We believe that we have, in the foregoing, conclusively shown that besides the true catarrhal influenza pneumonia, due to the bacillus of Pfeiffer and to the catarrhal streptococcic pneumonia, the fibrinous or cellular fibrinous, lobular and lobar pneumonia plays a considerable part as a complication or sequela of influenza.
If some physicians have observed only catarrhal pneumonia as the result of influenza, I can explain this remarkable statement only on the supposition that these observers regarded clinically every pneumonia as catarrhal, because they believed, on a priori grounds, that such was the only form of pneumonia occurring in influenza. The clinical course of croupous pneumonia occurring in influenza being frequently atypical, it was taken to be a catarrhal form, because of the "non pneumonic," generally purulent sputum and the gradual, lobular consolidation. How is it possible, however, to understand that such persons did not notice croupous pneumonia in the course of influenza upon the postmortem table, and in this way have cleared up their mistakes? To explain this I can only suppose that these observers saw the croupous lobar and lobular pneumonias, but did not recognize their relation to influenza, and consequently considered them to be cases of primary genuine croupous pneumonia.
For the present, of course, we must account for the great frequency of the croupous and the cellular croupous pneumonia in influenza by a mixed infection with the "cause of croupous pneumonia." Perhaps the time will come when the capability of the influenza bacillus to produce fibrinous inflammations of the lung will be proved. Speaking frankly, our present knowledge as to the "specific cause" of the different clinical pathologic forms of inflammation of the lung is still very uncertain and imperfect. Even the apparently well substantiated position of the " Diplococcus pneumoniae" as the cause of the endemic epidemic disease, "croupous pneumonia," is by no means so certain as the majority of persons to day believe. We need only mention the fact, which has been proved again and again, of the presence of streptococci only in croupous pneumonic infiltrations, of the exclusive presence of the Diplococcus pneumoniae in the catarrhal pneumonia of measles (H. Neumann); further, that Kreibich (from the Pathologic Anatomic Institute in Vienna), among 27 lobular aspiration pneumonias, found the diplococcus of pneumonia 23 times, and of these, 11 times this germ alone.
* Compare our influenza discourses, p. 44.
Only the combined activity of the clinician with the pathologist and bacteriologist will make it possible to clear up the vexed questions on which we have touched above.
We agree completely with the view which Wassermann (1893) has put forth in the following terms: "It would be premature to try at the present time to give a conclusive analysis of the inflammatory pulmonary affections on a basis of bacteriologic investigation. To arrive at this goal will require still much careful research in the laboratory as well as at the bedside. We are familiar at the present time with quite a number of parasites that are able to produce such disturbances; we know that just as the diplococcus of Frankel, so also the influenza bacillus of Pfeiffer, the bacillus of Friedlander, streptococci, and staphylococci are able to produce inflammations of the lung. At any rate the number of causative factors which may produce inflammatory conditions in the lung is large, and it is very uncertain, even unlikely, that all the causes of inflammations of the lung are known to us at the present time." clinical aspect and course of influenza pneumonia.
The manner in which pneumonia develops in influenza varies We have called attention to those cases where both diseases commence with a rigor, and called it the "pneumonic form of influenza." Tc this category belong the catarrhal as well as many of the true croupous inflammations. More frequently by far does pneumonia follow influenza. The development of pneumonia is then often insidious High fever without chill, increasing dyspnea, intense cough, all show the exacerbation of the influenza process, and soon after a circumscribec inflammatory area in the lung reveals its existence by the presence of crepitations. In a large number of cases the pneumonia follows on an attack of influenza. One, two, or even more days later a relapse occurs, sometimes but not always with a rigor; the influenza manifestations seem to recrudesce, but in reality they are the first signs of the slowly developing pneumonia. Many so called relapses depend upon this condition. In these cases the pneumonic attack often comes on the first time the influenza convalescent goes out; hence the universal view that the patient convalescing from influenza is very liable to catch cold and easily gets inflammation of the lungs.
While all symptoms-rigor, high fever, dyspnea, lancinating pain, and even the typical sputum-indicate the presence of pneumonia, it is sometimes impossible to locate it for several days. The first indications very often are noted in areas varying from the size of a silver dollar to that of a small plate, which, upon careful physical examination, are characterized by relative dulness, fine crepitant rales, subbronchial breathing, and weak bronchophony. I attach particular value to the last physical sign for facilitating the detection of small inflamed areas.
The pneumonic areas, both lobular and lobar, occasionally throughout the whole course of the pneumonia up to crisis or lysis, do not show absolute dulness and pure bronchial breathing, but for from six to eight days and even longer fine crepitant rales can be heard, together with only relative dulness and bronchophony (crepi tatio permanens).
A very frequent characteristic of all forms of influenza pneumonia, the croupous variety not excepted, is the lobular commencement-(that is, partially lobar), the gradual creeping character from lobule to lobule, and the frequent bilaterality of the pneumonia.