Special report on diseases of cattle

by United States. Bureau of Animal Industry; V. T. Atkinson; Dr. Dickson; A. Eichhorn; Richard W. Hickman; James Law; Lowe; C. Dwight Marsh; John R. Mohl

FOOTNOTES:

[3] The term "tumor" literally means a swelling, and thus has been applied to the prominence caused by an overdistended bladder, to the enlargement of pregnancy, to the swelling produced by an abscess, to the overgrowth of tissue (hyperplasia) associated with injury and consequent inflammation, and to numerous other phases of tissue enlargement directly connected with recognized disease processes. For this reason it is becoming more common for scientists to apply the word "neoplasm" to the new growths described in this chapter. Because of the still popular use of the word "tumor," it is retained in this chapter for the designation of those new growths to which the sevenfold characterization of our descriptive definition applies.

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DISEASES OF THE SKIN.

By M. R. Trumbower, D. V. S.

[Revised by John R. Mohler, V. M. D.]

GENERAL DISCUSSION.

The skin consists of two parts—a superficial layer, the epidermis, or cuticle, and the deep, or true, skin, the dermis, cutis vera, or corium.

The epidermis, cuticle, or scarf skin, is an epithelial structure, forming a protective covering to the corium. It varies in thickness, is quite insensible and nonvascular, and consists of a sheet of cells.

The epidermis is divided into a firm and transparent superficial and a deep, soft layer. The latter is the rete mucosum, whose cells contain the pigment which gives color to the skin. The deep surface of the epidermis is accurately molded on the papillary layer of the true skin, and, when removed by maceration, presents depressions which correspond to the elevations on the dermis. From the cuticle tubular prolongations pass into the sebaceous and sudorific glands; thus the entire surface of the body is inclosed by the cuticle.

The dermis, or true skin, is vascular and highly sensitive, containing the tactile ends of the nerves of touch. It is covered by epidermis and attached to the underlying parts by a layer of areolar tissue, which usually contains fat. The cutis consists of a fibro-areolar tissue and vessels of supply. It is divided into two layers, the deep, or true, corium and the upper, or papillary. The corium consists of strong interlacing fibrous bands, chiefly white; its meshes are larger and more open toward the attached surface, giving lodgment to the sweat glands and fat. The papillary, or superficial, layer is formed of a series of small conical eminences or papillæ, which are highly sensitive, and consists of a homogenous, transparent tissue. The blood vessels form dense capillary plexuses in the corium, terminating by loops in the papillæ. The papillary nerves run in a waving manner, usually terminating in loops.

Hair is an appendage of the skin and forms its external covering. It is a special modification of epidermis, having the same essential structure, and consists of a root, shaft, and point. The root has a bulbous extremity, is lighter and softer than the stem, and is lodged in a recess or hair follicle, which may either be in the corium or subcutaneous areolæ. The follicle is dilated at the bottom to correspond to the root bulb, and the ducts of one or more sebaceous glands open into it. At the bottom of each follicle is a conical, vascular papilla, similar in every respect to those on the surface of the dermis; this papilla fits into a corresponding depression in the root of the hair. The shaft consists of a center, or medulla, a surrounding fibrous portion, and an external coating, or cortex. The medulla consists of cells containing pigment or fat, is opaque, and deeply colored. All kinds of hair do not have this medulla. The fibrous portion occupies the bulk of the stem, and the cortex is merely a single layer of thin, flat, imbricated (shinglelike) scales.

The sebaceous glands, lodged in the corium, are most abundant in parts exposed to friction. They generally open into the hair follicles, occasionally on the surface of the body. Each gland consists of a small duct which terminates in a lobulated recess. These lobules vary, and are, as is the duct, lined with epithelium. They are filled with sebaceous matter which, as it is secreted, is detached into the sacs. They are very plentiful between the claws of cattle.

The sudorific glands, or sweat glands, are situated in the subcutaneous areolar tissue, surrounded by a quantity of fat. They are small, round, reddish bodies, each of which consists of one or more fine tubes coiled into a ball, the free end of the tube being continued up through the true skin and cuticle, and opening on the surface. Each sweat gland is supplied with a cluster of capillary blood vessels which vary in size, being very large when perspiration is excessive. The contents of the smaller ones are fluid, and of the larger, semifluid.

The skin may be regarded as an organ supplementary in its action to the lungs and kidneys, since by its secretion it is capable of removing a considerable quantity of water from the blood; it also removes small quantities of carbon dioxid, salts, and in certain instances during suppression of the renal secretions a small quantity of urea. The skin is also the chief organ for the regulation of animal heat, by or through conduction, radiation, and evaporation of water, permitting of loss of heat, while it also, through other mechanisms, is able to regulate the heat lost. The hair furnishes protection against extreme and sudden variations of temperature by reason of the fact that hairs are poor conductors of heat, and inclose between them a still layer of air, itself a nonconductor. The hairs are also furnished with an apparatus by which the loss of heat may be regulated; thus, in cold weather, through the contraction of unstriped muscular fibers of the skin, the hairs become erect and the external coat becomes thicker. Cold, too, acts as a stimulus to the growth of hair, and we find, in consequence, a thicker coat in winter than in summer. The hairs also furnish protection against wet, as they are always more or less oily from the secretion of sebaceous glands, and thus shed water. Through their elasticity they furnish mechanical protection, and through the thickness of the coat, to a certain degree, resist the attacks of insects. Finally, the hairs assist the sense of touch.

The sweat glands are constantly discharging a watery secretion in the form of insensible perspiration, and by their influence act as regulators of the temperature of the body; hence, in warm weather, the secretion of the skin is increased, which tends to prevent overheating. Sweating, in addition to regulating heat, is also an active agent in removing effete material from the blood; therefore this secretion can not be checked without danger. If the skin is covered with an impermeable coating of grease or tar, death results from blood poisoning, owing to the retention of materials destined to be excreted by the skin.

All secretion poured out by the skin is not only modified by the condition of the atmosphere but also by the character and quantity of the food, by the amount of exercise, and especially by the quantity of fluid taken.

The sebaceous secretion is intended to lubricate the skin and hairs. It consists of soft, fatty material suspended in water, and is characterized by an odor peculiar to the animal by which it is secreted.

I will not attempt to classify the various diseases of the skin, for in a work of this kind it would serve only to confuse the reader.

We shall first consider a class of diseases which are of an inflammatory type; next, those caused by faulty secretion and abnormal growth; then, diseases of parasitic origin; lastly, local injuries of the skin.

PRURITIS (ITCHING).

We shall consider pruritis first as a distinct subject. It is not a disease, only a sensation, and therefore a symptom. It is one of the symptoms accompanying the majority of the diseases which we will consider in this chapter. It is, then, a functional affection produced by slight irritation from without or by an internal cause acting upon the sensory nerves of the skin. Nothing characteristic is seen except the secondary lesions, produced mechanically by scratching or rubbing.

There are various forms of itching, the result of specific skin diseases, where the pruritis is a secondary symptom. In such cases it should not be regarded as an independent affection.

Causes.—Many causes may induce the condition which we recognize here as pruritis. The most common one is dirt on the skin, resulting from insufficient care. If the ceiling of the stable is open, so that dust and straw may fall, the skin is irritated and pruritis results. It also occurs in some forms of indigestion.

The parts of the body most exposed to this condition are the croup, the back, the top of the neck, and the root of the tail.

Another cause is found in affections of the liver and of the kidneys, when an increase of effete material has to be thrown off by the skin. Morbid materials circulating in the blood may produce a tickling or smarting sensation of the skin in their passage from the blood to the free surface of the skin. Certain irritating substances when eaten may be excreted by the skin, and coming thus in direct contact with the sensory nerves produce itching, or may go further and cause distinct inflammation of the skin. In another class of cases the pruritis may be ascribable to an atrophy, contraction, or hardening of the skin, when the nerves become irritated by the pressure. These conditions may be so slightly marked in a thick skin like that of the ox that they can not be recognized. It is frequently noticed that cattle rub themselves as soon as they pass from the stable into the open air—changing from a warm to a cold atmosphere. Again, we may find one that does all its rubbing in the stall. We may look for lice, but fail to find them. These conditions are generally attributable to high feeding and to too close confinement. They may be associated with inflammatory irritation or not; certainly we fail to discover any morbid changes in the skin. There is to some extent a delightful sensation produced by rubbing, and it may partly become a habit of pleasure.

Treatment.—We must place our chief reliance upon a change of food, plenty of exercise, and in most cases the administration of an active cathartic—1 to 1½ pounds of Epsom salt, a handful of common salt, a tablespoonful of ginger or pepper, mixed with 2 quarts of water, all of which is to be given at one dose. Afterwards half an ounce of hyposulphite of soda mixed with the feed may be given twice a day for a week. For an external application, when the skin is abraded or thickened from rubbing, a solution of borax, 4 ounces to the quart of water, may be used. Carbolic acid, ½ ounce to a quart of water, will give relief in some cases.

INFLAMMATORY DISEASES OF THE SKIN.

ERYTHEMA.

This is the simplest form of inflammation of the skin. It consists of an increased redness, which may occur in patches or involve considerable surface. The red coloration disappears when pressed by the finger, but soon returns after the pressure is removed. There is seldom much swelling of the affected part, though often there is a glutinous discharge which dries and mats the hair or forms a thin scale upon the skin. In simple erythema the epidermis alone is affected; when it becomes chronic, fissures form and extend into the corium, or true skin.

Causes.—Simple erythema, consisting of an inflammatory irritation, is seen in very young calves, in which the navels leak. The discharge being urine, it causes an irritation of the surrounding skin. Chafing, which is another form of erythema, is occasionally seen on the udders of cows from rubbing by the legs; chafing between the legs is not uncommon among fat steers. Chronic erythema is found in the form of chapped teats of cows and chapped lips in sucking calves. It frequently occurs in cows when they are turned out in winter directly after milking, and in others from chafing by the sucking calf. Some cows are peculiarly subject to sore teats. The fissures when neglected in the early stage of formation become deep, very painful, often bleeding at the slightest touch, and when milked in that condition cause the animal to become a kicker. Occasionally the lower portions of the legs become irritated and chapped when cattle are fed in a muddy or wet yard in winter, or if they are compelled to wade through water in frosty weather. Another form of erythema occurs in young cattle highly fed and closely stabled for a long winter. The erythema appears in patches, and as it is most common near the end of the winter it is known as the "spring eruption" or "spring itch."

Treatment.—In ordinary cases of erythema the removal of the cause and the application of benzoated oxid of zinc ointment, carbolized cosmoline, or ichthyol ointment applied a few times, will restore the skin to a healthy condition.

When there are fissures the zinc ointment is the best. If at the teats, a milk siphon ([Pl. XXIV], fig. 4) should be used instead of milking by hand, and the calf, if one is suckled, should be taken away. The calf should be fed by hand if its mouth is affected. When the legs are irritated or chapped, dry stabling for a few days and the application of tar ointment will soon heal them.

URTICARIA (NETTLE RASH, OR SURFEIT).

This is a mild, inflammatory affection of the skin, characterized by sudden development of patches of various sizes, from that of a nickel to one as large as the hand. The patches of raised skin are marked by an abrupt border and are irregular in form. All the swelling may disappear in a few hours, or it may go away in one place and reappear on another part of the body. It is always accompanied with a great desire to rub the affected part. In its simplest type, as just described, it is never followed by any serous exudation or eruptions, unless the surface of the skin becomes abraded from scratching or rubbing.

Causes.—Digestive derangements caused by overloading the stomach when the animal is turned out to graze in the spring, certain feed constituents, high feeding of fattening stock, functional derangement of the kidneys, spinal and other nervous affections, are the most common sources of nettle rash.

The disease consists in paralysis of the nerve ends that control the volume of the capillary vessels in certain areas of skin, thus permitting the vessels to expand, their contents in part to exude, and thus produce a soft, circumscribed swelling.

Treatment.—Administer a full dose of Epsom salt. Give soft, easily digested feed, and wash the affected parts with a solution of bicarbonate of soda (common baking soda), 8 ounces to the gallon of water twice a day, or diluted glycerin may be applied to the skin. If it assumes a persistent tendency, give a tablespoonful of the following powder in the feed three times a day: Cream of tartar, sulphur, and nitrate of potassium, equal parts by weight; mix.

ECZEMA.

Eczema is a noncontagious inflammation of the skin, characterized by any or all of the results of inflammation at once or in succession, such as erythema, vesicles, or pustules, accompanied with more or less infiltration and itching, terminating in a watery discharge, with the formation of crusts or in scaling off. The disease may run an acute course and then disappear, or it may become chronic; therefore two varieties are recognized, vesicular (or pustular) and chronic eczema.

Causes.—Eczema is not so common among cattle as in horses and in dogs, in which it is the most common of all skin diseases. Among cattle it is occasionally observed under systems of bad hygiene, filthiness, lousiness, overcrowding, overfeeding, excessively damp or too warm stables. It is found to develop now and then in cattle that are fed upon sour substances, distillery swill, house or garden garbage, etc. Localized eczema may be caused by irritant substances applied to the skin—turpentine, ammonia, the essential oils, mustard, Spanish-fly ointment, etc. Occasionally an eruption with vesiculation of the skin has been induced by the excessive use of mercurial preparations for the destruction of lice. It is evident that eczema may arise from local irritation to the skin or from an autointoxication. Cattle fed on the refuse from potato-starch factories develop a most obstinate and widespread eczema, beginning on the legs.

Symptoms.—In accordance with the variety of symptoms during the progress of the disease we may divide it into different stages or periods: (1) Swelling and increased heat of the skin; the formation of vesicles, which are circumscribed, rounded elevations of the epidermis, varying in size from a pinhead to a split pea, containing a clear, watery fluid; (2) exudation of a watery, glutinous fluid, formation of crusts, and sometimes suppuration, or the formation of vesicles containing pus (pustules); (3) scaling off (desquamation), with redness, and thickening of the skin. From the very beginning of the disease the animal commences to rub the affected parts; hence the various stages may not always be easily recognized, as the rubbing produces more or less abrasion, thus leaving the skin raw— sometimes bleeding. Neither do these symptoms always occur in regular succession, for in some cases the exudation is most prominent, being very profuse, and serve to spread the disorder over a large surface. In other cases the formation of incrustations, or rawness of the skin, is the most striking feature. The disease may be limited to certain small areas, or it may be diffused over the greater part of the body; the vesicles, or pustules, may be scattered in small clusters, or a large number run together. The chronic form is really only a prolongation of the disease, successive crops of pustules appearing on various portions of the body, frequently invading fresh sections of the skin, while the older surfaces form scabs, or crusts, upon the raw, indurated skin.

In old, standing cases the skin breaks, forming fissures, especially on portions of the body that bend—the neck and limbs. Thus the disease may be prolonged indefinitely. When eczema reaches its latest period, either acute or chronic, desquamation of the affected parts is the most prominent feature. The formation and shedding of these successive crops of scales constitute the character of the disease frequently denominated psoriasis.

Treatment.—The treatment of eczema is often anything but a pleasant task. There is no one method of treatment which always proves successful, no matter how early it is begun or how small an area is involved. We must endeavor to remove the cause by giving attention to the general health of the animal and to its environment. Feeding should be moderate in quantity and not too stimulating in character—green feed, bran mashes, ground oats, clean hay, plenty of salt. If the animal has been fed too high, give an active purgative—Epsom salt preferred—once a week, if necessary, and half an ounce of acetate or nitrate of potassium may be given in the feed twice a day. If the animal is in poor condition and debilitated, give a tablespoonful of the following mixture in feed twice a day: Powdered copperas, gentian, sulphur, and sassafras bark, equal parts by weight. If the animal is lousy, the parasite must be destroyed before the eczema can be cured. The external treatment must vary with the character of the lesions; no irritating application is to be made while the disease is in its acute vesicular, or pustular, stage, and, in the chronic stage, active stimulants must be used. Much washing is harmful, yet crusts and scales must be removed in order to obtain satisfactory results from the external applications. Both objects, however, can be attained by judiciously combining the curative agents with such substances as will at the same time cleanse the parts.

In the vesicular stage, when the skin is feverish and the epidermis peeling off, thus exposing the exuding dermis, an application of boric-acid solution, 2 drams of the acid to 8 ounces of water, often relieves the smarting or itching, and also serves to check the exudation and dry the surface. If this fails to have the desired effect compound cresol, 1 ounce to 2 quarts of water, should be used as a wash. Either of these washes may be used several times a day until incrustation is well established. Then compound cresol, 1 ounce to 2 quarts of sweet oil, or the benzoated oxid of zinc ointment, giving the affected surfaces a thorough application once a day, will be efficacious. When the eczema is not the result of an external irritant, it takes usually from one to two weeks to heal.

In chronic eczema, when there is a succession of scabs or scales, indolent sores or fissures, the white precipitate ointment, nitrate of mercury ointment, or blue ointment, mixed with equal parts of cosmoline or fresh lard, may be applied every second day, taking care to protect the parts so that the animal can not lick it off.

The internal administration of arsenic often yields excellent results in chronic eczema. Dissolve 1 dram of arsenic and 1 dram of carbonate of potassium in 1 pint of boiling water, and give 1 ounce of this twice a day in water, after feeding. An alkali internally may be of service. As such, one may give 2 ounces of bicarbonate of soda twice daily. Sublimed sulphur may also be tried in ounce doses twice daily.

PUSTULES (IMPETIGO).

Impetigo is an inflammatory disease of the skin, characterized by the formation of distinct pustules, about the size of a pea or a bean, without itching. The pustules develop from the papular layer of the skin, and contain a yellowish-white pus. After reaching maturity they remain stationary for a few days, then they disappear by absorption and dry up into crusts, which later drop off, leaving upon the skin a red spot that soon disappears. Occasionally the crusts remain firmly adherent for a long time, or they may be raised and loosened by the formation of matter underneath. The dry crusts usually have a brown or black appearance.

Causes.—Impetigo affects sucking calves, in which the disease appears upon the lips, nostrils, and face. It is attributed to some irritant substance contained in the mother's milk. Impetigo is also witnessed among grazing animals, regardless of age, and it especially attacks animals with white hair and skin. The mouth, face, and limbs become covered with pustules, which may rupture in a few hours, followed by rapid and successive incrustations; the scabs frequently coalesce, covering a large surface; pus may form under them, and thus the whole thickness of the skin become involved in the morbid process. This form of the disease is attributed to the local irritant properties of such plants in the pasture as St. John's wort (Hypericum perforatum), smartweed (Polygonum hydropiper), vetches, honeydew, etc. Buckwheat, at the time the seeds become ripe, is said to have caused it; also bedding with buckwheat straw.

Treatment.—Sucking calves should be removed from the mother, and a purgative given to the latter to divert the poisonous substance secreted with the milk. When the more formidable disease among grazing cattle appears, the pasturage should be changed and the affected parts of the animal thoroughly anointed once a day with sweet oil containing 2 drams of carbolic acid to the pint. This should be continued until the crusts soften and begin to drop off, then the parts may be cleansed thoroughly with warm water and soap. Subsequently the white precipitate ointment or carbolized cosmoline should be applied daily until the parts are healed.

PEMPHIGUS (WATER BLISTERS).

This is an inflammatory disease of the skin, characterized by successive formations of rounded, irregularly shaped water blisters, varying in size from a pea to a hen's egg.

Causes.—Obscure.

Symptoms.—The formation of a blister is preceded by a congestion or swelling of the skin. Yellowish-colored water collects beneath the cuticle, which raises the latter from its bed in the form of a blister. The blisters appear in a succession of crops; as soon as one crop disappears another forms. They usually occur in clusters, each one being distinct, or they may coalesce. Each crop usually runs its course in a week. The disease is attended with itching or burning sensations which cause the animal to rub, thereby frequently producing excoriations and formation of crust on the affected region.

Treatment.—Give a tablespoonful of the following-described mixture in feed twice a day: Saltpeter, cream of tartar, and sulphur, equal parts by weight. The blisters should be opened as soon as formed, to allow the escape of the serum, followed by a wash composed of chlorid of zinc, 1 dram to 15 ounces of water. When there is any formation of crusts, carbolized cosmoline should be applied.

FURUNCULUS (BOILS).

This is an acute affection of the skin, usually involving its whole thickness, characterized by the formation of one or more abscesses, originating generally in a sebaceous gland, sweat gland, or hair follicle. They usually terminate by absorption, or by the formation of a central core, which sloughs out, leaving a deep, round cavity that soon heals.

Causes.—Impoverished state of blood, the result of kidney diseases or of local friction or contusions, with the entrance of pus cocci through the damaged skin or through a hair follicle or a sebaceous gland.

Symptoms.—Boils in cattle usually appear singly, not in clusters; they may attain the size of a hen's egg. The abscess begins as a small round nodule, painful on pressure, gradually increases in size until death of the central portion takes place, then the surface of the skin gives way to internal pressure and the core is released and expelled. Constitutional symptoms are generally absent, unless the boils occur in considerable numbers, or by their size involve a great deal of tissue.

Treatment.—Poulticing to ripen the abscess. If this can not be done, apply camphorated oil two or three times a day until the core is formed. As soon as the central or most prominent part becomes soft, the abscess should be opened to release the core. Then use carbolized cosmoline once a day until the healing is completed. If the animal is in poor condition, give tonics—copperas, gentian, ginger, and sulphur, equal parts by weight, 1 tablespoonful twice a day. If the animal manifests a feverish condition of the system, give half an ounce of saltpeter twice a day, continuing it several days or a week.

FAULTY SECRETIONS AND ABNORMAL GROWTHS OF THE SKIN.

PITYRIASIS (SEBORRHEA, DANDRUFF, OR SCURF).

This is a condition characterized by an excessive secretion of sebaceous matter, forming upon the skin in small crusts or scales.

Causes.—It is ascribable to a functional derangement of the sebaceous glands, usually accompanied with dryness and loss of pliancy of the skin. The animal is hidebound, as it is commonly termed, thin in flesh, inclined to rub, and very frequently lousy. The condition is observed most often toward the spring of the year. Animals that are continually housed, and the skins of which receive no cleaning, generally present a coat filled with fine scales, composed of epithelium from the epidermis and dried sebaceous matter. This, however, is a physiological condition and compatible with perfect health.

Symptoms.—Pityriasis may affect the greater portion of the body, though usually only certain parts are affected—the ears, neck, rump, etc. The skin becomes scurfy, the hairy coat filled with branlike gray or whitish scales.

Treatment.—Nutritious feed, such as oil-cake meal, bran, ground oats, and clean hay. In the spring the disease generally disappears after the animal is turned out to pasture. When lice are present they should be destroyed.

ELEPHANTIASIS (SCLERODERMA).

This condition consists in a chronic thickening of the skin, which may affect one or more limbs or involve the whole integument. It is characterized by recurrent attacks of swelling of the skin and subcutaneous areolar tissue. After each attack the affected parts remain infiltrated to a larger extent than before, until finally the skin may attain a thickness of an inch, becoming wrinkled and fissured. In cattle this disease is confined to hot climates. The predisposing cause is unknown.

EDEMA (ANASARCA OF THE SKIN).

This is a dropsical condition of the skin and subcutaneous areolar tissue, characterized by pitting under pressure, the fingers leaving a dent which remains a short time.

Causes.—Edema generally results from a weakened state of the system arising from previous disease. It may also be dependent upon a functional derangement of the kidneys, upon weak circulation, or obstruction to the flow of blood through the lungs. In debilitated animals and in some animals highly infested with parasites there is swelling of the dewlap or of the fold of the skin between the jaws.

Symptoms.—Painless swelling of a limb, udder, lower surface of abdomen, or lower jaw becomes apparent. This may increase in dimensions for several days or may attain its maximum in less than 24 hours. Unless complicated with some acute disease of a specific character, there is not much, if any, constitutional disturbance. The deep layer of the skin is infiltrated with serum, which gives it the characteristic condition of pitting under pressure.

Treatment.—When the cause can be ascertained and removed we may expect to see the edema disappear. When no direct specific cause can be discovered and the animal is debilitated, give general tonic. If, on the contrary, it is in good flesh, give a purgative, followed by half an ounce of acetate of potassium twice a day. External applications are useless.

Edema may be distinguished from erysipelas or anthrax by the absence of pain and fever.

DERMOID AND SEBACEOUS CYSTS (WENS).

A dermoid cyst is formed by an involution of the skin with a growth of hair on the inner wall of the sac. It may become embedded deeply in the subcutaneous tissues or may just penetrate the thickness of the skin, where it is movable and painless. They are generally found within the ear or at its base, although they may form on any part of the body. Usually they have a small opening, from which a thick, cheesy matter can be squeezed out. The rational treatment is to dissect them out.

Sebaceous cysts appear not unlike the former. They are formed by a dilatation of the hair follicle and sebaceous duct within the skin, and contain a gray or yellowish sebaceous mass. The tumor may attain the size of a cherry stone or a walnut. Generally they are round, movable, and painless, soft or doughy in consistency, and covered with skin and hair. They develop slowly. The best treatment is to dissect out the sac with contents entire.

VERRUCA (WARTS).

Cattle are affected with two varieties of warts. One, the verruca vulgaris, is composed of a cluster of enlarged papillæ, covered with a thickened epidermis, the number of papillæ determining the breadth and their length its height. They are generally circular in figure, slightly roughened on the surface, and spring from the skin by a broad base. Occasionally large numbers of very thin, long, pedunculated warts grow from the skin of the ear, lips, about the eyes, and vulva. Another variety, the verruca acuminata, sometimes erroneously denominated epithelial cancers, are irregularly shaped elevations, tufted or club shaped, occasionally existing as thick, short, fleshy excrescences, giving the growth the appearance of granulation tissue. Their color is red or purplish, and oftentimes by friction they become raw and bleeding, emitting then a very offensive odor. They usually grow in clusters and their development is rapid.

Causes.—An abnormal nutrition of the skin, determined by increased energy of growth operating upon a healthy skin; at other times, upon a weak or impoverished skin.

Treatment.—When they are small and pedunculated, they may be snipped off with shears and the stump touched with nitrate of silver. When they are broad and flattened, they may be dissected out and the wound cauterized if necessary. If they are large and very vascular, they may be ligated, one by one, by taking a strong cord and tying it as firmly around the base as possible. They will then shrivel, die, and drop off. If there is a tendency to grow again, apply a red-hot iron or nitric acid with a glass rod. Very often warts quickly disappear if they are kept soft by daily applications of sweet or olive oil.

KELIS.

Kelis is an irregularly shaped flat tumor of the skin, resulting from hypertrophy—increased growth of the fibrous tissue of the corium, producing absorption of the papillary layer.

Causes.—It may arise spontaneously or follow a scar after an injury.

Symptoms.—Kelis generally appears below the knee or hock, and may occur singly or in numbers. There are no constitutional symptoms. Its growth is very slow and seldom causes any inconvenience. It appears as a flattened, irregular, or spreading growth within the substance of the skin, is hard to the touch, and is especially characterized by divergent branches or roots, resembling the claws of a crab; hence the name. Occasionally some part of it may soften and result in an abscess. It may grow several inches in length and encircle the whole limb.

Treatment.—So long as it causes the animal no inconvenience it is best not to meddle with it; when it does the animal ought to be fattened for beef, the meat being perfectly harmless to the consumer.

PARASITIC DISEASES OF THE SKIN.

RINGWORM (TINEA TONSURANS AND TINEA FAVOSA).

Ringworm is an affection of the skin, caused by a vegetable parasite.

The form known as tinea tonsurans is produced by the presence of a minute or microscopic fungus—the Trichophyton tonsurans, which affects the hair and the epidermic layer of the skin, and is highly contagious, being readily transmitted from one animal to another. This fungus consists of spores and filaments. The spores, being the most numerous, are round and seldom vary much in size. They are very abundant in the hair follicle. The filaments are articulated, waving, and contain granules. This disease is productive of changes in the root and shaft of the hair, rendering it brittle and easily broken off.

This disease becomes manifest by the formation of circular patches on the skin, which soon becomes denuded of hair. The cuticular layer of the skin in slightly inflamed, and vesication with exudation occurs, followed by the formation of scaly, brittle crusts. The patches appear silvery gray when incrusted, and are mostly confined to the head and neck. It is a common disease among young cattle in the winter and spring. Very early in the development of the patches the hairs split, twist, and break off close to the skin. This disease is attended with more or less itching. It is communicable to man.

Tinea favosa comes from another fungus, the Achorion schönleinii. This enters the hair follicle and involves the cuticle surrounding it, small crusts form which increase in diameter and thickness and then become elevated at their margin, forming a cup-shaped scab, the favus cup, which gives the disease its distinctive character. The number of these cups varies from a few to many hundreds. The hairs involved become brittle and broken, fall off with the crusts, leaving small bald patches. The crusts are of a pale or sulphur-yellow color at first; as they grow older they turn darker, or to a brown color. This form of ringworm has a peculiar odor, resembling that of mice or musty straw. It is occasionally communicated to cattle by man, mice, cats, etc., all being subject to it.

Treatment.—Remove all crusts by washing with soap and water, then apply acetic acid, sulphur ointment, tincture of iodin or nitrate of mercury ointment once a day. Cleanse the stable and whitewash it to destroy the spores scattered by the crusts.

OTHER PARASITES AND PARASITIC DISEASES OF THE SKIN.

For discussion of mange, itch, scab, lousiness, warbles (grub in the skin), buffalo gnats, hornfly (Hæmatobia serrata), ticks, flies, etc., see the chapter on "The animal parasites of cattle," page 502.

WOUNDS OF THE SKIN.

SNAKE BITES AND VENOMOUS STINGS.

[See discussion of these subjects in chapter on "Poisons and poisoning.">[

BURNS AND SCALDS.

This is a rare accident among cattle, yet in cases of fire it may occur. The application of heat, whether dry or moist, unless sufficient instantly to destroy the life of a part, is always followed by the development of vesicles or blisters, which contain a thin, watery fluid. The blisters may be isolated and not very large, or one blister may cover a very large surface. When the burn is very severe the skin may be wholly devitalized, or the injury may extend into the deeper structures of the skin. Then sloughs will occur, followed by a contraction of the parts in healing; if on a limb, this may render the animal stiff. When the burn or scald has been a severe one, the resulting pain is great and the constitutional disturbance very marked.

Treatment.—For a superficial burn use a mixture of equal parts of limewater and linseed oil, or common white paint—white lead ground in oil—to exclude the atmosphere and protect the inflamed skin. If it is not convenient to get anything else, chimney soot, flour, or starch may be spread on the wound (dry), and covered with cotton batting and light bandage. The blisters should be opened to let the contained fluid escape, but do not pull off the thin cuticle which has been raised by the blister. When the burn is extensive and deep sloughing occurs, the parts should be treated, like other deep wounds, by poulticing, astringent washes, etc. When the system has sustained much shock, the animal may require internal stimulants, such as 2 drams of carbonate of ammonia every hour until it rallies. When the pain is very great, hypodermic injections of 6 grains of morphia may be administered every six hours.

Frostbite on any portion of the body may be treated as recommended in the article on diseases of the ears.

EMPHYSEMA (AIR OR GAS UNDER THE SKIN).

Emphysema of the skin is not a true disease of the skin, but it is mentioned as a pathological condition. It is characterized by a distention of the skin with air or gas contained in the subcutaneous areolar tissue. It may depend upon a septic condition of the blood, as in anthrax or blackleg, or air may be forced under the skin about the head, neck, and shoulders, as a result of rupture of the windpipe. It occurs in the region of the chest and shoulders from penetrating wounds of the chest and lung, and occasionally follows puncture of the rumen when the escaping gas is retained under the skin.

Symptoms—The skin is enormously distended over a greater or less portion of the body; thus any region of the body may lose its natural contour and appear like a monstrosity. There is a peculiar crackling beneath the skin when the hand is passed over it, and on tapping it with the fingers a resonant, drumlike sound is elicited.

Treatment.—Puncture the distended skin with a clean, broad-bladed knife and press the air out. Further treatment must be directed with a view to the removal of the cause.

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DISEASES OF THE FOOT.

By M. R. Trumbower, D. V. S.

[Revised by Leonard Pearson, B. S., V. M. D.]

LAMINITIS (FOUNDER).

Laminitis denotes an active inflammation of the sensitive structures within the wall of the hoof, which in severe cases may result in suppuration and the loss of one or more claws. Owing to the simplicity of the structure of the foot of an ox compared with that of the horse, this disease is rarely seen in an acute form, but a mild form, commonly called "foot soreness," is not of infrequent occurrence.

Causes.—Laminitis in cattle may be caused by overfeeding, overheating, continued standing without exercise on a stone or cement floor without sufficient bedding, or by driving long distances over rough or stony soil.

Symptoms.—An unwillingness to maintain the standing position; the animal persists in lying down. The feet will be found unnaturally hot, and frequently some swelling may be noticed above the hoof. Pressure upon the hoof with blacksmith's hoof pincers causes pain and flinching. The general body temperature is increased and the breathing accelerated. Ordinarily the animal eats and drinks as usual. When it is made to move excessive tenderness of the feet becomes manifest, as is shown by reluctance to walk and by the very short, hesitating step. Founder affects the hind as well as the fore feet, although the front feet are more often exposed.

Treatment.—Cold packs to the feet, or if the animal can be made to stand in a stream of water, having a soft bottom, the inflammation is often relieved without the necessity of any additional treatment. It may be well, however, to give a full dose of Epsom salt, 1 to 1½ pounds, followed by half-ounce doses of saltpeter two or three times a day.

SORENESS (FOOT SORENESS).

Cattle that have been stabled or pastured on soft ground and are driven over stony roads soon wear down the soles of their feet and become lame from foot soreness. Draft oxen, for this reason, require to be shod. When the soreness is excessive it may develop into an active inflammation of all the sensitive structures of the foot—laminitis, or into a local bruise commonly called a "corn."

Treatment.—Rest, poulticing the feet with moistened clay, followed by astringent washes—strong white-oak bark or alum water.

If the pain and heat last several days, it is probable that pus has formed beneath the wall of the hoof. In this case it is necessary to cut through the wall, usually at the most prominent part of the sole, to allow the accumulation to drain out. The animal should then stand for several hours daily in a tub containing a 3 per cent solution of some good milky coal-tar disinfectant. When not in the disinfecting solution the foot should be dressed with pine tar and cotton and bandaged with bagging.

LOSS OF HOOF.

Cattle sometimes become fastened between planks or otherwise and pull off the wall of one or both claws in the effort to extricate themselves. The claws of one or more feet may be shed as the result of acute laminitis.

Treatment.—Wash the bleeding surface with an antiseptic and then with an astringent, such as a weak solution of alum, then apply a thick coating of pine tar; cover this with a layer of oakum or absorbent cotton; apply another coat of tar over this, and then bandage closely and firmly. This may remain without disturbance until the new growing wall becomes sufficiently strong to sustain the pressure and weight of the animal. If, however, at any time oozing or bad smell indicates that pus is forming under this dressing, the bandage should be removed and the suppurating surface freshly cleaned and dressed. This may have to be repeated every few days and should be continued so long as there is any pus formation. If the loss of hoof is owing to suppurative laminitis, the parts denuded of the horny covering must be thoroughly cleansed and disinfected with carbolic acid, lysol, or other antiseptic. Then apply a moderately thick layer of absorbent cotton and over this apply the tar and bandage. After this the antiseptic solution may be poured in daily at the top of the dressing. It will thus soak in and saturate the dressing and inflamed tissue. It may become necessary to remove all the dressing at daily or longer intervals to give the parts a fresh cleaning, and then to reapply it.

FOUL IN FOOT (FOOT ROT).

A variety of causes may produce inflammation of the foot between the claws or toes. It may be on account of overgrowth of the claws and inward pressure, as in ingrowing nail of man, or it may be caused by the irritation of stable filth by impaction and hardening of soil between the claws, or by other foreign substances becoming wedged in, causing inflammation and softening or ulceration of the skin in the interdigital space. Under some conditions several cattle in the same herd become affected, which has led some to think that the disease may be contagious. Occurrences have been reported in which foot rot of cattle has appeared within a short time among a large proportion of the cattle in a farming district. This disease is most frequently seen in the hind feet, though all four feet may become affected.

Symptoms.—The animal is observed to limp. On examination of the foot we discover heat and swelling above the hoof and of the soft parts between the claws which frequently spreads the claws apart to a considerable extent, or the inflammation may have advanced to softening and sloughing of the interdigital membrane. If the disease is neglected at this stage, deep abscesses may form and the pus burrow under the horny wall, or the joint within the hoof may become inflamed and the articular attachments destroyed, in which case the treatment will be difficult and recovery will be very tedious.

Treatment.—In the earlier stages of the disease, before pus burrows beneath the horn, a thorough cleansing and an application of a carbolic-acid solution—1 ounce to a pint of water—clean stabling, and laxative food will usually remedy the evil. Compound solution of cresol is an excellent remedy at this stage. It should be applied, in its pure or undiluted state, to the suppurating and putrefying tissue between the claws. It is best applied by means of a cotton swab on a thin stick. Care must be taken to keep it from contact with the skin about the coronary band or heels. If deep sloughing has taken place the carbolic solution should be used, and a wad of oakum or cotton smeared with pine tar should be secured firmly in the cleft. This can be done by taking a strip of strong cloth, 2 inches wide, passing the middle between the claws, then tying the ends after winding them in opposite directions above the hoof. Sometimes warm poulticing with flaxseed meal or bran is necessary to relieve excessive fever and pain. If the pus burrows under the horn, its channel must be followed by paring away the horn until the bottom is reached. The aftertreatment is the same as that already recommended. If the joint becomes diseased an amputation of that toe is the quickest and surest method to relieve the suffering of the animal, and offers the best chance for an early recovery.

ULCERATION OF THE HEEL.

Occasionally we find ulcers at the junction of the hair with the hoof at the heel, which present an elevated, raw, or ragged surface, and cause considerable lameness. This is generally caused by a bruise of the fibrous cushion of the back part of the foot. Subsequent sloughing or necrosis may occur, or pus may form deep within the wall and gain an exit at the margin of the heel. Sometimes, from no visible cause, large pieces of skin slough from the heel and pastern. This condition is caused by an infection with certain microorganisms (streptococci, necrosis bacilli) and may be contagious.

Treatment.—If there is a deep opening, inject carbolic solution once a day until it closes. If the ulcer is only superficial, wash with carbolic solution and apply a mixture of equal parts of blue vitriol and alum in dry powder.

FISSURE OF THE WALL (SPLIT HOOF).

This is rarely seen among cattle. It may occur in weak walls, in heavily bodied cattle, caused by stepping on an uneven surface, especially when the point of the toe is grown out long. One may find the point of the toe broken and the wall split almost up to the hair.

Treatment.—The divided sections may be brought into approximation and held in place by drilling a small hole from one side into and through the other, commencing half an inch back of the fissure on each side; then drive a light horseshoe nail through the hole and clinch it. Pare the injured claw as short as it will bear.

INTERDIGITAL FIBROMA.

Hard, nodular, fibrous tumors sometimes grow in the cleft of the foot, and cause inconvenience, lameness, absorption, or ulceration of the contiguous parts.

Treatment.—They should be dissected out and the wound dressed with carbolic-acid lotion and pine tar once a day until healing is completed.

DEFORMITIES.

Deformities in the feet of cattle usually consist in overgrowth of horn, generally from want of wear in animals which are stabled. The hoof may turn inward, outward, or upward, and may give rise to lameness, inability to walk, foul foot, etc. Bulls which are continually stabled and dairy cows very frequently have misshapen feet from want of an occasional trimming, and this deformity may eventually lead to permanent injury.

Treatment.—Cut the superabundant growth of horn down with saw, knife, or rasp, until the foot assumes its natural form.

PRICKS AND WOUNDS.

If an animal suffers with a penetrating wound from prick of fork or nail, the orifice of the wound should be enlarged to permit a free discharge of pus; then the foot should be soaked in a cresol compound solution (3 per cent) in a tub, or a flaxseed poultice applied, changing it three times a day until the fever has abated. The foot should be kept bandaged and dressed with pine tar and oakum; the animal must also be kept on a clean floor until the wound is closed and all or nearly all lameness has disappeared.

If an animal is cut in the foot with barbed wire, piece of glass, or any other substance, the wound, after proper cleansing, should be dressed with carbolic-acid solution, 1 ounce of the acid to 20 of water. If any uneven edges of horn, skin, or lacerated flesh project, trim them off, and in all cases when it can be done a tarred bandage should be applied. This will serve to sustain the cut surfaces in their place, exclude dirt, and protect against flies, maggots, etc.

When the wound has extended into a joint, surgical treatment, which will require the services of an educated veterinarian, may be necessary.

Occasionally an animal gets caught by the foot in a crevice and sustains severe bruising, wrenching, or fracture of some part of the foot. In such cases cold-water packs to the injured member are of service until the fever and swelling disappear. Afterwards the animal should rest until the usefulness of the foot is restored. Sometimes such an accident, causing fracture, renders necessary plaster bandages or amputation.

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DISEASES OF THE EYE AND ITS APPENDAGES.

By M. R. Trumbower, D. V. S.

[Revised by Leonard Pearson, B. S., V. M. D.]

DESCRIPTION.

For the sake of gaining a clear comprehension of the diseases of the eye it becomes necessary to review the anatomy of this important organ. The essential organ of vision, or globe of the eye, will be first described, then its receptacle or orbital cavity, the muscles that move it, the protective membranes, or eyelids, the membrana nictitans, or accessory eyelids, and, lastly, the lacrimal apparatus.

The globe or ball of the eye is almost spherical in form. On closer inspection, however, it appears to be made up of two combined portions from spheres of different sizes. The posterior portion, forming about five-sixths of the ball, is a sphere of comparatively large size with a small segment cut off it in front, and at this point there is applied to it the anterior portion, which, being a segment of a smaller sphere, projects at the front of the ball with a greater convexity than the posterior portion.

The eyeball consists of concentrically arranged coats and of refracting media inclosed in them. The coats are three in number, namely, (1) an external protective tunic made up of the sclerotic and cornea; (2) a middle vascular and pigmentary tunic, the choroid; (3) an internal nervous layer, the retina. The sclerotic is the white, opaque part of the outer tunic, of which it forms about the posterior five-sixths, being coextensive with the larger sphere already mentioned. The cornea forms the remaining one-sixth of the outer tunic, being coextensive with the segment of the smaller sphere. It is distinguished from the sclerotic by being colorless and transparent. The choroid coat will be recognized as the black layer lying subjacent to the sclerotic. It does not line the cornea, but terminates behind the line of junction of that coat with the sclerotic by a thickened edge—the ciliary processes. At the line of junction of the sclerotic and cornea the iris passes across the interior of the eye. This (which may be viewed as a dependency of the choroid) is a muscular curtain perforated by an aperture termed the pupil. The retina will be recognized as a delicate, glassy layer, lining the greater part of the choroid.

The refracting media of the eye are three in number, namely (1) the aqueous humor, a watery fluid inclosed in a chamber behind the cornea; (2) the crystalline lens and its capsule, a transparent, soft solid of a biconvex form, and placed behind the iris; (3) the vitreous humor, a transparent material with a consistence like thin jelly, and occupying as much of the interior of the eye as is subjacent to the choroid.

The sclerotic is a strong, opaque, fibrous membrane, which, in a great measure, maintains the form of the eyeball and protects the more delicate structures within it. Its interior portion, which is covered by the ocular conjunctiva, is commonly known as the "white of the eye." In form it is bell-shaped, and the optic nerve pierces it behind like a handle, the perforation being a little to its inner side. In front, the rim of the bell becomes continuous with the cornea. The outer surface of the membrane receives the insertion of the muscles of the eyeball. The coat is thickest over the posterior part of the eyeball, and is thinnest a little behind its junction with the cornea.

The cornea is the anterior transparent portion of the outer coat of the eyeball. It may be viewed as a part of the sclerotic specially modified to permit the passage of light into the interior of the eye. Its outline is elliptical, nearly circular, and its greatest diameter is transverse. At its periphery it joins the sclerotic by continuity of tissue, and as the edge of the cornea is slightly beveled and has the fibrous sclerotic carried for a little distance forward on its outward surface, the cornea is generally said to be fitted into the sclerotic like a watch glass into its rim. The venous canal of Schlemm runs circularly around the eyeball at the line of junction of the sclerotic and cornea. The anterior surface of the cornea is exquisitely smooth, and is kept moist by the lacrimal secretions. Its posterior surface forms the anterior boundary of the chamber in which the aqueous humor is contained. The cornea is of uniform thickness and is of a dense, almost horny, consistence. Save a few capillary loops of blood vessels at its margin the cornea is without vessels. Its structure is comprised of five distinct layers.

The aqueous humor occupies a chamber which is bounded in front by the posterior surface of the cornea and behind by the capsule and suspensory ligament of the lens and by the ends of the ciliary processes. It is across this chamber that the iris extends. The aqueous humor is composed of water, with a small proportion of common salt in solution.

The iris is a muscular, pigmented curtain extending across the interior of the eye and having about its center an aperture termed the pupil. By variations in the size of this aperture the amount of light transmitted to the retina is regulated. It varies somewhat in color, but is most frequently of a yellowish-brown tint. Its anterior face is bathed by the aqueous humor. The greater part of the posterior surface is in contact with the capsule of the lens and glides on it during the movements of the curtain. The circumferential border is attached within the junction of the sclerotic cornea. The inner border circumscribes the pupil, which varies in outline according to its size. When much contracted the pupil is a very elongated ellipse, the long axis of which is in the line joining the nasal and temporal angles of the eyelids. It contains muscular tissue, which, by contracting or relaxing, lessens or dilates the pupillary opening.

The choroid coat is a bell-shaped, dark membrane which lines the sclerotic. Its outer surface has a shaggy appearance, caused by the tunica fusca, which unites the two coats. Between the two the ciliary vessels and nerves pass forward. Behind it is pierced by the optic nerve; in front it is continued as the ciliary processes, which form, as it were, the rim of the bell. The ciliary processes form a fringe around the slightly inverted rim of the choroid.

The retina is the most delicate of the coats of the eyeball. It is formed by the expansion of the optic nerve on the inner surface of the choroid, and, like that coat, it is bell-shaped. Its inner surface is molded on the vitreous humor. The nervous structures of the retina terminate at a wavy line, the ora serrata, behind the ciliary processes. Ten distinct layers are described as composing the thickness of the retina.

The lens is situated behind the pupil and is contained within a capsule of its own.

The capsule is a close-fitting, firm, transparent membrane. The anterior surface forms the posterior boundary of the cavity containing the aqueous humor, and the iris in its movement glides on it. The posterior surface is in contact with the vitreous humor.

The vitreous humor occupies four-fifths of the interior of the eyeball. It is globular in form, with a depression in front for the lodgment of the lens. It is colorless, transparent, and of a consistency like thin jelly. It is enveloped by a delicate capsule—the hyaloid membrane—which is connected in front with the suspensory ligament of the lens, and ends by joining the capsule behind the lens.

The orbital cavity, at the side of the head, is circumscribed by a bony margin; posteriorly, however, there are no bony walls, and the cavity is often confounded with the depression above and behind the orbit—the temporal fossa. A fibrous membrane completes this cavity and keeps it distinct from the temporal fossa. This membrane—the ocular sheath or periorbita—is attached posteriorly around the opening in the back part of the orbital cavity (the orbital hiatus) and anteriorly to its inner face; then it becomes prolonged beyond the margin to form the fibrous membrane of the eyelids. When complete the orbital cavity has the form of a regular hollow cone, open at its base and closed at the apex. The opening of this cone is directed forward, downward, and outward. Independently of the globe of the eye, this cavity lodges the muscles that move it, the membrana nictitans, and the lacrimal gland.

The muscles of the eye are seven in number—one retractor, four straight, and two oblique. The retractor oculi envelops the optic nerve between the brain and the ball of the eye and becomes attached upon the external face of the sclerotic tunic. When this muscle contracts, it draws the globe back into the orbit, away from the light. The superior, inferior, external, and internal recti or straight muscles are attached to the back part of the orbital sheath and spread forward in four bundles over the globe of the eye, where they are inserted by a fibrous expansion into the sclerotic at the margin of the cornea. When they act singly, they turn the globe either upward, downward, inward, or outward. The great oblique, by its action, pivots the eye inward and upward in the orbit. The small oblique turns the eye outward and downward.

The eyelids are two movable curtains, superior and inferior, which cover and protect the eye in front. They are attached to the circumference of the orbit and have a convex external face formed by the skin and a concave internal face molded on the anterior surface of the eye and are lined by the conjunctiva, which is reflected above and below on the eyeball. The border of each lid is slightly beveled on the inner side and shows the openings of the Meibomian glands. These glands secrete an unctuous fluid, which is thrown out on the border of the lids, the function of which is to facilitate their movements and enable them to retain the tears in the ocular cavity. The eyelid is composed of a fibrous inner membrane ending in a stiff arch near the border, a muscle to close the lid, another to open it, the skin externally, and the conjunctival mucous membrane internally. The border of each lid is covered and protected by long hairs to prevent floating particles of matter in the atmosphere from gaining entrance to the eye.

The membrana nictitans, which is also named the third eyelid, winking eyelid, haw, etc., is placed at the inner angle of the eye, whence it extends over the eyeball to relieve it from foreign bodies which may fall upon it. It has for its framework a fibro-cartilage, irregular in shape, thick, nearly prismatic at its base, and thin anteriorly where it is covered by the conjunctiva; behind, it is loosely attached to a fatty cushion.

The lacrimal gland is situated between the orbital process and the upper part of the eyeball. It secretes the tears destined to lubricate the anterior surface of the eye. This fluid escapes upon the organ at the outer angle of the lids and is carried between them and the eyeball toward the inner angle.

The caruncula lacrimalis is a small round body, frequently entirely or partially black, situated in the inner angle of the eye, and is designed to direct the tears toward the puncta lacrimalia.

The puncta lacrimalia are two little openings, situated one in each eyelid, a short distance from the inner corner, which admit the tears into the lacrimal ducts leading to the lacrimal canal, whence they are emptied into the nasal passages.

CONJUNCTIVITIS (SIMPLE OPHTHALMIA).

This is an inflammation of the conjunctival mucous membrane of the eyeball and lids; in severe cases the deeper coats of the eye are involved, seriously complicating the attack.

Causes.—It may result from a bruise of the eyelid; from the introduction of foreign matters into the eye, as chaff, hayseed, dust, gnats, etc.; from exposure to cold; poisonous or irritating vapors arising from filthiness of stable. Dust, cinders, or sand blown into the eyes during transportation frequently cause conjunctivitis.

Symptoms.—A profuse flow of tears, closure of the eyelids from intolerance of light, retraction of the eyeball and corresponding protrusion of the haw, disinclination to move, diminution of milk secretion, etc. On parting the lids the lining membrane is found injected with an excess of blood, giving it a red and swollen appearance; the sclerotic, or white of the eye, is bloodshot and the cornea may be cloudy. If the disease advances, keratitis results, with its train of unfavorable symptoms.

Treatment.—Careful examination should be made to discover particles of chaff, etc., which may have lodged in the eye, and upon the discovery of such a cause prompt removal is indicated. This may be accomplished by flushing the eye with warm water by means of a syringe, or, if the foreign substance is adherent to the eyeball or lid, it may be scooped out with the handle of a teaspoon or some other blunt instrument. To relieve the congestion and local irritation, a wash composed of boracic acid in freshly boiled water, 20 grains to the ounce, or acetate of zinc, 5 grains to the ounce of pure soft water, may be used, to which may be added 20 drops of laudanum. A few drops of this should be placed in the eye with a camel's-hair pencil or soft feather three or four times daily. The animal should be placed in a cool, darkened stable; then a cloth folded into several thicknesses should be fastened to the horns in such manner as to reach below the eyes. This should be kept wet with cold water during the day and removed at night. If there is much fever and constitutional disturbance, it becomes advisable to administer 1 pound of Epsom salt dissolved in 1 quart of water.

INFECTIOUS CATARRHAL CONJUNCTIVITIS (SPECIFIC OPHTHALMIA).

This generally appears in an enzootic or epizootic form and affects a considerable number in the herd. It is distinctly a contagious disease and may be brought into a previously healthy herd by one infected animal. It may continue in a herd for a season or for several years, affecting all newly purchased animals. It is seldom seen in the winter months. It affects old and young animals alike.

Symptoms.—This form of catarrh conjunctivitis is characterized chiefly by a mucopurulent discharge from the eyes, an intense degree of inflammation of the mucous membrane, accompanied with swelling of the eyelids and an early opacity of the cornea. The flow of tears is mixed with pus, sometimes streaked with blood, and the skin of the face is kept moist and soiled. The eyes are kept continually closed. The implication of the cornea in the disease frequently blinds the animal for a time, and occasionally suppurative keratitis, ulcers of the cornea, or staphyloma supervene. The attack is marked from the onset by fever, partial loss of appetite, partial loss of milk, suspended rumination, and separation from the herd.

Treatment.—The animal should be housed in a cool, dark stable, supplied with plenty of fresh water to drink and soft, succulent feed. Administer 1 pound of Epsom salt—if a very large animal, use 1½ pounds—dissolved in 2 or 3 pints of water. For an eyewash, take boracic acid, 1 dram, and pour 4 ounces of boiling water over it. Use this as often as is convenient, applying it directly to the eye. In the majority of cases improvement becomes manifest in a few days, and the eye becomes clear and free from inflammation in 10 days or 2 weeks. Where the disease develops ulceration of the cornea, or well-marked, deep-seated keratitis, the treatment recommended for those conditions should be adopted.

Prevention.—Whenever this affection appears in a herd all the unaffected animals should be moved to fields which possess a different character of soil and feed. The water should also be changed, especially if they have been obtaining it from a stagnant pond.

KERATITIS (CORNEITIS).

This is an inflammation of the cornea proper, although the sclerotic at the corneal border becomes involved to some extent. It may be divided into diffuse and suppurative.

Causes.—The cornea constitutes the most prominent portion of the eyeball, hence it is subject to a variety of injuries—scratches, pricks, contusions, lacerations, etc. Inflammation of the cornea may also be due to the extension of catarrhal conjunctivitis or intraocular disease, and it may occasionally occur without any perceptible cause.

Symptoms.—Diffuse keratitis is characterized by an exudation into and an opacity of the cornea. The swelling of the anterior part of the eyeball may be of an irregular form, in points resembling small bladders, or it may commence at the periphery of the cornea by an abrupt thickening, which gradually diminishes as it approaches the center. If the whole cornea is affected, it has a uniform gray or grayish-white appearance. The flow of tears is not so marked as in conjunctivitis, nor is the suffering so acute, though both conditions often exist together. Both eyes usually become affected, unless it is caused by an external injury.

In favorable cases the exudate within the cornea begins to disappear within a week or 10 days, the eye becomes clearer and regains its transparency, until it eventually is fully restored. In unfavorable cases blood vessels form and are seen to traverse the affected part from periphery to center, vision becomes entirely lost, and permanent opacity (albugo or leucoma) remains. When it arises from constitutional causes recurrence is frequent, leaving the corneal membrane more cloudy after each attack, until the sight is permanently lost.

Suppurative keratitis may be a sequel of diffuse keratitis; more commonly, however, it abruptly becomes manifest by a raised swelling on or near the center of the cornea that very soon assumes a yellow, turbid color, while the periphery of the swelling fades into an opaque ring. Suppurative keratitis is seldom noticed for the first day or two—not until distinct pus formation has occurred. When it is the result of diffuse keratitis, ulceration and the escape of the contained pus is inevitable; otherwise the pus may be absorbed. When the deeper membranes covering the anterior chamber of the eye become involved, the contents of this chamber may be evacuated and the sight permanently lost.

Treatment.—Place the animal in a darkened stable, give green or sloppy feed, and administer 4 ounces of Glauber's salt (sulphate of soda) dissolved in a quart of water once a day. If the animal is debilitated a tablespoonful of tonic powder should be mixed with the feed three times a day. This may be composed of equal parts by weight of powdered copperas (sulphate of iron), gentian, and ginger. As an application for the eye, nitrate of silver, 3 grains to the ounce of soft water, with the addition of 1 grain sulphate of morphia, may be used several times a day. If ulceration occurs, it is well to dust powdered calomel into the eye twice daily, or apply to the eyelids a salve of yellow oxid of mercury, 5 per cent in lanolin. Some of this may go on to the cornea and beneath the lids. Apply twice daily. (See "Ulcers of the cornea.")

To remove opacity, after the inflammation has subsided, apply a few drops of the following solution twice a day: Iodid of potassium, 15 grains; tincture sanguinaria, 20 drops; distilled water, 2 ounces; mix.

Sometimes keratitis exists in a herd as a transmissible disease, spreading like infectious conjunctivitis. Calomel, applied to the eye, is especially useful in such cases.

ULCERS OF THE CORNEA.

An ulcer comes from erosion or is the consequence of the bursting of a small abscess, which may have formed beneath the delicate layer of the conjunctiva, continued over the cornea; or, in the very substance of the cornea itself, after violent keratitis, or catarrhal conjunctivitis. At other times it is produced by bruises, scratches, or other direct injury of the cornea.

Symptoms.—The ulcer is generally at first of a pale gray color, with its edges high and irregular, discharges instead of pus an acrid, watery substance, and has a tendency to spread widely and deeply. If it spreads superficially upon the cornea, the transparency of this membrane is lost; if it proceeds deeply and penetrates the anterior chamber of the aqueous humor, this fluid escapes, the iris may prolapse, and the lens and the vitreous humor become expelled, thus producing destruction of the whole organ.

Treatment.—It is of the greatest importance, as soon as an ulcer appears upon the cornea, to prevent its growing larger. The corroding process must be converted into a healthy one. For this purpose nothing is more reliable than the use of solid nitrate of silver. A stick of this medicine should be scraped to a point; the animal's head should be firmly secured; an assistant should part the lids; if necessary, the haw must be secured within the corner of the eye and then all parts of the ulcer should be lightly touched with the silver. After waiting a few minutes the eye should be thoroughly washed out with a very weak solution of common salt. This operation generally has to be repeated at the end of three or four days. If healthy action succeeds, the ulcer assumes a delicate fleshy tint, and the former redness around the ulcer disappears in proportion as the ulcer heals.

In superficial abrasions of the cornea, where there is no distinct excavation, this caustic treatment is not needed. The eye should be bathed several times a day with sulphate of zinc, 30 grains to half a pint of soft water, and protected against exposure to cold air and sunlight. Excessive ulceration sometimes assumes the form of fungous excrescence upon the cornea, appearing to derive its nourishment from loops of blood vessels of the conjunctiva. Under these circumstances the fungoid mass must be cut away and the wound cauterized with the nitrate of silver, or else the eye will soon be destroyed. When ulcers of the cornea appear indolent, with a tendency to slough, in addition to the treatment already prescribed, tonic powders of copperas, gentian, and ginger, equal parts by weight, should be given twice a day, mixed with the feed; dose, one tablespoonful.

STAPHYLOMA.

This is a disease of the eyeball, in which the cornea loses its transparency, rises above the level of the eye, and even projects beyond the eyelids in the form of an elongated, whitish, or pearl-colored tumor, which is sometimes smooth, at other times uneven.

Causes.—Inflammation is the only known cause, although it may not occur immediately; it frequently follows catarrhal conjunctivitis and keratitis as a sequela.

Treatment.—In a few cases restoration of sight may be effected by puncturing the projecting tumor and treating it afterwards with nitrate of silver in the same manner as prescribed for ulceration of the cornea. In some cases spontaneous rupture has occurred, and healing without any treatment at all.

CATARACT.

In cataract the crystalline lens becomes opaque and loses its transparency, the power of refraction is lost—the animal can not see.

Causes.—Cataract generally arises from a diminution (atrophy) or other change in the nutrition of the lens; it may occur as a result of inflammation of the deep structures of the eye. Cataract may be simple, or complicated with amaurosis, adhesions, etc.

Symptoms.—It is known by the whiteness or loss of transparency of the lens, although the pupil dilates and contracts. Sight may be totally lost; however, evidence is usually manifested that the animal distinguishes light when brought out of a darkened stable. For the most part the formation of cataract takes place slowly, the cases in which it originates very quickly being but few.

Treatment.—There is only one method for the treatment of cataract—a surgical operation for the removal of the lens; but this is not advisable, for the sight can not be perfectly restored, and objects would be seen imperfectly without the aid of glasses.

AMAUROSIS.

This is a paralysis of the nerve of sight or the expansion of the retina.

Causes.—This is the result of concussion from a blow upon the forehead, fracture of bone over the eye (causing downward pressure), rheumatic inflammation of the optic nerve, or from extension of deep inflammation of the eye involving the retina. It sometimes occurs as the result of excessive loss of blood or of great debility.

Symptoms.—In this disease observation is seldom made until the animal in its gait and by its action indicates blindness. Generally both eyes are affected. The eyeball remains clear, and the pupil is permanently dilated. No response to light is manifested.

Treatment.—If caused by debility, loss of blood, or associated with rheumatism, general blood tonics may be given in the feed, namely, powdered sulphate of iron, 1 dram; gentian, 2 drams; nux vomica, one-half dram; to be given twice a day. In cases of rheumatism, one-half ounce of saltpeter may be added.

FILARIA OCULI (WORM IN THE EYE).

Filaria oculi (provisionally taken as the larva of F. cervina) is a small white worm, found swimming in the aqueous fluid in the anterior chamber. It may be apparently harmless for a long time, but will eventually induce keratitis with inflammatory exudations.

Treatment.—The cornea may be punctured at its upper and outer margin, and the worm squeezed out with the aqueous humor. The latter will be formed again. This operation results disastrously unless the greatest care and skill are employed.

CORNEAL DERMATOMA (HAIRY TUMOR ON THE EYEBALL).

In a few instances this has been seen as a congenital growth. The tumor arises from the cornea or the sclerotic, covered by its respective membrane, with a growth of hair upon its surface. These tumors may be quite prominent or flattened, and are dark in color; the hair may protrude between the eyelids, giving the animal the appearance of having a double eyelid.

Treatment.—A surgical operation becomes necessary for their removal— one requiring a skilled operator.

STRABISMUS (SQUINTING).

This is a very rare affection among cattle. Strabismus may be either single or double—affecting one eye or both. It is caused by a paralysis, or a weakening of one of the straight muscles of the eyeball. Generally it is a congenital defect, and the squinting is toward the nose—strabismus convergens. It is best not to attempt to remedy the defect, as the risk in an operation is greater than the chances of success warrant.

PTERYGIUM.

This term is applied to a flesh-colored membrane, triangular in form, which most frequently grows from the inner angle of the eye and extends over the cornea, thus interfering with vision. It may grow from the outer angle, or even from either the superior or inferior hemisphere of the eyeball. The figure is invariably that of a triangle, with its base on the white of the eye and its apex more or less advanced over the cornea toward its center.

The distinguishing characteristics are the constancy of the triangular form, and the facility with which the whole of it may be taken hold of with a pair of forceps and raised into a fold on the cornea. Every other kind of excrescence attached to this membrane continues firmly adherent to it, and can not be folded and raised from the surface of the cornea in any manner whatever.

Treatment.—Raise the fold and dissect it away from all points of attachment.

TRICHIASIS (INVERSION OF THE EYELASHES).

In the simplest form the eyelashes bend inwardly, touching the eyeball, causing irritation and simple conjunctivitis. It may be also associated with entropion.

Treatment.—The offending eyelashes should be cut off or pulled out. In case the natural growth of the eyelashes is directed inward, an operation similar to that for entropion becomes necessary.

ENTROPION (INVERSION OF THE EYELID).

In inversion of the eyelid the eyelashes soon irritate the anterior face of the cornea and produce more or less inflammation and opacity. The inversion may be due to the growth of a tumor within or without the lid, to abscess, laceration, or injury, causing the lid to lose its natural conformity to the eyeball, ulcerations, etc. Surgical interference in either case becomes necessary to restore the lid to its natural direction.

ECTROPION (EVERSION OF THE EYELID).

This serves to injure the eye by permitting dust or other foreign substances to enter the eye and interferes with the natural removal of them.

Treatment.—A delicate surgical operation—the removal of an elliptic section of the palpæbral conjunctiva—may remedy the defect.

TUMORS OF THE EYELIDS.

Occasionally tumors form upon or within the substance of the eyelid. They may be of a fibroid nature and arise from the follicles of the hair as sebaceous tumors or may be in the form of an abscess. In debilitating diseases the lids sometimes become swollen and puffy, a condition which may possibly be taken for the growth of a tumor. This generally disappears with the improvement of the health of the animal. Warts not uncommonly appear on or about the eyelids of cattle.

Treatment.—The removal of a tumor in the vicinity of so delicate an organ as the eye should not be attempted by anyone not qualified to perform the operation.

LACERATION OF THE EYELID.

This accident is not uncommon where cattle are fenced in by barbed wire; an animal may be caught under the eyelid by the horn of another, or the laceration may occur in the stable by means of a projecting nail or splinter of wood.

Treatment.—The edges of the wound should be brought together closely and correctly, by means of pins pushed through very nearly the whole thickness of the lid, extending through each lip of the torn part; then a waxed silk or linen thread must be wound over each end of the pin, crossing the torn line in the form of the figure 8 ([Pl. XXVII], fig. 9); the pins should be placed about three-eighths of an inch apart. The projecting ends of the pins should be cut off close to the ligature, and the parts kept anointed with vaseline, to which 2 per cent of compound cresol has been added. In place of a pin suture, silver wire, catgut, or strong linen thread may be used in the way of an ordinary suture.

FOREIGN BODIES IN THE EYE.

Splinters of wood, hedge thorns, pieces of cornstalk or leaves, stems of hay or straw, twigs of trees, or weeds may penetrate into the eye, break off, and remain, causing inflammation, blindness, abscess, etc. These substances may penetrate the eyeball, but more frequently they glide off and enter between the eye and the ocular sheath.

Treatment.—Their removal becomes often a very difficult task, from the fact that the organ is so extremely sensitive, and the retracting power so strong as to necessitate casting the animal, or even the administration of sufficient chloroform to render it completely insensible. The removal, however, is of paramount importance, and the after treatment depends upon the extent and location of the injury—cold water compress over the injured eye, the application of mild astringent and cooling washes, such as acetate or sulphate of zinc, 5 grains to the ounce of water. When there is extreme suffering from pain a solution of atropia or morphia, 5 grains to the ounce of water, may be dropped into the eye, alternating with the cooling wash several times a day. When abscesses form within the orbit a free opening must be maintained for the discharge of pus. In deep penetrating wounds of the eye there is a great tendency to the formation of a fungous growth, which often necessitates the enucleation of the whole eyeball.

ORBITAL AND PERIORBITAL ABSCESS.

Orbital abscess may form outside the globe and within the orbital sheath, as the result of a previous wound of the parts or from fracture of the bony orbit, etc. Periorbital abscess commences outside the ocular sheath, beneath the periosteal membrane covering the bone, and is usually the result of a disease or fractured bone which enters into the formation of the orbital cavity.

Symptoms.—Orbital abscess is manifested by a pushing forward of the eyeball (exophthalmos), a swelling of the conjunctiva and eyelids. The bulging out of the eye is in proportion to the size of the abscess; the movement of the eye is fixed, due to the painfulness of any voluntary movement of the eyeball. Periorbital abscess generally pushes the eye to one side; otherwise the symptoms are similar to the foregoing. The pain generally is very great; paralysis of the nerve of sight may occur, and death may be caused by the abscess extending to the brain.

Treatment.—The treatment for either orbital or periorbital abscess is the same as that for abscess occurring in any other part of the body—a free opening for the escape of imprisoned pus. This should be made as soon as the true nature of the disease is recognized. Afterwards antiseptic injections may be needed to stimulate healthy granulation and to prevent septic infection of the ocular membranes. For this purpose a saturated solution of boric acid or listerine 1 part to 10 of water may be used. When the fever runs high, Glauber's salt (sulphate of soda) may be given in 4-ounce doses once a day. The animal should be kept in a darkened stable, on soft or green feed.

FRACTURE OF THE ORBIT.

This accident occasionally occurs among belligerent animals, or as the result of blows delivered by brutal attendants. The orbital process above the eye may be entirely crushed in, pressing down upon the eyeball. In such an event the depressed bone should be elevated into its proper place, and if it fails to unite it may have to be removed with saw or chisel. The margin of the orbit may be crushed at any point and cause periorbital abscess, or necrosis may result from the presence of a splinter of bone or the excessive destruction of bone. In all cases of fracture the animal should be kept by itself until the injured part heals.

NECROSIS OF THE BONY ORBIT.

As the result of fracture of the margin of the orbit a part of the injured bone may become necrosed (dead), and periostitis and periorbital abscess will follow as a consequence. The discovery of this disease will at first resemble abscess, but on making an examination with a probe after the abscess is open we find the bone rough and brittle at the point of disease. The discharge has a peculiar fetid odor, and is often mixed with blood.

Treatment.—The affected bone must be laid bare and all diseased portions removed by scraping or, if necessary, with saw or chisel, disregarding the extent of the injury or the size of the wound necessary to be inflicted. A large portion of the bony orbit may be removed without serious danger to the eye, provided the eyeball itself has not been previously affected by the disease or involved in the original injury.

TUMORS OF THE ORBIT.

A fungous tumor of the eyeball or orbit occasionally appears, which is designated fungus hæmatodes. This may arise without any appreciable cause, or as the result of a wound. It frequently commences within the eyeball as a small, red mass, eventually bursts through, and pushes its way outside the orbit as a large, dark-red mass, bleeding at the slightest touch. It has a peculiar, fetid odor, and early in its appearance destroys sight, involving all the contents of the orbit, not infrequently the bony wall itself.

Unless the tumor is totally removed in its early stage of growth, together with the eyeball, the disease will eventually cause emaciation and death of the animal. The enucleation of the eyeball should not be undertaken by anyone unacquainted with the anatomical structures involved in such an operation. When the operation is performed early enough the result is generally satisfactory.

Bony tumors of the orbit, the result of bruises, fractures, etc., are occasionally present in cattle. They may encroach upon the contents of the orbit, causing paralysis of the optic nerve—the condition known as amaurosis—or by pressure upon the posterior surface of the eyeball force it forward, or produce atrophy (shrinking). They may displace the eye in any direction, with or without disturbing vision.

Fibrous tumors growing within the orbit will produce symptoms similar to those of bony tumors.

Treatment.—When the outlines of the tumor, whether fungoid, bony, or fibrous, can be detected, an operation for its removal should be undertaken as soon as the sight of the eye is in any manner disturbed.

DISLOCATION OF THE EYEBALL.

The eyeball may be torn out of its socket by the horns of another animal, or it may be crowded out with the blunt end of a club, cane, or probe in the hands of a brutal attendant.

Treatment.—When the optic nerve is not lacerated and the retractor muscles at the back of the eye are intact, an attempt at reduction is advisable. This, however, must follow very soon after the injury—before swelling takes place. Divide the outer corner of the eyelid to enlarge the orifice, then by pressure with the fingers of both hands placed upon the sides of the eye the ball may be put into its place. Apply a firm compress over the injured eye and keep it constantly wet with cold water containing 1 dram of sugar of lead to each quart.

If the attempt at reduction proves unsuccessful the artery at the back of the eye should be ligated, and then the whole mass cut off as deep within the orbit as possible. The orbital cavity, after washing it out with a 3 per cent solution of carbolic acid or compound cresol, should be packed daily with fresh absorbent cotton.

INFLAMMATION AND ENLARGEMENT OF THE HAW.

The haw, or membrana nictitans, is subject to inflammation and swelling from the extension of conjunctivitis, or direct injury by foreign substances. It presents a red, swollen appearance, accompanied with considerable pain and a profuse flow of tears. A slight scarification with a sharp knife and the application of a cooling lotion, such as is recommended for conjunctivitis, will soon reduce the swelling and restore it to its normal function.

There is, however, a tendency for an inflammation of this membrane to take on a chronic character, which may eventually result in a permanent enlargement, resembling a tumor. When it attains sufficient size to protrude itself permanently over the eye, or project between the lids so as to obstruct the sight, its removal may become necessary. A threaded needle is passed through the body of the enlarged mass, by which the membrane is drawn out as far as possible, then with a blunt pair of scissors it may be dissected away from its attachments. The eye is afterwards treated with simple cooling lotions.

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DISEASES OF THE EAR.

By M. R. Trumbower, D. V. S.

[Revised by Leonard Pearson, B. S., V. M. D.]

Diseases of the ears of cattle are not very common, for the reasons probably that they are not subjected to the brutality of drivers so much as horses and that the horns to a great extent protect them against external violence.

OTITIS (INFLAMMATION OF THE INTERNAL EAR).

Inflammation of the deep part of the ear is often difficult to recognize in cattle. It may be caused by disease of bone in that region, from blows inflicted by drivers, or from injury by other cattle. Occasionally the ear becomes involved in actinomycosis (lumpy jaw), or the inflammation may be the result of a tuberculous affection.

Symptoms.—The animal will hold its head to one side, or shake it, while the ear itself is held immovable. The movement of the jaws in eating usually gives rise to a manifestation of pain; the base of the ear may be feverish and swollen, and very sensitive to the touch. If the inflammation has advanced to a suppurative stage, offensive matter will flow from the ear.

Treatment.—At first, hot fomentations to reduce pain and fever, followed by a sharp blister below the ear. Laudanum, 1 part to 10 of sweet oil, may be injected into the ear to relieve pain and to soften the secretions. If there is a discharge from the ear, it should be thoroughly washed out by injecting warm soapsuds until all the matter has been washed away; then inject the following mixture twice a day: Sulphate of morphia, 20 grains; water, 1 pint; glycerin, 4 ounces.

ABSCESS.

Abscesses, caused by contusions, sometimes form about the base of the ear, either inside or outside. A serous cyst is found occasionally between the cartilage and the skin on the base of the ear, which may be from a similar cause.

Treatment.—With the knife make a free incision into the most prominent part of the abscess or cyst, then, with a syringe, wash out the sac with carbolized water. If the abscess recurs, open it again, wash it out, and inject tincture of iodin, or fill it with iodoform.

FUNGOID GROWTHS.

As a result of laceration or wound of any kind, fungous growths, characterized by a raw, bleeding, granulating surface, with a tendency to become pendulous, may develop on the ear.

Treatment.—The whole tumor or diseased structure should be cut away, and the wound treated daily with a dressing of carbolized cosmoline or turpentine and sweet oil, 1 part of the former to 4 of the latter.

FOREIGN BODIES IN THE EAR.

Bugs have been known to gain entrance into the ears of animals. I once removed an acorn from the ear of a cow that had been roaming in the woods; also pieces of wood from a stanchion may be lodged accidentally in the ear.

Symptoms.—There is usually a continuous uneasiness or frequent shaking of the head, occasionally the manifestation of exceedingly great pain. The animal may rub the head and ear against trees or other objects in an endeavor to dislodge the offending body.

Treatment.—A careful examination reveals the cause, which may be removed with a pair of forceps or scraped out with a hairpin or piece of wire bent at one end. If much inflammation exists, the ear may be swollen so that the foreign substance is hidden from sight; then a probe may be inserted to feel for the object, which, when found, should be removed, even if it becomes necessary to split the ear at the base. Afterwards treat the ear with frequent warm water fomentations and the injection of soapy water or oil and water.

SCURFY EARS.

Cattle are subject to scurfy ears, which may be owing to a generally morbid condition of the skin, or may be confined to the ears alone. The affected animal shows an inclination to rub the ear; thick scales, which sometimes have the appearance of hard, dry, horny scales, of scurf collect on it. This condition is chiefly caused by a faulty secretion of the sebaceous glands of the ear. Thoroughly clean the ear with a stiff brush, then anoint it, so far as affected, with vaseline 4 parts to 1 part of white precipitate ointment. If the scurfy ears are only a part of a general scurfiness of the skin, the condition of the animal needs attention. (See "Pityriasis," [p. 329].)

FROSTBITE.

It is not uncommon among young cattle which are poorly nourished and exposed outdoors to storms and extreme cold to suffer frostbite of the ear, which may constitute actual freezing of the part.

Symptoms.—Frostbite presents naturally every degree of severity from the mere chilling of the tip of the ear to positive freezing and death of a portion. In a day or two after the freezing has occurred the ear becomes swollen and very painful; the dead part remains cold and begins to shrivel; a line of separation then forms between the inflamed and the dead or dying portion, and finally the piece destroyed drops off, leaving a raw healing surface. When the ear is only slightly affected by the cold, an excoriation or peeling off of superficial skin takes place, accompanied with some pain and itching.

Treatment.—A good liniment for frozen ears is a mixture of turpentine, ammonia, and chloroform, of each 1 part, added to 6 parts of sweet oil. Rub this on the ear several times a day. It will relieve pain and stimulate the circulation, thus favoring a recovery of the injured structures.

LACERATIONS OF THE EAR.

Aggressive dogs are the most frequent cause of lacerated ear, generally leaving a torn, ragged edge and bruised cartilage.

If the wound is extensive, a trimming of the ragged edges becomes necessary; then the edges should be fastened together with silver wire, catgut, or strong, thick, linen thread, taking a deep hold, and pine tar applied.

DISEASE OF THE CARTILAGE AND NECROSIS.

Occasionally the cartilages of the ear become affected, usually the result of a deep bruise; pus forms, burrows under the skin, and may find a discharge from any part of the ear more or less distant from the seat of the disease. When the cartilage has been extensively injured, pieces of it may become dead (necrosed) and dissolve, to be carried away with the pus, or it may lead to extensive sloughing and the formation of numerous running sores. In the disease of the cartilage there is seldom much swelling or great pain. The discharge is usually very offensive, and occasionally streaked with blood. Whenever there is a long-continued, persistent discharge from one or more openings in the ear, disease of the cartilage may be suspected.

Treatment.—The sinus formed by the passage of matter should be probed and searched to the bottom for the presence of a foreign substance or the evidence of decaying cartilage. When the probe touches necrosed cartilage it will feel like a piece of dry leather or partially softened wood. A counter opening must then be made at this place, and all diseased cartilage cut away with the knife. The subsequent treatment consists in keeping the artificial wound open for the discharge of pus, and the injection of chlorid of zinc, 5 grains to the ounce of water, once or twice a day, until the wound is healed.

ENCHONDROMA OF THE EAR.

This is an excessive growth of cartilage, found at the base of the ear in the form of a hard, painless tumor, firmly attached to the movable ear. The only recourse for its removal is the knife in the hands of one acquainted with the anatomy of the part involved in the operation.

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INFECTIOUS DISEASES OF CATTLE.

Revised by John R. Mohler, A. M., V. M. D.,

Chief, Bureau of Animal Industry.

GENERAL INTRODUCTION.

The importance, to the farmer and stock raiser, of a general knowledge of the nature of infectious diseases need not be insisted on, as it must be evident to all who have charge of farm animals. The growing facilities for intercourse between one section of a country and another, and between different countries, cause a wide distribution of the infectious diseases once restricted to a definite locality. Not only the animals themselves, but the cars, vessels, or other conveyances in which they are carried may become agents for the dissemination of disease. The growing tendency of specialization in agriculture, which leads to the maintenance of large herds of cattle, sheep, and hogs, makes infectious diseases more common and more dangerous. Fresh animals are being continually introduced which may be the carriers of disease from other herds, and when disease is once brought into a large herd the losses become very high, because it is difficult, if not impossible, to check it after it has once obtained a foothold.

These considerations make it plain that only by the most careful supervision by intelligent men who understand the nature of infectious diseases and their causes in a general way can these be kept away. We must likewise consider how incomplete our knowledge concerning many diseases is, and probably will be for some time to come. The suggestions and recommendations offered by investigators, therefore, may not always be correct, and may require frequent modification as our information grows more comprehensive and exact.

An infectious disease may be defined as any malady caused by the introduction, into the body, of minute organisms of a vegetable or animal nature which have the power of indefinite multiplication and of setting free certain peculiar poisons which are chiefly responsible for the morbid changes.

This definition might include diseases caused by certain animal parasites, such as trichinæ, for example, which multiply in the digestive tract, but whose progeny is limited to a single generation. By common consent the term "infectious" is restricted to those diseases caused by the invasion and multiplication of certain very minute unicellular organisms included under the general classes of bacteria and protozoa. Nearly all the diseases of cattle for which a definite cause has been traced are from bacteria. Among these are tuberculosis, anthrax, blackleg, and tetanus (or lockjaw). Some diseases, such as Texas fever and nagana, are traceable to protozoa, while others, like vactinomycosis and aspergillosis, are caused by fungi. Those diseases of which the cause is unknown or imperfectly worked out are pleuropneumonia, rinderpest, foot-and-mouth disease, rabies, cowpox, malignant catarrh, and dysentery.

Bacteria may be defined as very minute, unicellular organisms of a plantlike character. Their form is very simple, as may be seen from an inspection of the various species depicted on [Plate XXVIII]. The description of these figures will be found on [page 360]. The magnification there given will furnish the reader some idea of their very minute size. They multiply in two ways. The bacterium elongates and then divides in the middle to form 2 daughter cells. These go through the same process at once, and thus 4 cells are produced. The division of these leads to 8, the division of 8 to 16, and so on indefinitely. The rapidity with which this multiplication takes place depends upon the nature of the bacterium. The bacillus of tuberculosis multiplies very slowly, while that of anthrax does so with great rapidity, provided both are in the most favorable condition. Another mode of reproduction, limited to certain classes of bacteria, consists in the formation of a spore within the body of the bacterium. Spore formation usually takes place when the conditions pertaining to the growth of the bacteria become unfavorable. The spores are much more resistant to destructive agents than the bacteria which produced them. The anthrax spore may live several years in a dried state, but the anthrax bacillus perishes in a few days under like conditions. This matter will be referred to again when we come to discuss the subject of disinfection.

Of the protozoa which cause disease very little is at present known. One which produces Texas fever is pictured on [Plate XLV], in figs. 4 and 5. These parasites have a more complex life history than bacteria; and as they can not be grown in artificial media, their thorough investigation is at present hampered with great difficulties.

The differences in the symptoms and lesions of the various infectious diseases are due to differences in the respective organisms causing them. Similarly the great differences observed in the sources from which animals become infected and the manner in which infection takes place are due to differences in the life history of these minute organisms. Much discussion has taken place of late years concerning the precise meaning of the words "infection" and "contagion."

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VARIOUS BACTERIA WHICH PRODUCE DISEASE IN CATTLE.

DESCRIPTION OF PLATE XXVIII.

The bacteria on this plate are partly from tissues, partly from cultures, and stained artificially with aniline colors (fuchsin or methylene blue). Figs 6 and 7 are copied from Fränkel and Pfeiffer's atlas. All but fig. 7 are magnified 1,000 times; fig. 7, 500 times.

Fig. 1. Bacteria from pneumonia in cattle. These are also the cause of hemorrhagic septicemia and are closely related to swine-plague bacteria. These bacteria were drawn from a piece of spleen pulp (rabbit).

Fig. 2. Micrococci (streptococcus) which produce inflammation of the lining membranes of the abdomen, thorax, heart, brain, and joints. Frequently associated with the preceding bacteria in abscesses.

Fig. 3. Micrococci (staphylococcus) which produce inflammation and suppuration; also pyemia.

Fig. 4. Bacilli of blackleg. The pale oval bodies as well as the light spots in one end of the bacilli represent spores.

Fig. 5. Bacilli which produce tetanus or lockjaw. The light spot in the enlarged end of each rod represents a spore.

Fig. 6. Bacilli of tuberculosis. Microscopic sections of a pearly nodule from the lining membrane of the chest cavity. The bacilli are stained red and appear as small straight rods within the cells of the nodule or tubercle.

Fig. 7. Bacilli of anthrax. Bacilli from the spleen of a mouse inoculated with a culture. The bacilli were obtained from the blood of a cow which died of anthrax in Mississippi. The bacilli appear as rods stained blue. The round bodies are blood corpuscles, also stained artificially.

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These words, however, are now wholly inadequate to express the complex processes of infection, and it may be said that each species of bacterium or protozoon has its own peculiar way of invading the animal body, differing more or less from all the rest. There are, however, a few broad distinctions which may be expressed with the help of these old terms. Infection, as laid down above, refers at present in a comprehensive way to all microorganisms capable of setting up disease in the body. Some microorganisms are transmitted directly from one animal to another, and the diseases produced may be called contagious. Among these are included pleuropneumonia, rinderpest, foot-and-mouth disease, rabies, cowpox, and tuberculosis. Again, certain organisms are perhaps never transmitted from one animal to another, but may come from the soil. Among these are tetanus, blackleg, anthrax to a large extent, and perhaps actinomycosis in part. These diseases, according to some authorities, may be called miasmatic. There is a third class of infectious diseases, the specific bacteria of which are transmitted from one animal to another, as with the contagious diseases, but the bacteria may, under certain favorable conditions, find food enough in the soil and in the surroundings of animals to multiply to some extent after they have left the sick animal and before they gain entrance into a healthy one.

This general classification is subject to change if we take other characteristics into consideration. Thus tuberculosis, because of its insidious beginning and slow course, would not by many be considered contagious in the sense that foot-and-mouth disease is; yet, in either case, the bacillus must come from preexisting disease. The disease of rabies, or hydrophobia, is not contagious in the sense that rinderpest is, because the virus of rabies must be inoculated into a wound before it can take effect; yet, in both cases, the virus passes without modification from one animal to another, though in different ways.

Again, all the diseases under the second group, which seem to come from the soil and from pastures, are in one sense contagious in that the virus may be taken from a sick animal and inoculated directly, with positive results, into a healthy animal. Other illustrations may be cited which show that these old terms are not in themselves satisfactory. There are so many conditions which enter into the process of infection that no single classification will give a sufficiently correct or comprehensive idea of it. These statements will be easily understood if the different infectious diseases in the following pages are studied with reference to the way or ways in which each disease may be contracted. Enough has been said, therefore, to show that if we wish to make ourselves acquainted with the dangers of any given disease, we must study it and not rely upon any single work to tell the whole story.

Infectious diseases have, as a general rule, a period of incubation, which comprises the time elapsing between the exposure to the infection and the actual appearance of the disease. This period varies with the malady. The most common symptom of this class of diseases is fever. The severity of the fever is measured by the temperature of the animal; this is readily and accurately ascertainable by the clinical thermometer. (See [Pl. III], fig. 1.) The other symptoms are variable and depend upon the particular organ or organs most implicated. Loss of appetite, cessation of rumination and milk secretion, and general dullness are symptoms quite invariably present in most infectious diseases.

During the course of infectious diseases secondary diseases or complications may arise which are largely caused by bacteria other than those producing the original malady. These complications are often so severe as to become fatal. In general it may be stated that they are due to filthy surroundings, and hence cleanliness may become an important aid to recovery.

The treatment of infectious diseases is given under each malady so far as this is allowable or advisable. These diseases are not, as a rule, amenable to treatment. When the symptoms have once appeared the disease is liable to run its course in spite of treatment, and if it is one from which animals usually recover, all that can be done is to put them into the most favorable surroundings. Many infectious diseases lead sooner or later to death, treatment is useless so far as the sick are concerned, and it may be worse than useless for those not yet infected. All animals suffering with infectious diseases are more or less directly a menace to all others. They represent for the time being manufactories of disease germs, and they are giving them off more or less abundantly during the period of disease. They may infect others directly or they may scatter the virus about, and the surroundings may become a future source of infection for healthy animals. This leads us to the subject of prevention as the most important of all which claim our attention. In this place only a few general remarks will suffice to bring the subject before the reader.

The most important thing is to keep disease away from a herd or farm. To do this all sick or suspicious animals should be avoided. A grave form of disease may be introduced by apparently mild or trivial cases brought in from without. It is generally conceded that continual change and movement of animals are the most potent means by which infectious diseases are disseminated.

With some cattle diseases, such as anthrax, rinderpest, and pleuropneumonia, preventive inoculation is resorted to in some countries. This may be desirable when certain diseases have become established in any locality so that eradication is impossible. It should not be practiced in territories where a given disease may still be extirpated by ordinary precautions. Preventive inoculation is applicable to only a few maladies, and therefore its aid in the control of diseases is limited.

When an infectious disease has gained foothold in a herd the course to be pursued will depend upon the nature of the malady. A good rule is to kill diseased animals, especially when the disease is liable to run a chronic course, as in tuberculosis. The next important step is to separate the well from the sick by placing the former on fresh ground. This is rarely possible; hence the destruction or removal of the sick, with thorough disinfection of the infected locality, is the next thing to be done. As to the disinfectants to be used, special directions are given under the various diseases, to which the reader is referred. Here we will simply call attention briefly to the general subject.

DISINFECTION AND DISINFECTANTS.

Disinfection consists in the use of certain substances which possess the power to destroy bacteria or their spores, or both. Those which are cheapest and most available for animal diseases are ordinary freshly slaked lime or unslaked in powder, chlorid of lime, crude carbolic acid, corrosive sublimate, formaldehyde gas, formalin, and compound cresol solution.

(1) Slaked lime is perhaps the most easily procured, but its disinfecting power is limited. While it is capable of destroying all bacteria in their vegetative state, it is unable to destroy such spores as those of anthrax and blackleg. It is probable, however, that in incrusting spores it may destroy their vitality sooner or later. It is regarded as safe practice to use only spore-destroying substances for the virus of those diseases of which we have no definite knowledge. Nevertheless, in the absence of other disinfectants, lime is very useful. It may be employed as a whitewash on wood and stone and sprinkled as a dilute wash or in powder over yards, manure heaps, and over carcasses before they are buried, and over the ground on which they have lain to prevent other animals from carrying the infection away.

(2) Chlorid of lime is more efficient than simple slaked or unslaked lime, as it destroys spores. It is the ordinary bleaching powder of commerce and is quite unstable, hence old preparations, unless sealed, are of little value. A 5 per cent solution is sufficiently strong for all spore-bearing bacteria (3 ounces in 2 quarts of water). It may be efficiently applied to the walls and floor of an infected stable by mixing with limewash in the proportion of 6 ounces of the lime to each gallon of limewash. The ceilings and those portions of the walls which can not be reached should be disinfected by means of chlorin gas liberated from the chlorid of lime by crude carbolic acid. This is accomplished by making a cone of 5 or 6 pounds of chlorid of lime, in the top of which a deep crater is made for the placement of from 1 to 2 pints of crude acid. The edge of the crater is thereupon pushed into the fluid, when a lively reaction follows. The fumes of chlorin are strongly irritating to the respiratory tract and therefore all live stock should be removed before the work is started. Owing to the heat generated, it is advisable to place the lime in an iron crucible and to have nothing inflammable within a radius of 2 feet. The number and location of these cones of chlorid of lime depend on the size and structure of the building to be disinfected. As a rule, it may be stated that chlorin gas liberated from the above-sized cone will be sufficient for disinfecting 5,200 cubic feet of air space.

(3) Crude carbolic acid. The ordinary purified carbolic acid is too expensive to be used on a large scale, and the crude produce is a very good substitute. This is made more powerful by mixing with it an equal volume of commercial sulphuric acid. While the sulphuric acid is being added to the crude carbolic acid much heat is evolved, and if the glass jar in which the two are mixed is placed in cold water the resulting product is said to have a higher disinfecting power. The mixture is added to water enough to make a 5 per cent solution (about 7 ounces to 4 quarts of water). This is strong enough for all purposes. It may be kept in wood or glass, but not in metal, owing to the corroding action of the acid. It should be used freely on woodwork and on infected floors, and a force pump of the kind used by orchardists is very convenient as a means of applying the disinfectant. If the solution is warm when applied, it will penetrate the woodwork better than when cold, especially if the spraying is done during cold weather. The addition of air-slaked lime in any quantity that will dissolve in water to the above solution (say 1½ pounds of lime to 7 ounces of crude carbolic acid to each gallon of water) is preferred by many, as it makes any neglected places at once visible and leaves cleaner and better air within the buildings. In most cases in which its application becomes desirable—and this rule should apply to all disinfections—the disinfected stables, stalls, etc., should remain vacant as long as possible before cattle are again stabled therein.

(4) Mercuric chlorid, or corrosive sublimate, is a powerful disinfectant, but it is likewise very poisonous; hence its uses are limited. Cattle are especially susceptible to its action and caution must be used in its application. A solution of one-tenth of 1 per cent is usually sufficient (1 ounce to 8 gallons of water). It should not be placed in wooden pails, which would form the tannate of mercury, a weak antiseptic; nor, owing to its corrosive action, should expensive metal pails be used. Agate vessels or tin pails are to be preferred. All solutions should be labeled "poison," and to avoid accidents none should be kept on hand.

(5) Formalin and formaldehyde gas have been found very efficacious as sanitary agents. Formalin is the commercial name for the 40 per cent solution of formaldehyde gas in water, and is one of the most powerful antiseptic and disinfectants that we possess. Solutions of this strength are manufactured by different commercial houses and sold by the drug trade under the name of "formalose" and "formal." In this connection it should be mentioned that while the 40 per cent solution of formaldehyde gas and formalin are exactly the same thing, the former can be purchased at 33-1/3 to 64 per cent less than the latter. Formalin, diluted with water in the proportion of 1 pint to 30 parts of water, or 4 ounces to each gallon of water, may be applied, and it may thus be used as a wash or as a spray on all paints, metals, and woodwork, as well as on clothing and other fabrics, without injuring them. It may also be applied to floors, walls, and woodwork in whitewash by mixing 1 part to 30 parts of limewash, or 4 ounces to each gallon of limewash. Formalin has the appearance of water and in the strong solution is poisonous, but when diluted as recommended above it is not dangerous. The fumes given off by it, however, are very disagreeable and irritating to the eyes and nasal mucous membranes. One and one-half ounces of formalin added to 1 gallon of water is a valuable agent for the disinfection of the skin or septic wounds, but is somewhat painful and irritating to raw surfaces.

Formaldehyde is a gas which is soluble in 2½ parts of water (40 parts of formaldehyde gas to 100 parts of water); this solution constitutes the formalin of commerce. The use of formaldehyde gas is in most cases impracticable for stable disinfection. In case the stable is not too large and can be made almost air-tight the generation of formaldehyde gas, after removing all the animals, will be found very serviceable. It penetrates all parts of the stable—the walls, crevices, floors, ceiling—and is probably the best fumigating disinfectant that we have.

Probably one of the most simple and practical methods of liberating this gas is by means of the chemical reaction which takes place when formalin is poured upon permanganate of potassium. For each 1,000 cubic feet of air space, 16-2/3 ounces of crystallized or powdered permanganate of potassium is placed in a wide-surfaced pan; 20 ounces of formalin is then poured upon it, and the stable immediately closed for a period of 12 hours or longer. This method is efficient only when it is possible to seal tightly the place to be disinfected, and should be used only by experienced persons.

(6) Some coal-tar products are cheap, effective, and easily applied disinfectants, their action being due to the carbolic acid and creosote in their composition. They may be used in 3 to 5 per cent solution. As a rule they form a milky solution in water.

(7) Compound solution of cresol (liquor cresolis compositus), now recognized as an official preparation, is composed of equal parts of cresol and linseed-oil-potash soap. The mixture is a thick, dark, amber-colored fluid which mixes readily with water in all proportions to form a clear, soap solution. It is an efficient disinfectant in a 3 or 4 per cent solution, and in this strength it may be applied in the same manner as a 5 per cent solution of carbolic acid.

When it is desired to apply one of these above-mentioned agents to the stable or barnyard, a preliminary cleaning up of all débris and litter is advisable, together with the scraping of the floor, mangers, and walls of the stable with hoes; also the removal of all dust and filth. This should be followed by the burning of all such accumulations, inasmuch as this material likewise contains the infectious principle and is best destroyed by heat. Heat may be applied to the surface of the affected pen, byre, or barnyard by means of a cyclone burner, which consists of a tank, pump, hose, and cyclone nozzle for spraying with paraffin (gas oil). The latter is ejected in the form of spray, which when ignited gives a very hot and effective flame to be applied to the infected ground. Where such burning is impracticable the surface soil of the yard and surroundings should be removed to a depth of 5 or 6 inches and then placed in a heap and thoroughly mixed with air-slaked lime. The fresh surface of the soil thus exposed may then be sprinkled with the disinfectant.

In addition to these artificial substances there are several natural sanitary agents of great importance as destroyers of virus. These are cleanliness, ventilation, drying, and sunshine. All virus, excepting such as may live in the soil, is killed sooner or later by drying and sunshine, and the importance of these factors in the daily life of animals need not be insisted on here. Finally, all sanitary measures which contribute to the healthfulness of animal surroundings are directly or indirectly inimical to disease germs, and all carelessness in the keeping of animals may be regarded as an ally of these destructive organisms.

CONTAGIOUS PLEUROPNEUMONIA.

[[Pls. XXIX]-[XXXII].]

Definition and history.—This disease has been eradicated from the United States, and it is not probable that it will ever be seen in this country again. As, however, much interest was manifested in regard to it for a number of years, and as our cattle are still prohibited from some foreign markets on account of its previous existence here, the subject is treated at greater length than would otherwise be necessary.

The contagious pleuropneumonia of cattle is a specific, epizootic disease which affects bovine animals, and from which other species are exempt. It is characterized, when the disease results from exposure in the usual manner, by an inflammation of the lungs and pleuræ, which is generally extensive, and which has a tendency to invade portions of these organs not primarily affected and to cause death of the diseased portion of the lung. This disease is frequently called the lung plague, which corresponds to its German name of Lungenseuche. In French it is spoken of as the péripneumonie contagieuse.

The history of the contagious pleuropneumonia of cattle can not be traced with any certainty to a period earlier than the beginning of the eighteenth century. No doubt it existed and ravaged the herds of Europe for many years and perhaps centuries before that time, but veterinary knowledge was so limited that the descriptions of the symptoms and post-mortem appearance are too vague and too limited to admit of the identification of the maladies to which they refer. It has been supposed by some writers that certain passages in the writings of Aristotle, Livy, and Virgil show the existence of pleuropneumonia at the time that their works were composed, but their references are too indefinite to be seriously accepted as indicating this rather than some other disease.

It seems quite plain that as early as 1713 and 1714 pleuropneumonia existed in Swabia and several Cantons of Switzerland. There are even clearer accounts of its prevalence in Switzerland in 1732, 1743, and 1765. In 1769 a disease called murie was investigated in Franche-Comté by Bourgelat which undoubtedly was identical with the pleuropneumonia of to-day. From that period we have frequent and well-authenticated accounts of its existence in various parts of Europe. During the period from 1790 to 1812 it was spread throughout a large portion of the Continent of Europe by the cattle driven for the subsistence of the armies, which marched and countermarched in all directions. It was generally prevalent in Italy in 1800. It appears to have been unknown, however, in the Department of the Nord, France, until 1826, but during the years from 1820 to 1840 it penetrated into most parts of that country. During the same period it was introduced into and allowed to spread over Belgium and Holland.

This contagion is said to have been carried to Ireland from Holland in 1839, and is reported as existing in England in 1842. The disease was brought to the United States at several different times. Probably its first introduction was with a diseased cow sold in Brooklyn, N. Y., in 1843. It came to New Jersey by importing affected animals in 1847. Massachusetts was infected in the same way in 1859.

South Africa was infected by a bull brought from Holland in 1854, and Australia likewise received the contagion with an English cow in 1858. It is also reported as existing in various parts of the Continent of Asia, but the time of its first appearance and the extent of its distribution are very uncertain.

Some countries, such as Norway, Sweden, and Denmark, which had been infected for only a short time, have succeeded in eradicating the disease without much difficulty by slaughtering all affected and exposed animals. Other countries long infected and in which the contagion was thoroughly established, like Australia, South Africa, Italy, France, Belgium, and parts of Germany, have labored long, in some cases making no progress and in others being only partially successful. Holland was one of the first of the thoroughly infected countries to free itself from the contagion.

In the United States, Massachusetts eradicated pleuropneumonia during the period from 1860 to 1866. New York and New Jersey made an attempt to eradicate it in 1879, but were not successful. Late in 1883 the contagion was carried to Ohio, probably by Jersey cattle purchased in the vicinity of Baltimore, Md., to which place it had extended before 1868. From the herd then infected it was spread by the sale of cattle during 1884 to a limited number of herds in Illinois, to one herd in Missouri, and to two in Kentucky. The alarm caused among the stock owners of the United States by this widespread dissemination of a disease so much dreaded led to the adoption of active measures for its control and eradication. By cooperation between the United States Department of Agriculture and the authorities of the affected States it was found possible to prevent the further spread of the contagion and to eradicate it after a few months' delay.

In 1886 pleuropneumonia was discovered in some of the large distillery stables of Chicago and among cows on neighboring lots. This led to renewed efforts for the complete extirpation of this disease from the country. Congress in 1887 enlarged the appropriation available for this purpose and gave more extended authority. During the same year the disease was stamped out of Chicago, and has not since appeared in any district west of the Allegheny Mountains.

The work of eradication was at the same time commenced in all the infected States. Before the end of the year 1889 Pennsylvania, Delaware, Maryland, the District of Columbia, and Virginia had been freed from the disease. More difficulties, however, were encountered in the States of New York and New Jersey, on account of the larger territory infected and the density of the population. The long struggle was successful, however, and the last animal in which the disease appeared in the State of New York was slaughtered early in 1891, and the last one affected in New Jersey met the same fate early in the spring of 1892.

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During these same years a supreme effort had been made to stamp out this lung plague from Great Britain. From the official reports it appears that the number of infected districts and of diseased animals had rapidly diminished, but it was not until 1898 that the infection was finally eradicated.

The other infected European countries, though they maintain a veterinary sanitary service, are not making satisfactory progress in eradicating the disease. This is owing partly to delays in carrying out the provisions of the laws and partly to mistaken ideas as to the measures which are necessary to accomplish the object. The United States was the last of the countries having old infected districts which undertook to stamp out this contagion, and, except Holland, it was the first to reach success.

The cause (etiology) of pleuropneumonia.—This is a contagious disease, and arises only by contagion from a previously affected animal; consequently it can never be seen here except as the result of importing affected animals from the Old World. When thoroughly stamped out it does not reappear; and if imported animals continue to be properly inspected and quarantined, we have every reason to believe that pleuropneumonia will never again be seen in this country.

The exact nature of the virus or contagion of lung plague has never been determined. Various investigators have from time to time claimed the discovery of the specific organism of the disease, but it was not until 1898 that Nocard and Roux, by an ingenious method of cultivation, succeeded in obtaining a very feeble growth of an exceedingly minute microorganism. With these cultures the disease was produced in cattle.

Some investigators and writers are of the opinion that the disease can be contracted only by an animal coming near enough to a living diseased one to receive the contagion directly from it. They hold that the contagion is expired with the air from the affected lungs, and that it must be almost immediately inspired by another animal in order to produce the disease. Some experimental attempts to infect animals by placing them in stables where diseased animals have been, and by placing the diseased lungs of slaughtered animals in their feeding troughs have failed, and, consequently, apparently confirm this view.

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CONTAGIOUS PLEUROPNEUMONIA.

DESCRIPTION OF PLATES.

Plate XXIX. Upper or dorsal surface of the lungs of the ox, reduced to one-twelfth of the natural size: a, a', the right and left principal lobes. These are the largest and are situated posteriorly, resting upon the diaphragm; b, b', the ventral lobes, situated between the principal lobes; and c, c', c'' the most anterior, or cephalic, lobes. The right anterior is divided into two lobes (c, c'), the left is single (c''); d, trachea, or windpipe.
In the majority of the lungs examined in the laboratory of the bureau which were affected with contagious pleuropneumonia the principal lobes (a, a') were primarily affected.

Plate XXX. Bronchopneumonia. The ventral or middle lobe of the right lung affected with collapse and beginning bronchopneumonia. The light yellowish portions represent healthy lung tissue; the red represents the disease. It will be noticed that the lines between the lobules are quite faint, indicating little or no inflammation of the connective tissue between the lobules. The healthy lung tissue is seen to be raised above the level of the diseased portion. In contagious pleuropneumonia the exact reverse is the case, the diseased portions being very much larger than the healthy.

Plate XXXI. Contagious pleuropneumonia. Appearance of a cow's lung affected with contagious pleuropneumonia when sections or slices are made of it and cut surfaces examined.

Fig. 1. Transverse section through the right principal lobe in a case of acute pleuropneumonia. The area drawn includes the air tubes, veins, and arteries, and illustrates the great thickening of the interlobular connective tissue into broad whitish bands and of the walls of the air tubes, veins, and arteries: a, air tube cut obliquely; a', air tube cut directly across; b, arteries cut across; c, large vein completely occluded by a thrombus or plug formed during life. The great thickening of the walls of the artery and vein in this disease is especially brought out by stating that in the healthy lung they are so thin as to be easily overlooked.

Fig. 2. Transverse section of the principal lobe in a case of acute pleuropneumonia, illustrating the different kinds of hepatization or consolidation of the lung. These are indicated by the different colors from dark red to reddish yellow. This variation of color is regarded by some as the real marbling characteristic of pleuropneumonia, while the whitish bands penetrating the lung tissue in all directions constitute the true marbling according to other observers.

Plate XXXII. Contagious pleuropneumonia. This illustrates what are called infarctions. The right half of the figure shows nearly normal lung tissue. The left represents a blackish mass, in which the lung tissue is filled with blood and solidified. This is caused by the plugging of the vein carrying away the blood from this portion. The heart forces the blood through the artery into the tissue at considerable pressure, but owing to the fact that its return is prevented, the minute blood vessels rupture and the air vesicles become distended with blood, which coagulates and causes the firmness of the tissue.

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On the other hand, it is known that the serum from affected lungs retains its virulence and may be used successfully for inoculation weeks or months after the death of the animal from which it was taken. This is particularly the case when this liquid is hermetically sealed in glass tubes. Other investigators state that they have successfully infected cattle by placing, in the nostrils, sponges or pledgets of cotton saturated with such serum. Cattle have also, according to the best evidence obtainable, been infected from the clothing of attendants, from horns used in drenching, and from smelling about wagons which have been used to transport affected carcasses. In the work of eradicating pleuropneumonia from the United States many stables were found in which the disease would appear and reappear after the slaughter of affected herds, and in spite of any precautions which were adopted. These were always old stables, with woodwork in a decaying condition and with floors underlaid with filth which could not be thoroughly removed or disinfected. In every one of these cases the destruction of the stable, the burning of the lumber of which it was constructed, the removal of the accumulations beneath the floors, and thorough disinfection, prevented the recurrence of the plague in new stables built upon the same premises. This experience conclusively shows that under certain conditions, at least, stables may retain the infection for a considerable time, and that when restocked the disease may break out again from such infection.

As a rule, however, the disease is acquired by a healthy animal being near an affected one and receiving the contagion direct. Affected animals may give off the contagion in the early stages of the disease before the symptoms are apparent to the observer; also, they may retain this infectious character, if they survive the attack, for six months and probably for a year after all symptoms of the disease have disappeared.

Incubation.—The time which elapses between exposure to the contagion of pleuropneumonia and the first appearance of the symptoms of this disease varies greatly with different individuals and with different outbreaks of the disease. Ordinarily the symptoms of disease make their appearance within three to six weeks after exposure; they may be observed, however, within two weeks or they may not become apparent until nearly or quite three months. It is this long period of incubation and the great length of time that an animal may disseminate the contagion after apparent recovery which give the plague that insidious character so often spoken of, and which greatly increase the difficulties of eradication.

Symptoms.—The symptoms are such as would be expected with inflammation of the lungs and pleuræ, but they vary considerably, according to the type which the disease manifests. If the attack is an acute one, as is frequently seen in hot weather, the symptoms appear suddenly; the breathing becomes rapid and difficult, the animal grunts or moans with each expiration, the shoulders stand out from the chest, the head is extended on the neck, the back is arched, the temperature is 104° to 107° F., the milk secretion is suspended, there is no appetite, rumination is stopped, the animal may bloat and later be affected with a severe diarrhea. Such cases are generally fatal in 7 to 20 days.

Very often the attack comes on slowly and the symptoms are much less clear. In the mildest cases there is a cough for a week or two, but no appreciable loss of appetite or elevation of temperature. The lungs are but slightly affected and recovery soon follows. Such animals may disseminate the contagion for a long time without being suspected, and for that reason are the most dangerous of all.

A more severe type of the plague is the most frequently seen. In these cases the cough is frequent, more or less painful, the back somewhat arched, and the milk secretion diminished. The prominence of these symptoms increases, the appetite is affected, the animal loses flesh, the breathing becomes more rapid, the cough more painful, pressure of the fingers between the ribs shows tenderness, the hair loses its gloss and stands erect, the skin becomes adherent, little, if any, milk is secreted, and the temperature rises, varying in different animals from 103° to 107° F. Animals thus affected may continue to grow worse and die in from three to eight weeks, or they may after a time begin to improve and make an apparent recovery. The inflammation of the lung does not, as a rule, subside and the organ return to its normal condition, as is the case in ordinary pneumonia, but with this disease the life of the affected portion of the lung is destroyed, the tissue dies, and a fibrous wall is formed around it to shut it away from the living parts. The tissue, thus encysted, gradually softens, becomes disintegrated, and breaks down into pus. The recovery, therefore, is not complete; it is only apparent and partial.

To those accustomed to examining the lungs of cattle, other and extremely important symptoms may be apparent during the course of the disease. By applying the ear over the walls of the chest an area of a certain extent may be found in which the natural breathing sound is diminished or entirely lost. This represents the diseased portion of the lungs. In other cases a loud blowing sound may be heard, quite different from any sound produced when the lung is in a healthy condition. In some cases crepitation is heard near the border line of the diseased area and friction sounds produced by the roughened pleura; these can be appreciated, however, only by those whose ears have been trained to distinguish between the different sounds which reach the ear when applied to the chest wall. By percussion—that is, by pressing the fingers of the left hand firmly against the wall of the chest and tapping upon the middle finger with the ends of the fingers of the right hand—an area of dullness may be discovered corresponding to the portion from which the respiratory murmur has disappeared. This loss of respiration detected by auscul tation, and the dullness brought out by percussion, are the most important evidences of an inflamed or consolidated lung.

Seriously affected animals remain standing if they have sufficient strength, but those which lie down always lie on the affected side.

The proportion of animals which become affected after being exposed varies according to the virulence of the outbreak, the susceptibility of the animals, and the length of time during which exposure is continued. Sometimes not more than 15, 20, or 30 per cent will contract the disease when a large herd is exposed; on the other hand, however, 80 or 90 per cent may be affected. The proportion of cases in which the disease proves fatal also varies greatly—it may not exceed 10 and it may reach 50 per cent. In general, it may be said that about 40 per cent of the exposed animals will contract the disease and about one-half of these cases will prove fatal.

Post-mortem appearances.—Owing to the complexity of the structure of the lung tissue, its ramifications of bronchial tubes and blood vessels, and its abundant supply of lymphatics, the pathological changes in pleuropneumonia are interpreted with great difficulty. Furthermore, there are certain kinds of pneumonia which present some resemblances to pleuropneumonia and which may therefore be confused with it in some of its phases.

If we kill an animal affected with acute pleuropneumonia and examine the cavity of the chest and lungs, the following appearances will be noted:

The thorax may contain more or less serum, which may be clear or clouded. There may be firm adhesions of different parts of the lungs to the chest wall, the extent of which depends on the stage and severity of the disease. The diseased lobes are unusually large and exceedingly firm to the touch. The weight of a single large lobe may reach 40 pounds. Usually only one side is affected, often but a single lobe, and this most commonly the large or principal lobe. The pleura may be covered with one or more layers of a firm, elastic, grayish membrane, which varies in thickness and which sometimes may be pulled away entirely. Sometimes it is absent. The pleura, however, is opaque and apparently very much thickened. This is owing to the diseased condition of the connective tissue beneath the pleura, as will be explained later. When an affected lobe is cut through at right angles to its long diameter, the cut surface presents a variety of interesting changes. In the first place the spaces between the small subdivisions of the lung (the lobules), which in the healthy lung are barely visible, are distended with a yellowish-white, usually quite firm, substance, which is coagulated fibrin. The cut surface thus appears divided into small fields by yellowish-white bands of varying thickness running in various directions through the lung tissue and beneath the pleura. ([Pl. XXXI].) These bands may appear honeycombed and the spaces filled with yellowish fluid (serum) or they may be uniformly solid. It will also be noticed that the space immediately outside of and around the artery, vein, and air tube is similarly broadened by fibrinous deposits. Some authorities look upon these bands as constituting the so-called "marbling" of pleuropneumonia.

In addition to these changes which have taken place in the connective tissue between the lobules, the lung tissue itself may be markedly altered. Certain areas of the cut surface may be very firm in texture and of a brownish-red color. The cut surface is granular or roughened, not smooth to the eye. Other areas equally firm may be more grayish yellow and still others may be blackish. ([Pl. XXXII].) Besides these areas which represent solidified (hepatized) lung tissue there may be others which approach the normal lung tissue in color, are soft, and float in water. From these a milky, purulent fluid may often be expressed. These different shades are represented in [Plate XXXI], fig. 2, within a small compass. Some authorities are inclined to consider these variations in color on the same cut surface as the so-called marbling of pleuropneumonia. It matters not whether we regard the bands between the lobules or the varying shades of the lobules themselves as the marbling, provided either or both are peculiar to contagious pleuropneumonia. If we examine the blood vessels appearing on such cut surface they will usually be found plugged within the firmly hepatized regions. The artery contains a dark, soft, removable clot, the vein a grayish-pink, granular, fragile plug (thrombus), which adheres firmly to the wall of the vein, and if this is slit open, indications of a diseased condition of the inner coat will be readily detected. When large regions of the lung tissues are hepatized, the main air tube and its branches are usually filled with grayish, cylindrical branched masses of fibrin that are easily removed, as they do not adhere to the mucous membrane.

The views of pathologists differ as to the nature of the earliest changes in pleuropneumonia, and it is not within the scope of this work to present controverted or imperfectly developed theories. In the foregoing description we have taken as a type the acute pleuropneumonia in its fully developed phase, which can scarcely be mistaken for any other disease. We have seen that there is an inflammatory condition of the connective tissue between the lobules, resulting in the exudation of coagulable lymph. This inflammation is equally marked around the blood vessels and air tubes. It leads to inflammatory changes in the inner wall of the veins, and these cause the deposition of thrombi or plugs in the vessels, which prevent the return of the blood. The blood pumped into the lung tissue through the artery, but unable to get out by way of the vein, leaves the mesh-work of capillaries around the air vesicles, enters the latter, and produces the firm, hepatized condition so characteristic of this disease. If we bear in mind that the veins in different parts of the lung tissue are plugged at different times, and that, therefore, the affected regions are in different stages of disease, it will be easily understood how the different shades of color from dark red to grayish or yellowish red are produced.

The complete plugging of the veins may lead to the death of circumscribed masses of lung tissue. A line of separation forms between the living and the dead tissue and a thick cyst wall of fibrous tissue forms around the latter. The dead tissue for a time preserves the appearance of lung tissue, then undergoes disintegration and liquefaction. The softened mass is finally absorbed, and the walls of the cyst, or capsule around it, gradually collapse and form a cicatrix. This favorable termination takes place only when the dead mass is not too large. It may, however, involve over half of one of the large lobes. Under such circumstances recovery is improbable. A more favorable termination is the abundant growth of fibrous tissue around and into the hepatized masses. The formation of fibrous tissue may extend to the pleura, or lung covering, and cause firm adhesion of the lungs to the chest wall and to the pericardium, or heart case.

The same peculiar, inflammatory changes which take place between the lobules of the lung and around the bronchi and vessels may invade the pleural cavity, cause extensive membranous and spongy deposits on the pleura and firm deposits around the heart and large arteries, the gullet, and windpipe.

These are the main features of the lung disease caused by contagious pleuropneumonia. In the typical, acute cases there are a sufficient number of peculiarities to enable us to make a positive diagnosis. There are, however, many cases in which the disease is restricted to small areas, or to the interlobular tissue, or in which the changes are still imperfectly developed, or else so far advanced that doubts may arise as to the true nature of the affection. In such cases all obtainable facts, including the history of the case, the symptoms during life, and the pathological changes observed on post-mortem examination must be taken into consideration. Only one who has made a careful study of the disease is fitted to decide in such cases.

Other kinds of lung disease, because of certain features common to most lung diseases of cattle, may be confounded with pleuropneumonia. The inflammation of the connective tissue between the lobules is not infrequently observed in so-called interstitial pneumonia and may lead to the formation of whitish bands intersecting the lung tissues in various directions. On the cut surface these bands may give rise to a decidedly marbled appearance. Again, in traumatic pneumonia, caused, as its name implies, by the entrance of foreign bodies into the lung tissue, generally from the paunch, the connective tissue around the place of disease becomes inflamed and thickened, and the disease itself may simulate pleuropneumonia in its retrogressive stages when it is confined to a small portion of lung tissue. The filling up of the interlobular spaces with fibrin and connective tissue of inflammatory origin is not thus limited to pleuropneumonia, but may appear in a marked degree in other lung diseases. It must not be inferred from this statement that these interlobular changes are necessarily the same as those in pleuropneumonia, although to the naked eye they may appear the same. We simply note their presence without discussing their nature.

In general, the distinction between pleuropneumonia and bronchopneumonia is not difficult to make. In the latter disease the pneumonia generally invades certain lobes. The disease attacks the smaller lobes in their lowest portions first and gradually extends upward, i. e., toward the root of the lung or the back of the animal and backward into the large principal lobes. Again, both lungs in advanced cases are often symmetrically affected. In contagious pleuropneumonia the large principal lobe of one side is most frequently affected, and a symmetrical disease of both lungs is very rare, if, in fact, it has ever been observed. The lung tissue in bronchopneumonia is not enlarged, but rather more contracted than the normal tissue around it. This is well illustrated in [Plate XXX]. Normal, air-containing lobules may be scattered among and around the hepatized portion in an irregular manner. In pleuropneumonia the diseased and healthy portions are either sharply divided off, one from the other, or else they shade into each other by intermediate stages.

The hepatized lung tissue in bronchopneumonia when the cut surface is examined is visually of a more or less dark flesh color with paler grayish-yellow dots regularly interspersed, giving it a peculiar, mottled appearance. In the more advanced stages it becomes more firm, and may contain nodular and firmer masses disseminated through it. The air tubes usually contain more or less soft, creamy, or cheesy pus or a turbid fluid quite different from the loose, fibrinous casts of acute pleuropneumonia. The interlobular tissue may or may not be affected. It sometimes contains loose, fibrinous plugs, or it may be greatly distended with air, especially in the still normal portions of the lung. The pleura is seldom seriously diseased. If we contrast with these features the firm dark-red hepatizations, the plugging of the veins, the extensive interlobular deposits, and the well-marked pleuritis in pleuropneumonia, there is little chance for confusion between well-developed cases of these two lung diseases.

It should not be forgotten, however, that the lesions of the disease known as contagious pleuropneumonia may be confined to the serous membranes of the thorax, or they may be confined to the parenchyma of the lungs; they may affect a whole lobe, or only a small portion of it; they may or may not cause the so-called marbled appearance. In the same way bronchopneumonia may vary as to the parts of the lung affected, the extent of the lesions, the degree and kind of pathological changes in the interlobular tissue, the color of the lung on cross section and the amount of hepatization. In individual cases, therefore, it is often necessary to take into account the history of the animal, the course of the disease, and the communicability of the affection before a diagnosis can be made between the two diseases.

Prevention and treatment.—The prevention of pleuropneumonia, as of other contagious diseases, consists in keeping animals so that they will not be exposed to the contagion. As the disease arises only by contagion, there is no possibility of an animal becoming affected with it unless it has been exposed. If, therefore, pleuropneumonia exists in a locality the owner of healthy cattle should make every effort to keep his animals from coming near affected ones or which have been exposed. He should be equally particular not to allow persons who have been on the infected premises to visit his own pastures, stables, or cattle.

If pleuropneumonia breaks out in a herd, every animal in it should be slaughtered, the stables thoroughly cleaned and disinfected, and no other cattle allowed on the premises until a period of 90 days has elapsed.

Medical treatment of affected animals is unavailing and should not be attempted. No matter how valuable the diseased animals may have been before they contracted the disease, they should at once be destroyed and the contagion eradicated. This is the best policy for the individual as well as for the community.

The eradication of this disease by local or National Governments can be successful only when the same principles are adopted and carried out as here recommended for individual stables. It is then a difficult undertaking, simply because the contagion is generally widely disseminated before any measures are adopted, and because a great majority of cattle owners will never report the existence of the disease. Regulations must therefore be enforced which will insure the prompt discovery of every herd in which the disease appears, as well as the destruction of all diseased and exposed animals and the thorough disinfection of the premises.

To discover pleuropneumonia sufficiently early for this purpose, the district supposed to be infected should be clearly defined and inspectors should be constantly employed to inspect every herd in it at least once in two weeks, or, better, once a week. No bovine animal should be allowed to go out of the defined district alive, and all which enter it should be carefully inspected to insure their freedom from disease. As an assistance to the discovery of diseased herds, every animal which, from any cause, dies in the infected district and every animal which is slaughtered, even if apparently in good health, should be the subject of a careful post-mortem examination. Many affected herds will be found in this way.

In addition to these measures it is also necessary to guard against the removal of animals from one stable to another and the mixing of herds upon common pastures or in the public highways. The object must be to isolate every individual's cattle as completely as possible, or otherwise a single affected animal may infect a dozen or more herds. To prevent surreptitious sale or trading of cattle, each animal must in some way be numbered and recorded in the books kept by the official in charge of the district. In the work of the United States Department of Agriculture a numbered metal tag was fastened to each animal's ear and index books were so arranged that with a number given the owner could be at once ascertained, or from the owner's name the cattle for which he was responsible could be at once learned. In this way, if an animal was missing from a stable, the fact became apparent at once, or if one too many was found in a stable the number in its ear would indicate where it came from.

When pleuropneumonia is discovered by these means, the entire herd should be slaughtered as soon as the formalities of appraisement can be arranged. In country districts the carcasses should be buried, as it is generally impracticable to dispose of them in any other way. In city districts the animals may be taken to a slaughterhouse, with such precautions as are possible to prevent dissemination of the contagion. The animals should be slaughtered under the supervision of an inspector. The healthy carcasses may be utilized for food, but the blood, entrails, and all diseased carcasses should be heated to a temperature equal to that of boiling water or above, and then used for the manufacture of fertilizers.

The disinfection of premises should be thorough and should be carried out by a trained corps of men employed for the purpose. The floors of stables should be removed, the accumulations removed from beneath them, the contents of haylofts should be destroyed, and the woodwork and soil beneath the stables should be thoroughly drenched with a solution of bichlorid of mercury, 1 part to 2,000 of water. After the flooring is replaced the woodwork should be coated with limewash, containing one-fourth pound of chlorid of lime to the gallon of mixture.

Usually in these cases the owners are dependent upon their herd of cows for a living, and consequently it is difficult or impossible to hold the stables vacant for any considerable period. In a majority of instances cattle may be admitted at once to stables so disinfected, without the reappearance of the disease. Occasionally, however, it will reappear without apparent cause. For this reason the inspection and other measures must be maintained in the infected district for six months or a year after the last case of disease has been disposed of.

Many people have objected to the slaughter of diseased and exposed animals as an unscientific and expensive method of eradicating the disease. To these it may be answered that it is the only method which has ever proved successful, and that in the end it is much more economical than temporizing measures.

Inoculation has been adopted in many countries, and has undoubtedly lessened the death rate, but where this practice is allowed the disease is kept up and spreads. For this reason it should be prohibited wherever there is a possibility and disposition to eradicate the contagion.

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RINDERPEST.

Rinderpest, also known as cattle plague, is an acute, infectious disease of cattle, in which the digestive organs are mainly involved. Though unknown in this country, the importance of having near at hand a few definite facts concerning this disease, should it ever reach our shores, will be at once appreciated. A knowledge of such facts may aid in an early recognition of the disease. It must not be forgotten, on the other hand, that a superficial knowledge of diseases, such as the layman may gain through reading, not infrequently leads to confounding comparatively harmless, noninfectious maladies with such as are truly dangerous (foot-and-mouth disease, rinderpest, etc), and causes temporary panics among stock owners.

According to some authorities, rinderpest has its home in the territory around the Black Sea and the Volga River in Russia; according to others, in Central Asia. Thence it has been conveyed at various times by cattle to nearly every country of Europe and Asia, where it has proved to be a veritable bovine scourge. It probably visited Europe as early as the beginning of the Christian era, and since then the migrations of the people from the Far East have from time to time introduced the disease. Especially during the eighteenth century it was more or less prevalent in Europe, owing to the frequent wars, during which herds of cattle were brought from eastern Europe and Asia to supply the demands of the armies. It prevailed in Europe during the Franco-Prussian War. At present it exists in eastern Europe and in portions of Asia and Africa.

The virus is conveyed from one country to another chiefly by means of infected cattle, although infected hides, wool, and feed may play an important part in its dissemination. The railroad facilities of the present, which furnish the means of such rapid communication, are particularly liable to aid in the spread of the disease.

In the past rinderpest has been supposed to be identical with various human diseases, among them smallpox and typhoid fever. These suppositions are unfounded, and the view of authorities to-day is that it is a disease of a peculiar kind, not identical with any other known infectious disease.

The contagion of rinderpest.—The cause of rinderpest must be looked for among microorganisms—most likely bacteria. The investigations made thus far for this causal factor have been fruitless. However, certain recent experiments would indicate that the unseen microbe is of such dimensions that it is withheld by the dense bacterial filters, but passes through the more porous ones. Formerly it was supposed by various authorities that rinderpest virus appeared spontaneously under the influence of deteriorated feed and long and exhausting drives; also during unusual meteorological conditions. This view, however, is no longer maintained. It is probable that in its home in Asia the disease is perpetuated by continual infection of fresh animals, and some authorities go even so far as to believe that the disease would be entirely stamped out, even in its native haunts, by a destruction of all sick and infected herds. However this may be, the success of such an undertaking would largely depend on the nature of the cause. If a strictly parasitic organism, like the contagion of pleuropneumonia, it might be completely extirpated in this way. If, however, the germs or bacteria may live and multiply outside of the bovine body, in the soil, water, or in some other animal, extirpation would be impossible.

The virus may be transmitted in a variety of ways, both direct and indirect, from sick to healthy animals. It is said to be present in the various excreta, such as the discharges from the nose, and the saliva, the urine, and the manure, of the diseased. For months it retains its vitality in a moist state outside the body, and the disease is reported to have developed after feeding hay a year after it had lain in an infected stable; hence manure and the fodder and bedding soiled with discharges may convey it. Persons may carry the virus on their shoes, clothing, or implements. Even small animals, such as cats and rats, which frequent barns and stables, have been looked upon as carriers of the virus.

Cattle are very susceptible to the disease, and in its virulent type all those exposed are said to become infected. Buffaloes, sheep, and goats are likewise susceptible, but in a less degree.

It is also claimed that animals after having passed through one attack successfully resist future attacks. Inoculation with virus is said to produce immunity, but in many cases the process of inoculation itself is followed by death.

Symptoms.—The symptoms of rinderpest are not very characteristic, and hence the diagnosis of a suspected case in the beginning of an invasion is attended with difficulties. Certain appearances which are characteristic of one epizootic may be absent in another. Different observers are not quite agreed as to the most constant and important.

The period of incubation, i. e., the time between the exposure to infection and the earliest outward symptoms, varies from three to nine days. The first sign is a very high fever, which may reach 107° F. The heat of the skin varies in different parts of the body, and may be felt at the base of the ears and horns. Repeated chills are frequently observed. The pulse reaches 50 to 60 beats a minute, and in very severe attacks may rise to 90 or 100.

The animal manifests great debility. The head droops and rests on some object of support. One or both ears may droop. The coat is staring and the muzzle dry. The secretion of milk diminishes very rapidly. Within twelve to twenty hours the usual quantity may have become reduced one-half or two-thirds. The back is arched, and the four limbs are brought together under the body.

As the disease progresses, symptoms with reference to the digestive and respiratory organs become prominent. The mucous membrane of the mouth and the nose, as well as that of the rectum and vagina, becomes reddened, either in patches or diffusely, and assumes a scarlet hue. The discharges, at first firm, become softer, and soon diarrhea sets in. This is said to be one of the most constant symptoms. The rectum may become everted and paralyzed, and the bowels move spontaneously. The discharges become fetid, viscid, and streaked with blood. Coughing is a common symptom, and by some is considered characteristic. It is associated with discharges from the nose and vagina and dribbling of saliva from the mouth. The eyes also are affected. There is an increased formation of a viscid secretion which flows down the face.

Another series of changes prominent in some epizootics and mild or absent in others are the ulcers, or so-called "erosions," in the mouth. These begin as red patches and streaks. The mucous membrane in such localities is converted into a grayish-white slough, which, when shed, leaves a small erosion, or ulcer. At the same time similar changes may go on in the skin of the thighs, the udder, or the scrotum, or about the vagina, which lead to small sloughs.

In severe cases, which are the most common in the susceptible cattle of western Europe, death ensues four to seven days after the first appearance of the disease, and is preceded by great emaciation and debility, fetid, purulent discharges from the nose and mouth, and the relaxed rectum and vagina.

After death, if the animal is opened and the organs carefully examined, the chief changes are found in the digestive organs. The lining membrane of the mouth and pharynx is covered with mucus, is reddened in spots, and shows superficial, yellowish-gray, cheesy patches, which represent dead tissue, and when removed expose ulcerated depressions. The same reddening in spots and the yellowish-gray, cheesy deposits or patches are found in the fourth stomach, the small intestines, and more rarely in the cecum, while the third stomach, or manyplies, is more or less impacted with dry, hard feed. Similar changes may be found on the mucous membrane of the nasal cavity, larynx, trachea, the uterus, vagina, and rectum. The lungs may be injected, edematous, or pneumonic. The heart muscle is pale and flabby, and frequently hemorrhages are observed in its internal membrane. The liver may be pale or injected with blood, and at times shows hemorrhages beneath its capsule. The bile is thin and watery in consistence. The kidneys may be inflamed or contain small hemorrhages within their substance or under the capsule. The lymphatic glands may be swollen and injected or even hemorrhagic.

Treatment.—On account of the danger of spreading the infection, neither medicinal treatment nor inoculation is permitted in European countries, with the exception of Russia, where the disease is more generally diffused. The most effective method of exterminating rinderpest in those districts in which the disease is not indigenous has been found to be the slaughter of all affected and exposed animals. Where the disease is general, successful efforts adopted for its control have followed the immunization by inoculation of the exposed animals and a strict application of appropriate sanitary measures. This protective inoculation has been practiced with very gratifying results in Russia, South Africa, and in the Philippine Islands. An active immunity is thus induced in susceptible animals which lasts until the danger from exposure to the disease is over. This immunity may be attained (1) by the inoculation of pure bile from an animal which recently died of rinderpest, (2) by the inoculation of glycerinated bile, followed by pure bile or virulent blood, or (3) by the simultaneous inoculation of strong standardized serum and virulent blood.

The latter method has been adopted by the United States Government in its endeavor to exterminate the disease in the Philippines, and to protect the cattle and carabaos against rinderpest after their importation into those islands. Owing to the existence of this and other infectious diseases in the Philippine Islands, an order has been issued by the Department of Agriculture prohibiting the landing of any live stock or animals of any kind from the Philippines at any of the ports of the United States or the dependencies thereof. This prohibition removes the greatest source of danger to which the United States is exposed as the result of its intercourse with the islands. The introduction of rinderpest from those countries from which we import animals is rendered extremely improbable, especially in live animals, owing to its short period of incubation and to the 90-day quarantine for cattle (counting from date of shipment) and 15-day (counting from date of landing) quarantine for sheep and other ruminants and swine which are at present enforced in the United States at all ports of entry.

FOOT-AND-MOUTH DISEASE.

[[Pl. XXXIII].]

Foot-and-mouth disease, also known as aphthous fever, epizootic aphtha, and eczema contagiosa, is an acute, highly communicable disease chiefly confined to cloven-footed animals and characterized by an eruption of vesicles or blisters on the mucous membrane of the mouth and on the skin between the toes and above the hoofs. The vesicles rupture, forming erosions and ulcerations; there are also salivation, tenderness of the affected parts, loss of appetite, lameness, emaciation, and diminution in the quantity of milk secreted.

The tremendous ravages of the disease are seen in the number and variety of the species attacked. While it may be regarded as essentially a disease of cattle, hogs would seem to be as easy a prey. Almost in the same grade of receptivity are sheep and goats. Next in order of susceptibility come the buffalo, American bison, camel, chamois, llama, giraffe, and antelope. Horses, dogs, cats, and even poultry may occasionally become infected with the disease, the last three being particularly dangerous as carriers of the contagion. Man himself is not immune, and the frequency of his infection by coming in contact with diseased animals is established by numerous observations.

As with other communicable diseases, the source and origin of foot-and-mouth disease have given rise to much speculation. The disease had been known in Europe for centuries, but it was not until comparatively recent years that the erroneous conceptions of its spontaneous origin as a result of climatic and meteorological conditions, exhausting journeys, etc., were abandoned. It is now conceded that foot-and-mouth disease is propagated by a specific virus and that every outbreak starts from some preexisting outbreak.

So far investigators have been unable to identify or isolate the specific organism causing the disease, although numerous attempts have been made to cultivate and stain it by laboratory methods. Experiments have shown that the virus will pass through standard germ-proof filters, thus indicating its minute size and the reason it has not been detected by the staining methods. The contagion may be found in the serum of the vesicles on the mouth, feet, and udder; in the saliva, milk, and various secretions and excretions; also in the blood during the rise of temperature.

A wide distribution of the virus and a rapid infection of a herd is the result. Animals may be infected directly, as by licking, and in calves by sucking, or indirectly by such things as infected manure, hay, utensils, drinking troughs, railway cars, animal markets, barnyards, and pastures. Human beings may carry the virus on their shoes and clothing and transmit it on their hands when milking, since the udder is occasionally the seat of the eruption. It may also be carried by dogs, cats, rats, chickens, pigeons, etc. Milk in a raw state may also transmit the disease to animals fed with it.

The observations made by some veterinarians would lead us to suppose that the virus is quite readily destroyed. It is claimed that stables thoroughly cleaned become safe after drying for a short time; hence, litter of all kinds, such as manure or soiled hay and straw, may remain infective for a longer time because they do not dry out. Other authorities maintain that the virus is quite tenacious and may live in stables even so long as a year. They also state that animals which have passed through the disease may be a source of infection for several months after recovery.

Unlike most other infectious diseases, foot-and-mouth disease may repeatedly attack the same animals. The immunity conferred by an attack is of limited duration.

The period of incubation (that is, the time between the exposure of an animal to infection and the development of the disease) is variable, usually from three to six days. The disease may appear in 24 hours, or, in exceptional cases, not for 18 days or even longer.

Losses.—The highly contagious character of foot-and-mouth disease and its rapid spread to practically all exposed susceptible animals lead to heavy losses. Since the mortality is comparatively low, ranging from only 3 per cent or less in mild forms to 30 or 40 per cent in malignant cases, the havoc caused by the pestilence is sometimes underestimated. But there are other sources of loss which are much more important than the actual mortality. The fever and the difficulty of eating cause a rapid and extreme loss in flesh and a lessening or cessation of the milk secretion. The udders often become inflamed and ruined by the formation of abscesses, and cows affected in this way are sometimes rendered permanently valueless for milk production. The inflammation of the feet may cause the horn to drop from the toes, producing great lameness and lasting injury. Abortion is frequent, and typical lesions have been observed in the newly born at birth. Altogether these losses may amount to 20 or 30 per cent of the value of the affected animals.

In addition there are indirect losses of a commercial nature. Dairy farmers are put out of business for a time. Necessary quarantine restrictions greatly interfere with the movement of live stock and such commodities as hay, straw, hides, and farm produce. The business of the stockyards and slaughtering centers is greatly interfered with. Sometimes it is necessary to close stockyards for disinfection. The whole business of marketing, transporting, feeding, and slaughtering is interrupted and deranged. Losses of this character may reach enormous proportions.

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The disease in other countries.—Foot-and-mouth disease has prevailed in Europe for a great many years and has occasioned tremendous economic losses there.

In Italy, France, Switzerland, Germany, and Russia the plague has existed so long and has gained such a foothold that it is economically impossible to fight it with the American methods of slaughter and disinfection, for to do so would kill a large percentage of the live stock of those countries. In consequence, little or no progress toward eradication has been made by the authorities, though the severity of the disease in France appears to have abated somewhat in recent months.

The outbreak which appeared in Germany in 1888 increased steadily until 1892, when it diminished gradually for a few years, but the disease again reached great proportions in 1899. Thereafter it continued to exist to a greater or less extent until in 1911 it attained a virulence unequaled before. In that year 3,366,369 cattle, 1,602,927 sheep, 2,555,371 hogs, and 53,674 goats were affected. At that time the total number of cattle, sheep, swine, and goats in Germany was only 51,319,000, while there were in the United States 172,572,000, or between three and four times as many. It can readily be imagined, therefore, what it would mean to the United States if the disease were to gain the foothold here that it had in Germany, where, as these figures show, approximately one out of seven of the animals susceptible to the disease was affected.

The German Government, of course, has not left the disease to itself. It attempted to control some outbreaks by the method of slaughter, but the pestilence had gained too much headway and was too firmly established in too many portions of the country for this method to succeed, and the slaughter of the infected herds had to be abandoned. It now appears that there is no hope of getting rid of it until the virus has worn itself out. As soon as the animals' period of acquired immunity is over and favorable conditions present themselves, the contagion breaks out with renewed virulence. It has been impossible to control it by means of quarantines. One scientist has asserted that unless all the infected farms were absolutely isolated and the movement, not only of live stock but of persons, absolutely prohibited, the disease could not be stamped out. Such a quarantine is, of course, utterly impossible to enforce. In portions of Germany the farmers, realizing that the disease is inevitable, make haste to be done with it by exposing their stock deliber ately to mild cases in the hope that this will result in an immediate, mild attack and immunity for several years thereafter. Such immunity, however, is very uncertain.

Great Britain, Denmark, Norway, and Sweden, on account of their comparatively isolated positions, have been more successful in keeping out the disease. The outbreaks in those countries have been more sporadic, and by resorting to immediate slaughter the authorities have been able to stamp them out. Great Britain has applied both quarantine and slaughter for many years, and in an outbreak near Dublin in 1912 measures were adopted which were even more stringent than any that have been used in the United States. A British official (Cope) asserted in 1899 that after his country's experience with this disease it was "more dreaded by the farmers and stock raisers of Great Britain than cattle plague or pleuropneumonia, and they are now willing and ready to put up with any restrictions, of however drastic a character, considered necessary by the central department to stamp it out." The British authorities have succeeded in suppressing each outbreak, but reinfection often occurs from the neighboring continent. At the present time (April, 1922) Great Britain is having a siege of the disease, but is applying vigorous measures for its suppression.

In November, 1906, the disease reached Belgium from France, where it was quite prevalent, and by the end of the year every Province in Belgium was affected, and the Netherlands as well. Efforts to eradicate it from Belgium were unavailing. The Netherlands apparently succeeded in stamping it out for about six months, but it reappeared there.

The disease is also more or less prevalent in Central Europe, Spain, and in the Balkan countries.

Australia and New Zealand have remained free from it.

We have less accurate information regarding Asia and Africa, but the disease is known to prevail in Japan and China and in the Philippine Islands, and it is doubtful whether any considerable part of the Orient is free from it.

In South America it is reported as common in Brazil, Argentina, and Uruguay, and it probably exists in other countries.

Canada and Mexico are fortunately free from the disease.

Outbreaks in the United States.—Foot-and-mouth disease has appeared in the United States on six different occasions—1870, 1880, 1884, 1902, 1908, and 1914.

An extensive outbreak in 1870 was introduced by way of Canada, where the infection was brought by an importation of cattle from Scotland. It spread into the New England States and New York and appears to have been arrested within a few months. Its failure to spread more extensively and its early disappearance have been ascribed to favorable conditions, such as the movement of live stock from west to east, the limited trading at that period as compared with the present time, the restriction of traffic by winter weather, and the infrequency of travel which obtained at that time among people.

About 1880 two or three lots of animals affected by this disease were brought to the United States, but there was no extension from the animals originally affected.

In 1884, at Portland, Me., there was a small outbreak caused by imported cattle, and the disease spread to a few herds outside the quarantine station. Owing to the small number of animals affected and the limited area of territory covered by the disease, it was easily controlled by the ordinary measures of quarantine and disinfection.

It will be observed that in all these early outbreaks the contagion was introduced with imported animals. Since the development of a stringent system of inspection and quarantine of imported live stock, no instance of that kind has occurred. On subsequent occasions the infection has evidently been brought in with contaminated products or materials and not by means of live animals.

In November, 1902, the disease was discovered in Massachusetts and Rhode Island. The earliest cases were traced to Chelsea, Mass., near the docks, and it was suspected for a time that the infection was brought in with foreign shipping, by some such means as hay, straw, halters, ropes, hides, hair, wool, etc. Later developments, however, and especially investigations into the cause of the 1908 outbreak, led to the belief that a more probable source of the infection was cowpox vaccine virus imported from a country (probably Japan) where foot-and-mouth disease existed, the vaccine virus being contaminated with the virus of foot-and-mouth disease.

A Federal quarantine was declared by the Secretary of Agriculture on November 27, 1902, as soon as the nature of the disease was established, and steps for eradication were at once taken by the Bureau of Animal Industry of the United States Department of Agriculture in cooperation with authorities of the affected States. The methods followed consisted of inspection to trace and detect the disease, quarantine of infected premises and territory, slaughter and burial or burning of diseased and exposed animals, and disinfection of premises.

This outbreak involved Massachusetts, New Hampshire, Vermont, and Rhode Island, and was eradicated in about six months. Two hundred and forty-four herds, including 4,712 cattle, were found infected. Of these, 205 herds with 3,872 cattle, as well as 360 hogs and 220 sheep and goats, were slaughtered. The cattle infected but not slaughtered were those that either died or completely recovered before slaughtering could be carried out. The animals slaughtered were valued at $184,155.10, and the Federal Government reimbursed owners to the extent of 70 per cent, or $128,908.57. It is understood that the States paid the remainder. The total cost to the Department of Agriculture of stamping out the disease was about $300,000.

The next appearance of the foot-and-mouth disease was early in November, 1908, when it was observed in cattle near Danville, Pa. A Federal quarantine was issued November 12. The infection was traced back to the stockyards at East Buffalo, N. Y., and to Detroit, Mich. The disease appeared in the States of Michigan, New York, Pennsylvania, and Maryland. A careful and thorough investigation made by Mohler of the Bureau of Animal Industry and Rosenau of the Public Health Service demonstrated that the outbreak started from calves used to propagate vaccine virus at an establishment near Detroit, and that the source of the infection was contaminated Japanese vaccine virus.

Vigorous measures of eradication similar to those employed in 1902-3 were at once put into effect and the disease was stamped out in about five months at an expense of about $300,000 to the Department of Agriculture, and of about $113,000 to the States. The inspectors made 108,683 visits to farms, stockyards, etc., and inspected more than 1,500,000 animals (including reinspections). One hundred and fifty-seven premises were found infected, and 3,636 animals (2,025 cattle, 1,329 hogs, and 282 sheep and goats), valued at $90,033.18, were slaughtered. Owners were reimbursed for the value of their animals and property destroyed, one-third being paid by the States and two-thirds by the Federal Government.

The latest invasion was discovered in the vicinity of Niles, Mich., in October, 1914, after it had evidently been under way since August of the same year. This is the most serious and extensive outbreak ever known in this country. The disease extended to 22 States and the District of Columbia, at places ranging from the Atlantic to the Pacific coasts. The work of eradication was not completed for more than a year. The affected States were Connecticut, Delaware, Illinois, Indiana, Iowa, Kansas, Kentucky, Maryland, Massachusetts, Michigan, Minnesota, Montana, New Hampshire, New Jersey, New York, Ohio, Pennsylvania, Rhode Island, Virginia, Washington, West Virginia, and Wisconsin. Illinois had the largest infected area and the largest number of animals affected. The Union Stock Yards at Chicago became infected and were a source of dissemination of the contagion north, east, south, and west. These and other yards found infected were closed temporarily and disinfected.

The first Federal quarantine was issued October 19, 1914. A campaign to check the spread of the disease and to stamp it out was immediately begun by the United States Department of Agriculture in cooperation with the State authorities. Quarantines against the movement of animals and certain materials from the infected areas were declared, shipments were traced, rumors investigated, and thorough inspections made in an effort to discover all infected stock. As measures of eradication, diseased herds were slaughtered and buried and the premises disinfected. The owners of live stock and other property destroyed on account of the disease were reimbursed to the extent of the appraised value, half of which is paid by the Federal Government and half by the State. There were slaughtered 172,720 animals (76,575 cattle, 86,492 swine, 9,511 sheep, 133 goats, and 9 deer), in 3,482 herds. The total appraised value of these animals was more than $5,800,000. The expense to the Federal Government of eradicating this outbreak was about $4,540,000.

Symptoms.—In three to six days, or even longer, after the exposure of the animal to the infection the disease makes its appearance. It is usually first indicated by the animal suffering from a chill, quickly followed by an invasion of fever, which may cause the temperature to rise as high as 106° F. These symptoms are not always present, or may be in so slight a form as to escape notice. Following this in one or two days it will be noticed that small vesicles or blisters about the size of hempseeds or peas are making their appearance upon the mucous membranes of the mouth at the border and upper surface of the tongue near the tip, the inside of the cheeks, on the gums and the inner surface of the lips, or on the margin of the dental pad. These little blisters contain a yellowish, watery fluid and gradually become more extensive as the disease advances. Soon after the eruptions have appeared in the mouth of the animal considerable swelling, redness, and tenderness will be noticed about the feet, at the coronet, and between the digits of each foot. A day or two later eruptions similar to those within the mouth make their appearance upon these swollen regions of the foot, and at this stage it is usual to find that like lesions have made their appearance upon the perineum of the victim. In the case of milk cows the udder, and more particularly the teats, show the same vesicular eruption, but the latter as the result of milking soon become covered with reddened spots deprived of the superficial layer of skin and may develop deep, obstinate fissures.

As soon as the disease has become well established the patient evinces pain when attempting to eat; in fact, the appetite is often so seriously affected that all feed is refused, and the animal uneasily opens and shuts its mouth with a characteristic smacking sound, while strings of cohesive, ropy saliva hang suspended from the lips. With the advance of the disease the vesicles widen and extend until they may reach a diameter ranging from that of a dime to that of a silver dollar. These rupture soon after their appearance, sometimes on the first day, more rarely on the second or third day. After they have ruptured, the grayish-white membrane forming the blister may remain attached for a day or more, or disappear speedily and leave deeply reddened, sensitive spots or erosions, both within the mouth and upon the coronet and between the claws of the feet. Similar erosions, which quickly form scabs, as a rule, may be noticed in cases in which the teats of milk cows have become affected, and instances are reported in which sloughing of the tegument immediately around the lesions upon the udder has occurred. Owing to the tough, fibrous nature of the bovine skin, it is exceedingly rare for sloughing to occur upon any part of the body other than those mentioned.

The attack upon the feet of an animal is frequently manifested in all four feet at once, but one or more of the feet may entirely escape and remain unaffected throughout the course of the disease. The ulceration of the interdigital tissue may extend to the ligaments of the fetlock or produce disease of the joint or bone. As the feet become sensitive and sore the animal persistently lies down, and it has been found that bedsores develop with amazing rapidity in all such cases and wholly baffle all attempts at treatment until after the patient has regained its feet.

The disease may attack some of the internal organs before it appears upon any of the external tissues. These cases are very liable to prove quickly fatal. The animal dies from paralysis of the heart, due to the formation of poisonous principles within the system; it may suffocate by reason of the action of these same poisons upon the tissues of the lungs, or it may choke to death as a result of paralysis of the throat.

In cases of serious affection of the udder the erosions will often be found within the passages of the teats, resulting in a "caked" udder, and the same toxic poisoning which is the cause of death in the apoplectiform types just mentioned may arise from this source. In any event the milk from such cases is dangerous for use, causing fatal diarrhea in sucking calves or young pigs and serious illness in human consumers. The milk obtained from cows suffering with foot-and-mouth disease is not readily converted into either butter or cheese, but remains thick, slimy, and inert in spite of churning and attempts at curdling. Pregnant animals may abort. In pigs, sheep, and goats the lesions in the foot are most common, but both forms may be observed or only the mouth lesions.

When the disease has become fully established it will be found that the duration of the attack will vary greatly with different animals. From 10 to 20 days are usually required for the recovery of the normal appetite and spirits in mild outbreaks, while the return to a full flow of milk, in the case of milk cows, seldom occurs before the arrival of the following season.

In the malignant type of the disease it requires from three months to a year for an animal to recover. The mortality, as already stated, is usually low. The disease is more fatal in young animals that have been fed on infected milk, and produces death in from 60 to 80 per cent of these cases as a result of gastroenteritis. In the 1914 outbreak numerous new centers of infection started among hogs and calves which were fed on unpasteurized, infected milk from creameries.

Diagnosis.—The recognition of this affection should not, as a rule, be difficult, especially when the disease is known to be in the vicinity; in fact, the group of symptoms form a clinical picture too decided to be doubted. The combination of high fever, vesicular inflammation of the mouth, and hot, painful, swollen condition of the feet, followed 24 to 48 hours later by the appearance of numerous blisters varying in size from that of a pea to that of a walnut on the udder and feet and in the mouth should prevent any serious or long-continued error in the diagnosis; however, in the inoculation of calves we have a certain and final test. In 24 to 96 hours after inoculation the calves present the characteristic blisters. Such inoculation should be practiced, however, only by officials properly authorized to deal with contagious diseases.

Differential diagnosis.—The lesions of no other disease of cattle closely simulate the vesicular eruption of foot-and-mouth disease on the lining membrane of the mouth. When the blisters have ruptured, however, and the resulting lesions have become contaminated by numerous secondary forms of microorganisms, the correct recognition of the disease may be involved in considerable difficulty.

Cowpox or horsepox may be accidentally transmitted by inoculation. But the eruption of the "pox" goes on to the development of a pustule, while in foot-and-mouth disease the eruption is never more than a vesicle, even though the contained fluid may become turbid. The inoculation test in the case of cowpox does not respond with fever and eruption for at least 10 days, and often longer.

Necrotic stomatitis (sore mouth due to a germ) may be distinguished from foot-and-mouth disease by the fact that in the latter there is a rapid infection of the entire herd, including the adult cattle, as well as the infection of hogs and sheep. The characteristic lesion of foot-and-mouth disease is the appearance of blisters containing a serous fluid upon the mucous membrane of the mouth and upon the udder, teats, and feet of the affected animals. In necrotic stomatitis blisters are never formed, destruction of the tissues occurring from the beginning and being followed by the formation of yellowish, cheesy patches, principally found involving the lining membrane of the mouth, especially the tongue and cheeks.

In mycotic stomatitis (sore mouth due to a fungus or mold), portions of the lining membrane become inflamed and in a few days it changes to a croupous membrane which peels off, leaving a raw surface, while the thin skin between the toes may also be inflamed. The previous history of the case; the failure of the blisters, if any appear, to spread extensively; the absence of vesicular eruptions on other portions of the body, notably the udder and teats, and, characteristically, the hoof, together with the absence of rapid spread to practically all cattle in the herd and the complete negative character of inoculation of calves, distinguish between the local disease named and foot-and-mouth disease. Mycotic stomatitis occurs in only from 10 to 50 per cent of the animals in a herd, usually in the late summer or early fall after a dry spell, and it does not run a regular course.

The lesion, resulting from ergotism may be distinguished from those of foot-and-mouth disease by the lack of eruptions in the mouth and by the location of the disease at the tips of the ears, end of the tail, or upon the lower part of the legs, usually below the knees or hocks. The lesion of ergotism does not take the form of pustules or blisters, but manifests itself first as a swelling about the ankle, which later may slough and circumscribe the limb, forming a deep crack, extending entirely around the limb and forming a distinct line of demarcation between the healthy skin above and the diseased below. The absence of ulcerous sores on the coronet and between the claws, together with the healthy condition of the membranes of the mouth and the knowledge that the lesion upon the limb in question extends uninterruptedly around it, should point conclusively to a diagnosis of ergotism and to the exclusion of all fears of foot-and-mouth disease.

In foul foot or ground itch of cattle, the inflammation of the skin and toes is general and not in certain spots, as in foot-and-mouth disease. The mouth remains unaffected, and the presence of the disease may be traced to filth and poor drainage.

The severer forms of the disease might be confounded with certain general diseases. If gastrointestinal symptoms predominate, acute gastric catarrh or inflammation of the intestines might be thought of. Involvement of the lungs may lead to a diagnosis of acute congestion of the lungs or pneumonia. The distinction is apparent in these diseases by the lack of vesicular eruption on the mucous membrane or skin, and also by lack of evidences of infection in the herd or neighboring animals.

Prevention and eradication.—The measures to be adopted to prevent the spread of the affection must take into consideration the highly infectious nature of the disease, its ease of dissemination, and the liability of the virus to live for long periods outside the body of an animal. Great care should therefore be observed in keeping healthy animals unexposed to the contagion. When an outbreak occurs in a community the owner should make every effort to keep other animals from coming in contact with his diseased cattle. This especially applies to dogs, cats, goats, and poultry, which usually have access to the stables and barnyards and in this way furnish excellent means for disseminating the infectious principle. He should be equally particular in prohibiting any person from coming onto his premises, especially an attendant or owner or other person in any way connected with cattle. Such a herd may be placed under quarantine, with an inspector appointed to keep the premises under constant surveillance.

This method of quarantine alone, while very satisfactory in many instances, is rather tardy in obtaining the desired result. The experience of European Governments already mentioned shows that eradication by this method alone, when the disease has obtained a foothold, is practically impossible. For this reason, when the disease breaks out in a country like the United States, where the contagion is likely to spread rapidly by means of infected cars, manure, hay, and other feed, and where the results of its obtaining a firm foothold would be so disastrous, it seems that this method of temporizing is rather tedious, and more radical steps are required in order to suppress and eradicate completely the infection in the quickest and most thorough manner possible.

It would therefore appear better, after judicious appraisement, to concentrate the expense incident to the extermination of foot-and-mouth disease by purchasing and slaughtering all affected and exposed cattle. The carcasses of these animals should be totally destroyed, preferably by cremation, or otherwise by burying them in a hole 6 feet deep and covering them with air-slaked lime. The infected stable should be disinfected by thoroughly cleaning it, scrubbing the floor with hot water, brushing down all loose dust from the walls, and tearing off all woodwork which is partly decayed. Then the whole interior of the stable should be disinfected with one of the following substances:

• A 5 per cent solution of pure carbolic acid.
• Chlorid of lime, U. S. P. strength (30 per cent available chlorin), 1 pound to 3 gallons of water.
• Formaldehyde, 1 quart 40 per cent solution to 5 gallons of water.
• A 3 per cent solution of cresol compound, U. S. P., or accepted substitute therefor, containing at least 50 per cent cresylic acid.

All stable utensils should be thoroughly cleaned and disinfected by the application of a solution of one of the above-named disinfectants. The manure should be burned or disinfected and spread over ground (other than meadow land) that is to be turned under. No other cattle should be purchased for at least sixty days after the complete disinfection of the premises.

The success in eradicating the disease by combined quarantine, slaughter, and disinfection, as practiced in the United States, Denmark, Great Britain, and a few other countries, demonstrates in a striking manner the efficacy of slaughtering and the futility of relying upon quarantine alone to stamp out the disease.

Inoculation has been adopted in some countries in order to have the disease spread quickly through the herds, and while this practice has undoubted value where the disease is indigenous, it is not desirable in this country and should not be adopted.

As a rule medicinal treatment with a view of curing affected animals is not to be recommended under conditions prevailing in the United States, where the disease has not become established, and the first object is to stamp it out as quickly as possible. Even though most animals would recover, with or without treatment, it would be practically impossible, while they were being held for recovery, to prevent the spread of the infection to others. The disease would be liable to spread faster than it could be cured. As already pointed out, it has been found impossible to prevent absolutely the spread of the contagion by the strictest quarantine alone, under the usual farm conditions. In addition, the affected animals that have passed through the disease may become a source of further infection as virus carriers for weeks and months after they have apparently recovered, and are susceptible of reinfection, as one attack does not confer permanent immunity.

Foot-and-mouth disease in man.—Foot-and-mouth disease is primarily and principally a disease of cattle; secondarily and casually, a disease of man. It is transmissible to man through the eating or drinking of raw milk, buttermilk, butter, cheese, and whey from animals suffering from foot-and-mouth disease. It is also transmitted directly, though more rarely, from the salivary secretions or other infected material which may gain entrance through the mucous membrane of the mouth. It is doubtful whether the disease can be transmitted to man by cutaneous or subcutaneous inoculation, though it is probable that the infection may be communicated if the virus directly enters the blood through wounds of any kind. Children are not infrequently infected by drinking unboiled milk during the periods in which the disease is prevalent in the neighborhood, while persons in charge of diseased animals may become infected through contact with the diseased parts or by milking, slaughtering, or caring for the animals.

The symptoms in man resemble those observed in animals. There is fever, sometimes vomiting, painful swallowing, heat and dryness of the mouth, followed by an eruption of vesicles on the mucous membrane of the mouth, and very rarely by similar ones on the fingers. The vesicles appear on the lips, gums, cheek, and edge of the tongue, and are about the size of a pea. The vesicles soon rupture, leaving a small erosion which is soon covered by a thin crust under which the new formation of epithelium proceeds rapidly. The skin eruption mostly appears on the hands, tips of the fingers, base of the nails, and more seldom on the toes and other parts of the body. Besides these local changes, during the course of the disease headache, pain in the limbs, vertigo, abdominal cramps, vomiting, diarrhea, and weakness are occasionally observed. The disease is seldom fatal, usually appearing in a very mild form except in weakened children, in whom an accompanying intestinal catarrh may lead to a fatal termination.

Veterinarians who have had considerable experience with the disease among animals regard the human affection as by no means uncommon in countries where foot-and-mouth disease prevails, but the disturbance of health is usually too slight to come to the notice of the family physician.

But few outbreaks of the disease in man have occurred in the United States, and therefore cases of its transmission to man in this country are rather rare. Dr. James Law reports having observed the disease in man from drinking infected milk during the epizootic of 1870 in the Eastern States, but the outbreaks of 1880 and 1884 affected such a small number of animals and were so quickly suppressed that no instance of its transmission to man was recorded. A few cases have been reported by Brush accompanying the New England outbreak of 1902. Similar reports have been likewise received concerning the appearance of vesicular eruptions in the mouths of children during the 1908 and 1914 outbreaks, and the history of these cases incriminates the milk supply.

Experiments by Loeffler and Froesch, as well as recent experiments which have been made in Denmark and Germany, indicate that the infection is comparatively easy to destroy by heat or the usual antiseptics. Milk pasteurized at a temperature of 60° C. for 20 minutes is safe so far as infection by foot-and-mouth disease is concerned.

SEPTICEMIA AND PYEMIA.

These two names are applied to diseased conditions which are so nearly alike in their symptoms that it is sometimes difficult to distinguish the one from the other. Indeed, the name pyosepticemia, or septicopyemia, is often applied when it is impossible to make a distinction between septicemia and pyemia or where each is equally responsible for the diseased condition. The name septicemia is derived from two Greek words meaning "poison" and "blood," and signifies that the germ lives in the blood, hence the use of the term "blood poisoning" for this disease. Pyemia is likewise derived from two Greek words, meaning "pus" and "blood," and is that form of septicemia caused by pus-producing organisms and characterized by secondary abscesses.

Causes.—Neither of these diseases is brought about, strictly speaking, by any specific organism; hence neither can be looked upon as a specific disease. The organisms most frequently found in cases of septicemia are, on the whole, the same as those of pyemia, and may be pus cocci, the bacillus coli, or other pus-producing organisms. These organisms are often found as secondary invaders in other diseases, such as advanced cases of tuberculosis, in which cases they are responsible for the formation of pus.

Aside from the causative organism, or, in other words, the active cause, there are many secondary causes. The most important of these in pyemia is a break in continuity of the protective covering, as a wound, which affords an entrance into the tissues for the organisms. Among the different varieties of wounds may be mentioned cuts, bruises, punctures, burns, chemical or frozen wounds, and compound fractures of bones. Injuries received during parturition, stoppage of the milk ducts, and infection of the umbilicus in the newly born are also frequent causes of pyemia. Septicemia usually follows surgical wounds, local suppuration, enteritis, bronchitis—in fact, wherever there is a local lesion of any kind permitting germs to enter the blood. Septicemia was formerly applied to designate the condition in which the organisms were localized, but in which their toxins were diffused in the blood. Pyemia was made to represent that condition when the organisms were localized, but in which the pus was transported by the blood. These terms now are applied to conditions in which both the organisms and their toxins, or the pus, are present in the blood. The term septicemia is indicated when intoxication is the more pronounced symptom and pyemia if pus formation and metastatic or secondary abscess formation are observed.

Symptoms.—The symptoms of both diseases include primarily a high fever (104° to 107° F.). Coupled with this there is disinclination to move, the animal is depressed and not cognizant of its surroundings. The pulse is rapid, small, and feeble, respiration increased, mucous membrane injected, swollen, and of a yellowish tinge. Appetite is lost and death follows in the case of septicemia in from two to four days. In pyemia the symptoms come on more slowly and are not so intense as in septicemia, while the course of the disease is longer, lasting from six days to four weeks. The mortality is not so great as in septicemia, but the period of convalescence is always long.

Lesions.—Septicemia is characterized by the destructive changes in the blood, which is chocolate colored, noncoagulable, and swarms with bacteria. The lining membranes of the heart are studded with red spots, often running together to form a large hemorrhagic area. The lungs, liver, and kidneys may also show these hemorrhages. The spleen is enlarged and full of black blood. The cadaver decomposes very rapidly and in some cases forms great quantities of fetid gas. In pyemia, in addition to these lesions, abscesses are formed in the various organs throughout the body. If the disease develops slowly a post-mortem examination shows the abscesses to be the chief alterations. The pus content is usually greenish, stained with blood, and contains strings of fibrous tissue and necrosed matter.

Treatment.—Treatment is almost futile in advanced cases of either disease. Septicemia is usually fatal and pyemia frequently so. Prevention and the immediate treatment of local infections are the surest means of combating them. For local treatment of wounds the usual antiseptics are indicated, such as 3 per cent compound cresol or carbolic acid, or one one-thousandth bichlorid-of-mercury solution. For pyemia, where the abscesses are near the skin, they should be opened and treated antiseptically by injecting any of the previously mentioned germicides. General and heart stimulants are indicated, such as a drench containing digitalis 2 drams and alcohol 2 ounces. Quinin and calomel in repeated small doses of one-half dram each three times a day are sometimes beneficial. Camphor in the form of oil of camphor (camphor dissolved in 10 parts of sweet oil) is a good stimulant and has some antiseptic properties, which make it a valuable drug in combating these diseases when it is given in doses of 2 drams three times daily.

HEMORRHAGIC SEPTICEMIA.

Hemorrhagic septicemia is a name applied to a highly fatal, infectious disease existing in various species of domestic and wild animals, from a microorganism having definite biological characters and possessing the properties of producing clearly defined and characteristic lesions.

This causal agent, Bacterium bovisepticum, belongs to the same group of cocco-bacilli as those causing chicken cholera, swine plague, and rabbit septicemia, and may be described as an ovoid, nonmotile, polar-staining bacterium with rounded ends, 1/38000 of an inch wide by 1/20000 of an inch long, sometimes seen in pairs and sometimes in chains.

Various names have been applied to this disease, and though the causative agent and the distinctive lesions are well known, it is more than likely that the affection is seldom recognized. It was described by Bollinger in 1878, and named Wild und Rinderseuche, from its having affected deer, wild boars, cattle, and horses in an epizootic which swept over Germany at that time. Before this, however, several epizootics of what was evidently the same disease had been well described, notably that which occurred in England in 1854. Since then it has occurred in epizootic and enzootic forms in many sections of Europe, Asia, Africa, and America. In this country the disease has been observed in Texas, Tennessee, New York, Minnesota, Pennsylvania, District of Columbia, South Dakota, and Wisconsin. Other names given to it are game and cattle disease, buffalo disease, barbone, pasteurellosis bovina, ghotwa, and infectious pneumoenteritis.

In earlier times it was evidently confounded with gloss anthrax, and even now it is probably mistaken in a great many instances for anthrax, blackleg, cornstalk disease, and cerebrospinal meningitis.

The disease is essentially a septicemia, or blood poisoning, and the microbic invasion occurs from inoculation probably either through abrasions of the skin or by injury to the mucous membranes from coarse fodder, etc. Moore and Smith have found in the mouths and nasal cavities of healthy animals, including cattle, bacteria belonging to this group; but these organisms proved to be nonpathogenic. As is well known, however, many pathogenic germs at times exist in a saprophytic state, and it is not hard to conceive how a microbe may cease such existence and assume parasitic or pathogenic properties when the surroundings are eminently favorable. This may be a connecting link in the etiology of sporadic outbreaks of the disease in which all other hypotheses as to its genesis seem untenable. The disease seems to occur most frequently in swampy or mucky localities or in pastures receiving the overflow from infected fields. It is said to occur usually in the spring of the year, when the melting snows and rains bring to the surface the subterranean waters from rich soils containing nitrogenous materials in which the bacteria have been existing. In a great many instances there does not seem to be any plausible explanation for an outbreak of the disease and one can only surmise as to its origin.

Symptoms.—Three forms of the disease are recognized, based upon the distribution of the lesions—the superficial, or cutaneous, the pectoral, or thoracic, and the intestinal form. The last is a usual accompaniment of the other two and may be mild or severe. Naturally the symptoms vary according to the violence of the attack and to the particular form of disease with which the animal is affected. In the superficial, or cutaneous, form the presence of a swollen tongue, throat, and dewlap, or even of the lower portion of the legs, gives us a clew to the trouble. An entire loss of appetite occurs, and in milk cows there is a diminution of the milk secretion. The temperature may be only slightly elevated, but it is usually very high. Salivation is set up by the inflammation of the mouth and pharynx. Unsuccessful efforts at eating and swallowing are made. There may be difficulty in breathing, depending on the amount of involvement of the larynx, trachea, bronchi, or lungs. There may be a blood-stained discharge from the nostrils, and the mucous membrane thereof will often show punctiform hemorrhages. The pulmonary form shows the same symptoms as croupous pneumonia, with a frequent suffocative cough and oppressed breathing, or dyspnea. When the intestines are involved the patient strains to defecate, and passes shreds of intestinal mucus along with blood-stained feces. The urine also may be tinged with blood. Finally a severe diarrhea takes place, the animal becomes correspondingly weak, and death takes place in 24 to 36 hours. Cases may die in as short a period as six to eight hours, while in the pectoral form of the disease the animal may linger six or eight days. Cases have been reported which became chronic and in which death did not take place for a month or more. In some of the cases running an acute course, symptoms of toxemia are present; there is a lack of sensation of the skin, staggering gait, trembling, eyes fixed, neck at times bent to one side, and the eyes showing a wild expression. At times the animals appear as if in pain and look around at the flanks. In the pectoral form they may stand with the forelegs wide apart in evident effort to breathe more freely. Sometimes there is a champing of the jaws and a very free flow of glairy saliva dropping from the mouth.

The prognosis is decidedly unfavorable and 80 to 90 per cent of the cases result fatally.

Lesions.—The characteristic lesions of hemorrhagic septicemia consist of hemorrhagic areas in the subcutaneous, subserous, and muscular tissues, the lymph glands, and the viscera; in fact, they are distributed more or less widely throughout the body and vary in size from a mere speck to the diameter of a half dollar or even larger. The superficial form presents itself first as a doughy tumefaction of the skin about the region of the throat, neck, dewlap, or legs, which pits on pressure. This tumefaction consists essentially of a cerogelatinous exudate into the subcutaneous and intermuscular tissues.

Bloody extravasations may take place in subcutaneous tissues in various places, but they are usually seen about the lower portion of the neck. The mucous membranes and submucous tissues of the mouth, tongue, pharynx, and larynx become involved in the process and are greatly thickened, inflamed, and infiltrated with serum. The mucous membrane becomes reddish purple, and that of the nostrils may in addition show hemorrhagic spots on its surface. The lymphatic glands in this region are also swollen and infiltrated with bloody serum. The salivary glands are pale and dry. The pectoral type, though at times existing alone, may coexist with the cutaneous form. The inflammatory edema of the mouth extends to the mucous membrane of the trachea and bronchi, producing an extensive thickening and a yellowish infiltration. The lung shows interstitial thickening from the outpouring of serum into its meshes. It may become pneumonic.

The diaphragm, heart sac, and heart walls show numerous hemorrhagic points and larger bloody extravasations. Sometimes there is a serous pleurisy, with more or less fibrinous exudate. In the intestinal form the submucous and subperitoneal tissues show alterations from a few hemorrhagic spots to large bloody suffusions, or even gelatinous infiltrations. This latter is seen about the region of the pancreas and in the folds of the mesentery. There is a severe hemorrhagic inflammation of the intestines and a staining of the intestinal contents with blood. The muscular system throughout shows hemorrhagic areas. The abdominal viscera, liver, spleen, and kidneys often present hemorrhagic lesions.

Differential diagnosis.—Anthrax, which presents superficial swellings, like hemorrhagic septicemia, may be distinguished from that affection on post-mortem examination by the enlargement and engorgement of the spleen, the contents of which are soft and tarry. The blood of anthrax animals is very dark, and does not become light red on exposure to air, nor does it coagulate, while in hemorrhagic septicemia the blood is normal in appearance and coagulates. The detection of the anthrax bacillus in the blood would be final.

In blackleg the animals affected are usually under 2 years of age. The swellings are quite evident, and usually occur on the legs, above the knees or hocks, and are distended with gas, which crackles, or crepitates, when pressed upon. If one of these tumors is opened, a bloody serum will exude, and the gas gives off the odor of rancid butter. The internal hemorrhages are not general, although they may occur. A microscopic examination of the juices from the tumefaction will show the blackleg bacillus.

In cerebrospinal meningitis the causative agent is unknown, but probably exists in the feed. It may occur in any locality and at any season of the year. There are no local swellings, and cattle are not frequently affected.

Cornstalk disease may be differentiated from this affection from the fact that it always occurs after the cattle are turned into a cornstalk field, by its sudden onset, the absence of any characteristic symptoms or post-mortem lesions, and the failure to find the causative agent in the blood.

In making a post-mortem examination of animals affected with hemorrhagic septicemia, it would be well to examine the articular surfaces of the long bones, as it has been reported that they are frequently ulcerated. This should apply especially to those cases that have shown lameness.

Treatment.—Treatment is absolutely useless, so far as we know at present, and for all practical purposes prophylaxis alone should be relied upon. The same sanitary precautions, such as isolation, disinfection, and burial or burning of all dead carcasses, should be observed as for anthrax and other highly infectious diseases. All the premises, barns, stalls, litter, and stable utensils should be thoroughly disinfected. Separate the apparently well animals from the sick by placing them in a separate lot.

Experiments by the Bureau of Animal Industry toward protective inoculation of the exposed cattle on infected premises have been made and the results have been so satisfactory that several commercial houses handling biological products are manufacturing a vaccine for hemorrhagic septicemia in accordance with the Government's experiments on this subject. The method of preparing the vaccine is similar to that recommended by Lignières. It consists in growing the cultures of the organism of the disease at 42 to 43° C. and preparing from them growing at this temperature two different strengths of vaccine. The weaker vaccine, which is used for the first injection, is grown for five days at this temperature, whereas the stronger vaccine, for the second injection, is grown for only two days. These vaccines are used with an interval of 10 days between the injections, the dose being 1 cubic centimeter at each injection. The effect of this vaccine in abating outbreaks already in progress has been highly satisfactory and it is plain that the general introduction of preventive vaccination for hemorrhagic septicemia must be of material benefit to the cattle raisers in the infected districts.

VESICULAR ERUPTION OF THE GENITAL ORGANS.

This contagious disease is called coital exanthema or vesicular exanthema, and is more or less prevalent on the Continent. It has also been observed in the breeding districts of the United States. It is the subject of legislation in Germany, and governmental statistics are published annually concerning its distribution in the Empire. According to the reports from Hungary 492 head of cattle were attacked during 1898, 587 in 1899, and 207 in 1900.

A similar or perhaps identical disease of horses has the same distribution and is transmissible from horses to cattle and vice versa.

The disease may be defined as a highly contagious eruption situated upon the external genital organs of both sexes and accompanied with little or no general disturbance of health. The contagion, the nature of which remains still unknown, is transmitted mainly during copulation. The bull may have the disease and convey it to all the cows with which he comes in contact, or he may become infected by one cow, and, although not showing the disease, he may, during copulation, transmit it for several days after to all other cows. Simple contact between one cow and another may convey the disease, or the sponges used in cleaning the diseased may carry the virus to the healthy. It has also been conveyed to healthy cows by these animals lying with their hind quarters against infected wooden troughs.

Symptoms.—The period between the infection and the appearance of symptoms is somewhat variable. It is usually given as three to six days. It may be briefer or much longer. In cows the mucous membrane of the vagina and the vulva become swollen, inflamed, very tender, and covered with dark-red spots. The secretion is very abundant and consists at first largely of serum and mucus resembling the white of an egg. Small vesicles then appear, which rapidly burst and are converted into excoriations or deeper ulcerations. The secretion becomes more purulent and is apt to dry in crusts about the root of the tail. The eruption is accompanied with much itching and difficulty in urinating. The walk may be stiff and awkward. In bulls the eruption is situated on the prepuce and the end of the penis, and consists of pimples, vesicles, and ulcers, as in cows. It is accompanied with a little purulent discharge from the prepuce, itching, and difficulty in urinating. In severe cases the inflammation and swelling may extend backward to the scrotum and forward upon the abdomen.

The disease lasts from one to four weeks and always terminates in recovery. The acute stage lasts only four or five days, while the complete healing of the inflammation is slow. The eruption is usually accompanied with very little general disturbance. If the pain and irritation are severe, there may be some light loss of appetite and diminished milk secretion in cows. The disease rarely causes abortion. Chronic catarrh of the vagina and permanent sterility frequently follow as sequelæ.

Treatment need not be resorted to excepting in severe cases. The secretion and exudation should be washed off and a mild antiseptic applied, such as a 1 per cent solution of carbolic acid (1 ounce to 3 quarts of water) or 2 per cent solution of cresol compound in water. Care must be taken not to carry the disease from the sick to the well by sponges, etc., which have come in contact with the affected organs. These should be destroyed. To prevent the spread of the disease the infected animals should be kept isolated until they have recovered.

RABIES OF CATTLE.

Rabies is a disease preeminently affecting the canine race, although all warm-blooded animals, including man, are susceptible to the malady, which is always communicated through bites from a preceding case. It has required many years of patient, scientific research to lead the ablest investigators to a clear comprehension of the cause, nature, and characteristics of this affection. It was known and described several centuries prior to the beginning of the Christian era, and from the earliest dawn of history it has been feared and dreaded. Its terrible manifestations have always been surrounded with an atmosphere of awe and mystery, and it is not surprising that myths, fallacies, and misconceptions in regard to it have been common and widely accepted. As the investigations by which we have come to a tolerably clear understanding of the facts concerning rabies have been comparatively recent, and for the most part, have appeared in scientific periodicals, fallacies in regard to the disease continue to have a strong hold upon the public mind. For instance, it is still a widely prevalent belief that if persons or animals are bitten by a dog they are liable to become rabid if the dog should contract the disease at any future time. There is no foundation for this impression, and it would be a great comfort to many people who are now and then bitten by animals if the fallacy of this idea were known. All experience, both scientific and practical, goes to show that rabies is transmitted only by animals that are actually diseased at the time the bite is inflicted. Rabies is an infectious disease involving the nervous system and characterized by extreme excitability and other nervous disorders and always terminating in death. The contagion of this disease has never been isolated, but the fact that it is caused by a specific organism principally found in the nervous system is indisputable. For instance, if an emulsion of the brain of a rabid animal is filtered through a germ-proof filter, the filtrate will be harmless. This fact indicates that the infectious principle is not in solution, but is an organism withheld from the filtrate by the filter. This contagion can be propagated only in the body of an animal. It is transmitted naturally from one animal to another solely by bites, and the old idea of spontaneous appearance of the disease is absolutely fallacious. It may be produced artificially by inoculating susceptible animals with an emulsion of the brain or spinal cord, as well as the saliva, milk, and other secretions of the affected animal. The blood, on the contrary, seems to be free from the infectious principle. The saliva contains the virus, which, under natural conditions, is introduced into or under the skin on the tooth of the rabid animal. The disease is widespread, being found in many countries of Europe, Asia, and Africa, and in certain sections of the United States.

Owing to the rigid quarantine regulations enforced against dogs imported into Australia, that country remains absolutely free from the disease. Following the canine race, cattle seem to be the most frequently affected, probably because rabid dogs, next to their morbid desire to attack other members of their own race, have a better opportunity to bite grazing cattle than any other species of animal. The relative frequency of rabies in these two species of animals is indicated by the carefully compiled statistics of the German Empire, which shows that 904 dogs and 223 cows died of rabies in 1898, while in 1899 there were 911 cases in dogs and 171 in cattle. The latter receive bites most frequently on the hind legs and in the hips and about the lower jaw. These places are most accessible to dogs, owing to the habit of cattle to drive their tormentors away by lowering their heads and using their horns. Every animal bitten does not necessarily develop the disease, but the per cent of fatalities has been variously estimated, and averages from 25 to 30. This, however, depends on the location and size of the wound as well as the amount of hemorrhage produced, and various other conditions. In general, the nearer the bite is located to the central nervous system and the deeper the wound inflicted, the greater the danger of a fatal result. In cases in which the hemorrhage resulting from the bite is profuse, there is a possibility that the virus will be washed out of the wound and thus obviate the danger of subsequent appearance of the disease.

The virus after being deposited in the wound remains latent for an extremely variable period of time, which also depends on the size and depth of the wound as well as its location and the amount of the virulent saliva introduced. Experiments have proved that the virus follows the course of the nerves to the spinal cord and along the latter to the brain before the symptoms appear. Gerlach, having collected the statistics from 133 cases, has found this time, known as the period of incubation, to vary from 14 to 285 days. The great majority of cases, however, contract the disease in one to three months after the bite has been inflicted.

Symptoms.—As in dogs, both furious and dumb rabies are met with, the former being more common in cattle. A sharp line of distinction, however, can not be drawn between these two forms of the disease, as the furious form usually merges into the dumb, from the paralysis which appears prior to death. The typical cases of dumb rabies are those in which the paralysis appears at the beginning of the attack and remains until death. The disease first manifests itself by a loss of appetite and rumination, stopping of the secretion of milk, great restlessness, anxiety, manifestation of fear, and change in the disposition of the animal. This preliminary stage is followed in a day or two by the stage of excitation, or madness, which is indicated by increasing restlessness, loud roaring at times with a peculiar change in the sound of the voice, violent butting with the horns and pawing the ground with the feet, with an insane tendency to attack other animals, although the desire to bite is not so marked in cattle as in the canine race. A constant symptom is the increased secretion of saliva with a consequent frothing at the mouth, or the secretion may hang from the lips in long strings. Constipation is marked, and there is manifested a continual, although unsuccessful, desire to defecate. Spasms of the muscles in different parts of the body are also seen at intervals. About the fourth day the animal usually becomes quieter and the walk is stiff, unsteady, and swaying, showing that the final paralysis is coming on. This is called the paralytic stage. The loss of flesh is extremely rapid, and even during the short course of the disease the animal becomes exceedingly emaciated. The temperature is never elevated, it usually remaining about normal or even subnormal. Finally, there is complete paralysis of the hind quarters, the animal being unable to rise, and but for irregular convulsive movements lies in a comatose condition and dies usually from the fourth to the sixth day after the appearance of the first symptom.

Anatomy.—If animals which have succumbed to rabies are examined post mortem, very slight evidence of disease will be found in any of the organs, and, indeed, the absence of any specific lesions may be considered as characteristic. The blood is dark and imperfectly coagulated. The throat is frequently reddened, and there may be small spots of extravasated blood in the intestines. The stomachs are usually empty. In the spleen there may be hemorrhagic enlargements (infarcts). The cadavers rapidly undergo decomposition.

Differential diagnosis.—It is not an easy matter to decide definitely that a given animal has rabies, since the symptoms given above belong in part to a variety of other diseases, among which may be mentioned the excitement seen in young animals following close confinement, certain vegetable and mineral poisons, acute enteritis, and alterations of the central nervous system in cattle, the most common of which is tuberculosis of the brain and its covering membranes. The post-mortem lesions, however, should assist in making a correct diagnosis. Tetanus may readily be differentiated from rabies by the persistence of muscular cramps, especially of the face and abdomen, which cause these muscles to become set and as hard as wood. In tetanus there is also an absence of a depraved appetite or of a willful propensity to hurt other animals or to damage the surroundings. The cow remains quiet and the general muscular contraction gives her a rigid appearance. There is an absence of paralysis which marks the advanced stage of rabies. The form of dumb rabies in dogs is characterized by the paralysis and pendency of the lower jaw, while in tetanus the jaws are locked. This locking of the jaws in cattle renders the animal incapable of bellowing, as in rabies. Finally, tetanus may be distinguished from rabies by the fact that the central nervous system does not contain the infectious principle, while in rabies the inoculation of test rabbits with the brain or cord of a rabid animal will produce the disease with characteristic symptoms after an interval of 15 to 20 days. This period of incubation is much longer than in tetanus, since the inoculation of rabbits with tetanus cultures invariably results in death after a short period and usually within three days. The positive evidence that a rabid dog has been near cattle would greatly assist in making a decision in doubtful cases.

The disease in dogs is pretty well recognized by most people, but in case a suspected dog is killed it is desirable to open the animal and examine the contents of the stomach. While feed is absent, a variety of odd things may be present which the abnormally changed appetite of the rabid dog has induced it to swallow. Among such things may be straws, sticks, glass, rags, earth, pieces of leather, and whatever the animal may have encountered small enough to be swallowed. This miscellaneous collection in the stomach of dogs, together with absence of feed, is regarded by authorities as a very valuable sign, and in case of doubt may be made use of by laymen. In important cases, however, the head of the dog, cow, or other suspected animal should be removed and sent to the nearest biological laboratory, where a positive diagnosis can be made within 36 hours by the histological examination of the plexiform nerve ganglia, and within two or three weeks by the intracerebral inoculation of rabbits with an emulsion of the brain of the suspected animal.

Treatment.—This is useless after the first appearance of symptoms. When, however, a wound inflicted by a rabid animal can be discovered, it should be immediately cauterized or even completely extirpated, care being taken to cut entirely around the wound in the healthy tissues. For cauterizing the wound, fuming nitric acid, the hot iron, and 10 per cent solution of zinc chlorid are the most efficacious. To afford an absolute protection, this should be done within a few moments after the bite has been inflicted, although even as late as a few hours it has been known to thwart the development of the disease.

Pasteur originated and perfected a system of preventive inoculation against this disease which has greatly reduced the mortality in human subjects. Its application to animals, however, is difficult and requires considerable time and expense. A method of vaccination applicable to animals, consisting of a single injection of a suspension of "fixed" rabies virus, is now being quite extensively employed by veterinarians. Sanitary regulations which seek to control effectively the disease by exterminating it among dogs are most likely to prove successful. The measures which are adopted to this end can not be discussed in this place, but it is a striking fact that where the muzzling of all dogs has been rigidly enforced, as in England and in certain German districts, the disease has been practically stamped out.

TUBERCULOSIS.

[[Pls. XXXIV]-[XXXVIII].]

Tuberculosis is an infectious and communicable disease characterized in its early stages by the formation, in various organs of the body, of minute nodules or tubercles, which contain Mycobacterium tuberculosis, the cause of the disease.

The disease, in its various manifestations, has been known for many centuries, and legislative enactments having reference to the destruction of affected animals and forbidding the use of the flesh date far back into the Middle Ages. The opinions entertained regarding the nature and the cause of the malady varied much in different periods and very markedly influenced the laws and regulations in vogue. Thus, in the sixteenth century, the disease was considered identical with syphilis in man. In consequence of this belief very stringent laws were enacted, which made the destruction of tuberculous cattle compulsory. In the eighteenth century this erroneous conception of the nature of the disease was abandoned and all restrictions against the use of meat were removed. Since that time, however, its communicable nature has been established by many investigators, and the tide of opinion has again turned in favor of repressing the disease and prohibiting the sale of contaminated products.

Occurrence.—The statistics concerning tuberculosis show that it is a disease prevalent in all civilized countries. In some countries, such as the northern part of Norway and Sweden, on the steppes of eastern Europe and Russia, in Sicily and Iceland, and in Algiers, it is said to be quite rare.

The returns from testing British cattle with tuberculin, supplied by the Royal Veterinary College, as stated in March, 1900, showed that among 15,392 animals tested 4,105, or 26 per cent, reacted.

During the slaughter of cattle for pleuropneumonia careful examinations of the carcasses were made for tuberculosis. Of 300 head killed near Edinburgh 120, or 40 per cent, were tuberculous. Of 4,160 killed in England 20 per cent were tuberculous. Of one of these lots of cattle (451 animals) the president of the Lancashire Farmers' Association testified that they were fairly representative cattle—cows, heifers, and growing stock—a thoroughly mixed lot; 20 per cent of them had tuberculosis.

Of 398 bovine animals taken haphazard in the city of Manchester, 120, or 30 per cent, were tuberculous. Among them were 168 cows, 69, or 41 per cent, being tuberculous, and 2 having diseased udders.

The result of testing the Queen's herd at Windsor was that 36 out of 40, or 90 per cent, were found tuberculous.

The investigations made by the British Dairy Farmers' Association deserve particular attention, coming as they do directly from a cattle owners' organization. The council of this association "resolved to submit the general consideration of the question to a committee, with a view to some more definite understanding as to the possible extent to which tuberculosis exists in dairy cattle." The secretary was instructed to write to a number of dairy farmers being members of the association, asking their cooperation and the use of their herds for the application of the tests. Of the herds offered, 9 were selected, containing 461 cows and 12 bulls, and 188 of these animals reacted, being 40.8 per cent. There were among these cattle 335 Shorthorns, of which 119, or 35 per cent, reacted; 67 crossbreds, of which 28, or 42 per cent, reacted; 47 Ayrshires, of which 37, or 80 per cent, reacted.

Another experiment of much interest is that of the Cheshire County Council. The technical instruction committee set aside £250 to be used by a joint committee from the agricultural and horticultural schools and Worleson Dairy Institute for applying the tuberculin test to their herds. The tests were made February 15, 1899. The results were: Worleson herd of 54 animals, 16 diseased, or 29.6 per cent; agricultural school herd of 17 animals, 4 diseased, or 23.5 per cent. The Worleson herd consisted of Shorthorn cows. In each herd the purebred Shorthorn bull was tuberculous. The results of the tuberculin test were confirmed by the slaughter of the animals and examination of the carcasses.

Sir T. D. G. Carmichael, member of Parliament for Midlothian, gave evidence before the royal commission that his Polled Angus herd was tested in the spring of 1895. "The results of the test were fearfully unexpected and alarming." Of 30 tested 13 showed decided reaction—43 per cent. Again, he speaks of having 41 animals tested the same spring and 16 reacted—39.5 per cent.

Of 80 Shorthorn cattle intended for export which were tested 34 reacted, or 42 per cent.

Of a herd of 25 British Shorthorns recently tested in quarantine 40 per cent were found tuberculous.

The addition of these animals above referred to gives 20,930 head examined and 5,441, or 26 per cent, pronounced tuberculous. And these herds were not selected because they were supposed to be tuberculous, but represent the general cattle stock of the country. These animals included at least 470 head of Shorthorns, of which 170, or 34 per cent, were tuberculous.

To these facts may be added the evidence of Prof. Bang that in the first half of the nineteenth century tuberculosis was brought to Denmark by cattle from Switzerland, Schleswig, and England, and that the same thing is now going on in Sweden and Norway, particularly through English cattle. Also the evidence of M. Sivori, chief of section at the ministry of agriculture, Argentina, who has investigated tuberculosis in that country and who says that "30 or 40 years ago tuberculosis was unknown in Argentine cattle, and it is still unknown among the native (criollo) cattle. Its appearance dates from the introduction of pure breeding animals. Statistics prove that tuberculosis is observed among the grades— above all among those of the Durham and less among the Hereford."

Moreover, the reports of the royal commission of Victoria, Australia, and of the New Zealand department of agriculture show a large proportion of tuberculous cattle in those colonies, where the disease was almost certainly carried by British cattle.

In the same manner that tuberculosis has been carried from Great Britain to Denmark, Sweden, Norway, Argentina, and Australia, it has also been taken to Canada. In one herd of imported cattle slaughtered in the Canadian quarantine station, 13 of the 14 animals were found tuberculous. One of the largest Shorthorn herds in Canada was some time ago tested because an animal from it was condemned when offered for shipment to the United States. This herd was found to be very badly affected, and an effort is being made to eradicate the disease by the Bang method. A Canadian official publication says of another Shorthorn herd, which at one time had a very high reputation, that when an investigation in regard to tuberculosis was recently made the disease was found among ordinary cattle wherever animals from this herd had been introduced, and that this herd, which had been looked upon as one of the greatest benefits to the farming community, was really a danger, because it disseminated tuberculosis among the farmers' herds. Still another well-known herd recently attracted attention because four animals from it offered for export to the United States were all tuberculous.

From December 23, 1900, to February 19, 1901, the period that the department inspector tested all Canadian cattle intended for shipment to the United States, 140 purebred Shorthorns and 3 Shorthorn grades were tested, and of the total number 26, or 18 per cent, reacted. During the first month that this inspection was enforced, and when it may be assumed that the condition of the cattle most nearly represented what it had previously been, 74 cattle were offered for importation, and 18, or 24.3 per cent, were found tuberculous.

In justice to Shorthorn cattle it should be said in this connection that they are probably no more susceptible to tuberculosis than are other breeds, but the disease has been allowed to spread in certain herds and families to such an extent as to give a wrong impression concerning the breed as a whole.

The slaughterhouse statistics of Prussia show 14.6 per cent of the cattle and 2.14 per cent of the hogs to be tuberculous. In Saxony the percentage is 29.13 with cattle and 3.10 with hogs. In the city of Leipzig the figures are 36.4 for cattle and 2.17 for hogs. (Siedamgrotzky.) Of 20,850 animals in Belgium tested with tuberculin in 1896, 48.88 per cent reacted. (Stubbe.) Of 25,439 tested in Denmark from 1893 to 1895, 49.3 per cent reacted; and of 67,263 tested from 1896 to 1898, 32.8 per cent reacted. (Bang.)

Figures available in the United States allow us to make a reliable estimate of the extent of tuberculosis of cattle. The following summary is presented:

State.	Number tested.	Number tuberculous.	Per cent tuberculous.
Alabama	68,772	1,071	1.6
Arkansas	5,917	98	1.7
Colorado	1,959	76	3.9
Connecticut	29,286	4,695	16.0
Delaware	19,003	2,132	11.2
Florida	56,533	1,438	2.5
Georgia	46,522	998	2.1
Idaho	57,731	1,052	1.8
Illinois	92,781	6,112	6.6
Indiana	142,833	3,991	2.8
Iowa	158,514	9,958	6.3
Kansas	64,341	1,796	2.8
Kentucky	66,839	1,492	2.2
Louisiana	36,391	981	2.7
Maine	67,406	1,792	2.7
Maryland	65,888	5,491	8.3
Massachusetts	26,297	2,371	9.0
Michigan	163,323	5,361	3.3
Minnesota	240,888	7,555	3.1
Mississippi	99,245	503	.5
Missouri	196,208	2,587	1.3
Montana	165,640	3,346	2.0
Nebraska	125,162	3,947	3.2
Nevada	29,541	1,042	3.5
New Hampshire	16,623	1,697	10.2
New Jersey	32,184	2,542	7.9
New Mexico	3,897	39	1.0
New York	167,852	23,071	13.7
North Carolina	64,008	1,098	1.7
North Dakota	139,501	4,142	3.0
Ohio	97,612	4,470	4.6
Oklahoma	67,522	2,453	3.6
Oregon	123,792	2,581	2.1
Pennsylvania	102,465	6,322	6.2
Rhode Island	3,458	338	9.8
South Carolina	41,868	740	1.8
South Dakota	43,433	2,353	5.4
Tennessee	63,631	956	1.5
Texas	61,956	1,256	2.0
Utah	59,711	586	1.0
Vermont	160,361	11,486	7.2
Virginia	135,677	3,881	2.9
Washington	154,292	3,864	2.5
West Virginia	36,603	798	2.2
Wisconsin	285,269	8,166	2.9
Wyoming	22,811	322	1.4

Reports of tuberculin tests made on 400,000 cattle in the United States during the years 1893 to 1908 by Federal, State, and other officers with tuberculin prepared by the Bureau of Animal Industry show 37,008 reactions, or 9.25 per cent. These were mostly dairy cattle, and in some cases herds were suspected of being diseased.

Later reports of tuberculin tests made in the United States from July 1, 1917, to March 1, 1922, on 3,911,546 cattle by State, county, and Federal officers engaged in cooperative tuberculosis eradication work showed 153,046 reactions, or 3.9 per cent.

All cattle in the District of Columbia, numbering 1,701, were tested with tuberculin in 1909-10, and 18.87 per cent reacted. In 1909-11 herds in Maryland and Virginia supplying milk to the District of Columbia were tested, with 19.03 and 15.38 per cent of reactions, respectively, among 4,501 cattle.

All cattle in the District of Columbia were tuberculin tested in 1920-21, numbering 1,313, and 5 animals reacted, or 0.4 per cent, demonstrating that tuberculosis may be eradicated from all the herds in a circumscribed area.

The beef cattle of the United States show a much smaller proportion of the disease than dairy cattle, though the percentage of cattle found tuberculous in the Government meat-inspection service has increased considerably in recent years. This increase is due partly, but not wholly, to more stringent inspection. Of 7,781,030 adult cattle slaughtered under Federal inspection during the fiscal year ended June 30, 1911, 76,448 were found tuberculous, a percentage of 0.98.

From the statistics above referred to, and other data, it appears that in the more densely populated areas of Europe and America from 5 to 50 per cent of the dairy cattle are more or less affected with tuberculosis, while the proportion of beef cattle affected is distinctly less, ranging from 0.14 to 30 per cent. This difference is due to a number of causes. Beef cattle average younger when slaughtered. They are not so frequently stabled, and are for that reason less liable to infection, and as the males constitute a large proportion of this class of animals the effect of milk secretion in lowering the vital forces is not so apparent. In the United States it has been estimated that about 10 per cent of the dairy cattle are tuberculous, while only about 2 per cent of the beef cattle are so infected.

Cause and nature of the disease.—The cause of tuberculosis is the tubercle bacillus, which gains entrance to the body, lodges somewhere in the tissues, and begins to grow and multiply at that point. As this bacillus vegetates and increases in numbers it excretes substances which act as irritants and poisons and which lead to the formation of a small nodule, called a tubercle, at the point of irritation. As the bacilli are disseminated through the animal body they affect many parts and cause the formation of an enormous number of tubercles. By the union of such tubercles, masses of tubercular material are formed, which in some cases are of great size. The disease is called tuberculosis because it is characterized by the formation of these peculiar nodules, and the bacillus which causes the disease is for the same reason known technically as the Mycobacterium tuberculosis.

There are undoubtedly predisposing conditions which contribute toward the development of the disease; some of these are found in the animal body and others in the environment. An enfeebled condition caused by insufficient feed, exposure to great extremes of atmospheric temperature and insanitary surroundings, or the drain occasioned by heavy production of milk, appear to aid the development of the bacillus, and there is also a special individual susceptibility in some cases which may be otherwise described as an inability of the animal tissues to resist and destroy the bacilli when they have penetrated to the inner recesses of the body.

Among the conditions of environment which aid the development of tuberculosis may be mentioned stabling with lack of ventilation, damp buildings, the keeping of many animals together, drafts of air which cause colds and catarrhs, and, in general, everything which prevents the animals from developing and maintaining the highest condition of health. None of these conditions of body or environment are sufficient to cause the disease, however, unless the animals are exposed to the Mycobacterium tuberculosis and it penetrates the tissues of their bodies.

The ways in which the tubercle bacilli find their way into the body may be considered under four heads: (1) By inhalation into the lungs; (2) by taking into the digestive tract in the milk of tuberculous cows or with other contaminated feed; (3) during coition when the sexual organs are tuberculous; (4) from the tuberculous mother to the fetus in the uterus. The bacilli can reach the lungs by inhalation only when the bacilli are thoroughly dried and pulverized and in condition to be carried by currents of air.

It is well known that the bacilli withstand drying for months before they lose their power of producing disease. They leave the bodies of diseased animals in several ways. There may be a little discharge occasionally coughed up as a spray from the diseased lungs, or this material may be swallowed and the bacilli carried off with the excrement, or milk may be spilt, or there may be a discharge from the vagina when the genital organs are tuberculous. There may also be ulcers of the intestines, from which many bacilli escape with the feces. The bacilli from these sources may become dried and pulverized and carried in the air of the stable and into the lungs of still healthy cattle, where the disease then develops.

The disease of the stomach, intestines, and mesenteric glands is very probably the result of feed infection. Tubercle bacilli may have been scattered upon the feed by diseased animals, but the most common source of such infection is the milk of tuberculous cows. Calves may become infected in this way. The disease may remain latent until the animal becomes older. The not-infrequent occur rence of tuberculosis of the uterus and ovaries makes it probable that the disease may be transmitted by a diseased bull or carried by a healthy one from a diseased cow to a number of healthy cows.

The source of infection is always some previous case of the disease, for the disease can never rise spontaneously; hence, in those stables in which there is frequent change of cattle the introduction of tuberculosis by cattle coming from other infected stables is the most frequent source of infection. Since the bacilli when dried can be carried by the air, it is not necessary that healthy animals come in direct contact with cases of disease to become infected. In general, the greatest number of cases occur in the immediate environment of cities, where there are not only abundant opportunities for infection, owing to the frequent introduction of new animals into herds, but where the sanitary conditions may be regarded as the poorest.

The bacillus of tuberculosis was discovered by Robert Koch in 1882. It is a slender, rodlike body (see [Pl. XXVIII], fig. 6) from one-third to two-thirds the diameter of a red blood corpuscle in length. As already explained, when the bacillus has become lodged in any organ or tissue it begins to multiply, and thereby causes an irritation in the tissue around it, which leads to the formation of the so-called tubercle. The tubercle, when it has reached its full growth, is a little nodule about the size of a millet seed. It is composed of several kinds of tissue cells. Soon a change takes place within the tubercle. Disintegration begins, and a soft, cheesy substance is formed in the center, which may contain particles of lime salts. When these tubercles continue to form in large numbers they run together, forming masses of various sizes. The disintegration which attacks them leads to the formation of large cheesy masses of a yellowish color, containing more or less of lime salts in the form of gritty particles. These large tuberculous masses are surrounded by or embedded in layers of fibrous tissue which in some cases becomes very dense and thick.

The disease is thus a development of these tubercles in one or more organs of the body. The distribution and number of the tubercles determine the course of the disease.

In a large number of cases the changes are limited to the lungs and the serous membranes[4] of the thorax and abdomen. Pathologists have been in the habit of calling the lung disease tuberculosis and the disease of the serous membranes "pearly disease." Statistics have shown that in about one-half of the cases both lungs and serous membranes are diseased, in one-third only the lungs, and in one-fifth only the serous membranes. At the same time the lymphatic glands near the diseased organs are usually involved. Other organs, such as the liver, not infrequently contain tubercles. Though the disease may remain restricted to a single organ, it now and then is found generalized, affecting all organs of the body.

In the lungs ([Pl. XXXIV]) the changes observed vary according to the age and intensity of the disease process. They usually begin with the appearance of very minute tubercles. These may appear in large numbers on the surface of the lungs or within the lung tissue. Later the contents become cheesy and partly calcified. When these tubercles are sufficiently numerous to become confluent, large masses may be formed, which undergo the same retrogressive changes of caseation and calcification. In addition to the formation of tubercles in the lung tissue, certain other changes take place. There is usually bronchitis with abundant catarrhal secretion; this plugs up the smaller air tubes, and the lung tissue supplied with air by the tubes collapses. Subsequently it becomes filled with yellowish, cheesy matter, which greatly distends the small air tubes and air vesicles (bronchopneumonia). The connective tissue between the lung lobules, around the tubercles, and around the air tubes becomes thickened and indurated. In the larynx and the bronchi tubercles may vegetate upon the mucous membrane, and ulcers may result from their breaking down. The inflammatory irritation which the growth of the tubercles on the surface of the lungs arouses gives rise to adhesion of the lungs to the ribs and diaphragm. This adhesion is sometimes so firm and extensive that the lungs appear grown to the chest wall.

When, therefore, the lungs in advanced stages of the disease are cut open we observe large yellowish masses, from one-quarter to three-quarters of an inch in diameter, of a cheesy texture, in which calcified, gritty particles are embedded and which are surrounded by very firm connective tissue. The neighboring lung tissue, when collapsed and involved in bronchopneumonia, has the color and consistency of pale-red flesh. The air tubes, large and small, stand out prominently on the cut surface. They are distended with a pasty, yellowish, cheesy mass, surrounded and enveloped in thick mucus, and their walls greatly thickened. The larger bronchi may be sacculated, owing to the distention produced by the cheesy contents.

The disease usually attacks the bronchial glands, which are situated on the trachea and bronchial tubes at the bifurcation. The changes in the glands are the same as those going on in the lung tissue, and they frequently reach an enormous size.

The tubercle formation on the serous membranes covering the lungs and chest wall ([Pl. XXXVII], fig. 2), which may go on at the same time with the lung disease or independent of it, has been called "pearly disease," on account of the peculiar appearance of the tubercles. These begin as very minute, grayish nodules, which give the originally smooth, lustrous membrane a roughened appearance. These minute tubercles enlarge, become confluent, and project above the surface of the membrane as wartlike masses, attaining the size of peas. In this stage their attachment to the membrane is by means of delicate fibers. The attachment is loose, so that the tubercle hangs by a short pedicle or neck and may be moved slightly to and fro. Large masses are frequently formed by a coalescence of many tubercles and the secondary formation of the same. These may be found on the lungs, the ribs, and the diaphragm. These tubercles likewise undergo degenerative changes. The center partly softens and partly calcifies into a grayish mortarlike mass, and is gritty. Associated with the formation of tubercles on the pleura, those glands situated back of the center of the lungs between the two main lobes (posterior mediastinal) become greatly enlarged and the center cheesy. ([Pl. XXXVI], fig. 1.) They may compress the esophagus and interfere with swallowing. The size attained by these tumors and new growths is well illustrated by the fact that, taken together, they not infrequently weigh from 60 to 80 pounds. The bronchial glands, which in the healthy state are not so large as horse-chestnuts, have been found to attain a weight of more than 10 pounds.

In the abdominal cavity tubercles may be found, both in the organs and on the serous membranes covering them. They are situated usually on the omentum, or caul (see [Pl. XXXVI], fig. 2), the diaphragm, and the walls of the abdomen. In the liver large and small tubercular masses are occasionally encountered. (See [Pl. XXXV].) The mesenteric glands are occasionally enlarged and tuberculous; likewise the glands near the liver. Tubercles may also develop in the spleen, the kidneys, the uterus and ovaries, and the testicles.

Tubercular affection of the intestines seems to be quite rare, although ulcers of the large intestines have been observed. Nodules may also form under the serous covering of the intestines.

The brain and spinal cord are occasionally found tuberculous. Of 40 cases, Semmer found tuberculosis of the brain in 4. It is not improbable that, owing to the infrequency of exposing the brain and spinal cord, tuberculosis may have escaped the attention of pathologists, and it may be that it is not so uncommon as is generally supposed. The tubercles occur on the membranes of the brain as well as in the substance of the brain itself. They project into the ventricles as masses, varying in size from a pinhead to a hen's egg. They finally lead to various inflammatory changes. Jöhne has observed numerous small tubercles on the membranes of the spinal cord.

Very rarely tuberculous lesions have been observed in the bones and muscles of the body. Not so rare, however, is the affection of the lymphatic glands embedded in the muscular tissue, and those which can be felt beneath the skin. These are situated at the joints, under the jaw, and along the neck.

Of late tubercular disease of the udder in cows ([Pl. XXXVIII]) has received considerable attention from sanitarians, owing to the infection of the milk with the virus of tuberculosis. According to those who have given this subject special attention, the udder becomes swollen uniformly and quite firm. This swelling, which is painless, frequently attacks but one quarter, more rarely two, these being usually the hind quarters. The larger milk ducts contain yellowish, cheesy particles, in which are many tubercle bacilli. Later larger nodules can be felt within the udder, which undergo the various changes to which tubercles are subject. The udder may grow very hard to the touch and become very large, weighing in some cases up to 40 pounds. The milk, at first normal, becomes thin and watery after a month or so, and is mixed with flakes and tubercle bacilli.

As regards the frequency of the tuberculous processes in the different organs, the following carefully compiled statistics of the disease in Bavaria and Baden may serve as a guide:

Bavaria:	Per cent.
Tuberculosis of lungs and serous membranes	41
Tuberculosis of lungs alone	33
Tuberculosis of serous membranes alone (pearly disease)	17
Tuberculosis of other organs	8
Baden:
Tuberculosis of lungs alone	21
Tuberculosis of serous membranes alone	28
Both combined	39
Generalized tuberculosis	9
Tuberculosis of the sexual organs alone	3

Symptoms.—The beginning of the disease usually passes unnoticed, inasmuch as it is very slow and insidious and rarely accompanied with fever. When the lungs are involved a dull, short cough is noticed, which may later on become prolonged, convulsive, and very troublesome to the animal. The cough is more frequent in the morning after movement and drinking. The breathing varies. Only when much of the lung tissue is diseased is it labored and accompanied with active movements of the chest and nostrils. Discharge from the nose is rare or absent. At times, however, when the tubercles have broken down and cavities containing cheesy masses have formed in the lung tissue, or when the air tubes have become filled with cheesy and mucous masses, coughing will dislodge them and cause their discharge. In advanced stages the breath may have a disagreeable odor. Pressure on the chest wall may give rise to pain.

The general effect on the body is at first slight. In fact, animals may remain in good flesh for a considerable time. Invariably as the disease progresses loss of flesh and appetite and paleness of the mucous membranes become manifest. These symptoms are accompanied with a gradual diminution of the milk secretion. The debilitated condition of the animal is also manifested by a staring coat and a tough, dry, harsh skin (hidebound). Digestive disturbances are indicated by tympanites, or distention of the rumen by gas, colic, and diarrhea, alternating with constipation. The animal generally dies from exhaustion after a period of sickness which may last months or even years.

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TUBERCULOSIS.

DESCRIPTION OF PLATES.

Plate XXXIV. Tuberculosis of the lungs of cattle. The upper figure represents a large cheesy mass, surrounded by a capsule of connective tissue, the whole embedded in healthy lung tissue. The lower figure illustrates in section a mass of tubercles which have undergone cheesy degeneration, and some of which are surrounded by dense connective tissue.

Plate XXXV. Tuberculosis of the liver. A large portion of the lobe represented in the Plate has undergone tuberculous changes. Numerous nodules are shown in various stages of the disease, the majority of which, however, contain the yellowish, partly cheesy, partly gritty areas characteristic of advanced tuberculous degeneration. This large mass involves the surface of the liver, and also extends into the liver substance.

Plate XXXVI. Tuberculosis of lymph gland and of omentum (caul).

Fig. 1. A lymph gland from the region of the thorax behind or above the esophagus, or gullet (posterior, or dorsal, mediastinum). The gland is shown cut through and laid open. It is very much enlarged, and the yellowish cheesy masses which represent tissue undergoing tuberculous changes are well shown on the cut surface.

Fig. 2. Omentum, or caul, resting upon the paunch. The reddish nodules with which the membrane is beset are tubercles, the product of the disease.

Plate XXXVII.

Fig. 1. Tuberculosis of the sirloin and porterhouse cuts of beef. The grapelike tuberculous growths are mainly restricted to the lining membrane of the abdomen.

Fig. 2. Tuberculosis of the pleura of a cow, so-called "pearly disease." Notice the grapelike clusters of tubercular nodules scattered over the lining membrane of the chest (pleura).

Plate XXXVIII. Tuberculosis of cow's udder. The udder was uniformly swollen and quite firm. Small cheesy foci and yellowish lines of tuberculous material follow the course of the milk ducts. The mucous membrane of the milk cistern (a) is ulcerated and covered with yellowish cheesy particles. The supramammary lymphatic gland (b) is greatly enlarged and contains many miliary tubercular foci.

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Tuberculosis in the abdominal organs is often signalized by abortion and by abnormal sexual manifestations. When the brain is involved, the disease may cause convulsions, unconsciousness, paralysis, as well as peculiar movements in a circle, oblique position of the head, etc. Lydtin quotes the following description of the disease as taken from a Swiss sanitary order:

A dry, short, interrupted, hoarse cough, which the sick animals manifest, especially in the morning at feeding time, still more after somewhat violent exertion. At first these animals may be full blooded and lay on a considerable amount of fat when well fed. As the disease progresses they grow thin and show more and more those appearances which indicate diseased nutrition, such as a staring, lusterless, disheveled coat; dirty, tense skin, which appears very pale in those regions free from hair. The temperature of the skin is below normal. The loss of fat causes sinking of the eyes in their sockets. They appear swimming in water, and their expression is weak. The cough is more frequent, but never or very rarely accompanied with discharge. The body continues to emaciate, even with plenty of food and a good appetite, so that the quantity of milk is small. At times in the early stages of the disease, still more in the later stages, the diseased animals manifest considerable tenderness when pressure is applied to the front or the sides of the chest by coughing, moaning, etc. Often symptoms are wanting in spite of the existence of the disease.

Lydtin also quotes at length a description of the abnormal sexual desire occasionally observed among cows when affected with this disease.

Diagnosis.—A disease so varied in its attack upon the different organs of the body and in the extent of the disease process must necessarily lead to mistakes when diagnosis is attempted by ordinary means of examination. It has been confounded with the later stages of pleuropneumonia, with parasitic diseases of the brain, the lungs, the intestines, and with actinomycosis. A careful examination of the lungs by auscultation and percussion enables the expert to locate large tuberculous masses, owing to dullness, loss of respiratory murmur, and abnormal sounds, such as blowing, whistling, and creaking. The majority of cases of tuberculosis in cattle, however, including many in which the lungs are quite seriously involved, can not be detected in this manner.

THE TUBERCULIN TEST.

The tuberculin test, which is marvelously accurate in its indications, has been almost universally adopted for the detection of tuberculosis. Tuberculin is a drug prepared by sterilizing, filtering, and concentrating the liquids in which the tubercle bacillus has been allowed to vegetate. It contains the cooked products of the growth of these bacilli, but no living bacilli; consequently, when this substance is injected under the skin of an animal it is absolutely unable to produce the disease, cause abortion, or otherwise injure the animal. In case the injected animal is normal there is no more effect upon the system than would be expected from the injection of sterile water; however, if the animal is tuberculous, a decided rise of temperature will follow the use of tuberculin by the subcutaneous method. This substance, discovered by Koch, has the effect, when injected into the tissues of a tuberculous animal, of causing a decided rise of temperature or other manifestations while it has no such effect upon animals free from the disease. The value of tuberculin for this purpose was tested during the years 1890 and 1891 by Guttman, Roeckl and Schütz, Bang and Salomonsen, Lydtin, Jöhne and Siedamgrotzky, Nocard, and many others. It was at once recognized as a most remarkable and accurate method of detecting tuberculosis even in the early stages and when the disease had yet made but little progress. It is now quite generally employed.

The tuberculin test came into existence through the most careful and thorough scientific experimentation.

As a result of its use an accurate diagnosis may be established in more than 90 per cent of the cases tested. The relatively few failures in diagnoses are included among two classes of cattle. The first class contains those that are tuberculous, but which do not react either because of the slight effect of an ordinary-sized dose of tuberculin on an advanced case of the disease with so much natural tuberculin already in the system, or on account of a recent previous test with tuberculin which produces a tolerance to this material, lasting for about six weeks. The second class includes those that are not tuberculous, but which show indications of a reaction as a result of (a) advanced pregnancy, (b) the excitement of œstrum, (c) concurrent diseases, as inflammation of the lungs, intestines, uterus, udder, or other parts, abortion, retention of afterbirth, indigestion, etc., (d) inclosure in a hot, stuffy stable, especially in summer, or exposure to cold drafts or rains, (e) any change in the method of feeding, watering, or stabling of the animal during the test. Notwithstanding all these possibilities of error, the results of thousands of tests show that in less than 3 per cent of the cases tested do these failures actually occur. In the first class the chances of error are decidedly reduced by the skilled veterinarian by making careful physical examination and diagnosing clinically these advanced cases, and by the injection of double or triple doses into all recently tested cattle, with the taking of the after-temperature, beginning two hours following the injection and continuing hourly for 20 hours.

It is therefore apparent that tuberculin should be applied only by or under the direction of a competent veterinarian, capable not only of injecting the tuberculin but also of interpreting the results, and particularly of picking out all clinical cases by physical examination. The latter observation is extremely important and should always be made on every animal tested.

In the second class, where the temperature test is used, errors are avoided by eliminating from the test those cases that are nearing parturition or are in heat or show evidence of the previously mentioned diseases or exhibit temperatures sufficiently high to make them unreliable for use as normal. Where other methods of test are used these conditions do not have an important bearing on the results. In addition, a satisfactory tuberculin must be used; also an accurate thermometer and a reliable syringe, in order that a sufficient dose of tuberculin may be given. Finally, the number of apparent errors of the tuberculin test will be greatly diminished if a careful post-mortem examination is made, giving especial attention to the lymph glands. This low percentage of failures being the case, cattle owners should welcome the tuberculin test, not only for their own interest but for the welfare of the public as well. Where this method of diagnosing the disease has been adopted tuberculosis is gradually being eradicated. Without its use the disease can not be controlled and the owner is confronted with serious and continuous losses; with its use the disease can be eradicated from the herd, a clean herd established in a few years without very serious loss or hardship, and the danger of its spread to man removed. Tuberculin may therefore be considered a most beneficial discovery for the stock raiser.

Law has clearly stated the question when he says—

Many stock owners still entertain an ignorant and unwarranted dread of the tuberculin test. It is true that when recklessly used by ignorant and careless people it may be made a root of evil, yet as employed by the intelligent and careful expert it is not only perfectly safe, but it is the only known means of ascertaining approximately the actual number affected in a given herd. In most infected herds living under what are in other respects good hygienic conditions two-thirds or three-fourths are not to be detected without its aid, so that in clearing a herd from tuberculosis and placing both herd and products above suspicion the test becomes essential. * * * In skilled hands the tuberculin test will show at least nine-tenths of all cases of tuberculosis when other methods of diagnosis will not detect one-tenth.

Probably the most popular objection to tuberculin is that it is too searching, since it discovers cases in which the lesions are small and obscure. While this fact is admitted, it should also be remembered that such a small lesion to-day may break down and become widely disseminated in a relatively short period. Therefore any cow affected with tuberculosis, even to a slight degree, must be considered as dangerous not only to the other animals in the herd but also to the consumer of her products.

In 1898 Bang, of Copenhagen, one of the highest European authorities, in his paper presented to the Congress for the Study of Human and Animal Tuberculosis, at Paris, said:

Numerous tests made in almost every civilized country have demonstrated that in the majority of cases tuberculin is an excellent means for diagnosing the existence or nonexistence of the disease, but giving us no positive information as to the extent to which the disease has progressed. When tuberculin produces a typical reaction we may be almost sure that there exists in the body of the animal a tubercular process. The cases in which a careful examiner has not succeeded in finding it are very rare, and I am led to believe that when, notwithstanding all the pains taken, it has escaped discovery, the reason is that it is located in a portion of the body that is particularly inaccessible. Nevertheless, it is not to be denied that a fever, entirely accidental and of short duration, may in some rare cases have simulated a reaction. However this may be, the error committed in wrongly condemning an occasional animal for tuberculosis is of no practical consequence.

A worse aspect of the case is that there are some diseased animals in which tuberculin fails to discover the existence of tuberculosis. In most of these, no doubt, the deposits are old, insignificant, and generally calcified, or they are cases where the disease is arrested and perhaps in process of recovery, and which are possibly incapable of disseminating the contagion. But it is known that there are cases, not altogether rare, where tuberculin fails to cause a reaction in a highly tuberculous animal, and consequently one in which the disease exists in an extremely contagious form. For this reason a clinical examination should always be made of an animal which does not give a reaction but which shows symptoms indicating that, notwithstanding the test, it may suffer from tuberculosis.

Nocard, of Paris, wrote also in 1898 as follows:

The degree of certainty of the indications furnished may be stated in precise terms. The observation of a clear reaction to tuberculin is unequivocal; the animal is tuberculous. The pretended errors imputed to the method are explained by the extreme sensitiveness of the reagent, which is capable of detecting the smallest lesion. It often requires prolonged and minute researches in the depths of all the tissues to discover the few miliary centers, the presence of which has been revealed. The reaction is absolutely specific. In those cases where it is observed with animals which show lesions of another disease (actinomycosis, hydatid disease, verminous bronchitis, distomatosis), it may be affirmed that there exists, in addition to these conspicuous changes, a tuberculous center which alone has provoked the reaction.

The failure to react does not necessarily imply absence of tuberculosis. Such failures of tuberculin are very exceptional. They are seen most frequently with animals affected with tuberculosis in a very advanced stage and made evident by plain external signs. Sometimes, also, there are found at the post-mortem examination of animals which have not reacted small fibrous or calcified lesions in such a condition that one is tempted to believe them cured. Whether sterile or not, these lesions have no tendency to increase, and they are not very dangerous from the point of view of contagion.

These opinions of two eminent authorities, living in different countries, after long experience of their own and after studying the results of the many tests made in different parts of the world, should have great weight. They are essentially the same throughout.

In 1897 Voges compiled statistics of tuberculin tests, the accuracy of which had been determined by post-mortem examination. Of 7,327 animals tested, it appeared that errors had been made with 204, or 2.78 per cent. In the work of the Pennsylvania Live Stock Sanitary Board post-mortem examinations were made on about 4,400 reacting cattle and the disease was found in all but 8 of those which had given characteristic reactions.

The results of a much larger number of tests might be compiled at this time, but they would not materially change the average of those already mentioned. It is plain that tuberculin is a remarkably accurate test of tuberculosis, that the animals which react may be safely considered as tuberculous, and that when a careful clinical examination is practiced in addition to the test there are few animals in a dangerous condition which escape detection.

The first questions asked by those who oppose the adoption of the tuberculin tests are: Is this test infallible? and, if it is not infallible, why should it be forced upon the cattle owners of the country?

In answer to these questions it may be said that tuberculin is not absolutely infallible, and yet it is by far the best method of diagnosing tuberculosis that has been discovered. It is much better than any test known for pleuropneumonia when that disease was eradicated.

Practically all the animals that react are affected with tuberculosis and should be separated from the herd, not only in the interest of the public, but in the interest of the owner of the herd. The best authorities admit, after studying many thousands of tests, that there are few, if any, mistakes made in condemning cattle which show a typical tuberculin reaction. The errors are principally in the other direction—that is, some tuberculous animals are not discovered by the tuberculin test, but as the most dangerous of these may be picked out by ordinary clinical examination this fault of tuberculin is not so serious as it at first sight appears. This being the case, it should not be necessary to force the tuberculin test upon owners. They should be anxious to adopt it in their own interests and for the protection of their patrons. There is to-day no greater danger to the cattle and hog industries than that which confronts them in the form of tuberculosis, a disease already widespread and rapidly extending. Furthermore, in view of the results revealed by numerous tests covering vast numbers of animals, tuberculin must be considered as harmless for healthy animals. It has also been clearly demonstrated that tuberculin interferes in no way with the milking function in healthy cattle; neither in the quantity of milk nor in butter-fat value has any variation been detected. The conclusions of some of the best authorities on the subject of its harmlessness to healthy animals are given below.

Nocard and Leclainche state:

Direct experiments and observations collected by thousands show that the tuberculin injections have no unfavorable effect. With healthy animals the system is indifferent to the inoculation; with tuberculous animals it causes slight changes which are not at all serious.

Bang has written as follows on this question:

We will now consider the following question, a very important one, in the application of tuberculin, viz: Can the reaction produce a worse condition in tuberculous animals than before existed? Hess emphatically states that it can, and on this account he earnestly warns against its application. My attention has been directed to this question from the beginning. In my first publication on tuberculin injection I reported two cases in which acute miliary tuberculosis was proved in two high-grade tuberculous cows several weeks after the tuberculin injection. I then stated my suspicion that perhaps the tuberculin injection had some connection with this, just as is often supposed to be the case in human practice. With my present very large amount of material for observation at hand I may express the following opinion: Such an acute development of tuberculosis as a result of tuberculin injection is to be feared only exceptionally, and then in cases of advanced tuberculosis. It must not be forgotten that acute miliary tuberculosis by no means rarely accompanies an advanced tuberculosis of long standing. It is therefore impossible to offer strict proof of the causal connection with the injection, and only oft-repeated observation could make this probable. In support of my view I offer the following: In the course of the last three years I have made careful post-mortem examinations of 83 tuberculous animals, which have been removed from my experiment farm, Thurebylille. Among these were 18 (or, strictly speaking, 23) high-grade tuberculous animals. I have been able to prove miliary tuberculosis in only 4 of these. Among the others, which showed less developed tuberculosis, I have never found miliary tuberculosis, and with very many I have never found any sign of a more rapid development of the process. On the contrary, it has been proved that the disease was restricted locally, often for years, in spite of yearly repeated injections. Dissections were made at very different periods after the injections—in 17 cases from 4 to 12 days after the last test. In all of these cases earlier tests had been made months or years before. In 28 cases the injection took place from 19 days to 2 months before the butchering; in 3 of these cases earlier injections had been made. In 38 cases from two and one-half months to one year intervened between the last injection and the dissection. Dissection gives the best explanation of this question, but a clinical observation, continued for years, of a herd tested with tuberculin can render very essential aid. If Hess's opinion is correct, it is to be assumed that tuberculosis must take an unusually vicious course in such herds, but this I have been unable to prove. At Thurebylille there has existed for three years a reacting division, consisting originally of 131 head and now 69. Although these animals are yearly tested, and although most of them react every year, the division certainly appears to be made up of healthy animals, and the farm inspector has expressed the decided opinion that the tuberculosis in this division is no more developed than at the beginning of the experiment. The testimony of many owners of large herds of cattle which have long ago been injected is to the same effect. I will adduce statements from several. A farm tenant whose cattle were injected 20 months previously, when 82 per cent of the grown animals reacted, wrote me recently as follows: "Only 2 cows from the division of 100 head had been sold as decidedly tuberculous. The majority appeared afterwards, just as before, entirely healthy. The fat animals which had been slaughtered had been pronounced healthy by the butchers." Another farm tenant with a herd injected in 1894 had not been obliged to remove a single animal from the tuberculosis division, numbering 70 head. A large farm owner in Jutland stated in September that he had traced no undesirable result from the injection. His herd of 350 had been injected in February and about 75 per cent reacted. Similar answers have been given by other owners and veterinarians.

A veterinarian who had injected 600 animals, among them a herd of a large farm, 18 months previously, expressed the belief that the injection had produced in no single case an unusually rapid or vicious course of tuberculosis. In spite of a demand made months ago, I have received thus far no report from any veterinarian of an undesirable result.

On a large farm, on which before the injection tuberculosis had appeared in a vicious form, the owner had the impression that the severe cases had afterwards become more numerous. He had, however, not suffered severe losses, and 8 months later the large reacting division by no means made a bad impression. Finally, it is to be noticed that tuberculin has been employed on a large scale in Denmark for years, and still the demand from farmers constantly increases. This could certainly not be the case if the injections were generally followed by bad results.

Paige said, after the tests of the herd of the Massachusetts Agricultural College, that "its use is not followed by any ill effects of a serious or permanent nature."

Lamson, of the New Hampshire College Agricultural Experiment Station, said: "There is abundant testimony that its use is not in any way injurious to a healthy animal."

Conn, who made a special study of the present attitude of European science toward tuberculosis in cattle, reached the following conclusions:

It has been, from the first, thought by some that the use of tuberculin produces a direct injury upon the inoculated animals. This, however, is undoubtedly a mistake, and there is no longer any belief anywhere on the part of scientists that the injury thus produced is worthy of note. In the first place, the idea that it may produce the disease in a perfectly healthy animal by the inoculation is absolutely fallacious. The tuberculin does not contain the tubercle bacillus, and it is absolutely certain that it is impossible to produce a case of tuberculosis in an animal unless the tubercle bacilli are present. The use of tuberculin, therefore, certainly can never produce the disease in the inoculated animal.

It has been more widely believed, however, that the inoculation of an animal with this material has a tendency to stimulate an incipient case of tuberculosis. It has been thought that an animal with a very slight case of the disease may, after inoculation, show a very rapid extension of this disease and be speedily brought to a condition where it is beyond any use. The reasons given for this have been the apparent activity of the tuberculosis infection in animals that have been slaughtered shortly after inoculation. This has been claimed, not only by agriculturists who have not understood the subject well, but also by veterinarians and bacteriologists. But here, too, we must recognize that the claim has been disproved, and that there is now a practical unanimity of opinion on the part of all who are best calculated to judge that such an injurious effect does not occur. Even those who have been most pronounced in the claim that there is injury thus resulting from tuberculin have, little by little, modified their claim, until at the present time they say either that the injury which they formerly claimed does not occur or that the stimulus of the disease is so slight that it should be absolutely neglected in view of the great value which may arise from the use of tuberculin. Apart from two or three who hold this very moderate opinion, all bacteriologists and veterinarians unite in agreeing that there is no evidence for believing that any injury results. In Denmark, especially, many hundreds of thousands of animals have been inoculated, and the veterinarians say there is absolutely no reason in all their experience for believing that the tuberculin inoculation is followed by any injurious results.

In 1898 tuberculosis was found in the large Shorthorn herd belonging to W. C. Edwards, of Canada, who with commendable promptness and public spirit had his animals tested, and at once proceeded to separate the diseased from the healthy animals. They were all finely bred animals, and of the very class which we have been told are most susceptible to the injurious effects of tuberculin. After using this test regularly for two years, Mr. Edwards wrote as follows:

I have seen nothing to lead me to believe that the tuberculin test had any injurious influence on the course of the disease. It is by no means our opinion that the disease has been stimulated or aggravated by the application of the tuberculin test. All animals that we have tested two or three times continue as hale and hearty as they were previously, and not one animal in our herds has broken down or failed in any way since we began testing.

Mr. Edwards, in December, 1901, verbally stated that his views as to the harmlessness of tuberculin remained unchanged, and that he had not seen the least ill effect in any of his cattle from its use.

Those who have had most experience with tuberculin have failed to observe any injurious effects following its use upon healthy cattle. With tuberculous cattle it produces a fever of short duration, and in the great majority of cases all derangement of the system which it causes disappears within 48 hours after the tuberculin is administered. There appear to have been a very few cases in which the disease was aggravated, and a greater number in which it was benefited by the injection of tuberculin. The cases of abortion following the tuberculin test have not been numerous, even when cows were tested within a few weeks of the normal time of calving. The few cases of this kind which have occurred may be explained by the fact that abortion in cattle is a very common occurrence, and that it would inevitably happen sometimes after the tuberculin test as a mere coincidence and without any relation between the test and the loss of the calf. The cases of abortion which have been cited appear to be no more numerous than might be expected to have occurred among the same number of cattle within the same period if the test had not been applied.

At the present time there is ample evidence to show that tuberculin is the most reliable means of detecting tuberculosis in the living animal and that its use is not attended by any harmful aftereffects.

An act of Congress was approved July 24, 1919, for the purpose of controlling and eradicating tuberculosis of animals. The official means of detecting tuberculosis in the living animal is the tuberculin test, which may be applied by three different methods—the subcutaneous, the intradermic, and the ophthalmic. It is not necessary to discuss here the details of these three methods, which are made use of in the work of eradication of tuberculosis.

The plan adopted by the State and Federal authorities in eradication of the disease is known as "The Accredited-Herd Plan." Under this plan herds are tested under State and Federal supervision, the diseased animals are appraised, removed, and slaughtered under Federal inspection. Retests are then made after definite periods of time until two successive tests show all the animals to be free from the disease. At this time the herd owner is given a certificate of an accredited herd.

Details concerning the accredited-herd plan may be obtained by applying to the Chief of the Bureau of Animal Industry, Washington, D. C.

THE TUBERCULIN TESTS.

Testing animals with tuberculin is the process of introducing tuberculin into the animal and interpreting results according to well-known standards.

From the investigations and observations that have been mentioned, it may be safely concluded—

1. That the tuberculin test is a wonderfully accurate method of determining whether an animal is affected with tuberculosis.

2. That by its use the animals diseased with tuberculosis may be detected and removed from the herd, thereby eradicating the disease.

3. That it has no injurious effect upon healthy cattle.

4. That the comparatively small number of cattle which have aborted, suffered in health, or fallen off in condition after the test were either diseased before it was made or were affected by some cause other than the tuberculin.

THE SUBCUTANEOUS TEST (UNDER THE SKIN).

The most frequently used method of testing is the subcutaneous test, which consists in injecting the proper quantity of tuberculin underneath the skin into the subcutaneous tissue. If an animal is tuberculous, the action of the tuberculin causes a fever, which is indicated by a rise in temperature. This rise, under ordinary conditions, may occur any time between the eighth and twentieth hours after the tuberculin is injected, but in some cases it is desirable to measure the temperature before the eighth hour and continue to the twenty-fourth hour or longer.

The temperatures are measured at least 3 times in advance of the injection, at 2-hour intervals, to learn whether the animal is in proper condition to receive the test. The temperatures after injection are taken every 2 hours until the test is completed. The proper interpretation of the temperatures is made by the person applying the test, and a careful observance of any clinical changes is always important in determining the result. It can not be set forth too strongly that the test, including the two following methods, should be attempted only by those who are properly qualified to do the work.

THE INTRADERMIC TEST (INTO THE SKIN).

The intradermic test for detecting tuberculosis is used to a considerable extent, especially in area work and on range cattle not easily controlled. When made by those who have become skilled in its application, it is very accurate. In this test the tuberculin is injected between the layers of the skin, only a few drops being used, and it is usually applied in the region at the base of the tail, where the skin is soft and nearly hairless. The intradermic test is satisfactory also for the diagnosis of tuberculosis in swine and, when so used, the tuberculin is applied into the skin of the ear near its base.

The reaction from the intradermic test consists of a swelling at the point of injection and is observed from 72 to 150 hours after the injection. The character of the swelling varies, and a proper diagnosis of tuberculosis by this test can be made only by an experienced person.

THE OPHTHALMIC TEST (INTO THE EYE).

Still another method, known as the ophthalmic test, is used quite frequently and has been found to be of considerable value in what is known as "check" testing; that is, it is used in connection with either of the previously described methods. Sometimes a tuberculous animal that fails to react to those tests shows evidence of the disease upon the application of the ophthalmic test. The ophthalmic tuberculin is placed in one eye and the other eye is used as a check. A reaction is indicated by a characteristic discharge from the eye receiving the treatment, which may occur in from 3 to 10 hours after the application or even later. Some swelling and inflammation of the eye and lids are often noted.

TREATMENT OF TUBERCULOSIS.

Treatment of the disease is not seriously considered by any authorities at the present time.

The measures to be adopted to prevent the spreading of the disease must take into consideration not only the tubercle bacillus, but likewise all those circumstances that make cattle more susceptible to the disease, and which have already been dwelt upon. It would be useless to repeat here all that has been said above on the transmission of tubercle bacilli from one animal to another, and on the dangers of certain debilitating influences. A careful study of these influences will show how tuberculosis may, at least in some cases, be prevented. Great care should be bestowed upon the breeding, the surroundings, and the feed of the animal, so that the latter may be put into a condition to resist infection even when exposed to it. A tuberculin test should be applied to all strange cattle before they are introduced into the herd, and those which show a reaction should be refused.

A rigid exclusion of tuberculous animals is all that is necessary to prevent the appearance of the disease, provided cattle are not infected by consumptive persons and animals. The transmission of the disease from man to cattle is probably not frequent, but is regarded as a possible source of infection.

Tuberculosis in cattle must also be considered as bearing upon tuberculosis of other domesticated animals, particularly hogs. In Europe and the United States this disease is not uncommon among hogs, and appears to be on the increase. The reason for its existence may be looked for in the feeding of pigs with skim milk, buttermilk, and whey from creameries, with the offal of the abattoirs, with the household refuse generally, and behind tuberculous cattle. If tuber culosis is common among cattle, it is likely to be transmitted to hogs kept in this way.

The carcasses of animals which have died of tuberculosis should be buried deeply so that they can not be eaten by other animals. This is likewise true of all organs or tissues of slaughtered animals containing tubercles. These should never be fed to other animals, such as hogs, dogs, and cats, and should either be destroyed by fire or deeply buried.

When any of the animals in a herd of cattle show evident symptoms of tuberculosis, or when the tuberculin test proves that they are affected with this disease, the best method of procedure in most cases is to have the affected animals slaughtered and the stables disinfected. A large proportion of the animals which are slightly affected yield carcasses which are perfectly wholesome and fit for human food, but in all such cases there should be an inspection by an expert at the time of slaughter to determine which carcasses may be used and which should be destroyed.

The disinfection of stables may be accomplished by thoroughly cleaning them, scrubbing the floors with hot water, brushing down all loose dust from the walls, and tearing off all woodwork which is partly decayed. Then the whole interior of the stable should be covered with a good coat of limewash containing 1 part of formalin (which is a 40 per cent watery solution of formaldehyde) to 30 parts of the lime wash, or 4 ounces of formalin to each gallon of lime wash.

Similar precautions should be observed in removing the manure of the infected herd from the barnyard and other places accessible to cattle, since it is known that tuberculous cattle frequently eliminate large numbers of tubercle bacilli through the feces. The ground under the manure pile should then be disinfected, either by the above-mentioned formalin solution or by unslaked lime thickly sprinkled over the soil.

If all the animals which react are destroyed and the stables disinfected in this manner, the herd should remain free from the disease unless other affected animals are added to it. The introduction of the disease in this manner may be avoided by requiring a tuberculin test of all new animals admitted on the premises.

Unfortunately it is a fact that tuberculous animals which have been tested several times may become so accustomed to tuberculin that they will no longer react; consequently it is always advisable to purchase cattle from some one who is known to be reliable, as otherwise animals of this kind may be treated with tuberculin for the purpose of hiding the disease.

In the case of very valuable purebred animals and under exceptional circumstances it may be more advantageous to retain the reacting animals which are in good condition in order to breed from them and in that manner avoid the excessive loss which would follow from their immediate slaughter. This may be done if proper precautions are adopted.

The disposal of reactors depends upon the State laws and live-stock regulations of the State in which the herd belongs. If this policy is followed it should be attempted only after careful study of the plan known as the Bang method of controlling tuberculosis. The live-stock officials of the State should be frequently consulted and their advice followed; otherwise failure will surely ensue. The plan necessitates considerable trouble and is not recommended except under the circumstances mentioned.

BOVINE TUBERCULOSIS AND THE PUBLIC HEALTH.

The increasing amount of evidence pointing to the identity of human and animal tuberculosis, combined with the extraordinary mortality of human beings from this disease, often amounting to 10 to 14 per cent, has raised the question in all civilized countries as to how far animal, and especially bovine, tuberculosis is to blame for this high mortality. The medical and veterinary professions have approached this problem with equal zeal, and much has come to light within recent years which enables us to come to some conclusion. If this disease is transmitted from animals to man, how does the transmission take place? As comparatively few people come in direct contact with tuberculous cattle, it must be either through the meat, the milk, the butter, the cheese, or through all these products that the virus enters the human body. The question has thus narrowed itself down to the food products furnished by cattle.

It has become a very urgent question, especially in the poorer countries of Europe, whether all flesh from tuberculous animals is unfit for human food. It is argued there that if it can be shown that in the majority of cases of tuberculosis the bones and the muscular system are free from infection, there is no reason why the meat should not be put on sale under certain restrictions. The question may be resolved into two divisions: (1) How frequently does the disease invade those parts of the body which are used as food? (2) When the disease process is manifestly restricted to the internal organs, do tubercle bacilli circulate in the blood and lymph and can they be detected in the muscular tissue?

(1) Disease of the bones is not unknown, although very rare. According to Walley, it appears chiefly in the spongy bones of the head and backbone and in the long bones of the limbs. Occasionally the ends of the bones, where they are covered by the synovial membrane of the joints, are dotted with tubercles. The muscular system itself is very rarely the seat of tuberculous deposits, although the lymphatic glands lying near and among the muscles may be not infrequently diseased.

(2) Whether tubercle bacilli are found in muscle juice independent of any tuberculous deposits is a question which must be approached experimentally. There is on record a great variety of opinions on this matter, some authorities considering all flesh from tuberculous animals unfit for food, while others hold a contrary view. Experiments have shown that in rare cases the flesh of tuberculous cattle contains a small number of tubercle bacilli. In Germany the flesh of animals in which the disease is just beginning, or in which it is restricted to one or more related organs, is not rejected. When, however, the disease has affected the muscles or bones, or lymphatic glands situated on or between them, the flesh is condemned as unfit and dangerous. Animals are also rejected in which it is evident, from the general distribution of tubercles throughout the various organs, that the bacilli have been distributed by the blood and may have been carried into the muscular system (generalized tuberculosis).

Concerning the infectious nature of milk secreted by tuberculous cows, authorities have universally agreed that when the udder itself is in the slightest degree involved the milk possesses infectious properties, and is therefore dangerous. Tubercle bacilli in large numbers have been found in the milk and the udder under such circumstances. Unlike other affections of the udder, tuberculosis of this organ does not at once change the appearance and the quality of the milk secreted. Bang states that for at least a month after the disease has appeared the milk is normal in appearance and may be consumed and sold without arousing the suspicion of the owner. Considerable danger is, therefore, involved in this disease, and the necessity for the careful inspection of dairy cows seems more urgent than ever.

Authorities are, however, not fully agreed as to whether the milk from tuberculous cows in which the udder is apparently not invaded by the disease should be considered dangerous or not. Some incline to the belief that the milk secreted by healthy udders is never infectious, even when the lungs or other organs are affected; that, in other words, the tubercle bacilli are rarely, if ever, separated from the lesions which they produce, and that the udder itself must be diseased before tubercle bacilli can appear in the milk. Experiments made with the milk of tuberculous cows in which there were no indications of udder disease do not bear out this theory, since tubercle bacilli have been found in their milk. Some authorities still believe that the udder is diseased when the milk is infected, but that the disease escapes observation. However this may be, the fact that the udder may be diseased and the disease not recognizable simply casts suspicion upon all milk from tuberculous animals. We know that the milk of tuberculous cattle may or may not contain tubercle bacilli when the udder is apparently free from disease, but we have no rapid method of determining whether in any given case the milk contains tubercle bacilli or not. Moreover, the bacilli may be absent at one time and present at another in milk from the same cow. When we consider, therefore, the extent of tuberculosis and the hidden character of the disease, a certain degree of suspicion rests upon all milk from untested cattle. Fortunately, tubercle bacilli are readily destroyed by the temperature of boiling water, and hence both meat and milk are made safe, the former by the various processes of cooking, the latter by boiling for a few moments. It is incumbent upon all communities to have dairy cows examined and tested with tuberculin. If disease is detected, the affected animal should be killed at once or else all opportunity for the sale of such milk removed by appropriate measures. Where milk or cream is sold to the trade in large towns or cities pasteurization should be required as an additional safeguard.

Recently there has been much discussion of the question as to whether human and animal tuberculosis are identical diseases and as to the possibility of the tuberculosis of animals being transmitted to man or that of man being transmitted to animals.

The fact that tuberculous material from human subjects often failed to produce serious disease in cattle was observed by a number of the earlier investigators who experimented with such virus. It was the experiments and comparative studies of Theobald Smith, however, which attracted special attention to the difference in virulence shown by tubercle bacilli from human and bovine sources when inoculated upon cattle. Smith mentioned also certain morphological and cultural differences in bacilli from these two sources, and in the location and histology of the lesions in cattle produced by such bacilli. He did not conclude, however, that bovine bacilli could not produce disease in the human subject, but said:

It seems to me that, accepting the clinical evidence on hand, bovine tuberculosis may be transmitted to children when the body is overpowered by large numbers of bacilli, as in udder tuberculosis, or when certain unknown favorable conditions exist.

Koch, however, in his address at the British Congress on Tuberculosis, went far beyond this and maintained that "human tuberculosis differs from bovine and can not be transmitted to cattle." As to the susceptibility of man to bovine tuberculosis, he said it was not yet absolutely decided, but one was "nevertheless already at liberty to say that, if such a susceptibility really exists, the infection of human beings is but a very rare occurrence." He emphasizes this view in the following language:

I should estimate the extent of infection by the milk and flesh of tubercular cattle and the butter made of their milk as hardly greater than that of hereditary transmission, and I therefore do not deem it advisable to take any measures against it.

This conclusion was so radically different from the views of most experimenters and so out of harmony with facts which had apparently been demonstrated by others that it at once aroused opposition in the congress, followed by the adoption of dissenting resolutions, and led to numerous investigations in various countries. Koch's conclusions were based upon his failure to produce tuberculosis in cattle and other animals by inoculating them with tuberculous material of human origin and his success in causing progressive and fatal tuberculosis in the same kinds of animals when inoculated with tuberculous material of bovine origin. With such positiveness did he hold to the constant and specific difference between the human and bovine bacillus that he promulgated an experimental method of discriminating between them. Speaking of the etiology of intestinal tuberculosis in man, he said:

Hitherto nobody could decide with certainty in such a case whether the tuberculosis of the intestine was of human or of animal origin. Now we can diagnose them. All that is necessary is to cultivate in pure culture the tubercle bacilli found in the tubercular material, and to ascertain whether they belong to bovine tuberculosis by inoculating cattle with them. For this purpose I recommend subcutaneous injection, which yields quite specially characteristic and convincing results.

These important and comprehensive conclusions followed from a comparatively few experiments upon animals, and apparently no effort had been made to learn to what extent human tubercle bacilli may differ in their virulence for cattle or what grades of virulence there might be among bacilli of bovine origin. Vagedes had already shown that bacilli were sometimes present in human lesions which were as virulent as bovine bacilli, but his work was wholly ignored by Koch.

A considerable number of investigators, including Chauveau, Vagedes, Ravenel, De Schweinitz, Mohler, De Jong, Delépine, Orth, Stenström, Fibiger and Jensen, Max Wolff, Nocard, Arloing, Behring, Dean and Todd, Hamilton and Young, the German Tuberculosis Commission, and Theobald Smith, have found tubercle bacilli in the bodies of human beings who died of tuberculosis which proved to have about the same virulence for cattle as had the bacilli from bovine animals affected by the disease.

Kossel, in a preliminary report, stated that the German commission had tested 7 cultures of tuberculosis from cattle and hogs—4 from cattle and 3 from hogs. Two proved acutely fatal in cattle after eight to nine weeks; 4 likewise produced a generalized tuberculosis, but which certainly had a more chronic course, while 1 of the cultures caused only an infiltration at the point of inoculation, with some caseous foci in the adjoining prescapular gland and in one of the mediastinal glands, and there was lacking the spreading of the tuberculosis over the entire body which they were accustomed to see after the injection of cultures of bovine tuberculosis. "Hence," says Kossel, "among bovine tuberculosis bacilli there can also occur differences with regard to the virulence."

The German commission also tested 39 different freshly made cultures from tuberculous disease in man. Nineteen did not produce the slightest symptoms in cattle; with 9 others the cattle exhibited after four months very minute foci in the prescapular glands, which were mostly encapsuled and showed no inclination to progress; with 7 other cases there was somewhat more marked disease of the prescapular glands, but it did not go so far as a material spreading of the process to the adjoining glands. There were 4 cultures, however, which were more virulent and caused generalized tuberculosis in the cattle inoculated with them.

It would appear, therefore, that hereafter everyone must admit that it is impossible always to tell the source of a culture of the tubercle bacillus by its effect when it is inoculated upon cattle. One of the bovine cultures failed to produce generalized tuberculosis in cattle, and some of the human cultures did produce it in such animals. Moreover, while some of the human cultures caused no disease at all, others led to the development of minute foci in the prescapular glands, and still others to somewhat more marked disease of the glands. There were, consequently, four degrees of virulence noted in these 39 cultures of bacilli from human sources and three degrees of virulence in the 7 cultures from animal.

Now, if we accept the views of Koch as to the specific difference between human and bovine tubercle bacilli, and that the human bacilli produce only localized lesions in cattle, while bovine bacilli produce generalized lesions in them, must we not conclude that the one non-virulent bovine culture was in reality of human origin, and that the animal from which it was obtained had been infected from man? This is a logical deduction, but reverses the dictum laid down at London that human tuberculosis is not transmissible to cattle. Again, how are we to explain the human cultures of medium virulence? Are they human bacilli which, for some unknown reason, are increasing in virulence and approaching the activity of the bovine bacillus, or are they really bovine bacilli which have multiplied in the human body until their virulence has become attenuated? In whatever manner these questions are decided it would seem that the findings of the German commission, instead of supporting Koch's views that we can decide with certainty by the inoculation of cattle as to the source of any given bacillus, really show that this method of diagnosis is extremely uncertain in the present condition of our knowledge.

It is definitely admitted that 4 of the human cultures caused generalized tuberculosis in cattle; Kossel suggest, however, that it may be possible that the bacilli in cases of human tuberculosis under certain circumstances can likewise attain a very high pathogenic activity for cattle without being for that reason bovine bacilli. Undoubtedly the German commission is confronting the two horns of a dilemma, either one of which is fatal to the views of Koch as stated with such positiveness at London. If we accept this suggestion thrown out by Kossel, we must conclude that Koch was wrong in his claim that human tuberculosis can not be transmitted to cattle, and thus with one blow we destroy the entire experimental support which he had for his argument before the British Congress on Tuberculosis. If, on the other hand, we accept the conclusion which follows from the principle laid down by Koch for the discrimination between human and bovine bacilli, and which appears to be favored by Kossel, we must admit that bovine tuberculosis is an extremely important factor in the etiology of human tuberculosis. Of the 39 cases of human tuberculosis tested, 4, or more than 10 per cent, were virulent for cattle and would be classified as of bovine origin; however, these 4 cases, were all found among the 16 cases of tuberculosis in children which the commission investigated; hence it is plain that 25 per cent of the cases tested of tuberculosis in children would by Koch's method be classified as of bovine origin.

In the Bureau of Animal Industry two distinct lines of experiments have been carried on, in order that one might serve as a check against the other. There has been, however, no discrepancy in the results. De Schweinitz, in the Biochemic Division, Bureau of Animal Industry, isolated 9 cultures from human tuberculosis. Two were derived from human sputum, 3 from cases of generalized tuberculosis in adults, and 4 from cases of generalized tuberculosis in children. By comparing these cultures with a newly isolated virulent culture of bovine tuberculosis, there were found among them 2 cultures from children which were identical in their cultural and morphological characters with the bovine bacillus. These cultures also killed rabbits and guinea pigs in as short a time as did the bovine bacillus. Hogs which were inoculated subcutaneously with these 2 cultures from children died of generalized tuberculosis. Two calves weighing more than 300 pounds each were inoculated subcutaneously with these virulent human cultures, and as a result developed generalized tuberculosis. A yearling heifer inoculated with 1 of the cultures showed generalized tuberculosis when killed three months after inoculation. Both the cattle and the hogs had been tested with tuberculin and found to be free from tuberculosis before the inoculations were made. It is important to observe in this connection that 2 out of 4, or 50 per cent, of the cultures obtained from cases of generalized tuberculosis in children proved virulent for cattle.

Mohler, working in the Pathological Division, Bureau of Animal Industry, obtained 3 very virulent cultures of tubercle bacilli from the human subject. A goat inoculated subcutaneously with 1 of these cultures died in 37 days with miliary tuberculosis of the lungs involving the axillary and prescapular glands. This bacillus was obtained from the mesenteric gland of a boy. Of still greater interest is a bacillus isolated by Mohler from human sputum. A goat inoculated subcutaneously with a culture of this germ died in 95 days of pulmonary tuberculosis. A cat inoculated in the same manner died in 23 days of generalized tuberculosis. A rabbit similarly inoculated died in 59 days of pulmonary tuberculosis. Another rabbit inoculated with a bovine culture for comparison lived 10 days longer than the one inoculated with this sputum germ. Mohler also inoculated subcutaneously a 1-year-old heifer with a culture derived from the tuberculosis mesenteric gland of a boy 4 years of age. This culture was always refractory in its growth under artificial conditions, and the bacilli were short, stubby rods, corresponding in appearance to the bovine type. At the autopsy, held 127 days after the inoculation, the general condition was seen to be poor and unthrifty, and large, hard tumors were found at the points of inoculation. On the right side the swelling measured 3½ by 5 inches, and the corresponding lymph gland was 2¾ inches long by 1¾ inches in diameter. This gland contained numerous calcareous foci; one at the apex was an inch in diameter. The lesions on the left shoulder of the animal were very similar to those found on the right side, but the dimensions of the tumor were slightly less. The lungs presented an irregular mass of tuberculous nodules, and 7 or 8 grapelike nodules were seen on the parietal pleura. Bronchial and mediastinal lymph glands contained numerous tuberculous foci, and the pericardium, peritoneum, spleen, and liver also were affected.

In order to throw some light, if possible, upon the morphological constancy of the different types of tubercle bacilli, Mohler made comparative studies of bacilli from various sources, and which had been passed through various species of animals, by making the cultures upon dog serum after the method described by Theobald Smith. Some important results have been obtained. One culture of human bacilli which had morphological and cultural peculiarities similar to those of the bovine bacillus, and which produced only local lesions in cattle, was passed through a series of five cats. It was then found to be completely changed in its morphological characters, the rods being elongated, slender, more or less beaded, and entirely of the human type. Far from decreasing in virulence, however, as might be expected from its morphological appearance, this bacillus had so increased in its pathogenic activity that it produced generalized tuberculosis in a cow. This cow was inoculated subcutaneously in front of each shoulder with 2 cubic centimeters of a salt-solution emulsion of the tuberculous omentum of the last cat of the series. The cow rapidly lost flesh, had a temperature of 104° F., with the point of inoculation and adjacent glands greatly swollen. The autopsy revealed generalized tuberculosis, involving the lungs, mediastinal glands, spleen, liver, and kidneys. Tubercle bacilli of the bovine type obtained from the mesenteric glands of a sheep, hog, and cow were similarly transformed in their morphological appearance after being passed through a series of cats and recovered on dog serum. These bacilli also increased in virulence, as the last cat in the series invariably succumbed in a shorter time than the first of the series.

These experiments and observations indicate that the types of tubercle bacilli are very inconstant, and that under suitable conditions they readily change both in morphology and in virulence. A similar conclusion was reached by other investigators in working with the avian and porcine types of tubercle bacilli several years ago, and was reasonably to have been expected with the human and bovine types.

Later investigations made by Park and Krumweide, of the Research Laboratory of New York City, Novick, Richard M. Smith, Ravenel, Rosenau, Chung Yik Wang, and others tend to show the incidence of bovine infection in the human family. Chung Yik Wang stated in 1917 that studies of 281 cases of various clinical forms of tuberculosis in Edinburgh, Scotland, resulted in the isolation of the bovine tubercle bacilli in 78.4 per cent of cases under the age of 5 years, in 70.3 per cent between the ages of 5 and 16, and in 7.8 per cent over the age of 16. This investigator states that from the prophylactic point of view any measure resorted to in combating the disease should be directed not only against the human spread of infection, but also, more particularly in children's cases, against the bovine source of infection.

Ravenel, in summarizing the work of Drs. Park and Krumweide, as well as others throughout the world, gives the following results:

Of 63 children dying of tuberculosis at the babies' hospital 59 cases proved to be human infection and 4 bovine, a percentage of 6-1/3.

Of 9 children dying of tuberculosis at the foundling hospital 4 proved to have derived their infection from human sources and 5 from bovine, a percentage of 55.

Of a total of 88 children under 5 years of age who died of tuberculosis 77 proved to have derived their infection from human sources and 11 from bovine, a percentage of 12½.

Combining the cases studied in New York with those of other observers in different parts of this country and Europe, the following results are obtained:

Adults, 787 cases—777 human and 10 bovine infection.

Children, 5 to 16 years, 153 cases—117 human and 36 bovine infection.

Children under 5 years, 280 cases—215 human and 65 bovine infection.

The figures of the foundling hospital show the real danger of unprotected cows' milk.

The conclusion from these studies is inevitable, namely, that in children, in addition to the large number of deaths which occur from bovine infection, there are many cases of infection resulting in deformities, necessitating operations more or less severe in character and which frequently leave the patient disfigured permanently.

It must be plain to all, from these recent developments, that too much has been made of the slight differences in cultural characteristics, in morphology, and in virulence which have been observed in some cases in comparing the human and the bovine bacilli. The observations were interesting, and it was important that they be followed up until their significance was made entirely clear, but it was an almost unpardonable error, from a sanitary point of view, to promulgate sweeping generalizations calculated to arrest and abolish important measures for preventing human tuberculosis before the soundness of these generalizations had been established by a thorough course of experimentation.

When Koch said in the British Congress on Tuberculosis that he should estimate the extent of infection by the milk and flesh of tuberculous cattle and the butter made of their milk as hardly greater than that of hereditary transmission, and that he therefore did not deem it advisable to take any measures against it, he went far beyond what was justified by any experiments or observations which he reported, and he did a great deal of harm, which will be manifested for years to come, to those who endeavor to guard the human race from the dangers of animal tuberculosis. The researches which have been alluded to make these dangers more definite and certain than they have appeared before, and sanitarians should therefore most earnestly endeavor to counteract the erroneous and harmful impression which was made by Koch's address at London and his subsequent address at the International Conference on Tuberculosis at Berlin.

VACCINIA OR COWPOX.

Variola of cattle, more correctly vaccinia, is a contagious disease of cattle which manifests its presence through an elevation of temperature, a shrinkage in milk production, and by the appearance of characteristic, pustular eruptions, especially upon the teats and udders of dairy cows. Although this is a contagious disease, strictly speaking, it is so universally harmless and benign in its course that it is robbed of the terrors which usually accompany all spreading diseases, and is allowed to enter a herd of cattle, run its course, and disappear without exciting any particular notice.

The contagion of cowpox does not travel through the air from animal to animal, but is transfused only by actual contact of the contagious principle with the skin of some susceptible animal. It may be carried in this manner, not alone from cattle to cattle, but horses, sheep, goats, and man may readily contract the disease whenever suitable conditions attend their inoculation.

An identical disease frequently appears upon horses, attacking their heels, and thence extending upward along the leg, producing, as it progresses, inflammation and swelling of the skin, followed later by pustules, which soon rupture, discharging a sticky, disagreeable secretion. Other parts of the body are frequently affected in like manner, especially in the region of the head, where the eruptions may appear upon lips and nostrils, or upon the mucous surfaces of the nasal cavities, mouth, or eyes.

Variola of the horse is readily transmitted to cattle, if both are cared for by the same attendant, and, conversely, variola of cattle may be carried from the cow to the horse on the hands of a person who has been milking a cow affected with the disease.

The method of vaccination with material derived from the eruptions of cowpox as a safeguard against the ravages of smallpox in members of the human family is well known. The immunity which such vaccination confers upon the human subject has led many writers to assert that cowpox is simply a modified form of smallpox, whose harmless attack upon the human system is owing to a certain attenuation derived during its passages through the system of the cow or horse. The results of numerous experiments which have been carried out for the purpose of determining the relationship existing between variola of the human and bovine families seem to show, however, that although possessing many similar characteristics, they are nevertheless distinct, and that in spite of repeated inoculations from cattle to man, and vice versa, no transformation in the real character of the disease ever takes place.

Symptoms.—The disease appears in four to seven days after natural infection, or may evince itself in two or three days as the result of artificial inoculation. Young milch cows are most susceptible to an attack, but older cows, bulls, or young cattle are by no means immune. The attack causes a slight rise in temperature, which is soon followed by the appearance of reddened, inflamed areas, principally upon the teats and udder, and at times on the abdominal skin or the skin of the inner surface of the thighs. In a few cases the skin of the throat and jaws has been found similarly involved. If the affected parts are examined on the second day after the establishment of the inflammation numerous pale-red nodules will be found, which gradually expand until, within a few days, they reach a diameter of one-half inch or even larger. At this period the tops of the nodules become transformed into vesicles which are depressed in the center and contain a pale, serous fluid. They usually reach their maturity by the tenth day of the course of the disease and are then the size of a bean. From this time the contents of the vesicles become purulent, which requires about three days, when the typical pox pustule is present, consisting of a swelling with broad, reddened base, within which is an elevated, conical abscess varying from the size of a pea to that of a hazelnut.

The course of the disease after the full maturity of the pustule is rapid if outside interference has not caused a premature rupture of the small abscess at the apex of the swelling. The pustules gradually become darker colored and drier until nothing remains but a thick scab, which at last falls off, leaving only a slight, whitish scar behind. The total duration of the disease covers some 20 days in each animal, and owing to the slow spread of the infection from animal to animal, many weeks may elapse before a stable can be fully freed from it. The fallen scabs and crusts may retain their contagious properties for several days when mixed with litter and bedding upon the floor of the stable, and at any time during this period they are capable of producing new outbreaks should fresh cattle be brought into the stalls and thus come into actual contact with them. Again, the pustules may appear, one after another, on a single animal, in which case the duration of the disease is materially lengthened.

Treatment.—In herds of cattle that regularly receive careful handling, no special treatment will be found necessary beyond the application of softening and disinfecting agents to such vesicles upon the teats as may have become ruptured by the hands of the milker. Carbolized vaseline or iodoform ointment will be found well suited to this work. In more persistent cases it may be found desirable to use a milking tube in order to prevent the repeated opening of the pustules during the operation of milking. Washing the sores twice daily with a weak solution of zinc chlorid (2½ per cent solution) has been found to assist in checking the inflammation and to cleanse and heal the parts by its germicidal action. When the udder is hard, swollen, and painful, support it by a bandage and foment frequently with hot water. If calves are allowed to suckle the cows the pustules become confluent, and the ulcerations may extend up into the teat, causing garget and ruining the whole quarter of the udder.

As young cows are most susceptible to variola, the milker must exercise constant patience with these affected animals so long as their teats or udders are sore and tender, else the patient may contract vicious habits while resisting painful handling. The flow of milk is usually lessened as soon as the fever becomes established, but is again normal with the return of perfect health.

The practice of thorough cleanliness in handling or milking affected cattle may, in many instances, prevent the dissemination of the trouble among the healthy portion of the herd, but even the greatest care may prove insufficient to check the spread until it has attacked each animal of the herd in turn.

ACTINOMYCOSIS (LUMPY JAW)

[[Pls. XXXIX]-[XLI].]

Actinomycosis, also known as lumpy jaw, big jaw, wooden tongue, etc., is a chronic infectious disease characterized by the formation of peculiar tumors in various regions of the body, more particularly the head, and is due to the specific action of a certain fungus-like germ (actinomyces). This fungus is an organism which occurs in the tissues in the form of rosettes, and it has therefore been termed the "ray fungus." The disease is not directly transmitted from one animal to another, but it seems apparent that the fungus is conveyed into the tissues by various feedstuffs through slight wounds of the mucous membrane of the mouth, decayed teeth, or during the shedding of milk teeth. The ray fungus is found in nature vegetated on grasses, on the awns of barley, the spears of oats, and on other grains. Quantities of the fungi have been found between the vegetable fibers of barley which had penetrated the gums of cattle and on the awns of grain embedded in the tongues of cows.

Although actinomycotic tumors on cattle had been the object of study for many years, it was not until 1877 that the constant presence of actinomyces was pointed out by Bollinger, of Munich, and since that time considered the cause. This fungus was observed in these tumors as early as 1860 by Rivolta, and by others subsequently, without having been suspected as causing them.

Since Bollinger's publication much work has been done, many observations made, and many hitherto obscure disease processes brought into relation with this fungus. Furthermore, a similar disease in man was first definitely shown to be associated with the same fungus in 1878 by Israel, and in the following year Ponfick pointed out that the disease described by Bollinger in animals and that found by Israel in man were due to the same cause; that is, that the fungi described by these observers were one and the same.

The tumors and abscesses wherever they may be are all found to be the same in origin by the presence of the actinomyces fungus. When they are incised, a very close scrutiny with the naked eye, or, at most, a hand lens, will reveal the presence of minute grains which vary from a pale-yellow to a sulphur-yellow color. They may be very abundant or so few as to be overlooked. They are embedded in the soft tissue composing the tumor or in the pus of the abscess. With a needle they are easily lifted out from the tissue, and then they appear as roundish masses about one-half millimeter (1/50 inch) in diameter. To anyone familiar with the use of a microscope the recognition of these grains or particles without any previous preparation is a comparatively easy task.

When examined in the fresh condition under a microscope magnifying up to 250 diameters the general structure is made out without much difficulty. These grains consist of collections of minute, roundish masses. Their outer surface is made up of club-shaped bodies all radiating from the center of the mass (see [Pl. XXXIX], fig. 2), somewhat like a rosette. If the fungus is crushed, the interior is found made up of bundles of very fine filaments, which are probably continuous into the club-shaped bodies. The addition of a dilute solution of caustic soda or potash greatly aids the examination, as it removes the layer of cells adhering to the fungus, which obscures the structure. Now and then these grains are found to be in a calcified condition. The exterior is incrusted in lime salts, which are dissolved by adding some weak dilute acid, like acetic acid. Only by this procedure can the fungus be definitely recognized when in a mummified condition.

These are the bodies whose presence causes sufficient irritation in the tissues into which they find their way to set up inflammatory growths. These growths increase as the fungus continues to multiply until they reach enormous dimensions, if the affected animal is permitted to live long enough. The true nature of this parasite is not yet definitely settled, although many excellent observers have occupied themselves with it. According to earlier observers, it is a true fungus. Later ones are inclined to place it among the higher bacteria. Present knowledge concerning the actinomyces growth indicates that it should be classified with the higher bacteria or trichomycetes.

Whatever the situation of the disease caused by actinomyces may be, its nature is fundamentally the same and peculiar to the fungus. The pathological details which make this statement clear can not be entered upon in this place, nor would they be of any practical value to the farmer. We will simply dwell upon a few obvious characters.

The consistency of the tumor varies in different situations according to the quantity of fibrous or connective tissue present. When very little of this is present the tumor is of a very soft consistency. As the quantity of connective tissue is increased the tumor is firmer and of a more honeycombed appearance. The individual actinomyces colonies are lodged in the spaces or interstices formed by the meshwork of the connective tissue. There they are surrounded by a mantle of cellular elements which fill up the spaces. By scraping the cut surface of such a tumor these cell masses inclosing the fungi come away, and the latter may be seen as pale-yellow or sulphur-yellow specks, as described above.

Location of the disease.—In cattle the disease process may be located both externally, where it is readily detected, and in internal organs. Its preferred seat is on the bones of the lower and upper jaws, in the parotid salivary gland in the angle of the jaw, and in the region of the throat. It may also appear under the skin in different parts of the body. Internally it may attack the tongue and appear in the form of a tumor in the mouth, pharynx, or larynx. It may cause extensive disease of the lungs, more rarely of the digestive tract.

It appears, furthermore, that in certain districts or countries the disease seems by preference to attack certain parts. Thus in England actinomycosis of the tongue is most prevalent. In Denmark the soft parts of the head are most prone to disease, while in Russia the lips are the usual seat. In certain parts of Germany actinomycotic tumors are most frequently encountered in the throat region and in the jawbones.

A description of actinomycosis of the jaw (lumpy jaw) and of the tongue has already been given in a previous chapter, and hence they will be dealt with here only very briefly. When the disease attacks the soft parts of the head a rather firm swelling appears, in which are formed one or more smaller projecting tumors, varying from the size of a nut to that of an egg. These push their way outward and finally break through the skin as small, reddish, funguslike bodies covered with thin sloughs. Or the original swelling, in place of enlarging in the manner described, may become transformed into an abscess which finally bursts to discharge creamy pus. The abscess cavity, however, does not disappear, but is soon filled with fungus-like growths, which force their way outward through the opening.

When the tumors are situated within the cavity of the pharynx they have broken through from some gland, perhaps beneath the mucous membrane, where the disease first appeared, and hang or project into the cavity of the pharynx, either as pendulous masses with slender stems or as tumors with broad bases. Their position may be such as to interfere with swallowing and with breathing. In either case serious symptoms will soon appear.

The invasion of the bones of the jaws by actinomycosis must be regarded as one of the most serious forms of the disease. ([Pls. XXXIX], [XL].) It may start in the marrow of the bone and by a slow extension gradually undermine the entire thickness of the bone itself. The growth may continue outward, and after working its way through muscle and skin finally break through and appear externally as stinking fungoid growths. The growth may at the same time work its way inward and appear in the mouth. The disease may also begin in the periosteum, or covering of the bone, and destroy the bone from without inward.

Actinomycosis of the lungs is occasionally observed, and it is not improbable that at times it has been mistaken for tuberculosis. The actinomyces grains are, however, easily observed if the diseased tissue is carefully examined. The changes in the lungs as they appear to the naked eye vary considerably from case to case. Thus in one animal the lungs were affected as in ordinary bronchopneumonia as to the location, extent, and appearance of the disease process. The affected lobes had a dark-red flesh appearance, with yellowish areas sprinkled in here and there. (See [Pl. XLI], figs. 1, 2.) These latter areas were the seat of multiplication of the actinomyces fungus. In another case, of which only a small portion of the lungs was sent to the laboratory, they were completely transformed into a uniformly grayish mass, very soft and pulpy to the touch, and appearing like very soft and moist dough. ([Pl. XLI], fig. 3.) The actinomyces grains were exceedingly abundant in this tissue, and appeared when the tissue was incised as minute sulphur-yellow grains, densely sprinkled through the tissue, which readily came away and adhered to the knife blade. In still another case a portion of the lung tissue was converted into large, soft masses from 1 to 3 inches in diameter, each partly inclosed in very dense connective tissue. These soft, grayish-yellow masses likewise resembled moist dough in their consistency, and the actinomyces grains, though neither very distinct nor at all abundant, were easily fished out and identified as such. A portion of this growth, which was as large as a child's head, was converted into an abscess filled with creamy semiliquid pus.

This case differed from the preceding in that all appearance of lung tissue had disappeared from the diseased mass. Only on the exterior the lung tissue could be recognized, although even there it had been largely converted into very dense, whitish connective tissue inclosing the fungoid growth. In the other case the external form of the lung and the shape and outline of the lobules were preserved, but the lung tissue itself was not recognizable as such. In the case first mentioned the changes were still less marked, and actinomycosis would not have been suspected by a simple inspection. These few illustrations suffice to show that actinomycosis of the lungs may appear under quite different forms, and that the nature of the disease can be accurately determined only by finding the fungus itself. Rarely actinomycosis attacks the body externally in places other than the head and neck. Crookshank describes the case of a bull in which the flank was attacked and subsequently the scrotum became diseased. A large portion of the skin of the flank was destroyed and covered with a leathery crust. When this was pulled away the pus beneath it showed the actinomyces grains to the naked eye.

Actinomycosis may also involve the udder, the spermatic cord of castrated animals, the vagina, and, when it becomes generalized, the brain, liver, spleen, and muscular tissue.

Actinomycosis may in some cases be confounded with tuberculosis. The diagnosis does not offer any difficulties, since the presence of the actinomyces fungus at once removes any existing doubts. As has already been intimated, these grains, simulating sulphur balls, are visible to the naked eye, and their nature is readily determined with the aid of a microscope.

The course of the disease is quite slow. As the tumors grow they may interfere with the natural functions of the body. According to their situation, mastication, rumination, or breathing may be interfered with, and in this way the animal may become emaciated. Actinomycosis of the jawbones leads to destruction of the teeth and impedes the movements necessary to chewing the feed. Similarly, when the disease attacks the soft parts of the head obstructions may arise in the mouth by an inward growth of the tumor. If tumors exist in the pharynx they may partially obstruct the movements necessary to breathing, or close the air passages and cause partial suffocation. Actinomycosis of the tongue, in interfering with the many and varied movements of this important organ, is also a serious matter. There is no reason to suppose that the localized disease interferes with the general health in any other way than indirectly until internal organs, such as the lungs, become involved.

A very small proportion of the cases may recover spontaneously, the tumors being encysted or undergoing calcification. In most cases the disease yields readily to proper treatment, and about 75 per cent of the affected animals may be cured.

Prevention.—The question as to how and where animals take this disease is one concerning which we are still in the stage of conjecture, because so far we possess very little information concerning the life history of the actinomyces itself. The quite unanimous view of all observers is that animals become infected from the feed. The fungus is lodged upon the plants and in some way enters the tissues of the head, the lungs, and the digestive tract, where it sets up its peculiar activity. It is likewise generally believed that the fungus is, as it were, inoculated into the affected part. This inoculation is performed by the sharp and pointed parts of plants which penetrate the mucous membrane and carry the fungus with them. The disease is therefore inoculable rather than contagious. The mere presence of the diseased animal will not give rise to disease in healthy animals unless the actinomyces grains pass directly from the diseased into some wound or abrasion of the healthy or else drop upon the feed which is consumed by the healthy. Not only are these views deducible from clinical observation, but they have been proved by the positive inoculation of calves and smaller animals with actinomyces. The danger therefore of the presence of actinomyces for healthy animals is a limited one. Nevertheless an animal affected with this disease should not be allowed to go at large or run with other animals. If the fungus is being scattered by discharging growths we certainly can not state at this stage of our knowledge that other animals may not be infected by such distribution, and we must assume, until more positive information is at hand, that this actually occurs.

It is, however, the opinion of the majority of authorities that when actinomycosis appears among a large number of animals they all contract it in the same way from the feed. Much speculation has therefore arisen whether any particular plant or group of plants is the source of the infection and whether any special condition of the soil favors it. Very little positive information is at hand on these questions. It would be very desirable for those who live in localities where this disease is prevalent to make statistical and other observations on the occurrence of the disease with reference to the season of the year, the kind of feed, the nature of the soil (whether swampy or dry, recently reclaimed, or cultivated for a long time) upon which the animals are pastured or upon which the feed is grown.

It is highly probable that such investigations will lead to an understanding of the source of the fungus and the means for checking the spread of the disease itself. Veterinarian Jensen, of Denmark, made some observations upon an extensive outbreak of actinomycosis a number of years ago which led him to infer that the animals were inoculated by eating barley straw harvested from pieces of ground just reclaimed from the sea. While the animals remained unaffected so long as they pastured on this ground or ate the hay obtained from it, they became diseased after eating the straw of cereals from the same territory. Others have found that cattle grazing upon low pastures along the banks of streams and subject to inundations are more prone to the disease. It has also been observed that feed gathered from such grounds, even after prolonged drying, may give rise to the disease. Actinomycosis is not infrequent in cattle in the Southwest and is generally supposed to be the result of eating the prickly fruit of the cactus plant, causing wounds of the mucous membrane and subsequent infection with the parasite. Much additional information of a similar kind must be forthcoming before the source and manner of infection in this disease and its dependence upon external conditions will be known. It is not at all improbable that they may vary considerably from place to place.

Treatment.—Until recently this has been almost entirely surgical. When the tumors are external and attached to soft parts only, an early removal may lead to recovery. This, of course, can be undertaken only by a trained veterinarian, especially as the various parts of the head and neck contain important vessels, nerves, and ducts which should be injured as little as possible in any operation. Unless the tumor is completely removed it will reappear. Disease of the jawbones is at best a very serious matter and treatment is liable to be of no avail.

In March, 1892, an important contribution to our knowledge of this subject was made by Nocard, of the Alfort Veterinary School, in a communication to the French Central Society of Veterinary Medicine. He showed clearly that the actinomycosis of the tongue, a disease which appears to be quite common in Germany, and is there known as "wooden tongue," could be quickly and permanently cured by the administration of iodid of potassium. Nocard calls attention to the success of Thomassen, of Utrecht, who recommended this treatment so long ago as 1885, and who has since treated more than 80 cases, all of which have been cured. A French veterinarian, Godbille, has used the same remedy in a number of cases of actinomycosis in the tongue, all of which have been cured. Nocard also gives details of a case which was cured by himself.

All the cases referred to were of actinomycosis of the tongue, and no one appears to have attempted the cure of actinomycosis of the jaw until it was undertaken by Nörgaard, of the Bureau of Animal Industry. In April, 1892, he selected a young steer in fair condition which had a tumor on the jaw measuring 15½ inches in circumference and from which a discharge had already been established. This animal was treated with iodid of potassium, and the result was a complete cure.

The iodid of potassium is given in doses of 1½ and 2½ drams once a day, dissolved in water, and administered as a drench. The dose should vary somewhat with the size of the animal and with the effects that are produced. If the dose is sufficiently large signs of iodism appear in the course of a week or 10 days. The skin becomes scurfy, there is weeping from the eyes, catarrh of the nose, and loss of appetite. When these symptoms appear the medicine may be suspended for a few days and afterward resumed in the same dose. The cure requires from three to six weeks' treatment. Some animals, generally the ones which show no signs of iodism, do not improve under treatment with iodid of potassium.

If there is no sign of improvement after the animals have been treated four or five weeks, and the medicine has been given in as large doses as appear desirable, it is an indication that the particular animal is not susceptible to the curative effects of the drug, and the treatment may therefore be abandoned.

It is not, however, advisable to administer iodid of potassium to milch cows, as it will considerably reduce the milk secretion or stop it altogether. Furthermore, a great part of the drug is excreted through the milk, making the milk unfit for use. It should not be given to animals in advanced pregnancy, as there is danger of producing abortion.

The best results are obtained by pushing the drug until its effect is seen. The many tests to which this treatment has been subjected have proved, with few exceptions, its specific curative value. In addition to this the tumor should be painted externally with either the tincture of iodin or Lugol's solution, or the drug should be injected subcutaneously into the tumor.

Godbille has given as much as 4 drams of potassium iodid in one day to a steer, decreasing the dose one-fourth dram each day until the dose was 1¼ drams, which was maintained until the twelfth day of treatment, when the animal appeared to be entirely cured.

Nocard gave the first day 1½ drams in one dose to a cow; the second and succeeding days a dose of 1 dram in the morning and evening, in each case before feeding. This treatment was continued for 10 days, when the animal was cured.

Actinomycosis and the public health.—The interest which is shown concerning this cattle disease is largely due to the fact that the same disease attacks human beings. Its slow progress, its tendency to remain restricted to certain localities, and the absence of any directly contagious properties have thus far not aroused any anxiety in other countries as to its influence on the cattle industry, not even to the point of placing it among the infectious diseases of which statistics are annually published. Its possible bearing on public health has, however, given the disease a place in the public mind which it hardly deserves.

It has already been stated that the actinomyces fungus found in human disease is considered by authorities the same as that occurring in bovine affections. It is therefore of interest to conclude this article with a brief discussion of the disease in man and its relation to actinomycosis in cattle.

In man the location of the disease process corresponds fairly well to that in cattle. The majority of cases which have been reported in different parts of the world—and they are now rather numerous—indicate disease of the face. The skin, tongue, or the jawbones may become affected, and by a very slow process it may extend downward upon the neck and even into the cavity of the chest. In many cases the teeth have been found in a state of more or less advanced decay and ulceration. In a few cases disease of the lungs was observed without coexisting disease of the bones or soft parts of the head. In such cases the fungus must have been inhaled. The disease of the lungs after a time extends upon the chest wall, where it may corrode the ribs and work its way through the muscles and the skin. An abscess is thus formed discharging pus containing actinomyces grains. Disease of the digestive organs caused by this fungus has also been observed in a few instances.

Granting the identity of the disease in man and cattle, the question has been raised whether cattle are responsible for its occurrence in man. Any transmission of the infectious agent may be conceived of as taking place during the life of the animal and from the meat after slaughter. That human beings have contracted actinomycosis by coming in contact with diseased cattle is not shown by the cases that have been reported, for the occupations of most of the patients did not bring them into any relation whatever with cattle. While the possibility of such direct transmission is not denied, nevertheless it must be considered as extremely remote. Practically the same position is maintained at present by most authorities as regards the transmission of the disease to man by eating meat. Israel, who has studied this question carefully, found the disease in Jews who never ate pork,[5] and who likewise were protected from bovine actinomycosis by the rigorous meat inspection practiced by that race. Furthermore, it must be borne in mind that actinomycosis is a local disease, causing great destruction of tissue where the fungus multiplies, but which very rarely becomes generally disseminated over the body from the original disease focus. The fungus is found only in places where the disease process is manifest to the eye or becomes so in a very short time after the lodgment of the fungus. Only the greatest negligence would allow the actually diseased parts to be sold and consumed. Finally, this parasite, like all others, would be destroyed in the process of cooking. Most authorities thus do not believe that actinomycosis in man is directly traceable to the disease in animals, but are of the opinion that both man and animals are infected from a third source, which has already been discussed above. How far these views may be modified by further and more telling investigations of the parasite fungus itself no one can predict. There are still wide gaps in our knowledge, and the presentation above simply summarizes the prevailing views, from which there are dissenters, of course. An attempt to give the views of both sides on this question would necessitate the summarizing and impartial discussion of all the experiments thus far made—a task entirely beyond the scope of the present work.

Whether an animal affected with actinomycosis should be used for human food after all diseased organs and tissues have been thoroughly removed is a question the answer to which depends on a variety of circumstances. Among these may be mentioned the thoroughness of the meat inspection itself, the extent of the disease, and the general condition of the animal affected.

The Federal meat-inspection regulations require that carcasses of animals showing generalized actinomycosis shall be condemned. If carcasses are in a well-nourished condition, showing uncomplicated localized lesions of actinomycosis, they may be passed after the infected organs or parts have been removed and condemned. When the disease of the jaw is slight, strictly localized, and without pus formation, fistulous tracts, or lymph-gland involvement, the tongue, if free from disease, may be passed. The heads affected with actinomycosis (lumpy jaw), including the tongue, shall be condemned, except that when the lesions in the jaw are strictly localized and slight in extent, the tongue may be passed, if free from disease.

ANTHRAX.

Anthrax or charbon may be defined as an infectious disease which is caused by specific bacteria, known as anthrax bacilli, and which is more or less restricted by conditions of soil and moisture to definite geographical localities. While it is chiefly limited to cattle and sheep, it may be transmitted to goats, horses, cats, and certain kinds of game. Smaller animals, such as mice, rabbits, and guinea pigs, speedily succumb to inoculation. Dogs and hogs are slightly susceptible, while fowls are practically immune. The variety of domesticated animals which it may attack renders it one of the most dreaded scourges of animal life. It may even attack man. Of this more will be stated further on.

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ACTINOMYCOSIS (LUMPY JAW).

DESCRIPTION OF PLATES.

Plate XXXIX. Actinomycosis. (From Jöhne's Encyklopädie d. gesammt. Thierheilkunde.)

Fig. 1. Actinomycosis of the jaw. The lower jawbone has been extensively eaten away by the disease.

Fig. 2. Actinomyces fungus from a tumor of the jawbone in cattle, magnified 550 times.

Plate XL. Actinomycosis of the jaw. (Reduced one-half. From Jöhne's Encyklopädie d. gesammt. Thierheilkunde.) The lower jaw is sawed through transversely, i.e., from right to left, and shows the disease within the jawbone itself; a, within the mouth, showing the papillæ on the mucous membrane of the cheek; b, front view of a molar tooth; c, the skin covering the lower surface of the jawbone; d, the jawbone hollowed out and enlarged by the formation of cavities within it, which are filled with the soft growth of the actinomycotic tumor. The section makes it appear as if the bone were broken into fragments and these forced apart; e, a portion of the tumor which has broken through the bone and the skin and appears as a tumor on the cheek. The little roundish masses represent the granulomata (minute tumors) in which the fungus vegetates.

Plate XLI. Actinomycosis of the lungs.

Fig. 1. Transverse section of the ventral lobe of the right lung, from a case studied in the laboratory. The yellowish dots represent the places where the actinomyces fungus is lodged. The larger yellowish patches are produced by the confluence of a number of isolated centers. The entire lobe is of a dark flesh-red color, due to collapse and bronchopneumonia.

Fig. 2. The cut surface of a portion of the principal lobe of the same lung, showing the recent invasion of antinomycosis from the other lobe: a, large air tube; b, artery; c, a pneumatic lobule; d, lobule containing minute yellowish dots. In these the actinomyces fungus is lodged.

Fig. 3. Cut surface of a small portion of another lung, showing a few lobules, a. The fungus is sprinkled throughout the lung tissue in the form of yellowish grains, as shown in the illustration. The pleural covering of the lung tissue is shown in profile above.

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Cause.—The cause of anthrax is a microscopic organism known as the anthrax bacillus. (See [Pl. XXVIII], fig. 7.) In form it is cylindrical or rodlike, measuring 1/5000 to 1/2500 inch in length and 1/25000 inch in diameter. Like all bacteria, these rodlike bodies have the power of indefinite multiplication, and in the bodies of infected animals they produce death by rapidly increasing in numbers and producing substances which poison the body. In the blood they multiply in number by becoming elongated and then dividing into two, each new organism continuing the same process indefinitely. Outside the body, however, they multiply in a different way when under conditions unfavorable to growth. Oval bodies, which are called spores, appear within the rods, and remain alive and capable of germination after years of drying. They also resist heat to a remarkable degree, so that boiling water is necessary to destroy them. The bacilli themselves, on the other hand, show only very little resistance to heat and drying. It has long been known that the anthrax virus thrives best under certain conditions of the soil and on territories subject to floods and inundations. The particular kinds of soil upon which the disease is observed are black, loose, warm, humous soils; also those containing lime, marl, and clay, finally peaty, swampy soils resting upon strata which hold the water, or, in other words, are impervious. Hence fields containing stagnant pools may be the source of infection. The infection may be limited to certain farms, or even to restricted areas on such farms. Even in the Alps, more than 3,000 feet above sea level, where such conditions prevail in secluded valleys, anthrax persists among herds.

Aside from these limitations to specific conditions of the soil, anthrax is a disease of world-wide distribution. It exists in most countries of Europe, in Asia, Africa, Australia, and in our own country in the lower Mississippi Valley, the Gulf States, and in some of the Eastern and Western States. It seems to be gradually spreading in this country and every year occurs in new districts.

Meteorological conditions also have an important share in determining the severity of the disease. On those tracts subject to inundations in spring a very hot, dry summer is liable to cause a severe outbreak. The relation which the bacillus bears to these conditions is not positively known. It may be that during and immediately after inundations or in stagnant water the bacilli find nourishment enough in the water here and there to multiply and produce an abundant crop of spores, which are subsequently carried, in a dry condition, by the winds during the period of drought and disseminated over the vegetation. Animals feeding upon this vegetation may contract the disease if the spores germinate in the body.

Another source of the virus, and one regarded by many authorities as perhaps the most important, is the body of an animal which has died of anthrax. It will be remembered that in such bodies the anthrax bacilli are present in great numbers, and wherever blood or other body fluids are exposed to the air on the surface of the carcass there the formation of spores will go on with great rapidity in the warm season of the year. It will thus be readily understood how this disease may become stationary in a given locality and appear year after year and even grow in severity if the carcasses of animals which have succumbed to it are not properly disposed of. These carcasses should be buried deeply, so that spore formation may be prevented and no animal have access to them. By exercising this precaution the disease will not be disseminated by flies and other insect pests.

We have thus two agents at work in maintaining the disease in any locality—the soil and meteorological conditions, and the carcasses of animals that have died of the disease. Besides these dangers, which are of immediate consequence to cattle on pastures, the virus may be carried from place to place in hides, hair, wool, hoofs, and horns, and it may be stored in the hay or other fodder from the infected fields and cause an outbreak among stabled animals feeding upon it in winter. In this manner the affection has been introduced into far-distant localities.

How cattle are infected.—We have seen above that the spores of the anthrax bacilli, which in their functions correspond to the seeds of higher plants and which are the elements that longest resist the unfavorable conditions in the soil, air, and water, are the chief agents of infection. They may be taken into the body with the feed and produce disease which begins in the intestinal tract, or they may come in contact with scratches, bites, or other wounds of the skin, mouth, and tongue, and produce in these situations swellings or carbuncles. From such swellings the bacilli penetrate into the blood and produce a general disease.

It has likewise been asserted that the disease may be transmitted by various kinds of insects which carry the bacilli from the sick and inoculate the healthy as they pierce the skin. When infection of the blood takes place from the intestines the carbuncles may be absent. It has already been stated that since anthrax spores live for several years, the disease may be contracted in winter from feed gathered on permanently infected fields.

The disease may appear sporadically, i. e., only one or several animals may be infected while the rest of the herd remain well, or it may appear as an epizootic attacking a large number at about the same time.

Symptoms.—The symptoms in cattle vary considerably, according as the disease begins in the skin, in the lungs, or in the intestines. They depend also on the severity of the attack. Thus we may have what is called anthrax peracutus or apoplectiform, when the animal dies very suddenly as if from apoplexy. Such cases usually occur in the beginning of an outbreak. The animal, without having shown any signs of disease, suddenly drops in the pasture and dies in convulsions, or one apparently well at night is found dead in the morning.

The second type (anthrax acutis), without any external swellings, is the one most commonly observed in cattle. The disease begins with a high fever. The temperature may reach 106° to 107° F. The pulse beats from 80 to 100 a minute. Feeding and rumination are suspended. Chills and muscular tremors may appear and the skin show uneven temperature. The ears and base of the horns are cold, the coat staring. The animals are dull and stupid and manifest great weakness.

To these symptoms others are added in the course of the disease. The dullness may give way to great uneasiness, champing of the jaws, spasms of the limbs, kicking and pawing the ground. The breathing may become labored. The nostrils then dilate, the mouth is open, the head raised, and all muscles of the chest are strained during breathing, while the visible mucous membranes (nose, mouth, rectum, and vagina) become bluish. If the disease has started in the bowels, there is much pain, as shown by the moaning of the animal; the discharges, at first firm, become softer and covered with serum, mucus, and blood.

As the disease approaches the fatal termination the weakness of the animal increases. It leans against supports or lies down. Blood vessels may rupture and give rise to spots of blood on the various mucous membranes and bloody discharges from nose, mouth, rectum, and vagina. The urine not infrequently contains blood (red water), and death ensues within one or two days.

A third type of the disease (anthrax subacutus), which is rarely observed, includes those cases in which the disease is more prolonged. It may last from three to seven days and terminate fatally or end in recovery. In this type, the symptoms are practically as described in the acute form, only less marked.

In connection with these types of intestinal anthrax, swellings may appear in different parts of the body under the skin, or the disease may start from such a swelling, caused by the inoculation of anthrax spores in one of the several different ways already described. If the disease begins in the skin, it agrees in general with the subacute form in prolonged duration, and it may occasionally terminate in recovery if the swellings are thoroughly incised and treated.

Lesions.—These swellings appear as edemas and carbuncles. The former are doughy tumors of a more or less flattish form passing gradually into the surrounding healthy tissue. As a rule, they are situated beneath the skin in the fatty layer, and the skin itself is at first of healthy appearance, so that they are often overlooked, especially when covered with a good coat of hair. When they are cut open they are found to consist of a peculiar, jellylike mass of a yellowish color and more or less stained with blood. The carbuncles are firm, hot, tender swellings, which later become cool and painless and undergo mortification. The edemas and carbuncles may also appear in the mouth, pharynx, larynx, in the tongue, and in the rectum.

The bodies of cattle which have died of anthrax soon lose their rigidity and become bloated, because decomposition sets in very rapidly. From the mouth, nose, and anus bloodstained fluid flows in small quantities. When such carcasses are opened and examined it is found that nearly all organs are sprinkled with spots of blood or extravasations of various sizes. The spleen is enlarged from two to five times, the pulp blackish and soft and occasionally disintegrated. The blood is of tarry consistency, not firmly coagulated, and blackish in color. In the abdomen, the thoracic cavity, and in the pericardium, or bag surrounding the heart, more or less blood-stained fluid is present. In addition to these characteristic signs, the carbuncles and swellings under the skin, already described, will aid in determining the true nature of the disease. The most reliable method of diagnosis is the examination of the blood and tissues for anthrax bacilli, which requires a trained bacteriologist. The cases of fatal anthrax number from 70 to 90 per cent, and are usually more numerous at the first outbreak of the disease.

Differential diagnosis.—The diagnosis from blackleg may be made by noting the subcutaneous swellings which appear upon the patient. Those of blackleg are found to crackle under pressure with the finger, owing to the presence of gas within the tissues, while the tumors of anthrax, being caused by the pressure of serum, are entirely free from this quality and have a somewhat doughy consistence. The tumors of blackleg are usually on the shoulder or thigh and are not found so frequently about the neck and side of the body as are the swellings of anthrax. The blood of animals dead of blackleg is normal, and the spleen does not appear swollen or darkened, as in those affected with anthrax. The chief differences between anthrax and Texas fever are that the course of the former is more acute and the blood of the animal is dark and of a tarlike consistence, while in the latter it is thinner than normal. The presence of Texas-fever ticks on the cattle would also lead one to suspect that disease in regions where cattle are not immune from it.

Treatment.—In cases which originate from external wounds, the swellings should be opened freely by long incisions with a sharp knife and washed several times daily with carbolic-acid solution (1 ounce to a quart of water). Care should be taken to disinfect thoroughly any fluid discharge that may follow the incision. When suppuration has set in the treatment recommended in the chapter on wounds should be carried out.

In the treatment of animals showing symptoms of anthrax, the serum recommended under the next heading of "Prevention" should be administered in large doses. Animals showing only a high temperature with no other symptoms of the disease should be given from 30 to 50 cubic centimeters of the serum, but if the gravity of the disease is pronounced 100 cubic centimeters should be administered. In most instances a drop in temperature may be observed and a diminishing of the severity of the symptoms. At times, however, a relapse occurs about the second or third day following the serum injection, when it becomes necessary to administer another dose of serum. It has been proved that animals affected with anthrax may recover after injections of potent serum.

Prevention.—In this disease prevention is the most important subject demanding consideration. The various means to be suggested may be brought under two heads: (1) The surroundings of the animal, and (2) preventive inoculation.

(1) Surroundings.—What has already been stated of those conditions of the pastures which are favorable to anthrax, after a little thought, will suggest to most minds some of the preventive measures which may be of service in reducing losses in anthrax localities. All that conduces to a better state of the soil should be attempted. The State or Nation, by appropriate engineering, should do its share in preventing frequent inundations. If pools of stagnant water exist in the pastures, or if any particular portions are known by experience to give rise to anthrax, they should be fenced off. Efforts should likewise be made toward the proper draining of swamp lands frequented by cattle. Sometimes it has been found desirable to abandon for a season any infected or dangerous pastures. This remedy can not be carried out by most farmers, and it is liable to extend the infected territory. In some instances withdrawal of cattle from pastures entirely and feeding them in stables is said to have reduced the losses.

It is of the utmost importance that carcasses of animals which have died of anthrax be properly disposed of, as every portion of such animal contains the bacilli, ready to form spores when exposed to the air. Perhaps the simplest means is to bury the carcasses deep, where they can not be exposed by dogs or wild animals. It may be necessary to bury them on the pasture, but it is better to remove them to places not frequented by susceptible animals and to a point where drainage from the graves can not infect any water supply.

If they are moved some distance it must be borne in mind that the ground and all objects which have come in contact with the carcass should be disinfected. This is best accomplished with chlorid of lime. For washing utensils, etc., a 5 per cent solution may be prepared by adding 3 ounces to 2 quarts of water. This should be prepared fresh from the powder, and it is but little trouble to have a small tin measure of known capacity to dip out the powder, to be added to the water whenever necessary. The carcass and the ground should be sprinkled with powdered chlorid, or, if this is not at hand, an abundance of ordinary, unslaked lime should be used in its place.

The removal of carcasses to rendering establishments is always fraught with danger, unless those who handle them are thoroughly aware of the danger of scattering the virus by careless handling in wagons that are not tight. As a rule, the persons in charge of such transfer have no training for this important work, so that deep burial is to be preferred. Burning large carcasses is not always feasible; it is, however, the most certain means of destroying infectious material of any kind, and should be resorted to whenever practicable and economical. All carcasses, whether buried, rendered, or burned, should be disposed of unopened. When stables have become infected they should be thoroughly cleaned out, and the solution of chlorid of lime freely applied on floors and woodwork. The feed should be carefully protected from contamination with the manure or other discharges from the sick.

(2) Preventive inoculation.—One of the most important discoveries in connection with the disease was made by Louis Pasteur in 1881, and consisted in the new principle of producing immunity by the inoculation of weakened cultures of the bacillus causing the disease. This method has been quite extensively adopted in France, and to some extent in other European countries, and in the United States. The fluid used for inoculation consists of bouillon in which modified anthrax bacilli have multiplied and are present in large numbers. The bacilli have been modified by heat so that to a certain degree they have lost their original virulence. Two vaccines are prepared. The first or weaker, for the first inoculation, is obtained by subjecting the bacilli to the attenuating effects of heat for a longer period of time than in the case of the second, or stronger vaccine, for a second inoculation some 12 days later.

There are several difficulties inherent in the practical application of Pasteur's vaccine. Among them may be mentioned the variable degree of attenuation of different tubes of the vaccine and the varying susceptibility of the animals to be inoculated. The use of this vaccine is increasing, nevertheless, and has reduced the mortality in the affected districts from an average of 10 per cent in the case of sheep, to less than 1 per cent, and from 5 per cent with cattle, to less than one-half of 1 per cent.

It is very important to call attention to the possibility of distributing anthrax by this method of protective inoculation, as the bacilli themselves are present in the culture liquid. It is true that they have been modified and weakened by the process adopted by Pasteur, but it is not impossible for such modified virus to regain its original virulence after it has been scattered broadcast by the inoculation of large herds. It is obviously unsafe to have such vaccine injected by a layman; instead, it should be handled only by a competent veterinarian.

There are other disadvantages in this method of vaccination, and they all must be given due consideration. The unstable keeping quality of the Pasteur vaccine is a very important factor to be considered. Experience in this line has proved that Pasteur vaccine may deteriorate within a very short time after its preparation, and in repeated instances it has proved inert within three months of its preparation. When exposed to warm temperature and light, it deteriorates very rapidly; and when it is considered that the products of manufacturers may be stored under unfavorable conditions in branch houses and on the shelves of rural drug stores, the loss of potency can be readily explained. These deficiencies have been recognized by many investigators, and because of the superior keeping qualities particular attention has been directed toward the preparation of a spore vaccine by Zenkowsky of Russia, Detre of Hungary, and Nitta of Japan. For the purpose of producing a spore vaccine it is desirable to use a peptone-free agar medium, and after inoculation with an attenuated culture of the anthrax bacillus, it is allowed to grow at a temperature of 37° C. for 4 to 7 days. By this time an abundance of spores will have formed. The growth is then collected in sterile flasks and heated to a temperature of 60° C. for one-half hour to destroy the vegetative forms of the organism. If it is desired to use for vaccination one million spores, it is advisable to dilute the vaccine to a quantity of which 1 cubic centimeter would contain this number. Of such a vaccine 1 cubic centimeter would constitute the dose for cattle and horses. In all forms of vaccination against anthrax in sheep the greatest care must be exercised, as these animals are very susceptible to the disease, and at times vaccines which have no ill effects on cattle will prove fatal to sheep. Therefore the dose of the spore vaccine for sheep should not be more than one-fourth of that given to cattle.

Sclavo, Sobernheim, and others have established that injections of increasing quantities of virulent cultures into immune animals produced a serum which has great protective value against anthrax. Such protective serum may be produced in the various susceptible animals.

For immunization purposes it is advisable to use the simultaneous method; that is, both the spore vaccine and the anthrax serum should be injected. It is desirable to divide the herd to be treated into groups of ten or twelve and inject, first, each animal of the group with the serum, following this with the injection of the spore vaccine. The serum should be injected on one side, either on the neck or back of the shoulder, and the spore vaccine on the other side, injections being made subcutaneously. In herds in which the disease has already made its appearance it is necessary to take the temperatures of all the animals and to subject to the simultaneous vaccination only those that show no rise in temperature. All others should be given the serum-alone treatment in doses varying in accordance with the severity of the symptoms manifested by the individual animals. If the examination reveals a considerable number of infections, it is advisable to use the serum alone for all the animals, and in three or four weeks to revaccinate by the simultaneous method. The dosage should depend on the potency of the serum, serum of a high potency naturally being most desirable. Thus serum in 10 cubic centimeter doses for large animals, and 3 to 5 cubic centimeter doses for smaller ones, has been found to be effective in producing a temporary immunity.

As anthrax is entirely different from blackleg, vaccine for the latter does not act as a preventive against the former.

ANTHRAX IN MAN (MALIGNANT PUSTULE, OR CARBUNCLE).

Anthrax may be transmitted to man in handling the carcasses and hides of animals which have succumbed to the disease. The infection usually takes place through some abrasion or slight wound of the skin into which the anthrax spores, or bacilli, find their way. The point of inoculation appears at first as a dark point or patch, compared by some writers to the sting of a flea. After a few hours this is changed into a reddened pimple, which bears on its summit, usually around a hair, a yellowish blister, or vesicle, which later on becomes red or bluish in color. The burning sensation in this stage is very great. Later this pimple enlarges, its center becomes dry, gangrenous, and is surrounded by an elevated, discolored swelling. The center becomes drier and more leatherlike, and sinks in as the whole increases in size. The skin around this swelling or carbuncle is stained yellow or bluish, and is not infrequently swollen and doughy to the touch. The carbuncle itself rarely grows larger than a pea or a small nut, and is but slightly painful.

Anthrax swellings or edemas, already described as occurring in cattle, may also be found in man, and they are at times so extensive as to produce distortion in the appearance of the part of the body on which they are found. The color of the skin over these swellings varies according to the situation and thickness of the skin and the stage of the disease, and may be white, red, bluish, or blackish.

As sooner or later these carbuncles and swellings may lead to an infection of the entire body, and thus be fatal, surgical assistance should at once be called if there is well-grounded suspicion that any swellings resembling those described above have been caused by inoculation with anthrax virus. Inasmuch as physicians differ as to medicinal treatment of such accidents in man, it would be out of place to make any suggestions in this connection.

Extensive data are available, however, on the effectiveness of anthrax serum for the treatment of the disease in man. It is recommended that from 30 to 40 cubic centimeters of serum be injected in three or four different places. Should no improvement follow in 24 hours additional injections of 20 to 30 cubic centimeters should be administered.

In most instances the results are favorable, and this treatment is acknowledged to be superior to any other mode of treatment known for the disease.

To show that the transmission of anthrax to man is not so very uncommon, we take the following figures from the 1890 report of the German Government: The attention of the authorities was brought to 111 cases, of which 11 terminated fatally. The largest number of inoculations were caused by the slaughtering, opening, and skinning of animals affected with anthrax; hence, the butchers suffered most extensively. Of the 111 thus affected, 36 belonged to this craft. Infected shaving brushes also are very dangerous.

In addition to anthrax of the skin (known as malignant pustule), human beings are subject, though very rarely, to the disease of the lungs and the digestive organs. In the former case the spores are inhaled by workmen in establishments in which wool, hides, and rags are worked over, and it is therefore known as woolsorter's disease. In the latter case the disease is contracted by eating the flesh of diseased animals which has not been thoroughly cooked. These forms of the disease are more fatal than those in which the disease starts from the skin.

BLACKLEG.

[[Pl. XLII].]

Blackleg, black quarter, quarter ill, symptomatic anthrax, charbon symptomatique of the French, Rauschbrand of the Germans, is a rapidly fatal, infectious disease of young cattle, associated with external swellings which emit a crackling sound when handled. This disease was formerly regarded identical with anthrax, but investigations by various scientists in recent times have definitely proved the entire dissimilarity of the two affections, both from a clinical and a causal standpoint. The disease is produced by a specific bacillus, readily distinguishable from that causing anthrax. ([Pl. XXVIII], fig. 4.) Cattle between 6 months and 2 years of age are the most susceptible. Sucking calves under 6 months are rarely attacked, nor are they so susceptible to inoculation as older animals. Cattle more than 2 years of age may become affected, but such cases are infrequent. Sheep and goats may also contract the disease, but man, horses, hogs, dogs, cats, and fowls appear to be immune.

Like anthrax, blackleg is more or less restricted to definite localities. There are certain pastures upon which the disease regularly appears in the summer and fall of the year. As to any peculiarities of the soil nothing is definitely known. Some authors are inclined to regard moist, undrained, and swampy pastures favorable to this disease, but these theories will hardly hold, as it is found in all kinds of soil, in all altitudes, at all seasons of the year, and under various climatic conditions. It occurs in this country from the Atlantic to the Pacific and from Mexico to Canada, but it is more prevalent in the Western and Southwestern States. In Europe it exists in France, various parts of Germany, in Belgium, Norway, Denmark, Italy, and in the Alps of Switzerland. In Africa it occurs in Algeria and to some extent in Natal and bordering countries. In South America it prevails quite extensively throughout Argentina. Cattle in Cuba and Australia also suffer.

Cause.—The cause of the disease is a bacillus resembling in some minor respects the anthrax bacillus and differing but little from it in size. It also possesses the power of forming within itself a spore. In Plate XXVIII, figure 4, this is represented as an uncolored spot located in one end of the rod, which is enlarged so that the rod itself appears more or less club-shaped. What has already been stated concerning the significance of the spore of the anthrax bacillus applies equally well to these bodies. They resist destructive agents for a considerable time, and may still produce disease when inoculated after several years of drying. This fact may account for the occasional appearance of blackleg in stables. In order to meet the requirements for the development of the spores, which takes place only in the absence of the atmosphere, it is necessary that the wound be very small and deep enough to penetrate the subcutaneous tissue.

Several observers have found this organism in the mud of swamps. By placing a little of the mud under the skin, the disease has been produced.

Since the disease may be produced by placing under the skin material containing the specific bacilli and spores, it has been assumed that cattle contract the disease through wounds, principally of the skin, or very rarely of the mouth, tongue, and throat. Slight wounds into which the virus may find access may be caused by barbed wire, stubbles, thorns, briers, grass burs, and sharp or pointed parts of feed. Infection by way of digestive tract is also probable.

Symptoms and lesions.—The symptoms of blackleg may be either of a general or of a local nature, though more frequently of the latter. The general symptoms are very much like those belonging to other acute infectious or bacterial diseases. They begin, from one to three days after the infection has taken place, with loss of appetite and of rumination, with dullness and debility, and a high fever. The temperature may rise to 107° F. To these may be added lameness or stiffness of one or more limbs, due to the tumor or swelling quite invariably accompanying the disease. After a period of disease lasting from one to three days the affected animal almost always succumbs. Death is preceded by increasing weakness, difficult breathing, and occasional attacks of violent convulsions.

The most important characteristic of this disease is the appearance of a tumor or swelling under the skin a few hours after the setting in of the constitutional symptoms described above. In some cases it may appear first. This tumor may be on the thighs (hence "blackleg," "black quarter"), the neck, the shoulder, the breast, the flanks, or the rump; never below the carpal (or knee) and the hock joint. It more rarely appears in the throat and at the base of the tongue. The tumor, at first small and painful, spreads very rapidly both in depth and extent. When it is stroked or handled a peculiar crackling sound is heard under the skin; this is due to a collection of gas formed by the bacilli as they multiply. At this stage the skin becomes dry, parchment-like, and cool to the touch in the center of the tumor. If the swelling is cut into, a frothy, dark-red, rather disagreeable-smelling fluid is discharged. The animal manifests little or no pain during the operation.

As it is frequently desirable to know whether the disease is anthrax or blackleg, a few of the most obvious post-mortem changes may here be cited. The characteristic tumor with its crackling sound when stroked has already been described. If after the death of the animal it is more thoroughly examined, it will be noted that the tissues under the skin are infiltrated with blood and yellowish, jellylike material and gas bubbles. The muscular tissue beneath the swelling may be brownish or black, shading into dark red. ([Pl. XLII].) It is soft, easily torn and broken up. The muscle tissue is distended with numerous smaller or larger gas-filled cavities, often to such extent as to produce a resemblance to lung tissue. Upon incision it does not collapse perceptibly, as the gas cavities are not connected with one another.

In the abdomen and the thorax bloodstained fluid is not infrequently found, together with bloodstaining of the lining membrane of these cavities. Blood spots (or ecchymoses) are also found on the heart and lungs. The liver is congested, but the spleen is always normal in appearance.

Differential diagnosis.—Among the features of this disease which distinguish it from anthrax may be mentioned the unchanged spleen and the ready clotting of the blood. It will be remembered that in anthrax the spleen (milt) is very much enlarged, the blood tarry, coagulating feebly. The anthrax carbuncles and swellings differ from the blackleg swellings in not containing gas, in being hard and solid, and in causing death less rapidly.

It is difficult to distinguish between the swellings of blackleg and malignant edema, as they resemble each other very closely and both are distended with gas. Malignant edema, however, generally starts from a wound of considerable size; it usually follows surgical operations, and seldom results from the small abrasions and pricks to which animals are subjected in pastures. Inoculation experiments on guinea pigs, rabbits, and chickens will generally disclose the differences between the three diseases above, as all these species are killed by the germ of malignant edema, only the first two species by the anthrax bacillus, while the guinea pigs alone will succumb to the blackleg infection. Hemorrhagic septicemia may be differentiated from blackleg by its affecting cattle of all ages, by the location of the swelling usually about the region of the throat, neck, and dewlap, by the soft, doughy character of the swellings without the presence of gas bubbles, and finally by the characteristic hemorrhages widely distributed throughout the body. Other means of diagnosis, which have reference to the specific bacilli, to the inoculable character of the virus upon small animals, and which are of decisive and final importance, can be utilized only by the trained bacteriologist and veterinarian.

Treatment.—In this disease remedies have thus far proved unavailing. Some writers recommend the use of certain drugs, which seem to have been beneficial in a few cases, but a thorough trial has shown them to be valueless. Others advise that the swelling be opened by deep and long incisions and a strong disinfectant, such as a 5 per cent solution of carbolic acid, applied to the exposed parts; but this procedure can not be too strongly condemned. As nearly all those attacked die, in spite of every kind of treatment, and in view of the fact that when these tumors are opened the germs of the disease are scattered over the stables or pastures, thus becoming a source of danger to other cattle, it is obvious that such measures do more harm than good and should be put aside as dangerous. Bleeding, nerving, roweling, or setoning have likewise some adherents, but the evidence indicates that they have neither curative nor preventive value and therefore should be discarded for the method of vaccination which has been thoroughly tried and proved to be efficacious.

Prevention.—The various means suggested under "Anthrax" to prevent the spread or recurrence of this disease are equally applicable to blackleg, and hence do not need to be repeated here in full. They consist in the removal of well animals from the infected pasture to a noninfected field, the draining of the swampy ground, the burial or burning of the carcasses to prevent the dissemination of the germs over vast areas through the agency of dogs, wolves, buzzards, or crows, the disinfection of the stables and the ground where the animals lay at the time of death, and, if possible, the destruction of the germs on the infected pastures. One of the most effective methods for freeing an infected pasture from blackleg is to allow the grass to grow high, and when sufficiently dry to burn it off. One burning off is not sufficient to redeem an infected pasture, but the process should be repeated several years in succession. This method, however, is in many instances impracticable, as few cattle owners can afford to do it, and the only means left for the protection of the animals is vaccination.

Immunization by vaccination.—Three French veterinarians, Arloing, Cornevin, and Thomas, were the first to discover that cattle may be protected against blackleg by inoculation with virulent material obtained from animals which have died of this disease. Later they devised a method of inoculation with the attenuated or weakened blackleg spores which produced immunity from natural or artificial inoculation of virulent blackleg germs. Their method has undergone various modifications both in regard to the manufacture of the vaccine and in the mode of its application. Kitt, a German scientist, modified the method so that but one inoculation of the vaccine was required instead of two, as was the case with that made by the French investigators. The vaccine formerly prepared and distributed by the Bureau of Animal Industry combined the principle of Arloing, Cornevin, and Thomas, and the modification of Kitt.

By vaccination we understand the injection of a minute amount of attenuated—that is, artificially weakened—blackleg virus into the system. This virus is obtained from animals which have died from blackleg, by securing the affected muscles, cutting them into strips, and drying them in the air. When they are perfectly dry they are pulverized and mixed with water to form a paste, smeared in a thin layer on flat dishes, placed in an oven, and heated for six hours at a temperature close to that of boiling water. The paste is then transformed into a hard crust, which is pulverized and sifted and distributed in packages containing either 10 or 25 doses. This constitutes the vaccine, the strength of which is thoroughly tested on experiment animals before it is distributed among the cattle owners. This vaccine, which is in the form of a brownish, dry powder, is mixed with definite quantities of sterile water, filtered, and by means of a hypodermic syringe the filtrate injected under the skin in front of the shoulder of the animal. The inoculation is usually followed by insignificant symptoms. In a few cases there is a slight rise of temperature, and by close observation a minute swelling may be noted at the point of inoculation. The immunity conferred in this way may last for 18 months, but animals vaccinated before they are 6 months old and those in badly infected districts should be revaccinated before the following blackleg season.

The effect of the vaccine prepared by this bureau in preventing outbreaks of the disease and in immediately abating outbreaks already in progress was highly satisfactory, and it is not to be doubted that thousands of young cattle were saved to the stock owners during the 25 years in which the vaccine was distributed.[6] More than 47,000,000 doses were sent out during this period, and from reports received it is safe to conclude that more than 40,000,000 were actually injected, whereby the percentage of loss from blackleg has been reduced from 10 per cent, which annually occurred before using, to less than one-half of 1 per cent per annum. With these figures before us it is plain that the general introduction of preventive vaccination must be of material benefit to the cattle raisers in the infected districts. Moreover, there is every reason to believe that with the continued use of blackleg vaccine in all districts where the disease is known to occur, and an earnest effort on the part of the stock owners to prevent the reinfection of their pastures by following the directions given, blackleg may be kept in check and gradually eradicated.

Immunization against blackleg is now frequently accomplished by the use of the so-called blackleg aggressin and blackleg filtrates.

NECROTIC STOMATITIS (CALF DIPHTHERIA).

[[Pl. XLIII].]

Necrotic stomatitis is an acute, specific, highly contagious inflammation of the mouth occurring in young cattle, and characterized locally by the formation of ulcers and caseo-necrotic patches and by constitutional symptoms, chiefly toxic.

This disease has also been termed calf diphtheria, gangrenous stomatitis, ulcerative stomatitis, malignant stomatitis, tubercular stomatitis, and diphtheritic patches of the oral mucous membrane.

History.—During the last few years farmers and cattlemen in this country, especially in Colorado, Texas, and South Dakota, have increasingly noted the occurrence of enzootics of "sore mouth" among the young animals of their herds. Instead of healing, like the usual forms, of themselves, these cases, if untreated, die. Careful study of some of them has resulted in their identification with cases reported in 1877 by Dammann, from the shore of the Baltic; in 1878 by Blazekowic, in Slavonia; in 1879 by Vollers, in Holstein; in 1880 by Lenglen, in France; in 1881 by Macgillivray, in England; and in 1884 by Löffler, who isolated and described the microorganism which produces the disease. Bang obtained this organism from the diphtheritic lesions of calves in 1890, and Kitt likewise recovered the bacillus from similar lesions of the larynx and pharynx of calves and pigs in 1893.

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Etiology.—The cause of necrotic stomatitis, as demonstrated by Löffler and since confirmed by other investigators, is Bacillus necrophorus, often spoken of as the bacillus of necrosis. This organism varies in form from a coccoid rod to long, wavy filaments, which may reach a length of 100µ; the width varies from 0.75µ to 1µ. Hence it is described as polymorphic. It does not stain by Gram, but takes the ordinary anilin dyes, often presenting, especially the longer forms, a beaded appearance. A characteristic of the organism, of great moment when we come to treatment, is that it grows only in the absence of oxygen, from which fact it is described as an obligate anærobe.

Very few organisms exhibit a wider range of pathogenesis. According to clinical observation to the present time, Bacillus necrophorus is pathogenic for cattle, horses, hogs, sheep, reindeer, kangaroos, antelope, and rabbits. Experimentally it has been proved pathogenic for rabbits and white mice. The dog, cat, guinea pig, pigeon, and chicken appear to be absolutely immune. It is not pathogenic for man.

The importance of this bacillus is far beyond even its relation to necrotic stomatitis. Besides this disease it has been demonstrated as the causative factor in foot rot, multiple liver abscesses, disseminated liver necrosis, embolic necrosis of the lungs, necrosis of the heart, in cattle; gangrenous pox of the teats, diphtheria of the uterus and vagina, in cows; diphtheritic inflammation of the small intestine of calves. Among horses it is the agent in the production of necrotic malanders, quittor, and diphtheritic inflammation of the large intestine. In hogs it has caused necrotic or diphtheritic processes in the mucous membrane of the mouth, necrosis of the anterior wall of the nasal septum, and pulmonary and intestinal necrosis, accompanying hog cholera. Abscesses of the liver, gangrenous processes of the lips and nose, and gangrenous affections of the hoof have all been caused in sheep by this organism.

Pathology.—The principal lesions in necrotic stomatitis occur in the mucous membrane of the mouth and pharynx. The alterations may extend to the nasal cavities, the larynx, the trachea, the lung, the esophagus, the intestines, and to the hoof. The oral surfaces affected are, in the order of frequency, tongue, cheeks, hard palate, gums, lips, and pharynx. In the majority of cases the primary infection seems to occur in the tongue. ([Pl. XLIII].)

Infection takes place by inoculation. Some abrasion or break in the continuity of the mucous membrane of the mouth occurs. Very likely the origin may be connected with the eruption of the first teeth after birth, or, in animals somewhat older, the entrance of a sharp-pointed particle of feed. Gaining an entrance at this point, the bacilli begin to multiply. During their development they elaborate a toxin, or poisonous substance, which causes the death, or necrosis, of the epithelial, or superficial, layer of the mucous membrane and also of the white blood cells which have sallied forth through the vessel walls to the defense of the tissues against the bacillary attack. This destruction of the surface epithelium seems to be the essential factor in the production of the caseous patch, often called the false membrane. From the connective-tissue framework below is poured forth an inflammatory exudate highly albuminous or rich in fibrin-forming elements. When this exudate and the necrosed cellular elements come in contact, the latter furnish a fibrin ferment which transforms the exduate into a fibrinous mass. This process is known as coagulation necrosis, and the resulting fibroid mass, containing in its meshes the necrosed and degenerated epithelium and leucocytes, constitutes the diphtheritic or false membrane. Did the process cease at this point it would be properly called a diphtheritic inflammation, but it does not. A caseating ferment is supplied by the bacilli, and this, acting upon the fibroid patch, transforms it into a dry, finely granular, yellowish mass of tissue detritus resembling cheese.

Frequently this caseous inflammation results in the formation of one or more ulcers with thickened, slightly reddened borders, surmounted by several layers of this necrosed tissue. The floor of the ulcer is formed by a grayish-yellow, corroded surface, under which the tissue is transformed into a dry, friable, or firm cheesy mass. In the tongue this may progress to two fingers' thickness into the muscular portion; in the cheek it may form an external opening, permitting fluids to escape from the mouth; upon the palate it frequently reaches and includes the bone in its destructive course; upon the gums it has produced necrosis of the tooth sockets, causing loss of the teeth. In the advanced forms, caseous foci may be seen in the lung and in the liver and necrotic patches observed on the mucous membrane of the gastrointestinal tract.

Symptoms.—Necrotic stomatitis is both a local and a systemic affection. Primarily it is local. The local lesion is the caseo-necrotic patch or ulcer developed as a result of the multiplication of the bacilli at the point of inoculation. The general affection is an intoxication, or poisoning, of the whole system produced by a soluble toxin elaborated by the bacilli.

The stage of incubation is from three to five days. The first symptoms noted are a disinclination to take nourishment, some drooling from the mouth, and an examination of the mouth will show on some portion of its mucous membrane a circumscribed area of infiltration and redness, possibly an erosion. The latter gradually extends in size and depth, forming a sharply circumscribed area of necrotic inflammation. It may measure anywhere from the size of a 5-cent piece to that of a silver dollar or even larger. It has the appearance of a corroded surface, under which the mucous membrane or muscular tissue seems transformed into a dry, friable, or firm cheesy mass. It is grayish yellow in color and is bordered by a zone of thickened tissue slightly reddened and somewhat granulated. The necrotic tissue is very adherent and can be only partially peeled off. It is homogeneous, cheesy, and may extend two fingers' depth into the tissues beneath. The general symptoms are languor, weakness, and slight fever. In spite of plenty of good feed the calf is seen to be failing. It stops sucking, or, if older, altogether refuses to eat. The temperature at this time may be from 104° to 107° F. The slobber becomes profuse, swallowing very difficult, opening of the mouth quite painful, and a most offensive odor is exhaled. The tongue is swollen and its motion greatly impaired. Sometimes the mouth is kept open, permitting the tumefied tongue to protrude. One or more of the above symptoms direct the attention to the mouth as the seat of disease; or, having noticed the debility and disinclination to eat, an examination of the animal may show a lump under the neck or swelling of the throat or head. The following extract from a letter is characteristic:

I noticed my calves beginning to fail about the first week in December, but could not account for it, as they were getting plenty of grain and hay. My attention was first attracted by a swelling under the neck of one of the calves. I cast the animal and found that it was feed that had collected and the animal couldn't swallow it. I removed it, and in so doing noticed a large ulcer on the tongue and a very offensive odor. This was the first knowledge I had of anything being wrong with the calves' mouths. They may have been sick for some time before this.

Out of a herd of 100 belonging to this man, 70 were affected, and the letter emphasizes the insidious character of the onset.

The general affection at this time manifests itself by dejectedness, extreme weakness, and emaciation, constant lying down, with stiffness and marked difficulty in standing.

The disease frequently extends to the nasal cavities, producing a thin, yellowish, or greenish-yellow, sticky discharge which adheres closely to the borders of the nostrils. Their edges also show caseous patches similar to those in the mouth. Sometimes the nasal passage is obstructed by great masses of the necrosed exudate, thus causing extreme difficulty in breathing. When the caseous process involves the larynx and trachea there result cough, wheezing, and dyspnea, together with a yellowish mucopurulent expectoration.

When life is prolonged three or four weeks, caseous foci may be established in the lung, giving rise to all the signs of a bronchopneumonia. Many of these cases are associated with a fibrinous pleurisy. The invasion of the gastrointestinal tract is announced by diarrheal symptoms. This disease principally attacks sucklings not more than 6 weeks of age, but calves 8 and 10 months old are frequently affected, and several cases in adult cattle have been reported to this office.

In its very acute form many of the cases run their course in from five to eight days. In these the local lesions are not strongly marked, and death seems due to acute intoxication. In other enzootics the majority of the affected animals live from three to five weeks. These are cases that occasionally present the pulmonary and intestinal symptoms, and sometimes develop also caseo-necrotic lesions in the liver.

Ordinarily cases show no tendency to spontaneous cure. Left to themselves they die. On the contrary, if taken in hand early, the disease is readily amenable to treatment. In the latter event the prospects of recovery are excellent.

Differential diagnosis.—Necrotic stomatitis may be differentiated from foot-and-mouth disease by the fact that in the latter there is a rapid infection of the entire herd, including the adult cattle, as well as the infection of hogs and sheep. The characteristic lesion of foot-and-mouth disease is the appearance of vesicles containing a serous fluid upon the mucous membrane of the mouth and upon the udder, teats, and feet of the affected animals. In necrotic stomatitis vesicles are never formed, necrosis occurring from the beginning and followed by the formation of yellowish, cheesy patches, principally found in the mouth. Mycotic stomatitis occurs in only a few animals of the herd, chiefly the adult cattle, and the lesions produced consist of an inflammation of the mouth and lips and of the skin between the toes, followed in a few days by small irregular ulcers in the mouth. This disease appears sporadically, usually in the early fall after a dry summer, does not run a regular course, and can not be inoculated.

Prevention.—Prophylaxis should be carried out along three lines:

(1) Separation of the sick from the healthy animals.

(2) Close scrutiny and thorough disinfection once or twice daily for five days of the mouths and nasal passages of those animals that have been exposed.

(3) Complete disinfection of all stalls and sheds.

The disease appears to break out in winter and hold over to spring. It is conceivable that exposure to cold might so disturb the normal circulation of the oral tissues as to make the mucous membrane an excellent location for the causative factor of the disease. There is another possibility, however, which bears on the third line of prophylaxis. The so-called diphtheritic inflammations of the vagina and uterus in cows are caused by the same organism that induces necrotic stomatitis. A European writer has recently pointed out the almost constant relation of such attacks to previous occurrences of foul foot or foot rot in the same or other cattle on the place.

In all likelihood, in such cases, the stalls and sheds are the harborers of this germ. It is possible that many of these outbreaks have some relation to preceding cases of the above-mentioned diseases and the greater use in winter of the stalls and sheds, thus harboring the Bacillus necrophorus.

Treatment.—The treatment consists almost solely in careful and extensive cleansing and disinfection of the mouth and other affected surfaces. The mucous membrane of the mouth should be copiously irrigated with a 4 per cent solution of boracic acid in warm water at least twice daily. As exposure to oxygen kills the bacilli, one need have no fear about disturbing or tearing off the caseous patches or necrotic tissue during irrigation. The irrigation of the sores should then be followed by the application with a brush or rag on a stick of a paste made with 1 part of salicylic acid and 10 parts of water, or the affected areas may be painted with Lugol's solution of iodin (iodin, 1; potassium iodid, 5; water, 200). Frequent injections of 1 per cent carbolic-acid solution into the mouth make an excellent treatment. The internal administration of 2 grams of salicylic acid and 3 grams of chlorate of potassium three times a day has also proved to be very beneficial when accompanied with local antiseptic treatment.

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MALIGNANT CATARRH.

Malignant catarrh, or infectious catarrhal fever, is an acute infectious disease of cattle preeminently involving the respiratory and digestive tracts, although the sinuses of the head, the eyes, and the urinary and sexual organs are very frequently affected. It is relatively rare in this country, being more common on the continent of Europe. Outbreaks have occurred, however, in Minnesota, New York, and New Jersey. So far the causal agent of the disease has never been isolated, and inoculation experiments with the view of artificially reproducing the disease have proved negative in every case. In spite of the foregoing statements the consensus of opinion of eminent investigators points to malignant catarrh as being of specific origin; that is, due to some form of microorganism the contagious character of which is poorly developed. This accounts for the slow transmissibility of the disease from one animal to another. In fact, malignant catarrh is a type of that class of affections scientifically known as miasmatic diseases; that is, they remain stationary in stables with damp floors, low ceilings, poor ventilation, and bad sanitary conditions in general. Such places furnish a favorable seat of propagation for the infective material, and it will remain active for a long time, causing the loss of a few animals each year. One European veterinarian reports an instance in which the disease remained for 25 years on the same farm, attacking in all 225 animals, with a mortality of about 98 per cent.

The disease is most common in late winter and early spring, at all altitudes, and has a special preference for young, well-nourished cattle, although older animals are not immune. The time between the entrance of the infective principle into the body of the animal and the appearance of the first symptoms is relatively very long, averaging, according to German investigators, from 20 to 30 days. Fortunately, it is not a disease which spreads to any great extent or which causes severe losses, and hence legislative enactments do not seem to be necessary for its restriction.

Symptoms.—These are extremely variable according to the point of localization of the lesions. It is usually ushered in with a chill, followed by a marked rise of temperature (104° to 107° F.). The head droops, the skin is hot and dry, and the coat staring. Quivering of the muscles in various parts of the body is frequently observed. Marked dullness of the animal, passing, according to some observers, into an almost stupefied condition later on, is quite common. The secretion of milk stops in the beginning of the disease, and loss of flesh, invariably associated with the disease, is extremely marked and rapid. The lesions of the eyes may best be likened to moon blindness (periodic ophthalmia) in horses.

There is first an abundant secretion of tears, which run down the face. The lids are swollen and inflamed, and indeed this may be so marked as to cause involuntary eversion, exposing the reddened conjunctiva to view. Sunlight is painful, as is shown by the fact that the animal keeps the eyes continuously closed. This inflammation may extend to the cornea, causing it to assume a slightly clouded appearance in mild cases or a chalky whiteness in more severe affection. Cases of ulceration of the cornea followed by perforation and subsequent escape of the aqueous humor, leading to shrinking of the eyeball and permanent loss of sight, have been recorded, but these are relatively rare, although slight inflammation of the deeper structures of the eye (iris) are more frequent. In mild cases this inflammation may undergo complete resolution, but more frequently permanent cloudliness of the cornea, either diffuse or in spots (leucoma), is the result. The mucous membrane of the mouth, nose, sinuses of the head, throat, and lower respiratory passages are also involved. It is first catarrhal in character, but soon a false or diphtheritic membrane is formed, with the production of shallow ulcers. There is dribbling of saliva from the mouth and discharge from the nose, at first watery, becoming thicker and mixed with blood and small masses of cast-off croupous membrane, causing a very fetid odor. These croupous areas when they form in the throat, larynx, or windpipe, may lead to narrowing of the passages, with consequent difficult breathing and even suffocation. Various respiratory murmurs may also be heard, caused by the to-and-fro movement of mucus and inflammatory deposits along the air passages. There is also inflammation of the horn core with consequent loosening of the horn shell, and the horns are thus readily knocked off by the uneasy, blind sufferer. The animal may refuse all feed from the time of the initial rise of temperature, or in less severe cases, and especially when the lesions of the digestive tract are not so marked, the appetite may remain until the disease is well advanced. Constipation is quite common at the commencement of the attack, followed by diarrhea and severe straining, the evacuations becoming very soft, fetid, and streaked with blood. Cases of the evacuation of desquamated patches of diphtheritic membrane from the intestinal mucosa 6 to 9 feet in length have been reported. The kidneys and bladder are usually inflamed, the urine being voided with difficulty and the animal evincing signs of pain. Inflammatory elements, as albumen, casts, etc., may be seen on examination of the urine. In cows the mucous membrane of the vestibule is congested, swollen, and may contain ulcers and an excessive quantity of mucus. Abortion during advanced pregnancy is not infrequent, following a severe attack. In connection with these various symptoms there may be much uneasiness on the part of the animal, leading in some cases to madness and furious delirium, in others to spasms and convulsions or paralysis. A vesicular eruption of the skin may occur, seen principally between the toes and on the inside of the flank and in the armpits, with subsequent loss of hair and epidermis.

Like other infectious diseases, malignant catarrh pursues a longer or shorter course in accordance with the severity of the attack. In acute cases death is said to take place three to seven days after the appearance of symptoms. Recovery, if it occurs, may take three or four weeks. According to statistics, from 50 to 90 per cent of the affected animals die.

If animals which have died of this disease are examined, in addition to the changes of the mucous membrane of mouth and nasal cavities referred to above, shallow ulcers in these situations will be found occasionally. These necrotic processes may pass beneath the mucous membrane and even involve the underlying bony structure. In severe cases membranous (croupous) deposits are found in the throat. Similar deposits have been found upon the mucous membrane of the fourth stomach and intestine, which is always inflamed. There is more or less inflammation of the membranes of the brain, kidneys, and liver, and some fatty degeneration of the voluntary muscles. In countries where rinderpest occasionally appears it may be difficult to distinguish between it and malignant catarrh, owing to a general similarity of the symptoms. The principal points to be observed in differentiating between the two are the very slight transmissibility of the latter as compared with the intense contagiousness of the former, and the tendency of malignant catarrh to run a more chronic course than rinderpest, which usually results fatally in a very few days. Only a trained veterinarian who takes into consideration all the different symptoms and lesions of both diseases should decide in such cases.

Treatment.—There is no specific treatment for this affection. Copious blood letting in the earliest stages has been highly recommended, however, as this has a tendency to deplete the system and lessen the exudation of inflammatory products. Antiseptic washes, such as 4 per cent boric-acid solution to the eyes and Dobell's solution applied to the nose and mouth with ice poultices over the crest of the head and frontal region, have also proved efficacious. Calomel should also be given in 1-dram doses twice a day for three days, and in severe cases, involving the respiratory tract, a powder containing ferrous sulphate, quinin, and subnitrate of bismuth, given twice a day, will be found beneficial. At the same time it must be remembered that much greater success is to be looked for in the preventive treatment. This consists in the removal of the healthy from the infected animals (not vice versa) and thorough cleaning and disinfecting of the contaminated stables. If the floors are low and damp, they should be raised and made dry. If this can not be done, place a layer of cement under the stable floor to prevent water from entering from below. The stable should be well ventilated and the soil in the pastures thoroughly drained. If this is carefully carried out, the contagion should be destroyed and the danger of the reappearance of the disease in a great measure lessened.

MALIGNANT EDEMA.

Malignant edema, also termed gangrenous septicemia, is an acute, inflammatory disease of domestic and wild animals, resulting from the introduction of a specific organism into the deep connective tissues of a susceptible animal and proving fatal in many instances within 24 to 48 hours. The disease may be inoculated from one animal to another, but only by inserting the virus deeply below the skin. It is infrequently met with in cattle, but may follow operating wounds, as roweling, castration, and phlebotomy, which have become infected with septic matter, soil, or unclean instruments. In the pathological laboratory of the Bureau of Animal Industry the organism has also been obtained from the infected muscles of a calf that was supposed to have died of blackleg, and, as a result, all blackleg virus is thoroughly tested before it is made into blackleg vaccine in order to exclude the malignant-edema organism. The essential cause of malignant edema is a long, slender, motile, spore-bearing bacillus, resembling the bacillus of blackleg, and which can develop only in the absence of the atmosphere. Unlike the bacilli of anthrax and blackleg, which are confined to certain districts, this organism is widely distributed and found in ordinary garden soil, foul water, and in the normal intestinal tract of the herbivora. It may be brought to the surface of the soil by growing plants, rains, winds, or burrowing insects and rodents. In animals that have succumbed to the disease the germ is confined to the seat of infection, but a few hours after death it may migrate through the blood channels to other parts of the body. The bacillus may attack man, horses, asses, goats, sheep, pigs, cats, dogs, and poultry. Adult cattle, although refractory to experimental inoculation, suffer from natural infection, while calves are susceptible to both these methods of exposure. (Kitt.) The introduction of the bacillus into abrasions of the skin and superficial sores rarely does any harm, because the germ is quickly destroyed by contact with air. If, however, the organisms are inserted deeply into the subcutaneous tissues of susceptible animals, they quickly develop, producing a soluble poison, which is the fatal agent.

In lamb-shearing season, or after docking or castration, the mortality is higher among these animals because of wounds inflicted at such times. The application of antiseptics to wounds thus made will reduce the percentage of deaths to a minimum.

Symptoms.—Usually the first symptoms are overlooked. In the early stages the animal appears listless, disinclined to move about, and lies down in shady and quiet places. If forced to move about, the hind legs are drawn forward with a peculiar, stiff, dragging movement, and there may be slight muscular trembling over all the body, which becomes more intense as the disease progresses. When driven, the animal shows signs of fatigue, ultimately dropping to the ground completely exhausted. Breathing becomes fast and painful, with frequent spasmodic jerks.

The pulse is quick and weak and the temperature is 106° to 107° F. An edematous, doughy, and painful swelling appears at the point of infection. This tumefaction spreads more and more, and crackles on pressure. In case of an open wound, a fetid liquid and frothy discharge is observed. The center of the swelling may appear soft and jellylike, while the margin is tense, hot, and painful. The symptoms increase rapidly, resulting in coma and death.

Lesions.—After death the fat and subcutaneous tissues surrounding the infected area are infiltrated with a yellow gelatinous material containing an orange-colored foam, due to the presence of gas bubbles.

The muscles at this point are friable, spongy, and of a uniform brownish tint, dissociated by gas and with a blood-tinged exudate. This gangrenous tissue, when present before death, can be removed without pain to the animal. The intestines are generally normal, but, together with the peritoneum, they may be inflamed, and the lungs are usually the seat of an edema. The spleen, liver, and kidneys retain their normal appearance, in marked contrast with anthrax.

Differential diagnosis.—Unlike blackleg, this disease never appears as an epizootic but in isolated cases. It may also be differentiated from the former by the history of a recent parturition or surgical operation, by the presence of an external injury at the site of the swelling accompanied with a fetid liquid discharge, and the gangrenous appearance of the tumefaction. Man is susceptible to malignant edema, but not to blackleg. Malignant edema may also be easily differentiated from anthrax in that the blood and spleen are normal in appearance, while in the latter disease the blood is dark and of a tarlike consistency, and the spleen appears swollen, injected, and softened. The local tumor in malignant edema contains gas bubbles, which are absent in anthrax swellings. Inoculation experiments of guinea pigs, rabbits, and chickens will also disclose the differences among the above-mentioned three diseases, since all these species are killed by the germ of malignant edema, only the first two species by the anthrax bacillus, while the guinea pig alone will succumb to the blackleg infection.

Treatment.—Treatment is chiefly surgical and consists in laying the infected areas wide open by free incision, followed by a liberal application of a 30 per cent solution of hydrogen dioxid and subsequently a 5 per cent solution of carbolic acid. Usually the disease when observed has advanced to such an extent that medicinal interference is without avail. Preventive treatment is by far the most desirable, and consists, essentially, in a thorough disinfection of all accidental and surgical wounds, the cleansing of the skin, and the exclusion of soil, filth, and bacteria during surgical operations of any nature. Sheds, barns, and stables should receive a thorough application of quicklime or crude carbolic acid wash after all rubbish has been removed and burned. All dead animals should be burned or deeply buried and covered well with quicklime.

SOUTHERN CATTLE FEVER (TEXAS FEVER, TICK FEVER).

[[Pls. XLIV]-[XLIX].]

This disease, which is more commonly known as Texas fever, and sometimes as splenetic fever, is a specific fever communicated by cattle which have recently been moved northward from the infected district; it is also contracted by cattle taken into the infected district from other parts of the world. It is characterized by the peculiarity among animal diseases that the animals which disseminate the infection are apparently in good health, while those which sicken and die from it do not, as a rule, infect others.

It is accompanied with high fever, greatly enlarged spleen, destruction of the red blood corpuscles, escape of the coloring matter of the blood through the kidneys, giving the urine a deep-red color, with a yellowness of the mucous membranes and fat, which is seen more especially in fat cattle, by a rapid loss of strength, and with fatal results in a large proportion of cases.

This disease has various names in different sections of the country where it frequently appears. It is often called Spanish fever, acclimation fever, red water, black water, distemper, murrain, dry murrain, yellow murrain, bloody murrain, Australian tick fever, and tristeza of South America.

The earliest accounts we have of this disease date back to 1814, when it was stated by Dr. James Mease, before the Philadelphia Society for Promoting Agriculture, that the cattle from a certain district in South Carolina so certainly disease all others with which they mix in their progress to the North that they are prohibited by the people of Virginia from passing through the State; that these cattle infect others while they themselves are in perfect health, and that cattle from Europe or the interior taken to the vicinity of the sea are attacked by a disease that generally proves fatal. Similar observations have been made in regard to a district in the southern part of the United States.

The northern limits of this area are changed yearly as a result of the dissemination or eradication of the cattle tick along the border, but the infected area has gradually decreased, owing to the successful endeavors pushed forward to eliminate the ticks.

It was the frequent and severe losses following the driving of cattle from the infected district in Texas into and across the Western States and Territories which led to the disease being denominated Texas fever. It is now known, however, that the infection is not peculiar to Texas or even to the United States, but that it also exists in southern Europe, Central and South America, Australia, South Africa, and the West Indies.

When cattle from other sections of the country are taken into the infected district they contract this disease usually during the first summer, and if they are adult animals, particularly milch cows or fat cattle, nearly all die. Calves are much more likely to survive. The disease is one from which immunity is acquired, and therefore calves which recover are not again attacked, as a rule, even after they become adult.

When the infection is disseminated beyond the permanently infected district, the roads, pastures, pens, and other inclosures are dangerous for susceptible animals until freezing weather. The infection then disappears, and cattle may be driven over the grounds or kept in the inclosures the succeeding summer and the disease will not reappear. There are some exceptions to this rule in the section just north of the boundary line of the infected district. In this locality the infection sometimes resists the winters, especially if they are mild.

In regard to the manner in which the disease is communicated, experience shows that this does not occur by animals coming near or in contact with one another. It is an indirect infection. The cattle from the infected district first infect the pastures, roads, pens, cars, etc., whence the susceptible cattle obtain the virus secondhand. Usually animals do not contract the disease when separated from infected pastures by a fence. If, however, there is any drainage or washing by rains across the line of fence this rule does not hold good.

The investigations made by the Bureau of Animal Industry demonstrate that the ticks which adhere to cattle from the infected district are the only known means of conveying the infection to susceptible cattle. The infection is not spread by the saliva, the urine, or the manure of cattle from the infected district. In studying the causation and prevention of this disease, attention must therefore be largely given to the tick, and it now seems apparent that if cattle could be freed from this parasite when leaving the infected district they would not be able to spread the malady. The discovery of the connection of the ticks with the production of the disease has played a very important part in determining the methods that should be adopted in preventing its spread. It established an essential point and indicated many lines of investigation which have yielded and are still likely to yield very important results.

Nature of the disease.—Texas fever is caused by an organism which lives within the red blood corpuscles and breaks them up. It is therefore simply a blood disease. The organism does not belong to the bacteria but to the protozoa. It is not, in other words, a microscopic plant, but it belongs to the lowest forms of the animal kingdom. This very minute organism multiplies very rapidly in the body of the infected animal, and in acute cases causes an enormous destruction of red corpuscles in a few days. How it gets into the red corpuscle it is not possible to state, but it appears that it enters as an exceedingly minute body, probably endowed with motion, and only after it has succeeded in entering the corpuscle does it begin to enlarge. Plate XLV, figure 4, illustrates an early stage of this blood parasite. The red corpuscle contains a very minute, roundish body which is stained blue to bring it into view. The body is, as a rule, situated near the edge of the corpuscle. Figure 5 illustrates an older stage in the growth of the parasite, in fact the largest which has thus far been detected. It will be noticed that there are usually two bodies in a corpuscle. These bodies are in general pear-shaped. The narrow ends are always toward each other when two are present in the same corpuscle. If we bear in mind that the average diameter of the red blood corpuscles of cattle is from 1/4000 to 1/5000 inch, the size of the contained parasite may be at once appreciated by a glance at the figures referred to.

The various disease processes which go on in Texas fever, and which we may observe by examining the organs after death, all result from the destruction of the red corpuscles; this destruction may be extremely rapid or slow. When it is rapid we have the acute, usually fatal, type of Texas fever, which is always witnessed in the height of the Texas-fever season, that is, during the latter weeks of August and the early weeks of September. When the destruction of corpuscles is slower, a mild, usually nonfatal, type of the disease is called forth, which is only witnessed late in autumn or more rarely in July and the early part of August. Cases of the mild type occurring thus early usually become acute later and terminate fatally.

The acute disease is fatal in most cases, and the fatality is due not so much to the loss of blood corpuscles as to the difficulty which the organs have in getting rid of the waste products arising from this wholesale destruction. How great this may be a simple calculation will serve to illustrate. In a steer weighing 1,000 pounds, the blood in its body weighs about 50 pounds, if we assume that the blood represents one-twentieth of the weight of the body, which is a rather low estimate. According to experimental determination at the bureau station, which consists in counting the number of blood corpuscles in a given quantity of blood from day to day in such an animal, the corpuscles contained in from 5 to 10 pounds of blood may be destroyed within 24 hours. The remains of these corpuscles and the coloring matter in them must be either converted into bile or excreted unchanged. The result of this effort on the part of the liver causes extensive disease of this organ. The bile secreted by the liver cells contains so much solid material that it stagnates in the finest bile canals and chokes these up completely. This in turn interferes with the nutrition of the liver cells and they undergo fatty degeneration and perish. The functions of the liver are thereby completely suspended and death is the result. This enormous destruction of corpuscles takes place to a large extent in the kidneys, where a great number of corpuscles containing the parasites are always found in acute cases. This accounts largely for the blood-colored urine, or red water, which is such a characteristic feature of Texas fever. The corpuscles themselves are not found in the urine; it is the red coloring matter, or hemoglobin, which leaves them when they break up and pass into the urine.

Symptoms.—After a period of exposure to infected soil, which may vary from 13 to 90 days, and which will be more fully discussed under the subject of cattle ticks as bearers of the Texas-fever parasite, the disease first shows itself in dullness, loss of appetite, and a tendency to leave the herd and stand or lie down alone. A few days before these symptoms appear the presence of a high fever may be detected by the clinical thermometer. The temperature rises from a normal of 101° to 103° F. to 106° and 107° F. There seems to be little or no change in temperature until recovery or death ensues. The period of high temperature or fever varies considerably. As it indicates the intensity of the disease process going on within, the higher it is the more rapid the fatal end. When it does not rise above 104° F. the disease is milder and more prolonged.

The bowels are mostly constipated during the fever; toward the end the feces may become softer and rather deeply tinged with bile. The urine shows nothing abnormal during the course of the disease until near the fatal termination, when it may be deeply stained with the coloring matter of the blood. (Hemoglobinuria; see [Pl. XLV], fig. 3.) Although this symptom is occasionally observed in animals which recover, yet it may generally be regarded as an indication of approaching death. The pulse and respiration are usually much more rapid than during health.

Other symptoms in addition to those mentioned have been described by observers, but they do not seem to be constant, and only those described above are nearly always present. As the end approaches emaciation becomes very marked, the blood is very thin and watery, and the closing of any wound of the skin by clots is retarded. The animal manifests increasing stupor and may lie down much of the time. Signs of delirium have been observed in some cases. Death occurs most frequently in the night.

The duration of the disease is very variable. Death may ensue in from three days to several weeks after the beginning of the fever. Those that recover ultimately do so very slowly, owing to the great poverty of the blood in red corpuscles. The flesh is regained but very gradually, and the animal may be subjected to a second, though mild, attack later on in the autumn, which pushes the full recovery onward to the beginning of winter.

In the mild type of the disease, which occurs in October and November, symptoms of disease are well-nigh absent. There is little if any fever, and if it were not for loss of flesh and more or less dullness the disease may pass unnoticed, as it undoubtedly does in a majority of cases. If, however, the blood corpuscles are counted from time to time a gradually diminishing number will be found, and after several weeks only about one-fifth or one-sixth of the normal number are present. It is indeed surprising how little impression upon the animal this very impoverished condition of the blood appears to make. It is probable, however, that if two animals kept under the same conditions, one healthy and the other at the end of one of these mild attacks, are weighed, the difference would be plainly shown.

Pathological changes observable after death.—In the preceding pages some of these have already been referred to in describing the nature of the disease. It is very important at times to determine whether a certain disease is Texas fever or some other disease, like anthrax, for example. This fact can, as a rule, be determined at once by a thorough microscopic examination of the blood. The necessary apparatus and the requisite qualifications for this task leave this method entirely in the hands of experts. There are, however, a considerable number of changes caused by this disease which may be detected by the naked eye when the body has been opened. Put together they make a mistake quite impossible. The presence of small ticks on the skin of the escutcheon, the thighs, and the udder is a very important sign in herds north of the Texas-fever line, as it indicates that they have been brought in some manner from the South and have carried the disease with them, as will be explained later. Another very important sign is the thin, watery condition of the blood, either just before death or when the fever has been present for four or five days. A little incision into the skin will enable any one to determine this point. Frequently the skin is so poor in blood that it may require several incisions to draw a drop or more.

The changes in the internal organs, as found on post-mortem examinations, are briefly as follows: The spleen, or milt, is much larger than in healthy animals. It may weigh three or four times as much. When it is incised the contents or pulp is blackish (see [Pl. XLIV], fig. 1), and may even well out as a disintegrated mass. The markings of the healthy spleen (fig. 2) are all effaced by the enormous number of blood corpuscles which have collected in it, and to which the enlargement is attributable. Next to the spleen the liver will arouse our attention. (See [ Pl. XLV], fig. 2.) It is larger than in the healthy state, has lost its natural brownish color (fig. 1), and now has on the surface a paler, yellowish hue. When it is incised this yellowish tinge, or mahogany color, as it has been called by some, is still more prominent. This is owing to the large quantity of bile in the finest bile capillaries, and as these are not uniformly filled with it the cut surface has a more or less mottled appearance. This bile injection causes in many cases a fatty degeneration of the liver cells, which makes the organ appear still lighter in color.

In all cases the gall bladder should be examined. This is distended with bile, which holds in suspension a large number of yellow flakes, so that when it is poured into a tall bottle to settle fully one-half or more of the column of fluid will be occupied by a layer of flakes. If mucus is present at the same time, the bile may become so viscid that when it is poured from one glass to another it forms long bands. The bile in health is a limpid fluid, containing no solid particles.

If the animal during life has not been observed to pass urine colored with blood or red water, the bladder should be opened. This quite invariably, in acute cases, contains urine which varies in color from a deep port wine to a light claret. In many cases the color is so dense that light will not pass through even a thin layer. ([Pl. XLV], fig. 3.) The kidneys are always found congested in the acute attack. The disease exerts but little effect on the stomach and intestines beyond more or less reddening of the mucous membrane; hence an examination of them may be safely omitted. The lungs are, as a rule, not diseased. The heart usually shows patches of blood extravasation on the inside (left ventricle) and less markedly on the outer surface.

We have observed jaundice of the various tissues but very rarely. It has been observed by some quite regularly, however.

During the hot season about 90 per cent of the susceptible mature animals from a noninfected district die, but later, in the cool weather, the disease assumes a milder type, with a consequent decrease in the number of deaths.

The cattle tick, Margaropus annulatus, as the carrier of Texas fever. ([Pls. XLVI], [XLVII], and [XLVIII].) —The cattle tick is, as its name indicates, a parasite of cattle in the southern part of the United States. It belongs to the group of Arthropoda and to the genus Margaropus (or Boophilus), which is included in the order Acarina. Its life history is quite simple and easily traced from one generation to another. It is essentially a parasite, attaching itself to the skin ([Pl. XLVIII]) and drawing the blood of its host. It is unable to come to maturity and reproduce its kind unless it becomes attached to the skin of cattle, whence it may obtain its food.

The eggs laid on the ground after the female has dropped from the host begin to develop at once. When the embryo is fully formed within the shell it ruptures this and gains its freedom. The time required from the laying of the eggs to their hatching varies considerably, according to the temperature. In the laboratory in the heat of midsummer this was accomplished in about 13 days. In the late fall, under the same conditions, it required from four to six weeks. The larva after emerging from the egg is very minute, six-legged, and is just visible to the naked eye. ([Pl. XLVI], fig. 3.) If these larvæ are kept on a layer of moist sand or earth in a covered dish, they may remain alive for months, but there is no appreciable increase in size. So soon, however, as they are placed upon cattle growth begins.

On pastures these little creatures soon find their way on to cattle. They attach themselves by preference to the tender skin on the escutcheon, the inside of the thighs, and on the base of the udder. Yet when they are very numerous they may be found in small numbers on various parts of the body, such as the neck, the chest, and the ears. ([Pl. XLVIII] and [Pl. XLIX], fig. 1.)

The changes which they undergo during their parasitic existence were first studied by Dr. Cooper Curtice, of the Bureau of Animal Industry, in 1889. The young tick molts within a week, and the second or nymphal stage of the parasite's life is thus ushered in. After this change it has four pairs of legs. Within another week another molt takes place by which the tick passes from the nymphal to the sexual, or adult, stage. Impregnation now takes place, and, with the development of the ova in the body, the tick takes an increased quantity of blood, so that in a few days it becomes very much larger. That the rapid growth is due to the blood taken in may be easily proved by crushing one. The intestine is distended with a thick, tarry mass composed of partly digested blood. When the female has reached a certain stage of maturity she drops to the ground and begins to lay a large number of eggs, which hatch in the time given above.

The life of the cattle tick is thus spent largely on cattle, and although the young, or larvæ may live for a long time on the ground in the summer season, they can not mature except as parasites on cattle and horses. We have purposely omitted various details of the life history, including that of the male, as they are not necessary to an understanding of our present subject—Texas fever. How this is transmitted we will proceed to consider. Before the enforcement of the Federal quarantine southern cattle sent north during the spring and summer months carried on their bodies large numbers of the cattle ticks, which, when matured, would drop off and lay their eggs in the northern pastures. After hatching, the young ticks would soon get upon any northern cattle which happened to be on the pasture. So soon as they attached themselves to the skin they inoculated the cattle, and Texas fever would break out a week or more thereafter. For many years there had been a growing suspicion that the cattle tick was in some way concerned in the spread of Texas fever, and the facts which supported this supposition finally became so numerous and convincing that a series of experiments was inaugurated by the Bureau of Animal Industry which served to show that the tick is abundantly able to carry the disease to a herd of healthy cattle, and, in fact, is probably the only agent concerned in the transmission of the disease from southern cattle to susceptible northern animals.

Injurious effects of cattle ticks.—Unfortunately many cattle owners who have always been accustomed to see both ticks and ticky cattle on their farms are not inclined to attach much importance to these parasites, and, as a rule, through lack of appreciation of their damaging effects, placidly consider them as of little consequence. That ticks may be detrimental to their hosts in several ways has probably not suggested itself to these stockmen, who are most vitally affected, and it therefore seems necessary to emphasize the fact that, in addition to their relation to Texas fever, they may also be injurious to cattle as external parasites. While the power of transmitting Texas fever is undoubtedly the most dangerous property possessed by the cattle tick and is the principal cause for adopting stringent measures looking to its complete eradication, nevertheless there still remain other good reasons for the accomplishment of this achievement. These secondary objections to the presence of ticks on cattle consists in the physical harm they do to the host aside from the production of the specific disease of Texas fever. True, a few parasites may remain on cattle indefinitely without causing any noticeable effect, but it is not uncommon to notice bovine animals on pastures with their hides heavily infested with these pests. In such cases it can readily be seen that the continuous sucking of blood causes more or less impoverishment of the circulation. The animal must therefore be fed more in order to meet the demands of the parasites in addition to the ordinary needs of the host. If the ticks are removed from the body, the bites inflicted are often distinguished by small, inflamed or reddened areas somewhat swollen, with perforations of the skin which may allow the entrance of various kinds of disease germs, and showing that more or less irritation of the hide is produced by these parasites. This condition, together with the loss of blood, frequently induces an irritable state and evidence of uneasiness commonly known as "tick worry," which results in the loss of energy and other derangements of the animal's health. It may in some cases, especially in hot weather, become so pronounced that the animal will lose flesh in spite of good pasturing, thereby reducing the vitality and rendering it more susceptible to the inroads of disease. Moreover, if the infestation of ticks is not controlled, the cattle may be so reduced in condition that growth is retarded, and, in the case of young animals, they may never become fully developed, but remain thin, weak, and stunted—a condition that has been termed "tick poverty"—and easily succumb to other diseases as a result of lowered vitality. In milch cows this debilitating influence of the numerous ticks is shown in a greatly reduced milk supply. This should not appear strange when it is considered that some animals harbor several thousand of the bloodsucking parasites. If these parasites are crushed, it will be found that their intestines are completely filled with a dark, thick mass of blood abstracted from the animal host and containing nutriment that should go to the formation of milk, flesh, and the laying on of fat. In some rare cases the large number of bites on a limited area of skin may be followed by infection with pus-producing organisms, giving rise to small abscesses which may terminate in ulcers. The discharge from these sores, or in some cases the mere oozing of blood serum through the incision made by the mouth parts of the ticks, keeps the hair moist and matted together, and the laying and hatching of fly eggs in these areas give rise to infestation with destructive maggots, causing ulcers and other complications that require medical treatment. These statements regarding the secondary injurious effects of cattle ticks also apply to those ticks which have been previously spoken of as harmless so far as Texas fever is concerned, and, in fact, to all external parasites. Therefore, it is just as important to eradicate the cattle ticks for reasons other than those associated with Texas fever as it is to exterminate lice, fleas, and other vermin. Furthermore, cattle ticks, aside from the losses sustained by their purely parasitic effects, are the greatest menace to the profitable raising and feeding of cattle in the South, because they are an obstacle to cattle traffic between the infected and noninfected districts.

Loss occasioned by cattle ticks.—The economic aspect of the tick problem is unquestionably of the greatest practical interest, since the fundamental importance of all the other questions which surround it depends upon the actual money value involved. A careful and conservative estimate made in 1916 placed the annual loss caused by the ticks in the United States at $40,000,000, and indicated that the ticks also lowered the assets of the South by an additional $33,000,000. The principal items in these losses are set forth below.

It is well known that those animals coming from an infected district and sold in the "southern pens" of northern stockyards bring about one-half a cent less per pound than the quoted market price. The handicap that is placed on the southern cattle raiser as a result of this decrease in value of his stock will average at this figure $3 per head, allowing an individual weight of 600 pounds for all classes of animals. This decreased value reacts and fixes the valuation of all cattle which remain in the infected territory, thereby reducing the assets of the cattle industry of that section. In addition there is a very great loss from the decrease in flesh and lack of development of southern cattle occasioned by the parasitic life of the ticks from without and by the blood-destroying and enervating properties of the protozoan parasites from within.

The presence of the tick among the cattle of the South not only lessens the value of the cattle on the hoof but causes the gradings of hides that have been infested with ticks as No. 4 quality. The same hide, if free from tick marks, would grade No. 2. The difference in price between these two grades of hides is 3 cents a pound. As the hide of a southern steer weighs about 42 pounds, the presence of the tick in the hide causes a loss in the hide alone of more than $1.26 a hide. It has been shown that the cost of tick eradication is only about 50 cents a head, so that if the counties make a systematic campaign to eradicate the tick, the increase in value of the hide alone would pay for the cost of tick eradication and leave the farmer a net profit of about 76 cents a hide.

The shrinkage in the milk production of cattle harboring many ticks will average 1 quart a day, which in the aggregate is a heavy loss. The damage resulting to the southern purchaser of northern purebred or high-grade cattle is another item of no small moment. About 10 per cent of all such cattle taken into the South die of Texas fever, even after they are immunized by blood inoculations, and about 60 per cent of them succumb to Texas fever when not so treated. As they are usually very expensive animals and of a highly valued strain of blood, the loss in certain cases is excessive and in others almost irreparable, owing to the possible extinction of some particular type especially selected for the improvement of the herd.

Another instance in which it is difficult to figure the injury done by the ticks is in the case of death of nonimmune cattle in the tick-free pastures of the South. Such animals are as susceptible to Texas fever as nonimmune northern cattle, and inasmuch as there is in many States only one out of every four farms infested with ticks, the cattle on the remaining farms will in many cases contract Texas fever when exposed to the fever tick. These losses can scarcely be computed, as the death rate depends so much on the season of the year when exposure occurs and on the age of the animal affected. However, the deaths among such cattle are considerable, although this fact is little appreciated or understood by many outside the infected area.

On rare occasions a small outbreak of Texas fever occurs north of the quarantine line as a result of improperly disinfected cars, of unscrupulous dealers breaking the quarantine regulations, or of some accidental condition. Such damage, however, is slight, but should be considered in summing up the loss occasioned by the fever tick.

The advertisement which a breeder obtains and the sales which are made by having his stock in the show ring are usually lost to the cattle raiser in the infected area who aspires to display his animals in the North, as they are barred from most of these exhibitions. On the other hand, the southern farmer is not given an opportunity to see and be stimulated by the fine specimens of northern cattle which might be shown at southern stock exhibits, for the reason that the danger of contracting Texas fever is too patent to warrant such exposure. A heavy expense is incurred by the Government and the States in enforcing the regulations that apply to the quarantine line.

Another loss which is indirectly sustained by the southern cattle industry through increased freight rates is the cost, to the railroad companies, of cleaning and disinfecting the cars that carry cattle and in providing separate pens for them at various places.

These statements are sufficient to indicate that the loss to the quarantined section from the cattle tick is something enormous. Such a series of encumbrances as those recorded could be carried by the cattle industry of no other section of the country than the South, whose excellent pastures, rich soil, and salubrious climate are the only reasons for its ability to overcome such obstacles in meeting the competition of the West; and it is the inherent capacity of the South for greatly increasing its herds and enlarging its pasture lands that makes the actual loss even secondary to the potential loss from restrictions necessitated by the presence of the cattle tick. This potential loss may be described as the difference between the value of the cattle industry of the South to-day and the extent to which this industry would be increased if farmers and ranchmen were assured that their lands and cattle would not become infested with fever ticks. Could this assurance be given, the beneficial effects would extend over the entire country, because the market of the northern breeder would thereby become greatly extended.

These appalling losses and annual sacrifices of the cattle raisers of the infected district can be entirely effaced, and this at a small proportionate cost; for, with enthusiastic stockmen, satisfactory State legislation, sufficient money, and a corps of trained inspectors, the cattle tick may be exterminated, and every dollar expended in this work will be returned many times during each succeeding year.

The so-called period of incubation.—After the young ticks have attached themselves to cattle the fever appears about 10 days thereafter in midsummer. When the weather is cool, as in autumn, this period may be a little longer. The actual period of incubation may be shorter, for if blood from a case of Texas fever is injected into the blood vessels of healthy cattle the fever may appear within five days. When cattle graze upon pastures over which southern cattle have passed, the time when the disease appears varies within wide limits. When the animals have been put upon pastures immediately after southern cattle have infected them with ticks, it may take from 30 to 60 days, or even longer, before the disease appears. This will be readily understood when we recall the life history of ticks. The southern cattle leave only matured ticks which have dropped from them. These must lay their eggs and the latter must be hatched before any ticks can get upon native cattle. The shortest period is thus not less than 30 days if we include 10 days for the period of incubation after the young ticks have attached themselves to native cattle. When the infection of pastures with ticks has taken place early in the season, or when it is cold, the period is much longer, because it takes longer for the eggs to hatch.

If native cattle are placed upon pastures which have been infected with ticks some time before, the disease will appear so much sooner, because the young ticks may be already hatched and attack the cattle at once. It will be evident, therefore, that the length of time between the exposure of native cattle on infected fields and the appearance of the disease depends on the date of original infection, and on the weather, whether cold or hot. When native cattle are placed upon fields on which young ticks are already present, they will show the fever in 13 to 15 days if the season is hot.

The fever appears before the ticks have matured. In fact, they are still small enough to be overlooked. In any case very careful search should be made for them in those places which they prefer—the thighs, escutcheon, and udder. After the acute stage of the fever has passed the ticks begin to swell up and show very plainly. ([Pl. XLVI], figs. 6 and 7.)

Prevention.—It is generally accepted that if southern cattle are entirely free from that species of tick known as Margaropus annulatus they can be allowed to mingle with the most susceptible animals without danger. Furthermore, it has been learned from the study of the life history of the cattle tick and by observation that this tick infests pastures only transiently, never permanently, and will not mature except upon cattle or equines, that its extermination is possible, and that the disease it causes may be prevented. Therefore the various methods with these results in view should be directed toward the destruction of ticks on cattle as well as their eradication from the pastures.

METHODS OF ERADICATING THE TICKS.[7]

In undertaking measures for eradicating the tick it is evident that the pest may be attacked in two locations, namely, on the pasture and on the cattle.

In freeing pastures the method followed may be either a direct or an indirect one. The former consists in excluding all cattle, horses, and mules from pastures until all the ticks have died from starvation. The latter consists in permitting the cattle and other animals to continue on the infested pasture and treating them at regular intervals with agents destructive to ticks and thus preventing engorged females from dropping and reinfesting the pasture. The larvæ on the pasture, or those which hatch from eggs laid by females already there, will all eventually meet death. Such of these as get upon the cattle from time to time will be destroyed by the treatment, while those which fail to find a host will starve in the pasture.

Animals may be freed of ticks in two ways. They may be treated with an agent that will destroy all the ticks present, or they may be rotated at proper intervals on tick-free fields until all the ticks have dropped. The method most generally used is dipping the cattle in a solution of arsenic. The pasture-rotation method is not only more complicated, but the necessary tick-free fields are seldom available.

DIPPING.

The dipping vat is the best and cheapest means of applying the tick-destroying solution. The great advantage of dipping over spraying and applying remedies by hand lies in the fact that thoroughness of the treatment is practically assured.

When eradication is undertaken, all the cattle, and also the horses and mules if they harbor ticks, are treated regularly every two weeks during the part of the year that the temperature is favorable to treatment, until the ticks have disappeared. The purpose of the treatment is to destroy all ticks that get on the animals before they have had a chance to mature and drop, thus preventing them from reinfesting the pasture, farm, or range. If the treatment used were absolutely effective in destroying each and every tick on the animals treated there would be no renewal of the infestation after the treatment is begun. The cattle would act simply as collectors of ticks which would be destroyed regularly by the treatment applied every two weeks. It is probable, however, that in most instances, either because of the lack of efficiency of the dip or imperfect application, or because of failure to dip all cattle systematically, some ticks escape treatment and reproduce, thus prolonging the time that otherwise would be required for eradication.

If ticks apparently disappear from the cattle after they have been under treatment for some time, the dipping should not be discontinued until a number of careful inspections show that the cattle are free of ticks. If ticks continue on cattle until cold weather and then finally disappear it should be borne in mind that in all probability eradication has not been accomplished and that there may be engorged females, unhatched eggs, and inactive seed ticks on the farm or range, and that even if the cattle should remain free of ticks during the winter they may become reinfested the following spring. In any case in which ticks disappear from the cattle and treatment is discontinued, the cattle should be watched very carefully for ticks until ample time has elapsed to leave no doubt that eradication has been accomplished.

As a general rule it has been found that if dipping is begun in March and systematically and thoroughly done, all cattle being dipped every 14 days until November, complete eradication will be secured. In dipping, each animal should be completely covered by the dip. To prevent any animals from going through the vat without becoming wet all over, a man, provided with a forked stick, should be stationed at the middle of the vat to shove under those that have not been completely submerged.

Dipping is the only really satisfactory method of treating animals for ticks. In cases of emergency, however, or where there are not cattle enough within a radius of several miles to warrant the construction of a vat in which all the cattle of the community may be dipped, spraying may be advisable. In spraying animals the work should be done with great thoroughness and every portion of the body treated. An animal can not be sprayed properly unless it is tied or otherwise held, nor can good results be obtained unless the hair and skin are thoroughly wetted.

Preparation and use of arsenical dips.[8]—After experimenting for many years to discover a practical method for dipping cattle to destroy ticks without injury to the cattle, the Bureau of Animal Industry has developed a very satisfactory arsenical dip. Two formulas are given for homemade dips, one known as the "S-B" (self-boiled) and the other as the boiled dip. The former is the one usually employed.

The S-B dip.—The formula calls for two stock solutions, arsenic stock and tar stock, which must not be mixed except in the diluted dipping bath.

Arsenic stock requires the following materials ready to hand before starting:

	Pounds.
Caustic soda	4
White arsenic	10
Sal-soda crystals	10

There should be also some means for heating the solution in case, as sometimes happens because of impure materials, lack of skill, or some unforeseen circumstance, the heat created by mixing the materials should be insufficient to dissolve all the arsenic.

In a 5-gallon kettle or metal[9] pail place the 4 pounds of caustic soda, add 1 gallon of cold water, and stir with a stick until the caustic soda is practically all dissolved. Without delay begin adding the white arsenic, in portions of a pound or two at a time, as fast as it can be dissolved without causing the solution to boil, stirring all the time. If the liquid begins to boil, stop stirring and let it cool slightly before adding more arsenic. The secret of success is to work the arsenic in fast enough to keep the solution very hot—nearly but not quite at the boiling point. The result should be a clear solution, except for dirt. If the liquid persistently remains muddy or milky, it may be because the operation has been conducted so fast that much water has been boiled out and sodium arsenite is beginning to crystallize, so add another gallon of water and stir. If the solution does not then clear up, the caustic soda must have been very low grade, and the undissolved substance must be arsenic. In that case, put the kettle over the fire, heat nearly, but not quite, to boiling, and stir. As soon as the solution of arsenic is complete, dilute to about 4 gallons, add the sodium carbonate, and stir until dissolved.

Cautions.—It is necessary to avoid splashing. Hence never work hurriedly; stir deliberately and regularly; do not dump in the arsenic and sal soda, but carefully slide them in from a grocer's scoop held close to the side of the pail and to the surface of the liquid. Perform the whole operation in a well-ventilated place and avoid inhaling steam.

After the solution has become cold add water to make it to exactly 5 gallons,[10] mix well, let settle, and draw off into containers which can be tightly corked or otherwise closed. Jugs or demijohns are best, but tin cans will serve if occasionally inspected for leaks which may occur after a time through the action of the solution upon the solder of the can.

Tar stock is prepared thus: In a large metal pail dissolve three-fourths of a pound of caustic soda in 1 quart of water, add 1 gallon of pine tar, and stir thoroughly with a wooden paddle until the mixture, which at first looks streaked and muddy, brightens to a uniform, thick fluid somewhat resembling molasses. Test it by letting about a teaspoonful drip from the paddle into a glass of water (a glass fruit jar or a wide-mouth bottle will do) and stirring thoroughly with a sliver of wood. It should mix perfectly with the water. Globules of tar which can be seen by looking at the glass from underneath and which can not be blended with the water by repeated stirring indicate that more caustic-soda solution is needed. In that case make up more caustic-soda solution of the same strength and add it, not more than a pint at a time, with thorough stirring, until the desired effect is produced.

If an appropriate glass vessel for making the test is not at hand, take a little of the mixture between the fingers, then dip the fingers under water and try to rub off the tar. It should leave the fingers perfectly clean after a little rubbing with water. If an oily coating remains, more caustic-soda solution is needed. Such an extra addition of caustic soda will be required only in case of a very low-grade chemical or a very highly acid tar. The tar stock should be kept in closed containers, such as a pail with a friction top.

The quantity of S-B arsenic stock or of tar stock made in one operation can be varied as desired, provided the above-given proportions of the ingredients are adhered to. But one should attempt to work the S-B formula on a larger scale only after skill and experience have been acquired.

The boiled dip is less convenient than the S-B dip, but the final composition and effect of dipping baths prepared from the two are the same.

To make a 500-gallon bath provide:

Sal-soda crystals	24 pounds.
White arsenic	8 pounds.
Pine tar	1 gallon.

Put 25 gallons of water into a kettle or tank of from 40 to 50 gallons' capacity, heat to boiling, and add the sal soda. When this has dissolved add the white arsenic, then boil and stir for 15 minutes or longer, until the white arsenic has entirely disappeared. If intended for immediate use cool to 140° F. (by addition of cold water if desired), then pour in the pine tar in a thin stream while constantly and vigorously stirring the solution. Immediately empty the liquid into the dipping vat, which has already been three-fourths filled with water, and stir thoroughly.

All the utensils must be free from greasy or oily matter which would coat the arsenic and hinder its solution. The operation of boiling requires constant attention to avoid loss by foaming. Hard water may be used, but in that case considerable undissolved material, which, however, does not contain any arsenic, may be left after boiling.

For a stock solution to be kept on hand and used when needed add no tar, but after the solution has become cold make it up to 25 gallons, stir well, let settle, and draw off into containers which can be well closed. In this case the tar stock previously described is also required.

Diluting the dip.—First run water into the vat about three-fourths up to the dipping line, at which its capacity must be known. If tar stock is to be used the necessary amount will be one-third of a gallon for every 100 gallons of vat capacity. Measure it out, mix it with 2 or 3 times its volume of water and pour it along the surface of the water in the vat, stirring a little.

Every 100 gallons of standard-strength bath calls for 1-3/5 pounds white arsenic, which quantity is contained in four-fifths of a gallon of S-B stock or in 5 gallons of boiled stock. From these figures the quantity of arsenic or stock needed to charge the vat may be calculated. Or one may base the calculation on the following facts:

• One pound of white arsenic will make 62½ gallons of bath.
• One gallon of S-B stock will make 125 gallons of bath.
• One gallon of boiled arsenic stock will make 20 gallons of bath.

All solutions of arsenic are considerably heavier than water and if carelessly put into the vat they may plunge to the bottom and be difficult to mix. Therefore always pour the arsenic stock or a proprietary dip in a thin stream evenly along the vat except at the shallow exit end. Another precaution to be taken in handling proprietary dips is never to mix them first with small quantities of water, which may "break" them. Pour them directly into the water in the vat.

Finally, add water up to the dipping line and stir well. An excellent way to stir is by a pail tied to a rope. Sink it at the entrance end of the vat and haul it along the bottom to the exit. Then raise it, throw it back to the entrance end, and haul through again, repeating as many times as necessary but always hauling through in the same direction.

The standard-strength bath prepared as above contains practically 0.19 per cent arsenious oxid when fresh. After use oxidation may set in and weaken it, but it will not need to be strengthened so long as it tests not less than 0.175 per cent arsenious oxid.

To make up small quantities for spraying, to each 5 gallons of water measured out add first 2 fluid ounces (4 tablespoonfuls) of tar stock, and then 5-1/8 fluid ounces of S-B stock or 2-1/8 pints of boiled arsenic stock.

The standard strength of bath should be adhered to so far as possible because its effectiveness against ticks will effect eradication in the least time and with fewest dippings. But if time is not pressing it is sometimes best to begin with a lower strength, say 0.14 or 0.15 per cent, and gradually work up to full strength as the cattle become accustomed to the treatment. This is certainly a wise method for the individual cattle owner who is outside the area of cooperative work and who lacks aid and advice from experts. Weather conditions also need to be considered. Hot or moist weather is more trying to the cattle than cool or dry weather. The longer the time needed for the cattle to dry off after dipping, which of course primarily depends on the proportion of moisture in the air, the more liable they are to show blistering or other injury through the continued absorption of arsenic by the skin. The combination of heat and moisture is particularly bad, and under such conditions it may be desirable, unless other conditions prohibit, to use the bath somewhat weaker than standard strength. The following table shows the quantities of arsenic and stock solutions contained in 100 gallons of bath of different strengths, so that the quantities necessary to charge a vat of any size at any strength can be found by simple multiplication.

Composition of dipping baths.

Actual arsenious oxid.	Per 100 gallons of bath.			Actual arsenious oxid.	Per 100 gallons of bath.
	White arsenic.	S-B stock.	Boiled stock.		White arsenic.	S-B stock.	Boiled stock.
0.05	0.42	0.21	1.3	.15	1.25	.63	3.9
.06	.50	.25	1.6	.16	1.33	.67	4.2
.07	.58	.29	1.8	.17	1.41	.71	4.4
.08	.66	.33	2.1	.18	1.49	.75	4.7
.09	.75	.38	2.3	.19	1.58	.79	4.9
.10	.83	.42	2.6	.20	1.66	.83	..........
.11	.91	.46	2.8	.21	1.74	.87	..........
.12	1.00	.50	3.1	.22	1.83	.92	..........
.13	1.08	.54	3.4	.23	1.91	.96	..........
.14	1.16	.58	3.6	.24	2.00	1.00	..........

As dipping goes on the bath naturally needs replenishing, and its strength probably needs correction from time to time. Full directions on these points may be found in Farmers' Bulletin 1057.

Prepared dips.—Proprietary arsenical cattle dips appear now to have passed the experimental stage and to have become established as reliable and useful products. At any rate this can be said of the brands which have received permission for use in official dipping in place of the homemade dip. The formulas and standard samples of all such brands are in possession of the Bureau of Animal Industry and the manufacturers are required to guarantee that their products as placed on the market will be kept up to standard and that all requirements of the bureau will be observed. Like the homemade dip they all contain sodium arsenite as the active tick-killing agent. They do not all contain pine tar, because that substance is difficult to blend into a highly concentrated product, but they all contain some other substance or mixture of substances of such character and in such quantity as field trials have proved will produce the same effects.

They are not regarded as any more effective or any milder on the cattle than properly prepared homemade dips. None the less they are undoubtedly safer for general use because they offer decidedly fewer opportunities for making mistakes in the quantities used or in the operations gone through and also fewer chances for accidental poisoning or other injury from the handling of powerful chemicals. Whether their higher cost is sufficiently outweighed by these considerations is necessarily a matter for individual decision.

Precautions in the use of arsenic and arsenical dips.—The fact that arsenic is a violent poison is what renders it valuable, for the fever tick is hard to kill. But, like a keen-edged tool, it may be decidedly dangerous if ignorantly or carelessly handled. Three possibilities of danger must be kept constantly in mind; danger to oneself, danger to other persons, danger to animals.

The dry, powdered white arsenic should be kept in a tightly covered pail, plainly labeled. Paper bags are unsafe because they easily burst, and arsenic so scattered about looks harmless enough. In weighing or otherwise handling the arsenic avoid raising dust or breathing it in, if raised, and keep it off the skin and clothing. In mixing or boiling stock solutions work only in a well-ventilated place, and on the windward side of the kettle so that steam arising from it will not be inhaled.

The stock solutions are in some respects more dangerous than the original substance because the arsenic in them is already in solution and can act very quickly. If any gets on the skin or clothing it must be washed off without delay. Cattle must be kept away from such solutions or from anything that has been in contact with them, for cattle craving salt have been poisoned by licking the outside of leaky barrels and by licking the earth around dipping vats where a little concentrate had been carelessly spilled in charging the vat. All such poisoned earth must be removed, buried, and replaced by fresh.

The diluted bath is naturally much less dangerous, but no chances can be taken with it. No puddles from which animals may drink should be allowed to accumulate. The persons who do the dipping should not allow the skin or clothing to be wet by the dip any more or any longer than absolutely necessary. When spraying, the operator should see to it that neither he nor the animals inhale any of the spray.

When a vat is to be emptied the approved practice is to run the waste bath into a pit properly guarded by a fence, where it will gradually seep away under the surface and do no harm, provided only that seepage can not be carried to a well, stream, or spring from which any person or domestic animal may drink.

The symptoms of arsenical poisoning are rather variable and also depend on the size of the dose and the method of administration. If an animal sickens or dies shortly after dipping it by no means follows that arsenical poisoning or any other effect of the dipping is the cause. Very few cattle relative to the total number dipped have suffered undoubted arsenical poisoning and in most of the cases the cause could be traced to somebody's error or carelessness.

In regard to arsenical poisoning of human beings there is a standard antidote, which may be obtained at any drug store with directions for use. It should be kept on hand for emergencies. If the antidote is not at hand the poison must be removed from the stomach by encouraging repeated vomiting, and soothing drinks such as milk, white of eggs and water, or flour and water must be freely given meanwhile. A suspected case of arsenical poisoning must have the attention of a physician at the earliest possible moment, as sometimes the poison works very quickly.

Crude petroleum.—Various kinds of crude petroleum and emulsions of it have been used with more or less success in destroying ticks, but on account of the difficulty of obtaining suitable grades of oil and the liability of injury to cattle, their use has been practically abandoned.

Method of dipping.—The method usually adopted in dipping cattle is to construct a narrow swimming tank with a chute at one end for the entrance of the cattle, and a sloping exit at the other end when the cattle emerge after passing through the vat. (See [Pl. XLIX], fig. 2.) A drip chute, or floor, is connected with the exit, where the excess of dip is allowed to drip off the animals and to drain into the vat. Plans and specifications for installing dipping plants may be obtained from the Bureau of Animal Industry, Department of Agriculture, Washington, D. C.

TREATMENT.

When Texas fever has broken out, all animals, the sick as well as the healthy, should at once be removed to a noninfected pasture. While this may not cut short the disease, it may save the lives of some by removing them from the possibility of attack by more young ticks. Removal from infected pastures likewise prevents a second attack, in October or early in November, which is caused by another generation of ticks. Sick native cattle infect with a new generation of ticks the pasture to which they are removed, but these usually appear so late that they have but little opportunity to do any damage; hence, sick natives do not, as a rule, cause visible disease in other natives.

It is of importance to remove all ticks, so far as this is possible, from sick animals, since they abstract a considerable quantity of blood and thereby retard the final recovery.

Medical treatment of the sick has generally been unsatisfactory, although in chronic cases and those occurring late in the fall beneficial results have followed. If the animal is constipated, a drench containing 1 pound of Epsom salt dissolved in 1 quart of water should be administered, followed by sulphate of quinin in doses of 30 to 90 grains, according to the size of the animal, four times a day until the system is well saturated with it. Tincture of digitalis one-half ounce and alcohol 2 ounces may be combined with the quinin, according to indications of individual cases. An iron tonic containing reduced iron 2 ounces, powdered gentian 4 ounces, powdered nux vomica 2 ounces, powdered rhubarb 2 ounces, and potassium nitrate 6 ounces will be found beneficial in the convalescent stage when the fever has run its course. This tonic should be given in heaping teaspoonful doses three times a day in the feed. Good nursing is essential in treating these cases, and the animal should be given a nutritious, laxative diet with plenty of clean and cool drinking water and allowed to rest in a quiet place. If the stable or pasture is infested with ticks, the animal should be placed in a tick-free inclosure to prevent additional infestation with these parasites and the introduction of fresh infection into the blood. Furthermore, all ticks that can be seen should be removed from the sick cattle, as they keep weakening the animal by withdrawing a considerable quantity of blood, and thereby retard recovery.

QUARANTINE REGULATIONS.

The sanitary regulations issued by the Department of Agriculture for the control of cattle shipments from the infected districts have for their initial purpose the prevention of the transportation of ticks from infected regions to those that are not infected, either upon cattle or in stock cars or other conveyer. They are based upon the fact that Texas fever is carried north only by the cattle tick, and the exclusion of this parasite from the noninfected territory has in every instance been found a certain method of excluding Texas fever. The regulations governing the movement of cattle from below the quarantine line are made yearly by the Secretary of Agriculture, and they define the boundary of infected districts. The infected area as now determined is shown in maps issued periodically.

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SOUTHERN CATTLE FEVER (TEXAS FEVER, TICK FEVER).

DESCRIPTION OF PLATES.

Plate XLIV. Normal spleen and spleen affected by Texas fever.

Fig. 1. Spleen of an acute, fatal case of Texas fever. The narrow end of the spleen is here represented.

Fig. 2. Spleen of healthy steer. Though the latter animal weighed one-half more than the former, the weight of the diseased spleen (6-7/8 pounds) was nearly three times that of the healthy spleen (2-3/8 pounds).

Plate XLV. Texas fever.

Fig. 1. The cut surface of a healthy liver taken from a steer slaughtered for beef.

Fig. 2. The cut surface of the liver in Texas fever.

Fig. 3. Appearance of the urine in an acute, fatal case of Texas fever.

Fig. 4. Red corpuscles, magnified 1,000 diameters, containing the parasite of Texas fever. This appears as a blue point a near the edge of the corpuscle. The blood was taken from a skin incision. The case was nonfatal and occurred late in the fall.

Fig. 5. Red corpuscles from the blood of an acute, fatal case, 20 hours before death. The Texas-fever microbes a are shown as pear-shaped bodies, stained with methylene blue, within the red corpuscles. The larger body on the right b is a white blood corpuscle, also stained with methylene blue. (Magnified 1,000 diameters.)

Plate XLVI. The cattle tick (Margaropus annulatus), the carrier of Texas fever.

Fig. 1. A series of ticks, natural size, from the smallest, just hatched from the egg, to the mature female, ready to drop off and lay eggs.

Fig. 2. Eggs, magnified 5 times.

Fig. 3. The young tick just hatched (magnified 40 times).

Fig. 4. The male after the last molt (magnified 10 times).

Fig. 5. The female after the last molt (magnified 10 times).

Fig. 6. A portion of the skin of the udder, showing the small ticks. From a fatal case of Texas fever produced by placing young ticks on the animal. (Natural size.)

Fig. 7. A portion of the ear of the same animal, showing same full-grown ticks ready to drop off. (Natural size.)

Plate XLVII. The cattle tick (Margaropus annulatus).

Fig. 1. Dorsal view of male. (Greatly enlarged. Original.)

Fig. 2. Ventral view of male. (Greatly enlarged. Original.)

Fig. 3. Dorsal view of replete female. (Greatly enlarged. Original.)

Fig. 4. Ventral view of same.

Plate XLVIII. Portion of a steer's hide, showing the Texas-fever tick (Margaropus annulatus). (Natural size. Original.)

Plate XLIX.

Fig. 1. Tick-infested steer.

Fig. 2. Dipping cattle to kill ticks.

Plate L. Facsimile of poster used to show the difference between cattle of similar breeding raised on a tick-free farm in one case and on a ticky farm in the other.

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In consequence of the enforcement of these quarantine regulations, Texas fever has been practically prevented in the noninfected districts for several years, and little or no hardship has been caused to stockmen handling cattle from the infected areas. Prior to the adoption of these regulations the tick-infested district was rapidly extending northward, but since the quarantine line was established and rational regulations enforced it has gradually been moved farther south. This problem of still further reducing the infested area is of the greatest importance to the cattlemen of the South—in fact, to those on both sides of the line—and one which is receiving special consideration by this department as well as by many of the interested States.

TICK ERADICATION.

Systematic cooperative work by the Federal Government and the affected States for the eradication of the cattle ticks which transmit Texas fever was begun in the summer of 1906 under authority given by Congress in the appropriation act for the Department of Agriculture. The first Federal appropriation for the fiscal year ended June 30, 1907, was $82,500, and for the fiscal year 1908 an appropriation of $150,000 was made, then for several years $250,000, and this has been increased to $660,000 for 1922. Funds have also been provided by States and counties.

The original infected area amounted to 728,543 square miles. Of this territory there has been released from quarantine as a result of the work above mentioned 523,837 square miles (up to July 1, 1922). In other words, 72 per cent of the area has been freed from ticks in 16 years.

Great improvement has resulted from this work in the released territory. More cattle are being raised, and a better grade of breeding stock is being introduced; calves grow faster, and cattle put on flesh more rapidly during the grazing season and go into the winter in better condition because of the absence of the ticks; they can be marketed without quarantine restrictions, and higher prices are being obtained; dairy cows give a larger yield of milk; and values of farm lands are enhanced.

The difference between the prices realized for cattle from the tick-infested region and the prices of cattle of similar grades from above the quarantine line has ranged from $2.25 to $5 a head at the principal northern live-stock markets, without taking into account the improvement in quality and weight of cattle because of the eradication of the ticks. It can easily be seen that the extermination of the ticks means a large total annual increase in the prices obtained for southern cattle sold in northern markets. In addition to this, the increase in prices of cattle sold locally in the South would represent a large sum. This local increase has been found to amount to from $3 to $15 a head in territory freed from ticks. An agricultural official of one of the Southern States has reported that calves in the tick-free area bring double the prices that can be obtained for similar calves in the tick-infested region.

Heretofore it has been impracticable to improve the quality of southern cattle by introducing fine breeding animals from other sections, because such animals were liable to contract Texas fever and die unless protected by inoculation. Furthermore, it is impossible for animals to attain good growth and to thrive when they are heavily infested with ticks. With the eradication of the ticks, however, the southern farmers are enabled to introduce good breeding animals and to improve the grade of their stock.

There is no longer any doubt that it is entirely practicable to exterminate the ticks throughout the entire region, and the accomplishment of this result will be of tremendous economic advantage not only to the South but to the whole country. The rate of progress depends mainly on two factors— the amounts appropriated by the Federal and State Governments, and the cooperation of the people.

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CHRONIC BACTERIAL DYSENTERY.

Chronic bacterial dysentery is a chronic infectious disease of bovines caused by an acid-fast bacillus simulating the tubercle bacillus and characterized by marked diarrhea, anemia, and emaciation, terminating in death.

This disease was observed in the United States for the first time by Pearson in Pennsylvania cattle, and later by Mohler in Virginia cattle, and in an imported heifer from the island of Jersey at the Athenia quarantine station of the Bureau of Animal Industry.

Pearson proposed the name chronic bacterial dysentery for this affection, and it has also been termed Johne's disease, chronic bacterial enteritis, chronic hypertrophic enteritis, and chronic bovine pseudotuberculous enteritis by various European investigators. The disease was first studied in 1895 by Johne and Frothingham in Dresden, but they were inclined to attribute to the avian tubercle bacillus the cause of the peculiar lesions of enteritis which they observed. In 1904 Markus reported this disease in Holland, and subsequently it was observed in Belgium, Switzerland, Denmark, and Great Britain.

Cause.—The bacillus, which has been invariably demonstrated in the intestinal lesions and mesenteric lymph glands in this disease, is a rod about 2 to 3 microns long and 0.5 micron wide. It stains more or less irregularly, like the tubercle bacillus, and moreover the similarity goes further, in that the organism is also strongly acid-fast, which facts led Johne and Frothingham to surmise that the disease was caused by avian tubercle bacilli. However, it has now been plainly demonstrated that the bacillus of chronic bacterial dysentery is readily distinguished from the latter organisms, for while it resembles the tubercle bacillus in form and staining qualities, no one has succeeded in growing it in culture media or in reproducing the disease by injecting experiment animals.

Symptoms.—Probably the first symptom noticed is that the animal is losing condition despite the fact that its appetite is good and the food nourishing. This is soon followed by a diarrhea which, while moderate at first, soon becomes excessive and may be either irregular or persistent, the feces being of the consistency of molasses and passed frequently. In the meantime the hair becomes dry and harsh and the animal falls off considerably in weight. The temperature, however, remains about normal. The appetite does not seem to be greatly impaired until the last few weeks of life, but nevertheless emaciation continues, the animal becomes more and more anemic, great muscular weakness and exhaustion are manifested, and death follows, apparently as the result of the persistent diarrhea and great emaciation. The disease may continue for four or five weeks or may last for a year, or even longer, before death intervenes.

Lesions.—The lesions observed on post-mortem are remarkably slight and are out of all proportion to the severity of the symptoms manifested. The disease appears to start in the small intestines, especially in the lower portion, where the lesions are usually the most marked, but it also involves the large intestines, including the rectum. The mucous membrane may alone be affected, although usually in the long-standing cases the submucosa is also invaded and the entire intestinal wall is then much thicker than normal and the tissue infiltrated with an inflammatory exudate. The mucous membrane or inside lining membrane is markedly wrinkled or corrugated, showing large, coarse folds with more or less reddening or hemorrhagic patches or spots on the summits of the ridges, especially noticeable in the large intestines. The mesenteric lymph glands are usually somewhat enlarged and appear watery on section. The other organs do not appear to be affected except from the anemia present in the later stages of the disease.

Differential diagnosis.—The principal disease with which bacterial dysentery may be confused is tuberculosis, but the application of the tuberculin test will readily diagnose the latter disease, while no reaction will be noted in case the injected animal is suffering with the former affection. The disease may also be mistaken for the parasitic affections resulting from stomach worms (verminous gastritis) and intestinal parasites, especially uncinariasis, but a microscopic examination of the feces is necessary in order to establish definitely the diagnosis.

Treatment.—As with all other forms of infectious disease, it is advisable to separate immediately the diseased and suspected cattle from the healthy animals. The feces passed by the former animals should be placed on cultivated soil where healthy cattle will not be exposed to them, as the bacilli producing the disease are readily found in such manure. The stalls, stables, and barnyards should also be thoroughly disinfected, as has been described under "Tuberculosis," in this chapter, special attention being given to those places which have been soiled by feces. The administration of medicines has thus far been quite unsatisfactory, although treatment should be directed toward disinfecting the intestines with intestinal antiseptics, such as tannopin in 1 dram doses twice daily, and strengthening the animal by the use of stimulants such as strychnin in half-grain doses given twice daily hypodermically. Salol, turpentine, or subnitrate of bismuth in a starch or wheat-flour gruel may also give temporary relief, but the diarrhea is likely to reappear and cause the death of the animal. In all cases the feed must be carefully selected to assure good quality, and should consist preferably of nutritious dry feed.

NAGANA.

Nagana, also called tsetse-fly disease, is an infectious fever occurring chiefly in horses and cattle, characterized by alternating paroxysms and intermissions and produced by a specific flagellate protozoan (Trypanosoma brucei) in the blood. It is probably transmitted from animal to animal solely by the bites of the tsetse fly. This insect is something like a large house fly, and when it settles on a diseased animal, sucks the blood and infects its proboscis, it is enabled on biting a second animal to infect the latter by direct inoculation. This disease is found throughout a large portion of central and southern Africa, along the low-lying and swampy valleys. It has never occurred in the United States, nor is it known to be present in the Philippines, but its relation to surra and the possibility of its appearance in one of our island dependencies are the reasons for including a few remarks at this time.

Symptoms.—The chief symptoms in addition to the fever, which is usually about 104° to 105° F., are the muscular wasting, progressive anemia, and loss of power, together with the edema most marked about the head, legs, abdomen, and genital organs. The urine is yellow and turbid, and occasionally contains albumin and blood. There is paralysis of one or both of the hind legs, difficult urination and defecation, labored breathing, discharge from the eyes and nose, extreme thirst, and gradual extension of paralysis to other parts of the body. The disease runs a chronic course, lasting from three to six weeks in horses, and from one to six months in cattle. Besides these animals, the mule, ass, buffalo, antelope, hyena, camel, and dog contract the disease naturally, and sheep, goats, cats, and small laboratory animals succumb to artificial inoculation.

Lesions.—The spleen and lymphatic glands are enlarged. There are sero-fibrinous exudates in the body cavities, the liver is enlarged and engorged, heart flabby, and a catarrhal condition is present in the respiratory passages. Pathological changes occur in the spinal cord. The finding of the trypanosoma by microscopic examination of the blood will be conclusive evidence for diagnosis.

Treatment.—Treatment has not proved satisfactory. Quinin, arsenic, methylene blue, and other drugs have been used, but without success. Endeavors thus far made to produce immunity from this disease have likewise been unavailing.

CATTLE FARCY.

This is a chronic disease of cattle occurring in France and the island of Guadeloupe, West Indies. It is characterized by caseating nodular swellings, first of the skin and afterwards of the superficial lymphatic vessels and glands, finally proving fatal within a year by extension to the viscera. The swellings rupture and discharge a purulent yellowish fluid, which contains the causative organism. This affection, called farcin du bœuf by the French, resembles cutaneous glanders or farcy of horses, but is caused by an entirely different organism, the streptothrix of Nocard. Moreover, cattle are immune from glanders, and for this reason the name, unfortunately applied to this disease, should not lead to any confusion with the cutaneous glanders or farcy of horses. Although the disease has been described as occurring only in Guadeloupe and France, the possibility of its occurrence in American possessions warrants its mention in this chapter.

Treatment.—Treatment consists in making incisions into the swellings and syringing them out with 2 per cent compound cresol solution. The cavities may then be packed with cotton, soaked in 5 per cent zinc-chlorid solution. The swollen lymphatics may also be bathed or covered with cloths wrung out in this solution.

OTHER INFECTIOUS DISEASES.

The following are also infectious diseases of cattle, a discussion of which will be found in previous chapters:

	Page.
Contagious abortion	167
White scour of calves	261
Infectious ophthalmia (pink eye)	345