Chapter VII: Poisoning (1)

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.

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.

* =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).

=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.

* =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.

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.

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.

* =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.

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.

* =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.

POISONING BY WHITE LOCO WEED (ARAGALLUS SPICATUS).

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.

=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.