As soon as the lobes show this gray character and with the progressive development of an acute interstitial purulent pneumonia, the lung tissue becomes friable. All gradations of flabbiness may still be obtained and in the early stages while the cellular exudate is accumulating to change the color of the lung, little variation from the tough character of the pulmonary tissues can be recognized. When, however, a true gray character is assumed by a portion of the lobe, the tissue becomes so soft that it is handled with difficulty without rupture. The thumb can be pressed into the gray mass and pus will well up around the invading phalanx. The consistency in the late stages reminds one of the pulpy tissues in acute splenitis. In cutting such lobes it is almost impossible to obtain slices of the tissues, their own weight often breaking such a segment. When allowed to rest on the table for a few moments, the cut surface becomes coated with a dirty yellow slime representing pus and products of disintegration arising from the lung. The stroma and alveolar tissues are themselves involved in the inflammatory process and many of them have suffered complete or partial destruction so that they offer but little resistance to pressure and serve as a poor supporting stroma to the pulmonary tissues. The reaction which has taken place within the lung producing both the gray color and the destruction of the tissues is, indeed, an active suppurative one. One would not be surprised to obtain not only a purulent lesion wherein the cellular exudate occupies the air sacs and their walls but also a further stage leading to a destruction of the tissues to the extent that abscess cavities are produced. These we have met with in several instances, some of them being small while others were several centimeters in diameter. An abscess of larger extent and having a destructive process which involved the surrounding tissues so that one would speak of it as a process of gangrene, was observed by Dr. McMeans in one of his cases. A lobar distribution of the purulent lesion takes place where multiple involved lobules have fused in their periphery or where a suppurative flooding of the tissues in this violent late reaction has taken place.
The question at once comes to mind whether this gray stage is but the late event of what we have previously spoken of as influenza-pneumonia or whether this condition is superadded to what may begin as an influenza-pneumonia but end in a pulmonary inflammation with a mixed infection. Dr. Holman was not able to demonstrate a sufficient difference in the bacteriology of the lobes in the gray stages from those in the early acute stage to be able to say that the flora changes at a certain time during the progress of the disease in the individuals. It is possible, and there is some evidence in support of this, that the earlier stages of the pneumonic process represent the reaction to the influenza bacillus and that during this period the response is fairly uniform and similar owing to the fact that this infection has but a short incubation period and a high pathogenicity. In such an event the particular micro-organism may bring about a peculiar response of its own before the other organisms with which it is associated have the opportunity of producing damage. Subsequently, however, these secondary organisms impose their peculiar reactions upon an altered lung, thus inducing an inflammatory lesion which differs from the preceding reaction and also differs from the reaction usually induced by those organisms upon relatively healthy tissues. It is difficult to account for the very irregular distribution of the gray lesions by an explanation concerning the influenza bacillus alone, or by the characters peculiar to the secondary infection. There is an entire want of character to these gray lesions which makes them differ from other types of pneumonia known to us.
It is well to lay particular stress upon this peculiarity in the distribution and extent of the lesions within the lobes; and it is also important to appreciate the difference in the appearance of these gray areas from those of true lobar or broncho-pneumonia.
Finally there is another point in which this stage of the pneumonic process differs from that of pneumococcus lobar pneumonia. In frank lobar pneumonia the reactions taking place in the involved portion of the lung are fairly uniform in all its parts. The stage of red hepatization occupies about that amount of lung which subsequently shows itself in the state of gray hepatization. In other words, all of those areas which appear gray are preceded by this peculiar red consolidation, and all of the area occupied by the red hepatization will pass through the phases of gray hepatization before entering upon the final stage of resolution.
In influenza-pneumonia, on the other hand, the events taking place in a given lobe are not uniform and various stages and grades of the inflammatory reaction may be recognized at the same time, some appearing red, some congested, some flooded with blood in hemorrhage and others showing the purulent infiltration by the appearance of gray patches upon the background of red. Not only do the various reactions within the same lobe fail to show similar grades of intensity and similar stages or time of involvement, but we find that all of the red and hemorrhagic areas are not destined to pass through the gray stages. At times it is true an entire lung will enter into the purulent phase and if this becomes extreme abscess and gangrene are almost certain to develop. But often the purulent infiltration occupies only a few or scattered lobules and resolution may take place in a lung where the greater part of the lobes is occupied by the inflammatory œdema and hemorrhage and has never become truly consolidated by cellular and fibrinous exudate. This feature that the involved lung tissues need not pass through the sequence of events which is usually observed in frank lobar pneumonia is so distinctive that it differentiates the character of the inflammatory reaction very clearly. It may be that this is an indication of the unequal distribution of the micro-organism and that the first infection presumably by the bacillus influenzæ has been much more diffuse and of wider extent than the secondary invading bacteria which being distributed through the bronchial tree are more or less localized to those lobules most severely involved. It is impossible to claim for influenza-pneumonia as clear and sharp-cut stages as we obtain them in the pneumococcus lobar pneumonia.
During the period of the intense purulent reaction in certain portions of the lung, the intrinsic structures within the area also partake in the damage and response. The suppurative infiltration not only occupies the alveolar walls but also extends through the tissues of the bronchioles, the arteries and the veins. The polymorphonuclear leucocytes seem to migrate into all of the parenchyma indicating some damage by bacterial invasion. On more than one occasion have we observed partial or incomplete thrombosis of arterioles and capillaries whose walls showed an acute suppurative reaction. Some of these thromboses are of importance, being associated with the interference with a blood supply not compensated by adequate anastomosis. Necrosis and small areas of gangrene and abscess are to be found in the region of the circulatory disturbances. It is also during this period of the disease when the bronchi and their ramifications contain pus or muco-pus, that the exudate from the alveoli readily finds its way into the air passages and becoming mixed with the mucus from these tracts forms a tenacious discharge.
The presence of large amounts of exudate within the bronchi brought these structures into unusual prominence. This was particularly true in the purulent stage of the reaction when beads of sticky pus would well up from the cut bronchioles. We were tempted on a number of occasions to speak of this in terms of bronchiectasis but with the intense inflammatory reaction occupying the bronchial wall and modifying its contour on this account we avoided this diagnosis. In one instance, however, the lesion was unmistakable. This was a case of purulent pneumonia (764) dying on the ninth day of the disease. The distribution of his pulmonary lesions was distinctly lobular, apparently following the course of the bronchial distribution. The bronchi were followed longitudinally and irregular pouchings of the lumen were very apparent. The bronchi had suffered marked inflammatory reaction which had also infiltrated the muscular tissues of the tubes. Goodpasture and Burnett report finding two cases of acute bronchiectasis associated with abscess and ulceration of the bronchi. In our case the bronchiectasis was found bilateral but was more marked in the lower lobes than the upper.
The lymphatic channels within the lung tissue are found active in establishing an internal drainage to the neighboring thoracic glands. The lymph vessels were often found filled with leucocytes and variable amounts of serum. During this late stage only a few of the endothelial leucocytes were observed wandering to or from the lung with a load of pigment or cell debris. These wandering endothelial cells, however, appeared to become loosened from their normal situations and in the vicinity of lymphatic nodes or communicating channels where these cells are prone to localize with their carbon pigment, again assumed their spherical form and took on migratory properties entering into the nearby tissues and scattering themselves in the looser structures. It is an interesting point to note that these pigment carrying cells, ordinarily assuming a latent existence when their cytoplasm has been crowded with foreign particles will assume all the activities of migrating cells when the œdema of the tissues alters the physical properties not conducive to a stationary existence. These cells will then be found to enter the lung alveoli, often appearing as cells which have only recently picked up their carbon load. When, however, the conditions of the experiment, that is, the production of an inflammatory œdema in the lung, are produced in the tissues of an individual with much anthracosis, he will, during the period of his pneumonia and for some time during convalescence, bring up a greater number of these cells in his sputum than are ever obtained during the times when the lung is not involved. We are convinced that inflammatory conditions of the lung tend to reduce the total number of latent pigment bearing cells present in the involved tissues, and in this way somewhat reduce the grade of anthracosis.
A considerable discussion has arisen concerning the proper nomenclature for the pneumonia or pneumonias found in epidemic influenza. From some quarters have come the reports of a true lobar pneumonia, from others a lobular or broncho-pneumonia and others again claim that the reaction is an interstitial pneumonia of varying distribution. It appeared to us that the gross distribution of the lesions is not alone the criterion for a proper appreciation of the inflammatory states which may arise within the lung. I believe it has been amply demonstrated that the pneumonic reactions appearing in different regions of the United States as well as in different countries are not of a constant kind when viewed alone in the light of the gross picture nor are they constant from the standpoint of their bacteriology. We are of the opinion that the earlier phases of the pulmonary reaction are fairly constant in different places and that this constancy is dependent upon the common virus which initiates the respiratory lesion and which then permits a variety of micro-organisms invading as secondary agents. The secondary agents vary with the community and depending upon their nature the character of the reaction differs from that in other places. It has been well demonstrated that in some regions the hemolytic streptococcus is the important organism following the primary injury by the initial virus. In other places the pneumococcus or the staphylococcus or the M. catarrhalis is found to be of primary importance. Up to the present it has not been shown that the influenza bacillus is not the important organism causing the initial reaction and being responsible for the opportunity of secondary invaders leading to such diverse reactions in the lung. In our series we have met with lobar, lobular, interstitial and broncho-pneumonic types. We have not observed a case of the miliary bronchial reaction as described and illustrated by Goodpasture and Burnett and fully investigated by MacCallum. Moreover we have not met with the type of purulent bronchitis as a characteristic lesion preceding pulmonary involvement. The occurrence of pus within the bronchi occurred not early in the pulmonary lesion but later after the bronchi and bronchioles had passed through their stages of acute, serous and hemorrhagic pneumonia and were entering upon their secondary stage with pus production. The pulmonary lesion had long preceded the appearance of pus in the bronchi. We do not hold, however, that such relations between the pulmonary lesion and the purulent bronchitis do not exist for there is evidence that in particular regions this sequence of events was closely observed.
We cannot, however, correlate our findings with the classification of pneumonias as given by MacCallum. His claim for specific types of pneumonia as a sequel to influenza is based upon his statement that “no satisfactory evidence has been brought forward to show that the epidemic influenza is a bacterial infection. It is evidently a general or systematic infection not especially affecting the respiratory tract and analogous in many respects, as Bloomfield has pointed out, to the acute exanthematic diseases.” Thus we are confronted by two schools concerning the nature of influenza. The one claiming that epidemic influenza is essentially a disease of the respiratory system and the other completely denying this.