Читать книгу Plants Poisonous to Live Stock - Harold Cecil Long - Страница 8

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Soapwort (Saponaria officinalis L.). This plant is more or less poisonous, but is rarely, if ever, eaten by stock, and no recorded case of the poisoning of stock has been met with.

Toxic Principle. The whole plant, especially the root, contains the poisonous glucosidal Saponin (C₁₈H₂₈O₁₀)₄, a peculiar substance which causes intense frothing when stirred in water.

Symptoms. No symptoms of animal poisoning by the plant are recorded, but the action of Saponin in the blood stream is to induce dissolution of the red cells, with stupefaction and paralysis, as in the killing of fish by poisoning. It also causes vomiting and purging. Taken by the mouth it causes inflammation of the alimentary tract, the contents of which are fœtid and mixed with blood.

REFERENCES.

16, 63, 76, 81, 203, 235.

Corn Cockle (Agrostemma Githago L.). This well-known plant of cornfields must be regarded as poisonous, though experiments and reports as to its effects on the different classes of live stock vary widely. Though a poisonous principle is found in nearly all parts of the plant, the plant in the green state appears to be innocuous, and is in any case rarely likely to be eaten fresh by stock, which probably refuse it on account of its hairy character. The seeds, however, are by no means harmless. They are rather large, and somewhat troublesome to separate from cereal grains. When ground up with wheat they both discolour the flour and impart a grey tint and disagreeable odour to bread made from it. Further, flour containing a considerable quantity of cockle must, owing to the poisonous character of the latter, be held to be unfit for consumption. Fatal results have followed the use of bread containing Corn Cockle. The toxic principle therefore is not destroyed by heating, even in an oven in baking.

As regards domestic animals, Corn Cockle seeds have frequently been mixed with feeding stuffs and have caused many deaths. Cornevin’s experiments in feeding calves, pigs and fowls led to fatal results. He was able to say that the amounts of cockle flour necessary to cause death were:—

Calf	0·25	lb.	per 100 lb. live weight.
Pig	0·10	„
Dog	0·90	„
Fowl	0·25	„

Among other cases, Kornauth and Arche found that in their feeding trials pigs were not killed, but albuminoid metabolism was diminished and fat production increased. In 1893 pigs died in Germany with symptoms of acute poisoning, when fed on tailings containing six per cent. of cockle. In 1903–4 experiments showed that with the cow, sheep, pig and goat, cockle is not poisonous when fed in amounts usually found in feeding stuffs. Millspaugh gives a case in which two calves died on being fed with two lots of 14½ oz. each of wheat flour containing 30 per cent. and 45 per cent. of cockle seeds. About 1892 Nevinny concluded that six grammes of cockle seed consumed in 1200 grammes of bread were beyond doubt poisonous in effect, and that the sale of grain or flour containing it should be forbidden. Kobert held that the sale of feeding stuffs containing cockle should be forbidden by law. An extensive study of this question was made by Pesch, who concluded that “Under certain conditions Corn Cockle is injurious to domestic animals. The amount of the poisonous substance in the seed is variable, depending probably upon the season and the soil. Animals become accustomed to it, so that amounts of seed which at first cause sickness, later have no injurious effect. The susceptibility of animals to the poison varies both with the species and the individual. Young animals are more readily affected than older ones. It is believed that rodents and sheep are not susceptible, and, as far as is known, grown cattle are only slightly or not at all affected by the poison. Calves, swine, horses, and especially dogs, are more or less susceptible. Concerning birds and fowls there is some doubt.”

Though animals are reputed to become tolerant of the poison if the cockle is only taken in small regular doses, yet there appears to be a chronic form of poisoning due to this cause and termed Githagism, while there is an acute poisoning due to the ingestion of large quantities of the seeds which may cause death in 24 hours or less.

It is clear that the evidence is quite sufficient to warrant the statement that the ingestion of more than a very small quantity of cockle seed is dangerous, and the consumption of even small quantities should be avoided. Thus care should be taken to remove the seeds from cereal grains.

Toxic Principle. The dangerous substance contained in cockle seeds is the glucoside variously known as Githagin, Saponin, Agrostemmin, Sapotoxin, Agrostemma-Sapotoxin, or Smilacin (C₁₇H₂₆O₁₀)₂. This principle appears to occur chiefly in the seeds, which contain up to 6·56 per cent., but it has been found in small quantities in other parts of the plant. It is very freely soluble in water, in which it froths like soap when shaken up, and it has a sharp taste and no odour.

Symptoms. A sufficient quantity of the toxic substance may cause nervous debility and dysentery—according to Chesnut “intense irritation of the digestive tract, vomiting, headache, nausea, vertigo, diarrhœa, hot skin, sharp pains in the spine, difficult locomotion, and depressed breathing. Coma is sometimes present and may be followed by death. In animals chronic diarrhœa and gradual depression.”

The chronic form, which occurs when small doses are repeated over a long period (practically the only form found in human beings, but never in animals, except perhaps in the pig) is characterized by gradual wasting away, loss of breath, loss of strength, chronic diarrhœa, and nerve troubles, death taking place in marasmus and decline. The active principle acts as an irritant on the digestive tract, causing colic, diarrhœa and enterorrhagia.

Cornevin describes the symptoms in the acute form of the poisoning in the case of horses, cattle, pigs and dogs.

In the horse, if a small quantity only is taken, there is yawning, heavy colic, stamping and evacuation of rather soft fæces. If larger quantities are taken, the symptoms, which commence in about an hour, are salivation, frequent yawning and turning of the head, colic, pale mucus, hurried and weak pulse, rise in temperature and accelerated respiration. Some time later there are muscular tremors succeeded by pronounced rigidity, and the fæces are diarrhœic and fœtid. The animal lies down, and getting up is painful; it falls into a kind of coma, stretches itself to the utmost, and death takes place without convulsions.

In cattle, the symptoms observed one hour after eating are restlessness, salivation, and grinding of the teeth. Excitement and colic are followed sometimes by coughing, this state lasting from five to eight hours. There is then a period of coma, characterized by permanent decubitus, repeated fœtid diarrhœa, hurried and plaintive respiration, accelerated and gradually weakening pulse, a gradual loss of motor and sensory powers, and a progressive decline in temperature. Death occurs in twenty-four hours.

In the case of pigs, the animal grunts, lies down and remains thus with its snout embedded in the straw. There is vomiting, more or less violent colic and diarrhœa, the evacuation consisting of bad-smelling, spumous fæcal matter. At times there are clonic contractions. Young pigs are most susceptible.

Pott cites cases in which abortion was a feature of the poisoning, both in cows and pigs. The results of numerous experiments which he quotes (among others some carried out for the Prussian Ministry of Agriculture) are very contradictory, a small quantity causing death in some animals, while others of the same species were left unharmed by large quantities. He ascribes this to the very variable proportions of the poison present in the seeds.