The pathology of influenza

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

B. LESIONS OF THE LUNG

In the prosecution of the scientific study of any disease, the great temptation is to differentiate its various manifestations with the intention of elaborating a classification. While there may be more or less distinct types of pulmonary involvement in influenza, so many intermediary forms appear in an extensive series of cases, that any classification must necessarily be arbitrary. Here, such an attempt at classification is beset with unusual difficulty, because, in the vast majority of cases which come to anatomical observation, the disease is fulminating. The lesions are more uniform in character than in an experimental study where the material is arranged so as to include intermediary and chronic stages, which in man are only encountered when accident causes death. These gaps in the study cannot be supplemented with experimental observations, because attempts to reproduce this disease have failed, even in human subjects. From the literature it appears also that variations in the extent, and perhaps in the maturation, of the anatomical involvement may be represented in different proportions for different localities (1, 2, 17, 55, 92, 162). Therefore, no sharp differentiation may be drawn between the more or less definite stages which are seen at the post-mortem table; still, for convenience of description, certain of the lesions which occur more frequently and are more widely differentiated may be considered separately.

The disease, as has been indicated, may be confined to the bronchial tree. In these circumstances, it is almost necessary to suppose that the larger bronchi alone are involved. When the delicate bronchioles are affected, there is always a more or less extensive involvement of the pulmonary parenchyma (124), for the bronchioles have a more direct communication with the alveoli, and their walls present a less formidable barrier to the extension of the inflammation to the surrounding air sacs.

FIG. XI. AUTOPSY NO. 140. ILLUSTRATES A LATE CHANGE IN THE BRONCHIOLE; THE EXUDATE IS BEING ORGANIZED AND THE EPITHELIAL LINING IS PROLIFERATING AND HAS INVADED THE SURROUNDING LUNG TISSUE. COMPARE FIGURES [XLVIII] AND [XLIX].

FIG. XII. AUTOPSY NO. 209. A SMALL BRONCHIECTATIC CAVITY FILLED WITH PUS. THE GROSS APPEARANCE IS ILLUSTRATED IN FIGURE [L].

FIG. XIII. AUTOPSY NO. 96. RIGHT LUNG. A WATER COLOR DRAWING OF A GROSS LUNG IN THE ACUTE STAGE. NOTE THE SIZE OF THE LUNG, THE HEMORRHAGES ON THE PLEURAL SURFACE, AND THE BLUE AREAS OF CONSOLIDATION.

Clinically, there is reason to believe that the disease may begin with a period of general malaise, during which the respiratory symptoms may be more or less severe. In the fulminating cases, the malaise may be associated from the beginning, not only with a tracheobronchitis, but also with pulmonary involvement. In less severe types the malaise may be accompanied only by tracheobronchitis, and may present no symptoms referable to the pulmonary parenchyma; there may follow or not, a definite period of clinical improvement, after which pneumonic involvement becomes evident. However, even where a fulminating type of the disease is not associated with clinical evidence of pulmonary involvement, the post-mortem examination may show extensive change in the lung parenchyma (110).

Whether this grouping of the disease is correct or is based upon a fallacious deduction from more or less satisfactory clinical histories, is open to question; and a decision may be reached from comparison of the opinions based upon carefully observed cases treated in different institutions. From the report of the epidemic at the Johns Hopkins Hospital (Bloomfield and Harrop (14)), where two hundred sixty-eight cases were studied in which the complication of pneumonia was uncommon as compared with cases in other hospitals—the New Haven Hospital, for instance—and where the percentage of the deaths was low, the conclusion was reached that the disease is primarily a general one and that the pulmonary involvement is secondary, just as in an exanthem, like measles. By way of comparison, at the New Haven Hospital, where more than eleven hundred patients with influenza were observed, the type of disease described by Bloomfield and Harrop was relatively rare. Of course, there were cases of that type where general malaise, with or without respiratory symptoms, was followed by a period—usually of from two to three days—of definite improvement in the symptoms; and later extensive and serious pulmonary complications ensued. However, in another group, largely composed of individuals who entered the hospital seriously ill, the histories indicate an acute onset resembling that of lobar pneumonia and with early manifestations of pulmonary involvement (2, 17, 52, 145). This discrepancy, probably, may be explained in part by variations in the sensitivity to minor indisposition on the part of the different individuals.

The preceding review should aid in the correlation of the clinical types of the disease with the respiratory lesions. All pulmonary lesions, from the least to the most localized, may be explained either by a subsidence of a less acute initial and diffuse involvement of the parenchyma, or by a less rapid and progressive spread of the necrotizing and inflammatory process from the upper respiratory tract through the bronchioles to the alveoli. This conception does not take into account the significance of the period of malaise, interpreted by the clinician as the period of invasion, but attempts to correlate the respiratory symptoms with the pulmonary lesions and their etiology.

Our own experience, like that of other observers (26, 104, 162), is that all fatal cases of this disease show pulmonary involvement in the form of pneumonia. The lesion varies greatly in intensity and in the amount of pulmonary tissue affected. In the descriptions which follow, the more diffuse and intense processes will be discussed first, and later those in which the inflammation localized and terminated in pseudolobar, lobar, lobular, or peribronchial pneumonia.