Wound botulism is manifested by neurologic symptoms, as in foodborne botulism, but there are no GI symptoms or evidence implicating food as a cause. A history of a traumatic injury or a deep puncture wound in the preceding 2 wk may suggest the diagnosis. Careful search should be made for breaks in the skin and for skin abscesses caused by self-injection of illegal drugs. Cranial nerve deficits typically include ptosis, extraocular muscle palsies, weak cry, poor suck, decreased gag reflex, pooling of oral secretions, and an expressionless face. Severity varies from mild lethargy and slowed feeding to severe hypotonia and respiratory insufficiency.
Most cases are idiopathic, although some have been traced to the ingestion of honey.
C. botulinum spores are common in the environment, and many cases may be caused by the ingestion of microscopic dust. Electromyography is useful for diagnosis because it produces a characteristic augmented response to rapid repetitive stimulation in most cases. In foodborne botulism, the pattern of neuromuscular disturbances and ingestion of a likely food source are important diagnostic clues. The simultaneous presentation of at least two patients who ate the same food simplifies diagnosis, which is confirmed by demonstrating C. botulinum toxin in the serum or feces or by isolating the organism from feces. Finding C. botulinum toxin in suspect food identifies the source.