THE EFFECT OF ANESTHESIA AND OF SEDATIVES ON THE SERUM THERAPY OF EXPERIMENTAL BOTULISM

Abstract

When guinea pigs are fed large amounts of botulinus toxin, they develop symptoms of intoxication within 6 hours and die usually within 12 hours after the feeding of toxin. If very large amounts of toxin are introduced intraperitoneally, the animals may show symptoms of intoxication at the end of the 1st hour and die usually within 2 hours following the administration of toxin. If these animals are placed under anesthesia following the administration of toxin, the intoxication proceeds much more slowly. Anesthesia, by ether, is effective in this manner whether the toxin is given per os or intraperitoneally. The life of guinea pigs kept under ether after the administration of lethal amounts of toxin is prolonged by a period approximately equal to that during which the administration of the anesthetic is continued. When anesthesia is discontinued, the intoxication proceeds at its usual rate. It appears, therefore, that administration of ether delays the rate of intoxication but does not alter the toxin or the nature of the mechanism of intoxication. Anesthesia thus delays the progress of intoxication not only when administered immediately after the intake of toxin, but when administered much later after the intoxication has already progressed far enough to cause definite objective symptoms of poisoning. At this late stage of intoxication, the unsupported serum therapy of botulism in guinea pigs usually remains without effect. If, however, the animals are anesthetized at this time and kept under the influence of ether for some time, antitoxin therapy becomes effective. Indeed the antitoxin treatment can be delayed further for several hours, provided the animal is kept under anesthesia during the interval. Results of a similar nature were obtained with luminal sodium, nitrous oxide-oxygen mixture, and morphine used in place of ether. In view of the fact that the published data indicate that botulinus antitoxin has thus far failed to give beneficial results in the treatment of botulism in human beings because, as it would seem, of the rapid progress of intoxication, any method of delaying the progress of intoxication to supplement the antitoxin therapy deserves consideration.