Peer-reviewed veterinary case report
Immune cell patterns in dog brain diseases NME, NLE, and GME
By Park, E S et al.·Published in Veterinary pathology·2012·Department of Veterinary Pathology, Japan·View original on PubMed →
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Original publication title: Comprehensive immunohistochemical studies on canine necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalomyelitis (GME).
- Species:
- dog
Plain-English summary
A group of dogs with severe brain inflammation, including conditions like necrotizing meningoencephalitis (NME) and granulomatous meningoencephalomyelitis (GME), were studied to better understand their causes and effects. These dogs showed symptoms related to brain dysfunction, such as seizures or behavioral changes. Researchers examined brain tissue samples to identify the types of inflammatory cells present. They found that while the types of cells were similar across conditions, the location of the lesions varied significantly. Unfortunately, the study did not provide specific treatment outcomes for the dogs involved, but understanding these conditions can help veterinarians manage affected pets better in the future.
People also search for: dog brain inflammation symptoms · necrotizing meningoencephalitis treatment · granulomatous meningoencephalomyelitis in dogs
Abstract
In dogs, there are several idiopathic meningoencephalitides, such as necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalomyelitis (GME). Although they are often assumed to be immune mediated, the etiology of these diseases remains elusive. In this study, the histopathology of the lesions caused by these conditions and the inflammatory cell populations produced in response to them were examined among dogs affected with GME, NME, or NLE to understand their pathogeneses. The brain tissues of dogs with NME (n = 25), NLE (n = 5), or GME (n = 9) were used. The inflammatory cells were identified by immunohistochemistry using antibodies against CD3, IgG, CD20, CD79acy, and CD163. In NME and NLE, malacic changes were located in the cerebral cortex, as well as the cerebral white matter and thalamus, respectively. The distribution of the brain lesions in NME and NLE was breed specific. In GME, granulomatous lesions that were mostly composed of epithelioid macrophages were observed in the cerebral white matter, cerebellum, and brainstem. Although the proportions of IgG-, CD20-, and CD79acy-positive cells (B cells) were not significantly different among the GME, NME, and NLE lesions, that of CD3-positive cells (T cells) was increased in GME. In NME and NLE, CD163-positive cells (macrophages) had diffusely infiltrated the cerebral cortex and white matter, respectively. However, in GME, CD163-positive cells accumulated around the blood vessels in the cerebral and cerebellar white matter. The distributions of these lesions were quite different among GME, NME, and NLE, whereas there were no marked differences in the proportions of inflammatory cells.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/22262353/