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

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.

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 continued 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 being .034 gram. (dried) per kilo of body weight, while .103 gram. (dried) per kilo, was the average for the latter fungus.