There is no reason to doubt that the lobar pneumonia which we have found with influenza has been constantly caused by pneumococci. We have encountered no instance of lobar pneumonia caused by the capsulated bacillus of Friedländer. The incidence of different types of pneumococci in the lung with lobar pneumonia has been as follows: Type IV, 32.4 per cent; Type II, atypical, 26.5 per cent; Type III, 17.6 per cent; Type II, 5.9 per cent; Type I, 2.9 per cent; no pneumococci found 14.7 per cent. It is noteworthy that this distribution of types is in sharp contrast with the lobar pneumonia of civil life with which Types I and II constitute the cause of two-thirds of all instances, and is in agreement with the etiology of the pneumonias found in an army camp (Funston) in the absence of influenza in epidemic proportion.
Bronchopneumonia.—Bronchopneumonia is associated with intense bronchitis penetrating to the finest bronchioles and is characterized by consolidation distributed in such definite relation to the bronchial tree that dissemination of the inflammatory irritant by way of the bronchi is evident. Consolidation occurs (a) in foci affecting alveoli in immediate proximity to the respiratory bronchioles and in consequence clustered about the terminal bronchi, the intervening alveolar tissue containing air; (b) in foci of the same character surrounded by intraalveolar hemorrhage which occupies all alveolar tissue between adjacent foci; (c) throughout whole lobules or groups of lobules, intervening lobules being unaffected; (d) surrounding bronchi of medium size like a sheath.
The lobar pneumonia of influenza is characterized by frequent association with purulent bronchitis and bronchopneumonia. The bronchopneumonia of influenza exhibits characters which serve to distinguish it from other forms of bronchopneumonia; (a) The associated lesions of the bronchi are unusually severe; purulent exudate accumulates within the lumen and the lining membrane is destroyed. (b) Pneumonia is frequently hemorrhagic with accumulation of blood within the alveoli and within and surrounding the bronchi. (c) There is unusual susceptibility of the injured bronchi and of the pulmonary tissue to secondary invasion by streptococci and staphylococci with consequent necrosis and suppuration. (d) Bronchiectasis frequently accompanies bronchitis. (e) Bronchopneumonia frequently fails to resolve and the lesion assumes the character of a chronic pneumonia.
With bronchopneumonia pneumococci are found with B. influenzæ in the bronchi and lungs in nearly half and in the blood in approximately one-third of instances of the disease, but hemolytic streptococci, staphylococci, S. viridans, B. coli, M. catarrhalis and other microorganisms are very frequently found in various combinations: they undoubtedly have a part in the production of the lesion. Mixed infection of the lung and even of the blood with pneumococci and hemolytic streptococci is often found, and study of the sputum during life has repeatedly shown that pneumococci alone are present shortly after the onset of the disease, whereas hemolytic streptococci appear later or are first discovered at autopsy. In such instances pneumococci have not infrequently disappeared from the lung and at autopsy hemolytic streptococci alone are demonstrable.
The part which B. influenzæ has in the production of bronchopneumonia is of great interest. This microorganism is demonstrable by cultures in at least three-fourths of all instances of bronchopneumonia but is obtained from the inflamed lung tissue in less than half. In no instance of pneumonia have we found B. influenzæ unassociated with other microorganisms, whereas repeatedly pneumococci have been the only microorganism demonstrable in the lung and very frequently the only organism present in the blood. In view of the difficulty of demonstrating the microorganism in plates overgrown by other bacteria, it is probable that its incidence in the bronchi is much higher, if it is not constantly present, whereas its isolation from the lung is in part referable to its presence in the small bronchi where it can be readily demonstrated by cultures or by microscopic preparations. We have been almost uniformly unsuccessful in demonstrating the microorganism in the alveoli of the lung. Goodpasture and Burnett,[[106]] who have devised a special method for the demonstration of B. influenzæ in tissues, have found few of these microorganisms in the alveoli of the lungs.
Pneumonia characterized by the occurrence of small (peribronchiolar) spots of leucocytic pneumonia upon an almost homogeneous background of intraalveolar hemorrhage, was regarded by Pfeiffer as the characteristic lesion produced by his microorganism. B. influenzæ in our autopsies has borne the same relation to this lesion which it has exhibited to other forms of bronchopneumonia; pneumococci have been present with approximately the same frequency and hemolytic streptococci have often been found.
Streptococcus Pneumonia.—The occurrence of streptococcus pneumonia with suppuration occurring in the trail of influenza was frequently observed during the pandemic of 1889–90. It is now well recognized that the streptococcus concerned is one capable of causing hemolysis. Suppurative pneumonia referable to hemolytic streptococci is of two types which are readily separable by their anatomic characters: (a) One or several abscesses are situated below the pleura and accompanied by empyema. Their relation to severe lesions of the bronchi is not infrequently demonstrable, for a destructive lesion of the bronchial wall has penetrated into the surrounding alveolar tissue so that necrosis of tissue and subsequent abscess formation occur in continuity with the bronchial lumen. The localization of the abscess below the pleura is referable to the greater severity of the lesions of the small bronchi which are most numerous at the periphery, to the greater severity of these bronchial lesions at the bases of the lung, and to the relation of lymphatics within the interior of the lung to those of the pleura. It is not improbable that stasis of lymph caused by thrombosis of the lymphatics has a part in the production of abscess. Preceding or accompanying abscess formation, the lung tissue undergoes consolidation and in a wide area about the abscess has a homogeneous gray cloudy appearance occasionally mottled by opaque patches of necrosis. (b) Interstitial suppurative pneumonia is a lesion not infrequently found in association with influenza (21 times among 241 autopsies) and rarely, if ever, seen in its absence. There are few references to this lesion in the pathologic literature of the English language and those of German origin in great part refer to the period of the pandemic of 1889–90. The lesion is essentially suppurative lymphangitis, and both thrombosis and suppuration of the lymphatics are widespread throughout the affected lung. In proximity to the inflamed lymphatics and the surrounding interstitial septa, lung tissue throughout parts of the lobes or even throughout a whole (lower) lobe has undergone consolidation and has the gray, cloudy appearance of streptococcus pneumonia.
Staphylococcus Pneumonia.—Abscesses produced by staphylococci differ in anatomic characters and sequelæ from those caused by hemolytic streptococci. Small abscesses occur in one or several localized clusters; these abscesses are grouped about a bronchus and have their origin in its terminal branches. This relation may be readily demonstrated in microscopic sections. The lesion tends to remain localized and pneumonic consolidation is limited to the immediate neighborhood of the group of abscesses. There is no lymphangitis and the lesion is not accompanied by empyema.
Empyema.—Empyema is almost invariably associated with suppurative pneumonia caused by hemolytic streptococci. Among our autopsies purulent fluid has been found in the pleural cavity 55 times; it occurred 15 times among 178 instances of lobar or bronchopneumonia and 50 times among 60 instances of suppurative pneumonia referable to S. hemolyticus. In our experience hemolytic streptococci and pneumococci are the only microorganisms which exhibit a noteworthy capacity to penetrate from the lung to the pleural cavity. We have not found nonhemolytic streptococci (e. g., S. viridans) in association with empyema.
Staphylococcus has failed to invade the pleural cavity even when a pulmonary abscess has been present below the pleura, and in the only instances in which staphylococci have been isolated from the pleural cavity thoracotomy had been performed for empyema caused by hemolytic streptococci (2 instances) or an abscess communicating with both bronchus and pleura. B. influenzæ has been found in the pleural cavity with empyema only once and in this instance cannot be regarded as the cause of the lesion, for it has accompanied hemolytic streptococci.