Part 78

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.

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.