Toadstools, mushrooms, fungi, edible and poisonous; one thousand American fungi / How to select and cook the edible; how to distinguish and avoid the poisonous, with full botanic descriptions. Toadstool poisons and their treatment, instructions to students, recipes for cooking, etc., etc.

by Charles McIlvaine; Robert K. Macadam

In arriving at any conclusion we must bear in mind the variation of different animals in their susceptibility to poisons. Thus, to give the greatest difference observed, .085 gram. dried Amanita muscaria per kilo of body weight killed one dog in an hour, while in another dog .223 grams. of the same preparation per kilo only killed after 24 hours, the cardiac inhibition having disappeared one-half hour after the poison was injected. However, an average of six (6) experiments on cats and dogs with dried A. muscaria in which no antidote was given shows the lethal dose to be .103 gram. per kilo of body weight. The average of four (4) experiments, in which the fungus, dried in the same way, was used but atropine was given as an antidote, gives the lethal dose of .335 gram. per kilo and death only occurred late in each case. There can be no doubt, therefore, of the antidotal value of atropine for poisoning by Amanita muscaria.

It should be borne in mind, however, that it is not an infallible antidote even when given early, and that it does not prevent death from the late effects in severe cases, although given in large doses. In some experiments atropine was administered at the same time the poison was given and in others before it.

The important practical lesson is that too much reliance should not be placed upon atropine. It will be shown later that it has little value as an antidote to A. verna and A. phalloides. Probably these fungi contain less muscarine than A. muscaria. Although there is no drug so antagonistic in its physiological action to the poison of the A. muscaria as atropine, the use of other remedies should not be neglected. The symptoms have to be treated as they arise. Strychnia, alcohol in moderate amounts and suprarenal extract could all be used to advantage in restoring the circulation, especially late in the poisoning. Atropine merely removes the inhibition of the heart which occurs as an early symptom.

External heat should be applied if the body temperature is subnormal. The treatment of gastro-intestinal symptoms will depend upon the conditions of each individual case. The injection of a large amount of warm physiological salt solution (.6-.7 per cent. sodium chloride) into the subcutaneous tissues should also be tried in severe cases seen late in the poisoning.

POISONING BY AMANITA VERNA OR A. BULBOSUS VERNA BULL.

The symptoms appear from six to fifteen hours after the ingestion of the poison and may be largely choleraic in nature, i. e., vomiting and purging, the discharges from the bowel being watery with small flakes suspended and sometimes containing blood.

The disturbance of the circulation is somewhat similar to that caused by A. muscaria, viz., slow, strong pulse early, but rapid and weak later. Dizziness and faintness may be early symptoms. Sometimes the skin is pale and covered with cold, clammy sweat; at others there is great cyanosis. The body temperature is subnormal, unless nervous symptoms are very severe. Very prominent among the symptoms are tetanic convulsions, which may appear comparatively early and persist until the end.

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.