DIOSCORIDEÆ.
=Black Bryony= (_Tamus communis_ L.). The stem and foliage of Black
Bryony are apparently harmless, being browsed by sheep and goats with
impunity, but the scarlet fruits are decidedly poisonous and the starchy
root is acrid and purgative.
_Toxic Principle._ This is probably the glucoside _Bryonin_, which
occurs in _Bryonia dioica_ (p. 35).
_Symptoms._ Cornevin, in citing experiments on animals, states that
small quantities of the fruits cause uneasiness, somnolence, and
difficult locomotion. Larger quantities cause vomiting, intestinal
pains, and paralysis of hind quarters. Death is rapid. Müller, however,
remarks that paralysis of the hind quarters and convulsions may result
from small quantities, large quantities causing in addition inflammation
of the stomach and intestines.
REFERENCES.
73, 190.
LILIACEÆ.
=Herb Paris= (_Paris quadrifolia_ L.). Owing to its habitat—damp
woods—it is unlikely that stock will eat this plant, but it may be
possible where fields border open woods in which it grows. No records of
stock poisoning have been met with, but cases of poisoning in man are
recorded, one due to eating a considerable number (30 to 40) of the
berries, and symptoms of poisoning in a child four years of age who had
eaten a few berries. In smaller quantities they are very poisonous to
poultry. All parts are stated to be poisonous, especially the berries.
Fatal poisonings are nil, or very rare if recorded.
_Toxic Principle._ Walz isolated the glucoside _Paridin_; and Esser
states that the toxic property is due to a Saponin,—the bitter irritant
glucoside _Paristyphnin_ (C_{38}H_{64}O_{18}), which is convertible into
Paridin (C_{16}H_{28}O_{7} + 2H_{2}O) and sugar.
_Symptoms._ The plant is emetic, purgative, intensely acrid, and
narcotic. Poisoning up to the present only appears to have been recorded
in fowls, the symptoms being intense local inflammation, narcotic
effects, vomiting, colic, diarrhœa, stupefaction, convulsions, and
paralysis (Müller).
REFERENCES.
4, 16, 73, 76, 81, 130, 141, 190.
=Lily-of-the-Valley= (_Convallaria majalis_, L.). This beautiful plant
is only likely to induce poisoning of domestic animals at very rare
intervals, as it occurs wild in only a few woods from Moray southwards,
being, however, abundant in some districts. All parts are stated to be
poisonous, especially the flowers. It has an acrid, bitter taste. Few
cases of poisoning are recorded. Sheep and goats are believed to eat the
leaves with impunity. The extract is so poisonous that four drops
injected into the blood stream sufficed to kill a dog in ten minutes
(Cornevin). The leaves have been known to kill geese and fowls.
_Toxic Principle._ All parts of the plant contain the bitter poisonous
glucoside _Convallamarin_ (C_{23}H_{44}O_{12}), the glucoside _Paridin_
(C_{16}H_{28}O_{7} + 2H_{2}O), and the glucoside _Convallarin_
(C_{34}H_{62}O_{11})—the first a dangerous purgative, and the last a
cardiac poison resembling Digitalis. Convallamarin is a very poisonous
crystalline substance, with at first a bitter and afterwards a sweetish
taste.
_Symptoms._ The action of this plant on the animal organism is not yet
clearly known, but it is stated to have marked emetic and purgative
action. Taken in moderate quantities a period of retardation of the
heart and lung action is followed by a period in which the heart action
is intermittent, and there are stoppages in respiration, and vomiting.
Taken in large quantities, the first of these periods is extremely
short, the pulse soon becomes rapid and small, respiration is quickened,
and the heart action ceases (Cornevin).
Pott observes that the leaves cause stupefaction, convulsions, and death
after a few hours in the case of _geese_. He cites a case in which ten
_fowls_ ate the leaves and nine died.
REFERENCES.
52, 73, 76, 81, 190, 203, 205, 213.
=Meadow Saffron= (_Colchicum autumnale_ L.). The Meadow Saffron, Autumn
Crocus, or Naked Ladies, as it is variously named, occurs in meadows in
many districts in England and Wales. All parts are poisonous, both in
the green state and when dried, as it possibly may be, in hay. It has
caused extensive losses of live stock, and the greatest care should be
taken to eradicate it from grass land. The leaves and seed-vessels are
produced in spring, and the flowers from August to October—and it is at
these two periods that cases of poisoning by this plant are most
frequent, though, as stated, it may be included in hay. Many horses,
cattle, and pigs have been killed by Meadow Saffron, though cattle
commonly avoid it. Sheep and goats are believed to be very slightly
affected. Children and fowls died at Schorren (Canton Berne) from eating
the seeds, and there have been many cases of human poisoning due both to
eating the seeds and the bulbs. In Staffordshire, Mr J. C. Rushton
reported some years ago[4] that in one year a farmer lost seventeen
milking cows; in 1908 he lost seven calves; and in 1909 he lost a number
of sheep and cows. It was then discovered that the field in which the
animals grazed contained “any quantity of Meadow Saffron and Water
Hemlock,” and this was the cause of the losses. Horses and cattle are
more commonly poisoned than other domesticated animals. Johnson and
Sowerby record the case of a woman who ate the corms in mistake for
onions at Covent Garden, and died; and state that deer and cattle have
been killed by the leaves. Kanngiesser notes that this species is the
most toxic of German plants, and that in cases of human poisoning the
mortality is 90 per cent., children being chiefly affected. Cornevin’s
experiments showed that 8 to 10 grammes of green leaves per kilogramme
of live weight—say 3 to 5 lb. for an average cow—was sufficient to kill
ruminants; while 30 centigrammes of corms per kilogramme of live weight
sufficed to kill pigs—say 4½ oz. for a pig of 200 lb. live weight.
Barret and Remlinger (_Veterinary Journal_, 1912, p. 306) record the
sudden illness of 31 out of 51 cattle, and 5 of them died.
Footnote 4:
_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.
In the _horse_, there are spasmodic movements of the hind-quarters and
excessive excitement of the urinary genital organs. In _cattle_ there is
cessation of rumination, grinding of teeth, dryness of muzzle, ptyalism,
groaning, painful colic, dysentery, deeply sunken and watery eyes, anus
wide open, and evacuation of very fœtid, blackish, glareous matter round
the excrement. In _cows_ there may be suppression of milk, and abortion.
In the _pig_ there is abundant salivation and vomiting, and the animal
keeps its snout buried in the litter. There is also extremely fœtid
diarrhœa, with dysentery.
REFERENCES.
4, 16, 27, 73, 81, 128, 130, 141, 148, 151,
190, 192, 203, 217, 255.
GRAMINEÆ.
=Darnel= (_Lolium temulentum_ L.). The grass known as Darnel, of the
same genus as rye-grass, has been recognized for centuries as a harmful
species, and it is considered by some authorities that it is really the
tares of Scripture which the enemy sowed among the wheat. Its effect on
eyesight was known to the ancients[5], and its objectionable character
was noted by Shakespeare:—
Footnote 5:
E.g. Ovid says “Let the fields be clear of darnel that weakens the
eyes.” In Plautus’ comedy, _The Braggart Soldier_, one servant says to
another, “’Tis a wonder that you are in the habit of feeding on darnel
with wheat at so low a price.” “Why so?” “Because you are so dim of
sight.” [_Agric. Jour. Union of S. Africa_, Jan. 1914, p. 82.]
“Want ye corn for bread?
I think the Duke of Burgundy will fast
Before he’ll buy again at such a rate:
’Twas full of darnel: Do you like the taste?”
—I _Henry_ VI, Act III, Sc. 2.
Its effect when mixed with flour was also referred to by Gerarde (1597):
“The new bread wherein Darnell is, eaten hot, causeth drunkenness; in
like manner doth beere or ale wherein the seede is fallen, or put into
the mault.”
Before the seeding stage is reached Darnel seems to be quite suitable as
a food for stock, only the seed or grain being poisonous, and this not
invariably so. The chief danger perhaps is that the grain may not be
thoroughly removed from cereal grains, and may thus find its way into
bread or cereal stock foods. Though it has caused many cases of human
poisoning, fatal results seem to be rare: Dr. Taylor could record no
fatal case up to 1859. Darnel mixed with barley caused the poisoning of
pigs (_Veterinarian_, 1842). Johnson and Sowerby (1861) state that
Darnel has in several cases proved fatal to horses and sheep. The same
authorities quote a case in which 80 inmates of Sheffield Workhouse were
attacked by violent vomiting and purging from the use of oatmeal
containing Darnel. At the Veterinary School at Lyons a horse was killed
by giving it 2 kilogrammes (4·4 lb.) of Darnel. Cornevin concluded that
the amounts of Darnel necessary to kill certain animals would be as
follows:—
Horse 0·7 lb. per 100 lb. live weight.
Ruminants 1·5 to 1·8 lb. per 100 lb. live weight.
Poultry 1·5 to 1·8 lb. „ „
Dog 1·8 lb. „ „
He found pigs very little affected. As regards man 30 grammes (1 oz.) of
the flour appear to be about the most that can be taken without showing
dangerous symptoms.
The presence of Darnel flour in flour of the cereal grains may be
determined by an examination of the starch granules, which are given by
Cornevin as only 5 to 8µ; in diameter (compared with 25 to 4µ for rye),
simple in general, but sometimes in groups of 2 to even 5, polyhedral or
partly rounded, with a nucleus or fusiform nucleal cavity, and readily
coloured blue with iodine; they resemble those of maize but are only
about one-eighth the size.
_Toxic Principle._ The grains only are harmful, and contain the narcotic
alkaloid _Temuline_ (C_{7}H_{12}N_{2}O), which Hofmeister showed to be a
strong nerve poison, and which is said to occur to the extent of 0·08
per cent. in the seeds. Other authorities impute the toxic property to
_Loliine_, while Smith states that the toxic principle is _Picrotoxin_.
In relation to the grain fungal hyphæ have usually been found, though
not invariably, 20 to 30 per cent. of the plants sometimes being free
from it. The fungus (_Endoconidium temulentum_) is propagated
vegetatively by means of mycelium. It appears to live symbiotically in
the maturing grain, and perhaps to a slight extent renders possible the
assimilation of nitrogen from the atmosphere; but Freeman observed that
though generally stimulating to the Darnel, it is occasionally injurious
to it. Esser sums it up by saying that according to most authorities who
have investigated Darnel the fungus alone contains the toxic
substance—the Temuline—and hence the grains in which the fungus does not
occur should be harmless. The fungus is found in Darnel grain in all
countries—Chile, Brazil, S. Africa, Persia, Spain, France, Sweden,
Germany, etc. So far as can be ascertained there have been no feeding
experiments to determine the difference in toxic character between
fungus-infested and fungus-free grains. The dangerous properties are
said to be most pronounced in wet seasons.
_Symptoms._ In France Darnel is called _Ivraie_, because, when brewed
with barley, it acts as a narcotic intoxicant.
Darnel poisoning induces giddiness, drowsiness, uncertain gait, and
stupefaction (Müller), and, in the older animals, vomiting, convulsions,
loss of sensation and death (Pott).
The symptoms in the _horse_ are dilatation of pupils, vertigo, uncertain
gait, and trembling. The animal falls, the body is cold and the
extremities are stiff, respiration is laboured, the pulse is slow and
small, and there are convulsive movements of the head and limbs. There
is rapid enfeeblement, and death may occur within thirty hours.
In _pigs_, foaming, convulsions and paralysis have been observed; the
stomach and intestines were inflamed and the lungs congested.
REFERENCES.
4, 16, 73, 81, 106, 128, 130, 141, 190, 203, 204,
205, 213, 233, 235, 254.
EQUISETACEÆ.
=Horsetails= (_Equisetum_ sp.). A very great deal has been written on
the subject of Equisetosis or _Equisetum_ poisoning, and even at the
present day opinion is divided as to which species are poisonous and to
what extent. From the time of Linnæus there has been uncertainty as to
the species, which has generally been given as _E. arvense_. Two German
papers, by Weber and Lohmann respectively, published by the German
Agricultural Society in 1903 and 1904, have done much to remove doubt on
the matter, but cannot be said to have settled the question absolutely.
These two papers seem to have been overlooked by some recent writers on
the subject, but Lohmann’s appears to be the most authoritative paper
yet written. Both are referred to below.
It seems to be definitely proved that certain species of _Equisetum_
really are poisonous, hesitating statements notwithstanding. Chesnut and
Wilcox state that there are cases of poisoning of both horses and sheep
by _E. arvense_ in the United States, though they are not common, and
the opinion is expressed that “the plant, if deleterious, is evidently
so only on account of its harsh scouring action in the mouth and
intestinal tract.” On the other hand Rich and Jones record poisoning of
horses by _E. arvense_ in hay, but while adding that horses seem to
develop a depraved appetite for the weed, they state that they have no
evidence that horses grazing upon _the green plant_ are poisoned.
Güssow’s experience has been that cattle do not suffer any inconvenience
at all from this species, or only very slight disturbance of the
digestive organs, but that horses are conspicuously subject to fatal
poisoning by it. Examination of hay on which a considerable number of
poisoned horses were fed revealed in every case the presence of _E.
arvense_. When the food was changed, horses, if not too seriously
affected, made rapid recovery. (Treatment suggested is to change to
easily digested food, give a sharp purgative, and follow by small doses
of nux vomica three times a day.) Pammel says that in recent years a
disease of horses in Vermont has been attributed to hay and fodder
containing the weed; that it is proved by experiment that when ingested
in sufficient quantity _E. arvense_ is capable of causing fatal
poisoning in horses, and is at times the cause of extensive losses; and
that young horses are most susceptible, while grain-fed horses are less
susceptible than others. He adds that sheep are supposed to be slightly
affected, but cattle eat hay in which it occurs in large proportion with
impunity.
Coming to the two German reports, it is stated by Weber (1903) that _E.
palustre_ contains a specific poison for cattle and other ruminants, but
sheep and goats are able, owing to their fine muzzles, to separate it in
fodder, and hence suffer less. Horses and pigs, he says, seem to suffer
very little. Young animals and stock, from districts where the species
does not occur, suffer more than those from places where it occurs—the
latter appearing to learn early to avoid it.
Lohmann conducted feeding experiments with guinea-pigs with _E.
arvense_, _E. palustre_, _E. pratense_, _E. sylvaticum_, _E. maximum_,
and _E. heleocharis_ (not British). He also fed _E. arvense_ and _E.
palustre_ to horses, cattle, sheep, pigs, and geese in considerable
quantities for many days on end; and made experiments with aconitic acid
on guinea-pigs and horses. The feeding experiments with guinea-pigs
showed that of the species named only _E. palustre_ and to a less extent
_E. sylvaticum_ are poisonous plants (to guinea-pigs). With the large
domestic animals the experiments showed _E. arvense_ to be a harmless
plant, and _E. palustre_ to be really injurious to cattle but avoided by
other stock. Lohmann considers that the many statements in the
literature agree in part with this result, and that the divergent
observations may be traced to various causes, among which perhaps an
abnormal chemical composition of the weed fed plays a principal part.
In this connection, however, the American results must be carefully
borne in mind, and _E. arvense_ must not too hastily be regarded as
blameless.
_Toxic Principle._ It was for some years believed that the apparent
toxic symptoms induced by Horsetails were due to Silica or to Aconitic
acid—the latter a substance found by Matz and Ludwig. The conclusion
come to by Weber, however, was that the poisoning by _E. palustre_ is of
an organic character, not due to silica. The young shoots, which contain
little silica, were found in general to be much more poisonous than the
old plants, which contain much silica. It was long since found by
Wiggers that dried plants of _E. palustre_ contained 8·88 per cent. of
silica, but all species contain this substance in greater or less
degree, and it varies considerably in amount, even in the same species.
The feeding experiments conducted by Lohmann, with certain species of
_Equisetum_, and the observed symptoms of illness after the consumption
of some of them, particularly _E. palustre_, serve to show that the ill
effects are neither to be attributed to greater or less digestibility,
nor to the silica present. Neither are the aconitic acid and other
organic substances, in part found in previous investigations,
responsible for the poisoning. However, an active compound named
_Equisetine_, a substance belonging to the alkaloid group, was isolated;
this occurs usually, perhaps only, in _E. palustre_, at any rate in
sufficient quantity to be dangerous to animals. Lohmann then, following
up the investigations of Paucerzynski, Matz, Meyer, Weber and others,
ascertained definitely that _E. palustre_ contains an alkaloidal nerve
poison, to which the name _Equisetine_ was given, and the experiments
were held to decide that this is the poisonous substance in this
species. (As stated above, _E. arvense_ was held to be harmless.)
_Symptoms._ At first, excitement and anxiety, followed by uncertainty of
movement, reeling and staggering; paralysis of hind limbs at least,
falling, possibly general paralysis, insensibility to external
irritants, unconsciousness, and coma. Pulse accelerated, appetite at
first normal, but in course of time great disturbance of nutrition;
sugar in the urine. Course sometimes very acute, death occurring in a
few hours, but sometimes protracted (two to eight days), and at times
even chronic (one to several weeks).
In _cattle_, after excessive eating, continuous diarrhœa is
characteristic, with paralysis; while, if the food be persisted with,
cachexia and hydræmia combined with weakness bordering on paralysis make
their appearance (Friedberger and Fröhner, _via_ Pammel). In addition to
cachexia, Pott also mentions colic, stoppage, bloody urination,
abortion, and loss of teeth.
Young animals appear to succumb sooner than older ones, while grain-fed
animals are more resistant than others. Referring to _E. arvense_ Pammel
says it produces paralysis of the rear extremities, and when death
occurs spasms are noted. In relation to the poisoning of _horses_ by the
same species in hay Rich and Jones note unthriftiness, the animal
appearing thin and the muscles wasted. In from two to five weeks,
according to the age of the horse and the manner of feeding, the animal
begins to lose control of the muscles, and there is swaying and
staggering, though the eye is bright and the appetite good. If the plant
is regularly ingested the horse loses the power of standing, becomes
nervous, struggles to rise, the legs become more or less rigid, and at
times all the muscles of the body seem convulsed. Even in this condition
one well-nursed patient lived two weeks. The horses are generally
willing to eat, although unable to rise, but become sore and tired from
struggling, finally dying from exhaustion. Life is much prolonged by
turning from side to side three or four times in twenty-four hours, thus
preventing congestion. The pulse is slow till near the end, when it is
rapid and weak; the temperature is below normal at first, but when the
animal is down there is fever; the extremities are usually cold; and the
lining membrane of the mouth, nose, and eye becomes pale.
Of _Equisetum_ sp. Stebler and Schroeter say that they induce diarrhœa
in cattle, which become poor, and in cows the milk yield is checked or
ceases. Weber also refers to the effect on milk yield of _E. palustre_,
which he says causes the milk of affected cows to become watery, poor in
fat, and gives rise to a greasy, unappetising butter, while the yield
may soon quite fail.
REFERENCES.
2, 20, 57, 111, 176, 203, 204, 213, 220, 221, 222, 237, 260, 261.
FILICES.
=Bracken= (_Pteris aquilina_ L.). The Bracken, Brake Fern, or “Fern” is
of very considerable importance to farmers for four reasons: (1) It is a
most pernicious weed; (2) it forms an excellent litter for stock and
treads down into good manure; (3) it is said to have been successfully
converted into silage; but (4) it has been accused of poisoning cattle.
In regard to possible poisonous properties, it must be said that the
facts are at present somewhat uncertain, but a number of authorities
clearly regard the Bracken as poisonous. (_a_) Müller (1897) records the
poisoning of horses which ate it for some weeks with chaff—and some
died. (_b_) Chesnut and Wilcox (1901) say that cases of poisoning of
horses and cattle have been reported from England and a few localities
in the United States. (_c_) Pott states that when eaten in quantity by
cattle Bracken causes hæmaturia, and in horses nervous symptoms (brain
trouble), sometimes with fatal effects. (_d_) Pammel also remarks on the
believed poisonous character of this plant. (_e_) In view of its
suspected poisonous character feeding experiments were conducted by the
Board of Agriculture and Fisheries with a large quantity of Bracken, but
the results were negative, yielding no experimental proof of the plant
being poisonous. One animal—a heifer—consumed 60 lb. of Bracken between
Aug. 14 and Aug. 20, and after two meals containing about 30 lb. of
Bracken showed only symptoms of indigestion. After the 60 lb. there were
no symptoms of illness. It has been thought possible that the so-called
Bracken poisoning is due to _Potentilla Tormentilla_ (_q.v._).
In 1893 Storrar dealt with the question and expressed the view that any
disorder due to Bracken was probably not a toxic effect but a digestive
trouble simply (_Jour. Comp. Path._, 1893).
_Toxic Principle._ Continental authorities say that Bracken contains the
poisonous _Pteritannic acid_, which is identical with the _Filicic acid_
of the Male Fern (_Aspidium filix-mas_).
_Symptoms._ In the cases of horses which died Müller gives the symptoms
as timidity, slower movement or action, loss of balance, dilated pupils,
reddening followed by yellowing of the conjunctivæ, and slowing of the
pulse.
Pammel notes Bracken as an astringent and anthelmintic, and also says it
causes enteritis, spasms, and paralysis.
REFERENCES.
10, 25, 57, 190, 203, 204, 213.
FUNGI[6].
=Ergot= (_Claviceps purpurea_). This fungus, parasitic on rye and a
number of grasses, has long been known to induce distinct poisonous
effects on man and domestic animals when ingested in sufficient
quantity.
Footnote 6:
Poisonous parasitic fungi generally are not dealt with in this volume,
but ergot is included because it is widely distributed and perhaps the
best known, while its effects have been fully studied.
Ergot must be regarded as a cause of abortion in cows, though somewhat
divergent views have been expressed as to the facts, some authorities
considering the belief well founded, while others consider that there is
little ground for it. It is quite clear, however, that when taken in
sufficient quantity Ergot induces serious poisoning of domestic animals.
Horses have died in two or three days from eating ergoted hay and wild
rye. Extensive outbreaks of ergotism have occurred in the United States,
and serious losses have been recorded in the Central and Western States.
Ewart remarks that “a comparatively small number of fresh Ergot grains
suffice to injure or kill a horse, cow, or sheep.” The effects of the
poisoning of animals will be found under _Symptoms_ below.
_Toxic Principle._ Ergot of rye is used in medicine. It contains 0·20 to
0·25 per cent. of _Ergotinine_. In the British Pharmaceutical Codex,
1911, the grains (sclerotia) of Ergot (see Frontispiece) are described
as longitudinally furrowed, 1 to 4 cm. long, slender, curved, tapering
to both ends; they break with a short fracture, and are somewhat
triangular in transverse section; they have a characteristic and
disagreeable odour and taste, are dark violet to black in colour, and
whitish within. Ergot contains the physiologically active alkaloid
_Ergotoxine_ or _Hydroergotinine_ (C_{35}H_{41}O_{6}N_{5}), also known
as _amorphous Ergotinine_, and, when formerly obtained in an impure
state, as _Cornutine_ and _Ecboline_. It is the hydrate of the
crystalline base Ergotinine (C_{35}H_{39}O_{5}N_{5}). There are also
other physiologically active constituents derived from amino-acids.
_Symptoms._ In man Ergot has induced two types of epidemic ergotism,
caused by the prolonged use of ergoted rye bread. The two forms are
rarely or never found together. One is a gangrenous form characterized
by agonizing pain in the extremities, followed by dry gangrene of the
peripheral parts of the body. The second type of ergotism is much more
rare—a nervous epidemic characterized by paroxysmal epileptiform
convulsions.
Owing to the fact that at the outset ergotism causes irritation in the
hands and feet it is termed “Kribbelkrankheit” in Germany.
The three substances noted above as isolated by Kobert are stated to
cause poisoning—the first producing inflammation of the serous and
mucous membranes, disintegration of the red blood cells, and widespread
ecchymoses; the second excites the central nervous system and causes
general convulsions; and the last induces gangrene.
In one case a horse ate ergoted hay: next day the left hind leg was
stiff, and moist with cold sweat; on the second day it was badly swollen
and gangrene of all the tissues became apparent, and after the skin of
the leg and a considerable part of the muscular tissue had sloughed off
the animal died on the third day. In other cases horses showed symptoms
twenty-four hours after eating ergoted hay: fatigue, indisposition to
work, cold sweat, particularly on the neck, paralysis of the tongue and
muscles concerned in swallowing, and then generalized paralysis, very
slow and deep respiration, subnormal temperature, normal pulse at first
and then weaker till scarcely distinguishable, death in six or eight
hours (Chesnut and Wilcox).
According to Pammel ergotism manifests itself among animals chiefly in
the chronic form, the poison being acquired in small amounts and
accumulation taking place slowly. Two distinct forms of the disease are
recognized, the spasmodic and gangrenous. “Symptoms referable to the
digestive tract, such as nausea, vomiting, colic, diarrhœa, or
constipation occur in both forms. Pregnant animals very frequently
abort.”
“In the spasmodic type of the disease, symptoms due to overstimulation
of the central nervous system appear. These are tonic contraction of the
flexor tendons of the limbs, anæsthesia of the extremities, muscular
trembling, general tetanic spasms, convulsions and delirium. Death
usually occurs from secondary causes.”
“Gangrenous ergotism is characterised by coldness and anæsthesia of the
extremities, followed ultimately by dry gangrene of these parts. The
effects of this dry gangrene are often very serious and amount to
sloughing of the feet, tips of the ears, tip of the tail, shedding of
the hair, teeth, etc. Death takes place from exhaustion.
“Acute poisoning is characterized by vomiting (in dogs), profuse
salivation, dilatation of the pupils, rapid breathing and frequent
pulse. The animal cries out, has convulsive twitchings, staggering gait,
paraplegia, intense thirst and coma, terminating in death.”
In an extensive outbreak of ergotism in the United States in 1884 Law
and Salmon reported as a prominent symptom ulceration of the mucous
membrane of the tongue and mouth cavity, this and lesions on the
extremities giving the appearance of foot-and-mouth disease. Affected
animals showed weakness, dullness, and paralytic conditions of certain
groups of muscles. When in pregnant animals the uterus is acted upon,
labour pains occur, and the fœtus is expelled. The straining in those
cases is often very painful and may be so severe that prolapsus of the
uterus or even the rectum is the result. When Ergot produces gangrene,
it usually affects the extremities, like the lower parts of the legs,
the ears, tail or teats in cattle, and the comb, wattles, toes, wings or
tongue of poultry. It is preceded by redness, coldness, and painful
swelling of the parts affected. After a while sensibility of the dying
region is lost and the line of demarcation between it and the living
tissue becomes manifest. The dead portion commonly dies and is cast off.
In some cases the gangrene is accompanied by symptoms of a septic
nature.
“The possible result of the poisoning depends largely on the amount of
Ergot taken and on the severity of the symptoms produced thereby. When
small amounts are taken and only a slight dullness or digestive
disturbance results the outlook may be quite favourable. Even Ergot
abortion with rather severe symptoms usually is followed by recovery,
but in the gangrenous cases, fatal terminations are common. The animals
which through this cause have lost one or more parts are not only
crippled, but septic or embolic complications may lead to a fatal
termination. Paralytic cases do not permit of a favourable prognosis,
especially if muscle groups containing important functions are
involved.” (_N. Dakota Exp. Sta. Rept._)
REFERENCES.
1, 4, 13, 16, 35, 57, 81, 82, 128, 154, 161, 203, 242, 251.