Concurrent leukoencephalomyelitis and polyneuritis in a Maltese terrier: resembling combined central and peripheral demyelination in humans (original) (raw)
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Spongiform leukoencephalopathy in an adult mixed breed female dog
2020
Leukoencephalomyelopathy is a nonspecific lesion characterized by widespread vacuolation of central nervous system white matter. It is mainly of genetic basis, occurring in young pure breed dogs. This report describes a neurodegenerative disease associated to demyelination in an adult mixed breed female dog. After 20 days in a kennel with 12 other dogs, the dog showed progressive nervous signs with ataxia and inability to maintain balance. No other dog was affected. After 15 days, the animal was euthanized in extremis and necropsied. No macroscopic lesions of diagnostic relevance were present. Microscopically, status espongiosus was observed in white matter throughout the length of the neuroaxis, from frontal brain lobe to lumbar spinal cord. Specific stains of Kluver Barrera and immunohistochemistry for the detection of phosphorylated and non-phosphorylated neurofilaments, microglia, astrocytosis, oligodendrocytosis and myelin proteins in brain and spinal cord sections showed demyelination, axonal fragmentation and degeneration, microgliosis and decrease of oligodendrocytes. The anatomopathological study and epidemiological data suggests a primary demyelination due to decrease in number and function of oligodendrocytes, which is probably of genetic basis with late onset.
Journal of Veterinary Medical Science, 2003
Canine necrotizing meningoencephalitis (NME) and granulomatous meningoencephalomyelitis (GME) were compared pathologically. Gross observation exhibited lateral ventricular dilation and discoloration, malacia and/or cavitation of the cerebrum in NME. On the contrary, gross changes were milder in GME, except for occasional visible granulomatous mass formation. Histopathologically, the lesions of NME were distributed predominantly in the cerebral cortex and various degrees of inflammatory and necrotic changes were observed according to clinical stages. Besides, microscopic lesions of GME were mainly distributed in the white matter of the c erebrum, cerebellum and brainstem, which are characterized by perivascular cuffing, multiple granulomas and leptomeningeal infiltrates. Although macrophages and lymphocytes were predominant in the inflammatory lesions of both disorders, macrophages in GME transformed into epithelioid cells and exhibited more massive infiltration. Although lectin RCA-1-reactive cells were numerous in both disorders, lysozyme immunoreactive cells in NME were fewer than that in GME. Parenchymal infiltration of MAC387-positive cells was common in GME and limited in NME. The number of CD3-positive lymphocytes in the GME lesions tended to be greater than in NME, though the difference was not statistically significant. Morphological and immunohistochemical differences of the lesions, in particular, the characteristics of infiltrative macrophages may reflect these different pathogeneses of the two disorders.
Journal of Veterinary Internal Medicine
Background: Presumed autoimmune diseases affecting the central nervous system (CNS) of dogs are common. In people, antibodies against neuronal cell surface antigens that are associated with a wide variety of neurological syndromes have been identified. The presence of cerebrospinal fluid (CSF) autoantibodies that target neuronal cell surface proteins has not been reported in dogs with neurologic disorders. Objectives: Autoantibodies to neuronal cell surface antigens can be found in the CSF of dogs with inflammatory CNS disease. Our aim was to determine whether 6 neuronal cell surface autoantibodies were present in the CSF of dogs diagnosed with inflammatory and noninflammatory CNS disease. Animals: Client-owned dogs with CNS disease and complete diagnostic evaluation including magnetic resonance imaging and CSF analysis were included. One healthy dog was included as a negative control. Methods: Cerebrospinal fluid was tested for 6 antigenic targets with a commercially available indirect immunofluorescence assay test kit. Results: There were 32 dogs with neurological disease, 19 diagnosed with inflammatory disease (encephalitis and meningitis), 10 with noninflammatory disease (neoplasia, intervertebral disk disease, degenerative myelopathy, and epilepsy), 2 with no diagnosis, and
Journal of Veterinary Science, 2015
In the present study, the use of dogs with experimental autoimmune encephalomyelitis (EAE) as a disease model for necrotizing encephalitis (NE) was assessed. Twelve healthy dogs were included in this study. Canine forebrain tissues (8 g), including white and grey matter, were homogenized with 4 mL of phosphate-buffered saline for 5 min in an ice bath. The suspension was emulsified with the same volume of Freund's complete adjuvant containing 1 mg/mL of killed Mycobacterium tuberculosis H37Ra. Under sedation, each dog was injected subcutaneously with canine brain homogenate at four sites: two in the inguinal and two in the axillary regions. A second injection (booster) was administered to all the dogs using the same procedure 7 days after the first injection. Clinical assessment, magnetic resonance imaging, cerebrospinal fluid analyses, necropsies, and histopathological and immunohistochemical examinations were performed for the dogs with EAE. Out of the 12 animals, seven (58%) developed clinically manifest EAE at various times after immunization. Characteristics of canine EAE models were very similar to canine NE, suggesting that canine EAE can be a disease model for NE in dogs.
Clinical and Pathological Findings of Necrotizing Meningoencephalitis in a Maltese Dog
A 2-year-old, intact female Maltese dog was presented to the veterinarian with a history of acute neurological signs. On neurological examination the dog showed deficit of mental status (apathy and depression), seizures, constant howling, head turn and compulsive circling to the right side and falls to the left side. The treatment protocol using prednisolone (for seizures remission) and cyclosporine (initiated in the chronic stage) did not stop the progression of the disease and euthanasia was elected 65 days later. Necropsy revealed mild cerebral asymmetry, and in the frontal (more affected) parietal and occipital lobes of the right hemisphere there were friable, depressed and yellowish areas characterizing malacia. The left contralateral frontal lobe was edematous and slightly yellowish. At histopathology, the lesions were characterized by marked, multifocal to coalescing necrotizing meningoencephalitis, characterized by focally extensive areas of malacia, especially in the cortex of the frontal and right parietal lobes. Extension of lesions to white matter was observed only in the caudal region of the right frontal lobe. Plasma cells and lymphocytes infiltration was observed around vessels, leptomeninges and in the neuroparenchyma. In addition, the non-cavitation areas were also characterized by neuropil vacuolization, neuronal necrosis, neuronophagia, astroglyosis with various gemistocytes, endothelial hyperplasia and hypertrophy. The immunohistochemical analysis showed predominance of CD3 positive T lymphocytes in proportion to CD79 positive cells. Clinical signs, character and distribution of neurological lesions were compatible with necrotizing meningoencephalitis (NME). This condition, initially reported only in Pugs, currently affects other breeds and attention should be given to the differential diagnosis with other neuropathies in dogs.
Research in Veterinary Science, 2007
The clinical diagnosis of distemper is difficult in dogs presented with nervous deficits in the absence of extraneural signs and myoclonus. The aim of this study is to verify how the clinicopathological findings may suggest distemper encephalomyelitis in such cases. We prospectively investigated 20 necropsied dogs presented with neurological signs without those characteristic signs of distemper at the time of hospital admission. Eight out of 20 dogs were diagnosed with distemper encephalomyelitis at post mortem by reverse transcriptionpolymerase chain reaction (RT-PCR) and histological examination. Cerebellar and/or vestibular signs progressing to tetraparesis/plegia were frequent neurological signs. Abnormalities in hematologic findings were non-specific, nevertheless the cerebrospinal fluid evaluation could suggest canine distemper virus (CDV) infection by a lymphocytic pleocytosis. At post mortem chronic CDV encephalomyelitis was predominant. Our clinical results, as well as the predominance of chronic encephalomyelitis, differ from other studies about CDV encephalomyelitis with naturally infected dogs presenting extraneural signs and myoclonus.
Necrotizing Meningoencephalitis in Atypical Dog Breeds: A Case Series and Literature Review
Journal of Veterinary Internal Medicine, 2013
Background: Canine necrotizing meningoencephalitis (NME) is a fatal, noninfectious inflammatory disease of unknown etiology. NME has been reported only in a small number of dog breeds, which has led to the presumption that it is a breed-restricted disorder. Hypothesis/Objectives: Our objective was to describe histopathologically confirmed NME in dog breeds in which the condition has not been reported previously and to provide preliminary evidence that NME affects a wider spectrum of dog breeds than previously reported. Animals: Four dogs with NME. Methods: Archives from 3 institutions and from 1 author's (BS) collection were reviewed to identify histopathologically confirmed cases of NME in breeds in which the disease has not been reported previously. Age, sex, breed, survival from onset of clinical signs, and histopathologic findings were evaluated. Results: Necrotizing meningoencephalitis was identified in 4 small dog breeds (Papillon, Shih Tzu, Coton de Tulear, and Brussels Griffon). Median age at clinical evaluation was 2.5 years. Histopathologic abnormalities included 2 or more of the following: lymphoplasmacytic or histiocytic meningoencephalitis or encephalitis, moderate-to-severe cerebrocortical necrosis, variable involvement of other anatomic locations within the brain (cerebellum, brainstem), and absence of detectable infectious agents. Conclusions and Clinical Importance: Until now, NME has only been described in 5 small dog breeds. We document an additional 4 small breeds previously not shown to develop NME. Our cases further illustrate that NME is not a breedrestricted disorder and should be considered in the differential diagnosis for dogs with signalment and clinical signs consistent with inflammatory brain disease.