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The opportunity presented for a correlated study of the clinical features, bacteriology, and pathology of pneumonia following influenza throughout the period of the epidemic at Camp Pike from September 6, 1918, to December 15, 1918, made it evident that this pneumonia could be regarded as an entity in only one respect, namely, that influenza was the predisposing cause. Clinically, bacteriologically, and pathologically it presented a very diversified picture ranging all the way from pneumococcus lobar pneumonia to hemolytic streptococcus interstitial and suppurative pneumonia with the picture modified to a varying extent by the preceding or concomitant influenzal infection.

One hundred and eleven consecutive cases in which careful clinical and bacteriologic studies were made form the basis of the material presented. Of these cases, 38 came to necropsy so that ample opportunity was presented to correlate the clinical and bacteriologic studies made during life with the pathology and bacteriology at necropsy. It has seemed advisable to group the cases primarily on an etiologic basis with secondary division according to clinical features in so far as this can be done. Bacteriologic studies showed that at the time of onset these pneumonias were either pneumococcus pneumonias or mixed pneumococcus and influenza bacillus pneumonias in nearly all instances. Certain of these cases later became complicated by a superimposed hemolytic streptococcus or a staphylococcus infection. In a few instances hemolytic streptococcus pneumonia directly followed influenza without an intervening pneumococcus infection. B. influenzæ was present in varying numbers in nearly all cases. In only 2 instances however, was it found unassociated with pneumococci or hemolytic streptococci, once alone and once with S. viridans.

Clinically the cases fell into four main groups: (1) Lobar pneumonia; (2) lobar pneumonia with purulent bronchitis; (3) bronchopneumonia (pneumococcus); (4) bronchopneumonia (streptococcus). It should be borne in mind, however, that the picture was a complex one and that correct clinical interpretation was not always possible, since many cases did not conform sharply to any one type and superimposed infections during the course of the disease often modified the picture.

Pneumococcus Pneumonia Following Influenza.—Bacteriologic examination of selected and washed specimens of sputum coughed from the lungs at time of onset of pneumonia showed the various immunologic types of pneumococcus to be present in 105 cases. The incidence of the different types is shown in Table XIV.

Table XIV
Types of Pneumococcus in 105 Cases of Pneumococcus Pneumonia Following Influenza
	LOBAR PNEUMONIA	BRONCHOPNEUMONIA	TOTAL	PER CENT
Pneumococcus, Type I	8	0	8	7.6
Pneumococcus, Type II	3	1	4	3.8
Pneumococcus, II atyp.	12	7	9	18.1
Pneumococcus, Type III	3	3	6	5.7
Pneumococcus, Group IV	32	36	68	64.8

The most noteworthy feature of the figures in Table XIV is the high proportion of pneumonias due to types of pneumococci found in the mouths of normal individuals, 93 cases or 88.6 per cent, being caused by Pneumococcus Types II atypical, III, and IV. This is in harmony with the results generally reported and is in all probability due to the fact that in patients with influenza pneumococci, which under normal conditions would fail to cause pneumonia, readily gain access to the respiratory tract and produce the disease. It is also of interest that with one exception the highly parasitic pneumococci of Types I and II were associated with pneumonias clinically lobar in type.

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.

(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.