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Abstract. A 6-year-old, 30-kg, female German Shepherd Dog, living in a leishmaniasis enzootic area, was presented with a severe rear limb motor disorder and a medical history of acute onset of fever. Routine hematology indicated neutrophilia. Spinal survey radiographs were consistent with osteomyelitis and discospondylitis. Because of the poor clinical prognosis and the painful nature of the lesions, the dog was euthanized at the owners' request. At necropsy, T13-L1 vertebrae had large areas of necrosis within the vertebral bodies. Histopathological findings were consistent with chronic, severe, fungal osteomyelitis and discospondylitis. Polymerase chain reaction identified Scedosporium apiospermum, a eutrophic filamentous fungus now recognized as an emerging agent of severe infections in immunosuppressed human patients.

A 2-year-old male ferret was presented with central nervous system signs. Computed tomography (CT) of the brain revealed a well-defined contrast-enhancing lesion on the rostral forebrain that appeared extraparenchymal. Surgical excision of the mass was performed and the ferret was euthanised during the procedure. Histopathology of the excised mass showed multiple meningeal nodular lesions with infiltrates of epithelioid macrophages, occasionally centred on degenerated neutrophils and surrounded by a broad rim of plasma cells, features consistent with pyogranulomatous meningitis. The histopathological features in this ferret were similar to those in cats with feline infectious peritonitis. Definitive diagnosis was assessed by immunohistochemistry, confirming a ferret systemic coronavirus (FSCV) associated disease. This is the first case of coronavirus granuloma described on CT-scan in the central nervous system of a ferret.

This report describes a spinal cord epidural and synovial lipomatosis in a 3‐year‐old neutered male Eurasian dog. This dog presented for ambulatory paraparesis and was previously treated with immunosuppressive dosages of prednisolone for 2 years. Computed tomography (CT) myelography and magnetic resonnance imaging (MRI) images identified dorsal compression of the thoraco‐lumbar spinal cord by hypertrophic epidural fat. Histological examination identified extensive well‐differentiated mature adipose tissue in the subepithelial area of the tarsal synovium. Prednisolone is a reported predisposing factor in humans with lipomatosis.

Liposarcomas are rare malignant tumors of the adipose tissue which are well described in humans and animals. Wide margin excision is the recommended treatment for these infiltrative, slow to metastasize tumors. Primary liposarcoma with ocular localization is a very rare tumor in humans, dogs and cats. This report describes, for the first time, a palpebral liposarcoma in a 18-month old guinea pig that presented with a large palpebral mass and purulent discharge in the right eye. The ophthalmic evaluation revealed a one-centimeter infiltrating subcutaneous mass within the upper eyelid, a severe chemosis and hyperhemia of the palpebral and bulbar conjunctiva of the right eye. Cytologic examination of the mass revealed only epithelial cells. Histologic examination interpreted the lesion as a xanthogranulomatous reaction possibly secondary to meibomian gland rupture or inflammation. One month later, the mass had increased in size and the animal had stopped eating. Euthanasia was performed and a large biopsy was submitted for another histological examination. Histopathology revealed polygonal to rounded cells with a large, empty intracytoplasmic vacuole, and an ovoid, eccentrically located nucleus. The histology was consistent with a well-differentiated liposarcoma. Given the unusual location, immunohistochemistry was performed to ascertain the mesenchymal nature of the neoplasm.

Background: Copper-associated hepatitis (CAH) is a well-documented chronic hepatic disease in dogs. In some breeds, the disease results from an inherited defect in copper metabolism. In others, it is unclear whether its acummulation is a primary or secondary condition. Reports of copper accumulation in dog breeds that are not genetically predisposed are increasing.Aim: To describe the epidemiology, clinical and laboratory findings, liver biopsy techniques, and treatment response in dogs with CAH.Methods: A retrospective study was performed, drawing upon medical records from CAH dogs at a Veterinary Referral Hospital in Paris, France. The diagnosis of CAH had been confirmed in these patients by positive rhodanine staining of hepatic tissue obtained through biopsy. Medical records were mined for the following data: age at presentation, sex, breed, chief presenting complaints, abdominal ultrasound (US) findings, and rhodanine staining pattern.Results: A total of 17 dogs were included in the study. Median age at presentation was 8-year old (4–11). No sex predisposition was found. Terriers (4/17) and German Shepherd Dogs (GSD, 3/17) were overrepresented. American Staffordshire Terriers and Beauceron had not previously appeared in case reports on CAH; two of each breed were identified in this study. Clinical signs of affected dogs were non-specific. An incidental identification of increased liverenzymes was observed in 5/17 dogs. A heterogeneous, mottled liver was frequently described (5/17) on abdominal US. Liver biopsies were performed by US-guided percutaneous approach in 10/17 dogs, laparoscopy and laparotomy in 6/17 and 1/17, respectively. The rhodanine staining pattern was centrilobular (zone 3) in 8/17 dogs and periportal (zone 1) in 3/17 dogs. The pattern was considered multifocal in 6/17 dogs.Conclusion: Increased liver enzymes may be the only clinical finding in dogs with copper-associated hepatitis, reflecting the silent progression of this disease. Centrilobular pattern of rhodanine staining was observed in the majority of cases suggesting the primary condition of the disease. Results of this study are consistent with the current literature, which reports that terriers and GSD are predisposed to CAH. This is the first  description of CAH in Beauceron and American Staffordshire Terrier dogs. Keywords: American Staffordshire Terrier, Beauceron, Copper-associated hepatitis, Liver biopsy, Rhodanine.

Abstract. A hepatic mass was identified in a 5-year-old, female mixed-breed cat that died spontaneously after a clinical history of progressive emaciation, ptyalism, and persistent coryza. At necropsy, a 7-cmdiameter, yellow-brown, firm, multilobulated tumor was identified in the liver. Microscopically, the mass consisted of neoplastic cells arranged in small, closely packed nests within a thin fibrovascular stroma. These cells were of medium sized and polygonal, with fine argyrophilic cytoplasmic granules. Nuclei were predominantly round with finely stippled chromatin and indistinct nucleoli. Mitotic figures were numerous. Immunohistochemically, most of the neoplastic cells were immunoreactive for chromogranin A, neuronspecific enolase (NSE), and cytokeratin AE1/AE3 and weakly labeled for synaptophysin. The tumor was negative for glial fibrillary acidic protein (GFAP), vimentin, and cytokeratins 5, 6, 8, and 17. Vascular emboli and intrahepatic micrometastasis were also identified with chromogranin A. All these features were consistent with a hepatic neuroendocrine carcinoma and emphasized the importance of using a panel of antibodies to diagnose such rare tumors.

Background: Gain-of-function mutations in KIT are driver events of oncogenesis in mast cell tumours (MCTs) affecting companion animals. Somatic mutations of KIT determine the constitutive activation of the tyrosine kinase receptor leading to a worse prognosis and a shorter survival time than MCTs harbouring wild-type KIT. However, canine MCTs carrying KIT somatic mutations generally respond well to tyrosine kinase inhibitors; hence their presence represents a predictor of treatment effectiveness, and its detection allows implementing a stratified medical approach. Despite this, veterinary oncologists experience treatment failures, even with targeted therapies whose cause cannot be elucidated. The first case of an MCT-affected dog caused by a secondary mutation in the tyrosine kinase domain responsible for resistance has recently been reported. The knowledge of this and all the other mutations responsible for resistance would allow the effective bedside implementation of a deeply stratified and more effective medical approach. Case presentation: The second case of a canine MCT carrying a different resistance mutation is herein described. The case was characterised by aggressive behaviour and early metastasis unresponsive to both vinblastine-and masitinib-based treatments. Molecular profiling of the tumoural masses revealed two different mutations; other than the already known activating mutation p.Asn508Ile in KIT exon 9, which is tyrosine kinase inhibitor-sensitive, a nearly adjacent secondary missense mutation, p.Ala510Val, which had never before been described, was detected. In vitro transfection experiments showed that the secondary mutation did not cause the constitutive activation by itself but played a role in conferring resistance to masitinib. Conclusions: This study highlighted the importance of the accurate molecular profiling of an MCT in order to improve understanding of the molecular mechanism underlying tumourigenesis and reveal chemoresistance in MCTs for more effective therapies. The detection of the somatic mutations responsible for resistance should be included in the molecular screening of MCTs, and a systematic analysis of all the cases characterised by unexpected refractoriness to therapies should be investigated in depth at both the genetic and the phenotypic level.