An 11 year old neutered female cat in good health, then started to vomit, became depressed and rapidly developed acute nystagmus extending to tetraparesis and death.
Example Histopathological Description:
In this transverse section of one half of the brain at the level of the thalamus and hippocampus there are multifocal, moderate to severe, haemorrhagic and malacic changes in the thalamic nuclei, and to a lesser extent the cerebrocortex. Pathological changes are confined to the grey matter. There are numerous haemorrhages in the thalamus and the surrounding grey matter is pale and vacuolated. Perivascular oedema is evident, along with erythrophagocytosis and the presence of a few Gitter cells in some perivascular spaces. Some affected vessels show endothelial hypertrophy and some of those severely affected have fibrinoid necrosis. There is mild diffuse gliosis in affected areas. Neuronal necrosis is present in the thalamus, cerebral cortex and in the hippocampus.
Polioencephalomalacia, subacute, multifocal, severe
Feline thiamine deficiency encephalopathy.
These lesions are typical of thiamine-deficiency encephalomalacia which is well recognised in Australia. However, other causes of polioencephalomalacia (e.g. endotoxaemia) cannot be completely excluded.
The absence of the characteristic pathological changes in feline cuterebriasis, as described by Williams et al (Vet Pathol 1998, 35:330), i.e. parasitic track lesions, cerebral infarction, subependymal rarefaction and gliosis, and subpial astrogliosis, mitigate against this possibility. Vascular thromboembolism is more typically associated with localised areas of haemorrhage and infarction than is present in this case. Trauma is unlikely due to the absence of meningeal haemorrhage and the distribution of lesions. Generalised ischaemia (e.g. anaesthetic accident during surgery) is possible – cerebrocortical malacia and hippocampal neural necrosis support the diagnosis but the history and presence of thalamic haemorrhage and malacia do not.
Intramural haemorrhage, fibrin and oedema in medium sized blood vessels in the thalamus, gliosis and the presence of a few Gitter cells, suggests a subacute rather than acute duration.
Tissue from an aged dog with a slow growing mass on the left elbow.
Example Histopathological Description
The section consists of a multi-lobulated, non-encapsulated mass containing a dense population of pleomorphic cells that range from polygonal to spindloid. Throughout there are mostly thin fibrovascular septa within the lobules. However, some of these bands have dense collagen and may represent the remnants of tendon tissue. Some scattered areas of reduced cell density have myxomatous or hyaline fibrillar matrix. There is evidence of clefting throughout, with the clefts lined by flattened cells. Where the tumour cells are arranged in dense sheets they are predominantly spindle-shaped with distinct cell borders, a small amount of eosinophilic cytoplasm and small, oval nuclei. In areas predominated by polygonal cells there is abundant matrix and cell nuclei are evenly spaced but occasionally arranged in chains and clusters. In some areas there is moderate anaplasia, with binucleated and multinucleated cells. In other foci there are larger epithelioid cells with round nuclei containing a large amount of pale cytoplasm which is often vacuolated. Mitotic figures occur at a rate of approximately 1 per 40x field of view. There are small foci of haemorrhage and necrosis scattered throughout. The neoplastic mass extends to the margins in this section.
Probable synovial cell sarcoma. However, articular histiocytic sarcoma is also possible – special staining is recommended to differentiate.
Both synovial cell sarcoma (SCS) and articular histiocytic sarcoma (AHS) have a poor prognosis if untreated. They are almost impossible to excise successfully. Hence, amputation of the limb is the usually performed. If special stains suggest a histiocytic sarcoma, then exploration beyond the regional lymph nodes for other neoplastic foci is also recommended.
The features that support a diagnosis of SCS/AHC in this case include the age of the dog, location, multinodular structure, presence of clefts, and presence of dense strands of collagen representing probable residual tendon. To favour SCS were the biphasic nature of the cell population, the absence of sheets of anaplastic histiocytes, occasional pockets of myxoid differentiation, foamy cytoplasm in some tumour cells, and low mitotic index.
The tumour cells in this case were not immunophenotyped by the contributing laboratory – being an archival case (1966), the options for immuno-staining were not available at the time. However, a number of studies since then have helped to characterise tumours of this type in dogs, and immuno-labelling is now readily available. A recent article by P Moore (‘A Review of Histiocytic Diseases of Dogs and Cats’, Veterinary Pathology 2014, 51(1):167-184) should be consulted.
The mass is either a SCS (arising from synovial fibroblasts) or an AHS (arising from interstitial dendritic cells). Immunophenotyping would differentiate these choices since the spectrum of histomorphology for each can overlap considerably. Moore offers valuable advice on the interpretation of a CD18 stain which can be conducted on formalin-fixed tissue.
There is also some morphological overlap between SCS and pleomorphic soft tissue sarcoma (see review by Dennis et al Vet Pathol 2011, 48:73-84); however, storiform patterns were not present in this mass. While it is possible for chondroid matrix to be minimal in anaplastic chondrosarcoma, there was little other than location to prompt this as a stand-alone diagnosis.