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.