clear cells and were individually located in the epidermal basal layer of all regions examined. Clusters of Merkel cells were often observed adjacent to the sinus hair of the face and carpus. Immunohistochemically, Merkel cells were positive for cytokeratin (CK) 20, CK18, p63, neuron-specific enolase, synaptophysin, and protein gene product 9.5. Merkel cell carcinoma was detected as a solitary cutaneous mass in 3 aged cats (13 to 16 years old). On cytology, large lymphocyte-like cells were observed in all cases. Histologic examinations of surgically resected tumors revealed nests of round cells separated by various amounts of a fibrous stroma. Tumor cells were commonly immunopositive for CK20, CK18, p63, neuron-specific enolase, and synaptophysin, representing the characteristics of normal Merkel cells. 29 Merkel cells are located in the hair discs (Haarscheiben), hair follicles, interfollicular epidermis, and glabrous skin in humans. 20,21 However, a previous study reported that Merkel cells were absent in hair follicles in the body skin of mice and present only in the epidermal hair discs and whisker hair follicles.20 Most Merkel cells possess synaptic connections with the enlarged terminal endings of myelinated sensory nerve fibers. Neurotransmitters or neuromodulators are secreted from Merkel cells through exocytosis in response to mechanical stimuli to the skin, thereby suggesting a function of Merkel cells as a mechanoreceptor of tactile sensation. 10,12 Difficulties have been associated with identifying Merkel cells on routine hematoxylin and eosin (HE)-stained sections. 20Merkel cells express various neuropeptides and neuroendocrine markers, such as neuron-specific enolase (NSE), chromogranin A, synaptophysin, and protein gene product 9.5 (PGP9.5) in humans, making them identifiable by immunohistochemistry. 7,9,17,24 Cytokeratin (CK) 20 is assumed to be the most specific marker for Merkel cells in the skin of humans and mice. 5In humans, CK20-positive Merkel cells are distributed in the palms and hairy skin of embryos and fetuses and in the ventral midline of adults (the incision line of a routine autopsy). 14,20 To the best of our knowledge, the presence and distribution of CK20-positive Merkel cells have not yet been examined in normal cat skin.Merkel cell carcinoma is a rare cutaneous tumor showing both epithelial and neuroendocrine differentiation. Although Merkel cell carcinoma is considered to arise from Merkel cells, recent findings indicated that primitive epidermal stem cells or early B cells were the origin of Merkel cell carcinoma. 13,27,30 Only 3 cases of feline Merkel cell carcinoma have been reported to date and were diagnosed by examining biopsy samples. Two cases were accompanied by pulmonary and lymph node metastases showing malignant behaviors, 22,23 while the

ABSTRACT. Neuroaxonal dystrophy (NAD) was examined in two Papillon dogs and a mix breed dog between Papillon and Chihuahua. In addition, cerebellar cortical abiotrophy (CCA) in a Papillon dog, which had similar clinical and magnetic resonance imaging (MRI) features to those of NAD, was also investigated. The common clinical symptoms of all dogs affected with NAD and CCA, were pelvic limb ataxia and cerebellar ataxia including intention tremor, head tremor, and hypermetria in the early onset. These clinical signs were progressed rapidly, and two dogs with NAD were euthanized by owner's request and the other two were died by aspiration pneumonia. MRI examinations and gross observations at necropsy revealed moderate to severe cerebellar atrophy in all cases of NAD and CCA. The most typical histological change of NAD was severe axonal degeneration with marked spheroid-formation in the dorsal horn of the spinal cords, the nuclei gracilis, cuneatus, olivalis and its circumference in the medulla oblongata. The spheroids were characterized as large eosinophilic or granular globes within the enlarged myelin sheaths, sometimes accompanied by moderate accumulation of microglias and/ or macrophages. In contrast, such spheroid formation was minimal in the brain of CCA. In the cerebellum, mild to moderate loss of the Purkinje and granular cells were recognized in three dogs with NAD, whereas these changes were more prominent in a dog with CCA. Although the clinical signs and MRI findings relatively resembled between NAD and CCA, the histopathological features considered to be quite differ, suggesting distinct pathogenesis and etiology. Since both NAD and CCA are proposed as the autosomal recessive hereditary disorders, careful considerations might be needed for the breeding of Papillon and Chihuahua dogs.