34 Journ. de méd. vét. de Lyon, 1850, p. 249.
MORBID ANATOMY.—Either the membrane or the granular infiltration is characteristic of diphtheria. The statement that the former occurs only when atmospheric air can gain access thereto, as A. d'Espine and C. Picot still hold,35 is plainly contradicted by its appearance on the mucous membrane of the lower intestines. The condition of the membrane is not unalterable, any more than the clinical symptoms of the disease, for, according to different circumstances, epithelium, mucus, blood, and vegetable parasites are added thereto. The membrane can either be lifted from the mucous membrane on which it lies or is imbedded into and underneath it. In the first instance, it consists to a great extent of fibrin, the result either of epithelial changes or derived directly from the exuded blood-serum. E. Wagner, who makes no anatomical distinction between croup and diphtheria, considers epithelial changes the principal source. The pavement epithelium becomes altered in a peculiar manner. It becomes turbid, larger, dentated, and dissolves into a network; it is at first uninhabited, but serves later as the vehicle of newly-formed cells; there also occurs a considerable infiltration of the mucous membrane pus-cells and granules; besides, the cellular tissue is studded with granules, the granular degeneration resulting sometimes in necrotic destruction, which is looked upon by Virchow as the most important element in severe forms of diphtheria. The several conditions or degrees may occur independent of each other, associated or in succession. Classen shares Wagner's views, but, according to Boldygrew, the pseudo-membrane consists of successive coagulations of a fibrinous fluid which exudes from the diseased surface. Steudener also opposes the views of Wagner. He does not believe in the probability of an exclusively endogenous origin of the cellular elements of croup membrane; in fact, he doubts the occurrence of an endogenous formation of pus-globules in epithelium. Croupous membrane, according to him, is formed by the migration of numerous white blood-globules through the walls of the vessels in the mucous membrane, and by a direct formation of fibrin from the transuded plasma. In addition to this, the mucous membrane is stripped of its epithelium (except at the mouths of the acinous glands) and infiltrated with migrating cells. Fresh croupous membrane consists of a delicate network of homogeneous structure and shining appearance, in which numerous cells and the epithelium of the various layers of the trachea are imbedded. In old membranes the cells are destroyed by granular degeneration and general maceration. Tenacious mucus with pus-cells and detritus are then found. C. Weigert looks upon the deposits as analogous to those on serous membranes. Every inflammation yields an exudation which may coagulate when the coagulating ferment is added. This latter is probably produced by the white blood-cells when in disintegration. But he does not say why it is that there is no such coagulation in suppurative processes, where the leucocytes are more numerous. He believes himself justified in establishing pathological differences of croup, pseudo-diphtheria, and diphtheria. A croupous inflammation means destruction of epithelium, which gives rise to a fibrinous exudation upon the surface, while the cellular tissue remains intact. The only difference between it and the pseudo-diphtheritic inflammation is looked for in the larger number of emigrated white blood-cells. The superficial deposit consists, to a great part, of them and the fibrinous exudation. When there are but few leucocytes the deposit is a network of fibrillæ (croup). When there are many, the masses are more solid and voluminous (pseudo-diphtheritis). When, however, the tissue is changed into a hard substance resembling coagulated fibrin, when the exudation does not exist on the surface, but takes place into the mucous membrane, the process is diphtheria. Zahn also establishes three varieties—viz. 1st, such as result from a peculiar degeneration of pavement epithelium; 2d, such as originate in the solidification of a muco-fibrinous, and, 3d, of a fibrino-purulent, exudation. Each of these varieties may contain colonies of micrococci, but these organisms are neither essential nor are they constantly found.
35 Man. prat. des mal. de l'enfance, 1877, p. 81.
The diphtheritic process does not merely consist of the membranous changes in the pharynx and air-passages. Its fatal cases have afforded marked evidence of the implication of most of the organs. Reimer's 17 cases give the following post-mortem results: the lungs were hyperæmic in 8 cases, twice the seat of pneumonia, and three times of embolic infarctions; in addition, emphysema in 12, oedema in 6, atelectasis in 7, subpleural ecchymoses in 7, pericardial ones in 4. The heart-muscle had undergone fatty degeneration in 6, and was the seat of ecchymoses of the size of a pin's head in 3. In addition to frequent hyperæmic conditions of the abdominal viscera, emboli of the liver in 3 (with capillary hemorrhages of the peritoneal covering in 1), emboli of the spleen in 5, desquamative nephritis in 7 (in 6 of which there were colonies of micrococci in the uriniferous tubules), cellular hyperplasia of the cervical and mediastinal glands in 14 (complicated in 6 with capillary hemorrhages in the glandular tissue). The blood was frequently normal, very often watery and dark, at times leucocythæmic. Thus the disease exerts its influence everywhere.
Rindfleisch defines diphtheritic inflammation as that form of inflammation which produces a coagulating necrosis in the tissues by the immigration of schizomycetæ. The coagulating necrosis differs from the usual form of necrosis in this, that the change from life to death is accompanied with the coagulation of fluid albuminoids. This process takes place mainly in the interior of cells and other parts of tissues, and therein differs from the coagulation of fibrin. In the cells there is taking place a peculiar homogenization of protoplasm; at the same time the nuclei disappear, and are changed into irregular masses liable to cohere and form membranous conglomerates, which owe their peculiar wax color to the invasion of a solid albuminoid endowed with a strong tendency to refract the light. Coagulating necrosis is found in circumscribed localities, and gives rise, in the neighborhood, to a marked amount of inflammation and suppuration, which leads to the expulsion of the necrotic part, with more or less loss of substance—either mild or phagedenic ulceration.
Leyden describes a gray degeneration of the muscular tissue which he believes to be truly inflammatory, and Unruh has lately published an account of some cases in which myocarditis occurred. In Leyden's cases, the muscular nuclei were increased, became atrophied, and underwent fatty degeneration, giving rise thereby to extravasations, softening, dilatation and debility of the heart, with general debility, collapse, and—probably by reflex action on other branches of the pneumogastric—vomiting. Micrococci he found neither in the heart nor in the kidneys.
In the heart, particularly on the right side, numerous thrombi are frequently found in various stages of development; its muscular tissue is often in a state of fatty degeneration or the seat of parenchymatous inflammation and hemorrhages. Bridges first called attention to the occurrence of endocarditis in diphtheria.36 This complication, which, however, occurs more frequently with rheumatism, puerperal fever, diphtheria of wounds, pyæmia, and old valvular affections than in the course of an acute diphtheria, does not, as found in the latter affection, consist simply of a fatty degeneration and subsequent ulceration, but is considered a genuine diphtheritic process (Virchow), affecting the mitral valve more frequently than the tricuspid or pulmonary valves. It begins with hyperæmia and the exudation of plasma in the cellular elements, so that they appear larger and darker. The granulations which form are frail and easily destroyed, so that ulcers form on which fibrin is deposited, and whence it is conveyed as emboli into the terminal arteries (Cohnheim) of the spleen, nerves, brain, and eye. Infarctions may also occur in the valveless veins of these organs, giving rise rather to small multiple abscesses than to large purulent collections. Suppuration but rarely takes place in the heart; the granular mass found there resists the action of æther and alcohol, and spreads throughout the cardiac parenchyma, so that perforation of the septum and of the right auricle and aorta has been observed.
36 Med. Times and Gaz., ii. p. 204.
Bouchut and Labadie-Lagrave, out of 15 cases of diphtheria, met in 14 with a plastic endocarditis, which became the source of emboli. Thus, there were infarctions of the lungs, at times in their centre colorless, at other times in a state of purulent degeneration; superficial thrombi of the small veins of the heart, subcutaneous connective tissue, pia mater, brain, and liver; and in addition, moderate leucocytosis.
The lungs exhibit (post-mortem) all sorts of inflammatory and congestive conditions, with their consequences, as oedema, catarrh, broncho-pneumonia, atelectasis, emphysema, ecchymoses, and large infarctions.