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ically defined cases of wound botulism. Wheeler and colleagues surely know wound botulism when they see it, because they consult on most wound botulism cases, and to the mind of most experts familiar with the diagnostic challenges of botulism, they are fully justified in using clinical diagnosis as the gold standard against which to measure the mouse bioassay’s limited sensitivity. The sensitivity calculated in the article is not the intrinsic sensitivity of a test under ideal laboratory conditions, but rather that of the clinical setting, calculation of which depends on a complicated set of real-world factors. This calculation must take into account the quality of the gold standard clinical diagnosis, which depends on the initial astuteness of the admitting physician and the diagnostic skill of the California Department of Public Health consultant, and variations in toxin levels in clinical samples, which depend on the timeliness of sample collection, the size of the Clostridium botulinum colony in the infected wound, kinetics of toxin absorption from the abscess, its migrations to the extracirculatory compartment, and possibly other factors. One must also keep in mind that the sensitivity of mouse bioassay results may be different for the other principal forms of botulism—foodborne botulism and infant botulism. Most foodborne botulism cases are diagnosed by other expert con

Diagnosis and Treatment of Botulism: A Century Later, Clinical Suspicion Remains the Cornerstone