CHAPTER VII.. Poisoning.

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.

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.

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.

=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.

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.

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.

* =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).

=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.

* =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.

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.

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.

* =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.

* =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).

* =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.

* =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.

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).

=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.