The University of Georgia College of Veterinary Medicine

eorgia Veterinary Scholars Program

GVSP Summer 2007 Scholars

Georgia Veterinary Scholar	Faculty Mentor

Wesley Campbell University of Georgia Class of 2010	Dr. Scott Schatzberg

Polymerase Chain Reaction of Cerebrospinal Fluid for Vector Borne Diseases in Dogs with Meningoencephalitis of Unknown Etiology
M. Wesley Campbell *, Qiang Li, Craig Greene, Adam Birkenheuer, Simon Platt, Marc Kent, Edward B. Breitschwerdt, Scott J. Schatzberg, Department of Small Animal Medicine, The University of Georgia, Athens, Georgia. USA
Abstract
The canine meningoencephalitides of unknown etiology (MUE) include pathologic conditions characterized as granulomatous meningoencephalitis (GME), necrotizing meningoencephalitis (NME), and necrotizing leukoencephalitis (NLE). The inciting causes for these inflammatory disorders of the canine central nervous system (CNS) are unknown, and typically they are fatal without aggressive immunosuppressive therapy. Based on limited supportive data, these idiopathic disorders typically are labeled as autoimmune diseases. The etiologies for the majority of cases of meningoencephalitis remain elusive, in part due to current limitations in routine diagnostic testing for pathogens in the canine CNS.
Histopathologic lesions present in canine MUE are similar to those present in several types of human infectious meningoencephalitis. However, most available antemortem tests for canine meningoencephalitis are non-specific and insensitive, and etiological agents are identified rarely. The polymerase chain reaction (PCR) method applied to cerebrospinal fluid (CSF) has revolutionized pathogen detection in human CNS disorders. Epidemiolgic data suggests that vector borne diseases including Rocky Mountain Spotted Fever, Lyme Disease, Ehrlichiosis, Bartonellosis, and Anaplasmosis are common in the southeastern United States, making these pathogens important etiological candidates for canine MUE.
The objective of this investigation was to assess for the presence of DNA from Ehrlichia spp., Bartonella spp., Borrelia spp., Anaplasma phagocytophilum, and Rickettsia rickettsii in CSF from 50 dogs with MUE using degenerate and specific PCR approaches. DNA extracted from CSF from 25 dogs with non-inflammatory neurological disorders was used as negative controls. The 50 dogs with MUE were negative for all pathogens tested, with the exception of 1 dog which was PCR positive for Bartonella spp. The CSF from the 25 negative control dogs produced no PCR amplicons for any of the pathogens tested. Additional studies testing for other bacterial and viral pathogens are warranted to gain insight into the etiologies of canine MUE. The identification of infectious etiologies for MUE should lead to more targeted antimicrobial therapies accompanied by improved prognoses and survival rates.