_Staffordshire Weekly Sentinel_, Aug. 21st, 1909.
The toxic principle is cumulative, that is, small quantities of the plant eaten regularly may result in poisoning, owing to the poison being slowly eliminated by the kidneys. Indeed, cases have been recorded in which the poison has been secreted and eliminated in the milk of cows and so has caused poisoning of both calves and infants.
_Toxic Principle._ Meadow Saffron contains in all parts the acrid, poisonous alkaloid _Colchicine_ (C_{ 22}H_{ 25}NO_{ 6}) stated by Esser to occur to the extent of 0·2 per cent. in the corms, 0·4 to 0·6 per cent. in the seed coats, but only traces in the leaves. Hertel obtained 0·38 to 0·41 per cent. of alkaloid from the _seeds_, Farr and Wright from 0·46 to 0·95 per cent., and Carr and Reynolds 0·12 to 0·57 per cent.; the U.S. Pharmacopœia, 1905, required a Colchicine content of 0·45 per cent. in the _seeds_, and 0·35 per cent. in the _corms_ (Allen).
_Symptoms._ After small, but not fatal doses there is loss of appetite, suppression of rumination, salivation, light colic, diarrhœa and voiding of small quantities of urine. Blood has been observed in the milk of affected cows. Larger and fatal quantities cause total loss of appetite and sensation, stupefaction, loss of consciousness, dilatation of pupils, unsteady gait, and even paralysis of limbs, sweating, severe colic, and bloody diarrhœa, strangury and bloody urination; rapid, small, and finally imperceptible pulse, laboured breathing; and death in from one to three days. Where recovery takes place it is very slow (12 to 14 days according to Cornevin).
Cornevin draws attention to the fact that, as the symptoms do not occur until several hours after ingestion, by which time the poison must be partly distributed, the poison is very dangerous and difficult to combat, attempts at vomiting or evacuation, whether spontaneous or caused therapeutically, having little chance of ridding the organism of the poison. Cornevin’s account of the symptoms shows that at first there is abundant salivation, with constriction of the throat, and dysphagia; then nausea with vomiting; colic; abundant, repeated and diarrhœic evacuations, which at the end become dysenteric with painful tenesmus; abundant urination; short, accelerated and difficult respiration, with incoordination in the thoracic and abdominal movements. The circulatory functions are modified only in fatal cases, when the pulse is small and intermittent towards the end. There is finally a notable drop in temperature, shown by the coldness of the skin. Death occurs in from 16 hours to 6 days after ingestion. During the last few hours the animals are stretched at full length and are incapable of getting up. There may be prolapsus of the rectum; the eye is deeply sunk; sensibility is deadened and death is due to stoppage of respiration.