Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical features, magnetic resonance imaging, histopathology, and immunohistochemistry.

The purpose of this study was to identify time-related changes in clinical, MRI, histopathologic, and immunohistochemical findings associated with ischemic stroke in dogs. Additionally, the association of cerebrospinal fluid (CSF) and tissue levels of interleukin (IL)-6 with clinical prognosis was assessed. Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAO) in nine healthy experimental dogs. The dogs were divided into three groups according to survival time and duration of the experimental period: group A (survived only 1 day), group B (1-week experimental period), and group C (2-week experimental period). Neurologic status was evaluated daily. Magnetic resonance imaging (MRI) was performed according to a predetermined schedule. Concentration of IL-6 in CSF was measured serially after ischemic stroke. Postmortem examination was performed for all experimental dogs. During histopathological examination, variable degrees of cavitation and necrosis due to neuronal cytopathic effects, such as pyknotic nuclei and cytoplasmic shrinkage, were observed on the affected side of the cerebral cortex in all dogs. Immunohistochemistry specific for IL-6 showed increased expression in the ischemic lesions. CSF IL-6 concentrations and ischemic lesion volumes 1 day after ischemic stroke were significantly higher in group A compared to groups B and C.

A study of experimental autoimmune encephalomyelitis in dogs as a disease model for canine necrotizing encephalitis.

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.

Unsuccessful cyclosporine plus prednisolone therapy for autoimmune meningoencephalitis in three dogs.

A 4-year-old female Maltese (case 1), a 9-year-old castrated male shih tzu (case 2) and 2-year-old female Pomeranian (case 3) presented with neurological signs, such as head tilt, ataxia, circling and paresis. The three cases were tentatively diagnosed as having meningoencephalitis of unknown etiology based on computed tomography scan and cerebrospinal fluid analysis. All patients were managed with cyclosporine plus prednisolone therapy. The survival times of the three patients were 170, 70 and 21 days, respectively. After the cases died, we performed necropsy and histopathological examination for definitive diagnosis. Based on the necropsy, histopathological and immunohistochemical examinations, cases 1, 2 and 3 were definitely diagnosed as having necrotizing meningoencephalitis, necrotizing leukoencephalitis and granulomatous meningoencephalitis, respectively. This case report demonstrated the clinical findings, brain CT characteristics and histopathological and immunohistochemical features of NME, NLE and GME in dogs and discussed the reason for the relatively short survival times under cyclosporine plus prednisolone therapy.