When influenza attacked the encampment, about 50,000 troops were quartered in it, and for a considerable period no more troops were brought into the camp and none left it. All cases of pneumonia occurring among these troops were brought to the base hospital so that the autopsies which were studied were representative of all the pneumonias following influenza in this limited group of men. It is noteworthy that autopsy disclosed no instance of fatal influenza unaccompanied by pneumonia.
Pneumonia of Influenza.—Knowledge concerning the bacteriology of the pneumonia of influenza dates from the study of the epidemic of 1889–90. The frequency with which Diplococcus lanceolatus occurred in association with influenzal pneumonia was well recognized, although several observers, notably Finkler[[57]] and Ribbert,[[58]] found Streptococcus pyogenes so often that they attributed the pneumonia of influenza to this microorganism.
During a subsidiary outbreak of influenza occurring in 1891–92 Pfeiffer[[59]] discovered the microorganism which he believed was the cause of the disease. Pneumonia, he believed, was caused by the invasion of this microorganism into the lung, and the pneumonia of influenza, if death occurred at the height of the disease, was characterized not only by the presence of the bacillus of influenza, but was recognizable by its anatomic peculiarities. He described lobular patches of consolidation which were separated from one another by air containing tissue or were confluent, so that, although the lobular character was still recognizable, whole lobes might be affected. The consolidated tissue was dark red and within each lobular area were small, yellowish gray spots varying in size from that of a pinhead to a pea. In the mucus of the larynx and trachea were numerous microorganisms, including diplococci and streptococci, among which influenza bacilli were predominant; in the larger bronchi, bacteria other than influenza bacilli were less abundant, whereas in the finer bronchi filled with purulent fluid and in the lung tissue influenza bacilli had undivided sway. Pfeiffer stated that the changes described were found when death occurred at the height of the disease, whereas other pulmonary lesions might be sequelæ of this typical influenzal pneumonia.
Observations upon the pathology of influenzal pneumonia made during the epidemic of 1889–92 have been collected in the monograph of Leichtenstern[[60]] published in 1896. He combats the opinion held by some observers that pneumonia with influenza is always catarrhal and cites many writers to prove that lobar pneumonia not infrequently accompanies the disease. Indeed, some have found “croupous” pneumonia more often than “catarrhal.” Krannhals[[61]] at Riga found typical fibrinous pneumonia in 53 instances, doubtful forms in 22 and bronchopneumonia in 37. Cruickshank[[62]] in England found croupous forms predominant. Among 43 autopsies performed upon individuals dead with influenza Birch-Hirschfeld[[63]] found 11 instances of croupous lobar pneumonia, 8 instances of croupous lobular pneumonia and 24 instances of catarrhal pneumonia. Leichtenstern thinks that the atypical symptomatology of lobar pneumonia with influenza—for example, the purulent character of the sputum—has led many physicians to believe that lobar pneumonia rarely occurs. It is equally true that many instances of confluent lobular pneumonia are mistaken for lobar.
There appears to be no comprehensive description of the pneumonias of influenza based upon the epidemics of 1889–92. Descriptions dating from this period are much obscured by attempts to separate croupous or fibrinous from catarrhal pneumonias. Croupous lobular pneumonia has been recognized, for example, by Birch-Hirschfeld. Leichtenstern describes a form of pneumonia which he regards as neither lobar nor lobular although it implicates whole lobes; the consolidated tissue is homogeneous and varies in color from fleshy red to bluish red; it is tough and elastic in consistency. The author thinks that it is an error to regard this lesion as a confluent lobular pneumonia.
Kuskow[[64]], who has discussed the pathology of influenza in considerable detail, has seldom seen lobar pneumonia but has almost invariably found, even when there is lobar distribution of the lesion, lobular patches of consolidation involving groups of lobules, single lobules or only parts of lobules; the lung tissue has been hyperemic and in places edematous.
Opinions concerning the pathology and bacteriology of the pneumonias of influenza, published since the recent epidemic, have varied almost as much as those just cited. Few observers have had the opportunity of making a considerable number of observations under conditions which determine the relation of the pulmonary lesions to the primary disease.
Keegan[[65]] has found with influenza a massive and confluent bronchopneumonia, frequently resembling lobar pneumonia but distinguishable particularly in its early stages when the cut section of the consolidated lung has a finely granular character and each bronchiole stands out as a grayish area with intervening dark red alveolar tissue.
Symmers[[66]] states that the pneumonia of influenza is a confluent lobular exudative and hemorrhagic pneumonia which bears a close resemblance to the pneumonic variety of bubonic plague.
Our commission[[67]] published a preliminary report on pneumonia following influenza observed at Camp Pike. The occurrence of purulent bronchitis, distention of lungs, peribronchial hemorrhage and bronchiectasis were described. B. influenzæ was isolated from the bronchi in approximately 85 per cent of instances of influenzal pneumonia but from the consolidated lung in less than half this number of autopsies. Lobar pneumonia was present in a large proportion of autopsies but was less frequent than bronchopneumonia. Bronchopneumonic consolidation is in part red, lobular and confluent, in part nodular; pneumococci have a predominant part in the production of these lesions. Three types of suppurative pneumonia are described: (a) Abscess caused by hemolytic streptococci usually in contact with the pleura and accompanied by empyema; (b) Suppuration of interstitial tissue of the lung caused by hemolytic streptococci and accompanied by empyema; (c) multiple foci of suppuration clustered about a bronchus of medium size and caused by staphylococci. We have expressed the opinion that B. influenzæ descends into the bronchi; pneumococci, usually Type IV, may enter the lung and produce either lobar or bronchopneumonia. Hemolytic streptococci may descend and infect the pneumonic lung causing death often before suppuration has occurred. Epidemics of such superimposed streptococcus pneumonia in wards of the hospital were described.