SECTION II. (continued 3)

“We have no doubt that the condition is primarily an affection of the bronchi and bronchioles, and not of the alveoli, though the alveoli may be affected later if the patient survives long enough. In a typical post-mortem examination it would be difficult, or almost impossible, to define the actual cause of death unless one knew the clinical history.”

Abrahams and his collaborators describe in detail eight consecutive cases. A study of the type of onset may be of help in determining the character of the disease. The first patient had been subject to bronchitis for years. He had been ill with cough and some pyrexia for five days previous to his admission. There is no further description of his admission symptoms. Case two was admitted on March 17th, having taken ill the previous day with shivering, cold and pain in the chest. The temperature was 104°, the pulse-rate 118, and the respirations were 44. The patient was very restless and had much dyspnoea but was not cyanosed. The third patient had taken ill three days previous to admission with symptoms of cold in the head and a sore throat. He complained of headache and dry cough without expectoration, shortness of breath, and a pain behind the sternum.

124Case four was admitted with a history of having been out of sorts with a cold and bronchial cough for ten days previously. On admission his temperature was 103°, pulse-rate 112 and respiration-rate 36. He had abundant blood-stained purulent sputum.

Case five is the first case that shows a type of onset distinctly resembling that of influenza. The patient had been ill three days with headache, cough and generalized pain previous to his admission. The temperature on admission to the hospital was 103°, pulse-rate 112, respiration-rate 20. There were no abnormal physical signs in the chest on admission. They did appear two days later. Case six related that he had been sleeping under canvas for three nights before coming to the hospital, and that during the first of these nights he was taken ill with a cold which became associated with a cough and increasing shortness of breath. On admission there was slight cyanosis, and dyspnoea was very pronounced. Shortly afterwards he became orthopnoeic, with heliotrope cyanosis. On the slightest exertion, such as turning over in bed, the cyanosis increased markedly, and although the respiration-rate remained under forty when he was at rest, on the least exertion it increased to nearly sixty. The sputum was purulent and abundant, pale yellow, not frothy and not blood-stained, and the day after admission contained Bacillus influenzae, pneumococcus and Micrococcus catarrhalis.

Case seven had been ill seven days before admission with cough and fever. On admission his temperature was 105°, pulse 116, respiration 24. Case eight gave a history of having had a cough for eight days previous to admission. This cough had not incapacitated him much at first, but he became progressively worse during the four days before admission, with increasing shortness of breath and abundant yellow sputum which he found it difficult to raise. On admission dyspnoea with cyanosis was very evident.

Even from these detailed clinical descriptions it is impossible to say definitely whether the disease was or was not influenza. There is no doubt, however, but that clinically the disease resembled more the so-called streptococcus pneumonias that were observed in the United States camps in the winter of 1917–18. The descriptions of the mode of onset are particularly at variance with the onset as we know it in influenza.

Those who believe that the influenza bacillus is the cause of influenza maintain that the finding of this organism in a large per cent. of cases by both groups of observers is valuable evidence. For reasons previously stated we cannot agree.

125Description of the epidemic features is not detailed enough to be of assistance. The first group of authors remark that the disease constituted “almost a small epidemic.” The second group say that six out of eight cases in their series of candidly reported patients came from one command. The former report on twenty cases, the latter on eight. The latter remark that although they have dealt with only eight cases in detail, they had a much larger number altogether. Presumably there were a decidedly larger number of patients in both hospitals, but the actual number is not stated. In short, we do not know whether the disease appeared to be more or less epidemic than the apparently similar disease among our troops in the winter of 1917–18.

Both groups of observers have described in some detail the pathology of the cases which were necropsied. The author in attempting to obtain further comparative information has submitted the pathologic descriptions given by the British authors to Dr. E. W. Goodpasture, who has very kindly pointed out the points of similarity and difference between the gross and microscopic findings in these cases of purulent bronchitis, and the same findings in typical influenza. He says that the lung picture, as described, is not the same as that which was typical of the acute influenza observed in the autumn of 1918 and again in the winter of 1920. The characteristic picture in the latter is primarily an extensive involvement of the alveolar structure, while as Abrahams and his associates remarked, the condition in their case is primarily “an affection of the bronchi and bronchioles, and not of the alveoli, though the alveoli may be affected later, if the patient survives long enough.” Goodpasture states that the pathology as described by the British authors is very similar to the lung picture in interstitial bronchopneumonia described by MacCallum for the post-measles and primary bronchopneumonia among our troops in the winter of 1917–18. The streptococcus and the influenza bacillus were dominant organisms in MacCallum’s series. It also resembles the pathologic picture described by Pfeiffer in his original article on one of the late recurrences of the 1889–93 epidemics of influenza.

In summing up, we must admit that it is impossible to reach a definite conclusion, but that both clinically and pathologically the disease described among the British troops in 1916 and 1917 was not typical of influenza as we have known it more recently. The similar conclusion reached by Carnwath, presumably chiefly from epidemiologic considerations, has already been described. We do not deny that this “purulent bronchitis” may have been influenza. On the 126contrary, it is a part of our hypothesis that influenza under the proper conditions may become epidemic in practically any land. But we do believe that the evidence has not shown that the disease among the British troops in 1916 and 1917 was an etiologic precursor of the great pandemic.

To return to a discussion of influenza in China, we quote from an article by Cadbury in the China Medical Journal: “Unfortunately no health reports are available for the greater part of the Chinese Republic. We have consulted, however, the Health Reports of the Shanghai Municipal Council from 1898 to 1917, and among the total foreign deaths we find that only the following were attributed to influenza: 1899, one death; 1900, one death; 1907, four deaths; 1910, one death. After this no deaths are recorded from this cause up to and including the year 1917.

“In the Hongkong Medical and Sanitary Reports, which give the total deaths registered in the Colony, we have examined the records from 1909 to 1917. During these nine years only two deaths were attributed to influenza, and both occurred in 1909.

“From a personal letter from Dr. Arthur Stanley, Health Officer in Shanghai, dated February 11, 1919, I quote the following:

“‘As to influenza we had an attack beginning at the end of May and lasting through June and again in the latter part of October and lasting through November. The latter was somewhat more severe. The noteworthy features were general absence of catarrhal symptoms, congestive pharynx frequent, as also was a slight erythematous blush on the neck and chest, which made one think at first of scarlet fever. Fatal pneumonia common among the Chinese and Japanese, but among Europeans very little pneumonia.’

“In his report for May, 1918, Dr. Stanley says that the disease was reported to have reached Peking before it came to Shanghai, but subsequent reports showed that most of the river ports were almost simultaneously infected, the rate of spread conforming to the rate of conveyance by railways and boats of infected persons. The mortality was very low.

“Newspaper reports indicate that a third appearance of the disease in Shanghai occurred from the middle of February, 1919, which was still prevalent in April. The symptoms were much more severe.

“For Hongkong I quote from a personal letter from Dr. Hickling, the Principal Medical Officer of Health, dated January 29, 1919:

“‘The epidemic of influenza in the spring was a very mild one, so far as we can judge. The disease did not last more than a few days in 127most cases. The recent epidemic (October, November, December and January) has been much more severe, often lasting two or three weeks.’

“Only one death, which occurred on May 14th, was reported from Hongkong in the spring. In the later epidemic the deaths reported were as follows: October, 70; November, 95; December, 67. The first of these deaths occurred on October 5th. The figures for January had not been compiled, but the disease was diminishing.

“Dr. C. W. McKenny of Hongkong has kindly furnished me with the following facts: ‘During the first five months of 1918 there were twenty-two admissions for influenza to the Civil and Tung Wa hospitals (3 in May). In June there were 269 cases with three deaths. In July, August and September, 43 cases; and during October-November, 130 cases with four deaths....

“‘The June epidemic in Canton appeared first at the Pui Ying School, then among the employees of the Post Office, the staff of the Canton Hospital, the Canton Christian College, and the Kung Yee Hospital. The other schools entirely escaped. Eleven days were taken by the disease to spread from one part of the city to the various other parts.’”

Plague appeared in the north of China in 1917, originating apparently in inner Mongolia. The spread extended over quite an area, and it is reported that this epidemic of pneumonic plague has been more extensive than any since that of 1910–11. The disease was first reported prevalent in Patsebolong December 6, 1917. The diagnosis was confirmed bacteriologically, and there can be little doubt but that the cases of plague reported in various parts of China even up to March 18th were true plague, and not unrecognized influenza.