Chapter 43

When it is desired to apply one of these above-mentioned agents to the stable or barnyard, a preliminary cleaning up of all dÈbris 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 pleurÊ, 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 pÈripneumonie 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-ComtÈ 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.

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 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.