The records of 75 dogs with fibrocartilaginous embolism of the spinal cord were evaluated retrospectively. The diagnosis was confirmed histopathologically in 21 dogs (group A) and remained suspected in 54 patients (group B). The two groups were compared. Particular emphasis was placed on the description of physiotherapy procedures, recovery rates and prognostic criteria. Results demonstrated that fibrocartilaginous embolism affected mainly middle-aged, large- or giant-breed dogs. Clinical signs were peracute in onset, non-progressive and often asymmetric. Cerebrospinal fluid analysis was normal in the majority of dogs. Intramedullary swelling was the only abnormality detected on myelograms of these patients. A positive correlation was found between a poor prognosis and the involvement of intumescences, symmetrical clinical signs and decreased deep pain sensation. However, physio/hydrotherapy instituted immediately after the diagnostic work-up seemed to have a major influence on the recovery rate.

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In this report we document the results of several independent studies testing the sensitivity, specificity and reliability of the Prionics Western blotting (PWB) procedure to detect bovine and ovine disease-specific, protease-resistant prion protein (PrP(Sc)). Validation of the technique was obtained by blind analysis of samples from cattle affected with bovine spongiform encephalopathy (BSE), clinically normal animals or cattle with neurological diseases unrelated to BSE. Overall, very high sensitivity, specificity and reliability was observed. It became clear that sampling of the correct brain region and the method used for protein extraction are important factors for correct diagnosis. Furthermore, we tested the usefulness of the PWB technique as an instrument for surveillance purposes. We analyzed animals from a culling scheme as well as older animals from abattoirs to determine the number of subclinical BSE cases detectable by histopathological examination, immunohistochemistry for PrP(Sc) and PWB. In both studies, BSE-affected animals with no overt clinical symptoms were detected. These results demonstrate the usefulness of the PWB procedure in surveillance systems serving as a rapid diagnostic tool to identify animals subclinically infected with BSE.

The clinical records of 38 cats (1985-1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age 35 months) and had either generalized or complex-partial seizures of acute onset and rapid progression. The seizures had a tendency to become recurrent and to present as clusters or even status epilepticus later in the course of the disease. Fourteen cats died spontaneously, and 24 were euthanized. Histopathologic examination revealed bilateral lesions restricted to the hippocampus and occasionally the lobus piriformis. The lesions seemed to reflect different stages of the disease and consisted of acute neuronal degeneration to complete malacia, affecting mainly the layer of the large pyramidal cells but sometimes also the neurons of the dentate gyrus and the piriform lobe. The clinical, neuropathologic, and epidemiologic findings suggest that the seizures in these cats were triggered by primary structural brain damage, perhaps resulting from excitotoxicity. The cause remains unknown, but epidemiologic analysis suggests an environmental factor, probably a toxin.

During the past six years these authors have observed a distinctive multifocal non‐suppurative necrotizing encephalitis in Yorkshire terriers. Histopathological findings were different from those in canine encephalitides of known and unknown causes. Clinically, the Yorkshire terriers presented primarily brain stem signs or evidence of cerebral involvement, including seizures. The course of the disease was mostly chronic and progressive. Protozoal, bacterial and mycotic organisms were not found on histopathological examinations. The morphology of the lesions was strongly suggestive of a viral aetiology. Immunocytochemistry as well as in situ hybridisation failed to provide evidence for canine distemper virus infection. Likewise, canine herpesvirus was not detected by immunocytochemistry. Other known canine encephalitides could be excluded on clinical and morphological grounds; however, certain similarities may exist to pug dog encephalitis.