Abstract. Clinical and pathologic features of a sporadic, necrotizing meningoencephalitis affecting adolescent and mature pug dogs are described. Many of the affected animals were closely related. Acute and chronic forms occur, with clinical signs reflecting the pathologic affinity of the disease for the cerebral hemispheres. No etiologic agent has been identified. The extensive necrosis and affinity for the cerebral hemispheres are similar to alphatype herpesvirus encephalitides of other species.For more than 20 years we have observed in pug dogs a unique non-suppurative meningoencephalitis associated with extensive cerebral necrosis. Except for one brief account5 the disease has not been described. Because of its unusual nature and because of some confusion about the disease, we present this retrospective study. Included are some speculations on etiology, based on lesions. Case HistoriesThe study material comprised 17 naturally occurring cases of this disease in pug dogs from northern California (all from within 160 km of Sacramento). All dogs were patients of our Veterinary Medical Teaching Hospital. Six were males and 11 were females. They ranged in age from 6 months to 7 years (two aged 6 months, five aged 1 year, seven aged 2 to 3 years, and three aged 5 to 7 years). At least 11 of the dogs were born in the same kennel, and their pedigrees revealed numerous common ancestors, including one male that appeared at least once in the three generations preceding each affected dog. Pedigree data on the other six dogs were incomplete and not contributory.Ten dogs showed signs for 2 weeks or less, one for a month, and six for 4 to 6 months. Thus, over half were acute and about a third quite chronic. The most common clinical sign was generalized seizures; these occurred in 16 of the 17 dogs. In some cases, seizures were the initial sign ofillness reported by the owners; in others, seizures began after variable periods of lethargy and/or ataxia. Some form of depressed consciousness, progressing from lethargy early in the disease to coma terminally, occurred in all dogs. Other signs seen frequently included walking in circles, head-pressing, blindness with normal pupillary light reflexes, cervical rigidity (resistance to passive movement of the head and neck), and opisthotonus.Hemograms of 12 dogs did not reveal significant abnormalities. Various blood chemistries, including liver enzymes, plasma proteins, and serum electrolytes, were done in seven cases but did not reveal abnormalities. No abnormalities were found in the urine of six dogs examined by routine urinalysis.Cerebrospinal fluid (CSF) was collected from the cerebellomedullary cistern of 16 of the dogs. Analysis of 12 of these specimens included total and differential cell counts and total protein determination (Table 1). In all 12 specimens the total white blood cells were increased (mean = 374 ? 178.2), and the predominant cell type was the small lymphocyte, which constituted from 71% to 989' 0 of the nucleated cells (Table 1). Complete examinations were n...
Abstract. In 27 adult dogs with a distinctive chronic granulomatous meningoencephalomyelitis there were locomotor problems, cervical meningitis and blindness. Lesions were widespread, but most severe in cerebral and cerebellar white substance and in the cervical spinal cord. Lesions were characterized by the development of epithelioid cell granulomas arising from mononuclear cuffs. There were secondary edema and necrosis in severe cases and eventual fibroplastic repair in chronic cases. The cause is unknown.
An arteriovenous malformation and two hemangiomas in the canine spinal cord were found in three dogs. The malformation was ventral, extramedullary and largely subdural. Chronic hypoxia, consequent upon the shunt, had led to extensive local edema, necrosis and hemorrhage at T13-L1. Prominent intramedullary perivascular fibrosis, mineralization and obliteration were the presumed consequences of the hemodynamic insult. The hemangiomas, one of which was multiple, were deep lesions that produced compressive changes in the adjacent cord tissue. The masses were regarded as benign neoplasms with central sclerosis. These conditions appear not to have been reported previously in the dog.
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