Plants Poisonous to Live Stock

by Harold Cecil Long

PAPILIONACEÆ.

Laburnum (Cytisus Laburnum L.). The well-known and much admired Laburnum must be regarded as one of the most poisonous species of British plants. By numerous experimental researches Cornevin proved that all parts of the plant are poisonous—root, wood, bark, leaves, flowers, and seeds, especially the seeds. In his experiments the horse, ass, sheep, goat, dog, cat, fowl, duck and pigeon, were utilized, seeds being given. He found that 80 centigrammes per kilogramme live weight would be necessary to kill a horse (say 1 lb. for an animal of 1200 lb. live weight), 60 centigrammes per kilogramme live weight to kill an ass (say 6 oz. for an ass weighing 600 lb.); and 6 grammes in the case of a fowl (say 0·4 oz. for a fowl weighing 4½ lb.). The sheep and goat he was not able to kill, as they refused the food after a certain point; the dog and cat he was not able to kill because they so readily vomited; and the duck and pigeon vomited with extreme facility.

Many cases of the poisoning of children have occurred through the ingestion of the flowers and seeds. In 1908 a case was recorded by the Board of Agriculture and Fisheries, in which two horses were alleged to have been poisoned in North Wales by laburnum seeds, a very small quantity of which was found in their stomachs after death.

Müller states that in Dalmatia goats which had eaten Cytisus Weldeni, though themselves uninjured, produced milk which was poisonous to man.

Toxic Principle. All parts contain the toxic alkaloid Cytisine (C₁₁H₁₄N₂O), said by Moer and Partheil to be identical with Ulexine; it is found in the seeds to the extent of 1·5 per cent. Cornevin states that the root, wood and bark are nearly constant in toxicity, but that the leaves and pods present remarkable seasonal variations owing to the migration of the poison into the seeds. The toxic property is not destroyed by drying of the plant.

Symptoms. Laburnum poisoning is of the acrid, narcotic type, with, in man, nervous symptoms, abdominal pain, vomiting, purging, tetanic spasms and convulsions.

Cornevin’s observations show that the symptoms occur in three consecutive stages,—(1) excitement, (2) coma and incoordination of movement, and (3) convulsions. The order of the appearance, their duration, and the association of each with the others depend upon the susceptibility of the animal and the quantity ingested. Thus the symptoms of excitement may be present alone if only a small quantity is eaten; the duration of the symptoms in this case is never considerable, and the normal is gradually regained. In general, however, the symptoms are associated in pairs; thus when an average quantity is fed there is excitement and coma but no convulsions; when large quantities are fed the first stage is suppressed or is so short as to be almost imperceptible, the coma and convulsions being present simultaneously. As regards temperature, there is, in stage (1) a rise, in stage (2) a drop, and in stage (3) a rise again near death. In stages (2) and (3) there is a slackening of respiration, the arterial tension is raised, there is an increase in the number of pulsations and a modification of the rhythm. In stage (3) near death there is a lowering of the arterial tension, and the pulsations become gradually less perceptible, but with a uniform rhythm; there is a slackening in respiration, and by the time this finally ceases the heart beats have become imperceptible.

When horses, asses or mules have eaten a small quantity of the seeds or leaves, there is simply yawning and uncertain gait, these symptoms lasting for two hours, and the normal being regained after urination. Considerable (but not fatal) quantities cause unsuccessful attempts at vomiting, sometimes opisthotonos in asses, sweating, muscular tremors, and then a deep coma which may last 15 hours. Fatal quantities cause yawning, sexual excitement, accelerated and noisy respiration, wheezing, muscular tremors followed by contractions which commence in the posterior limbs and spread to the anterior limbs, facial contractions, staggering and copious sweating. A rapid fall in temperature follows, but there is a slight rise during the period of convulsions; the pulse is at first quicker and stronger, but the number of beats rapidly comes back to the normal, to rise again shortly before death; the rhythm of the pulse is at first regular (in groups of 2, 3 or 4) but becomes irregular again just before death. The animal at length falls, and cannot get up, the nostrils are distended, the mouth is wide open, respiration becomes gradually slower, and death takes place in great agony.

In cases of poisoning of horses and asses noticed by Pott animals that could not vomit died very quickly. The symptoms were excitement, nausea, coma, slower breathing, convulsions, paralysis of the motor nerves, and finally cessation of the action of lungs and heart.

Ruminants are much less susceptible than horses. Cornevin’s attempts at poisoning failed through their refusal of the plant. Müller observed in a case of cattle poisoning, bloating, paralysis of the limbs (especially fore limbs), sleepiness, dilatation of pupils, and later salivation, nausea, coma and occasional convulsive movements of the muscles of the extremities. These symptoms persisted through several days and then disappeared.