There is ample evidence that both the lymphadenoid and myeloid tissues of the body are affected. The lymph glands at the hilum of the lung naturally are involved with the extensive pulmonary changes. Also, a similar change may be found in distant nodes, perhaps associated with drainage from focal lesions or perhaps brought about by general intoxication.
The myeloid involvement is unassociated with focal lesions and finds its early expression in the equation of the white blood cells of the peripheral blood. The two groups of changes, those involving the lymphadenoid and those of the myeloid structures, should be discussed separately.
By far the most extensive lesions are encountered in the lymph glands of the lung and its hilum, and from here the mediastinal and deep nodes along the trachea are affected to a greater or lesser extent. The glands are very large and succulent (2, 157, 162, etc.). Very frequently, indeed, they are hemorrhagic on cross section (34, 108) (Fig.XXXVII), and there exudes a sanguinous fluid, usually thin and syrupy in character. The cut surface projects slightly, and the edge of the gland everts. The architecture is often obscured by hemorrhage—a diffuse red color—but very frequently near the periphery, translucent or more opaque, yellowish points are visible. Rarely, larger, opaque, yellow foci are found in the gland; these may be softened and purulent in exceptional cases (2, 47, 157).
Microscopically, the picture presented by the gland is that of a non-suppurative lymphadenitis. The peripheral sinuses are markedly distended and the channels through the gland share in the change (66). The sinuses contain serum, red blood cells, and mononuclear cells for the most part, but occasionally polymorphonuclear leucocytes are also encountered. More rarely still, a megalokaryocyte finds its way into the sinus. The most characteristic feature is the presence of phagocytosed cells,—a picture comparable with that found in the typhoid lymph node. The nuclei of the phagocytic cells are vesicular and usually stand out sharply in contrast with the pyknotic nuclei of the included cells. There is conclusive evidence that the phagocytes arise from the lining cells of the channel wall, as in typhoid fever, for these cells are frequently in process of division (Fig.LIV). The blood vessels of the lymph gland, greatly congested, contain almost exclusively red blood cells. As a rule, the lymph follicles and the lymph cords take little part in the process. If there is any change in these structures, it is a rarefication. Occasionally, hemorrhage is encountered in a follicle or even in a cord, and this hemorrhage may involve not only the cells of the cord, but its supporting reticular structure, and may form the nucleus of a subsequent necrotizing or suppurative focus.
FIG. XXXI. AUTOPSY NO. 100. ACUTE FULMINATING BRONCHIOLITIS AND BRONCHOPNEUMONIA. NOTE THE NECROTIC ALVEOLAR WALLS AND THE MASSES OF BACTERIA IN THE EXUDATE. COMPARE FIGURESVIII,XVII, ANDXXXII.
FIG. XXXI. AUTOPSY NO. 100. ACUTE FULMINATING BRONCHIOLITIS AND BRONCHOPNEUMONIA. NOTE THE NECROTIC ALVEOLAR WALLS AND THE MASSES OF BACTERIA IN THE EXUDATE. COMPARE FIGURESVIII,XVII, ANDXXXII.
FIG. XXXI. AUTOPSY NO. 100. ACUTE FULMINATING BRONCHIOLITIS AND BRONCHOPNEUMONIA. NOTE THE NECROTIC ALVEOLAR WALLS AND THE MASSES OF BACTERIA IN THE EXUDATE. COMPARE FIGURESVIII,XVII, ANDXXXII.
The picture that has been detailed is subject to modification in those cases particularly where a leucocytic reaction is associated. Then, there may be more polymorphonuclear leucocytes in the sinuses, and necrotizing foci may be converted into miliary abscesses.
The change in the bronchial lymph glands cannot be considered other than an expression of an aplastic, inflammatory reaction. It finds an analogue especially in diseases like typhoid fever. The most constant picture includes an edematous, hemorrhagic reaction in which there is phagocytosis of sieved-out cells by the scavengers generated within the gland. Where necrosis or suppuration occurs, and this is rare, it may be considered as a complication.
Elsewhere in the body, the lymph glands rarely show the same degree of change as those of the thorax. The same general picture, however, is present to a greater or lesser extent, except that extensive necrosis and suppuration have not been encountered.
The lymphadenoid tissues of the alimentary canal share in the process only to a minor extent. In a number of cases, there is no question that the Peyer’s patches and solitary follicles are hyperplastic. Grossly, they stand out prominently, and are pale pinkish-grey in color. Histologically, there is hyperplasia, chiefly apparent from the large germinal centers in the follicles, and a slight distention of the lymph channels. This picture, so commonly found in every type of general infection, is in no way characteristic of influenza.
The spleen is the seat of the usual manifestations in generalized acute infections. In no case is the organ markedly involved, although considerable increases in its size may occur (2, 108, 141, 157, 162). It is not feasible to introduce a detailed discussion of this mild grade of splenic tumor, for there are natural variations in the size of the spleen and frequently it is modified in this respect by subsidiary conditions. In every instance the capsule of the spleen is smooth and there is no acute or chronic perisplenitis attributable to influenza. The capsule usually retracts slightly and the splenic pulp, in slight excess, is much more frequently red or garnet than grey in color. Occasionally, the splenic tumor is grey as in pneumonia. The more minute changes in the organ consist of congestion of the sinuses, increase of the mononuclear cells of the pulp, and prominence of the germinal centers of the Malpighian corpuscles (140). Hemorrhages, found occasionally (47), are more frequent in the pulp, but also occur in the corpuscles.
One of the clinical features of influenza is a leukopenia, which persists often in the face of acute pyogenic pulmonary infection (12, 138, 143, etc.). In this series of ninety-five cases, the vast majority had this type of blood picture, but occasionally a leucocytosis (14) was demonstrable even during the early part of the disease and in those cases which terminatedfatally within a period that may be called acute. In almost all instances where fatal termination was delayed, the leucocyte count ultimately was elevated either with remission or to a constant high level. The blood studies have not been sufficiently complete to allow further discussion, though there is reason to believe that these might have yielded interesting results. The blood changes in this series are similar to those presented in the reports of the epidemic from other sources.
In the majority of cases where the marrow was studied, it was aplastic (12). Occasional, focal, hemorrhagic lesions of the marrow (47) similar to those discussed below in the skeletal and parenchymatous systems were encountered and there was an apparent increase in the number of megalokaryocytes. The usual hyperplasia of the myeloid elements of the marrow associated with pyogenic change was not present.