- Hamster exposure was associated with autoimmune cerebellar ataxia in a hospital-based case-control study.
- This relationship was not seen with exposure to dogs, cats, or other animals.
- Exposed patients showed distinctive neurologic signs and inflammatory cerebrospinal fluid findings.
People with autoimmune cerebellar ataxia were more likely to have been exposed to pet hamsters versus a control group, a hospital-based study in China suggested.
Among patients matched on age and sex, hamster exposure was more common in those with autoimmune cerebellar ataxia compared with those with other autoimmune central nervous system disorders (56.1% vs 4.5%;adjusted OR 38.46, 95% CI 10-142.86, P<0.001), reported Hongzhi Guan, MD, PhD, of the Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing, and co-authors.
This relationship was not seen with any other animals, the researchers wrote in the Journal of Neurology, Neurosurgery & Psychiatry. “There is no significant correlation between other pets and autoimmune cerebellar ataxia, including dogs and cats,” Guan noted in an email.
The median duration of hamster exposure was 12 months. Eleven patients had a history of hamster bites, and the median interval from bite to ataxia onset was 6 months.
Compared with other autoimmune ataxias, pyramidal signs, diplopia, and peripheral neuropathy or radiculopathy were more common in hamster-associated ataxia, and cerebrospinal fluid (CSF) white blood cell counts, protein concentrations, and positive rates for oligoclonal bands were higher.
CSF pathogen testing was negative in all patients. Neuronal autoantibodies were detected in nine autoimmune cerebellar ataxia patients exposed to hamsters, the researchers added. HLA-A*24:02 and HLA-B*15:01 had nominal correlations with hamster exposure, which were not significant after correcting for false discovery rate.
“Autoimmune cerebellar ataxia is an immune-mediated disorder characterized by rapid onset and progression of double vision, slurred speech, gait problems, and limb incoordination that has variable prognosis,” noted Andrew McKeon, MB, BCh, MD, of the Mayo Clinic in Rochester, Minnesota, who wasn’t involved with the study.
Autoantibodies detected in serum, CSF, or both can help diagnose autoimmune cerebellar ataxia, McKeon said. “Many disorders are of unknown cause, but a history of non-neurological autoimmune disease is a risk factor,” he told MedPage Today. “Other patients have an occult cancer in the body expressing mutated neural antigens that may trigger autoimmune ataxia known as paraneoplastic disorders.”
The most recent diagnostic criteria for primary autoimmune cerebellar ataxia were published in 2020 by a task force on immune-mediated ataxias. The task force pointed out that while about 20% of ataxia cases are classified as idiopathic sporadic, a significant number of these are likely autoimmune cerebellar ataxia.
“In clinical practice, we observed that some patients with autoimmune cerebellar ataxia had a history of keeping pet hamsters,” Guan and co-authors noted.
For this case-control study, the researchers studied patients at the Peking Union Medical College Hospital from January 2024 to February 2026 who met diagnostic criteria for primary or autoantibody-associated autoimmune cerebellar ataxia. Controls included patients with anti-NMDA receptor encephalitis, anti-LGI1 encephalitis, myelin oligodendrocyte glycoprotein antibody-associated disease, GAD antibody-spectrum disorders, or other disorders.
Of the 57 patients with autoimmune cerebellar ataxia, 32 had hamster exposure and 25 did not. Exposure was defined as daily or near-daily contact with hamsters for at least 2 months. Exposed ataxia patients had a mean age of 31, and 40.6% were male.
Pyramidal signs occurred more frequently in patients with versus without hamster exposure (90.6% vs 48.0%, P<0.001), as did diplopia (65.6% vs 36.0%, P=0.026), and peripheral neuropathy or radiculopathy (25.0% vs 0%, P=0.021). These patients also had higher CSF white blood cell counts (45 vs 3 cells/μL, P<0.001) and protein concentrations (0.90 vs 0.36 g/L, P<0.001). Oligoclonal bands were detected in 93.5% of ataxia patients with hamster exposure versus 52.2% of those without it (P<0.001).
“Although pet rodents can transmit various pathogens, hamster-associated autoimmune cerebellar ataxia in our cohort did not appear to be caused by a neuroinvasive pathogen,” Guan and co-authors observed. Immunotherapy effectiveness, neuronal autoantibody detection, and relapse in approximately half of the cases support an autoimmune pathogenesis, they added.
“We therefore hypothesize that hamsters may trigger abnormal autoimmune responses through an as-yet unidentified mechanism, leading to cerebellar ataxia,” the researchers wrote. “Comparable mechanisms are seen in other neuroimmune diseases, such as Guillain-Barré syndrome triggered by Campylobacter jejuni or cytomegalovirus, in which molecular mimicry and dysregulation of immune responses may contribute to autoimmunity.”
The study was limited by its small sample size, the researchers acknowledged. Hamster exposure was assessed retrospectively and included contact with the animals, urine or stool, food pellets, and dust or aerosols.
