CELASTRACEÆ.
=Spindle Tree= (_Euonymus europæus_ L.). According to Cornevin the
spindle tree is poisonous in all its parts, especially the fruits, which
are emetic and strongly purgative. Sheep and goats have been injured
from eating the leaves, and children have suffered from eating the
fruits.
_Toxic Principle._ This plant does not appear to have been closely
studied from the toxicological point of view; contrary to the statements
generally made in the literature Van Rijn remarks that this species does
not contain the doubtfully classed _Euonymin_.
_Symptoms._ Ingestion of the plant induces symptoms and lesions such as
are due to violent vegetable purgatives.
REFERENCES.
63, 81, 205, 252.
RHAMNACEÆ.
=Buckthorn= (_Rhamnus Catharticus_ L.) and (_R. Frangula_ L.). The
berries of both species are toxic and purgative, but both are uncommon
and rarely eaten by stock.
_Toxic Principle._ The berries and bark contain the glucosides
_Frangulin_ (C_{21}H_{20}O_{9}) and _Rhamnetin_ (C_{16}H_{12}O_{7}).
_Symptoms._ The berries are purgative, and there is some danger from
large quantities, which may induce superpurgation. The leaves are
astringent and may arrest milk secretion (Cornevin). Müller states that
the inflammation of the stomach and intestines may terminate fatally.
REFERENCES.
4, 63, 76, 190, 203.
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_
(C_{11}H_{14}N_{2}O), 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.
REFERENCES.
4, 16, 63, 64, 81, 128, 144, 161, 190, 205, 213.
=Broom= (_Cytisus Scoparius_ Link.). This very plentiful and widely
distributed plant is undoubtedly to some extent poisonous, though
perhaps only feebly so in the quantities likely to be eaten by domestic
animals. Blyth records 400 cases of poisoning from it, however. Very
hungry animals might eat too much of it, and hence show symptoms of
poisoning.
_Toxic Principle._ The plant contains the alkaloid _Cytisine_
(C_{11}H_{14}N_{2}O); also the volatile alkaloid _Sparteine_
(C_{15}H_{26}N_{2}), a single drop of which, according to Blyth, killed
a rabbit, which showed symptoms similar to those of nicotine poisoning.
_Symptoms._ Taken in sufficient quantity broom induces narcotic
poisoning, with symptoms resembling those caused by Coniine, with
central nervous paralysis.
Cornevin gives the symptoms as similar to those due to _C. Laburnum_.
REFERENCES.
4, 16, 82, 128, 203.
=Indian Peas= (_Lathyrus sativus_ L.). A type of poisoning that deserves
attention here is that known as _Lathyrism_, since it is due to the
consumption of peas of the genus _Lathyrus_, the most dangerous being
the “Indian Pea,” _L. sativus_. The peas of this plant (see
Frontispiece) are small and dark-coloured, and are imported largely from
India and other countries under the general name of Mutter peas, a name
which they share with the ordinary pea _Pisum sativum_. In addition to
the seeds of this species the seeds of two South European and North
African species—_L. Cicera_ and _L. Clymenum_—have commonly caused
poisoning both in man and in animals, not infrequently leading to fatal
results. Horses, cattle, sheep and pigs have been affected—horses
particularly so—and many cases have been recorded in the veterinary
journals since 1885. Very heavy losses have occasionally resulted from
the use of the raw peas as a food for stock. For example, in 1884
Messrs. Leather of Liverpool had 35 out of 74 cart horses ill through
eating Indian peas at the rate of 3 to 4 lb. per head per day. Of the 35
no less than 19 died, and 2 were slaughtered, while 14 recovered. In the
famous Bristol Tramways case (1894) 123 out of 800 horses became ill
owing to being fed on the peas of _L. sativus_, and many died. There are
few records of harm to cattle, sheep and pigs, and Watt quotes Don to
the effect that pigeons lose their power of flight by feeding on the
peas. Very large quantities of the peas are used for feeding purposes,
and the fact that the losses are not larger is probably because the peas
only comprise a small proportion of the ration or are cooked before use.
After boiling or roasting the peas appear to be less harmful, as they
are eaten in India when cooked, or ground into flour and converted into
bread—though Cornevin states that drying and cooking does not destroy
the toxicity, while boiling for some time showed that at any rate part
of the toxic substance passed into the water, which became toxic and
caused death, the boiled seeds losing the greater part of their
poisonous property and not causing accidents when the water was
rejected. MacDougall states that as far as experimental evidence was
available (1894) it seemed to show that boiling the seeds before use
renders them innocuous.
Lathyrism usually only supervenes when the use of the peas for food is
prolonged, and the peas are taken in considerable quantity, but it is
possible that there is wide variation in the toxicity of different
samples, owing to differences in soil, climate, and other factors. In
man, Lathyrism is stated to be common in Spain, Italy, Russia and India,
owing to continued use of bread from flour of the three species of
_Lathyrus_ mentioned above. It is said especially to affect males.
_Toxic Principle._ Nothing certain as to the poisonous properties is
known, attempts to isolate the toxic substance having failed (Kobert),
though Smith gives it as prussic acid, apparently indicating a
cyanogenetic glucoside. This, however, can hardly be so, as the poison
is cumulative, and may not show its effects for weeks or months, or, in
man, even years—according to the quantity of peas eaten.
_Symptoms._ Lathyrism is only produced when the ration consists largely
of the pea for a considerable period (see above); in the horse fed
exclusively on the pea, the tenth day; but when one or two quarts are
given daily, only towards about the 80th day. Moreover, the malady may
declare itself as long as fifty days after the cessation of the pea
feeding (Lander).
In general Lathyrism is marked by paralysis of the lower extremities in
man and the hind limbs in animals, owing to the degeneration of the
muscle fibres, and possibly to affection of the nerves. In _horses_
there is paralysis of the hind limbs, dyspnœa and roaring—with paralysis
of the recurrent laryngeal nerve, and transverse myelitis. The horse
thus shows weakness of the hind quarters, staggering in the effort to
stand, difficulty in breathing, abnormally fast and irregular pulse,
open mouth, distended nostrils. Tracheotomy often gives almost immediate
relief.
Lander mentions in cart horses grinding of teeth, and convulsive
movements of the eyes, recalling epilepsy. In one outbreak there was
thick wind, staggering gait, weakness of hind quarters, and general
signs of intoxication; and sudden violent attacks of laryngeal paralysis
and dyspnœa during which there was palpitation, frothing, tongue
protruded, eyes staring, bluish tint of buccal membranes, and
palpitation. Paroxysms sometimes proved fatal.
An attack among 125 _lambs_ is mentioned by Cornevin. The lambs could
not stand on their fore legs and were obliged to go down on their knees.
On setting them up again, they were only able to keep up while
motionless or moving slowly. There was loss of sensibility in the front
members. In spite of this the eye was alert, they were attentive to
everything that went on around them, and were easily frightened.
In _pigs_ paralysis of posterior members has been observed.
In _cattle_ there was staggering, blindness, and stiffness of the lower
joints. In _sheep_ and _pigs_ there was also paralysis of the hind
limbs.
REFERENCES.
63, 82, 137, 170, 179, 190, 203, 205.
=Yellow Vetchling= (_Lathyrus Aphaca_ L.). To what extent this vetchling
is poisonous to stock is not clearly known, but it is cultivated in
India as a fodder for cattle. The seeds, however, are not altogether
safe when ripe, and MacDougall says “The seeds and pods have been known
to be used in soup in their young state and without harm resulting, but
the ripe seeds are narcotic and cause sickness and headache.”
=Lupines= (_Lupinus_ sp.). Different species of _Lupinus_ have been
found to cause poisoning of live stock, more particularly sheep, which,
when fed largely on lupines, develop a chronic type of poisoning known
as _Lupinosis_, or poisoning may be acute and rapid in its effects, as
in the United States. Records of large numbers of sheep being affected
at a time date from 1872, in various parts of the German empire. In
Europe by far the most harmful species is the Yellow Lupine (_L.
luteus_), which has been the cause of heavy losses of sheep, though
horses, cattle and goats may also be affected. The Blue Lupine (_L.
angustifolius_) and White Lupine (_L. albus_) may also be toxic. _L.
luteus_ has caused lupinosis in Germany since 1860, and Cornevin states
that in 1880 no less than 14,138 out of 240,000 sheep fed upon it (or
5·89 per cent.) died. Of 44 horses affected 11 died.
It must not be thought that all crops of lupine are poisonous, as
lupines are extensively grown on the Continent for fodder purposes and
are usually harmless. Even where Lupinosis occurs, considerable
quantities of the lupine must be ingested to cause poisoning. The
toxicity appears to vary according to soil and certain indefinite
conditions, and sometimes even a kilogramme (2·2 lb.) of the plant would
suffice to kill a sheep. Poisonous symptoms may sometimes be observed
after a single meal. Desiccation does not render the plant innocuous,
the seeds and hay being poisonous.
In the United States species of _Lupinus_ have caused great loss. In
1898 no fewer than 1,150 of a flock of 2,500 sheep died from eating one
species; one sheep farmer lost 700 sheep from the same cause; and 1,900
out of 3,000 sheep died from Lupine poisoning in Montana in 1900. Lupine
hay is found to be less harmful to horses and cattle, and Chesnut and
Wilcox suggest that this is possibly because as a rule they avoid the
pods, while sheep eat them. Lupines in America are very rapid in their
action on sheep, which may often die in one-half to three-quarters of an
hour after eating a quantity of the pods. Further, there is evidence
that sheep may gradually become immune to the poison by eating Lupines
regularly, since sheep fed regularly on hay nearly half lupine were
unaffected, but others eating the same hay for the first time died in
considerable numbers. The lupines are certainly far the most dangerous
when they bear ripe seeds—cut and made into hay before the pods form
they are much less dangerous.
In regard to _L. luteus_ Lander says: “According to the German
authorities a daily ration of 1 pound of the whole plant, ⅗ pound of
empty pods, or 1⅕ pound of seeds, will produce poisoning.”
Various means have been tried to render Lupines harmless, and success is
stated to follow heating with steam under a pressure of 2 to 2½
atmospheres.
_Toxic Principle._ A very full account of Lupine poisoning is given by
Pott, and from this a brief summary may be made. Siewert and Wildt
(1879) found two substances very like the alkaloids of _Conium
maculatum_—one like Coniine and the other like Conhydrine, the former
only being proved to be very poisonous. Baumert states that in _L.
luteus_ there are only two bitter alkaloids, _Lupinine_ (C_{10}H_{19}ON)
and _Lupinidine_ = _Sparteine_ (C_{15}H_{26}N_{2}). Many investigators
(_e.g._ Kühn at Halle) held that lupinosis was not identified with the
presence of lupine alkaloids. Then, in 1883, Arnold and Schneidemühl
caused the disease (lupinosis) in sheep with lupines freed from all
alkaloids, and they isolated from the seeds a substance they named
_Lupinotoxin_, which they found to be poisonous. The nature of the
poison cannot yet be said to be fully understood. The Lupine does not
always appear to be poisonous—only under certain conditions which are
not too well defined. One farmer had Lupines on the same soil for twelve
years without ill effects when fed to sheep, and then of 450 sheep 120
were severely ill, and 80 died; they had had unthrashed Lupine, not
quite ripe, to the extent of one-fourth of the ration. It is held to be
definitely established that the presence of this poison is due in turn
to the presence of a saprophytic fungus; when the fungus is absent or
only present in small quantity the lupine is not at all or only slightly
poisonous.
_Symptoms._ The disease is either acute or chronic according to the
amount of poison ingested. Most writers describe the disease in sheep,
but symptoms given vary somewhat.
In the acute form sheep become ill suddenly. There is loss of appetite,
dyspnœa, intense fever, hæmaturia, circulatory and digestive troubles,
grinding of teeth and trembling, which may pass into spasmodic
contractions. Vertigo is sometimes present. Jaundice then appears and is
evidenced by the yellow colour of the mucous membranes. Tumefaction of
the eyelids, lips and ears is common, but not invariably present.
Micturition is frequent, but not abundant, and the urine contains
albumen; the excrements are few and dry. There is collapse, and loss of
condition progresses rapidly, death occurring on the fourth to the sixth
day after the commencement of the illness.
In the chronic form the interstitial hepatitis predominates. Tumefaction
of the head may also appear as in the acute form. Digestive troubles
indicate chronic gastro-enteritis. This condition lasts for from 15 to
20 days, during which the cephalic œdemæ are eliminated by gangrene and
the animals remain listless and without appetite. The illness in sheep
is grave, and affected animals are rarely completely cured. The
mortality in other species does not seem to be less than in sheep.
(Cornevin.)
In describing the acute form of lupinosis Pammel adds that the initial
temperature may be as high as 104° to 106° F., but that it is
intermittent and gradually falls just before death. The pulse may reach
130 per minute and the respirations 100. A bloody froth may issue from
the nostrils. Animals apparently prefer the recumbent position, extend
the head on the ground, and seem entirely oblivious to all surroundings.
At first there is constipation, but later diarrhœa may set in and the
excreta be tinged with blood. In the chronic form the symptoms are not
so violent. Jaundice may be entirely absent, and emaciation and anæmia
may be the chief signs.
Chesnut and Wilcox record a case in which two sheep were each given 150
medium-sized pods of a native lupine, and seemed to like them. In 45
minutes, however, they became frenzied and died an hour later. They give
the symptoms as practically the same as those caused by European species
of _Lupinus_; acute cerebral congestion, with great mental excitement,
the sheep rushing about and butting into things; following is a stage
characterized by irregularity of movement, violent spasms, and falling
fits; in most cases collapse and death occur within half-an-hour to an
hour and a half; the pulse is strong and regular; the convulsions
resemble to some extent those caused by strychnine; the excretion of the
kidneys is much increased and sometimes bloody. In post-mortem
examination the kidneys are found affected, the lungs slightly
congested, the cerebral membranes in all cases congested, and in violent
cases small blood vessels are ruptured in different parts of the body.
REFERENCES.
4, 16, 20, 21, 42, 57, 63, 69, 82, 93, 128, 161, 166, 170, 190, 203,
213.
=“Java” Beans= (_Phaseolus lunatus_). Though not native to Great
Britain, the so-called Java Beans have been imported in considerable
quantities for stock feeding, and in the past nine years have caused the
death of a large number of animals. For example, in March, 1906, the
Board of Agriculture and Fisheries published an account of the poisoning
of animals by these beans at eight centres; at six of the centres 133
cattle were involved and 43 died. The beans are of varying origin, and
pass under the name of Java beans, Rangoon beans, Burma beans, Lima
beans, and Paigya beans. They are considerably different in colour
according to origin, the _Java_ beans being pale brown to almost black;
_Rangoon_, _Burma_ or _Paigya_ beans smaller, plumper, and lighter in
colour (“red Rangoon beans” are pinkish with small purple splotches, and
“white Rangoon beans” are pale cream); and _Lima_ beans are much larger
than the last-named and pale cream or white in colour (see
Frontispiece).
It has long been known that beans of certain forms of _Phaseolus
lunatus_ are poisonous, and the fact is noted by Church (_Food Grains of
India_, 1886), and by Watt (_Dictionary of the Economic Products of
India_, 1889–96). The coloured forms, and particularly the wild forms,
are the most dangerous, the white types being in general safe for stock
feeding. Some forms have a general similarity to butter beans and
haricots, and have hence been favourably regarded by farmers, but it is
a sound plan to purchase under a guarantee beans with such names as
those given.
_Toxic Principle._ It was shown in 1903 (_Proc. Roy. Soc._, Vol. 72)
that the seeds of _P. lunatus_, uncultivated in Mauritius, contained a
cyanogenetic glucoside, _Phaseolunatin_ (C_{10}H_{17}O_{6}N). This
glucoside, under favourable conditions, such as are present when the
beans are moist, masticated and ingested at the temperature of the
animal body, gives rise to prussic acid, which is the direct cause of
poisoning. The seeds of the wild forms yield, like bitter almond seeds,
considerable quantities of prussic acid, while the cultivated forms
resemble sweet almonds in yielding only traces of the acid, or none at
all. Determinations of the yield of prussic acid by various
investigators show percentages of from 0·027 to 0·137 in _Java_ beans,
and 0·004 to 0·02 in _Burma_ beans. The largest proportion therefore
occurs in the coloured beans, while the white forms contain much less or
none at all, and may be generally regarded as safe for stock.
_Symptoms._—The symptoms given by Damman and Behrens (_Veterinary
Journal_, 1906) were vertigo, tympany, and falling, with death in most
cases. Mosselmann (_Vet. Jour._, 1908) observed the symptoms due to the
ingestion of a small quantity of the beans by six head of cattle. They
were: great excitement, salivation, swelling, slight diarrhœa, quick
pulse and respiration, muscular spasms, and paralysis of the hind
quarters in one instance; all recovered rapidly.
REFERENCES.
5, 38, 76, 77, 107, 109, 125, 129, 144, 255.
=Castor Oil Plant= (_Ricinus communis_ L.). The beans (see Frontispiece)
of this exotic are toxic, and poisoning is only likely to occur if they
are sold in error as a feeding stuff, or from the use for feeding
purposes of the press-cake after the extraction of the well-known castor
oil, a purgative commonly used medicinally, of which the beans contain
about 50 per cent. According to Cornevin four seeds suffice to cause
accidents in man, eight lead to very grave results, and beyond that
number death may ensue. Pigs and poultry have been poisoned by the
seeds, and M. Audibert (near Beaucaire) reported the death of 80 sheep
from eating the press-cake, which is stated to have more pronounced
properties than the oil. It has been found as an impurity in linseed
cake and maize meal. (_Jour. Roy. Agric. Soc._, 1892.)
_Toxic Principle._ The toxic properties of the bean are due to _Ricin_,
a toxin which is similar to bacterial toxins, and the activity of which
is destroyed by heating to 100° C. The beans also contain the alkaloid
_Ricinine_ (C_{8}H_{8}O_{2}N_{2}), the toxic properties of which are
regarded as doubtful. (See Deane and Finnemore, _Yearbook of Pharmacy_,
1905, p. 473.)
_Symptoms._ These usually appear some days after the ingestion of the
beans or press-cake. There is generally purging. Broad observed in an
affected horse loss of appetite, shivering, cold extremities, dejection,
abdominal pain, constipation, temperature 103° F., pulse 70, and death
in about three days.
REFERENCES.
4, 16, 66, 73, 128, 205.
ROSACEÆ.
=Cherry Laurel= (_Prunus laurocerasus_ L.). This exceedingly common
ornamental shrub has caused the poisoning of numerous cattle and sheep
on the Continent, but is apparently less harmful in Great Britain—and in
any case animals are not much given to eating the foliage of this shrub,
the strong smell of the leaves when bruised affording a warning of its
unwholesome character. Gerlach recorded the intoxication of 25 sheep.
Bibbey also records the poisoning of 15 sheep by laurel, some of them
dying (_Farmer and Stockbreeder_, Jan. 29, 1912). On the other hand,
Henslow wrote of his cows that they “completely ruined a long laurel
hedge adjoining the field in which they lived; but this abnormal food
did no harm either to themselves or the milk they produced.”
_Toxic Principle._ So long ago as 1803 Schrader showed that the cherry
laurel contains a substance yielding prussic acid. The leaves contain
the cyanogenetic glucoside _Prulaurasin_ (C_{14}H_{17}O_{6}N), and an
enzyme-emulsin which, by its action on the cyanogenetic glucoside,
induces the formation of prussic acid, which is the actual cause of
poisoning. The percentage of the glucoside appears to be greatest about
July and August. By a microchemical examination Peche has clearly
localised hydrocyanic acid compounds in the leaf parenchyma.
_Symptoms._ In poisoning by Cherry Laurel there is bloating, inability
to rise, loss of sensation, difficult breathing, convulsions and
dilatation of pupils, and the results may be fatal if unattended to,
prussic acid being formed.
In the case of poisoning of ewes Aggio observed (_Veterinary Journal_,
1907) loss of appetite, vomiting, and inability to rise, followed by
several deaths. In 1871 Adsetts described (_Veterinarian_, 1871)
symptoms of poisoning in the horse: indistinct and feeble pulse;
congested mucous membranes, difficult respiration, uneasiness,
prostration, coldness of the extremities, loss of appetite,
constipation, diminished urination, and acute pain, eventuating in death
in three days. In sheep Bibbey observed salivation, grinding of teeth,
brain symptoms, paralysis in the back, coma, and death.
REFERENCES.
4, 16, 73, 76, 81, 128, 129, 130, 132, 170, 205, 232, 254, 255.
CUCURBITACEÆ.
=Bryony= (_Bryonia dioica_ L.). This widely distributed hedge climber,
which produces large quantities of scarlet berries, is a highly irritant
plant, with an unpleasant odour and a nauseous juice. The large fleshy
tuberous rootstocks have caused the poisoning of whole families who have
eaten them in mistake for turnips and parsnips. The berries may tempt
children, and cases of poisoning have occurred. Cornevin estimated that
15 berries would cause the death of a child and 40 that of an adult. No
deaths of domestic animals have been observed in searching the
literature, but animals may possibly eat it along the hedgerows at times
when grass is scarce. Pigs might possibly eat sufficient of the
rootstock, or poultry of the berries, to cause poisoning.
_Toxic Principle._ The plant contains the bitter and poisonous glucoside
_Bryonin_ (C_{34}H_{48}O_{9}).
_Symptoms._ The symptoms are those resulting from inflammation of the
stomach and intestines, together with convulsions. According to Cornevin
consumption of the plant promotes sweating, and causes a livid hue,
nausea, diuresis and abundant painless, watery defæcation, to which are
added in cases of poisoning nervous symptoms of stupor and tetanic
convulsions. There may be superpurgation or a suppression of defæcation.
Lander states that 2 lb. of fresh or 6 to 8 oz. of dried root given to
_horses_ did not cause purging, but there was abdominal pain, loss of
appetite, accelerated breathing, fever, dullness and copious urination.
Cases may end fatally.
REFERENCES.
73, 76, 81, 141, 170, 233.
UMBELLIFERÆ.
=Cowbane= or =Water Hemlock= (_Cicuta virosa_ L.). This plant is
undoubtedly exceedingly poisonous, and fatal cases have occurred in both
man and farm live stock. It has been mistaken by man for parsley, celery
or parsnip, with fatal results, many persons having succumbed to it. The
rootstock is attractive to children on account of its sweetish taste.
Pott says that either fresh or dry it is poisonous to all animals when
only a small quantity is eaten, and often causes rapid death. Sheep and
goats appear to be less readily affected than other domestic animals,
and cattle to be most sensitive. The loss of eleven animals in Brittany
was noted in the _Veterinarian_ in 1877, and a number of cattle died in
Ireland (_Veterinary News_, 1911), death in both cases being due to
Cowbane. It is clearly dangerous to grazing animals which have easy
access to it, especially if ordinary herbage is scarce. Hedrick (Canada)
is quoted as stating that a piece of the root about the size of a walnut
is sufficient to kill a cow in about fifteen minutes; and Müller says
that the quantity of dried plant sufficient to kill a horse appears to
be about 1 lb. According to Kanngiesser the mortality in human poisoning
due to this plant amounts to 45 per cent. of the cases.
_Toxic Principle._ The poisonous character of Cowbane has not been fully
investigated, and the toxic principles are given as the alkaloid
_Cicutine, with Oil of Cicuta_, and _Cicutoxine_. The last is a bitter
resinous substance classed by Cushny in the picrotoxin group; it occurs
in the dry root to the extent of 3·5 per cent. The toxicity is stated to
vary with season and climate; the rootstock is most poisonous in spring.
_Symptoms._ In man the yellow poisonous juice in the rhizome induces
epileptic convulsions, followed by death. The cicutoxine gives acrid
narcotic symptoms quickly followed by fatal results. The symptoms
usually appear within two hours, and death ensues in half-an-hour to
several hours. The symptoms which appear in an hour or so are given as
loss of appetite, salivation, vomiting (in swine), nausea, colic (in
horse), bloating (in cattle), diarrhœa, irregular pulse and heart,
dilatation of pupils, rolling of eyeballs, vertigo, reeling in circles,
twisting of neck, falling down, automatic movement of limbs, opening and
shutting of mouth, and death, usually with convulsions, in from half an
hour to an hour after first manifestation of symptoms.
For _cattle_, Lander gives hurried respiration, collection of froth at
the mouth and nostrils, and tympanites. The limbs are extended and
alternately stiffened and relaxed.
In his description of the symptoms Esser states that swallowing is
difficult, the tongue is stiffened, there is salivation, and death takes
place after loss of consciousness and convulsions.
REFERENCES.
31, 73, 81, 123, 141, 151, 170, 190, 203, 205, 213, 233, 238.
=Water Parsnip= (_Sium latifolium_ L.). The leaves and especially the
root of this species are regarded as poisonous, and the plant is
described as “poisonous” by Strasburger.
According to Müller the symptoms resemble those produced by
_Chaerophyllum_ (p. 40). After eating the roots _cows_ showed symptoms
of excitement, leading, in some instances, very quickly to death. The
milk, according to Cornevin, is of a disagreeable flavour.
The related _S. angustifolium_ has also been mentioned as objectionable.
As regards the toxic principle these plants have not been closely
studied, and it is not possible to give detailed symptoms.
REFERENCES.
73, 81, 190, 235.
=Water Dropwort= (_Oenanthe crocata_ L.). This weed of marshes, ditches,
and similar wet spots, has been a frequent cause of loss of stock. Cases
of fatal human poisoning have also occurred, owing to the leaves having
been mistaken for celery and the rootstock for parsnips. Several cases
of the poisoning of cattle have been recorded in the veterinary
journals, and sheep and cattle died on a farm near Bristol (_Jour. Roy.
Agric. Soc._, 1898). Horses have also been poisoned. Johnson and Sowerby
(1861) record the poisoning of 17 convicts near Woolwich, the leaves and
roots being eaten in mistake for celery and parsnips respectively. Nine
suffered from convulsions and became insensible; one died in five
minutes, a second in a quarter of an hour, a third in an hour, and a
fourth a few minutes later, while two more died during the next few
days.
Cornevin says that this plant causes the poisoning of animals every
year—they eat it willingly, showing an enfeebled instinct owing to
domestication. The plant is poisonous in all its parts, the root being
the most toxic, and drying does not destroy the toxic property. Cornevin
gives the following quantities of the fresh root as necessary to poison
various animals:—
Horse 0·100 per cent. of the live weight.
Ox 0·125 „ „ „
Sheep 0·200 „ „ „
Pig 0·150 „ „ „
Rabbit 2·000 „ „ „
Holmes described _Oenanthe crocata_ as the most dangerous and virulently
poisonous of all our native plants (_Pharm. Jour._, 1902).
Other species of _Oenanthe_ are also poisonous in a less degree—_e.g._
_O. fistulosa_ L., and _O. Phellandrium_ Lamk.
_Toxic Principle._ Poehl (1895) obtained from the root of this species
an amorphous neutral product which he designated _Oenanthotoxin_. The
latest investigation is that by Tutin, who examined entire dried plants
collected in early spring, and the experiments confirmed the conclusion
arrived at by Poehl, that the toxic principle is a neutral resin. A
dark-coloured, viscid resin, insoluble in water, and equal to 3 per
cent. of the weight of the plant, was extracted, and it is stated that
the neutral portions of the petroleum and ether extracts of this resin
represent the toxic principle of the plant. As there is no evidence of
the homogeneity of this product, and it is probably complex in
character, it was given no name or formula. The fact that it has
poisonous properties was ascertained by administering the various
products to guinea pigs _per os_.
_Symptoms._ In poisoning by _O. crocata_ the symptoms generally appear
very quickly, and in serious cases death may follow in from one hour to
a few hours. In Tutin’s experiments on guinea pigs the extracts referred
to above rendered the animal hypersensitive in two to four hours, while
marked convulsions, with trismus soon appeared; the heart-beat became
very noticeably slow and the convulsions persisted until death ensued.
There is great restlessness, difficult breathing, convulsions, loss of
sensation, blindness and stupefaction (Müller); Lander says the symptoms
recall hemlock poisoning, with the addition of green fœtid diarrhœa.
In _cattle_, one hour after eating, there is depression and accelerated
respiration; the conjunctivæ are injected, the eye turns in its orbit,
the pulse is weak but rapid, and there is foaming. Later, there is
colic, and spasmodic contractions of limbs and jaws. If the quantity
ingested is sufficient to cause death, the animal falls, but still moves
its limbs. There is bellowing, contraction of pupils, insensibility, and
death in convulsions—or, if not fatal, cattle may remain paralysed.
In the _horse_, the appearance of the symptoms and the course of the
illness are much more rapid and the nervous symptoms are accentuated.
If the _pig_ has consumed only a small quantity it soon gets rid of the
poison by vomiting; but if the quantity is considerable there is no
vomiting and death is as rapid as with cyanide poisoning (Cornevin).
REFERENCES.
10, 14, 73, 81, 141, 146, 170, 190, 205, 209, 213, 235, 246.
=Fool’s Parsley= (_Aethusa Cynapium_, L.). Much has been written about
the toxic properties of this weed of cultivated fields, principally
because, owing to the fact that the foliage has often been mistaken or
misused for parsley and the roots for radishes (!), it has been the
cause of human poisoning, though it seems to be one of the least active
of the poisonous Umbellifers. Its poisonous character is undoubted, but
it is unlikely to cause the poisoning of stock, which seem to refuse it.
Some authors regard it as strongly poisonous, but others as more or less
harmless. Johnson and Sowerby cite a case in which a child of five years
old died within an hour after eating the root, and a second death (in
Germany) within twenty-four hours from the use of the leaves in soup.
The most complete account of this plant is that by Power and Tutin,
issued from the Wellcome Chemical Research Laboratories in 1905. Many
authors since 1807 are cited as writing of its poisonous properties, and
of cases of poisoning, two of which terminated fatally. Miller (1807)
says that “most cattle eat it, but it is said to be noxious to geese.”
Bentley and Trimen write that “in all recorded experiments with it on
animals, it has had poisonous effects.” Dr. John Harley (1876 and 1880),
after experiments on a child and adults, concluded that the plant was
absolutely free from the noxious properties attributed to it. In 1904,
however, a case of severe poisoning by it was recorded (_Brit. Med.
Jour._, July 16, 1904, p. 124).
_Toxic Principle._ This has for many years been stated to be the
alkaloid _Cynapine_. For their investigation Messrs. Power and Tutin
collected the plant round London in July and August, with the fruits
still green, and after thorough chemical examination found 0·015 per
cent. of an _essential oil_ of rather unpleasant odour; 0·8 per cent. of
_resinous substances_; and an exceedingly small amount of a _volatile
alkaloid_ having the peculiar characteristic odour of _Coniine_. The
amount of hydrochloride of the alkaloid obtained showed that if the base
were Coniine it would correspond to only 0·00023 per cent. of Coniine in
the plant. In a degree this confirms the statement by Walz (1859) that
the fruit “contains a volatile base, very similar in odour and chemical
behaviour to Coniine, and probably identical with it.” The investigators
suggest that the alkaloid is Coniine, and the small amount would justify
the opinion, but there may be variation in toxic property according to
stage of development and climate. The authors conclude that “it cannot
be considered improbable that under favourable conditions of growth, the
proportion of alkaloid may be increased to such an extent as to impart
to the plant the poisonous properties ascribed to it.”
_Symptoms._ In a child which died, there were abdominal pain, a feeling
of sickness, and a tendency to lockjaw, and death supervened within an
hour; and in a German case, vomiting, diarrhœa, lockjaw, and death in 24
hours. (Johnson and Sowerby.) The plant causes convulsions and stupor,
with nausea and vomiting (Henslow).
The symptoms observed in _cows_ are loss of appetite, salivation, fever,
uncertain gait, and paralysis of hind limbs (Müller).
Pott refers to a case which occurred in Guernsey among _horses_. Animals
with white muzzles and feet had diarrhœa, while other horses remained
healthy. All white places on the body were badly inflamed. Pammel states
that the plant causes stupor, paralysis and convulsions in domestic
animals.
REFERENCES.
45, 73, 81, 121, 130, 141, 190, 203, 213, 214.
=Chervils= (_Chaerophyllum_ sp.). No investigation of these plants
appears to have been undertaken, but _C. sylvestre_ L., though eaten by
some animals, including the ass and the rabbit, is stated by a German
observer (_vide_ Cornevin) to have caused the death of pigs. Müller
states that according to the literature both cows and pigs have been
poisoned, even fatally, by _C. temulum_ L. The plants have a strong
odour and acrid taste.
_Toxic Principle._ This, if any, appears to be unknown, though Müller
(1897) says that _C. temulum_ contains in all its parts the little known
_Chaerophyllin_ (? alk.).
_Symptoms._ The pigs referred to above as having died were said to show
paralysis, dilated pupils, and enteritis, and to refuse food. Postmortem
examination showed acute gastro-intestinal inflammation. In the case of
cows there are similar symptoms.
REFERENCES.
73, 190.
=Hemlock= (_Conium maculatum_ L.). This plant, famous from ancient times
as extremely poisonous, has a fœtid, disagreeable odour—a mousy
smell—especially noticeable when the plant is bruised. It has caused
human poisoning in three ways: the seeds have been eaten in error for
anise, the leaves for parsley, and the roots for parsnips.
Animals rarely appear to eat this plant, but cases have been recorded.
It is stated that in the United States many domestic animals have been
killed by it; and Ewart says that it is responsible for poisoning a
number of cows in Victoria. Goats are believed to be largely immune to
the poison, or are less harmed than other animals, and sheep are stated
to eat the plant with impunity, though cases of poisoning are recorded.
Johnson and Sowerby state that horses have occasionally swallowed
considerable quantities without apparent effect, while Cornevin remarks
that to cause death a horse would need to eat 4 to 5½ lb. of the fresh
plant, or a cow 8¾ to 11 lb.
Hemlock is probably most dangerous to live stock in the spring, when
green herbage is least plentiful and the young shoots of hemlock are
fresh and short. Chesnut says that the root is nearly harmless in March,
April and May, but dangerous later, especially in the first year of
growth; but Esser states that it is only poisonous in the spring. The
foliage is more poisonous before flowering than after, when the
poisonous principle passes to the fruits, which are more poisonous
before ripening (three quarters ripe) than afterwards. Pott remarks that
after eating hemlock cows give milk with a bad taste.
_Toxic Principle._ Early in summer the toxic principle appears to be
chiefly contained in the foliage, but later in the fruit, particularly
when still green. Among the substances contained in hemlock are the
toxic alkaloid _Coniine_ (C_{8}H_{17}N), the poisonous _Coniceine_
(C_{8}H_{15}N), _Conhydrine_ (C_{8}H_{17}NO), the alkaloid
_Methylconiine_ (C_{9}H_{19}N), _Pseudoconhydrine_ (C_{8}H_{17}ON).
Coniine may be described as an oily, colourless, quite volatile liquid,
quickly turning brown on exposure to the air, and giving a mousy odour
to the whole plant. The amount of Coniine in the fresh leaves is given
(Pammel) as 0·095 per cent., but in the ripe seeds 0·7 per cent. English
fruits contain much more of the total alkaloids than imported fruits.
Owing to the volatile character of the poisons hemlock largely loses its
toxicity when dried in hay, and is therefore the less likely to prove
injurious to domestic animals.
_Symptoms._ Hemlock is a dangerous narcotic plant. Even the smallest
quantities may cause inflammation of the digestive organs, paralysis and
death. The general symptoms are salivation, bloating, dilatation of
pupils, rolling of eyes; laboured respiration, diminished frequency of
breathing, irregular heart action; loss of sensation, convulsions,
uncertain gait, falling, and at the end complete paralysis. Death occurs
after a few hours. The poison acts on the motor nerve endings, causing
paralysis, dyspnœa resulting from paralysis of the pectoral nerves, and
acceleration of the heart from that of the inhibitory fibres of the
pneumogastric.
Small quantities cause in the _horse_ a little prostration, yawning,
acceleration of pulse, dilatation of pupils and sometimes muscular
spasms of the neck and shoulders. Large quantities cause nausea,
unsuccessful attempts to vomit, gritting of teeth, accelerated
respiration and dyspnœa, and muscular tremors commencing in posterior
members and spreading to anterior members and spine. There is next
difficulty of locomotion, sweating (but not continual), falling,
paraplegia, then paralysis, loss of feeling, lowering of temperature,
rapid pulse, increasingly difficult respiration, and death from stoppage
of respiration.
With _cattle_ there is ptyalism, cessation of digestion, bloating,
constipation, weakness and stupor. Pregnant cows have been observed to
abort; the milk of cows has an unpleasant flavour. There are bloody
evacuations in some instances in the case of the ox. In cows Chesnut
says that there was “loss of appetite, salivation, bloating, much bodily
pain, loss of muscular power, and rapid, feeble pulse.”
In _sheep_ the abdomen is tucked up, the animal has a dazed appearance,
there is dilatation of pupils, unsteady gait, the hind limbs being
dragged, coldness, and death after a few convulsive movements.
In the _pig_ there is prostration and inability to move, coldness, slow
breathing, livid mucous membranes, imperceptible pulse, paralysis,
particularly of the posterior members, and no convulsions.
REFERENCES.
4, 16, 52, 53, 73, 81, 82, 91, 128, 141, 161, 203, 205, 213, 238.