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Although neurological signs have been reported sporadically in dogs with systemic
Lyme disease, it is unknown if neuroborreliosis occurs in dogs. The current study systematically evaluates canine brains for evidence of Borrelia burgdorferi infection. Twelve Beagles were experimentally challenged with B. burgdorferi-infected ticks at 18 weeks of age, and 2 unexposed dogs served as controls. One of the uninfected dogs and 6 infected dogs were each given 5 daily immunosuppressive doses of dexamethasone starting at 153 days post-infection. Eleven dogs were confirmed as infected by skin punch biopsy polymerase chain reaction (PCR) and serology. Neurological signs were not seen in any dogs through the end of the 190-day study. Whole blood, serum, cerebrospinal fluid (CSF), and brains from all dogs were collected. DNA was extracted from blood, CSF, and brain and evaluated by PCR for B. burgdorferi. Formalin-fixed brain tissue was examined by histopathology, immunohistochemistry, and PCR. Immunohistochemical staining for B. burgdorferi antigen was negative in all cases. The CSF analysis was normal, and PCR was uniformly negative for B. burgdorferi in all dogs. Six of the 11 (45%) infected dogs had mild to moderate lymphoplasmacytic choroid plexitis, which was more pronounced in the immunosuppressed dogs. The lack of B. burgdorferi DNA and immunohistochemical evidence of organisms, including within the choroid plexus lesions, suggests that B. burgdorferi does not have a direct role in the etiopathogenesis of canine central nervous system pathology.