Diagnosis and Treatment

Presentation is usually 12–24 hours after ingestion and starts with gastrointestinal complaints of nausea, vomiting, and distention. Gradually, neurologic symptoms follow, with bulbar symptoms (CN IX, X, XI and XII), diplopia, and bilateral symmetric descending paralysis from cranial nerves to limbs. Frequently, pupillary mydriasis and ptosis are observed.⁴ Forty to 70 percent of affected individuals require intubation for respiratory muscle paralysis.¹ Mentation and sensation remain normal, and cardiovascular effects are rarely seen until respiratory compromise occurs.

Botulism is commonly confused with the Miller Fisher variant of Guillain-Barré syndrome, but differential diagnosis should include poisoning by aminoglycoside, anticholinergics, carbon monoxide, diphtheria, organophosphates, or thallium, as well as myasthenia gravis, Guillain-Barré, inflammatory neuropathies or myelopathies, stroke, tetanus, or tick paralysis.⁴

Diagnosis is clinical until botulinum toxin can be detected in serum, stool, or food samples. Tensilon testing and electromyography (EMG) are normal early on, though motor response to EMG testing will be diminished gradually but conduction velocity will remain unimpaired. Samples of stool, blood, gastric contents, vomitus, and foods should be checked for both C. Botulinum spores and toxin. Physicians should contact the CDC at 770-488-7100 if botulism is suspected.

Presentation is usually 12–24 hours after ingestion and starts with gastrointestinal complaints of nausea, vomiting, and distention. Gradually, neurologic symptoms follow, with diplopia and bilateral symmetric descending paralysis from cranial nerves to limbs. Frequently, pupillary mydriasis and ptosis are observed.

Management is supportive, particularly of the respiratory system, as intubation is required in at least 40 percent of individuals.¹ A trivalent antitoxin is no longer available, but bivalent (types A and B) and monovalent (type E) antitoxins are.⁴ One should bear in mind that the antitoxins are equine-derived, so the usual serum sickness precautions remain. Both are obtained on a named-patient basis from one of the nine CDC regional centers. Usually, they are flown to the nearest airport, and a courier service hand-delivers them directly to you. The CDC coordinates the vast majority of this once they have the patient’s name and know that you suspect botulism.

Many patients have long-lasting side effects years after diagnosis, especially in perceived strength and respiratory fitness.⁹ Most patients return to near baseline function within several months to a year.

“There are old home canners, and there are bold home canners, but there are no old, bold home canners.”

Color-enhanced transmission electron micrograph (TEM) of Clostridium botulinum. C. botulinum grows in badly preserved canned foods, notably meat and fish, and produces the potent exotoxin that causes botulism poisoning. The toxin affects the central nervous system of humans; in fatal cases death results from heart and lung failure due to malfunctions in the cardiac and respiratory centers of the brain. Magnifcation 50,000x at 10 cm.

Case Resolution

The patient’s primary care physician, who had admitted the patient’s wife, was contacted, as were infectious disease and neurology. Once I mentioned the word “botulism,” their response was dramatically prompt. I had, oddly enough, seen an entire family with an outbreak in medical school and had the experience of calling the state defense lab and the CDC to coordinate delivery of the antitoxin. The statistical likelihood of seeing two independent outbreaks of botulism in my career is something I leave to the statisticians (back-of-the-napkin math puts it around 4*1013:1).