Human Botulism Caused by Clostridium Botulinum Type E: The Birmingham Outbreak

Abstract

Four elderly patients developed botulism following ingestion of tinned Alaskan salmon contaminated with Clostridium botulinum type E. Severe skeletal muscle paralysis, occurring within 18 hours in peripheral, respiratory and facial, extrinsic ocular and pharyngeal muscles, resulted in progressive respiratory failure, ptosis, loss of eye movements, dysphonia and dysphagia. In addition, the development of intestinal ileus, loss of vagal cardiac control, hypotension and lack of vasomotor response to either postural change, stimulation by cold or the Valsalva manoeuvre indicated dysfunction of both parasympathetic and sympathetic nervous systems. Sensation was unimpaired and no alteration of consciousness occurred despite the presence of extensive abnormal delta activity in the EEGs of all patients. The diagnosis of botulism was confirmed by demonstration of Cl. botulinum type E toxin in the serum of all four patients and in salmon remnants from the suspect tin, in which Cl. botuilnum type E spores were also identified. Standard supportive intensive care and antitoxin therapy were complemented by the use of a novel neuromuscular blockade antagonist, 4-aminopyridine. This agent was shown by electromyography to be effective in restoring neuromuscular transmission and, clinically, to produce almost complete reversal of peripheral paralysis. However, this effect was transient and there was no detectable effect on respiratory muscle. Administration of 4-aminopyridine by constant infusion produced sustained improvement in peripheral muscle power, but there was no additional effect on respiratory muscle, and convulsive phenomena occurred following treatment. Despite these latter problems, 4-aminopyridine produced a greater response in peripheral muscle than might have been expected with guanidine and further studies, possibly with less neurotoxic analogues, are indicated.