Wassermann obtained similar results: "The opinion that influenza pneumonia is caused only by a mixed infection with pneu mococci and streptococci would be tenable only if we were always to find pneumococci and streptococci in influenza pneumonia. But this is not the case; on the contrary, these micro organisms are almost always absent, so that in pure and uncomplicated cases a pure culture of influenza bacilli is found in the pneumonic sputum. Therefore this form of pneumonia-and it is by far the most frequent in an epidemic-is not to be considered as a foreign complication of influenza, but simply as a continuation of one and the same process from the bronchi into the pulmonary tissues. In other words, influenza pneumonia is quite independent of ordinary croupous pneumonia, and is a separate variety.
Thus at last was influenza pneumonia, in the strict sense of the term, rightly classified from a bacteriologic point of view.
Anatomically this true pneumonia caused by the influenza bacillus is, according to Pfeiffer, Beck, and Wassermann, entirely catarrhal.
We cannot here consider further the exhaustive description which Pfeiffer has given of the pneumonia caused by influenza bacilli. It is but a repetition of what we have known long regarding the anatomic course of a pure catarrhal pneumonia.
As the inflammatory process proceeds from the bronchi into the pulmonary tissues, there arise, as always under such conditions, lobular areas of inflammation, which either remain separated by tissues containing air, or coalesce to secondary lobar areas whose origin from lobular foci can still be recognized. The cut surface is quite smooth, and on pressure drops of yellow pus ooze from the severed bronchi. Microscopically, "the whole appearance is one of catarrhal suppuration in optima forma. The alveolar lumina and septa, as well as the peribronchial connective tissue, are so infiltrated with round cells that apparently the lung structure is entirely obliterated. In the alveoli surrounding these purulent infiltrations, besides containing round cells, the alveolar epithelium is much swollen. In preparations stained by Weigert's method the absence of fibrin (or its occurrence at most in traces) in the areas of infiltration is very evident."
No doubt most of the bronchopneumonia caused by influenza accords with the bacteriologic anatomic description of Pfeiffer. Nevertheless, there is also no doubt that much influenza bronchopneumonia is accompanied by streptococci, possibly also with diplococci, which settle along with the influenza bacilli and may even overgrow them. Only thus can we explain the numerous cases of influenza pneumonia in which streptococci and diplococci were found during the time of the pandemic of 1889-1890. Albu emphasizes the frequency of the secondary bronchopneumonias arising from the invasion of streptococci, and considers "this mixed infection as pathognomonic of influenza."
The pneumonia just described and caused by the influenza bacilli is a purely catarrhal form, and is by no means the only one which occurs in influenza. A very large number of cases are of the croupous variety, and a third not less extensive group consists of certain mixed pneumonias-that is, catarrhal croupous or, as they may be called, cellular fibrinous. We shall return to these varieties later.
Up to the present it has not been shown that the influenza bacillus, besides giving rise to a catarrhal inflammation, can produce also a fibrinous exudate in the pulmonary alveoli. The bacillus has not yet been found in croupous infiltrations. We must for the present assume that the croupous pneumonia which occurs so frequently in influenza is due to a mixed or secondary infection with those cocci which alone can produce the croupous inflammatory condition (Diplococcus lanceolatus s. pneumoniae). We agree with the general prevailing opinion that this diplococcus is the main cause of croupous pneumonia, but we cannot overlook the fact that this question is as yet by no means settled.
A point upon which there has been much difference of opinion is the relative frequency of catarrhal and croupous inflammations of the lung in influenza. The reasons for contradictory opinions on this point are obvious. They depend upon the facts that at the bedside it is often impossible to differentiate between these two forms of inflammation; and that the anatomic differential diagnosis also is by no means always easy or certain.
It is in influenza especially that mixed and transitional forms of lobular and lobar infiltration, whose anatomic character, viz., whether catarrhal or croupous, is often extremely difficult, either macroscopic ally or microscopically, to recognize. In these mixed, that is to say, cellular fibrinous, pneumonias, there are found, besides characteristically catarrhal pneumonic areas, also just as characteristic fibrinous fine- and coarse grained foci in the same lobe of the lung; in some of the affected areas are found alveoli which contain catarrhal and fibrinous masses intermixed, so that the naked eye appearance is not characteristic of either variety of pneumonia. But even microscopically the differentiation is often difficult. In the sections stained by Weigert's method several alveoli or groups of the same may show catarrhal inflammation (a cellular exudate with little or no fibrin), while other alveoli situated near by are infiltrated with round cells, or these are even irregularly distributed among the alveoli, which may be filled with fibrin and thus exhibit the characteristics of true fibrinous pneumonia.
We cannot here dwell longer on the unsettled question of the pathologic anatomy of pneumonia, but we will quote some authors who refer to these mixed forms:
Ziegler states that "the exudate of catarrhal bronchopneumonia may frequently have a hemorrhagic character, and that croupous exudations with fibrinous plugs also occur. These are cases, therefore, in which the cut surface shows a more or less pronounced pneumonic granular surface."
Sahli points out that "bronchopneumonia, apart from its macroscopic dissemination, is histologically often difficult to differentiate from croupous pneumonia, and especially from croupous pneumonia in which there is hemorrhagic exudation, with a more or less appreciable amount of fibrin. In the sputum of such cases Frankel's pneumococcus is not infrequently found, often also all or any of the other forms of microorganisms which give rise to inflammation."