Abstract. Two dogs with rapidly progressing paralysis had polyarteritis involving mediumsized to large arterioles and small arteries of the spinal meninges. Rupture of structurally weakened vessels caused massive hemorrhage with compression and infarction of the spinal cord. The cause of the vasculitis was not determined.There are few reports of spontaneously occurring disseminated necrotizing vasculitis involving the central nervous system of dogs [9, 201. Although it presumably is rare, its incidence and clinical significance have not been determined. We describe two dogs with severe neurologic disease resulting from necrotizing arteritis involving the spinal vasculature. Case HistoriesDog 1, a 10-month-old female Boxer, had been treated when 6 months old for demodicosis, which went into clinical remission. Three months later the dog developed a temperature of 41 O C and was treated for tonsillitis with penicillin, streptomycin, and antipyretics. Three weeks later, after apparent recovery, fever and tonsillitis recurred. Hematologic examination showed a mild leukocytosis and regenerative left shift. Despite therapy and tonsillectomy, the fever persisted. During the third succeeding week, the dog had pain in the region of the cervical and thoracic spine. She became paralyzed shortly thereafter and was killed and necropsied. Dog 2, a 4-month-old Labrador Retriever referred to in a previous paper [20], had fever, tonsillitis and enteritis and was treated for three days with no favorable response. On the third day a rapidly progressive hind limb paralysis developed, accompanied by increasing tonicity of the front limbs, mild opisthotonus and abdominal muscular spasms. The dog was killed and necropsied.
In 10 of 16 domestic cats with spontaneous non-suppurative encephalomyelitis, lesions were multifocal but relatively few and were considered nonspecific as to cause, although viral agents could not be excluded. Six cats had polioencephalomyelitis or polioencephalitis suggestive of viral infection. The clinical and morphological features are compared with those of previous reports of feline encephalitis possibly of viral origin. Some previously reported epidemiological and serological surveys suggest a possible role for arboviruses.
Absrrucr. A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.
Levamisole was given orally to 3 groups of dogs, totaling 56 animals. Drug administration period varied from 1 to 120 days. All animals were killed and the central nervous system was examined histologically. Lesions were found in 44 of 56 dogs. These consisted of disseminated perivascular cuffing with mononuclear cells throughout the brain and meninges. The severity of the perivascular cuffing varied considerably and could not be correlated to the length of the drug administration period nor to any other variables. There was no damage to the neural tissues associated with the perivascular cuffing. There was evidence of regression of the lesions whether levamisole treatment was continued or not. The changes observed in this study were considered to be related to the known immunomodulating properties of levamisole. The pathogenesis of this change in uncertain.
Two young zebra siblings from consecutive pregnancies suffered from neurological disease, characterized by ventral deviation of the neck and tetraparesis which progressed to tetraplegia within a few weeks. On histological examination widespread neuronal degeneration was observed in the ventral horns of the spinal cord and in the lower brain stem. Ultrastructurally the neuronal degeneration was characterized by accumulation of neurofibrillary material resembling neurofilaments. The findings are compared to other diseases with neurofibrillary accumulation in man and animals.
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