The epidemic of influenza, prevalent in Europe during the Great War, was watched with interest everywhere, not only because of its military importance, but also because of the danger of its spreading to other continents. The prediction that this would occur, made months before its realization, was verified on an even larger scale than had been anticipated, for in the autumn of 1918, this acute respiratory infection passed over the United States like a huge wave, taking a tremendous toll in human lives; later smaller waves followed leaving in their wake corresponding degrees of devastation. The first cases of the disease appeared on the New England coast, and New Haven was among the cities to be early invaded, though here the epidemic was somewhat less severe than in other cities along the Atlantic Seaboard.

Forewarned and alert to the danger, medical men spared no effort in studying the disease; as a result, no malady, perhaps, has ever been investigated so intensively and from so many different points of attack in an equal length of time. Proof of this appears in the abundant literature issuing from every quarter. Among the various contributions to this subject, many include the anatomical changes associated with the disease. In general, however, these are brief; and although they serve their special purpose well, they have not been elaborated sufficiently to close the chapter.

During a period of about three months beginning with September 18, 1918, while the epidemic raged and waned in New Haven, there were approximately eleven hundred cases of the disease admitted to the New Haven Hospital. As is so often true, only the more critically ill sought hospital care, and few, if any, patients affected by other respiratory infections are included in these statistics. The mortality here, as elsewhere, was very high; of two hundred eighty (280) cases that ended fatally, eighty-two (82) were investigated at the post-mortem table. An attempt was made to make the studies very complete, and this was favored since the headquarters of the Yale Army Laboratory School, under the command of Colonel Charles F. Craig, were located at the Brady Laboratory where a large number of men were being instructed in Pathology and Bacteriology. It was also fortunate that competent illustrators were available who made a splendid series of water-colors and drawings of the characteristic lesions, both gross and microscopic.

The number of autopsied cases at the New Haven Hospital was augmented by a series of acute fatalities from the same disease at the United States General Hospital No. 16, at Allingtown, West Haven, where the anatomical studies were carried on by the same group of men. The latter autopsies offered nothing new, but served to corroborate the conclusions reached at the New Haven Hospital.

The majority of the fatalities occurred in the acute stage of the disease, the anatomical aspects of which have been elaborated more or less completely.^[1] Other cases survived for a longer period and in these, anatomical changes existed, which, as will appear later, were prognosticated from the acute lesions. Moreover, these findings suggested that certain progressive anatomical changes occur even when the disease runs a much less severe clinical course; for example, in cases where respiratory symptoms persist for a long period before they are brought to a fatal conclusion.

History, too, suggests such a chain of events; namely, in the record of the delayed crop of respiratory disorders that followed the harvest of the epidemic of ’90.

Previous studies of experimental pneumonia in normal and aplastic animals by one of the authors (160) give a background for the interpretation of the histology of some phases of this disease, but more important are the studies of the respiratory inflammatory processes initiated by the inhalation of toxic gases. This subject, introduced into human Pathology with the use of poisonous gases in modern warfare, necessitated elaborate investigations which have just been concluded (159).

The pathology produced by the inhalation of these poisonous vapors is analogous to that found in influenzal pneumonia. This is said with a full comprehension of the criticism that may follow such a statement, and with the knowledge that a similar analogy has been drawn between influenzal and plague pneumonia (Symmers, 141). It is, however, a criticism that is welcomed and which will be met in the body of the paper.

For the reasons just cited, it has seemed desirable to contribute to the Pathology of various phases of influenzal pneumonia and to attempt to correlate this with other types of acute respiratory inflammation, in the hope that the prognostications which suggest themselves may be of aid in the prophylaxis and possibly in the treatment of the more insidious and progressive pulmonary changes that may follow this disease.

A large part of the text is devoted to a description of the gross and more minute pathology of the respiratory tract associated with influenza and its complications, both in the acute and in the subacute or chronic stages. Incidental lesions of less importance in other portions of the body that have occurred in these cases are presented briefly, and emphasis is placed upon a number of special subjects. The order of discussion will be as follows:—

I. The Pathology of the Respiratory Tract in Influenza.

(A) Lesions of the Trachea and Bronchi.

(B) Lesions of the Lung.

(1) Acute Diffuse Fulminating Type.

(2) Localization and Necrotization of the Pneumonic Process.

(3) Organization of the Bronchiolar and Pneumonic Processes.

II. Influence of the Respiratory Complications of Influenza upon Tuberculosis of the Lung.

III. Extrarespiratory Lesions in Influenza.

(A) Lesions of the Hematopoietic System.

(B) Lesions of the Vascular System, Parenchymatous Organs, Alimentary Tract, and in the Walls of Other Hollow Viscera.

(C) Miscellaneous Lesions.

IV. Comparison between the Respiratory Lesions of Influenza and those Initiated by the Inhalation of Poisonous Gases with Special Reference to:—

(A) The Inflammatory Response versus the Systemic Capacity to Compensate.

(B) The Primary Injury.

(C) The Tendency to Organization of Bronchiolar and Alveolar Exudates with Bronchiolitis and Bronchiolectasis as SequelÆ.

(D) The Importance of the Trachea and its Ramifications as a Protective Mechanism against Infection of the Pulmonary Parenchyma.

V. Peculiarities of the Histology of Influenzal Pneumonia.

(A) The Extent of the Initial Pulmonary Lesion.

(B) The Hemorrhagic Exudate—The Relation of Red to Grey Hepatization.

(C) The Aplastic Exudate.

(D) The Hyaline Necrosis of the Pulmonary Tissue.

(E) The Organization Process.

VI. Infection as a Possible Etiological Factor for Malignant New Growths.

VII. The Bacteriology of Influenzal Pneumonia.

(A) Organisms Associated with Influenzal Pneumonia.

(B) The Relation of the Type of Organism to Pleural Involvement.

(C) The Relation of Different Organisms to the Type of Pneumonia.

(D) Summary and Discussion.

VIII. Conclusions.

IX. Bibliography.

X. Illustrations.