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Updated: Oct 20, 2026

Cerebellar Regional Dissection for Molecular Analysis
Published on: December 5, 2020
Cerebellar ataxia following whooping cough
Abstract:
Bordetella pertussis (BP), the agent of whooping cough, has not been recognized so far as a cause of permanent cerebellar ataxia in human. We describe three patients who developed a disabling and permanent cerebellar syndrome soon after whooping cough. In two patients, diagnosis of BP infection was confirmed by culture of nasopharyngeal secretions. The infection occurred between the age of 13 and 15 years, with neurological symptoms beginning after a delay varying from 3 weeks to 3 months. In our three patients, the cerebellar syndrome was characterized by dysmetria of ocular saccades, scanning speech and ataxic gait. Brain MRI demonstrated a pancerebellar atrophy. The pathogenesis of this cerebellar degeneration is not established. Experimental studies have demonstrated that the cerebellum is particularly vulnerable to lymphocytosis-promoting factor (LPF), one of the exotoxins from BP. The mechanism of this toxicity might be a marked increase in the cellular levels of 3',5'cyclic guanosine monophosphate (cGMP). Since whooping cough is a bacterial exotoxin-mediated disease, this is the first report of a cerebellar syndrome triggered by a bacterial exotoxin.
Insights
Bordetella pertussis (BP), the cause of whooping cough, can lead to permanent cerebellar ataxia in adolescents. This study details three cases of disabling cerebellar syndrome following BP infection, highlighting a potential link between bacterial exotoxins and neurodegeneration.
Area of Science:
- Neurology
- Infectious Diseases
- Toxicology
Background:
- Bordetella pertussis (BP) is the causative agent of whooping cough.
- BP infection is typically associated with respiratory symptoms.
- Permanent cerebellar ataxia has not been previously linked to BP infections in humans.
Observation:
- Three adolescent patients developed a disabling and permanent cerebellar syndrome after whooping cough.
- Neurological symptoms appeared 3 weeks to 3 months post-infection.
- Clinical presentation included dysmetria of ocular saccades, scanning speech, and ataxic gait.
Findings:
- Diagnosis of BP infection was confirmed by culture in two patients.
- Brain MRI revealed pancerebellar atrophy in all three patients.
- This is the first report of a cerebellar syndrome triggered by a bacterial exotoxin.
Implications:
- Suggests a potential neurotoxic effect of BP exotoxins, specifically lymphocytosis-promoting factor (LPF).
- Highlights the vulnerability of the cerebellum to BP-associated toxins.
- Underscores the need for further research into the pathogenesis of BP-induced cerebellar degeneration.
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