The rest of the history was remarkable for hypertension, non-insulin-dependent diabetes, gastroesophageal reflux, osteoporosis, mild dementia, and a prior cerebrovascular aneurysm that was clipped, as well as a VP-shunt. The family was unsure why the shunt had been placed and later removed.

The patient asked me for a cup to spit into. “I’m having trouble swallowing my spit real good today,” he said. “I’m sure it’s nothing. I’m not throwing up yet either, but if you had something for nausea, I’d take it.” I paused again. The alarm had turned into a Klaxon. Difficulty swallowing with a sudden onset in relation to neurologic complaints usually doesn’t go into the “benign” folder in my brain. Heart, lungs, and stomach all seemed unremarkable. Neurologic is where the answer lay, but central or peripheral?

No dysdiadochokinesia. No ataxia. Good gait. Plantar flexion and dorsiflexion seemed weak. Patellar, Achilles, and Babinski seemed normal. Bicep and tricep reflexes seemed diminished. Grip strength was poor, but bicep and tricep strength felt all right. Tongue wasn’t deviated, but speech was “different” according to the family. Eyes were normal individually, diplopia was present. No matter where I went or where he looked, he saw double. This was interesting.

Form took shape, observations started rolling together.

Peripheral. Small muscles. Diffuse. Ocular. Tongue. Nausea. Someone else in the house with something similar—the cogs aligned.

I whispered an expletive under my breath. “Do you and your wife can food?” I asked.

“Eh, I don’t know. I just eat it. She makes good pasta sauce,” he said. I turned toward the family and tried again a bit more specifically. “Does your mom grow tomatoes, cook them into sauce, and then can the pasta sauce?”

“Oh, yeah, spaghetti sauce—they do that all the time! Why?”

“Because I’m pretty sure that they have botulism!”

The alarm in my head grew louder. Diffuse weakness, more of the distal and smaller muscles. Eyes, tongue, fingers this didn’t sound like stroke.

The Facts

Foodborne botulism is a rare clinical entity, with about 1.25 cases per 10 million people annually.¹ It frequently affects a single individual, as reported in 70 percent of cases from 1975 to 1988, but averages 2.7 cases per outbreak.² In 2012, 25 cases were reported to the Centers for Disease Control and Prevention (CDC), with four outbreaks with more than one individual and one death.³ The botulinum toxin is frequently cited as the most potent known toxin, with a LD50 of 1μg/kg, and works by inhibiting release of acetylcholine from autonomic and presynaptic motor nerves.^4,5 Most cases in adults result from ingestion of the toxin, whereas infantile and wound botulism are due to the ingestion or infiltration of toxin-forming spores. There are seven separate types of botulinum toxin: types A, B, C, D, E, F, and G. Types A, B, E, F, and G are absorbed from the gastrointestinal tract, and most cases are secondary to types A, B, and E. Type A is usually found west of the Mississippi River, type B east of the Mississippi (in the Allegheny Mountains particularly), and type E in the Pacific Northwest and Great Lakes states.^6-8