• Open Access

Seroprevalence of Various Infectious Agents in Dogs with Suspected Acute Canine Polyradiculoneuritis

Authors


  • This study was presented in two parts in poster form at the American College of Veterinary Internal Medicine Forum, Dallas, TX, May 2002, and San Antonio, TX, June 2008. This study was performed at Colorado State University (CSU), Veterinary Teaching Hospital, Fort Collins, Colorado. Cases referred to in this study were seen at CSU, University of Wisconsin—Madison Veterinary Teaching Hospital, or by surrounding local veterinarians.

Corresponding author: Dr Natalee Holt, DVM, Tufts University Cummings School of Veterinary Medicine, 200 Westboro Road, North Grafton, MA 01760; email: natalee.holt@tufts.edu.

Abstract

Background: Acute canine polyradiculoneuritis (ACP) is considered to be an animal model of the acute axonal form of Guillain-Barré syndrome (GBS) in humans. Various antecedent events have been associated with GBS, including bacterial or viral infection. The relationship between ACP and previous infection requires additional attention.

Hypothesis: We hypothesized a relationship between ACP and serological evidence of exposure to Ehrlichia canis, Borrelia burgdorferi, Toxoplasma gondii, Neospora caninum, Campylobacter jejuni, and canine distemper virus (CDV).

Animals: Eighty-eight client-owned dogs, 44 with ACP, 44 age-matched controls.

Methods: Retrospective study with stored serum samples. Serum antibodies against the target organisms were measured with commercially available assays. Sera from dogs with and without ACP that were positive for T. gondii IgG by ELISA were assayed by an IgG heavy chain-specific, Western blot immunoassay.

Results: Dogs with ACP (55.8%) were more likely to have T. gondii IgG serum antibody titers than dogs without ACP (11.4%). Serum antibodies from 8 affected dogs and 11 control dogs bound to T. gondii antigens with apparent molecular masses of 67, 61, 58, 45, 33, 24, 9, and 6 kDa. An antigen with an apparent molecular mass of 36 kDa was recognized by 2 dogs with ACP but none of the control dogs.

Conclusions: Results of this study suggest that ACP in some dogs, like GBS in some humans, may be triggered by T. gondii and a prospective study should be performed to further evaluate this potential association.

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