Toadstool Poisoning and its Treatment 



In animals the effect of this toadstool is entirely different from that of 

 A. muscaria. Perhaps the most striking difference is the frequency 

 with which convulsions appear. Convulsions occurred repeatedly in 

 mammals and in nearly every frog to which the toadstool was given. 

 This fungus seems to contain some poison that acts upon the spinal cord 

 very much as strychnia does, though less powerfully, of course. 



The circulatory conditions are also different. The inhibition of the 

 heart may be pronounced as an early condition, but the pressure does 

 not return to the normal after this disappears, either from giving 

 atropine or from cutting the pneumogastric nerves. Section of these 

 nerves removes the cardiac inhibition much more completely than after 

 poisoning by the A. muscaria. There is often a fall of pressure without 

 cardiac inhibition. In other words, there is a much greater permanent 

 fall of blood-pressure due to paralysis of the nerve center controlling 

 the blood vessels (vaso-motor center). This condition will last a long 

 time and does not show the same tendency to disappear as after A. 

 muscaria. Moreover it is produced by comparatively small amounts 

 of the A. verna. 



The respirations are very slow. The blood is poorly oxygenated and 

 this probably causes the cyanosis sometimes observed in men poisoned 

 by this fungus. 



Bloody fluid is sometimes vomited or comes from the nose. It may 

 also occur in the discharge from the bowel. 



Retching and purging occurred more frequently as early symptoms 

 than in animals poisoned by A. muscaria. 



Coma appeared early and continued until death. The administration 

 of atropine soon after giving the poison when cardiac inhibition was 

 present, caused a slight temporary rise of blood pressure but did not 

 affect the dilated condition of the blood vessels. The pressure con- 

 tinued low notwithstanding the atropine. Although the experiments 

 with this fungus were not as numerous as with the A. muscaria because 

 of difficulty in obtaining it, yet it seems clear that atropine is of very 

 little value as an antidote. Death very rarely resulted from the cardiac 

 inhibition occurring early but usually came on late after that condition 

 had disappeared. The lethal dose was no larger when atropine was 

 given than when no antidote was used. 



Amanita verna is very much more toxic than A. muscaria, the average 

 of four experiments in which the former was given without an antidote 



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