The receptivity of different breeds has been discussed and the Holsteins and Shorthorns have been thought to show the greatest susceptibility. These are among the cattle that are most prized, bought and sold, and exposed to infection. The Shorthorn especially has a great development of the circulatory system, including the connective tissue with its great lymph sacs and channels, and the microbe we are dealing with shows a marked preference for the lymph system, in which it finds its appropriate field of development. Susceptibility is greatly encreased by a warm climate or hot season, under which large herds may die without a single exception, the disease running a fatal course in two or three days. In cooler climates 20 per cent. will often escape at first (French Commission Experiments, 1849).
Lesions. If death has taken place early, the lesions are usually essentially pulmonary, though they may implicate the pleuræ and mediastinum. In many cases the lung alone is involved, yet even then the predilection of the microbe for the lymph network of the interlobular tissue is strongly manifested in the serous infiltration of that, rather than of the lung structure proper. This determines the much talked of marbled lung, the pulmonary lobules standing out at first as a more or less deep red brown or black, while the marbling is caused by the yellowish or grayish infiltrated tissue surrounding each pulmonary lobulette which appear set in, as in mosaic on the surface of a section. Sometimes a blood extravasation discolors the interlobular exudate as well, yet it retains its soft liquid appearance which sufficiently distinguishes it from the firmer lung tissue. These yellowish interlobular markings vary much in thickness, but in acute cases this may be up to half an inch or even more. In the lesions of longer standing the interlobular exudate has usually coagulated, or even undergone fibroid organization, so that it compresses and condenses the lobules which it surrounds.
The pulmonary lobules may show the earliest changes of the alveolar and lobular capillaries, with formation of an exudate, and an active proliferation of small round cells in and around the alveoli. Later the exudate coagulates, forming the familiar red hepatization, and this in its turn may pass into the gray, or it may liquefy and undergo absorption and resolution. Other changes are not uncommon. The excess of interlobular exudate will compress the pulmonary lobules so as to reduce their size and expel the blood from their structure, giving them a pale color, or this compression becomes still greater, completely arresting the circulation and inducing lobular gangrene. Thrombi in the afferent and efferent vessels contribute to the necrotic change, and sequestra of varying size, from that of a nut to that of an infant’s head or larger, are formed. The earliest stage of this necrosis is usually infarction of the lung, a definite area of which becomes saturated with dark blood cells so that in contrast with the rest of even the hepatized lung, it is almost as characteristic as the marbling. The further progress of this necrosis is varied. Most commonly the exudate surrounding the necrotic mass becomes organized into white fibrous tissue and forms an investing sac in the interior of which is the dead lung tissue, showing for a time distinctly, the bronchia, blood vessels, lobulettes, and interlobular tissue. This gradually becomes detached and floating in a liquid debris, slowly undergoes solution, and is absorbed, the sac meanwhile closing in on the cavity. A large sequestrum may be a year or sixteen months in undergoing complete solution. In other cases the pulmonary lobulettes undergo an individual softening while the interlobular tissue becomes organized and when cut across, the lung presents a distinct honeycombed appearance. In still other cases a considerable area of both lobulettes and interlobular tissue is necrosed and liquefied, while the exudate, around the bronchial tubes, that supplied it, becomes organized, and on the necropsy the latter are found to constitute a thick branching mass of a very characteristic appearance.
The newly affected lobulettes have a watery or gelatinoid or dropsical appearance and if freely incised give out a large amount of serum and flatten down in doing so. When hepatized the cut surface is granular, and microscopic examination shows the terminal bronchia and alveoli filled with a fibrinous exudate containing great quantities of red blood globules and leucocytes. The distension of the lung is enormous, so that when the entire organ is infiltrated it may weigh from 50 to 100 pounds.
In recent cases the lung may be extensively affected without affecting the pleuræ; in other cases both are early involved. In advanced cases the pleuræ are always implicated. First there is the subpleural infiltration over the affected part of the lung; later the pleural surface has reddened arborescent patches, with a slight solid exudate, and a yellowish (sometimes blood-stained) serum collects in the bottom of the cavity; later still the affected portion of the lung is covered more or less thickly with false membranes, while others cover the organ or the parietal pleura below this level, and hang in shreds or bind the lung to the ribs. In old standing and recovered cases these may be largely represented by dense, white fibrous investments covering the lung or the rib, or establishing permanent adhesions. The amount of pleural effusion may be about two gallons in bad cases, and like the invasion is either unilateral or bilateral. The pericardium is usually more or less involved in pleuritic cases.
The larger bronchia sometimes contain false membranes.
The bronchial, prepectoral and mediastinal lymph glands are often enlarged, congested and infiltrated with an abundant exudate.
Similar infiltration of the lymph glands of the pharynx, mesenteries. sublumbar region and groin are described, together with hypertrophy and congestion of the intestinal follicles, and congestion of the muscles and intermuscular tissue, of the articular and tendinous synovial sacs, and even of the meninges of the brain and cord. I know of no facts to show that these conditions result from anything else than the toxins and the general constitutional disorder. The indications are that the microbes are speedily destroyed in the circulating blood, and intravenous injections and caudal inoculations alike fail to cause the characteristic lesions in the lung, their favorite point of casual election.
Incubation. This usually lasts from 6 to 30 days, being greatly abridged by hot weather and often prolonged in the cold. Delamotte claims to have seen it extend to 5 months, and in one case a calf turned out on Montauk Point, L,. I., from an infected place was noticed ill on the 104th day. Australia, South Africa and Norway were each infected by cattle that had been three months out of their native infected land. I have seen cattle pass three or four months after purchase in an unthrifty condition, yet without cough or other recognized diagnostic symptom and then come down with lung plague. Such doubtless explain the alleged protracted incubations, the system has been invaded, ill health ensues, but the lungs are only slightly affected for a length of time. In other cases one animal in a herd has had a mild attack, which escaped notice, and it was only later that the disease was recognized in a second victim, infected from this first.
The bearing of this on imported animals is evident. An animal imported alone should be kept under surveillance for a month or two after quarantine, while in any considerable herd the disease would certainly manifest itself during the prescribed three months detention.