Abstract
We thank Dr Kerstin Baiker and Dr Kaspar Matiasek for their comments on our article. 2 We would like to focus on 3 important discussion points.
As they mentioned, the immune response in canine necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalomyelitis (GME) is very complicated. Despite their unique distribution patterns (NME, NLE, and GME), breed predispositions (NME and NLE), and histopathologic features, the populations of the inflammatory cells detected by immunohistochemical analysis are not significantly different among these canine central nervous system (CNS) disorders. We agree with their statements that further examinations will be needed to know the “real” etiologies of these diseases. Actually, we recently examined several cytokine levels within the fresh brain tissues from NME, NLE, and GME cases and found that these 3 diseases have quite different cytokine profiles. We therefore hope to publish the data and receive specific comments from researchers in this field.
Concerning the etiology of GME, we did not mean at all that the Borna virus infection might be associated with the canine disease, but some viral infections, such as canine distemper, have some possibility to act as a trigger of an irregular immune response.
A previous study on a canine CNS disease named subacute necrotizing encephalopathy, caused by combined respiratory chain defect mitochondrial transfer RNA mutations in Yorkshire Terriers, 1 was very interesting for us, although the relationship between the genetic changes and CNS lesions in the affected dogs might remain unclear. The clinical course, canine breed, and distribution of the lesions seemed to be in conformity with those of NLE in Yorkshire Terriers, described in our article and other previous reports.