469 - Neuromuscular weakness secondary to Botulism.

Case Diagnosis: Botulism

Case Description: 70-year-old male with history of hypertension, non-CPAP dependent OSA and GERD. Patient presented with complaints of diplopia, dry mouth, difficulty opening eyes, dysarthria, unsteady gait and postnasal drip. His exam was notable for bilateral upper visual field defect and left eye lateral gaze palsy. Patient had a rapid mental decline on admission with seizure like activity. Stroke workup including EEG was negative. Patient developed acute hypoxic and hypercapnia respiratory failure with significant respiratory acidosis requiring intubation. Patient was found to have descending weakness/paralysis manifesting as a bulbar palsy with progressive involvement of the extremities. Tracheostomy was done due to neuromuscular dysphagia. Complete bacterial, viral and antibodies workup was negative except for elevated GM1 antibody. Patient was started on antitoxin empirically. Stool toxin assay was positive for Clostridium Barataii consistent with botulism. Patient received six sessions of plasmapheresis. After completion of three weeks of acute rehabilitation, patient had complete neurological recovery.

Discussions: Our patient did report some typical symptoms of botulism including cranial nerve dysfunction, muscle weakness and respiratory difficulty although he did not have clear exposure to a potential source of botulism. The acute decline in mental status is likely attributed to hypercapnia. It is not uncommon for lab and imaging to be normal in patients with botulism. Elevated GM1 antibody is associated with motor and sensorimotor neuropathies and was of no clinical significance in this case. Botulism should be suspected in patients with absence of fever and at least one specific sign and symptom of cranial neuropathy.

Conclusions: Presumptive clinical diagnosis of botulism can be made in any patient with acute onset of unexplained cranial nerve abnormalities, symmetric muscle weakness and without sensory neuropathy.