Abstract
Molecular mimicry is hypothesized to play a key role in the pathogenesis of acute polyradiculoneuritis (APRN) in dogs, as in Guillain-Barré syndrome (GBS). GBS is linked to Campylobacter jejuni and cytomegalovirus, while Parvovirus B19 shows temporal and serological associations. In dogs, the cause of APRN is often unknown, although recent vaccination or ingestion of raw poultry contaminated with Clostridium perfringens is documented. Antiganglioside antibodies are potential serum biomarkers for APRN. Eight 2.5-month-old Sprocker littermates and a 3-month-old female Cockapoo developed severe gastrointestinal clinical signs and tested positive for canine parvovirus-2 (CPV-2) infection. Six littermates died, while two pups (one male, one female) and the Cockapoo recovered. Seven days later, the male puppy developed pelvic limb weakness progressing to flaccid tetraparesis over 24 h, followed by thoracic limb contracture. Both female pups, 10 days after recovering from illness, developed neuromuscular clinical signs that deteriorated for 9 days before improving. They presented with a short-strided, choppy gait with kyphosis, and the Cockapoo developed dysphonia. Both female puppies improved over several months. Antiganglioside antibodies were not detected in the two littermates at 1 and 3 months after clinical onset. Treatment included supportive care. Both littermates received prednisolone and methocarbamol, with only the female responding. The male was euthanized due to poor quality of life. Post-mortem examination revealed widespread muscular atrophy and axonal degeneration, with active regeneration detected on semi-thin tissue sections of nerves. This study described a peripheral neuropathy temporally associated with CPV-2 infection. Although a causal relationship cannot be established, the clinical course and pathological features are compatible with a post-infectious neuromuscular process.