The pathology of influenza

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

If the atrium of an infection and its specific etiological agent are undetermined, the narrator of the pathology of a specific disease is confronted immediately with serious obstacles in the elaboration of a complete picture. Some writers assume that the respiratory tract is the portal of entry in influenza (162), though the specific agent is still unknown.[^[2]] Whatever the agent, unquestionably it attacks the respiratory tract at a very early stage in the disease and produces a lesion which becomes responsible for the most serious aspect of influenza, whether this phase be primary or only a complication.

Among the lesions which will be considered, therefore, those of the respiratory tract chiefly will be emphasized. They include the changes in the large air passages, as well as the pulmonary, alveolar, and interstitial involvement. Unquestionably, a very close association exists between the lesions of the larger air passages and those of the alveoli, but probably it is equally true that the former may occur alone; in many instances also they are the forerunners of the latter lesions. Consequently, it seems logical to begin with an exposition of the lesions in the trachea and its ramifications, including the bronchioles.

A. LESIONS OF THE TRACHEA AND BRONCHI

Gross Picture.

Early in the disease the congestion and the hemorrhages that have been described in the mucous membrane of the nasopharynx (14 and 94) are also conspicuous features in the lining of the trachea and bronchi (Fig. [I]). This membrane is swollen, turgid, red, and covered by a copious, mucous exudate which may be clear, but much more frequently is blood-stained or opaque and yellowish in color. The blood, variable in amount, may be fresh and red; and after the mucous exudate on the surface is removed, more intense red foci stand out on the congested base (47, 90, 157). Frequently, as the bronchi are approached, the red color of the mucosa becomes more intense and may have a garnet tinge. Membranes such as are encountered in the more usual necrotizing inflammatory processes, like diphtheria, have not occurred in the trachea and larger bronchi in this series (108, 128, 157).[^[3]] The exudate peels off readily, and as indicated above, leaves a velvety red surface, dotted here and there with darker or more intensely red foci. Small ulcerations of the mucosa occur, but are inconspicuous (82, 156). As the finer ramifications of the bronchi are approached, the accumulation of the exudate in their lumina becomes more and more marked, and on cross section of the lung, they often stand out conspicuously on account of their increased size and projecting, seromucous, blood-stained content (101, 149, 162).

It is remarkable how long this picture in the trachea and bronchi may persist without showing any marked variation. It is encountered, not only in the most acute and fulminating types of the disease (that have been examined), but a similar picture may be present in cases which end fatally only after a period of weeks of severe illness. In the latter cases, however, the exudate, particularly in the bronchioles, assumes a more purulent character and after this accumulation is wiped away from the surface of the tube, the intensity of the dark red color of its lining membrane presents an even more striking contrast on account of the opaque, yellowish-green exudate in the lumen. At this stage, too, the bronchioles are more distended with pus, which oozes from each one when the lung is sectioned (1, 108, 110). In the cases still more chronic, the terminal bronchioles may be sharply outlined with a thick grey wall which surrounds the dilated opening from which the accumulated yellowish exudate oozes as soon as the pressure is relieved (Figs. [XXXIX] and [XL]).

Histological Picture.

The changes are less marked, perhaps, in the trachea than in its finer ramifications. The mucosa is constantly more or less destroyed and large areas, usually focal, are entirely devoid of their epithelial covering. This is replaced by a sparse exudate, composed largely of red blood cells, mucus, a small amount of fibrin, and nuclear fragments (Fig. [II]). It may dip into the submucosa for a short distance, but usually these indentures are associated with the ducts of the mucous glands into which the inflammatory reaction extends. A more striking feature than the exudate, however, is the edema and the congestion of the submucosa. The loose areolar tissue of the submucosa is spread widely apart, and throughout it distended blood vessels are very conspicuous. Occasionally such a vessel is broken and actual hemorrhage appears in the submucosa. Occasionally, too, the inflammation extends down the duct to the mucous gland itself, and here, also, aplastic inflammatory reaction is evident, inasmuch as the acini now stain intensely red with the cells undifferentiated from each other and specked here and there by broken remains of the dead nuclei (Fig. [III]). After the disease has continued for a short period, even at the end of five or six days, some regeneration of the epithelial lining may be seen (3) (Fig. [IV]). But despite this, the acute picture persists, and there goes on, side by side, an attempted repair characterized by epithelial regeneration and the same evidence of acute change. Since the lesion is essentially a superficial one, scars or contractures of any extent are not encountered in the trachea, even in examples of the disease that have ended fatally only after many weeks.[^[4]]

FIG. VIII. AUTOPSY NO. 97. ALTHOUGH THE EPITHELIUM IS STILL VISIBLE AS A HYALINE BAND LIFTED FROM THE UNDERLYING MUCOSA, BOTH MUCOSA AND SUBMUCOSA ARE INVOLVED IN A NECROTIZING PROCESS. BACTERIA ARE ABUNDANT IN THE DEAD TISSUE.