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PLATE 5.

FIG. I.-A Normal So-called "Fetal Gelatinous Nodule" at the Line of Closure of the Mitral Valve of the New-born. 70. The connective tissue is very cellular; ground substance partly myxomatous in character; in it are seen (1) a number of thinwalled blood-vessels.

FIG. II.-A Section of an Acutely Inflamed Mitral Leaflet in Mycotic Endocarditis. 80. 1, Necrotic tissue of the leaflet ; 2, new formed blood-vessels growing into the connective tissue. Between the spindle-shaped, connective-tissue cells are seen many large protoplasmic epithelioid cells.

lial defects which incite thrombotic precipitation. Usually, a clear, finely granular mass of closely packed conglutinated blood-plates is deposited directly on the cells; over this layer there forms a fibrinous network or clumpy masses appear, which inclose leukocytes. Upon the surface of this irregularly shaped vegetation a thin cluster of leukocytes and bacteria in various numbers also accumulate.

In the subsequent course of verrucose endocarditis organization of the thrombotic deposit, which leads to healing, takes place. From the attachment of the valves. blood-vessels grow between the connective-tissue lamellæ toward the excrescences; they send numerous shoots between the fibroblasts toward the thrombotic mass. (Plate 6, Fig. I.) These consist at first of extraordinarily fine, solid processes, which later become hollow and filled with red blood-corpuscles. Gradually, the thrombotic mass becomes completely infiltrated with granulation tissue, which is made up of fibroblasts, small round cells, and blood-vessels. Later, this richly cellular and vascular granulation tissue is transformed into fibrous scar tissue, in which single blood-vessels may remain present for some time. In this manner are produced nodular and diffuse thickenings of the valves. Sometimes these processes of

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healing lead to various changes in the form of the valves, which produce valvular insufficiency; or the new tissue may cause the valves to become adherent to each other and thus produce narrowing or stenosis of the orifice. Subsequently, lime salts may be deposited upon the sclerosed tissue in the form of irregular and ridge-like projections.

Ülcerative endocarditis in the early stages can not be distinguished from the verrucose, except that almost from the very first micro-organisms are present in much greater numbers and are demonstrable in the form of dense, dark balls or masses of micrococci. The further differences of the course depend upon the specific action of the microbes, which, on the one hand, is essentially chemotactic, and, on the other, necrotic. We find the connective-tissue lamellæ of the valves infiltrated to a considerable extent with leukocytes, which in places are so dense that there result minute abscesses in the valvular tissue with soften

ing of the fibers. In the neighborhood of the masses of

cocci the tissue does not stain nor does it contain nuclei -it is necrotic. This zone is marked off from the surrounding tissue by intense aggregations of leukocytes.

Suppuration and necrosis lead to more or less extensive destruction, to ulceration, and to loss of continuity in the inflamed valve. The latter may become perforated, and after complete necrosis and suppurative softening whole fragments may be detached and swept into the bloodstream. Hence, this malignant type of endocarditis usually leads to a fatal end, because metastatic abscesses develop in various organs of the body through the process of embolism; and, moreover, the individual becomes profoundly affected by the toxic action of the ever multiplying bacteria.

The micro-organisms observed in verrucose and ulcerative endocarditis are the staphylococci, streptococci, diplococci pneumoniæ, and, in rare cases, the gonococci.

PLATE 6.

FIG. I.-Acute Verrucose Mycotic Endocarditis of the Mitral Valve. Section through the valve and vegetation. Stained by Gram's method. 16. Bird's-eye view. 1, Connective tissue of the valve; 2, a vegetation composed of conglutinated blood-cells, fibrin, and, at the periphery, aggregations of staphylococcal colonies, 3, around which leukocytes have accumulated; 4, disintegrated and partly necrotic valve tissue with infiltrated leukocytes.

FIG. II.-Verrucose Endocarditis of the Mitral Valve, Organizing. × 40. 1, Connective tissue of the mitral valve with increased number of cells; 2, endocardial efflorescence; 3, blood-vessels growing through the valve and penetrating into the excrescence; 4, leukocytic accumulations.

Diseases of the Pericardium.

Both layers of the pericardium are frequently the seat of inflammatory processes, which are accompanied by an outpouring of a fluid exudate into the pericardial cavity and with a deposit of fibrin upon the opposing serous surfaces. Most frequently, pericarditis results from extension of the inflammation from the pleura, the lung, the mediastinum, or also from the heart; or from metastases (embolic) in certain infectious diseases (articular rheumatism, septicopyemia), and from chemic irritants, as in uremia. In the last case micro-organisms are not met with.

Microscopically, we find in the early stages intense congestion of the pericardial blood-vessels. Sometimes the lumen of the vessel is filled with a network of fibrin or with leukocytic thrombi. At the same time, there are seen cloudiness and loosening of the endothelium, which, later, is rapidly destroyed, so that in advanced cases only fragments of endothelial cells are found in areas, mostly detached from the underlying membrane. Upon the endothelial lining, as well as below it, appear, at first, single

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