The pathology of influenza

by M. C. Winternitz; Frank P. McNamara; Isabel M. Wason

FIG. XVI. AUTOPSY NO. 112. BACTERIA DEVELOP IN THE HYALINE NECROTIC EPITHELIUM OF THE TERMINAL BRONCHIOLES. HERE THEY FORM CIRCUMSCRIBED MASSES THAT SIMULATE NUCLEI. COMPARE FIGURES [V], [VIII], [XV], AND [XVII].
HELIOTYPE CO. BOSTON

FIG. XVIII. AUTOPSY NO. 155. ILLUSTRATES A MILD FORM OF PULMONARY INTERSTITIAL EMPHYSEMA.

FIG. XXII. AUTOPSY NO. 175. AN ALMOST PURE FIBRINOUS EXUDATE. THE ALVEOLAR WALLS ARE SLIGHTLY HYALINIZED AND THEIR EPITHELIUM IS ALMOST ENTIRELY LACKING.

There are, of course, variations in the extent of the serum, the fibrin, and the hemorrhage in the exudate of the alveoli, and while these different types may occur as pure forms, often they are associated. In still other areas and varying in prominence, one finds as characteristic an exudate, not only of serum, strands of fibrin, and red blood cells, but also a diffuse dotting of the exudate with bacteria, singly, in pairs, clumps, and chains (92, 164) (Fig. [XXI]). This type of reaction is uncommon in pulmonary disease. It resembles more closely a streptococcus cellulitis such as is encountered frequently in the subcutaneous tissues, for example, a woody phlegmon, or a sero-hemorrhagic exudate like the avirile response to a rapidly fatal hemolytic streptococcus serositis. A similar reaction has been reproduced experimentally in animals which have been rendered aplastic with benzol previous to pulmonary insufflation, and it is conceivable that the lack of polymorphonuclear response in the inflammatory exudate may be associated with some such general destruction or temporary suspension of leucocytic formation (160).

A more striking picture, however, even than this aplastic alveolar exudate appears in the terminal bronchioles. In many instances, these are conspicuous on account of their size, for they are dilated to form prominent, often irregular, sacs (Fig. [XV]). The distention of these terminal bronchioles may be so great that the surrounding alveoli are compressed. What makes them even more conspicuous is their lining, once epithelium, but now a swollen, thick, homogeneously staining material, with complete loss of architecture; the material forms (with hematoxylin and eosin) a red band limiting the lung tissue and sharply demarcating it from the exudate within the bronchioles (48, 92). However, this ribbon of red, often thickened by fibrin deposition, is not always pure, for bacteria thrive in the dead tissue. They occur singly, paired, in chains, and also as circumscribed, dense masses which in size and position, simulate nuclei (162) (Fig. [XVI]). This same hyalinization of the epithelium, it will be recalled, occurs in the larger bronchi (Fig. [V]), and there, too, bacteria frequently develop in the dead tissue (Fig. [VIII]). In the smallest bronchiolar ramifications, acute epithelial necrosis is not infrequently encountered, even when the surrounding lung tissue is relatively normal (Fig. [XVI]). That the process does not stop with the epithelium, but, as in the larger bronchi, may extend through the entire structure of the bronchioles, is manifest. Even the alveolar walls may be involved and frequently homogeneous pink or red bands, now the phantom of the former viable lung tissue, mark the presence of the old wall of the alveolus (Fig. [XVII]). Occasionally, some architecture remains in this pink ribbon and then the involvement seems to be primarily in the vessels of the wall. Not all the vessels are involved, and next to a hyaline thrombus in one, there may be fresh blood, usually red blood, in its neighbor. The alveolar epithelium is usually denuded and thus accentuates the intensity of the change.

The acute death which involves the tracheal, bronchial, and bronchiolar epithelium and which may extend beyond the epithelium into the walls of these structures and kill en masse the walls of the alveoli, is a lesion which does not occur in other types of acute pulmonary infection. However, in influenza, as after exposure to pulmonary irritating gases, it is the lesion of characterization (158,159). The effects of this change, of course, where it involves the alveolar wall, will vary with the extent of the process; but given an absolutely necrotic wall, as yet unstrengthened by inflammatory reaction, an expected result would be its rupture with respiratory movement. The point of rupture is important, but where so many alveoli are involved, disturbance of continuity will occur, occasionally in such position that the result will be the escape of air into the interstitial tissues.[^[7]] There is ample evidence that this happens. Indeed, among the clinical manifestations of the disease, interstitial emphysema of the lung spreading through the fascial planes to the subcutaneous tissues of neck and thorax is well known; the phenomenon is more frequent and extensive in influenza than in any other disease (8, 17, 52, 143).

Interstitial emphysema is very striking at the post-mortem table. The escaped air appears as beads along the interlobular septa, but on account of their size they are always most conspicuous between the lobes and along the vessels toward the hilum (162) (Fig. [XVIII]). Histologically, a small bubble of escaped air confined to the interlobular septum compresses the surrounding tissue with almost complete atelectasis of many neighboring alveoli (Fig. [XIX]).