=The prognosis= is not hopeful. Statistics show that almost all the

affected animals die, and that those exceptional cases which survive

remain puny and sickly. There is no economic advantage in attempting to

save them.

The mothers of affected calves seldom show any sign of illness, though

the after-birth is often retained.

=Lesions.= The macroscopic lesions are of very trifling importance

compared with the gravity of the disease. The digestive tract appears

congested throughout. The intestinal mucous membrane is moderately

swollen, but without gross lesions. The intestinal contents exhale a

sickly, fœtid odour. The smaller vessels and capillaries forming the

peripheral vascular network appear distended, as in septicæmia. The

carcases putrefy with extreme rapidity.

Curative =treatment= is very uncertain. Varying results have been

obtained with doses of 4 to 5 drams of slight purgatives like

borotartrate of potassium, sodium sulphate, and magnesium sulphate;

small doses of intestinal antiseptics like salicylic acid, 15–grain

doses of salicylate of soda, 45 to 75 grains of carbolic acid, 2 per

cent. carbolic solution in doses of 7 to 12 drams; 1 per cent. Lysol

solution in doses of 2 to 4 ounces; benzo-naphthol, lactic acid 45 to 75

grains, tar water, lime water, etc. Although all these preparations,

when carefully used, generally give good results in the early stages of

simple diarrhœa, they appear to fail in dysentery of new-born calves.

Prophylactic measures are more reliable. They consist:

(1.) In scrupulous disinfection of the byres when the first case of

abortion occurs;

(2.) In successively isolating cows which are about to calve in a small

specially detached stable;

(3.) In carefully disinfecting the genital organs of cows which have

aborted, firstly with boiled water at a temperature of 100° Fahr., and

then with 1 per cent. iodine solution.

Calves which are infected when born cannot be saved, but abortion can be

prevented and dysentery so stamped out.

DIARRHŒIC ENTERITIS IN CALVES.

This disease is usually called “simple sporadic diarrhœa.” It may appear

at any time before weaning, and can usually be cured if treated early

before the patients show bodily wasting.

=Causation.= Indigestion from failure of the abomasum to deal with the

milk usually precedes diarrhœic enteritis; it may terminate without

complications, but very often is followed by diarrhœa. Anything which

produces milk indigestion, therefore, favours the occurrence of

enteritis. Such predisposing influences include over-distension of the

abomasum, milk of bad chemical composition, milk tainted by keeping or

by storage in dirty and infected pails, etc. The addition to the milk of

nutritive substances which the abomasum and intestine are not yet

capable of digesting, such as wheat, rye, barley, or maize meals, very

often produces diarrhœa even when the meal is well cooked.

Chills, privations, irregular feeding, and badly-managed weaning may

facilitate its development, but none of these causes, however important

they may be, seem to play any other part than that of favouring the

multiplication of the numerous varieties of microbes to be found in the

intestinal tract. Vascular disturbance occurs, either as a result of

direct irritation of the intestinal mucous membrane or of the action of

toxic products contained in milk which has served as a culture medium

for these microbes; this is followed by secretory disturbance, and the

intestinal contents being modified in character, the microbes normally

present undergo changes in number and quality. Inoffensive organisms

assume pathogenic qualities and secrete toxic principles, normal

digestion is disturbed, the intestinal defence becomes less perfect,

toxic principles which the liver is incapable of destroying are

absorbed, and diarrhœic enteritis is set up.

=Symptoms.= Diarrhœic enteritis appears during the second week of life,

towards the end of the first month, or even later. It is characterised

by the passage of fæces consisting of mucus and containing little clots

of milk.

This is the first stage of alimentary diarrhœa, also termed “white

diarrhœa” or “white scour.” It may prove unimportant; it may last a day

or two and then cease. Most commonly diarrhœa increases and assumes a

mucous and then a serous character, whilst the dejecta exhale a very

characteristic repulsive smell. The excrement becomes greenish brown,

and after several days or a week or more may appear blood-stained. The

number of evacuations varies enormously, depending on the gravity of the

condition. The ejected material is irritant, and the parts soiled by it,

like the perineum, hocks, and back of the cannon bones, become slightly

inflamed as though blistered; later, the hair falls away.

The general health then begins to suffer. Fever remains moderate, but

the mouth is pasty, the tongue coated, and the breath fœtid.

The patients become thin, and lose their appetite and spirits. Palpation

of the abdomen, especially of the right flank, is slightly painful, and

the pulse is accelerated.

The diarrhœa may spontaneously diminish if the animal’s constitution

prove sufficiently strong; but if it follows its course, the little

patient becomes weaker, eats less, the evacuations increase and are

accompanied by tenesmus. In seven to eight days, in rare cases in four

to five, the animal dies from toxi-intoxication of intestinal origin, or

from infection resulting from intestinal germs, particularly the

bacterium _Coli communis_, obtaining entrance into the circulation. On

the other hand, the diarrhœa may continue for weeks.

=The diagnosis= is easy, and there should be no difficulty in

distinguishing this disease from dysentery and from umbilical phlebitis,

which are also accompanied by diarrhœa.

=The prognosis= is grave, unless treatment is early undertaken. In the

latter case there is a good chance of recovery.

=Lesions.= The macroscopic lesions are not of much interest, being

confined to congestion of the intestinal mucous membrane, superficial

desquamation of the epithelium, small vascular erosions, and general

wasting.

The mesenteric lymphatic glands are swollen and œdematous.

After death from general infection, it is not uncommon to find pleural,

peritoneal, and pericardial exudation or even endocarditis.

Even in cases where no post-mortem change has had time to occur cultures

from the blood yield varieties of the bacterium _Coli communis_.

=Treatment.= The meals should be given at fixed hours, and regulated

both as regards quantity and quality. These precautions alone suffice to

prevent the appearance of diarrhœic enteritis.

Curative treatment has every chance of succeeding when undertaken at the

outset. Delafond and Trasbot recommend mild purgatives, which act more

rapidly than intestinal antiseptics. These comprise borotartrate of

potash in doses of 4 to 5 drachms, sodium sulphate in doses of 2½ to 4

drachms, sulphate of magnesia, etc. By evacuating the bowel and removing

a large number of the germs which have multiplied there, they arrest

intoxication and prevent infection. Nevertheless, they should not be

administered for long, and after one or two doses should be followed by

antiseptics like benzo-naphthol, in doses of 15 to 30 grains, salicylic

acid in doses of 5 to 10 grains, or salicylate of soda 45 to 60 grains.

Mucilaginous and sweetened drinks containing lactic acid in doses of 45

to 75 grains per day may be given between the meals, or at intervals if

the calf is sucking.

Laudanum in doses of 6 to 10 drops per day administered in rice water,

extract of opium, weak solutions of tannin, etc., are also of value.

Filliàtre has successfully used tar water in the first stages. The

solution consists of vegetable tar 6 drachms, boiling water 1 quart.

This solution is used tepid in the proportion of 1 part to 3 parts of

warm milk.

Decoctions of spiked purple loosestrife, willow bark, etc., are also of

great value in certain districts.

The drug which appears least dangerous, however, is that so often

successfully used in young children—viz., subnitrate of bismuth. It can

be given in doses of 30 to 45 grains per day, with lactic acid in doses

of 75 to 150 grains, according to the size of the patients. If the

animals are greatly exhausted and have been ill for some time there is

less chance of recovery, and under these circumstances Dr. Lesage’s

anti-colic serum might be used.

It gives excellent results in infants, and it has proved successful in

simple diarrhœa of calves.

CHAPTER VII.

POISONING.

Accidental poisoning is frequent in domesticated animals. It may present

no visible lesions, and it is therefore very important to recognise the

symptoms which indicate the secret lesion.

POISONING DUE TO FOOD.

Under this title are included all forms of poisoning resulting from the

ingestion of bad fodder. Such expressions as “intestinal typhus” and

“typhic gastro-enteritis” only indicate a special stage in the

condition, which is never twice the same.

=Causation.= The most important changes in the food ingested do not

consist in a mere modification in its chemical composition, but in the

presence of various parasites which develop in grain and forage, after

moistening, or after abnormal fermentation in the interior of the

grains. These parasites are chiefly represented by fungi belonging to

the genus Mucor: _Aspergillus_ or _Penicillium_; blight—_Puccinia

graminis_, _Uredo linearis_; smut—_Tilletia caries_, _Ustilago segetum_,

_Ustilago maydis_; yeasts of different kinds resulting from the

fermentation of brewers’ grains; and, finally, unrecognised microbes

which act by means of the poisons they secrete.

=The symptoms= are always very vague. At first the only marked symptom

is loss of appetite, accompanied by dryness of the mouth and muzzle,

depression and constipation. The animals never clearly show signs of

gastro-enteritis; nevertheless, the changes in general health point very

clearly to a digestive origin.

In cases of acute poisoning the symptoms develop rapidly. Torpor becomes

more marked, the movements of the heart tumultuous, and the temperature

rises to 105° Fahr. (40·5° C.), diminishing later until death occurs.

In chronic forms of poisoning constipation is present at first, but is

soon followed by profuse, fœtid, blackish diarrhœa, sometimes containing

streaks of blood and accompanied by abdominal pain.

In exceptional cases these digestive symptoms are amplified by the

presence of broncho-pneumonia, pleuro-pneumonia, nephritis, and

cystitis, as in poisoning by tannin and essential oils. These

complications are of infectious origin.

In young animals, like lambs and young pigs, still with their mothers

alimentary intoxication may also occur though the mothers show no signs

of illness. The passage of poisonous principles into the milk cannot be

disputed. Moussu has seen numerous cases of alimentary intoxication in

lambs whose dams were fed with decomposed beet pulp, and in sucking pigs

whose mothers had received bad maize, turnips, etc.

=Diagnosis.= Careful examination of the substances with which the

animals are fed, and consideration of the history, prevent confusion

with ordinary poisoning. Anthrax as a cause can easily be eliminated.

=The prognosis= is grave, unless the practitioner is summoned early.

=The lesions= are those of acute gastro-enteritis—congestion of the

mucous membrane, abomasum, and intestine, submucous infiltration,

shedding of the epithelium, which sometimes attains the stage of

ulceration, suffusion and intestinal or superficial hæmorrhage,

dilatation of the capillaries, etc.

The symptoms of poisoning are produced by the absorption of toxic

products, which pass from the intestine into the blood current.

Poisoning is frequently complicated by infection produced in a similar

manner.

=Treatment.= The first point is to change the food. This alone is often

sufficient to dispose of the digestive disturbance in a week or two. In

addition, mustard plasters may be applied, and purgatives, stimulants

and mucilaginous drinks may be given. Finally, diuretics are useful in

eliminating the toxic products accumulated in the blood. They comprise

general stimulants like wine, alcohol, tea, coffee, etc. Subcutaneous or

intravenous injection of physiological salt solution is indicated.

POISONING BY CAUSTIC ALKALIES.

=The cause= consists in the administration of insufficiently diluted

solutions of ammonia in cases of tympanites, or the ingestion of

quick-lime, used for disinfecting stables, by animals suffering from

depraved appetite.

=The symptoms= indicate injury to the anterior part of the digestive

tract. They consist in salivation, loss of appetite, colic, indigestion,

diarrhœa, and progressive loss of strength.

=Diagnosis= is only possible when the history is clear.

=The prognosis= is grave if the doses swallowed have been so large as to

cause severe burning of the mouth, œsophagus, rumen, etc. The local

lesions are grey and soft.

=Treatment= consists in immediately giving acidulated draughts

containing vinegar or 1, 2 or 3 per cent. of hydrochloric acid, and

emollient, mucilaginous drinks containing opium for the purpose of

calming the irritation.

POISONING BY CAUSTIC ACIDS.

Cases of this kind are rare. Gerlach described a case of poisoning by

straw which had been removed from sulphuric acid carboys. Abadie saw a

number of cases which were traced to the unskilful treatment of two

empirics.

=The symptoms= point to the existence of stomatitis, œsophagitis, and

gastro-enteritis. Death occurs rapidly, with a running-down pulse. On

post-mortem examination one discovers more or less deep burning of the

mucous membrane of the digestive tract.

=The diagnosis= is difficult in the absence of information.

=The prognosis= is grave.

=Treatment= comprises administration of alkaline draughts, solutions of

bicarbonate of soda, calcined magnesia, etc., and of mucilaginous drinks

containing opium, chalk, etc. This may produce temporary relief.

Water mixed with whipped whites of eggs is also extremely valuable, but

it is often better to slaughter the animal as soon as the condition is

diagnosed.

POISONING BY COMMON SALT.

This form of poisoning is rare in oxen on account of the large quantity

of salt which can be ingested without producing bad effects. It is

commonest in animals to which old brine has been given or which have

received rough salt containing toxic substances (sheep and pigs). Beef,

pork, or fish brine, four or five months old, is especially dangerous

because of the toxins it contains. Half a pint is a fatal dose for a pig

(Reynal). The symptoms include marked thirst, vomiting and diarrhœa; at

a later stage motor and nervous disturbance appears, resulting from

poisoning of the cerebro-spinal system. Paralysis, epileptiform

convulsions, trismus, coma and death characterise extremely acute cases.

To the naked eye, the =lesions= are those of acute gastro-enteritis;

and, in many cases, of marked congestion of the brain and medulla and of

the mucous membrane of the bladder.

=The treatment= is prophylactic and hygienic. Old brine and salt of

doubtful purity should be avoided. The symptoms should be treated by

administering diuretics, preferably soda bicarbonate, which does not

irritate the kidney, and by giving mucilaginous drinks with anodynes.

POISONING BY THE NITRATES OF POTASH AND SODA.

This form of poisoning has frequently been described as following the

ingestion of water used for washing sacks which have contained chemical

manures. Occasionally it results from the administration of medicines

containing excessive doses of nitrate of potash. The symptoms vary in

severity with the purity of the salt, with its nature, and with the

degree of concentration of the solution: nitrate of potash is more

dangerous than nitrate of soda.

The chief =symptoms= may be grouped as follows:—

Salivation, indigestion and tympanites, nausea, vomiting, diarrhœa, and

(especially) intense polyuria: the kidney may be irritated to such a

degree as to produce albuminuria and hæmaturia. Intense dulness and

general weakness precede death, which sometimes occurs in four to twelve

hours after the poison has been taken.

The =lesions= are to be found in the digestive and urinary apparatus.

The kidneys are congested and hypertrophied, or present changes

indicating epithelial nephritis. The ureters and the bladder may show

similar lesions.

=Treatment= comprises removal of the cause, and the administration of

emollients, narcotics, and diffusible stimulants.

POISONING BY TARTAR EMETIC.

Tartar emetic is sometimes given for the purpose of favouring secretion

and restoring rumination; occasionally the proper dose is exceeded and

poisoning occurs. Given repeatedly, tartar emetic is apt to accumulate

in the deeper portions of the gastric compartments and to produce

general symptoms of super-purgation, and such local symptoms as

ulceration and even perforation of the walls of the stomach, which in

turn is followed by abscess formation in the abdominal wall.

=Diagnosis= is easy. =The prognosis= is grave.

=Treatment= is confined to the administration of mucilaginous and

diuretic fluids. Tannin has been recommended.

POISONING BY ARSENIC.

Overdoses of Fowler’s solution produce rapidly fatal results, in

twenty-four to forty-eight hours. Lesions are little marked.

Arsenious acid acts like tartar emetic by accumulating and producing

local gastritis; it may also cause acute poisoning, being in that case

characterised by severe colic with tympanites, salivation, and fœtid,

sometimes blood-stained, diarrhœa. The urine becomes albuminous, and

remains scanty. Incomplete paralysis is sometimes produced, and various

forms of hæmorrhage result from changes in the constituents of the

blood.

If the gastric compartments are perforated, an abscess may develop in

the abdominal wall. The =lesions= are those of acute gastro-enteritis.

The contents of the stomach exhales an odour resembling garlic. The

parenchymatous organs—the liver, kidney, and heart—show fatty

degeneration in chronic cases.

In prescribing arsenic, one should begin with small doses, which can

gradually be increased as the animal becomes accustomed to the drug.

Curative =treatment= consists in administering antidotes, such as

hydrated oxide of iron, sulphate of iron, and calcined magnesia.

Haubner described a form of chronic arsenical poisoning produced in the

neighbourhood of blast furnaces near Freiberg. Similar forms of

poisoning may perhaps occur in the neighbourhood of chemical and

smelting works in England.

PHOSPHORUS POISONING.

Though the chronic form is common in men, phosphorus poisoning only

occurs accidentally in animals through eating phosphorus paste, used as

a poison for rats, or as a consequence of excessive doses given

medicinally. Some cases have been described by Maury.

=The symptoms= comprise salivation, loss of appetite, alliaceous odour

of the buccal cavity, arrest of intestinal peristalsis, indigestion,

colic, diarrhœa, exhaustion and death in a state of coma. Albuminuria

and icterus also occur.

=The lesions= are the same as those of arsenical poisoning—viz.,

stomatitis, pharyngitis, and gastro-enteritis. The specific changes

consist in fatty degeneration of the liver and kidneys, and the peculiar

odour resembling garlic exhaled by the flesh.

Death is a consequence of deoxygenation of the blood, which appears

black, and when spectroscopically examined reveals only the lines of

reduced hæmoglobin.

=Treatment.= Oil and milk dissolve phosphorus and render it more easily

assimilable; they should never be administered. Large doses (up to six

fluid ounces) of essence of turpentine have been recommended. This

prevents the phosphorus absorbing oxygen at the expense of the blood.

Saline purgatives assist in eliminating the poison.

MERCURIAL POISONING.

Mercurial poisoning may result either from the administration of

medicines or from accident. Cases of the former kind follow the internal

use of sublimate or calomel. Doses of 2 to 2½ drams of calomel, if

repeated for a certain time, may prove toxic in the ox. Accidental

poisoning results from the use of mercurial ointment as a parasiticide

over large surfaces. Poisoning, however, rarely occurs unless the animal

is able to lick the parts. Some authors have tested this point by freely

applying mercurial ointment over parts likely to absorb it readily,

without having seen any bad effect.

=Symptoms.= Free salivation, the saliva gradually becoming fœtid and

blood-stained. The slight irritation of the buccal membrane first seen

is soon replaced by congestion of the gums, then by gingivitis and

periostitis, with local ulceration and hæmorrhage. The portion of the

gums surrounding the teeth becomes violet, and suppurative alveolitis

may follow.

As a consequence of disturbance in the digestive secretions digestion

ceases, defæcation becomes irregular, the fæces are often hard and

coated, and can only be passed with difficulty, though sometimes there

is profuse fœtid diarrhœa.

Respiration is difficult, jerky, or even dyspnœic, and is accompanied by

discharge from the nose and by expectoration. The gait is irregular, and

paralysis may follow. Finally the skin shows an eruption resembling that

of impetiginous eczema; vesico-pustules, covered with yellowish crusts,

appear over the entire surface of the body.

=Lesions.= The lesions of hæmorrhagic gastro-enteritis are sometimes

accompanied by catarrhal tracheo-bronchitis, and even intra-pulmonary

hæmorrhage. The muscles are discoloured, appear as though boiled, and

are covered with ecchymoses. Blood effusions occur beneath the

eczematous crusts, but the rest of the skin is anæmic.

=Treatment= includes administration of raw eggs, or, better still, of

white of egg beaten up in water; the albumen in coagulating imprisons

the mercury. Failing these, other bodies, like flowers of sulphur and

iodide of potassium, which with mercurial salts form soluble and

harmless compounds, may be given. Chlorate of potash has also been

recommended.

Complications like stomatitis and gastro-enteritis are treated by the

usual methods.

LEAD POISONING: SATURNISM.

Lead poisoning is very rare, and seldom occurs except near camps or

factories. It then results from swallowing lead “spray” mixed with the

grass or from inhalation of lead vapour.

=The symptoms= comprise salivation, nausea, colic, obstinate

constipation, tympanites, and arrest of milk secretion. A peculiar form

of trembling affects the head; epileptiform convulsions, amaurosis, and

paralysis may also occur. General sensibility diminishes, and death

follows.

The disease may assume a chronic form, characterised by a blue line

around the gums, changes in the joints, albuminuria, and bodily wasting.

=The lesions= are those of ulcerative stomatitis, anæmia of the mucous

membranes, and fatty degeneration of the epithelium. In the chronic form

the kidneys are atrophied.

=Treatment= consists in giving substances which form insoluble compounds

with lead. It comprises the administration of dilute sulphuric acid,

solutions of sodium sulphate or magnesia, milk, eggs, and iodide of

potassium.

COPPER POISONING.

This is a rare form of poisoning. It may follow ingestion of food stored

in copper vessels, licking of ointments containing copper salts, or

ingestion of vine leaves, or leaves of other plants which have been

sprayed with sulphate or acetate of copper to prevent “mildew.”

=The symptoms= comprise vomiting of green-coloured material, colic,

diarrhœa, muscular weakness, and convulsions. The urine contains

dissolved albumen and hæmoglobin.

=The lesions= are those of acute enteritis and dilatation of the

stomach. The essential lesion consists in decomposition of the blood

with the formation of methæmoglobin. Nephritis and granular degeneration

of the muscles form secondary symptoms.

=Treatment= consists in administering raw eggs, albumen, milk, mucilage,

flowers of sulphur, or calcined magnesia.

CARBOLIC ACID POISONING.

Carbolic acid poisoning sometimes follows the use of carbolic acid

solutions in the form of injections, enemas, or baths.

=Symptoms.= Administered in over-doses or for too long a time, carbolic

acid produces stomatitis, œsophagitis and vomiting.

True poisoning is characterised by changes in the kidneys and bladder;

the urine becomes brown and turbid, and possesses a well-marked carbolic

odour, the animals suffer from severe trembling and appear stupid, and

coma and paralysis precede death.

The specific =lesions= consist in parenchymatous nephritis, sometimes

accompanied by renal hæmorrhage, cystitis and hyperæmia of the lung and

brain. The flesh has an odour of carbolic acid, which renders it unfit

for human consumption.

=Treatment= consists in giving stimulants and slight diuretics, such as

ether, alcohol, wine, coffee, saline sulphates, or Glauber’s salt. The

last named forms phenyl-sulphuric acid, which is not toxic. Olive, rape,

or linseed oil has been recommended. All these drugs are useless if the

kidney lesions have become too pronounced.

POISONING BY ALOES.

This form of poisoning is caused by administering over-doses of aloes.

Apart from the accidents possible in pregnant female animals, large

doses of aloes produce symptoms of super-purgation—profuse diarrhœa,

running down pulse, and nervous prostration.

=The lesions= are those of gastro-enteritis, the intestine being empty,

and its mucous membrane of red colour.

=Treatment= is confined to administering drugs like camphor, rice,

bismuth, opium, chloral, and emollients, which diminish peristalsis and

lessen secretion.

IODOFORM POISONING.

=The causes= are limited to the licking of wounds which have been

dressed with iodoform.

=The symptoms= include gastric disturbance, somnolence, coma, and the

signs of iodism.

The only =lesions= are those of fatty degeneration of the kidneys and

liver.

=Treatment= comprises the exhibition of vomitants, stimulants, and

diuretics.

IODINE POISONING: IODISM.

Death by iodine poisoning is absolutely exceptional: the complications

described under the name of iodism are rather to be referred to

saturation of the organism than to true poisoning.

=The cause= of iodism is unduly prolonged administration of iodide of

potassium, or of iodine in solution.

=The symptoms= include discharge from the eyes, coryza, hypersecretion

from all the mucous membranes, and gastric disturbance. The cutaneous

eruption exhibits special peculiarities, including desquamation of the

epidermis in the form of branlike scales, and pruritus.

The first indications in =treatment= are to discontinue the drug and to

administer stimulants and nutrients like milk, cod liver oil, etc.

STRYCHNINE POISONING.

Strychnine poisoning is most commonly due to over-doses of the drug

accidentally given during treatment.

=The symptoms= comprise tetanic convulsions, hyperæsthesia and dyspnœa.

As a result of muscular rigidity, the ribs cannot be moved, and death by

asphyxia follows.

=Treatment= comprises the use of anæsthetics, and the administration of

chloral hydrate, as long as the contractions continue. Bromide of

potassium, tobacco, tannin, etc., are also useful.

* * * * *

The chief part of the botanical descriptions in the following list have

been extracted, by permission, from the Annual Report for 1898 of the

United States Bureau of Animal Industry, p. 392. To Dr. D. E. Salmon,

who gave this permission, and who also kindly supplied the blocks, the

writer (Mr. Dollar) desires to express his very sincere thanks.

Considerable modifications have been made, and in the case of the more

important poisonous plants, details of symptoms and treatment have been

added.

LIST OF PLANTS POISONOUS TO STOCK.[2]

Footnote 2:

The names of plants proved beyond doubt to be poisonous to stock are

marked with an asterisk. The evidence in regard to the toxic

properties of others is not in every case entirely convincing, though

there is good ground for strong suspicion.

PERISPORACEÆ (ROT-MOULD FAMILY).

=Aspergillus glaucus.=—This is the common flocculent woolly mould which

sometimes develops to a dangerous extent on corn, oats, and other food

grains which have either been harvested before full maturity or been

stored in a damp place. The mouldy growth is pure white at first, but

changes with the ripening of the spores to gray and then green. The

spores are apparently the cause of the so-called enzootic cerebritis, or

“staggers,” of horses, which, during the winter of 1898–99, was reported

as having caused very heavy losses in the southern portion of the United

States. European investigators have shown that the spores of this mould

will grow within the living body if they are introduced into the blood.

Death is probably caused by some poison which is simultaneously produced

with the mould in the body of the animal.

HYPOCREACEÆ (ERGOT FAMILY).

* =Claviceps purpurea.=—This, the most common species of ergot, infests

various species of native and cultivated grasses. It sometimes causes

great losses of stock.

POISONING BY ERGOT OF RYE: ERGOTISM.

=Causation.= This form of poisoning is due to the presence of ergot in

grain or forage.

=Symptoms.= The symptoms are seldom very marked. In mild cases pregnant

females may abort; grave cases are indicated by local gangrene of the

mucous membrane and gangrene of the extremities, particularly in

poultry, in consequence of the constrictive action of the drug on the

peripheral blood-vessels, on the vaso-motor centres, and on unstriated

muscular fibres.

=Treatment.= The use of chloral and morphine has been suggested in this

condition; but as the lesions when discovered are established and

permanent, this treatment seems illusory. More is to be expected from

preventive measures and the avoidance of ergotised food.

USTILAGINACEÆ (SMUT FAMILY).

=Ustilago maydis.=—The black powdery fungus known as corn smut is common

throughout the corn-producing districts of the central United States,

and is occasionally reported as being fatal to stock. Experiments made

in Wisconsin and elsewhere show that it is not a very active poison when

eaten in moderate quantity. When given in gradually increasing amounts

up to 2 lbs., no effect was noted, but 4 lbs. on each of two successive

days caused the sudden death of one cow. Since corn smut has been shown

to be less fatal when wet, it seems probable that its physical and not

its chemical character may be responsible for the death of cattle which

have eaten it in considerable quantity.

[Illustration: $1]

POISONING BY SMUT OF BARLEY.

=Causes.= The presence of smut in straw, in millers’ grains, or in

damaged kiln-dried grains which have fraudulently been added to grain

sold for feeding, represents the principal source of this form of

poisoning.

=The symptoms= are very vague. There is indigestion, with a tendency to

nausea, and vomiting. Diarrhœa may be present: At a later stage the

heart and nervous system are affected. The gait becomes hesitating, the

animals show general dulness and spasm of the pharynx; death, when

occurring, is by cardiac or respiratory syncope.

=Treatment= consists in giving an entire change of food, and

administering stimulants and purgatives.

AGARICACEÆ (MUSHROOM FAMILY).

=Amanita muscaria.=—The well-known fly amanita (fly fungus; deadly

amanita) may be found from spring to early winter in pine forests

throughout the United States. Cows are supposed to be killed by eating

it, and almost every year the daily papers chronicle the death of

several human beings who were led to eat the fungus through mistake for

some edible species. The fresh cap is frequently rubbed up with milk and

used to poison flies.

PHALLACEÆ (STINK-HORN FAMILY).

* =Clathrus columnatus.=—In an article published in the _Botanical

Gazette_ (Vol. XV. p. 45), Dr. Farlow, of Harvard University, gives an

account of an investigation of a case of poisoning in hogs which was

caused by eating this peculiar fungus. It grows in patches in oak woods

and openings, and is quite common throughout the Southern States.

POLYPODIACEÆ (FERN FAMILY).

=Pteris aquilina.=—In July, 1895, nineteen cattle died in Maryland,

which were supposed to have been poisoned by eating the common bracken

fern. Very few similar cases are on record, but one European authority

cites one in which five horses were killed by eating hay contaminated

with this fern, and another states that cases are quite frequent among

cattle in England.

EQUISETACEÆ (HORSETAIL FAMILY).

=Equisetum arvense.=—The field horsetail was reported from Connecticut

in 1871 as being poisonous to horses. Cases are very rare, and it is

probable that this plant is deleterious only when eaten in considerable

quantity, and then perhaps only on account of its physical character.

Experiments made in Europe show that a similar species (_E. palustre_)

is fatal to horses when fed in considerable quantity with hay.

TAXACEÆ (YEW FAMILY).

=Taxus minor.=—The common yew, or ground hemlock, is called poison

hemlock in some places. The leaves of this shrub are probably poisonous

to stock, as are those of the European yew. This species is more

accessible to stock than the western yew (_Taxus brevifolia_), which

grows only in deep cañons.

YEW POISONING (TAXUS BACCATA).

The leaves of yew, when eaten in any considerable quantity, are very

poisonous. Two ounces to eight ounces, according to the size of the

animal, slow the heart’s action, produce weakness, staggering, and

apoplectic congestion, which may have a fatal result in less than an

hour. The bark is less injurious, and the fruit is scarcely poisonous at

all.

The early =symptoms=, which are only seen in chronic cases, consist in

excitement, followed by somnolence and muscular weakness, with slowing

of the respiration and circulation.

POACEÆ (GRASS FAMILY).

=Lolium temulentum.=—The seed of the darnel, or poison rye grass, an

introduced annual especially abundant on the Pacific Slope, is

considered poisonous to both man and animals.

=Stipa robusta.=—This is a perennial plant which is known in Arizona and

New Mexico as sleepy grass. It produces a narcotic effect on horses and

cattle that feed upon it, but stock bred in that region rarely touch it.

=Zea mays.=—The numerous deaths that are frequently attributed to Indian

corn are mostly due, not to any poison inherent in the plant, but rather

to parasitic or saprophytic fungus growths, as noted under _Aspergillus_

and _Ustilago_. The green fodder is very apt to cause severe and even

fatal tympanites if the animal’s diet is not properly regulated. Death

has also been attributed to the presence of nitre (potassium nitrate) in

the growing stalks. It is supposed that in very rich soil this substance

will sometimes accumulate in the stalks in considerable quantity during

prolonged drought.

POISONING BY THE MALE TUFTS OF MAIZE.

The green tufts alone are toxic; the toxicity disappears after drying.

Prolonged administration produces nephritic colic and renal lithiasis.

POISONING BY SWEET SORGHUM GRASS.

This form of poisoning is characterised by attacks of trembling,

tympanites, and frequent attempts to urinate. The heart beats feebly,

and the pulse grows progressively weaker, until at last it becomes

imperceptible.

MELANTHACEÆ (BUNCH-FLOWER FAMILY).

* =Chrosperma muscætoxicum.=—The bulbous portion of the fly poison, or

crow poison, an eastern plant, is sometimes eaten by cattle with fatal

results. The bulbs, when crushed with molasses, are used to stupefy

flies.

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* =Veratrum viride.=—The leaves of the common swamp hellebore (American

white hellebore; false hellebore; Indian poke) of the eastern and

northern portions of the United States have proved fatal to man and to

horses. Sheep eat the young leaves and shoots with apparent relish. The

seed is poisonous to chickens.

=Zygadenus venenosus.=—The name death camas has been applied to this

plant in the North-West of America to distinguish it from the true camas

(_Quamasia quamash_), which is highly esteemed for food by the Indians.

In Oregon it is erroneously called “lobelia” by most stockmen and

farmers. Horses, cattle, and sheep, as well as man, are poisoned by

eating the bulb.

=Zygadenus elegans.=—The bulbs, and perhaps the leaves, of the _Glaucous

zygadenus_, or alkali grass, are poisonous to cattle.

CONVALLARIACEÆ (LILY OF THE VALLEY FAMILY).

_Convallaria majalis._—All parts of the lily of the valley are

powerfully poisonous, and are liable to injure cattle and horses.

HÆMODORACEÆ (BLOODWORT FAMILY).

=Gyrotheca capitata.=—This is the red root, or paint root, of the

Atlantic coast and Cuba, so called on account of the red colour of its

sap. White hogs are supposed, throughout the Southern United States, to

be particularly subject to the poison contained in the plant.

FAGACEÆ (BEECH FAMILY).

=Quercus sp.=—In Europe the acorns of various species of oak cause

sickness and death in hogs and cattle. This effect may possibly be due

to tympanites, but may also be due in some way to the tannin or the

bitter principle which they contain.

POISONING BY ACORNS.

The acorn, or fruit of the oak (_Quercus robur_ and _Quercus

sessiliflora_), is much valued as a food for swine. “A peck of acorns a

day with a little bran will make a hog, ’tis said, increase a pound

weight _per diem_ for two months together.” Though largely consumed by

swine with no apparent ill effects, acorns constitute a dangerous food

for young cattle, especially when eaten before they are ripe and when

herbage or other feeding is scanty or restricted.

=The symptoms= comprise dulness, loss of appetite, constipation,

followed by diarrhœa, with straining and colicky pains, head carried

low, eyes retracted, with mucus about the eyelids and blood-stained

discharge from the nose. Frequently the abdomen is distended.

Temperature normal.

=The lesions= are, abrasions of the buccal membrane on the palate,

cheeks, etc.; impaction and intense congestion of the omasum.

=Treatment.= Change of pasture. Alkalies—potash or soda bicarbonate,

magnesia; tonics and stimulants.

URTICACEÆ (NETTLE FAMILY).

* =Urtica gracilis.=—The slender nettle covers thousands of acres of

reclaimed swamp land in Michigan and Wisconsin, which is made nearly

worthless by its dense growth, horses refusing to pass through it to

cultivate the soil.

CHENOPODIACEÆ (GOOSEFOOT FAMILY).

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=Sarcobatus vermiculatus.=—Black greasewood, or chico, is a scraggy

shrub which grows in strongly alkaline soil in the south-western and

western portions of the United States. A correspondent in New Mexico

states that on one occasion he counted as many as 1,000 sheep that had

been killed by eating the leaves of this plant. It is claimed that cows

are not affected by eating it at any time, and that sheep can eat it

quite freely in winter. Death is perhaps due more to tympanites rather

than to any poisonous substance which the plant contains.

PHYTOLACCACEÆ (POKEWEED FAMILY).

* =Phytolacca decandra.=—The leaves of the common pokeweed (poke;

garget; American nightshade) of the eastern half of the United States is

occasionally eaten by cattle with fatal results.

ALSINACEÆ (PINK FAMILY).

* =Agrostemma githago.=—The common corn cockle (cockle; mullein pink) is

a weed common to both the United States and Europe. Poultry and

household animals are occasionally poisoned by eating the seeds or the

bread made from wheat contaminated with the seeds.

MAGNOLIACEÆ (MAGNOLIA FAMILY).

=Illicium floridanum.=—The leaves of this species of anisetree are

supposed to be poisonous to stock.

RANUNCULACEÆ (CROWFOOT FAMILY).

* =Aconitum napellus.=—Aconite (monkshood; wolfsbane) is very commonly

cultivated in gardens, and is therefore capable of doing great damage to

stock. Horses and cattle have frequently been poisoned by eating the

leaves and flowering tops.

* =Aconitum columbianum.=—The Western aconite, or monkshood, is native

in the north-western portion of America, where it sometimes poisons

sheep.

=Anemone quinquefolia.=—The common wind flower, which grows throughout

most of the United States, is extremely acrid and poisonous. Cattle

seldom touch it. The plant loses most of its poison in drying.

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* =Delphinium tricorne.=—The dwarf larkspur, or stagger weed, of the

north-eastern quarter of the United States has been especially reported

from Ohio as fatal to cattle in April, when the fresh leaves appear.

* =Delphinium consolida.=—The seeds of the commonly introduced field

larkspur are well known to be poisonous; the leaves are known in Europe

to be fatal to cattle.

* =Delphinium menziesii.=—The purple larkspur of the north-western

quarter of the United States is very common throughout Montana. In one

case of poisoning reported by Dr. E. V. Wilcox, of the Montana

Experiment Station, over 600 sheep were affected, 250 of which were

claimed to have been killed by the weed. An experiment made by Dr. S. B.

Nelson, Professor of Veterinary Sciences in the Washington State

Agricultural College, shows that it is possible to feed as much as 24¾

lbs. of the fresh leaves to a sheep within a period of five days without

any apparent ill effect taking place. An experiment made by Dr. Wilcox

shows that the extract from less than an ounce of the dried leaves

killed a yearling lamb in two hours, the dose having been given by way

of the mouth.

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LARKSPUR POISONING IN SHEEP.[3]

Footnote 3:

The following account is summarised from a bulletin of the Montana

Experiment Station by Dr. Wilcox.

Severe losses have from time to time been recorded, especially in

America, from larkspur poisoning, the number of animals lost amounting

to thousands. The first signs of poisoning are slight general stiffness

and straddling gait, especially of the hind legs. The stiffness becomes

more and more pronounced, until walking is difficult and evidently

painful. Soon there are manifested various involuntary twitchings of the

muscles of the legs and sides of the body, and loss of control or

co-ordination of the muscles. Ordinarily there is no increase in the

quantity of the saliva, no dribbling of saliva from the mouth, no

champing of the jaws or attempts at swallowing. The sheep manifest none

of the mental disturbances frequently seen in cases of poisoning from

other sources, as for example loco weed and lupine. There is no

impairment of the special senses. The sheep seem to hear and see as well

and as correctly as under normal conditions of health.

No indications of any disturbances of the digestive functions are to be

seen. The appetite remains good, and the sheep eat up to the very last.

They were observed eating industriously during the intervals between the

attacks of spasms which they have during the last stages.

At first the frequency of the pulse and of the respiratory movements is

lessened and the temperature is lowered. The pulse remains very weak,

but in the later stages becomes very rapid, in some cases 130 per

minute. Toward the last also the respiration is very shallow and rapid.

During the final convulsions the respiration is sometimes 120 per

minute, but so shallow that the air is simply pumped up and down the

windpipe. The air in the lungs is therefore not renewed, and the animal

dies by asphyxia or suffocation.

So long as the sheep can stand on its feet, or walk, it keeps up with

the flock as nearly as possible. The exercise, however, excites it,

makes its respiration more rapid, and it has frequently to lie down for

a moment and then get up and hobble along after the flock. The worst

cases can thus easily be detected, since they straggle behind the rest

of the flock.

The later stages follow rather rapidly. The involuntary movements become

more frequent and more severe. All four legs tremble and shake

violently. In fact, all the muscles of the body contract spasmodically

until the animal totters over on its side and dies in the most violent

spasms.

Larkspur has the effect of arresting the heart’s action and respiration

and of paralysing the spinal cord.

=Treatment.= Place the animal by itself in a cool, quiet, shaded place

and avoid all excitement. Of the drugs tested, atropine sulphate

dissolved in camphor water has given the best results. Wilcox (Bull. 15,

Montana Ex. Station) recommends for sheep from ¹⁄₂₀ to ¹⁄₁₅ grain in the

earlier, and ⅙ to ¼ grain in the later convulsive stages. Cattle require

from four to five times these doses. Inhalations of ammonia vapour, and

small doses of alcohol and ether, are also useful.

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In other cases very good results have been obtained from giving

permanganate of potash in the form of a drench: 5 to 10 grains for an

adult sheep or pig, 15 to 20 grains for a horse, and 30 to 50 grains for

an ox, dissolved in a pint or two pints of water.

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* =Delphinium geyeri.=—The Wyoming larkspur is well known throughout

Wyoming, Colorado, and Nebraska under the name of poison weed. It is

reported to be the most troublesome plant to stock in Wyoming, the

dark-green tufts of foliage being especially tempting in spring when the

prairies are otherwise dry and barren.

=Delphinium recurvatum.=—This species of larkspur grows in wet subsaline

soil in the southern half of California. It has been reported from San

Luis Obispo county as fatal to animals.

=Delphinium scopulorum.=—The tall mountain larkspur of the Rocky

Mountains has been reported to the Canadian Department of Agriculture as

poisonous to cattle in the high western prairies of Canada.

=Delphinium trolliifolium.=—This plant is common throughout the coast

region of northern California, Oregon, and Washington. In Humboldt

County, Cal., it is known as cow poison, on account of its fatal effect

on cattle. Its toxic character has been questioned. Perhaps it is not

equally poisonous throughout all stages of its growth.

* =Helleborus viridis.=—The green hellebore is a European plant,

sometimes self-sown from gardens. All parts of the plant are poisonous.

Cattle have been killed by eating the leaves.

POISONING BY HELLEBORE.

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This form of poisoning is of slow progress, the plant producing

irritation of the digestive mucous membrane. The =symptoms= consist in

loss of appetite, blackish, glairy diarrhœa, and intermittence of the

pulse.

* =Ranunculus sceleratus.=—The cursed crowfoot, or celery-leafed

crowfoot, is found throughout the eastern half of the United States and

also in Europe. Cattle generally avoid all of the buttercups, but fatal

cases of poisoning from this plant are recorded in European literature.

When dried in hay, the plant appears to be non-poisonous. The bulbous

crowfoot (_R. bulbosus_) and the tall crowfoot (_R. acris_) are

well-known to be very acrid in taste, and it is probable that all of the

species which grow in water or in very marshy land are poisonous.

POISONING BY RANUNCULACEÆ.

Poisoning only occurs when the green plants are eaten. Drying causes

certain essences contained in them to disappear, and thus destroys their

toxicity.

This form of poisoning is indicated by yawning, colic, blackish, fœtid

diarrhœa, and rapid loss of strength.

The animals suffer from stertorous breathing, weakness of the pulse, and

aberration of vision. They die in convulsions.

BERBERIDACEÆ (BARBERRY FAMILY).

=Podophyllum peltatum.=—The leaves of the common mandrake, or May apple,

of the eastern half of the United States, are sparingly eaten by some

cattle. Cases of poisoning are very rare, but the experience of one

correspondent shows that the milk from a cow that had been feeding on

the plant off and on for about three weeks was so extremely laxative as

to be positively poisonous. The accident occurred to a baby, fed

exclusively on cow’s milk. The physiological effect of the milk was

precisely like that of mandrake. It was shown that the cow ate the

plant, which was abundant in one pasture, and when the animal was

removed to a pasture free from the plant the child’s illness stopped at

once.

BUTNERIACEÆ (STRAWBERRY-SHRUB FAMILY).

=Butneria fertilis.=—The large oily seeds of the calycanthus, or

sweet-scented shrub, contain a poisonous alkaloid, and are strongly

reputed to be poisonous to cattle in Tennessee.

PAPAVERACEÆ (poppy family).

=Argemone mexicana.=—The Mexican poppy is reputed to be poisonous to

stock both in the United States and in New South Wales. The seeds are

narcotic, like opium.

* =Chelidonium majus.=—The yellow milky sap of the celandine, an

introduced weed common in the eastern United States, contains both an

acrid and a narcotic poison. Both are powerfully active, but cases of

poisoning are rare, as stock refuse to touch the plant. Reeks, of

Spalding, however, describes (_J. Comp. Path. and Therap._, Dec. 1903,

p. 367) an outbreak of poisoning by common celandine in which twenty-one

valuable cows were affected and three died. The symptoms comprised

excessive salivation and thirst, convulsions, unconsciousness and

epileptiform movements.

* =Papaver somniferum=, opium poppy, or garden poppy: =P. rhœas=, field

poppy, red poppy, or corn poppy.—These plants are sometimes self-sown

from gardens. Both contain acrid and narcotic poisons, and European

literature records the death of various animals from eating their leaves

and seed pods.

POISONING BY POPPIES.

The consumption of poppies causes arrest of peristalsis, secretion of

foamy saliva, colic, depression, coma, and in severe cases death by

stoppage of respiration.

PRUNACEÆ (PLUM FAMILY).

* =Prunus caroliniana.=—The laurel cherry, or mock orange, is native in

the south-eastern quarter of the United States, and is there often

cultivated for hedges. The half-withered leaves and the seeds yield

prussic acid, and are poisonous when eaten by animals.

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* =Prunus serotina.=—The wild black cherry is a valuable forest tree

which ranges throughout the eastern half of the United States. Cattle

are killed by eating the partially withered leaves from branches thrown

carelessly within their reach or ignorantly offered as food. The leaves

of various other wild and cultivated cherries are probably poisonous to

cattle in the same way.

VICIACEÆ (PEA FAMILY).

=Aragallus lambertii.=—The Lambert, or stemless loco weed, is, next to

the following species, the best known representative of a large group of

closely related plants which are native to the western half of the

United States, and are known as loco weeds on account of the peculiar

excited condition which they induce in animals that eat of their leaves.

Horses and cattle are both affected, but the chief damage is done to

horses. After being permitted to graze on any of these plants the animal

acquires an unnatural appetite for them, and soon refuses all other

kinds of food. It rapidly becomes unmanageable, shows brain symptoms,

and finally dies from lack of proper nourishment.

=Astragalus mollissimus.=—This, the woolly loco weed, is perhaps the

best known of all the loco weeds. It is the species most abundant in

Colorado, where from 1881 to 1885 nearly $200,000 was paid out in

bounties in an attempt to exterminate it. The plant is still abundant in

that State, and reports of the damage done by it continue frequent.

Specimens of the three following species of _Astragalus_ have been

forwarded to the Division of Botany with the information that they were

causing great financial loss in the districts noted. It is quite

probable that other species are dangerous also.

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POISONING BY WHITE LOCO WEED (ARAGALLUS SPICATUS).

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This is an erect tufted perennial, 4 to 18 inches high, with pinnately

divided leaves and spikes of white or cream-coloured flowers, shaped

like those of the pea. The pod is one-celled, and when shaken produces a

rattling sound, which gives the plant the name of “rattle weed” in some

localities. The white loco weed is exceedingly common throughout

Montana. It occurs most abundantly on the northern slopes of foothills

up to an altitude of about 8,000 feet. Its preferred habitat is for the

most part in rather dry situations. The habit of the plant varies in

different parts of Montana. In some localities the flowers are pure

white, while in others they are decidedly yellow.

In Colorado the plant which is most ordinarily known as loco weed is

_Astragalus mollissimus_, while in Montana the species already named is

perhaps most important; but there are others which have a rather wide

distribution and are known to produce the same effects. Among these may

be mentioned _A. splendens_, _A. lagopus_, and _A. besseyi_.

The losses caused from the loco disease are very heavy in nearly all the

Rocky Mountain States. The locoed condition is so commonly observed

among sheep and horses that cases are not reported, and it is

practically impossible to learn the exact extent of the disease. In the

Judith Basin one prominent stockman was nearly ruined financially by the

prevalence for a number of years of the loco habit among his sheep. In

another instance the raising of horses was abandoned over a large tract

of country on account of the loco weeds.

The loco disease occurs under two forms—an acute and a chronic. An acute

case of loco disease was observed by Dr. Wilcox in a two-year-old ewe

with a lamb at its side. The ewe was observed eating large quantities of

white loco weed on May 22nd, 1900. During the afternoon of the same day

it became unmanageable, and the lamb was badly affected. An examination

of the ewe at this time showed that it was completely blind and was

affected with dizziness. It walked around in long circles to the right,

and after a short period remained standing for a few moments in a sort

of stupor. At the beginning of each attack the head was elevated and

drawn to the right; eyelids, lips, and jaws were moved rapidly. Each

attack lasted from one to two minutes and the intervals between the

attacks lasted about five minutes. The second day the attacks became

more severe and of longer duration, the head being turned more decidedly

to the right and the animal sometimes falling upon the ground. Similar

symptoms, accompanied by digestive disturbances, were manifested by the

lamb during the second day, and it died during the afternoon. On the

morning of the third day it was found that the ewe was pushing against

the fold, and had apparently been in that position during the greater

portion of the night. The animal then began to whirl round to the right.

Later it became unable to stand, and the spasmodic movements were

largely confined to the legs. On the morning of the fourth day it died.

The pupil of the eye was at no time dilated, and the expression was

nearly normal. The pulse was at first very irregular, but on the second

day became again regular and of normal frequency. The only remedy which

was tried was frequent injections of one-quarter grain doses of

morphine, but this was without effect. Two other ewes ate smaller

quantities of loco weed at the same time and were similarly affected,

but less severely. In these cases morphine was tried with better

success. The lambs, however, died from the poisonous properties

contained in the milk of the mother.

The general =symptoms= of loco disease are quite familiar to all stock

raisers. Perhaps the most characteristic are those of cerebral origin,

and are shown in peculiarities of gait and action, which may be compared

to a drunken condition. The brain disturbances may consist in impairment

of the special senses or in irregular motor impulses, which produce

incoherent muscular action. In some cases the animal becomes blind. More

frequently the animal makes errors in judgment of the size and distance

of objects. These visual disturbances are often quite ludicrous. The

animal often takes fright, apparently at imaginary objects, or at

objects which under ordinary circumstances would cause no alarm. Locoed

horses are somewhat dangerous for driving purposes on account of their

tendency to run away. Such horses are frequently attacked with kicking

fits without any apparent cause. The sense of hearing is often affected,

and the response to sounds is irregular and out of proportion to the

volume and character of the sound. Irregularities in muscular movements

of sheep may assume a variety of forms. The animal may simply carry its

head in an extended or otherwise unnatural condition. In some cases the

back is arched. Trembling is a characteristic symptom. In locoed horses

a great difficulty is sometimes experienced in persuading them to go

backward. Locoed sheep are exceedingly difficult to manage. The

different members of the flock may suddenly take a notion to run away in

different directions, with the result that it is almost impossible for

the shepherd to prevent their becoming separated. In cattle the disease

appears to be rare, although symptoms, so far as observed, are

essentially the same as those in sheep and horses. Occasionally locoed

cattle manifest dangerous symptoms, and attack men and other animals.

In chronic cases of loco the animal gradually becomes more emaciated and

crazy. In sheep the fleece may be shed in patches or as a whole. The

animal becomes unable to care for itself, and is apt to fall into the

water while attempting to drink. Fits of trembling are of frequent

occurrence, and the animal finally dies of inadequate nutrition and

total exhaustion. In chronic cases of loco disease in horses the animal

is usually left to its own resources on the range. During the later

stages it may remain for weeks at a time upon a small area of ground

without taking water. Dr. Wilcox saw a number of such cases in horses

that were almost unable to walk. Under such circumstances the animals

seldom or never lie down. One horse which was seen remained for a period

of two weeks, in 1897, upon a piece of ground about 150 feet square.

During this time the horse had no water.

Numerous autopsies on locoed sheep and horses revealed slight congestion

of the brain membranes in all cases. The lungs and heart were in normal

condition. Fatty tissue was considerably reduced in quantity, and the

muscles were paler in colour than under normal conditions.

The most serious mistake in connection with loco disease is made in

allowing locoed sheep to remain with the rest of the flock. The loco

habit is apparently learned by imitation of locoed animals, and so long

as locoed sheep are allowed to remain with other sheep the loco habit

rapidly spreads. An experienced sheep raiser, after being nearly ruined

financially through the loco disease, adopted the method of immediate

isolation and the feeding of locoed sheep for mutton. His stock was

replaced with sheep that were free from the loco habit, and the trouble

has been entirely eradicated from his range.

No specific remedy for the loco disease has been discovered, and in the

nature of the case no such remedy is likely to be found. In the present

state of knowledge concerning the subject the only rational =treatment=

to be recommended is that of confinement and feeding with a nutritious

diet. By separating the locoed sheep at once from other sheep the

spreading of the habit will be prevented, and the locoed animals may be

fattened and thus prevented from becoming a total loss. Although locoed

animals may readily be fattened and sold for mutton, their recovery from

the loco habit is apparent only, and is due to their inability to obtain

the loco weed. Such animals when allowed to run upon the range again

almost invariably return to their old habit of eating loco weed. Animals

which have once been locoed are, therefore, unsuitable for stocking the

range.

In combatting the loco disease the most rational methods include

providing salt for the sheep, the immediate removal of locoed sheep from

the band, confining them in a fold, and feeding them upon a nutritious

diet. They may thus be fed for market, and their pernicious habit will

not spread to other sheep. In the case of locoed horses, an apparent

recovery takes place if they are confined in a stable and fed on

ordinary cultivated forage or allowed to run in pastures where no loco

weeds are found. Such horses are always somewhat dangerous, and more apt

to run away or become unmanageable than horses which have not become

affected with this disease.

* =Crotalaria sagittalis.=—The rattlebox (rattle weed; wild pea) is an

annual weed which grows on sandy soil throughout most of the eastern

half of the United States. In some years it is especially abundant in

the bottom lands of the Missouri Valley. Horses and sometimes cattle are

killed in this region by eating grass or meadow hay which is

contaminated with the plant.

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=Lupinus leucophyllus.=—This herbaceous shrub is a representative of a

very large genus of plants, many of which are widely and abundantly

distributed throughout the western United States, and are generally

known as lupines. The above species is very abundant in Montana, where

it is said to have caused the death of a very large number of sheep.

There is some question whether the animals are killed by a poisonous

constituent of the plant or merely by tympanites. The seeds of all the

lupines are probably deleterious in the raw state. In Europe, however,

the seeds of _Lupinus albus_, after the bitter taste has been removed by

steeping and boiling, are eaten by human beings as well as by cattle.

POISONING BY LUPINES (LUPINUS LEUCOPHYLLUS; L. SERICEUS; L. CYANEUS).

These plants are commonly known by the names blue pea, blue bean, and

wild bean. They are coarse, silky-haired perennial herbs, with blue

flowers arranged in conspicuous terminal racemes, which blossom in June

and July, with long-stemmed leaves, which are divided into from seven to

eleven leaflets radiating from a common point. The fruit is a hairy,

several-seeded pod, and the seeds are small and somewhat flattened.

As a rule these plants do not occur in the flat river bottoms. They

occur most abundantly on the foothills and mountain ranges at moderate

elevations.

During the season of 1900 the lupines in Montana began to bloom about

May 20th, and the first full pods were collected on June 5th. Lupines

are not very extensively eaten by sheep during the spring and summer,

except when they are unusually hungry or are being driven from one range

to another. Lupines are more often eaten by sheep in summer on the

mountain sides, and in the fall and early winter after early frosts have

opened the pods and the seeds have fallen out. Lupine hay is greedily

eaten by all kinds of stock during the winter, and large quantities of

this hay have been fed for the past fifteen or twenty years. Lupine hay

is cut in different years at dates ranging from the 1st of July to the

middle of September. When cut during the first half of July the newly

ripe pods, full of seeds, are secured in the hay. When, however, the

harvesting of lupine hay is postponed until September, the pods become

ripe and split open, and the majority of seeds fall out. A striking

variation in the quantity of pods containing seeds is noted during

different years. During seasons in which May and June are wet the

quantity of pods is usually large. When, however, these months are dry

only a few pods are found on each plant, and a vast majority of the

flowers fail to be fertilised.

Dr. Wilcox has observed that sheep are especially fond of the pods of

various leguminous plants before they become mature and while they are

still in a succulent condition.

Dr. Wilcox saw a flock of sheep which while being driven from one range

to another, in a hungry condition, was allowed to feed upon an area of

lupines in a nearly ripe condition. Within two hours the sheep

manifested violent symptoms of poisoning, and ultimately 100 out of the

lot of 200 died. He afterwards saw many hundreds of fatal cases in sheep

and a number in horses, both from eating green lupines and lupine hay.

As an experiment two sheep were given each 150 medium-sized lupine pods

(_L. leucophyllus_) which were entirely full of ripe seeds. The sheep

ate the pods readily. Both sheep became frenzied within about forty-five

minutes after feeding upon the lupine pods, and died about one hour

later. The symptoms in these cases were the same as those observed in

poisoning under natural conditions.

=The symptoms= of lupine poisoning are so well known in Europe that

chronic lupine poisoning has been given the name _lupinosis_. It is

characterised by loss of appetite, fever, dyspnœa, constipation, and

yellowness of the visible mucous membranes. Diarrhœa, sometimes of a

sanguinolent type, appears later. The urine becomes albuminous, tinted

with bile products or stained red by hæmoglobin, and the head shows

œdema. Death occurs in a few days. In America the chronic form has not

been observed. In cases of lupine poisoning in Montana there was noted

acute cerebral congestion, accompanied with mental excitement. The sheep

rushed about in different directions, butting one another and other

objects. The first stage of frenzy was soon followed by a second stage,

characterised by pronounced irregularity of movement, spasms, and

falling fits. In the majority of cases death occurred in from one-half

to one and one-half hours. In extensive cases of lupine poisoning it was

uniformly observed that a number of the sheep lingered on from two to

four days before they died. The muscular convulsions resembled those

caused by strychnine. The excretion of the kidneys was much increased

and frequently was bloody. Post-mortem examinations of sheep poisoned by

lupines revealed conditions similar to those in acute forms of loco

disease, with the addition of a congested condition of the kidneys.

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No remedies have been tried in cases of poisoning from American species

of lupine, but it seems reasonable to suppose that potassium

permanganate would probably destroy the lupine alkaloids in the stomach

if administered promptly after the first signs of poisoning. Experience

and observation indicate that lupine hay is always dangerous for sheep

if cut at a time when the seeds are retained in the hay. The evidence

thus far collected regarding this matter indicates that the seeds are

the most poisonous part of the plant.

POISONING BY VETCHES (LATHYRUS SATIVUS): LATHYRISM.

In the horse this disease is due to feeding on grain containing the

seeds of vetches, but in the ox to eating the green portions of the

plants. Feeding has to be continued for at least a month to produce

accidents.

The earliest =symptoms= consist in suppression of milk secretion, and

somnolence. Nervous symptoms—from which alone the horse suffers—soon

make their appearance. The neuro-muscular system is attacked.

Interference with the nervous system is followed by inco-ordination of

movement, and later by paraplegia of the hind quarters. Roaring is not

noticeable, probably because the patients rarely move rapidly.

=The lesions= have been little studied, but appear to consist in

congestion and infiltration of the meninges, cord, and roots of the

lumbo-sacral plexus.

=Treatment.= If the animals are paralysed, treatment is rarely of value;

otherwise it is sufficient to remove the cause and to administer

purgatives and diuretics, with the object of eliminating toxic products.

Recovery follows in three to four weeks.

=Robinia pseudacacia.=—The common locust tree is native in the central

and eastern parts of the United States, and is extensively cultivated

for ornamental purposes throughout the Union. The bark and leaves

contain a powerful poison, and persons have been killed by eating these

parts.

* =Sophora secundiflora.=—The beautiful bright-red beans of the

frijo-lillo, or coral bean of southern and western Texas contain a

powerfully poisonous alkaloid. The plant is said to have poisoned stock

in Texas and in northern Mexico.

LINACEÆ (FLAX FAMILY).

=Linum rigidum.=—The large-flowered yellow flax is reported from Pecos

Valley, Texas, as poisonous to sheep. An investigation made by the

Bureau of Animal Industry, U.S.A., showed that the plant is poisonous.

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MELIACEÆ (UMBRELLA-TREE FAMILY).

* =Melia azedarach.=—The Chinese umbrella-tree is much cultivated for

ornament, and sometimes grows wild in the South. A correspondent from

Arizona stated that three of his hogs were poisoned by eating the seeds,

which were ignorantly offered to them for food.

EUPHORBIACEÆ (SPURGE FAMILY).

=Euphorbia.=—There are many species of spurge native to the United

States, nearly all of which contain an acrid milky juice. Stock

generally avoid them, but cattle have been poisoned by drinking water

into which the plants have been thrown. The juice of _E. marginata_ and

_E. bicolour_ is used to some extent in Texas to brand cattle, it being

held to be superior to a red-hot iron for that purpose, because screw

worms will not infect the fresh scar and the spot heals more readily.

* =Jatropha stimulosa.=—The seeds of the spurge nettle of the Southern

States are extremely poisonous. Stock avoid the plant on account of its

stinging hairs.

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* =Ricinus communis.=—The castor oil plant is quite commonly cultivated

in the warmer portions of the United States, and grows wild in the

South. The seeds have been accidentally eaten by horses with fatal

effect, and they have been strewn on pasture lands in the North-West for

the purpose of killing sheep that were trespassing thereon. A Frenchman

has discovered a method of making cattle immune to the effects of the

toxalbumin contained in the seeds, so that they may be fed to stock

without causing any apparent ill effect. A note on poisoning by castor

oil cake will be found hereafter.

BUXACEÆ (BOX FAMILY).

* =Buxus sempervirens.=—The leaves of the common box, cultivated for

hedges, are poisonous to all kinds of stock.

ÆSCULACÆ (HORSE-CHESTNUT FAMILY).

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=Æsculus californica=, California buckeye: =Æ. glabra=, Ohio buckeye;

fœtid buckeye: =Æ. hippocastanum=, horse-chestnut: =Æ. pavia=, red

buckeye.—The leaves and fruit of these species are generally regarded as

poisonous to stock. The fruit may be easily converted into food by

washing and boiling. It is believed that a small quantity of the

unprepared fruit of the California buckeye will cause cows to slip their

young.

HYPERICACEÆ (ST. JOHN’S WORT FAMILY).

* =Hypericum perforatum.=—The common St. John’s wort is commonly

believed to cause disagreeable eruptions on cows’ udders and on the feet

of white haired animals. This species and the spotted St. John’s wort

(_H. maculatum_) were brought into the United States Bureau of

Agriculture by Dr. G. W. Bready, from Norwood, Maryland, who stated that

five horses were poisoned in May, 1898, by eating meadow hay which

contained nearly 50 per cent. of these plants. One horse died from the

effects of the poison, and two were killed to prevent their further

suffering.

POISONING BY ST. JOHN’S WORT.

The ingestion of St. John’s wort produces excitement followed by

dulness, interference with vision and hearing, and by visual

hallucinations with a tendency to lean backwards, the front limbs

remaining fixed in position. The patient often sits down on the hind

quarters like a dog.

APIACEÆ (CARROT FAMILY).

* =Cicuta maculata.= This is the water hemlock (spotted hemlock; beaver

poison; cowbane), which grows most abundantly throughout the United

States. It is one of the best known poisonous plants. Stock are not

infrequently killed by eating the fleshy roots or hay with which the

plants are mixed.

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* =Cicuta vagans.=—Cattle are frequently killed in Oregon and Washington

by eating the large fleshy rootstocks which have been washed, frozen, or

dug out of the soil, or by drinking water in marshes where the roots

have been trampled upon. The roots of the other species of _Cicuta_ are

undoubtedly poisonous, but cases have been reported against one other

species only, namely, _C. bolanderi_. It grows in marshy land in

California.

* =Conium maculatum.=—The well-known poison hemlock, or spotted hemlock

of Europe, is an introduced weed not uncommon in the north-eastern

section of the United States and in California. The plant is generally

avoided by stock on account of its bad odour, but animals have been

killed by eating it in the fresh state. Since the poisonous constituent

is volatile, the dry plants are not so dangerous.

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POISONING BY HEMLOCK AND WILD CHERVIL (ANTHRISCUS SYLVESTRIS).

Poisoning only results from ingestion of the green plants. It is

characterised by salivation, nausea, dyspnœa, generalised trembling and

vertigo, paraplegia, and symptoms of gastro-enteritis.

POISONING BY FENNEL.

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This disease, seen in Algeria, and recently studied by Bremond and

Bojoly, need only be mentioned. The information at present available is

indefinite, and the symptoms so closely resemble those of Texas fever

that there seems a possibility of confusion having arisen.

=The lesions= are those of hæmorrhagic gastro-enteritis.

=Treatment= consists in giving tannin, opium, and emollients.

=Oxypolis rigidus.=—The cowbane is natural in swamps throughout the

eastern half of the United States. The leaves and roots are reputed to

be poisonous to cattle.

=Sium cicutæfolium.=—The leaves of the hemlock water parsnip, which is

more or less common throughout the United States, are said to be

poisonous to stock.

ERICAEÆ (HEATH FAMILY).

=Andromeda polifolia.=—The wild rosemary, or moorwort, is a plant native

to the northern regions of Europe, Asia, and America, entering the

United States only in the extreme north-east. The leaves, which have

been eaten by sheep with fatal effect, contain a narcotic poison known

as andromedotoxin. The plant is not very dangerous in its native

habitat, because it grows in bogs which are inaccessible to stock.

* =Azalea occidentalis.=—The California azalea is very much dreaded by

sheep men who drive their flocks into the southern Sierras for pasture.

Investigation has shown that the leaves contain a poisonous substance.

* =Kalmia angustifolia.=—The narrow-leaf laurel is abundant in the

north-eastern section of the United States, where it is also well known

as sheep laurel and lamb-kill. The leaves contain andromedotoxin, and

sheep and calves are frequently poisoned by eating them.

* =Kalmia latifolia.=—The broad-leaf laurel is native throughout the

greater part of the eastern half of the United States, and is known by a

great variety of common names, the most important of which are laurel

and ivy. The latter name is most commonly used south of Maryland. Scores

of cattle and sheep are poisoned annually by eating the plant. It is

probably the most dangerous of all the shrubs belonging to the heath

family.

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* =Leucothoë catesbæi.=—This is the branch ivy, hemlock, or calf-kill,

of the Allegheny Mountains. It is well known in that region to be fatal

to all kinds of stock.

* =Leucothoë racemosa.=—The swamp _Leucothoë_ of the Atlantic and Gulf

States has been reported from New Jersey as especially fatal to calves.

* =Pieris mariana.=—The stagger bush of the Atlantic Coast region,

Tennessee, and Arkansas is commonly known to be poisonous to calves and

to sheep. The name stagger bush was applied to the shrub on account of

the peculiar intoxicating effect of the leaves.

* =Rhododendron californicum.=—The California rhododendron is native on

the Pacific Slope from San Francisco to British Columbia. The plant is

reported from Oregon as poisonous to sheep. It is quite probable that

the leaves contain andromedotoxin, but they have not been tested.

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* =Rhododendron maximum.=—The great laurel (rosebay; mountain laurel;

rhododendron) is a large evergreen bush or small tree which is quite

commonly cultivated for ornament, and is found native in the Allegheny

Mountains. The leaves contain andromedotoxin, and they are occasionally

eaten by stock with fatal effect.

PRIMULACEÆ (PRIMROSE FAMILY).

=Anagallis arvensis.=—The pimpernel is a European plant which has

obtained a specially strong foothold in California, where it grows

luxuriantly and is sometimes known as poison weed. It is suspected of

having caused the death of a horse at Santa Ana. Chemists have isolated

a powerfully poisonous oil and a strongly active ferment from the plant.

OLEACEÆ (OLIVE FAMILY).

=Ligustrum vulgare.=—The privet, or prim, is a garden shrub, introduced

from Europe and Asia, which is much used for hedges, and has escaped

from cultivation in western New York and southward to North Carolina.

Accidents have been occasioned in children both by the fruit and the

leaves. The plant is to be suspected in cases of poisoning in animals.

APOCYNACEÆ (DOGBANE FAMILY).

=Apocynum androsæmifolium=, spreading dogbane: =A. cannabinum=, Indian

hemp.—These plants are generally distributed throughout the United

States. Stock generally avoid them in pasture fields on account of their

acrid milky juice. When dry they are not so poisonous as when in the

fresh state.

=Nerium oleander.=—The oleander is a common house plant throughout a

large portion of the United States. It grows freely out of doors in the

Southern and Western States, and has probably escaped from cultivation

in some places. It grows wild in northern Mexico. The leaves are well

known to be most powerfully poisonous, and stock are occasionally killed

by eating them.

ASCLEPIADACEÆ (MILKWEED FAMILY).

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* =Asclepias eriocarpa.=—This is the plant with broad mullein-like

leaves which is known as milkweed in California. Several authentic

accounts of the poisoning of sheep have been secured against the plant

in Mendocino County. It is especially feared on very warm days by sheep

men when they are compelled to drive their flocks through dry, barren

valleys. It sometimes grows on cultivated land, and is cut with hay.

* =Asclepias syriaca.=—This is the common milkweed, or silkweed, of the

north-eastern quarter of the United States. Experiments show that the

milky juice so abundant in all parts of the plant is very acrid and

poisonous. It is listed among the poisonous plants of Europe.

SOLANACEÆ (POTATO FAMILY).

* =Datura stramonium=: =D. tatula=.—These two species very closely

resemble each other, and are most commonly known in the United States by

the name of jimson weed. They are European plants which have become

weeds in waste grounds and about dwellings throughout the greater

portion of the country. One or two instances are recorded in which

cattle have been poisoned by eating hay containing the young leaves.

* =Hyoscyamus niger.=—The black henbane is an ill-smelling plant, a

native of Europe, now naturalised in Michigan, and from New York

northward. One or two cases are recorded in European literature in which

stock have been poisoned by eating the plant of their own accord, but

there is very little danger from it, on account of its ill odour and

harsh texture.

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* =Nicotiana tabacum.=—This is the tobacco most commonly cultivated in

the United States. It is native to South America and has escaped from

cultivation to some extent in the Southern States. According to some

authorities stock are not always disposed to shun this plant on account

of its characteristic ill odour and taste, but, on the contrary, will

eat a small amount of the leaves with apparent relish, especially when

they are somewhat fresh. Stock have, however, been poisoned by eating

leaves which were placed within their reach to dry, and also by eating

food contaminated with the juice of the leaves. Considerable precaution

should be used in applying tobacco juice to fresh cuts or bruises in

stock, as the poison is easily absorbed into the system and may prove

fatal. There are several native species of tobacco in the western half

of the United States, all of which are undoubtedly poisonous if eaten

even in moderate quantity.

TOBACCO POISONING.

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Tobacco poisoning may be produced by baths or lotions containing tobacco

juice, which is often used as a parasiticide. The ingestion of tobacco

leaves in forage may also produce poisoning. Doses of 1 ounce in the

goat and 10 ounces in the ox are toxic.

=The symptoms= consist in salivation, vomiting, nausea, diarrhœa,

cardiac palpitation and dyspnœa.

=The lesions= are those of gastro-enteritis with cerebral congestion.

=Treatment= consists in giving tannin, black coffee, etc.

=Solanum dulcamara.=—The bittersweet, or climbing nightshade, is a

European weed, now introduced in the north-eastern quarter of the United

States. The leaves are suspected of being poisonous to stock.

* =Solanum nigrum.=—The black nightshade (common nightshade; garden

nightshade) is a common weed in cultivated fields throughout the greater

portion of the United States. Cattle seldom eat the plant, but a few

cases of poisoning are recorded for calves, sheep, goats, and swine.

* =Solanum triflorum.=—The spreading nightshade is a native of the Great

Plains (United States), and also a common garden weed from Arizona and

Texas to British America. Complaints of the poisoning of cattle by this

plant have been sent to the Department of Agriculture from Nebraska.

Experiments show that the berries are poisonous.

=Solanum tuberosum.=—The small, immature tubers of the common cultivated

potato and those that have turned green from exposure to the sun are

slightly poisonous. The green fruit and the white sprouts from mature

potatoes are likewise poisonous. In all of these cases the deleterious

substance may be removed or destroyed by thorough boiling.

SCROPHULARIACEÆ (FIGWORT FAMILY).

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=Digitalis purpurea.=—The purple foxglove is a common garden plant which

has sparingly escaped from cultivation and is naturalised to some extent

on Cape Breton Island. Horses are occasionally poisoned in Europe by

nipping the plants from gardens or by eating hay contaminated with it.

=Gerardia tenuifolia.=—The slender gerardia is native to the eastern

half of the United States, and has been specially reported as poisonous

to sheep and to calves in the Southern States.

=Gratiola officinalis.=—The hedge hyssop of the Southern States contains

an acrid poison. The same plant grows in Europe, and is there regarded

as poisonous to stock.

=Pedicularis.=—The plants of this genus are commonly called lousewort.

In Europe several species are suspected of being slightly poisonous to

stock. One of these, _P. palustris_, occurs in Labrador, and there are

over thirty species native to the United States, largely Western. They

should all be suspected of being poisonous.

CAMPANULACEÆ (BELL-FLOWER FAMILY).

=Lobelia inflata=, Indian tobacco: =L. kalmii=, brook lobelia: =L.

spicata=, pale-spiked lobelia: =L. syphilitica=, great lobelia.—All of

the species in this genus contain an acrid and usually milky juice, and

are poisonous. None has been specially reported as poisonous to stock,

but the above-named species are to be suspected, because they frequently

occur in grass and are sometimes found in meadow hay.

AMBROSIACEÆ (RAGWEED FAMILY).

=Xanthium canadense.=—The young seedlings of the American cocklebur are

reported from Texas as being rapidly fatal to hogs.

=Xanthium spinosum.=—The spiny clotbur is suspected of being poisonous,

but few cases have been definitely recorded against it. The seeds

apparently contain a toxic compound.

=Xanthium strumarium.=—The young seedlings of the broad cocklebur are

reported from Georgia as being fatal to hogs. Experiments seem to show

that the seed is poisonous.

CARDUACEÆ (THISTLE FAMILY).

* =Helenium autumnale.=—Sneezeweed (sneezewort; autumn sneezeweed;

stagger weed; false sunflower) is found throughout the greater portion

of the United States, being most abundant in the Southern and Eastern

States. Sheep, cattle and horses that are unfamiliar with the plant are

often poisoned by it when driven to localities where it is abundant.

Stock avoid it, as a rule, but it is claimed that they sometimes develop

a taste for the plant, and are killed quickly by eating it in large

quantity.

=Senecio jacobæa.=—The tansy ragwort, or stagger wort, is a European

plant which grows as a weed in ballast about New York and Philadelphia.

Farther north, in Nova Scotia, it has become extensively naturalised,

and it is there regarded by stock men as poisonous. It is interesting to

note that _S. guadalensis_ of Mexico is also considered fatal to stock.

COLCHICUM POISONING.

Fodder of bad quality often contains leaves, flowers, and particularly

seeds of colchicum, which produce nausea, vomiting, colic and diarrhœa.

The colchicine acts particularly on the kidney and heart, producing

specific disturbance, indicated by hæmaturia, polyuria, and cardiac

palpitation, with lowering of the body temperature.

Even when poisoning is not fatal, it is very apt to produce abortion.

POISONING BY ANNUAL MERCURY.

Annual mercury given in green fodder is stated to produce indigestion,

diarrhœa, vesical and intestinal hæmorrhage, and early death. Some

authors, however, deny that it has such toxic properties.

POISONING BY BRYONY.

In large doses all parts of the bryony plant are toxic—the root, stalk,

and leaves.

Bryony is sometimes used as a purgative. Poisoning is characterised by

nausea, sweating, diuresis, frequent action of the bowels, and, in grave

cases, by tetaniform convulsions followed by death.

POISONING BY CASTOR OIL CAKE.

=Causation.= Excessive use of this form of cake is the usual cause of

such poisoning, though bad quality is also an important factor. The

castor oil beans are often insufficiently crushed and compressed, so

that a considerable amount of oil is contained in the cakes as sold; but

the most dangerous constituent is undoubtedly the material known as

ricin, which, in some specimens of cake, may exist in highly dangerous

quantity.

The oil contained in the cake, like every other fatty substance, favours

intestinal peristalsis and the onward movement of the digested food. The

laxative principle excites secretion, and if the cake be given for

considerable periods, the most serious consequences may ensue.

Cakes prepared from mixed rape seed and castor beans act in a similar

way, though in a longer or shorter time, according to their richness in

ricin.

The earliest =symptom= consists in purgation, which gradually develops

into super-purgation, and is followed by direct irritation of the mucous

membrane, indicated by serous, fœtid, and sometimes sanguinolent,

diarrhœa. The symptoms may appear in twenty-four hours. They are usually

accompanied by a rise in temperature of 2° to 3° Fahr. Secretion of milk

ceases, and animals heavy with young sometimes abort. In exceptional

cases death follows.

=The lesions= are those of hæmorrhagic enteritis.

=Treatment= is principally of a preventive character. The cakes should

be examined, and if they contain insufficiently crushed seeds or beans

should be discontinued or given in smaller quantities. The proportion of

ricin in mixed rape and castor cakes should be determined.

Curative treatment consists in removing the cause and treating the

enteritis. The latter is best controlled by giving emollients,

diuretics, and mucilaginous drinks prepared from linseed, marsh-mallow,

barley, etc.

POISONING BY COTTON CAKE.

Cotton cake forms a rich food, which fattens animals very rapidly, but

given in excess may produce true poisoning, and if prepared from

undecorticated seed may produce mechanical irritation ending in

obstruction of the bowel.

The latter accident occurs only in the sheep. It consists in obstruction

of the omasum (œsophageal gutter), and particularly of the abomasum, by

the woody seed covering, the fibres of which become agglutinated and

close the pyloric opening, just as do the fragments of wool or the hairs

in animals affected with the licking habit (pica, depraved appetite).

The mass thus formed passes into the intestine, and is apt to become

fixed at some point and to cause death.

In the ox, as in the sheep, true poisoning may result from the action of

an injurious principle which Cornevin discovered in the seed and

particularly in the meal. The relative rarity of such accidents is

explained by the composition of the cakes, which are rich in husks but

poor in meal.

In the first series of accidents the =symptoms= resemble those produced

by the intestinal obstructions peculiar to the licking disease; in the

second they appear about the eighth to the fifteenth day, and are

indicated by sensitiveness of the abdomen and by efforts to pass urine.

The urine is albuminous; at a later stage it becomes darker in colour,

reddish, and stained with hæmoglobin. The mucous membranes exhibit a

sub-icteric tint.

=Lesions.= The liver shows interstitial hepatitis, consequent on changes

in the hepatic cells due to the poisonous principle. The kidney first

shows lesions of interstitial, but afterwards of epithelial, nephritis;

the endothelium of the tubes appears to be undergoing proliferation.

=Treatment= should only be undertaken when the organic lesions seem

trifling, and suggest the possibility of cure without excessive outlay.

Under such circumstances it is sufficient to remove the cause and to

supply proper diet.

POISONING BY MOLASSES REFUSE.

Molasses refuse is much used about Paris and in the department of Le

Nord for fattening or simply for feeding animals. Added to rough fodder,

even of poor quality, the refuse renders it palatable, and thus forms an

economic food; it also improves the condition of animals with broken

wind. Its poverty in nitrogenous materials (the refuse consists of 60

per cent. of hydrocarbons; 10 to 12 per cent. of potash and soda salts)

renders it necessary to enrich it in this respect. Moreover, only a

limited quantity should be given. If given in larger amounts than 2 to

2½ parts per 500 parts of body weight it may produce bad effects. In

this case the earlier symptoms point to interference with the urinary

apparatus, the digestive apparatus being affected later; both accidents

are due to the potash and soda salts present in the refuse, and may

become so well marked as to constitute true poisoning.

=The symptoms= consist in abundant diuresis, resulting from the excess

of potash and soda salts, and are followed by albuminuria.

Superpurgation is usually present.

=Lesions.= On post-mortem examination one finds lesions of irritant

gastro-enteritis, and of chronic nephritis.

=Treatment= consists in withdrawing the molasses refuse, and giving

milk, mucilaginous fluids, barley-water, and cereals, which soothe the

kidney.

DISEASES PRODUCED BY DISTILLERY AND SUGAR FACTORY PULP.

This disease, which is very common in France and Germany, results from

feeding on distillery and sugar factory residues, consisting for the

most part of beet pulp.

In 1860 Guionnet described it under the name of disease of the abomasum,

and more recent work by Butel, Rossignol, and Arloing has thrown a great

deal of light on its exact nature.

=Causation.= Guionnet attributed the injurious action of beet pulp,

etc., to excess of acidity, due to the addition of sulphuric acid during

manipulation in the factory; but it has since been shown that this

acidity, if existing, is specially due to various fermentation products,

the results of lactic, butyric, and acetic fermentation, etc.

Rossignol regarded the symptoms as wholly due to the excessive

proportion of water, viz., 90 per cent.; but this does not explain the

general symptoms of poisoning.

The real cause is to be sought in the manner of preserving the pulp in

simple earth silos or in cemented silos, where it undergoes fermentation

and putrefaction. The contained liquid is then extremely toxic. Filtered

through porcelain and injected under the skin, it produces vaso-motor

and vaso-paralytic disorder, identical with that seen in acute forms of

the disease; in other cases it excites abnormal secretion, and leads to

permanent diarrhœa and chronic gastro-enteritis.

This liquid, if injected intravenously, may prove toxic in doses of 2 to

3 cubic centimètres per kilogram of bodily weight. Its injurious effect

is due to toxins secreted by special bacilli, which were isolated and

studied by Arloing. The toxicity diminishes as the pulp becomes older,

and can be avoided by adding antiseptics like common salt, which prevent

fermentation. These experiments of the Lyons professor are certainly

very interesting, and, although perhaps not identical with what occurs

in practice, sufficiently indicate the way in which poisoning occurs.

Pathological disturbance only follows the use of decomposed pulp.

Animals reared on farms where distillery and sugar factory pulp is

regularly given become accustomed to it, and are rarely affected. The

chief sufferers are those recently imported, or recently placed on such

food; in them the disease may assume either the acute, nervous,

subacute, or chronic form.

=Acute form: Symptoms.= This form is exceptional in the ox, but is more

frequent in the sheep. In oxen the earlier symptoms point to digestive

disturbance, and consist of dulness, loss of appetite, colic,

sensibility of the abdomen, cessation of rumination (without

tympanites), and constipation. The excreta are hard, coated, and

blackish in colour, but not blood-stained.

Diarrhœa follows, is accompanied by aggravation of the general symptoms,

the temperature rises to 104° or 106° Fahr. (40° or 41° C.), and

exhaustion is pronounced. Other, less characteristic, symptoms, such as

grinding of the teeth and mastication without food being present in the

mouth may accompany the above and arouse fears of peritonitis. In sheep

the dulness and prostration shown at first suggest the existence of

anthrax—a view strengthened by the fact that the respiration becomes

very frequent and the fever intense, whilst death may be rapid, and may

sometimes occur with startling suddenness.

=Lesions.= Bacteriological examination, or even a naked-eye examination,

made immediately after death enables one easily to differentiate between

the two conditions. When the animals have died very rapidly—in one

night—lesions of enteritis alone are present. More marked cases exhibit

thickening and intense congestion of the mucous membrane of the

abomasum, which may be of a deep mahogany colour.

The intestine itself is affected, and even though the glandular

epithelium is little changed, the intercellular spaces show ecchymoses

and multiple hæmorrhages, which give the contents of the digestive tract

the appearance of wine lees.

The abdominal viscera scarcely present any characteristic lesions. The

liver has the appearance of having been boiled, as in many forms of

poisoning. The kidney is congested and blackish; the spleen only appears

hypertrophied when post-mortem examination has been delayed and

microorganisms from the intestine have invaded the circulatory system.

After death the kidneys and spleen very rapidly undergo softening.

=Nervous form: Symptoms.= Whilst in the first form the symptoms appear

especially due to diastatic ferments present in the pulp liquid, in the

nervous form they appear rather to result from the convulsing and

paralysing action of ptomaines.

The ox seems more particularly susceptible to the action of the latter.

It shows symptoms resembling those of horses suffering from a severe

abdominal form of influenza: profound depression, mahogany-coloured

conjunctiva, lachrymation, infiltration of the cornea, high temperature

(104° to 106° Fahr.—41° to 41·5° C.), strong action of the heart, but

small pulse. The cerebral symptoms are especially marked. The animal

suffers from vertigo, and when excited, or when attempts are made to

administer medicine, it thrusts its head against the wall, as though

suffering from a cerebral tumour. It also shows hyperæsthesia, slight

colic, and sensitiveness of the abdomen.

In sheep the symptoms consist in alternate extreme depression and

extreme excitability.

In both species the termination is always rapid: death occurs in a few

days.

The abdominal =lesions= are identical with those of the acute form. They

consist in gastro-enteritis, or, rather, intense congestion of the

abomasum and intestine, with extravasation of blood around the acini of

the glands and beneath the mucous membrane, etc., and in more or less

marked desquamation of epithelium.

The annexed organs sometimes present secondary changes: in the nervous

centres the lesions are more marked; the meninges are congested, in some

cases inflamed, and cerebro-spinal fluid is present in increased

quantity.

=Subacute or Chronic form: Symptoms.= This form is equally frequent in

the ox and sheep; it develops insidiously, and for a time may escape

detection.

The symptoms are those of slight gastro-enteritis without tympanites;

but this condition is succeeded by serous, fœtid, uncontrollable

diarrhœa, which weakens the animal and causes death from excessive

wasting and hydræmia.

The sensitiveness of the entire right side of the abdomen, the special

diarrhœa, the cardiac disturbance, and the widely distributed œdema,

usually suffice to prevent confusion with the ordinary forms of

gastro-enteritis. In sheep the diarrhœa is blackish, sometimes

blood-stained, and is accompanied by a sub-icteric or icteric tint of

the mucous membranes, of the skin, and of all the tissues. The intensity

of coloration affords a guide to the rapidity of development of the

disease. The urine is also bile-stained, and there appears to be an

exchange of functions between the two great depurative organs, the liver

and kidney. The urine may become sanguinolent, because it contains

either unchanged blood or simply dissolved hæmoglobin.

=The lesions= are similar to those previously described, but with

modifications of intensity. When diarrhœa has been marked and

persistent, the digestive mucous membrane is hardened, indurated, and

appears as though tanned. This is due to chronic inflammation, probably

to the gastro-enteritis with which the condition begins. The liver

appears as if cooked; the fat, the majority of the tissues, and

especially the conjunctiva, exhibit a light yellow tint, pointing to

hepatic disturbance.

=The diagnosis= is generally easy in all three forms, provided that the

food be examined.

=The prognosis= varies; the acute and nervous forms are usually fatal.

But when the disease develops slowly, recovery may occur.

=Pathogeny.= Practical observation and laboratory researches show that

the above conditions result from poisoning. Histological examination of

livers from sheep which have died rapidly shows complete degeneration of

the hepatic cells, which become incapable of performing their function.

The biliary acids, no longer being withdrawn from the circulating blood,

produce general intoxication, destruction of the blood corpuscles, and

the appearance of hæmaphæic icterus and hæmoglobinuria.

=Treatment.= Being convinced that acidity alone caused this disease, the

older practitioners suggested the administration of salines. In reality

it is necessary to check fermentation. Drainage of the silos in which

beet pulp is stored is often sufficient for this purpose; but if badly

arranged, drainage rather assists the growth of moulds and various

organisms in the mass, which affords a medium favourable to their

multiplication. Complete desiccation would undoubtedly give much better

results, but cannot economically be effected. The best practical measure

consists in storing the pulp in special silos, divided into compartments

by lattice work partitions. The escape of liquid is facilitated by

forming the floors of the silo with a sufficient slope. Preservation,

however, is not perfect, and some compartments are always found damaged.

Excessive fermentation can be checked by adding ordinary salt to the

pulp in the proportion of ·2 per cent.

Curative treatment comprises restricted diet for several days, and the

administration of milk, carbonate of soda, and stimulants, which favour

excretion of the toxins. Some patients may be saved by subcutaneous

injections of large quantities of normal salt solution. When poisoning

is pronounced, and the viscera are clearly injured, it is more

economical to slaughter the animals, provided that the icterus does not

render the flesh useless for sale.

CHAPTER VIII.

PARASITES OF THE DIGESTIVE APPARATUS.

Parasites of the digestive apparatus are extremely common in ruminants,

some, like the infusoria of the rumen, being of no importance, others,

on the contrary, appearing to play a predominating part in the

development of certain forms of anæmia and serious wasting diseases,

such as the various forms of gastro-intestinal strongylosis, coccidial

enteritis, etc.

GASTRO-INTESTINAL STRONGYLOSIS IN SHEEP.

PARASITIC GASTRO-ENTERITIS. OVINE PASTEURELLOSIS.

Verminous diseases of the abomasum are common in the sheep and goat, but

(in France at least) appear rare in the ox.

=Causation.= Gastro-intestinal strongylosis is produced by various

parasites of the genus Strongylus, such as _Strongylus contortus_,

_Strongylus convolutus_, _Strongylus instabilis_, _Strongylus

circumcinctus_, _Strongylus filicolis_, which occur not only in the

abomasum, but also in the small portions of the first intestine,

sometimes in very large numbers.

The first is a threadlike worm, pointed at both extremities, and from ½

to 1 inch in length. It exhibits a red tint, which zoologists refer to

the presence of blood in its digestive apparatus, derived from the

host’s intestinal mucous membrane. Some doubt has been thrown on the

nature of this coloration, however; and certain Italian authors, in

common with Lignières, have declared it due to a certain red pigment

developed in the tissues of the parasite, the spectroscopic reaction of

which differs from that of hæmoglobin.

The strongyles are said not to penetrate the mucous membrane, but simply

live on the intestinal contents. This may be true of certain varieties,

but it is none the less certain that others penetrate the mucous

membrane deeply, even to the extent of becoming half-embedded in it.

Particularly is this the case with _Strongylus circumcinctus_, found in

the epizooty which occurred at Grignon, and also found by Moussu in

grave epizooties which he has from time to time investigated.

According to Lignières this gastro-intestinal strongylosis only plays a

trifling part in the development of the above-mentioned disease, which

he declares to be due to infection with a cocco-bacillus of the

Pasteurella group, the development of which alone, he states, explains

all the symptoms.

In France the disease now under consideration has never extended beyond

limited regions, but in Argentina, where Lignières carried out his

investigations, it is said to be very fatal. Lignières bases his opinion

on the following facts:—

Firstly, that experimental verminous infection of young animals does not

produce either anæmia or cachexia.

Secondly, that animals in excellent condition may prove to be infested

with large numbers of parasites.

Thirdly, that animals which have succumbed to this disease, hitherto

regarded as verminous, sometimes prove to harbour few or no parasites.

Fourthly, that this grave and fatal disease, and the symptoms by which

it is clinically recognised, can be produced with cultures of the

cocco-bacillus, which he has isolated.

These statements are very precise, but Moussu declares that he has never

yet been convinced of the reliability of the last statement referring to

experimental transmission, any more than of the data regarding alleged

protective vaccination.

=The symptoms= of gastro-intestinal strongylosis or ovine pasteurellosis

point to a progressive pernicious anæmia of chronic or subacute form.

Rapidly progressive cases are exceptional.

In France the form seen is almost invariably chronic. The animals appear

dull, sluggish, and feeble; they lose appetite, waste, become anæmic,

then cachectic, and, after several months, die of exhaustion and

wasting, after having shown diarrhœa during the later stages.

The fæces are pasty, and exhale a very marked putrefactive odour. There

is little room to doubt that auto-intoxication from resorption of

intestinal products is continually going on.

The animal’s general appearance is bad, the ears are pendant, the wool

is dry and dull, and can be removed in handfuls by the slightest pull.

There are no other external symptoms, and the diagnosis can only be

arrived at by discovering the eggs of the parasite in the fæces.

=Lesions.= Post-mortem examination reveals all the general lesions of

advanced cachexia and of gastro-enteritis of varying intensity. The

abomasum and first portions of the small intestine usually contain a

considerable number of strongyles; tæniae are often present in the

intestine, and Moussu declares that he has always found a certain number

of hooked worms and œsophagostomes.

The peritoneal, pleuritic, and pericardial exudates common in most

wasting conditions are always present, but the quantity of exudate in

each cavity varies within wide limits. The liquid may even resemble that

due to inflammation or infection; sometimes it is light pink or red in

colour.

Pulmonary lesions usually exist. Moussu has almost always found gastric

strongylosis associated with pulmonary or tracheo-bronchic strongylosis,

but Lignières asserts that the Argentine cases showed nodules of

hepatisation which had nothing to do with the pulmonary strongylosis,

and which appeared to result from areas of pneumonia produced by the

specific cocco-bacillus and other organisms. He has even found abscesses

and cavernous spaces in the lung.

[Illustration: $1]

=Pathogeny.= According to Lignières the specific agent of pernicious

anæmia is a cocco-bacillus which stains well with fuchsin, violet, blue,

safranin, etc., but does not take Gram, and which in cultures assumes

either the strepto-bacillary form or occurs in barrel-shaped masses. It

grows in simple bouillon at 38° C., but better still in peptonised

bouillon, which turns turbid for five or six days, afterwards becoming

limpid in consequence of the organisms falling to the bottom of the

vessel. It does not coagulate milk. On agar the culture is thin, bluish,

shows an iridescent reflection, and when old appears whitish. Grown on

gelatine, the appearances are similar—the gelatine is not liquefied; on

serum the pellicle is scarcely visible.

The organism is said to be pathogenic for guinea-pigs, rabbits, dogs,

and, of course, for sheep. Moussu, however, does not consider that the

reported cases of transmission through the blood stream or by

subcutaneous injection are really convincing or characteristic. He does

not question the fact that Lignières discovered a special pathogenic

agent in all cases and in all his patients; but what appears to him

debatable is the exclusive part which Lignières attributes to that

agent.

The fact that in Argentina, just as in France, strongyles have always

been discovered in epizootics of this nature of itself constitutes

something; and causes the second fact, that it has never yet been proved

that any heavy mortality occurred in the absence of parasitic

infestation, to assume considerable importance. Moussu regards these two

facts as the greatest obstacles to Lignières’ theory. He states that in

his view the verminous affection is the essential, primordial and

primitive affection, and that microbic infection is only secondary, and

an almost inevitable result of grave verminous infestation.

It is quite certainly wrong to think that verminous affections may

continue with scarcely any injury to the animal, especially when such a

belief is based on observation of a few parasites which are not of a

predatory character. In most cases of the kind now under consideration,

the various parasites found (_Strongylus circumcinctus_ and _filicolis_,

_Anchylostomes_, etc.) cause more or less grave lesions.

These intestinal wounds facilitate the infection to which the fatal

course of the disease is due. The disease, then, is not a special

unvarying infection, but consists of multiple superposed infections.