Chapter XX: Part 20

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 pleurÊ, 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 auscultation, 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.

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.

_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 deliberately 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.