B114 



(leaf 2) 



foliage, but develops rapidly from the union of substances released 

 when the leaves are crushed and moistened, as occurs in an animal's 

 stomach during digestion. 2 3 4 The foliage is poisonous over a long 

 period; its virulence does not decrease until the end of August, al- 

 though the plants are harmless by October. Unfortunately, the 

 leaves of the young shoots, which are the most palatable, are also 

 the most harmful. The Nevada Agricultural Experiment Station 2 

 determined that a little over one-fourth of a pound of leafage was 

 fatal to sheep and iy 2 pounds was sufficient to kill a 500-pound 

 cow. This amount, however, must be consumed at a single feeding, 

 as the animals are able to eliminate the effects of smaller quantities 

 rapidly and to escape harmful results even though total consump- 

 tion at various periods during the day may exceed the lethal dose. 

 Continued use of chokecherry foliage, however, does not establish 

 immunity against hydrocyanic acid poisoning. Ordinarily, the 

 poisonous acid is released as soon as the foliage is eaten, but some- 

 times, on dry ranges, lethal quantities are eaten without apparent 

 discomfort, until the animal goes to water. The water consumed 

 moistens the dry food mass in the stomach with resultant formation 

 of the acid, which quickly kills the animal. Fleming and associates 2 

 report the following symptoms: 



The poisoned animal becomes very uneasy, staggers, falls, goes into con- 

 vulsions, breathes with increasing difficulty with eyes rolling and tongue hang- 

 ing out. Then it becomes quiet, bloats, and dies, usually within less than an 

 hour after eating the leaves. 



Post-mortem examinations easily serve to identify the poison as 

 the stomach contents, when stirred, emit the strong, bitter-almond 

 odor characteristic of hydrocyanic acid. 



Various remedies have been suggested, such as administrations of 

 starchy foods or ordinary corn sirup, 3 or a drink composed of freshly 

 mixed sodium carbonate and iron sulphate. 2 5 However, most anti- 

 dotes have proved of little value, as the poisonous action is usually 

 well advanced before the animal can be treated, particularly on the 

 open range. Furthermore, the convulsions and paralysis of the 

 respiratory system of the poisoned animal make administration of 

 the antidote difficult. Most authorities 1 2 believe that livestock 

 losses from chokeberry poisoning can be largely avoided by proper 

 range management, as poisoning usually occurs in areas which are in 

 a depleted condition. The use of overgrazed ranges, or locally over- 

 used areas such as watering places, bedgrounds, and along driveways, 

 which are infested with western and black chokecherries, should be 



1 See footnote on preceding page. 



2 Fleming, C. E., Miller, M. K., and Vawter, L. R. THE COMMON CHOKECHERHY (PRUNUS 



DEMISSA) AS A PLANT POISONOUS TO SHEEP AND CATTLE. N6V. Agr. Expt. Sta. Bull. 109, 



30 pp., illus. 1926. 



8 Morse, F. W., and Howard, C. D. POISONOUS PROPERTIES OF WILD CHERRY LEAVES. 

 N. H. Agr. Expt. Sta. Bull. 56: [111]-123, illus. 1898. 



4 Couch, J. F. POISONING oir LIVESTOCK BY PLANTS THAT PRODUCE HYDROCYANIC ACID. 

 U. S. Dept. Agr. Leaflet 88, 4 pp. 1932. 



5 Raring, C. M. PRECAUTIONS AGAINST POISONING BY JOHNSON GRASS AND OTHER SOR- 

 GHUMS. Calif. Agr. Expt. Sta. [Unnumbered Leaflet], [4] pp. [1917.] 



Fleming, C. E., and Dill, R. THE POISONING OF SHEEP ON MOUNTAIN GRAZING RANGES 



IN NEVADA BY THE WESTERN CHOKECHERKY (PRUNUS DEMISSA). NeV. Agr. Expt. Sta. Bull. 



110, 14 pp., illus. 1928. 



