Pneumonia is the most frequent and most important complication of influenza. It is the decisive factor in influencing the mortality of the disease.

The question regarding the relation of influenza to pneumonia has at all times, and more particularly at the beginning of the pandemic of 1889, been answered in a variety of ways. When the generally received opinion that influenza was a harmless disease made way for the recognition that it could give rise to grave and fatal inflammations of the lung, there were, nevertheless, some authorities who attempted to explain the coexistence of influenza and pneumonia as purely accidental, and due to the simultaneous existence of an influenza epidemic and an independent pneumonia epidemic.

A glance at the history of influenza teaches that there has never been any epidemic which has not been marked by frequent pneumonic complications. Already in the epidemic of 1580 this had been emphasized by Bockel, and even more by Sydenham (1675), Arbuth not (1732), Huxham (1737), Whytt (1758), and others. But the epidemics of 1830 to 1837 especially gave rise in France to a lively discussion regarding the character of the influenza pneumonia. The question whether pneumonia was only a complication, " une maladie surajoutee" (Vigla, Petrequin, Nonat), or the localization of the pathologic process in the lung, "une symptome essentiel de la grippe" (Landau, Piorry, Gouraud), was discussed at that time just as vigorously as it is at the present time. The reports of the French physicians at that time form a veritable mine of accurate observations concerning the peculiarities of influenza pneumonia, and the ways in which it differs from pneumonia. The pneumonia of influenza had been designated already by Sydenham as "sub alio sidere nata,"

Another view was that the influenza bronchitis merely brought about the disposition and prepared the soil upon which the ubiquitous pneumonia germs could settle and develop (secondary infection). Certain instances that could not be ignored, in which unmistakable influenza and pneumonia set in together, were explained by the supposition of a simultaneous double infection with the bacilli of both influenza and pneumonia. This view gained many supporters when bacteriologic examinations showed the presence of the well known micro organisms of pneumonia in influenza produced inflammations of the lung.

Remarkable differences of observation occurred here. The majority (Weichselbaum, Bouchard, Netter, Menetrier, Birch-Hirsch feld, and many others) found the Diplococcus lanceolatus almost exclusively, while others (Finkler and Ribbert, Vaillard and Vincent, and others) found only the Streptococcus pyogenes. To explain these facts it was assumed that the first group of observers met only with croupous influenza pneumonia, in which the diplococcus is supposed to be the free dominant organism, while the other group came across only catarrhal or bronchopneumonias, in which the streptococcus is supreme. Numerous other observers found both diplo cocci and streptococci besides; occasionally, staphylococci and Fried lander's bacillus. In order not to disturb anatomic and bacteriologic classification, we must suppose that these were cases of mixed pneumonia, croupous catarrhal, or, as we shall call it for the future, cellular fibrinous mixed pneumonia.

The doctrine that pneumonia was due exclusively to either mixed or secondary infection seemed thus so firmly established that it required some courage to go against the stream and to assume that the still unknown exciting cause of influenza was in itself capable of causing an inflammation of the lungs. Was there any reason why this microbe, which was evidently able to cause the most intense inflammation of the bronchial mucous membrane, even extending into the finest bronchioles, should not also penetrate into the alveoli ? Were the alveoli actually accessible only to the diplococci and the streptococci that cause pneumonia? Reflections such as these, but especially a series of clinical and anatomic experiences, led me, in December 1889, to put forward the theory which, in earlier epidemics, already had been precisely stated by the physicians at that time (Gray, 1782), namely: "There is a primary influenza pneumonia (that is, an inflammation of the lung caused by the influenza toxin) whose onset is often simultaneous with the typical manifestations of influenza." I called this "the pneumonic form of influenza."

Similar views were put forward at that time (1890) by Drasche, Runeberg, and Heitler. Drasche says: "Although in the majority of cases influenza pneumonia is preceded by bronchitis, from which the inflammation extends into the lung tissue, nevertheless clinical observation shows that the lung affection may occur as a direct result of the infection without any sign of bronchitis." Heitler states: "From our knowledge at the present time regarding the character of pneumonia there is no reason from a clinical, anatomic, or bacteriologic standpoint, for not considering many cases of croupous pneumonia during the influenza epidemic as a direct result of the causative agent of influenza."

Our view was not accepted at that time by the bacteriologists, who insisted upon mixed infection with the known micro organism of pneumonia, and it was condemned as "untenable."

Two years later, when the influenza bacillus was discovered, the question of the etiology and pathogenesis of influenza pneumonia assumed a different aspect. First R. Pfeiffer and then Beck and Wassermann showed that in the pneumonic exudate within the alveolar lumina, as well as in the alveolar septa (and here particularly inclosed in round cells), influenza bacilli were to be found in "remarkable numbers." Pfeiffer describes his discovery in the words: "In smear preparations that have been prepared from the secretion adhering to the mucous membrane of the larynx and trachea there is generally a mixture of various varieties of bacteria, streptococci, diplococci, etc., but even here the influenza bacillus is by far the most numerous. In the larger bronchi the admixture of other bacteria becomes less; in the bronchioles filled with purulent material the influenza bacillus is predominant; so, too, in the pulmonary tissues. The other micro organisms, streptococci and diplococci, are not seen, in recent (pneumonic) attacks, either in sections or in smear preparations.