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Death from lobar pneumonia, bronchopneumonia and measles, fatal with few exceptions in consequence of complicating pneumonia, constituted in 1916 approximately one-sixth (16.8 per cent) of the mortality in the army,¹ whereas in 1917 the same diseases were responsible for nearly two-thirds (61.7 per cent) of all deaths. During the first half of 1918 the incidence of pneumonia steadily increased and in some army camps there were extensive outbreaks of unusually severe pneumonia.

In July, 1918, the Surgeon General assigned a group of medical officers to the study of the pneumonias prevalent in the army and stationed them at Camp Funston, Kansas. At the base hospital of this camp all cases of pneumonia occurring among troops assembled in the camp were studied, but during the month of August there were few cases of pneumonia and these were of mild type.

Pneumonia which occurred at Camp Funston during August was almost wholly limited to recently recruited colored troops from southern states (Louisiana, Mississippi). There was a low rate of mortality, and few complications. This pneumonia exhibited a noteworthy difference in etiology from that usually seen in civil life, for it was associated with a high incidence of those types of pneumococci which occur in the mouths of healthy men, namely, Pneumococcus atypical II,² Type III, and the group of microorganisms represented by Type IV. Pneumococcus Type I was encountered in only a few instances and Type II was not found, although these two microorganisms are responsible for two-thirds of the lobar pneumonia which occurs in civil life.

During the investigation at Camp Funston the Commission had the courteous cooperation of Major Willard Stone, Director of Medical Service, and received much valuable assistance from Lieutenant A. McGlory, Registrar of the Base Hospital.

A review of the accurately compiled records of the base hospital was made in order to obtain a history of the pneumonias and other respiratory diseases which had occurred throughout the existence of the camp, established in September, 1917. It soon became evident that a disease recognized as influenza had been prevalent throughout this period and its incidence had shown a close parallel with that of acute bronchitis. At the same time there had been much pneumonia and a high death rate from this disease. The chart³ which was constructed showed that the disease which had been designated influenza assumed epidemic proportions in March, 1918. Any doubt that may have been entertained concerning the nature of the disease is dispelled by the characters of this epidemic which, beginning at the end of February, reached its height on March 12 and rapidly subsided; 1,127 men with influenza entered the base hospital between March 4 and March 29 and many more were treated in the infirmaries of the camp. In April there was a second wave of influenza and in May a third, each in large part limited to newly drafted men brought into the camp shortly before these outbreaks. Corresponding to the epidemic of influenza there was a great increase of pneumonia, reaching a maximum about one week after the height of the incidence of influenza; subsequently the incidence of pneumonia increased after each one of the secondary waves of influenza. Pneumonia following measles occurred throughout the history of the camp; in November and December, 1917, there was a severe outbreak of pneumonia following measles and the mortality was high. Our conclusions in regard to the pneumonias which occurred during the history of Camp Funston were as follows:

1. Pneumonia of a relatively stationary camp population, such as that which occurred among white troops during the period of our investigation, was in considerable part caused by Pneumococcus Types I and II and resembled the pneumonia of civil life.

2. Pneumonia of newly drafted colored troops from southern states during the period of our investigation was caused in great part by pneumococci of those types which occur in the mouths of healthy men, namely, Types IV, III and atypical II.

3. Pneumonia caused by influenza occurred after the epidemic of influenza which we have described. The report states: “With the information available it is not possible to draw a sharp line between (1) the pneumonia of the stable camp population, (2) the pneumonia of the newly drafted southern troops, and (3) the pneumonia following influenza. It is possible that influenza, in greater or less degree, also acts as a predisposing factor in the production of the first and second varieties.”

4. Pneumonia with measles was a frequent and unusually fatal type of the disease. The most important causes of pneumonia during the history of the camp were influenza and measles.

Evidence is not lacking that influenza occurred in epidemic form in other widely separated camps in the United States during the spring of 1918. Vaughan and Palmer⁴ state that a disease strongly resembling influenza became prevalent in the Oglethorpe camps about March 18, 1918, and continued three weeks; during this time the number sent to hospital or to quarters with this disease was 1,468 in a total strength of 28,586. Pneumonia does not appear to have followed this epidemic.

Miller and Lusk⁵ found the ordinary type of pneumonia prevalent at Camp Dodge, Iowa, until March 18 to 20, 1918, when abruptly the streptococcus type predominated and there was a great increase in the rate of mortality. A mild tracheitis, they state, was widespread in the camp during March.

In March, 1918, one member of our commission saw an outbreak of influenza at Fort Sam Houston which was identical in its clinical characters with the disease which appeared as a pandemic in the fall of 1918.

The report of the Surgeon General⁶ for 1919 shows that there was a sharp increase of the incidence of influenza in the army during March, reaching a maximum in April. The rate of influenza for 1,000 troops fell to its original level through May and June and finally rose to a great height in September and October.

Influenza in epidemic form made its appearance in the army camps of the United States during March, 1918. The symptomatology of the disease associated with its peculiar epidemiology as seen at Camp Funston make its recognition unquestionable. The disease had doubtless been present in this camp since its establishment in September, 1917, but did not assume epidemic proportions until the spring of 1919.

Pneumonia followed the epidemics of influenza which occurred in the spring of 1918 and exhibited characters similar to those of the pneumonias which followed the pandemic of September and October, 1918. In both instances the height of the outbreak of pneumonia has been one week after the maximum incidence of influenza.

Influenza became epidemic in Spain about the middle of May and in other countries received the name “Spanish influenza” which is not more applicable than the designation “Russian influenza” often applied to the disease during the pandemic of 1889–90.

The studies of MacNeal⁷ have shown that the first epidemic of influenza in the American Expeditionary Force in France occurred about April 15, 1918, at a rest camp near Bordeaux, reached its height on April 22 and ceased May 5. The disease was of a mild character with few complications. Localized epidemics were reported from various camps and hospitals during May and June, when the disease, MacNeal states, had become widespread in all sections of the American Expeditionary Force in France and in the French and British armies as well. Influenza had become epidemic in the Italian navy in the first two weeks of May. The belief that the disease was introduced from America, the author thinks, is “probably completely disproved by the fact that the epidemic was subsequently introduced into America in August and September and found there a most fertile soil for its spread.” This view is disproved by the demonstration that influenza had appeared as scattered epidemics in the army camps in March, 1918. There is little reason to doubt that influenza in the American Expeditionary Force was brought from America.

At the end of August our commission was transferred from Camp Funston to Camp Pike, where throughout the history of the encampment pneumonia had been so prevalent that it had given the camp the rank of third in death rate from lobar pneumonia and fourth in death rate from bronchopneumonia among 32 camps established in this country. We arrived at Camp Pike September 5 and were stationed at the base hospital. Our work was facilitated by the hearty cooperation of the commanding officer, Major Morton R. Gibbons, who neglected no opportunity to promote the investigation. Our work was cordially aided by Major Carl R. Comstock, Director of the Medical Service, and by Major Henry H. Lissner, who later occupied this position. Work in the laboratory of the hospital received the valuable cooperation of Major Allen J. Smith, Director of the Laboratory, who placed at our disposal every facility available. Lieutenant James R. Davis, who was for a time in charge of the laboratory, effectively assisted the work.

The commission consisted of the following officers: E. L. Opie, Colonel, M. R. C.; Allen W. Freeman, Major, M. C.; Francis G. Blake, Major, M. R. C., James C. Small, Lieutenant, M. C. and Thomas M. Rivers, Lieutenant, M. C. Major Freeman acted as epidemiologist and will publish a report upon the epidemiology of influenza and pneumonia at Camp Pike. On October 11 the laboratory car “Lister” in charge of Lieutenant Warren H. Butz was assigned to the commission. Lieutenant Harry D. Bailey was attached to the commission on October 14 and later assisted in its work. Valuable technical assistance was given by Sergeant Charles Behre, by Wm. E. Hoy, detailed from the Army Medical Museum, and by Thomas Payne.

Study of the pathology of the lesions concerned was completed in the Pathological Laboratory of Washington University School of Medicine.

The existence of an epidemic of influenza at Camp Pike was recognized on September 23, when 214 cases of influenza were admitted to the base hospital. Preceding this date and beginning September 1 there had been a gradual increase of the number of patients admitted with the diagnosis of acute bronchitis. It is noteworthy that the demonstration of B. influenzæ had been regarded as essential for a diagnosis of influenza and since this microorganism had not been found, instances of acute inflammation of the respiratory passages with the symptoms of influenza were classified under a variety of names.

After September 23 influenza was recognized by its symptoms. The number of cases increased with great rapidity and on September 27 reached over 1,000 per day; this number was approximately maintained during one week and after October 3 the epidemic gradually subsided. Among 52,551 men in the camp, including those who arrived during October, 12,393 were attacked by influenza; of these 1,499 suffered with pneumonia and 466 died. The height of the outbreak of pneumonia followed approximately one week after that of influenza. The statistics from September 20 to October 14 collected by Major Freeman show that pneumonia following influenza, like the pneumonia at Camp Funston during the interepidemic period, has a conspicuous tendency to select men who have been in the camp less than one month, designated in Table I as new recruits:

Table I
	POPULATION	INFLUENZA	PNEUMONIA
No.	Per cent.	No.	Per cent.
Men in camp more than one month	27,782	4,462	15.6	493	1.7
New recruits	23,769	7,263	30.6	1006	4.2
Total	51,551	11,725	22.7	1499	2.9

New recruits were nearly two and a half times as susceptible to pneumonia as men who had been in camp more than one month. This statement does not take into consideration differences in the environment and mode of living of the new men.

In view of the existing uncertainty concerning the bacteriology of influenza and its associated pneumonias, the commission has availed itself of the opportunity afforded by the epidemic of influenza to determine what bacteria were present in the nasopharynx and sputum in these diseases. The examinations have been necessarily limited to a small proportion of the immense number of patients admitted to the hospital with influenza and pneumonia. Autopsies on those who have died with pneumonia have offered a more direct means of determining the relation of bacteria to inflammation of the bronchi and lungs. An attempt has been made to classify the pneumonias following influenza and to determine their relation to the complex bacterial flora of the injured respiratory passages. These studies have shown very early the threatening prevalence of streptococcus pneumonia, and appropriate measures have been taken to combat the spread of this infection. No better illustration could be furnished to demonstrate the value of routine performance of autopsies as a means for the recognition of obscure epidemic disease.

In view of the wide difference of opinion concerning the pathology of influenzal pneumonia special study has been given to the lesions of the disease, because the epidemic has furnished the unique opportunity of examining all instances of pneumonia accurately referable to an epidemic of influenza attacking a large but definitely defined group of individuals (50,000 troops). In a civil hospital there is often great difficulty in deciding, even in the presence of an epidemic, if death from pneumonia is the result of influenza, but at Camp Pike the relation of the heightened death rate to the epidemic has excluded all save a trivial error in determining the relation of fatal pneumonia to influenza.

At the direction of Col. F. F. Russell, who has promoted the work of the commission by unfailing aid, a special study has been made of the relation of hemolytic streptococcus to the complications of measles.

During the later period of the investigation at Camp Pike experiments were performed on monkeys to determine the pathogenicity of B. influenzæ and of microorganism isolated from the pneumonias following influenza. Typical lobar pneumonia was produced in monkeys by intratracheal injection of pneumococci. These experiments are described in an appendix.

The Surgeon General has approved the publication of this report but the authors alone are responsible for the views expressed.

Eugene L. Opie.

Washington University

School of Medicine