Primary and secondary nervous system involvement occurs in 4% and 5%-12%, respectively, of all canine non-Hodgkin lymphomas. The recent new classification of canine malignant lymphomas, based on the human World Health Organization classification, has been endorsed with international acceptance. This histological and immunocytochemical classification provides a unique opportunity to study the histologic anatomic distribution patterns in the central and peripheral nervous system of these defined lymphoma subtypes. In this study, we studied a cohort of 37 dogs with lymphoma, which at necropsy had either primary (n = 1, 2.7%) or secondary (n = 36; 97.3%) neural involvement. These T- (n = 16; 43.2%) or B-cell (n = 21; 56.8%) lymphomas were further classified into 12 lymphoma subtypes, with predominant subtypes including peripheral T-cell lymphoma (PTCL) or diffuse large B-cell lymphoma (DLBCL), respectively. This systematic study identified 6 different anatomically based histologically defined patterns of lymphoma infiltration in the nervous system of dogs. Different and distinct combinations of anatomical patterns correlated with specific lymphoma subtypes. Lymphoma infiltration within the meningeal, perivascular, and periventricular compartments were characteristic of DLBCL, whereas peripheral nerve involvement was a frequent feature of PTCL. Similarly cell counts above 64 cells/μL in cerebrospinal samples correlated best with marked meningeal and periventricular lymphoma infiltration histologically. Prospective studies are needed in order to confirm the hypothesis that these combinations of histological neuroanatomic patterns reflect targeting of receptors specific for the lymphoma subtypes at these various sites.

Canine leishmaniasis (CL) is a cutaneous, mucocutaneous, or visceral disease caused by intracellular Leishmania protozoan parasites that are transmitted by the bite of female sand flies. Domestic dogs are the main reservoir hosts. The clinical signs are very variable, ranging from subclinical infections to generalized disorders characterized by hyperthermia, anemia, weight loss, polydipsia, hepatomegaly, splenomegaly, hypergammaglobulinemia, generalized lymphadenopathy, cutaneous lesions, and other lesions. 2,4 In visceral CL, parasites and their lesions are found throughout the host organism, producing proliferative inflammatory reactions causing an immune imbalance. Among the inflammatory infiltrates, macrophages predominate, and occasionally amastigotes are found within them. Many organs have been observed to be affected, especially the lymph nodes, liver, spleen, and skin.2 It is thought that a humoral response and deposition of immune complexes are likely responsible for the pathogenesis 2,4 including the systemic necrotizing vasculitis that has been described in affected dogs. 17 Occasionally, neurological signs and/or histopathological lesions have been observed affecting the central nervous system (CNS) in CL, 2,9,11 giving rise to the term cerebral leishmaniasis. 8 However, except for the choroid plexuses 13 and meninges, 19 Leishmania amastigotes, to the authors' knowledge, have not been observed in either the CNS parenchyma or peripheral nerves in CL. The current study described a dog with radiculoneuritis, myelitis, and mild meningoencephalitis associated with Leishmania spp. amastigotes in the peripheral and central nervous systems.A 4-year-old male Labrador Retriever suffered an episode of left hemiparesis 9 months before presentation. Blood analysis at that time showed thrombocytopenia and mild hyperglobulinemia. Enzyme-linked immunosorbent assay (ELISA) a for anti-Leishmania antibodies and indirect fluorescent antibody test (IFAT) b for Leishmania were negative. The animal responded favorably to chronic treatment with prednisolone.c Seven months later the animal relapsed, and blood analysis revealed anemia, hyperproteinemia, hypoalbuminemia, and hyperglobulinemia. A second ELISA a test was performed and the result was again negative. Serology for Toxoplasma and Neospora was negative. At that time, treatment was begun with clindamycin, d and an improvement in the clinical signs was noted.Forty-five days later, the dog was referred to the Al Sur Veterinary Hospital with a 10-day evolution of tetraplegia. Clinical examination showed hypothermia, dehydration, tachypnea, and cachexia. The animal was depressed, and postural reactions were absent. Carporadialis and flexor reflexes in the forelimbs were absent; bilateral Horner syndrome was also observed. Atrophy of the supra and left spinal nerves. Microscopically, nerve fiber destruction together with mixed inflammatory infiltration was observed in the spinal nerves. Cervical spinal cord sections showed multifocal, diffuse granulomatous inflammation ...

Finding a marker of neural stem cells remains a medical research priority. It was reported that the proteins doublecortin and nucleostemin were related with stem/progenitor cells in central nervous system. The aim of the present immunohistochemical study was to evaluate the expression of these proteins and their pattern of distribution in canine brain, including age-related changes, and in non-nervous tissues. We found that doublecortin had a more specific expression pattern, related with neurogenesis and neuronal migration, while nucleostemin was expressed in most cells of almost every tissue studied. The immunolabeling of both proteins decreased with age. We may conclude that nucleostemin is not a specific marker of stem/progenitor cells in the dog. Doublecortin, however, is not an exclusive marker of neural stem cells, but also of neuronal precursors.

The molecular pathogenic mechanisms of prion diseases are far from clear. Genomic analyses have revealed genetic biomarkers potentially involved in prion neuropathology in naturally scrapie-infected sheep, a good animal model of infectious prionopathies. However, these biomarkers must be validated in independent studies at different stages of the disease. The gene and protein expression profiles and protein distribution of six potential genetic biomarkers (i.e., CAPN6, COL1A2, COL3A1, GALA1, MT2A and MTNR1B) are presented here for both the early and terminal stages of scrapie in five different brain regions. Gene transcription changes were confirmed in the medulla oblongata, and the expression profiles were generally similar in other central nervous system regions. The changes were more substantial in clinical animals compared to preclinical animals. The expression of the CAPN6 protein increased in the spinal cord and cerebellum of the clinical and preclinical brains. The distribution of the GALA1 was identified in glial cells from the cerebellum of scrapie-infected animals, GALA1 protein expression was increased in clinical animals in the majority of regions, and the increase of MT2A was in agreement with previous reports. The downregulation of MTNR1B was especially marked in the Purkinje cells. Finally, although collagen genes were downregulated the protein immunostaining did not reveal significant changes between the scrapie-infected and control animals. In conclusion, this study of gene transcription and protein expression and distribution confirm CAPN6, GALA1, MTNR1B and MT2A as potential targets for further prion disease research.