[591] Zeitschr. f. rat. Med. (3 R.), Bd. xxvi., S. 1, 1866.
§ 560. The nerium oleander has several times caused grave symptoms of poisoning, and they have usually fairly agreed with those produced by foxglove. For example, Maschka[592] relates the case of a boy, two years old, who ate two handfuls of the nerium oleander. The effects commenced in ten minutes, the child was uneasy, and vomited. In six hours a sleepy condition came on; the face was pale, the skin cold, the pupils contracted, and the pulse slow and irregular. After the sickness the boy woke up, but again fell asleep, and this occurred frequently; coffee was given, which appeared to do good. The pulse was intermittent. On the following day the child was still ill, with an intermittent pulse, frequent vomiting, feebleness, sleeplessness, and dilatation of the pupil; there was no diarrhœa, on the contrary, the bowels were confined. On the third day recovery followed.
[592] Vierteljahrsschrift f. gericht. Med., Bd. ii., No. 17, 1860. Brit. and For. Med. Chir. Review, vol. xxvi. p. 523, 1860.
In an Indian case,[593] the symptoms were altogether peculiar, and belonged rather to the convulsive order. A wood-cutter, aged thirty-five, near Kholapore, took, for the purpose of suicide, a little over an ounce of the expressed juice of the oleander. The symptoms began so rapidly that he had not time to walk five yards before he fell insensible; he was brought to the hospital in this state; the face on his arrival was noticed to be flushed, the breathing stertorous, there were violent spasmodic contractions of the whole body, more marked on the left than on the right side. The effect of this was remarkable. During the intervals of the spasm, the patient lay evenly on his back, and when the convulsions commenced the superior contraction of the left side threw him on to the right, in which position he remained during the paroxysm, after the subsidence of which he fell back into his old position. The evacuations were involuntary and watery; the man was insensible, with frequent convulsions of the kind described, for two days, but on the third day became conscious, and made a good recovery.
[593] Transac. of Med. and Phys. Soc. of Bombay, 1859.
In any case of poisoning, the methods by which neriin and oleandrin are separated from the plant can be applied to separate them from the tissues with more or less success. Here, as in all the other digitalin-like glucosides, physiological tests are alone of value in the final identification.
§ 561. The Madagascar Ordeal Poison.—To this group may also belong the poison of the Tanghinia venenifera, a tree in the Island of Madagascar, the fruit of which is used as an ordeal poison. It may be obtained in crystals; it is insoluble in water, and very poisonous. The upas of Singapore is also said to contain with strychnine a glucoside similar to antiarin.
§ 562. Erythrophlein is an alkaloid, not a glucoside, and is obtained from the bark of the Erythrophlœum guineense (West Africa). It acts on the heart like digitalis, and has also effects similar to picrotoxin.
§ 563. The term “saponin” of late years has been applied to a class of glucosides which possess the common property of being poisonous, and, when dissolved in water, forming solutions which froth on shaking like soap-suds.
The substances which have these properties are not all of the same series chemically, but those of the general formula, CnH2n-8O10, are most numerous, and the following is a list:—
Possibly also dulcamarin C22H34O10 and syringen C17H26O10 may belong to this series.
There are some 150 distinct plants which thus yield saponins; a few of these plants are as follows:—Saponaria officinalis, Gypsophila struthium, Agrostemma githago (corn cockle), Polygala senega, Monimia polystachia, the bark of Quillaja saponaria, and Chrysophyllum glycyphleum.
The saponin separated from Saponaria, and from the corn cockle will be here described.
§ 564. Properties.—Saponin is a white amorphous powder, very soluble in water, to which it gives the curious property of frothing just like soap solution. To obtain this effect there must be at least 1 mgrm. in 1 c.c. of liquid. Saponin is neutral in reaction, it has no odour, but causes sneezing if applied to the mucous membrane of the nose; the taste is at first sweet, and then sharp and acrid. It is almost entirely insoluble in absolute alcohol, but dissolves in hot alcohol of 83° to separate again nearly completely on cooling. It is precipitated by basic lead acetate, and also by baryta water, but in each case it is advisable to operate on concentrated solutions. Picric acid, mercuric chloride, and alkaloidal “group reagents” give no precipitate. When a little of the solid substance is treated with “Nessler” reagent, there is a greenish or yellow colour produced. A drop of strong sulphuric acid, mixed with a minute quantity of saponin, strikes slowly a bright red colour, which, on heating, deepens to maroon-brown. Nordhausen sulphuric acid shows this better and more rapidly. If saponin is boiled with dilute acid it breaks up into sapogenin and sugar, and therefore the liquid after neutralisation reduces “Fehling.” This reaction is probably after the following equation:—
2C17H26O10 + 2H2O = 2C8H11O2 + 3C6H12O6.
Sapogenin may be separated by evaporating the neutralised liquid to dryness, treating the dry residue with ether, which dissolves out the sapogenin, and finally recovering the substance from the ethereal solution, and crystallising it from hot alcohol. Crystals are readily obtained if the alcoholic solution is allowed to evaporate spontaneously. A solution of saponin exposed to the air gets turbid, and develops carbon dioxide; not unfrequently the solution becomes mouldy.
§ 565. Effects.—Pelikan[594] has studied the effects of various saponins on frogs. One to two drops of a saturated watery solution of saponin applied subcutaneously to the leg, caused, in from five to six minutes, great weakness, accompanied by a loss of sensibility; but strong mechanical, chemical, or electrical stimuli applied to the foot excited reflex action, for the ischiatic nerve still retained its functions. Nevertheless, from the commencement, the excitability of the poisoned muscles was much weakened, and just before death quite disappeared. Section of the ischiatic nerve delayed the phenomena. Curarine did not seem to have any effect on the poisonous action. A concentrated solution applied to the heart of a frog soon arrests its beats, but weaker doses first excite, and then retard.[595]
The author has studied the general action of saponin on kittens, insects, and infusoria. Small doses, such as from 13 to 32 mgrms. (1⁄5 to 1⁄2 grain), were injected beneath the loose skin of the back of the neck of a kitten, when there were immediate symptoms of local pain. In from five to ten minutes the respiration notably quickened, and the animal fell into a lethargic state, with signs of general muscular weakness; just before death the breathing became very rapid, and there were all the signs of asphyxia. The pathological appearances after death were fulness in the right side of the heart, and intense congestion of the intestinal canal, the stomach generally being perfectly normal in appearance, and the kidneys and other organs healthy. The least fatal dose for a kitten seems to be 13 mgrms., or ·04 grm. to a kilogram.[596]
[596] The action of saponin when applied in concentrated solution to flies is that of an intense irritant. There is protrusion of the sucker, and progressive paralysis. The common infusoria live for some time in dilute solutions of saponin—this is also true of some of the higher forms; for example, a Cyclops quadricornis seemed in no way affected by a 2 per cent. solution.
§ 566. Action on Man.—The effects of saponin on man have been but little studied; it has been administered by the mouth in doses of from ·1 to ·2 grm., and in those doses seems to have distinct physiological effects. There is increased mucous secretion, and a feeling of nausea; but neither diaphoresis nor diuresis has been observed. From the foregoing study it may be predicated that 2·6 grms. (40 grains), if administered subcutaneously to an adult, would endanger life. The symptoms would be great muscular prostration, weakness of the heart’s action, and probably diarrhœa. In fatal cases, some signs of an irritant or inflammatory action on the mucous membranes of the stomach and intestines would be probable.
§ 567. Separation of Saponin.—Saponin is separated from bread, flour, and similar substances by the process given at p. 153, “Foods.” The process essentially consists in extracting with hot spirit, allowing the saponin to separate as the spirit cools, collecting the precipitate on a filter, drying, dissolving in cold water, and precipitating with absolute alcohol. In operating on animal tissues, a more elaborate process is necessary. The author has successfully proceeded as follows:—The finely divided organ is digested in alcohol of 80 to 90 per cent. strength, and boiled for a quarter of an hour; the alcohol is filtered hot and allowed to cool, when a deposit forms, consisting of fatty matters, and containing any saponin present. The deposit is filtered off, dried, and treated with ether to remove fat. The insoluble saponin remaining is dissolved in the least possible quantity of water, and precipitated with absolute alcohol. It is also open to the analyst to purify it by precipitating with baryta water, the baryta compound being subsequently decomposed by carbon dioxide. Basic lead acetate may also be used as a precipitant, the lead compound being, as usual, decomposed by hydric sulphide; lastly, a watery solution may be shaken up with chloroform, which will extract saponin. By some one of these methods, selected according to the exigencies of the case, there will be no difficulty in separating the glucoside in a fairly pure state. The organ best to examine for saponin is the kidney. In one of my own experiments, in a cat poisoned with a subcutaneous dose of saponin (·2 grm.), evidence of the glucoside was obtained from the kidney alone. The time after death at which it is probable that saponin could be detected is unknown; it is a substance easily decomposed, and, therefore, success in separating it from highly putrid matters is not probable.
§ 568. Identification of Saponin.—An amorphous white powder, very soluble in water, insoluble in cold alcohol or ether, having glucosidal reactions, striking a red colour with sulphuric acid, imparting a soap-like condition to water, and poisonous to animals, is most probably a saponin.
§ 569. Santonin (C15H18O3) is a neutral principle extracted from the unexpanded heads of various species of Artemisia (Nat. Ord. Compositæ). The seeds contain, according to Dragendorff, 2·03 to 2·13 per cent. of santonin, and about 2·25 per cent. of volatile oil, with 3 per cent. of fat and resin. Santonin forms brilliant, white, four-sided, flat prisms, in taste feebly bitter. The crystals become yellow through age and exposure to light; they melt at 169°, and are capable of being sublimed; they are scarcely soluble in cold water, but dissolve in 250 parts of boiling water, freely in alkaline water, in 3 parts of boiling alcohol, and in 42 parts of boiling ether. Santonin is the anhydride of santonic acid (C15H20O4). Santonin unites with alkalies to form santonates. Sodic santonate (C15H19NaO4 + 31⁄2H2O) is officinal on the Continent; it forms colourless rhombic crystals, soluble in 3 parts of cold water.
§ 570. Poisoning by Santonin.—Eighteen cases of poisoning, either by santonin or santonin-holding substances, which F. A. Falck has been able to collect, were nearly all occasioned by its use as a remedy for worms. A few were poisonings of children who had swallowed it by accident. With one exception those poisoned were children of from two to twelve years of age; in five the flower heads, and in thirteen santonin itself was taken. Of the eighteen cases, two only died (about 11 per cent.).
§ 571. Fatal Dose.—So small a number of children have died from santonin, that data are not present for fixing the minimum fatal dose. ·12 grm. of santonin killed a boy of five and a half years of age in fifteen hours; a girl, ten years old, died from a quantity of flower heads, equal to ·2 grm. of santonin. The maximum dose for children is from 65 to 194 mgrms. (1 to 3 grains), and twice the quantity for adults.
§ 572. Effects on Animals.—Experiments on animals with santonin have been numerous. It has first an exciting action on the centres of nerves from the second to the seventh pairs, and then follows decrease of excitability. The medulla is later affected. There are tetanic convulsions, and death follows through asphyxia. Artificial respiration lessens the number and activity of the convulsions, and chloroform, chloral hydrate, or ether, also either prevent or shorten the attacks.
§ 573. Effects on Man.—One of the most constant effects of santonin is a peculiar aberration of the colour-sense, first observed by Hufeland in 1806. All things seem yellow, and this may last for twenty-four hours, seldom longer. According to Rose, this apparent yellowness is often preceded by a violet hue over all objects. If the lids are closed while the “yellow sight” is present, the whole field is momentarily violet. De Martiny,[597] in a few cases, found the “yellow sight” intermit and pass into other colours, e.g., after ·3 grm. there was first the yellow perception, then giving the same individual ·6 grm., all objects seemed coloured red, after half an hour orange, and then again yellow. In another patient the effect of the drug was to give “green vision,” and in a third blue.
[597] Gaz. des Hôpit., 1860.
Hufner and Helmholtz explain this curious effect as a direct action on the nervous elements of the retina, causing them to give the perception of violet; they are first excited, then exhausted, and the eye is “violet blind.” On the other hand, it has been suggested that santonin either colours the media of the eye yellow, or that there is an increase in the pigment of the macula lutea. I, however, cannot comprehend how the two last theories will account for the intermittency and the play of colours observed in a few cases. To the affections of vision are also often added hallucinations of taste and smell; there is headache and giddiness, and in fourteen out of thirty of Rose’s observations vomiting occurred. The urinary secretion is increased. In large and fatal doses there are shivering of the body, clonic, and often tetanic convulsions; the consciousness is lost, the skin is cool, but covered with sweat, the pupils dilated, the breathing becomes stertorous, the heart’s action weak and slow, and death occurs in collapse—in the case observed by Grimm in fifteen hours, in one observed by Linstow in forty-eight hours. In those patients who have recovered, there have also been noticed convulsions and loss of consciousness. Sieveking[598] has recorded the case of a child who took ·12 grm. (1·7 grain) santonin; an eruption of nettle rash showed itself, but disappeared within an hour.
[598] Brit. Med. Journ., 1871.
§ 574. Post-mortem Appearances.—The post-mortem appearances are not characteristic.
§ 575. Separation of Santonin from the Contents of the Stomach, &c.—It is specially important to analyse the fæces, for it has been observed that some portion goes unchanged into the intestinal canal. The urine, also, of persons who have taken santonin, possesses some important peculiarities. It becomes of a peculiar yellow-green, the colour appearing soon after the ingestion of the drug, and lasting even sixty hours. The colour may be imitated, and therefore confused with that which is produced by the bile acids; a similar colour is also seen after persons have been taking rhubarb. Alkalies added to urine coloured by santonin or rhubarb strike a red colour. If the urine thus reddened is digested on zinc dust, santonin urine fades, rhubarb urine remains red. Further, if the reddened urine is precipitated by excess of milk of lime or baryta water and filtered, the filtrate from the urine reddened by rhubarb is colourless, in that reddened by santonin the colour remains. Santonin may be isolated by treating substances containing it with warm alkaline water. The water may now be acidified and shaken up with chloroform, which will dissolve out any santonin. On driving off the chloroform, the residue should be again alkalised, dissolved in water, and acidified with hydrochloric acid, and shaken up with chloroform. In this way, by operating several times, it may be obtained very pure. Santonin may be identified by its dissolving in alcoholic potash to a transitory carmine-red, but the best reaction is to dissolve it in concentrated sulphuric acid, to which a very little water has been added, to warm on the water-bath, and then to add a few drops of ferric chloride solution to the warm acid; a ring of a beautiful red colour passing into purple surrounds each drop, and after a little time, on continuing the heat, the purple passes into brown. A distinctive reaction is also the production of “iso-santonin”; this substance is produced by warming santonin on the water-bath with sulphuric acid for a few hours, and then diluting with water; iso-santonin is precipitated, and may be crystallised from boiling alcohol. Iso-santonin melts at 138°; it has the same composition as santonin. It is distinguished from santonin by giving no red colour when treated with sulphuric or phosphoric acids.
§ 576. The Daphne Mezereum (L.).—Mezereon, an indigenous shrub belonging to the Thymeleaceæ, is rather rare in the wild state, but very frequent in gardens. The flowers are purple and the berries red. Buckheim isolated by means of ether an acrid resin, which was converted by saponifying agents into mezereic acid; the acrid resin is the anhydride of the acid. The resin is presumed to be the active poisonous constituent of the plant, but the subject awaits further investigation. There are a few cases of poisoning on record, and they have been mostly from the berries. Thus, Linné has recorded an instance in which a little girl died after eating twelve berries. The symptoms observed in the recorded cases have been burning in the mouth, gastroenteritis, vomiting, giddiness, narcosis, and convulsions, ending in death. The lethal dose for a horse is about 30 grms. of powdered bark; for a dog, the œsophagus being tied, 12 grms.; but smaller doses of the fresh leaves may be deadly.
§ 577. Ergot is a peculiar fungus attacking the rye and other graminaceous plants;[599] it has received various names, Claviceps purpurea (Tulasne), Spermœdia clavus (Fries), Sclerotium clavus (D.C.), &c. The peculiar train of symptoms arising from the eating of ergotised grain (culminating occasionally in gangrene of the lower limbs), its powerful action on the pregnant uterus, and its styptic effects, are well known.
[599] Some of the Cyperaceæ are also attacked.
The very general use of the drug by accoucheurs has, so to speak, popularised a knowledge of its action among all classes of society, and its criminal employment as an abortive appears to be on the increase.[600]
[600] The Russian peasantry use the drug for the same purpose. Vide Mackenzie Wallace’s “Russia,” i. p. 117.
The healthy grain of rye, if examined microscopically in thin sections, is seen to be composed of the seed-coating, made up of two layers, beneath which are the gluten-cells, whilst the great bulk of the seed is composed of cells containing starch. In the ergotised grain, dark (almost black) cells replace the seed-coat and the gluten-cells, whilst the large starch-containing cells are filled with the small cells of the fungus and numerous drops of oil.
§ 578. The chemical constituents of ergot are a fixed oil, trimethylamine, certain active principles, and colouring-matters.
The fixed oil is of a brownish-yellow colour, of aromatic flavour and acrid taste; its specific gravity is 0·924, and it consists chiefly of palmitin and olein; it has no physiological action.
Trimethylamine is always present ready formed in ergot; it can also be produced by the action of potash on ergot.
With regard to the active principles of ergot considerable confusion still exists, and no one has hitherto isolated any single substance in such a state of purity as to inspire confidence as to its formula or other chemical characters. They may, however, be briefly described.
C. Tamet[601] has separated an alkaloid, which appears identical with Wenzel’s ergotinine. To obtain this the ergot is extracted by alcohol of 86°, the spirit removed by distillation, and the residue cooled; a resin (which is deposited) and a fatty layer (which floats on the surface) are separated from the extractive liquor and washed with ether; the ethereal solution is filtered and shaken with dilute sulphuric acid, which takes up the alkaloid; the aqueous solution of the substance is then filtered, rendered alkaline by KHO, and agitated with chloroform. The ergotinine is now obtained by evaporating the chloroform solution, care being taken to protect it from contact with the air. It gives precipitates with chloride of gold, potassium iodohydrargyrate, phosphomolybdic acid, tannin, bromine water, and the chlorides of gold and platinum. With moderately concentrated SO4H2, it gives a yellowish-red coloration, changing to an intense violet, a reaction which does not occur if the alkaloid has been exposed to the air. The composition of the base is represented by the formula C70H40N4O12, and a crystalline sulphate and lactate have been obtained.[602]
Wenzel’s Ecboline is prepared by precipitating the cold watery extract of ergot with sugar of lead, throwing out the lead in the usual way by hydric sulphide, concentrating the liquid, and adding mercuric chloride, which only precipitates the ecboline. The mercury salt is now decomposed with hydric sulphide, and after the mercury precipitate has been filtered off, the filtrate is treated with freshly precipitated phosphate of silver, and refiltered; lastly, the liquid is shaken up with milk of lime, again filtered, and the lime thrown out by CO2. The last filtrate contains ecboline only, and is obtained by evaporation at a gentle heat. It is an amorphous, feebly bitter substance, with an alkaline reaction, forming only amorphous salts.
The most recent research by Dragendorff on ergot tends to show that Wenzel’s alkaloids, ergotinine and ecboline, are inactive. Dragendorff describes also (a.) Scleromucin, a slimy substance which goes into solution upon extraction of the ergot with water, and which is again precipitated by 40 to 45 per cent. alcohol. It is colloidal and soluble with difficulty in water. It contains nitrogen, but gives no albuminoid reaction, nor any reaction of an alkaloidal or glucosidal body; it yields to analysis—
| 8 | ·26 | per cent. | Water. |
| 26 | ·8 | „ | Ash. |
| 39 | ·0 | „ | Carbon. |
| 6 | ·44 | „ | Hydrogen. |
| 6 | ·41 | „ | Nitrogen. |
(b.) Sclerotic Acid.—A feebly-acid substance, easily soluble in water and dilute and moderately concentrated alcohol. It passes, in association with other constituents of the ergot extract, into the diffusate, when the extract is submitted to dialysis; but after its separation in a pure state it is, like scleromucin, colloidal. It is precipitated by 85 to 90 per cent. alcohol, together with lime, potash, soda, silica, and manganese; but after maceration with hydrochloric acid, the greater part of the ash constituents can be separated by a fresh precipitation with absolute alcohol. The sample gave 40·0 per cent. of carbon, 5·2 per cent. hydrogen, 4·2 per cent. nitrogen, 50.6 per cent. oxygen, with 3·4 per cent. of ash. Sclerotic acid forms with lime a compound that is not decomposed by carbonic acid, and which upon combustion leaves from 19 to 20 per cent. of calcium carbonate. Both these substances are active, although evidently impure. Sclerotic acid is sold in commerce, and has been employed subcutaneously in midwifery practice in Russia and Germany for some time.
The inert principles of ergot are—(1.) A red colouring matter, Sclererythrin, insoluble in water, but soluble in dilute and strong alcohol, ether, chloroform, dilute solutions of potash, ammonia, &c. It can be obtained by dissolving in an alkali, neutralising with an acid, and shaking up with ether. Alcoholic solution of sclererythrin gives with aluminium sulphate, and with zinc chloride, a splendid red mixture; with salts of calcium, barium, and many of the heavy metals, it gives a blue precipitate; the yield is only ·1 to ·05 in a thousand parts.
(2.) Another colouring-matter, dissolving in concentrated sulphuric acid with the production of a fine blue violet colour, the discoverer has named Scleroidin. This is not soluble in alcohol, ether, chloroform, or water, but dissolves in alkaline solutions, potash producing a splendid violet colour; yield about 1 per 1000.
(3, 4.) Two crystalline substances, which may be obtained from ergot powder, first treated with an aqueous solution of tartaric acid, and the colouring-matters extracted by ether. One Dragendorff names Sclerocrystallin (C10H10O4); it is in colourless needles, insoluble in alcohol and water, with difficulty soluble in ether, but dissolving in ammonia and potash solutions. The other crystalline substance is thought to be merely a hydrated compound of sclerocrystallin. Both are without physiological action.
Kobert recognises two active substances in ergot, and two alone; the one he calls sphacelic acid, the other cornutin.
§ 579. Detection of Ergot in Flour (see “Foods”).—The best process is to exhaust the flour with boiling alcohol. The alcoholic solution is acidified with dilute sulphuric acid, and the coloured liquid examined by the spectroscope in thicker or thinner layers, according to the depth of colour. A similar alcoholic solution of ergot should be made, and the spectrum compared. If the flour is ergotised, the solution will be more or less red, and show two absorption bands, one in the green, and a broader and stronger one in the blue. On mixing the original solution with twice its volume of water, and shaking successive portions of this liquid with ether, amyl alcohol, benzene, and chloroform, the red colour, if derived from ergot, will impart its colour to each and all of these solvents.
§ 580. Pharmaceutical Preparations.—Ergot itself is officinal in all the pharmacopœias, and occurs in grains from 1⁄3 to 1 inch in length, and about the same breadth, triangular, curved, obtuse at the ends, of a purple colour, covered with a bloom, and brittle, exhibiting a pinkish interior, and the microscopical appearances already detailed. Ergot may also occur as a brown powder, possessing the unmistakable odour of the drug. A liquid extract of the B.P. is prepared by digesting 16 parts of ergot in 80 parts of water for twelve hours, the infusion is decanted or filtered off, and the digestion repeated with 40 parts of water; this is also filtered off, and the residue pressed, and the whole filtrate united and evaporated down to 11 parts; when cold, 6 parts of rectified spirit are added, and, after standing, the liquid is filtered and made up to measure 16. A tincture and an infusion are also officinal; the latter is very frequently used, but seldom sold, for it is preferable to prepare it on the spot. The tincture experience has shown to be far inferior in power to the extract, and it is not much used. Ergotin is a purified extract of uncertain strength; it is used for hypodermic injection; it should be about five times more active than the liquid extract.
§ 581. Dose.—The main difficulties in the statement of the medicinal dose, and of the minimum quantity which will destroy life, are the extreme variability of different samples of ergot, and its readiness to decompose. A full medicinal dose of ergot itself, as given to a woman in labour, is 4 grms. (61·7 grains), repeated every half hour. In this way enormous doses may be given in some cases without much effect. On the other hand, single doses of from 1 to 4 grms. have caused serious poisonous symptoms. The extract and the tincture are seldom given in larger doses than that of a drachm as a first dose, to excite uterine contraction. In fact, the medical practitioner has in many cases to experiment on his patient with the drug, in order to discover, not only the individual susceptibility, but the activity of the particular preparation used. From the experiments of Nikitin, it is probable that the least fatal dose of sclerotic acid for an adult man is 20 mgrms. per kilogrm.
§ 582. Ergotism.—Ergotised cereals have played a great part in various epidemics, probably from very early times, but the only accurate records respecting them date from the sixteenth century. According to Dr. Tissot,[603] the first recorded epidemic was in 1596, when a strange, spasmodic, convulsive disease broke out in Hessia and the neighbouring regions. It was probably due to spurred rye. In Voigtländer, the same disease appeared in 1648, 1649, and 1675; in 1702 the whole of Freiberg was attacked. In Germany and in France successive epidemics are described throughout the eighteenth century. In France, in 1710, Ch. Noel, physician at the Hôtel Dieu, had no less than fifty cases under treatment at the same time.
[603] Dr. Tissot in Phil. Trans., vol. lv. p. 106, 1765. This is a Latin letter by Dr. Baker, and gives a good history of the various epidemics of ergotism.
It is generally said that in 1630, Thuillier, in describing an ergot epidemic which broke out in Cologne, first referred the cause of the disease to spurred rye.
It is interesting to inquire into the mortality from this disease. In 1770, in an epidemic described by Taube, in which 600 were affected, 16 per cent. died. In a nineteenth-century epidemic (1855), in which, according to Husemann, 30 were ill, 23·3 per cent. died. In other epidemics, according to Heusinger, out of 102, 12 per cent. died; according to Griepenkerl, out of 155, 25 or 16 per cent. died; and, according to Meyer, of 283 cases, 6 per cent. died.
There are two forms of chronic poisoning by ergot—one a spasmodic form, the other the gangrenous form.
§ 583. The convulsive form of ergotism mostly begins with some cerebral disturbance. There are sparks before the eyes, giddiness, noises in the ears, and a creeping feeling about the body. There is also very commonly anæsthesia of the fingers and toes, and later of the extremities, of the back, and even of the tongue. Diarrhœa, vomiting, colic, and other signs of intestinal irritation seldom fail to be present; there are also tetanic spasms of the muscles, rising in some cases to well-marked tetanus; epilepsy, faintings, aberrations of vision, amaurosis, and amblyopia are frequent; the skin becomes of a yellow or earthy colour, and is covered with a cold sweat; boils and other eruptions may break out; blebs, like those caused by burns or scalds, have in a few cases been noticed. Death may occur in from four to twelve weeks after the eating of the spurred grain from exhaustion. In those individuals who recover, there remain for some time weakness, contractions of groups of muscles, anæmia, or affections of vision.
§ 584. The Gangrenous Form of Ergotism.—In this form there is generally acute pain in the limb or limbs which are to mortify; and there may be prodromata, similar to those already described. The limb swells, is covered with an erysipelatous blush, but at the same time feels icy cold; the gangrene is generally dry, occasionally moist; the mummified parts separate from the healthy by a moist, ulcerative process; and in this way the toes, fingers, legs, and even the nose, may be lost. During the process of separation there is some fever, and pyæmia may occur with a fatal result.
Fontenelle described a case in which a rustic lost all the toes of one foot, then those of the other; after that, the remnant of the first foot, and lastly the leg. But probably the most extraordinary case of gangrene caused by the use of ergot is that which occurred at Wattisham, Suffolk, in the family of a labouring man named John Downing. He had a wife and six children of various ages, from fifteen years to four months. On Monday, January 10, 1762, the eldest girl complained of a pain in the calf of her left leg; in the evening, her sister, aged 10, also experienced the same symptoms. On the following Monday, the mother and another child, and on Tuesday, all the rest of the family except the father became affected. The pain was very violent. The baby at the breast lived a few weeks, and died of mortification of the extremities. The limbs of the family now began to slough off, and the following are the notes on their condition made by an observer, Dr. C. Wollaston, F.R.S., on April 13:—
“The mother, aged 40. Right foot off at the ankle, the left leg mortified; a mere bone left, but not off.
“Elizabeth, aged 13. Both legs off below the knees.
“Sarah, aged 10. One foot off at the ankle.
“Robert, aged 8. Both legs off below the knees.
“Richard, aged 4. Both feet off at the ankle.
“Infant, four months old, dead.”
The father was also attacked a fortnight after the rest of the family, and in a slighter degree—the pain being confined to the fingers of his right hand, which turned a blackish colour, and were withered for some time, but ultimately got better.
As a remarkable fact, it is specially noted that the family were in other respects well. They ate heartily, and slept soundly when the pain began to abate. The mother looked emaciated. “The poor boy in particular looked as healthy and florid as possible, and was sitting on the bed, quite jolly, drumming with his stumps.” They lived as the country people at the time usually lived, on dried peas, pickled pork, bread and cheese, milk, and small beer. Dr. Wollaston strictly examined the corn with which they made the bread, and he found it “very bad; it was wheat that had been cut in a rainy season, and had lain in the ground till many of the grains were black and totally decayed.”[604]
[604] In the Phil. Trans. for 1762 there are two strictly concordant accounts of this case; and in the parish church of Wattisham, there is said to be a memorial tablet, which runs as follows:—“This inscription serves to authenticate the truth of a singular calamity which suddenly happened to a poor family in this parish, of which six persons lost their feet by a mortification not to be accounted for. A full narrative of their case is recorded in the Parish Register and Philosophical Transactions for 1762.”
§ 585. Symptoms of Acute Poisoning by Ergot.—In a fatal case of poisoning by ergot of rye, recorded by Dr. Davidson,[605] in which a hospital nurse, aged 28, took ergot, the symptoms were mainly vomiting of blood, the passing of bloody urine, intense jaundice, and stupor. But in other cases, jaundice and vomiting of blood have not been recorded, and the general course of acute poisoning shows, on the one hand, symptoms of intense gastro-intestinal irritation, as vomiting, colicky pains, and diarrhœa; and, on the other, of a secondary affection of the nervous system, weakness of the limbs, aberrations of vision, delirium, retention of urine, coma, and death.