Contagious and destructive nature of the disease. Mode of extension from the mouth and pharynx. Causes: bacillus diphtheriæ columbarum; its characters: pathogenesis to birds, mice, rabbits, Guinea pigs; dogs, rats, and cattle immune; diagnosis from bacillus diphtheriæ. American disease. Incubation. Symptoms: prostration; wheezing breathing; sneezing; difficult deglutition; false membrane on fauces; necrotic changes in mucosa; perforations; lesions of internal organs; blood infection; nostrils stuffed; bill gapes; lesions on eye, tongue, gullet, crop, intestine; diarrhœa; vomiting. Skin lesions. Course, acute, chronic. Paralysis. Mortality. Prognosis. Diagnosis from coccidiosis, from croupous angina of Rivolta, from aspergillus disease. Treatment: isolation; destruction of carcasses; hatching; destruction of dead wild birds and rabbits; exclusion of living; quarantine of new birds; disinfection; locally, antiseptics by inhalation, swabbing, and internally, iron in water.

This affection prevails in certain countries and causes heavy losses among young pigeons, so that it might with great propriety be included among animal plagues, which should be dealt with by the State. The malady is a local inflammation leading to the formation of false membranes and its usual course is to progress from the mouth and pharynx, to the nasal passages, lachrymal ducts and sacs, the larynx, trachea, bronchia, intestines and skin.

Causes. The essential cause of the disease is held by Löeffler to be the bacillus dipththeriæ columbarum, which is a short bacillus with rounded ends, a little longer than the bacillus of fowl cholera and not quite so broad. It is usually found in irregular clusters, especially in the interior of the hepatic capillaries. It is ærobic, non-motile, non-liquifying, and grows on nutrient gelatine, blood serum or potato. In gelatine it forms a white surface layer, and spherical colonies along the line of puncture, which show a yellowish brown tint under the microscope. On blood serum and potato it forms a grayish white layer.

Pathogenesis. The bacillus is inoculable on other pigeons and as it usually appears in the young birds in the nest, still fed by the parent bird, it is probable that no inflammation nor abrasion is necessary to make it take. Pure cultures inoculated in the mouth gave rise to the usual local type of the disease. When inoculated subcutem it caused a local necrotic inflammation.

In mice subcutaneous injections proved fatal in five days with general dissemination of the bacillus. There are congested and hemorrhagic spots on the lungs, enlarged spleen, and the liver is marbled by numerous necrotic white masses, in the centre of which the capillaries are found to be blocked with the bacilli. This is so pathognomonic that Löffler looks on the inoculation of mice as the best means of diagnosis.

Inoculated rabbits showed inflammation in the seat of inoculation and sometimes fibrinous peritonitis and enlarged spleen. Inoculation on the cornea produced a false membrane.

In Guinea pigs induration and ulceration occurred in the seat of inoculation but recovery followed in 14 days.

Sparrows inoculated in the pectoral muscles died in three days with yellowish necrotic tissue highly charged with bacilli.

Inoculation of the chicken by Löffler and Megnin produced a circumscribed redness which soon disappeared. On the other hand Krajewski, Colin, Loir and Ducloux seem to have inoculated chickens successfully, and Cadeac says that the cultures are infecting for sparrows, pigeons, turkeys, chickens and ducks. It rests uncertain therefore whether the pseudomembranous pharyngitis of hens is a distinct disease as alleged by Löffler and Megnin or if the chickens used by these observers were not already immune by reason of a prior attack.

Löffler’s experiments showed that dogs and rats were immune. Loir and Ducloux failed to infect cattle.

In infected dove-cots a comparative immunity is attained by the older pigeons, which continue to harbor the germ, but do not suffer materially from its presence. They however communicate it to the susceptible young in the milky secretion produced in the crop and with which they feed them, and these accordingly perish in large numbers. Thus pigeons that are themselves in fine condition become the propagators of the bacillus to the more impressible.

Sparrows and other small birds are also held to be common propagators of the germ, and if they too can secure an individual immunity and yet harbor the bacillus, their passage from yard to yard may be attended with great danger. The grains soiled by their bills and not swallowed are common media of transmission.

Loir and Ducloux found the affection transmissible between man and pigeon. The identity of the bacillus with that of genuine diphtheria in man appears to have been thoroughly disproved by the observations of Roux and Yersin.

The following differential characters have been noted:

It may be accepted as demonstrated that the common diphtheria of birds is essentially distinct from the genuine diphtheria of man, and that when such diphtheria of the bird is conveyed to man as has been often alleged (Richter, Gips, Bonig, Gerhart, etc.), it is one of the forms of pseudo diphtheria that is produced, and not that which is caused by the Klebs-Löffler bacillus. Dr. V. A. Moore, who has cultivated specimens of the bacillus diphtheriæ Columbarum obtained from Germany, considers the germ as belonging to the group of the bacillus coli communis, and as not the cause of the chicken diphtheria in America. Further investigation must settle whether the bacillus diphtheriæ Columbarum is the one cause of this affection in Europe, and what is the microbian cause or causes of the disease in America.

Incubation. This is very variable. False membranes may form in twenty-four hours in some cases; in other cases they may be delayed from four to fourteen days (Colin, Babes, Puscarin, Marinescu).

Symptoms. There is dullness, prostration, sunken head, ruffled feathers, altered hoarse voice, drooping wings, wheezing breathing, difficult deglutition, sneezing, and patches of dark red congestion in the fauces covered with a thin film, at first translucent, but soon becoming dense, adherent, opaque, whitish or yellowish. As it becomes older this deposit becomes granular, wrinkled, dry and friable. It is more adherent in chickens than in pigeons and causes bleeding when detached. Necrotic changes may take place in the mucosa leading to considerable loss of tissue, and even to perforations of the soft palate, pharynx or œsophagus. It may remain circumscribed by the region of the mouth and end in an early recovery, or it may extend to the organs of the chest and abdomen, or the germs may proliferate largely in the blood and induce fatal results. On the other hand it may become subacute or even chronic, and, as already noted in the case of the parent pigeons, it may persist as an infecting disease without materially injuring the general health of a comparatively immune animal.

The affected nasal passages become filled by frothy liquid and blocked by false membranes, so that the bird is driven to breath through the open mouth. The skin around the nares, and eyelids and the cavity beneath the eye may be covered with the false membrane, by the increase of this product the bones may be driven out of place, so that the palatines press downward, the eyeball is pressed outward and the root of the beak may seem swollen. The false membranes that form on the skin or reach the surface are soft, creamy, cheesy, or dry, granular and friable.

When the eye is specially affected there are swelling of the lids, profuse lachrymation, closure of the lids by adhesion, and formation around their borders or on their inner surface and on the membrana nictitans of false membranes which press the lids outward more or less unevenly, and may be easily recognized when the lid is everted. The cornea and even the interior of the eye may suffer, leading to perforation, internal tension, and in some cases atrophy, with permanent blindness.

The tongue may suffer on the tip as in pip, or on its dorsum, from which the disease extends to the larynx, trachea and even the air sacks, which become filled with false membranes, that are coughed up, and decomposing in the mouth, add to the infection and fœtor. Dyspnœa and cyanosis of comb and wattles are marked features.

The extension may take place downward along the alimentary track, the false membranes forming on the gullet or crop and interfering with swallowing or digestion, or on the intestine and determining a fœtid, often greenish or bloody diarrhœa with indications of false membranes. Vomiting may be a marked symptom.

The skin is usually attacked secondarily around the margin of the beak, the eyelids, the nares, the ears, the comb, the wattles, the anus, but it may develop at any point where the infecting material has touched an abraded surface.

Trinchera found that in acute cases the acme was reached in fifteen days after which improvement might be looked for. A chronic form affecting the gullet might however persist indefinitely in pigeons without proving incompatible with good health.

Paralysis of the wings or limbs may remain after the healing of the local lesions.

Mortality. Prognosis. The disease is very fatal to both pigeons and chickens, 50, 70 or even 100 per cent. perishing when a flock is attacked for the first time. In flocks that have previously suffered, on the other hand, a large number are practically immune, and even if they contract the disease it assumes a mild form, and they survive but may retain the germ and continue to communicate it to others. Even the young of such immune flocks suffer less severely, coming as they probably do from less susceptible and therefore surviving birds, or having already perhaps contracted a mild (non-fatal) type of the disease from their parents.

Differential Diagnosis. From psorospermosis (coccidiosis) it is distinguished by its origin on the mucous membranes, and not on the skin, the skin lesion being a secondary one. In psorospermosis the primary lesion is usually on the skin, from which it extends to the mouth and especially along its floor. In psorospermosis the morbid deposit assumes the form of rounded warty-like masses, on comb or wattles; is easily propagated by inoculation, is promptly checked by antiseptics, does not tend to produce internal extension nor generalization, and on microscopic examination shows numerous spheroidal coccidia intermingled with the epidermic cells and possessing amœboid movement. By virtue of this automatic movement they make their way between and into the epidermic cells in which they multiply.

From the croupous angina of Rivolta it is distinguished by the absence of the infusoria (monocercomonas gallinæ) to which he, Delprato and Pfeiffer attributed that affection. The monocercomonas is a flagellate organism 14 μ to 25 μ in length and 5 μ to 7 μ in breadth. Its rounded end bears one flagellum as long as the body, and its acute end three flagella which give it active motions. These are found in the yellowish white swellings of the mucosa, which vary in size from a millet seed to a pea, covering a hyperæmic spot and composed of epithelial cells, blood globules—white and red,—leucocytes, granules and the infusoria. The false membrane is remarkable for its lack of consistency and its tendency to invade the mouth and gullet rather than the air passages. These infusoria are not colored by picrocarminate of ammonia, but stain by methyl-violet and then appear as round or slightly irregular hyaline bodies.

From aspergillus disease of pigeons, by the absence of the characteristic, miliary, white nodule of that disease showing caseated contents intermixed with an abundant mycelium of aspergillus fumigatus. The aspergillus disease attacks especially the mouth but may also implicate the gullet, lungs, liver, intestine and kidneys. The microscopic examination of the exudate is conclusive, by reason of the presence of the bacillus diphtheriæ columbarum, and the comparative absence of the filamentous mycelium.

Treatment. This is mainly prophylactic. The first step must be to separate the sick and healthy, destroying the former, or shutting them up in a special enclosure apart from all other birds. In the case of valuable chickens, their eggs may be set under other hens and the young raised apart from the suspected flock. This may even be attempted in pigeons, the common eggs being removed and the valuable ones put in their place under a healthy sitting dove. In the case of pigeons that have been recently through the disease they should be kept strictly by themselves, even though they may appear to have regained perfect health. The dead bodies must be burned or deeply buried. Sparrows and even rabbits dying in the vicinity must be similarly disposed of, and where the disease prevails sparrows and small birds may be exterminated as probable bearers of infection.

The purchase of strange birds must be carefully guarded, none being taken that show weeping eyes, nasal discharge, labored or wheezing breathing, and all new birds should be placed by themselves in quarantine for ten to fifteen days. Finally a thorough disinfection of the place where the sick have been is of first importance. Thorough cleaning of the poultry house, followed by a coat of white-wash, every gallon of which contains four ounces of chloride of lime, or one drachm of mercuric chloride will usually prove effective. The poultry runs should be liberally sprinkled with a solution of sulphuric or hydrochloric acid, one part to 1000. The same may be used on the building, which may further be fumigated by burning sulphur.

Poultry shows should be kept under the most rigorous sanitary supervision.

Curative treatment is only profitable in the case of specially valuable birds, and even then only, as a rule, when the disease is confined to the nose, mouth, larynx and pharynx. The affected parts may be brushed with a solution of chloride of iron (1 dr. of the tincture to 1 oz. water), nitrate of silver (2 grs. to 1 oz. water), sulphide of calcium (½ dr. to 1 oz. water), tannin (10 grs. to 1 oz.). Tincture of iodine may be applied direct, or a solution of carbolic acid or of creosote or creolin (1 part to 50) will often succeed. Thomassen recommends the removal of the false membranes and the application of boric acid followed by dry sulphur. Benoist says the majority recover when made to inhale the fumes of oil of turpentine evaporated at a gentle heat twice a day.

As internal medication, or to correct the intestinal affection, sulphate of iron may be dissolved in the drinking water, or salicylic acid may be given in pill form with molasses.

CHRONIC PHARYNGITIS.

Sequel of acute: or subacute from the first. Due to œstrus, in cattle to summer catarrh, tubercle or actinomycosis. Lymphatic horses predisposed; attends chronic indigestion; in swine tonsilitis. Symptoms: chronic cough, easily roused, wheezy or mucous; nasal discharge; low condition; lack of spirit. Lesions: congestion; softenings; erosions; cicatrices; tonsilitis; abscesses; specific deposits. Treatment: hygienic; antiparasitic; astringent; antiseptic; derivative; counter-irritant; tonic inhalations and electuaries. Bitters. Iron.

Causes and Nature. Chronic pharyngitis in animals may be a simple continuation of the acute, in a milder form, or it may assume a subacute or chronic type from the first and never rise to the intensity that would characterize the acute. It may be a simple catarrhal affection or it may become more or less follicular or glandular. Again in horses it is not infrequently a result of the hibernation form of the œstrus (bots) attached to the delicate pharyngeal mucosa, and in cattle from the extension of the chronic summer catarrh, or from the local development of tubercle or actinomycosis in the walls of the pharynx or in the adjacent lymph glands. Horses of a soft, lymphatic constitution, with a heavy coat, confined in close warm stalls, and which perspire abundantly are especially liable to the affection. It may also be an accompaniment and result of chronic gastric indigestion. In swine the affection is commonly associated with tonsilitis.

Symptoms. In many cases the main symptom is a chronic cough which is aroused by any cause of irritation, feed, especially dry or fibrous fodder, cold drinking water, sudden passing from the hot stable to the cold outer air, reining in, pressure on the throat, or sudden active exertion. If the cartilages are calcified it may be impossible to rouse the cough by pressure. The cough is often dry and wheezy, rather than soft and gurgling as in the second stage of acute pharyngitis, and is repeated several times paroxysmally. In the intervals there is more or less stertor or wheezing, or a distinct rattle especially when the neck is curved by drawing the nose inward. Deglutition may be interfered with but this shows most with the first swallow, which in the case of liquids may be returned through the nose, whereas those that follow go down without difficulty. A lateral swelling of the parts above the larynx or a bulging of the parotids is not uncommon. Discharge from the nose of a mucopurulent character is usually present, but often so scanty as to be overlooked. There is usually loss of flesh and lack of vigor even if the subject is well fed.

Lesions. In the simple catarrhal form the mucous membrane of the lateral pharyngeal walls, the posterior pillars of the palate and the back of the soft palate, is red, congested, with arborescent vessels, thickening, and puckering into rugæ. The epithelium has lost its translucency, become opaque and granular, and its desquamation in spots and patches may leave erosions, ulcers more or less deep, and white drawn cicatrices. When the follicles and mucous crypts are involved (follicular) they stand out like millet seed, peas or beans, and may show ulceration or minute abscess. In pigs especially, tonsilitis is liable to be present, and the tonsillar follicles are filled and distended with tenacious mucous, a caseous granular debris, or even a cretaceous material. In the vicinity of the tonsils, minute abscesses may exist in or beneath the mucosa.

Ulceration may be the result of tubercle, glanders, actinomycosis, aspergillus, sarcoma, or some local infection, and attendant symptoms of one or other of these diseases will guide the diagnosis. Thus in tubercle there will be the implication of the adjacent lymph glands and usually of distant ones; in glanders the deposits in the nose, submaxillary lymph glands and lungs will enable one to diagnosticate; in actinomycosis the hardness of the neoplasm and the presence of the yellowish tufts which present under the microscope the concentrically arranged club-shaped elements, will show its nature; and in sarcoma or carcinoma the structure of the new tissue will decide its character. The pharyngeal muscles are the seat of granular or fatty degeneration or of fibroid change. Friedenreich speaks of a fold from the vault of the pharynx which had nearly closed the passage and had killed the horse by inability to swallow.

Treatment. Chronic pharyngitis is usually a very obstinate affection and demands careful hygienic as well as medicinal treatment. Hot, foul stables, unduly thick coats, unwholesome food, irregular feeding, excessive meals at long intervals, overwork, undue exposure to cold and wet, lack of sunshine or of grooming are to be corrected. Next, the removal of mechanical irritants such as pharyngeal bots, actinomycosis growths, etc., will be in order. Then the use of astringents and antiseptics internally and of derivatives externally will be demanded. An occasional embrocation of mustard, or the application of ammonia and oil, will often serve a good purpose, and in obstinate cases the hot iron in points will sometimes prove effective.

Internally the inhalation of the fumes of tar, carbolic acid, creolin, oil of turpentine, or of burning sulphur kept up continually or frequently repeated. Giving all drink in the form of tar water will often have a good effect. Electuaries made with boric acid, salicylate of soda, ammonium chloride or iodide, borax, with honey, molasses, liquorice, Iceland moss, or gum arabic will often prove beneficial. Agents that stimulate the mucosa may follow, such as balsams of Peru or Tolu, copaiba, cubebs, pilocarpin, wild cherry bark, or these may be combined with the former. Finally a course of tonics are usually of the first importance; iron sulphate, copper sulphate, arsenious acid, arsenite of strychnia may furnish examples.

DEPRAVED APPETITE. STUMP SUCKING. PICA. LICKING DISEASE.

Common features of group. Ruminants; depraved appetite; objects swallowed: hair balls. Sheep eating wool in winter. Pigs eat bristles. Puppies swallow marbles, etc., wantonly. Solipeds swallow hair, plaster, earth, sand, and lick manger or rack. Fowls eat their feathers. Causes: soil exhaustion, lack of lime, soda, potash, phosphorous; relation to osteo malacia; granitic or sandy soils, peat, muck, causative; digestive disorder; faulty food; yearly breeding and heavy milking; constant stabling; dry seasons. Course: chronic. Lesions; emaciation; anæmia; serous exudate; catarrh of the bowels. Treatment: soil; good fodder; salts of soda, potash and lime, phosphates; tonics; apomorphine. Wool eating; example: digestive disorders; emaciation. Treatment: open air; good fodder; salts of the bones and soft tissues; clip nurses; apomorphine.

Definition. We have here a class of morbid habits, which cannot be referred to any constant lesion or group of lesions, and which appear in certain cases to result from example and to constitute nothing more than a bad habit.

Symptoms. Ruminants without any appreciable cause, lick the clothes of their care-takers, chew and swallow articles of clothing of all kinds, bones, old shoes, gloves, socks, cuffs, collars, small forks, pocket-knives, nails, wires, needles, coins, stones, lumps of clay, hair, which may give rise to secondary troubles of a more or less serious kind. Pregnant cows are especially subject to this infirmity. The small pointed objects like pins, needles, ends of wires, etc., which are mostly taken by accident with the food are especially apt to be entangled in the alveoli of the reticulum and make their way to the heart, with fatal effect, or through the abdominal walls creating a fistula. Hair aggregates with saliva, mucus and phosphates, to form balls in the first two or three stomachs. Other indigestible objects may also become encrusted and prove sources of irritation. Licking the skin of another animal is doubtless at times encouraged by the taste of the salts of perspiration, but in other cases it has all the appearance of a mutual kind service as the cow with itching head will walk up and present it to its fellow which rarely fails to respond to the invitation. Stump licking is not uncommon.

Sheep shut up in the winter get in the habit of chewing each other’s wool, thus virtually depilating their fellows and accumulating wool balls in their stomachs.

Pigs when running at large eat human fæces often infecting themselves with the cysticercus cellulosa, and devour their own or their fellows’ bristles, which form ovoid and irritating aggregations in the stomach.

Puppies are proverbial for swallowing every small object that comes in their way, coal, pebbles, marbles, leather, hair, etc., with the result of inducing nausea and vomiting, or more seriously, wounds of the stomach, gastritis and enteritis. In older dogs the habit is more likely to imply rabies.

Solipeds will lick and swallow each others hair, eat off the hair from each other’s tails and manes, eat their clothing, lick the wall plaster, earth or sand, and even the manger or rack. The last named habits are usually connected with disease.

Fowls can digest almost anything they swallow, but if they take to picking their feathers, they create serious injury to the skin and indirectly to the general health.

Causes and Nature. In general terms it may be said that the causes of depraved appetite are very numerous, so that the trouble must be looked upon as a symptom of many morbid conditions in place of a disease sui generis.

Heredity has been invoked as a cause, mainly, it would appear, because the disease appears enzootically on certain exhausted soils, or in herds kept in the same unhygienic conditions. In such cases the real cause is usually to be found in faulty conditions of soil, water, buildings, food, etc., on the correction of which the trouble disappears. When, however, from a long continuance of unhygienic conditions, a weakness of constitution is transmitted from parent to offspring, such hereditary debility may be accepted as a predisposing factor.

An exhausted soil, lacking especially the elements of lime and phosphorus, is a common cause, though by no means the only one. Nessler who analyzed the hay and water, furnished to cattle suffering from this disease in the Black Forest found a notable absence of the soda salts. In others in which osteo malacia was the prominent symptom the lack was in phosphate of lime as well. In the nature of things the soil that has been continuously cropped to exhaustion is robbed of both earthy and alkaline salts, and the animals fed on its exclusive products suffer not only as regards the nutrition of the bone, but also of the soft parts. Hence Trasbot says that in osteo malacia, pica is never absent. Roloff and Röll hold that it is the first symptom of osteomalacia. In South Africa where the land has been cropped with oats year after year without manure and as long as it will bear, the disease became prevalent in the street car horses fed on the oats, and was corrected by the addition of phosphates, or phosphate bearing food, to the ration. In the older dairying farms of New York which have been kept under grass for a great length of time, and all the milk products sold off, depraved appetite in all its forms is quite frequent. Where the land is originally light and sandy and naturally deficient in lime, osteo malacia is often a concurrent disorder. The two conditions may however occur independently of each other, and especially may pica appear alone, in keeping with the greater solubility of the soda and potash salts and the readiness with which these can be washed out of the soil, while the less soluble lime salts in part remain.

Lemcke, Haubner and Siedamgrotzky attribute the disease to a nervous disorder. Lemcke indeed traces the disorder to a lack of phosphorus, and claims that osteomalacia only supervenes where the rheumatic diathesis is also present.

It may be shortly stated that the disease prevails especially on granitic or sandy soils, or on those which are mainly composed of organic debris (peat, muck). Limestone soils and those which contain any considerable proportion of potash or soda are usually exempt.

Digestive disorder though starting from a different point may tend to the same end. A hyperacidity of the stomach has been observed to coincide with the malady, and by interfering with easy and normal digestion, it may stand in the way of such assimilation as is necessary to vigorous health.

Faulty food operates in a similar manner. The exhausted soils, and their products deficient in alkaline and earthy salts have been already referred to; we must also note the evil effect of fibrous fodders, the main nutritive elements of which have been washed out by intemperate weather after they were cut, the rank aqueous products of wet or swampy soils, the fibrous and siliceous plants (rushes, carex, equisetums, etc.) which grow on poor, wet or soured soils, the innutritious and fermented products of beet sugar factories, and generally the spoilt food which has undergone fermentation.

Yearly breeding and constant milking, by undermining the general health, predisposes so strongly that in many cases the affection is seen in dairy cows, while oxen and young cattle escape. The last period of gestation when the demands for the growing calf are greatest, is the period of especial danger.

Permanent stabling which denies the invigorating influence of sun, exercise and pure air contributes toward the general debility and therefore, in animals that are closely stabled for the winter the spring is especially to be feared, when compulsory inactivity, poor feeding, gestation and milking have combined to reduce the system.

Dry seasons have been noticed to increase the affection manifestly by reducing the supply of food.

Course. The affection is chronic and unless arrested by the supervention of more favorable conditions, may last for a year or more. Spontaneous recovery may set in when turned out to pasturage and open air life, and especially if a rich grain feeding is added. Without change in the conditions however, the tendency is to a fatal result.

Lesions. The victims of the disorder are emaciated, the fatty tissue contains a yellow serum, there is little blood, and that is thin and watery and coagulates loosely, the muscles are pale and flabby, and the gastro-intestinal mucous membrane is the seat of catarrh.

Treatment. To treat rationally and successfully we must adapt the measures to the obvious causes. When the soil has been scourged and exhausted, a change of pasture, and of land used for hay or soiling crops is the first consideration. If these cannot be secured then grain and seeds rich in protein, and alkaline and earthy salts should be added to the ration. Wheat bran, middlings, peas, beans, cotton seed meal, linseed meal, rapecake may be named among available resorts, or in their absence, daily doses of phosphate of lime, and sodium chloride or bicarbonate, or potash salts may be allowed, or even bone dust.

If imperfect digestion is a manifest factor, sodium chloride, or potassium chloride, calcium phosphate, iron and bitters will serve a good end. In hyperacidity, limewater, chalk, or magnesia may be given. If the digestion is torpid, hydrochloric acid with bitters may be resorted to.

Feser and especially Lemcke strongly recommend apomorphia. It is used hypodermically in doses of 2 grains for horse or cow repeated daily for three days.

Secondary Symptoms in Wool-eating Lambs. Lambs from two to six weeks old especially such as suck ewes with woolly udders (merino, Cotswold) first swallow the wool inadvertently, and then acquire a liking for the saline matters in the abundant yolk (merino), till finally the accumulating wool balls produce digestive and nervous disorder and a craving for the indulgence. Thus the breed must be considered in estimating the symptoms. For the same reason the wool about the hips or elsewhere soiled with salts of the urine or liquid fæces prove attractive to the victim. The proximity of other wool eaters is another cause which starts others to follow the bad example. The general conditions of debility, exhausted soil, and the absence of alkaline and earthy salts must be borne in mind. So too with prolonged confinement indoors in winter, the absence of invigorating exercise and the restriction of the animals (dams) to food which is deficient in saline matters.

Beyond the mere eating of the wool and the destruction of fleeces, the lambs do not usually suffer seriously. But if the consumption of wool is excessive the accumulating balls of the size of marbles in the stomach, and the blocking of the pylorus and small intestine, may give rise to intermittent constipations and diarrhœas, deranged digestion, muco-enteritis, mucous covered stools, loss of condition, emaciation and retarded development.

Treatment consists first in the securing of a more healthy regimen. This is but one of the evils of the close winter confinement of an animal preëminently adapted to freedom and exercise. Turning out in a wide range, especially if pasture is available, is a prime consideration. The separation from the flock, of the first wool eaters, will check the propagation of the vice by imitation. Food that is defective in one or more constituents must be supplemented by that which will correct the deficiency. Salt, potassic salts and above all phosphate of lime or bone meal will sometimes benefit. May recommends the separation of the lambs from the ewes except when nursing, three times a day. Finally Lemcke claims for apomorphia the same curative effect as in other animals. The dose is 2 grains, subcutem, as in the cow and may be repeated three days in succession.

LACERATION OF THE PHARYNX.

Trauma of pharynx from objects swallowed; from whip or other instrument in choking; lesions. Symptoms: swelling; rapidly extending; dysphagia; salivation; retching; dyspnœa; roaring; asphyxia. Treatment: as for pharyngitis; open pouch, suture laceration; use antiseptics; liquid diet.

Laceration of the velum palati has been already referred to, and the remaining walls of the pharynx sometimes suffer in the same way and from identical causes. Pins, needles, and other sharp pointed bodies taken with the food sometimes perforate the walls and determine an advancing ulceration which furnishes a way for their escape externally in the region of the throat. In other cases a rigid staff, a whip, or even a probang introduced to overcome choking, is forced through the walls of the pharynx forming a pouch for the accumulation and septic fermentation of ingesta, and extensive ulcerative and gangrenous lesions.

Lesions and Symptoms. These depend mainly on the extent of the laceration. If there is a mere abrasion, superficial laceration or prick of the mucosa, it determines a prompt inflammation, with exudation which covers or closes the wound and a speedy healing may ensue. When, however, the whole thickness of the mucosa has been extensively lacerated and a pouch has been formed beneath it, it becomes filled with decomposing mucus and ingesta, and the resulting septic products determine ulceration, abscess, or gangrene. The result is too often a general and fatal septic infection.

In the milder forms there are only the common indications of a moderate pharyngitis. In the more severe form, the throat swells at first on the lacerated side and later all around. This swelling soon fills the intermaxillary space and extends over the face and the entire head. From the first, deglutition is extremely difficult or impossible, liquids are returned through the nose and saliva flows abundantly from the mouth. Retching is not uncommon and saliva mixed with alimentary matters is discharged by the nose (solipeds) or mouth (other animals). The swelling of throat and head has a doughy, œdematous feeling, it is very tender, and soon causes rattling, wheezing breathing, roaring, dyspnœa and asphyxia.

Necropsy shows the general œdematous exudate, the laceration of the pharyngeal walls, and the collection of debris and pus in the lacerated cavity. The pus may have extended between the muscles following the course of the gullet and trachea as far as the chest. Extensive patches of necrosis may also be shown. Treatment. In the slighter cases the ordinary treatment for catarrhal pharyngitis is demanded. In the more severe the lesions are so redoubtable and their progress so rapid that a fatal result is virtually inevitable. As a desperate resort the septic pouch may be opened from without, its contents removed, the pharyngeal wound sutured if possible, and a thorough irrigation with antiseptics (acetate of aluminium solution) employed at frequent intervals to check if possible the septic process. The animal should be fed with well boiled milk or other liquid which will not add to the fermentation, and this may be given through a stomach tube, or by the rectum when deglutition is impossible.