Chapter 44

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.