Botulism can occur naturally as a food-borne illness caused by ingestion of pre-formed botulinum toxin, typically types A, B or E from Clostridium botulinum. Clostridium baratii as a causitive agent of human botulism has been reported only rarely in the medical literature(1). We report an unusual case of botulism caused by type F toxin produced by C. baratii.
A 26 year old, previously healthy white man awoke the morning of admission with a complaint of diplopia, then developed shortness of breath and mild dysarthria. He was transferred to our facility after intubation for hypercapneic respiratory failure at another institution. The patient arrived awake and able to follow commands. He remained intubated with no respiratory effort over the ventilator. Physical exam revealed bilateral opthalmoplegia, with bilateral abducens palsies, loss of upgaze, non-reactive 6mm pupils, mild ptosis and weakness of eye closure. Biceps and triceps strength were decreased to 4/5, but all other muscle testing was normal. Sensory and reflex examinations were normal. Admitting laboratories and brain imaging by computed tomography and magnetic resonance were normal. Lumbar puncture revealed elevated protein at 50mg/dL but no other abnormalities. Nerve conduction studies with electromyography found markedly decreased muscle compound action potentials in all muscle groups with normal sensory action potentials and normal repetitive stimulation. The differential diagnosis included Botulism and Miller-Fisher Syndrome. The patient was treated with botulinum anti-toxin against toxins A,B and E. Additionally he received 5 days of IVIG. Stool and serum samples were sent for botulism toxin assay and anti-ganglioside GQ1B antibody. The patient progressed to bilateral upper extremity flacid paralysis but began to recover extremity motor function on day 4. His course was complicated by acute renal failure secondary to osmotic nephrosis from IVIG and a prolonged ileus. He was extubated on hospital day 9 and discharged home on day 20. Botulism toxin assay was positive for type F toxin. Culture suggested C. baratii. Confirmatory testing by the CDC is pending. Anti-GQ1B antibody tests were negative.
Botulism is caused by neurotoxins produced by the organisms C. botulinum, C. baratii or C. butyricum against proteins involved in synaptic vesicle release. Food-borne illness from botulinum toxin is rare, with only 33 reported cases in the United States in 2001(2). Food-borne illness from C. baratii type F toxin is even more unusual, with only 4 reported cases(1). Compared with classic Botulism from C. botulinum type A toxin, type F toxin may produce a much shorter clinical course, approximately 7 days, as noted in our patient and in previously published case reports(1). This difference may be due to the differential rates of replacement of the cleaved neuronal proteins. C. baratii type F toxin cleaves synaptobrevin, while type A toxin cleaves synaptosomal-associated protein of 25 kilodaltons (SNAP-25). Both proteins participate in synaptic vesicle release. In experimental rat cerebellar neuron preparations, synopatobrevin function is restored within 7 days while restoration of SNAP-25 function requires greater than 30 days(3). Finally, anti-toxin against type E toxin may provide benefit in type F toxin disease due to toxin heavy-chain sequence homology(1).
This patient developed Botulism secondary to a rare toxin. The unique characteristics of type F toxin and its site of action provide insight into the clinical course of this patient.
D.S. Hagg, None.