To investigate whether exposure to pet hamsters may act as a potential trigger for autoimmune cerebellar ataxia (ACA).
We conducted a hospital-based case–control study based on our institutional ACA cohort. 57 patients were enrolled in the ACA group and 67 age-matched and sex-matched patients with other autoimmune central nervous system disorders served as controls. Clinical and paraclinical data were collected. Exposure to hamsters and other animals was defined as daily or near-daily contact for at least 2 months.
Hamster exposure was significantly more common in the ACA group than in controls (56.1% vs 4.5%, p<0.001; adjusted OR 38.46, 95% CI 10 to 142.86, p<0.001), whereas exposure to other animals did not differ between groups. Among patients with ACA with hamster exposure, the median interval from contact to ataxia onset was 12 months and 11 patients had a history of hamster bites. Compared with patients with ACA without hamster contact, those with hamster exposure more frequently presented with pyramidal signs, diplopia and peripheral neuropathy/radiculopathy, together with higher cerebrospinal fluid (CSF) white blood cell counts, protein concentrations and positivity rates for oligoclonal bands. CSF pathogen testing was negative in all subjects. Neuronal autoantibodies were detected in nine patients with ACA with hamster exposure. HLA-A*24:02 and HLA-B*15:01 showed nominal correlations with hamster exposure, but these did not remain significant after Benjamini-Hochberg false discovery rate correction.
Pet hamster exposure may be a risk factor for ACA. Hamster-associated ACA showed distinctive clinical and CSF inflammatory features. These findings support pet hamster exposure as a novel potential environmental trigger for ACA.