Botulism Type F, a Rare Type of Botulism that Can Masquerade as a Posterior Fossa Stroke.
Source: PubMed, NCBI / U.S. National Library of Medicine
Botulism is a rare, life-threatening condition caused by potent neurotoxins that inhibit the release of acetylcholine into the neuromuscular junction, resulting in cranial nerve palsies, flaccid paralysis, and respiratory compromise. Most cases are caused by type A and B toxins produced by Clostridium botulinum. Here, we describe a 41-year-old woman who presented with acute onset binocular diplopia, nausea/vomiting, slurred speech, and unsteady gait, symptoms that resemble a posterior fossa stroke. The patient was initially admitted to the stroke service; however, her symptoms quickly progressed to flaccid quadriparesis with generalized areflexia, fixed and dilated pupils, and respiratory failure requiring intubation, raising concerns for neuromuscular junction disorders. Stool and rectal swabs were sent for botulinum toxin screening. Repetitive nerve stimulation showed decremental compound muscle action potential (CMAP) response with 3 Hz stimulation, mild incremental response to exercise, and incremental response with 50 Hz stimulation, findings suggestive of presynaptic pathology. The CDC was contacted and the patient received botulinum antitoxin on the second day of hospitalization. Positive PCR testing on rectal swab was reported on day 4, and the patient was ultimately diagnosed with Type F botulism, an exceedingly rare variant of the disease typically associated with Clostridium baratii. The patient was extubated after two weeks. No source of the toxin was identified.
Abstract
Botulism is a rare, life-threatening condition caused by potent neurotoxins that inhibit the release of acetylcholine into the neuromuscular junction, resulting in cranial nerve palsies, flaccid paralysis, and respiratory compromise. Most cases are caused by type A and B toxins produced by Clostridium botulinum. Here, we describe a 41-year-old woman who presented with acute onset binocular diplopia, nausea/vomiting, slurred speech, and unsteady gait, symptoms that resemble a posterior fossa stroke. The patient was initially admitted to the stroke service; however, her symptoms quickly progressed to flaccid quadriparesis with generalized areflexia, fixed and dilated pupils, and respiratory failure requiring intubation, raising concerns for neuromuscular junction disorders. Stool and rectal swabs were sent for botulinum toxin screening. Repetitive nerve stimulation showed decremental compound muscle action potential (CMAP) response with 3 Hz stimulation, mild incremental response to exercise, and incremental response with 50 Hz stimulation, findings suggestive of presynaptic pathology. The CDC was contacted and the patient received botulinum antitoxin on the second day of hospitalization. Positive PCR testing on rectal swab was reported on day 4, and the patient was ultimately diagnosed with Type F botulism, an exceedingly rare variant of the disease typically associated with Clostridium baratii. The patient was extubated after two weeks. No source of the toxin was identified. This rare type of botulism Type F (less than 1% of all botulism cases) is characterized by a more rapid progression of symptoms compared to typical Type A/B botulism and might present clinically like a posterior circulation stroke. Therefore, maintaining high clinical suspicion for neuromuscular disorders (especially in patients presenting with stroke-like symptoms of the posterior fossa) and early administration of antitoxin are critical factors for mitigating disease severity and improving clinical outcomes.