Superimposed infection of the lungs with other types of pneumococci than those primarily responsible for the development of pneumonia occurred not infrequently in this group of cases either during the course of the disease or shortly after recovery from the first attack of pneumonia. Pneumococcus Type II infection was superimposed upon or shortly followed pneumonia caused by Group IV pneumococci in 4 instances, by Pneumococcus II atypical in 1 instance. In 1 case pneumonia due to Pneumococcus II atypical occurred three days after recovery from a Pneumococcus Type I pneumonia, in another case Pneumococcus Type III infection was superimposed upon a pneumonia originally due to a pneumococcus of Group IV. These cases are presented in detail in another section of this report, and in several instances were shown to be directly due to contact infection from patients in neighboring beds.
In a similar manner, superimposed infection with S. hemolyticus at some time during the course of the pneumonia occurred in 13 cases in this group, with fatal result in all but one. Streptococcus infection occurred in pneumonia due to Pneumococcus II atypical once, to Pneumococcus Type III once, and to pneumococci of Group IV eleven times. Nine of these cases were free from hemolytic streptococci at the time of onset of the pneumonia, 4 showed a very few colonies of hemolytic streptococci in the first sputum culture made.
B. influenzæ was found in the sputum coughed from the deeper air passages in the majority of cases, being present in 80, or 76.2 per cent, of the 105 cases. In the 58 cases of lobar pneumonia it was found 41 times, or 70.7 per cent, in the 47 cases of bronchopneumonia 39 times, or 82.9 per cent. The abundance of B. influenzæ in the sputum varied greatly in different cases. Microscopic examination of stained sputum films and direct culture of the sputum on blood agar plates showed that in general it was more abundant in the mucopurulent sputum from cases of bronchopneumonia than in the mucoid rusty sputum from cases of lobar pneumonia. This was by no means an invariable rule, however, since in the former the bacilli were sometimes very few in number, in the latter quite abundant. Whether B. influenzæ shared in the production of the actual pneumonia in these cases is difficult to decide and cannot be stated on the basis of the bacteriologic and clinical observations which have been made.
Clinical Features.—One of the most striking aspects of pneumococcus pneumonia following influenza was the diversity of clinical pictures presented. These varied all the way from the classical picture of lobar pneumonia to that of bronchopneumonia of all grades of severity from the rapidly fatal coalescing type to that of very mild character with very slight signs of consolidation. For this reason it is questioned whether there is any real justification for speaking of a typical influenzal pneumonia, an opinion that seems well supported by the diversified picture found at the necropsy table.
For purposes of presentation, pneumococcus pneumonia following influenza may be divided into three clinical groups: (1) Lobar pneumonia; (2) lobar pneumonia with purulent bronchitis; (3) bronchopneumonia. No accurate data are available as to the relative frequency with which these three types occurred at Camp Pike. In the group of 105 cases studied there were 58 cases of lobar pneumonia, 11 of which had purulent bronchitis, and 47 cases of bronchopneumonia. The majority of these cases, however, occurred during the early days of the epidemic of influenza and probably show a considerably higher proportion of lobar pneumonias than actually occurred in the total number of pneumonias throughout the epidemic. This is indicated by the fact that of 100 consecutive cases of influenza selected for observation at the height of the epidemic, 3 developed clinical evidence of lobar pneumonia and 12 of bronchopneumonia.
(1) Lobar pneumonia presenting the typical clinical picture with sudden onset, tenacious rusty sputum, sustained temperature, and physical signs of complete consolidation of one or more lobes occurred in 47 cases; 36 cases in this group definitely followed influenza. In 11 cases no certain clinical evidence of a preceding influenza was obtained, and it is probable that some of these represent cases of pneumonia occurring independently of the epidemic of influenza.
The onset of pneumonia in this group of cases occurred from four to nine days after the onset of influenza and with few exceptions was ushered in by a chill and pain in the chest. In several instances the patient had apparently recovered from influenza as evidenced by fall of temperature to normal. After twenty-four to seventy-two hours of normal temperature the patient would have a chill and develop lobar pneumonia. In the majority of cases, however, lobar pneumonia developed while the patient was still sick with influenza. The course of the disease, symptomatology and physical signs were quite characteristic of lobar pneumonia and require no special comment. Recovery by crisis occurred in 21 cases, by lysis in 8. Pneumococcus empyema developed in 3 cases, fibrinopurulent pericarditis in 3 and all but 1 of these 6 cases terminating fatally.
In Table XV 5 fatal cases of lobar pneumonia, which illustrate some of the unusual features of the disease when it follows influenza, have been summarized. The first 2 cases represent examples of recurring attacks of pneumonia which developed shortly after recovery from the first attack, in both instances being due to types of pneumococci different from those causing the first attack. The third case represents an example of superimposed infection of the lungs with hemolytic streptococci and staphylococci during the course of a pneumonia due to Pneumococcus IV and disappearance of the latter organism from the tissues so that it was not found at time of necropsy. The last 2 cases are examples of fulminating rapidly fatal cases of lobar pneumonia associated with mixed infections of pneumococci and hemolytic streptococci, the streptococci probably being secondary in both cases. Cases like the few examples cited above, which occurred not infrequently throughout the epidemic of influenza, serve to illustrate the difficulties which may be met in attempting to correlate the clinical, bacteriologic and pathologic features of pneumonia following influenza unless careful bacteriologic examinations are made both during life and at the necropsy table in the same group of cases.
| Table XV | |||||||
|---|---|---|---|---|---|---|---|
| Cases of Lobar Pneumonia Following Influenza | |||||||
| CASE | ONSET OF INFLUENZA | ONSET OF PNEUMONIA | SPUTUM EXAMINATION | COURSE OF PNEUMONIA | NECROPSY | ||
| DATE | BACTERIOLOGY | DIAGNOSIS | BACTERIOLOGY | ||||
| Pul | Sept. 7 | Sept. 9 1st attack bronchopn. | Sept. 10 | Pn. IV ++++ B. inf. +++ | Recovery by crisis on Sept. 14. On Sept. 21 developed lobar pneumonia. Died Sept. 30 | Lobar pneumonia. Gray hepatization L.L, L.U, R.L. | H.B. Pn. II Br. Pn. II ++++ B. inf. +++ R.L. Pn. II + + |
| Lew | Sept. 16 | Sept. 20 chill | Sept. 22 | Pn. I +++ B. inf. + | Lobar pn., recovery by crisis Sept. 29. Developed 2nd attack lobar pn. on Oct. 2. Died Oct. 8 | Lobar pneumonia. Gray hepatization R.U. Fibrinopurulent pleurisy | H.B. Pn. II atyp. Br. B. inf. ++++ Pn. IIa +++ S. hem. + Staph. + R.U. Pn. IIa ++++ |
| Col | Sept. 20 | Sept. 24 | Sept. 27 | Pn. IV ++ | Severe lobar pneumonia. Died on Sept. 30 | Lobar pneumonia. Red hepatization all lobes. Serofibrinous pl., rt. 125 c.c. | H.B. S. hem. Br. S. hem. ++++ Staph. + L.L. S. hem. ++++ Staph. + |
| Gar | Sept. 23 | Sept. 28 | Sept. 30 | Pn. IV ++ S. hem. + B. inf. + | Fulminating rapidly fatal lobar pneumonia. Died Sept. 30 | Lobar pneumonia. Engorgement and red hepatization L.U., R.U. | H.B. S. hem. Br. S. hem. ++++ B. inf. +++ L.U. S. hem. ++++ |
| Hol | Sept. 25 | Sept. 30 | Sept. 30 | Pn. III ++ B. inf. ++ | Fulminating rapidly fatal lobar pneumonia. Died Oct. 1. | Lobar pneumonia. Engorgement all lobes | H.B. sterile Br. B. inf. ++++ Pn. III ++ S. hem. + R.L. Pn. III ++++ B. inf. ++ S. hem. + |
| L.L. R.L., etc., indicates lobes involved. H. B. = Heart’s blood. Br. = bronchus. | |||||||
(2) There were 11 cases of lobar pneumonia with purulent bronchitis in the group studied. Clinically, they closely resembled the cases in the preceding group except in so far as the picture was modified by the presence of the purulent bronchitis. All directly followed influenza. The sputum, instead of being rusty and tenacious, was profuse and mucopurulent, usually streaked with blood. Stained films and direct culture on blood agar plates showed pneumococci in abundance and B. influenzæ in varying numbers, in only two instances the predominant organism. The physical signs were those of lobar pneumonia with, in addition, those of a diffuse bronchitis as manifested by medium and coarse moist râles throughout both chests. Five cases recovered by crisis; 6 terminated fatally and in all of them the clinical diagnosis of lobar pneumonia with purulent bronchitis was confirmed at necropsy.