(3) Forty-seven cases in the group studied presented the clinical picture of bronchopneumonia. The onset of pneumonia in these cases was in most instances insidious and appeared to occur as a continuation of the preceding influenza. The temperature, instead of falling to normal after from three to four days, remained elevated or rose higher, the respiratory rate began to rise, a moderate cyanosis appeared, the cough increased, and the sputum became more profuse, usually being mucopurulent and blood streaked, sometimes mucoid with fresh blood. The pulse showed little change at first, being only moderately accelerated. Pleural pain, so characteristic of the onset of lobar pneumonia, was rarely complained of, but a certain amount of substernal pain was common, probably due to the severe tracheobronchitis. Physical examination at this time revealed small areas showing relative dullness, diminished or nearly absent breath sounds, and fine crepitant râles. These areas usually appeared first posteriorly over the lower lobes.
The subsequent course of the disease showed the widest variation from mild cases with limited pulmonary involvement going on to prompt recovery in four or five days with defervescence by lysis or crisis to those presenting the picture of a rapidly progressive and coalescing pneumonia with fatal outcome. In the milder cases the diagnosis of pneumonia depended in considerable part upon the general symptoms of continued fever, increased respiratory rate, and slight cyanosis. Definite pulmonary signs were always present if carefully looked for, though sometimes not outspoken. Areas of bronchial breathing and bronchophony often appeared late, sometimes not until the patient was apparently recovering. In the severe cases cyanosis became intense and an extreme toxemia dominated the picture. In certain of these cases there was an intense pulmonary edema. The respiratory rate showed wide variation, the breathing in some cases being rapid and gasping, in others comparatively quiet. Progressive involvement of the lungs occurred with the development of marked dullness, loud bronchial breathing and bronchophony. Abundant medium and coarse moist râles were heard throughout the chest, probably due in considerable part to the extensive bronchitis almost universally present. An active delirium was not uncommon. Signs of pleural involvement, even in the most severe and extensive cases, rarely occurred, except in those cases in which a hemolytic streptococcus infection supervened.
Of the 47 cases in this group, 29 recovered; 14 by crisis, 15 by lysis. The average duration of illness from the onset of influenza until recovery from the pneumonia was ten days, the majority of these cases being relatively mild in character with pneumonia of three to six days’ duration. Empyema with ultimate recovery occurred in 1 of these cases, Pneumococcus Type II being the causative organism.
There were 18 fatal cases in the group. Nine of these are summarized in Table XVI as illustrative of the frequently complex character of bronchopneumonia following influenza and because of the interest attaching to the bacteriologic examinations made during life and at necropsy. Case 70 is a typical instance of the rapidly progressive type of confluent lobular pneumonia with extensive purulent bronchitis, intense cyanosis, and appearance of suffocation, with which pneumococci, in this case Pneumococcus IV, and B. influenzæ are commonly associated. Case 59 is illustrative of the small group of bronchopneumonias following influenza which die, often unexpectedly, after a long drawn out course, in this instance three weeks after onset. Examination of the sputum at the time the pneumonia began, showed Pneumococcus Type IV and B. influenzæ. At necropsy there was a lobular pneumonia with clustered small abscesses, probably due to a superimposed infection with S. aureus. There was a well-developed bronchiectasis in the left lower lobe. Cultures taken at autopsy showed a sterile heart’s blood, which is not infrequently the case in cases of pneumococcus lobular pneumonia after influenza. Cultures from the consolidated portions of the lung showed no growth, the pneumococcus having disappeared as might be expected from the duration of the case. B. influenzæ together with staphylococci were found in the bronchi. In Cases 50 and 56 a second attack of pneumonia caused by a different type of pneumococcus from that responsible for the first attack occurred, the second attack in both instances being due to contact infection with Pneumococcus Type II from a patient in a neighboring bed suffering with Pneumococcus Type II pneumonia. Both cases showed at necropsy the type of confluent lobular pneumonia so commonly found in pneumococcus pneumonias following influenza. Case 107 illustrates well the extent to which mixed infections may occur, especially when cases are treated in crowded hospital wards. The sputum at time of onset showed Pneumococcus IV in abundance and a few staphylococci. At necropsy there was a confluent lobular pneumonia with clustered abscesses, purulent bronchitis, and bronchiectasis in the left lower lobe. The heart’s blood was sterile, the lungs showed Pneumococcus Type III and staphylococci. B. influenzæ was not found, but through oversight, no cultures were taken from the bronchi. Cases 92, 99, 102, and 104 are all examples of superimposed hemolytic streptococcus infection occurring in the presence of a Pneumococcus Type IV pneumonia, with the picture of interstitial suppuration, abscess formation, and empyema due to S. hemolyticus on the background of a pneumococcus lobular pneumonia found at necropsy. All showed abundant pneumococci and B. influenzæ in the sputum and were free from hemolytic streptococci at time of onset of pneumonia, except Case 92 which showed 2 colonies of S. hemolyticus in the first sputum culture made. At time of death the pneumococci had disappeared in all cases and were replaced by hemolytic streptococci.
| Table XVI | |||||||
|---|---|---|---|---|---|---|---|
| Cases of Bronchopneumonia Following Influenza | |||||||
| CASE | ONSET OF INFLUENZA | ONSET OF PNEUMONIA | SPUTUM EXAMINATION | COURSE OF PNEUMONIA | NECROPSY | ||
| DATE | BACTERIOLOGY | DIAGNOSIS | BACTERIOLOGY | ||||
| 70 | Sept. 18 | Sept. 21 | Sept. 22 | B. inf. ++++ Pn. IV ++ | Diffuse bronchitis with rapidly progressive confluent bronchopneumonia. Died Sept. 24 | Nodular and diffuse confluent lobular pneumonia. Purulent bronchitis. Bronchiectasis | H.B. sterile Br. B. inf. ++++ Pn. IV ++ Lun. B.inf. +++ Pn. IV +++ |
| 59 | Sept. 13 | Sept. 18 | Sept. 19 | Pn. IV +++ B. inf. + | Bronchopneumonia with long drawn out course. Died Oct. 4 | Lobular pneumonia, with clustered abscesses. Bronchiectasis | H.B. sterile Br. B.inf. +++ Staph. ++ R.L. no growth. |
| 50 | Sept. 14 | Sept. 17 | Sept. 18 | Pn. IV +++ | Mild bronchopneumonia improving on Sept. 24. On Sept. 26 became suddenly worse and died on Sept. 30 | Nodular and confluent lobular pneumonia. Purulent bronchitis | H.B. sterile Br. B.inf. +++ Staph + R.L. Pn. II +++ B.inf. + L.U. Pn. II +++ |
| 56 | Sept. 10 | Sept. 17 | Sept. 18 | Pn. IIa +++ | Bronchopneumonia with recovery by crisis on Sept. 19. Developed a second attack of pneumonia and died Sept. 29 | Confluent lobular pneumonia | H.B. Pn. II Br. Pn. II +++ B.inf. ++ L.L. Pn. II +++ B.inf. + |
| 107 | Sept. 27 | Sept. 29 | Oct. 1 | Pn. IV +++ B. inf. + Staph. + | Diffuse bronchitis and severe bronchopneumonia. Died Oct. 5 | Confluent lobular pneumonia with clustered abscesses. Pur. bronchitis and bronchiectasis | H.B. sterile R.L. Pn. III ++ Staph. ++ L.L. Staph. ++ |
| 92 | Sept. 23 | Sept. 28 | Oct. 1 | B. inf. +++++ Pn. IV +++ S. hem. 2 col. | Severe bronchopneumonia with empyema. Died Oct. 5 | Lobular pneumonia. Empyema. Purulent bronchitis | H.B. S.hem. Br. B.inf. +++ S.hem. +++ R.L. S.hem. +++ B.inf. ++ Emp. S.hem. |
| 99 | Sept. 24 | Sept. 29 | Oct. 1 | B. inf. ++++ Pn. IV ++ S. vir. + | Diffuse purulent bronchitis with bronchopneumonia. Died Oct. 7 | Bronchopneumonia. Purulent bronchitis | H.B. S.hem. Br. B.inf. +++ Lun. S.hem. +++ S.hem. ++ B. inf. + |
| 102 | Sept. 24 | Sept. 28 | Oct. 1 | Pn. IIa +++ B. inf. ++ | Severe bronchopneumonia with empyema. Died Oct. 4 | Lobular pneumonia with interstitial suppuration. Pur. bronchitis. Empyema | H.B. S.hem. Br. B.inf. +++ S.hem. +++ R.L. S.hem. +++ |
| 104 | Sept. 26 | Oct. 1 | Oct. 1 | B. inf. ++++ Pn. IV +++ | Diffuse purulent bronchitis with severe bronchopneumonia. Developed streptococcus empyema. Died Oct. 11 | Nodular bronchopneumonia with interstitial suppuration. Pur. bronchitis and bronchiectasis. Empyema. | H.B. S.hem. R.L. S.hem. ++++ Emp S.hem. |
The cases cited in the preceding paragraph are illustrative examples from a series of over 250 necropsies which are described in another section of this report. They serve to indicate clearly the extent to which mixed and superimposed infections of the lungs may occur in pneumonia following influenza and leave little doubt that a considerable proportion of the deaths from influenzal pneumonia are due to this circumstance.
Hemolytic Streptococcus Pneumonia Following Influenza
But 4 cases of hemolytic streptococcus pneumonia directly following influenza without an intervening pneumococcus infection of the lungs occurred in the group of cases studied clinically. Superimposed infection with S. hemolyticus, however, occurred not infrequently during the course of pneumococcus pneumonia following influenza, as has been stated above. This occurred 3 times in lobar pneumonia and 10 times in bronchopneumonia, with fatal outcome in all but 1 case.
Bacteriology.—Bacteriologic examination of the sputum in the 4 cases of streptococcus pneumonia directly following influenza showed S. hemolyticus present in abundance. B. influenzæ was also present in large numbers in 3 cases, but was not found in the fourth. In 1 case a Gram-negative micrococcus resembling M. catarrhalis was also present in large numbers in the sputum. Pneumococci were not found either by direct culture on blood agar plates or by inoculation of the sputum intraperitoneally in white mice.
In the 13 cases of superimposed hemolytic streptococcus infection occurring during the course of pneumococcus pneumonia, bacteriologic examination of the sputum by direct culture and by mouse inoculation shortly after onset of the pneumonia showed Pneumococci (atypical II once, Type III once, Group IV eleven times) B. influenzæ present in large numbers, and no hemolytic streptococci except in 4 instances in which a very few organisms were present. Subsequent invasion of the lower respiratory tract by S. hemolyticus was shown to occur by means of cultures of empyema fluids or by cultures made at necropsy.