Part 15

That the meningococcus should be classed in this group is certain. The author observed at Camp Sevier cases of epidemic meningitis occurring in various influenza wards scattered throughout the hospital, with no demonstrable relationship. Usually there was but one case in a ward and almost invariably meningitis occurred when convalescence was beginning. No epidemic occurred in any ward. Others have reported actual epidemics of meningitis following influenza. Moss found that a large proportion of his influenza cases had the meningococcus in the circulating blood, as demonstrated by culture. Fletcher cultivated meningococci from the lungs in all of eleven autopsies, and in all eleven cases the influenza bacillus was also present.

In considering the effect of influenza on the death rate in general, and in considering the relationship of influenza to other diseases in general, it is important to distinguish those diseases which are apparently unrelated and those diseases which occur as direct complications or sequelae. Bronchopneumonia, bronchitis, empyema, otitis media, frequently tonsillitis and sometimes erysipelas, occur as sequelae. Meningitis should frequently be included in this group.

Not only is there an increase in certain other diseases following influenza outbreaks, genetically related, as we have seen, but also some observers, particularly Crookshank, believe that previous to epidemic influenza prevalences there occurs an increase in the incidence of other entirely unrelated infectious diseases, such as poliomyelitis. This theory of simultaneous increase in invasiveness of many apparently unrelated germs is comparatively new and will probably receive deep consideration in the future. For the present the information on the subject is so limited that attempted conclusions would have no value.

ORIGIN OF THE 1918 PANDEMIC.

In discussing the spread of the 1918 pandemic over the earth, the author has traced it from an apparent origin in the United States. Localized early epidemics are reported simultaneously in the United States, France, and China. From the literature at his disposal he has been unable to find convincing proof of an earlier origin in Asia, but he did emphasize at the time the necessity of a much more thorough study of influenza in all countries to be made by more competent statisticians. Nevertheless it is highly interesting to formulate an hypothesis which appears to meet all demands, on the assumption that the disease originated in America. In order to hold a theory with this basis we must assume that the third of our previously mentioned hypotheses of the origin of the disease is the more nearly correct.

Let us assume that in the interpandemic periods the influenza virus is widely distributed over the earth, existing in an avirulent form. The basis for this assumption is the previously described occurrence of localized epidemics in interpandemic periods. The occurrence of solitary cases, although of interest, could scarcely be considered as evidence of the widespread distribution of the virus, but in the case of the small outbreaks as in 1900, 1907 and 1915, and as in the numerous small outbreaks described by Hirsch, the character of the epidemic curve is characteristic. Let us, then, assume that the disease has been endemic in the United States, together with other localities. It requires no keen observation to discover in the years 1917 and 1918, Theobald Smith’s “movement of individuals and masses from one part of the world to another, whereby the partly adapted parasites become planted, as it were, into new soil, and the original equilibrium is disturbed.” Not only was there a tremendous redistribution and concentration of individuals in our camps in this country, but also there was a further disturbance of the equilibrium in the outbreak of other infectious diseases, particularly measles. The effect of the measles epidemic on the virulence of the streptococcus and allied organisms has been discussed; presumably the same occurred with respect to the influenza virus. Howard and Love report that approximately 40,512 cases of influenza were reported in the United States Army during 1917. They write:

“In 1917, the death rate for the acute respiratory diseases (influenza, pneumonias and the common types) increased to 1.71. During the fall of 1917, after the camps were filled with drafted men, acute epidemic diseases swept through a number of them. Measles was one of the most prevalent and one of the most fatal of the infectious diseases that occurred. It was noted during the fall and early winter that there were a number of cases of pneumonia which were unlike the pneumonia that ordinarily occurred. This was apparent both to the physicians in civil life and in the army camps. It was reported by all classes of practitioners that numerous cases of pneumonia were occurring which resembled the pneumonia following measles, but occurring among men who had not had measles recently. In a number of the camps, both in the north and in the south, rather extensive epidemics of pneumonia occurred and a number of deaths resulted. The same variety of pneumonia occurred in the late winter and spring of 1918. In many of the camps pneumonia was practically epidemic during March and April. In many camps a number of cases occurred later in the spring and summer. It was again reported by a number of medical men that these cases of pneumonia that were occurring were different from the types of pneumonia ordinarily encountered and very similar to pneumonia following measles, but, again, that the cases occurred among men who had not had measles recently.”

MacNeal has observed similar conditions in the American Expeditionary Forces in France in 1917:

“The American troops in France in 1917 began to show, as early as October, 1917, a very considerable rise in the influenza morbidity. The data available in the office of the Chief Surgeon, A. E. F., show an influenza morbidity per 100,000 of 321 in July, 438 in August, and 404 in September, rising to 1,050 in October, 1,980 in November, and 2,480 in December, 1917, in which month the total number of new cases of influenza reported was 3,520. That a considerable proportion of these cases were actual infections with the bacillus of Pfeiffer is proven by the necropsy findings in fatal cases of bronchitis and bronchopneumonia, especially those performed by Major H. E. Robertson at Army Laboratory No. 1, Neufchateau, in November and December, 1917, and January, 1918. In these cases the bacillus of Pfeiffer was found in the scattered patches of lung involved in the bronchopneumonia and also with great frequency in the cranial sinuses. These necropsy findings were, at the time, recognized as essentially new for young adult Americans, and, in a discussion at Army Laboratory No. 1, during December, 1917, they were considered as being of possible important significance for the future morbidity of American soldiers in France. In the British Army in France there is definite evidence of epidemics showing the same pathologic condition, during the winter of 1916–17, and at Aldershot in September, 1917. There can be little, if any doubt that this disease was essentially the same which attacked the American soldiers late in 1917.”

Schittenhelm and Schlecht have reported that a disease was studied among the German troops on the Eastern front which resembled greatly the influenza. It occurred from the beginning of August to the middle of October, 1917. It attacked simultaneously and in epidemic form units and divisions very widely separated over a large territory. It was characterized clinically by a very sudden onset, in the greater number of cases with chill, headache, pain in the extremities, sometimes thoracic pain and cough. The fever lasted seven to nine days. The spleen was enlarged in 11 per cent. of the individuals. There was diarrhea in 12 per cent., frequently conjunctivitis, and quite often a scarlatiniform rash. Bacteriologic examination of the blood was negative. There was usually leucopenia. No treatment seemed especially efficacious. Aspirin gave the best results. The authors call attention to the close similarity to influenza and also suggest that it might have been due to transmission by insects as in pappataci fever or in dengue.

Carnwath concluded that the finding of influenza bacilli in necropsies in British soldiers in 1917 was without epidemiologic significance in considering the origin of the 1918 pandemic. He had studied the disease among the British in detail and appeared to be of the opinion that the first influenza morbidity of significance among the British troops did not appear previous to April, 1918.

MacNeal further says: “The influenza rates per 100,000 of 1,050 in November and 2,480 in December, 1917, really indicate a greater relative prevalence of influenza at that time in the A. E. F. than occurred in the fall of 1918, when the respective morbidity rates were 826 in September, 2,176 in October, and 1,356 in November. The total number of American troops in France was relatively small during that winter—141,995 effective mean strength in December—so that the prevalence of influenza did not lead to the recognition of an actual epidemic. Furthermore, the overcrowding in quarters, which seems to have had a definite relation to many of the later explosive outbreaks, had not become such a distinct feature at that time. In addition, the cold, wet weather, exposure and unusual living conditions furnished explanations for the morbidity which were no longer adequate during the hot weather of May and June, 1918. Until May, 1918, therefore, the prevalence was that of an endemic disease, with perhaps an occasional outbreak suggesting epidemic character.”

We admit that MacNeal’s report furnishes excellent evidence of an independent origin in France. Two points should be borne in mind. First, that MacNeal’s figures are not for the French, but for the Americans who were transported to that country, and that we may consequently consider influenza among the American Expeditionary Forces as being possibly from the same source as influenza among the troops in our own country,—that the American Expeditionary Forces may be considered a subdivision of the American Army in the United States, equally well as a subdivision of the French population; second, that we have been unable to find detailed evidence of similar conditions occurring among the French troops or French population, where the conditions have been ripe in a way since 1914. MacNeal records that in March and April, 1918, there was a great increase in the number of troops brought over from the United States to France. Previous to that time there had been 287,000 in that country and during the two months 150,000 were added, with a consequent increase of more than fifty per cent.

We should insert a word of caution regarding the diagnosis of influenza among troops in the absence of any sign of an epidemic. Internists who served in base hospitals during the war will agree that a diagnosis of influenza is very frequently made on the admission card when the disease turns out to be some other malady. This was not equally true in all camps, but regimental surgeons could often be found who would transfer a patient to the hospital with the diagnosis of influenza used almost interchangeably with the diagnosis “Fever of unknown origin.” It would be interesting to see statistics from one or two of those base hospitals which were manned with especially competent internists, as to the frequency with which the admission diagnosis of influenza remained unchallenged in the hospital, during the year 1917.

There would be such cases in greater or smaller numbers. The magnitude of this number would not influence our hypothesis.

Aside from this discussion of the disease among our troops in France it is most important that we establish, if possible, the identity of the disease reported among British troops in Northern France during the winter of 1916–1917 and designated by the name “Purulent Bronchitis.” The disease first appeared in December, 1916. It reached its height during February and early March of 1917, and appears to have disappeared early in the spring. Hammond, Rolland and Shore report that during February and early March 45 per cent. of the necropsies under observation showed the presence of purulent bronchitis, and they remarked that the disease assumed such proportions as to constitute almost a small epidemic. They described the clinical aspects as follows:

“The cases which came under our notice can be divided broadly into two types: The first and more acute presents a clinical picture which closely simulates ordinary lobar pneumonia with a sustained temperature of about 103°, and expectoration at first blood-streaked—rather than rusty—which, however, rapidly becomes quite purulent. The pulse-rate in these cases is out of all proportion to the temperature in its rapidity. Dyspnoea and cyanosis are prominent features. The patient usually dies from ‘lung block,’ resulting in embarrassment of the right side of the heart on the fifth or sixth day. For the last day or two there is often incontinence of the feces, due, no doubt, to the condition of partial asphyxia. The mental state is one of torpor; delirium is the exception.

“The second and less acute type is marked by a more swinging temperature with a range of two or three degrees. The expectoration at first may be frothy and mucopurulent, but it very soon assumes the typically purulent character. This form may run a long course of from three to six weeks, during which time the patient wastes a great deal and has frequent and profuse sweats; indeed, at a certain stage the illness is most suggestive of acute tubercular infection, and it is only by repeated examination of the expectoration that the clinician can satisfy himself he is not really over-looking a case of acute pulmonary tuberculosis. The majority of our cases conforming to this type have ultimately recovered, but the convalescence is slow and tedious.

“Onset.—Whilst a history of a previous catarrhal condition lasting for a few days is often obtained, the disease quickly assumes an acute character; we have been able to observe this in patients admitted into this hospital with purulent bronchitis; we find the temperature is between 102° and 103°, the pulse 120 or over, and the respiration about 35. The patient frequently complains of shivering and looks pathetically miserable, but we have not seen an actual rigor. Despite his obvious shortness of breath, the sisters have noticed that, at any rate at first, he prefers a lateral position low down in the bed, and resents any attempt to prop him up.

“Cough.—This for the first day or two may be irritable and distressing, with a little frothy expectoration, but as the latter becomes more purulent the cough is less troublesome, and soon the patient is expectorating easily and frequently, until the later stages are reached; when owing to increasing asphyxia the patient becomes more and more torpid, the cough subsides, and hardly any secretion is brought up. This failure becomes an added factor in bringing about a rapidly fatal termination.

“Expectoration.—The sputum, with its yellowish-green purulent masses, is very characteristic, and may be one of the first indications of the serious nature of the illness the patient is suffering from.

“Temperature.—The fever of this complaint does not follow any very constant type. In nearly all our cases the pyrexia was of sudden onset, and for the first few days was more or less sustained at about 103°. Later it conformed more to the swinging type with a range of several degrees. In a few cases a curious gradual ante mortem drop has been observed.

“Pulse.—Tachycardia is a very constant feature throughout the illness. The rate is frequently well over 120, though the volume may remain surprisingly good until immediately before death.

“Some degree of dyspnoea is always present, and is usually progressive, though towards the end in the fatal cases when the mental acuteness is dulled by the increasing asphyxia the patient is not distressed by its presence. In some cases there have been paroxysmal exacerbations of the breathlessness, accompanied by a state of panic, in which the patient struggles wildly and tries to get out of bed in order to gain relief. Cyanosis is another prominent feature throughout the illness. At first it may not be more than duskiness, but in the later stages it becomes very evident. It is only slightly relieved by oxygen; this, no doubt, is partly explained by the difficulty in giving the oxygen efficiently, owing to the patient’s objection to any mouthpiece that fits at all tightly, and partly by the blocked condition of the bronchioles interfering with the absorption of the oxygen.

“The condition usually begins with the presence of a moderate number of sharp crepitant râles, often first heard in the region of the root of the lung; these quickly become generalized. In the majority of the cases signs of bronchopneumonia patches can be made out; these are generally situated near the root of the lungs. In a certain number of cases these patches spread and become confluent, giving practically all of the physical signs of a lobar pneumonia. As the disease progresses the air entry is diminished; on listening one is often struck by the small volume of sound heard. The resonance of the lungs may also be lessened. A slight pleuritic rub was heard in a few of our cases, but this was soon masked by the bronchitis signs.”

Detailed sputum examination in twenty cases showed the presence of the influenza bacillus in eighteen, and in ten out of these eighteen the organism was isolated by culture. The next most frequent organism found was the pneumococcus, which was present in thirteen cases. The streptococcus was found in five.

Abrahams, Hallows, Eyre and French report the same epidemic:

“A typical case is as follows. The onset is usually acute; the early symptoms are those of a ‘cold in the head.’ The temperature may be 101 or 102°, but there are no features to distinguish the condition from acute ‘coryza’ or febricula, so that in the majority of cases the patient does not report sick for two or three days, by which time he is sent to the hospital. At this state two features attract particular attention. First, the character of the expectoration: this consists of thick pale yellow, almost pure pus, not the frothy expectoration familiar in ordinary bronchitis; it has no particular odor and it becomes increasingly abundant until in a day or two it may amount to several ounces in the twenty-four hours. Secondly, the rapidity of the patient’s breathing: this may be so evident that pneumonia suggests itself, yet on examining the chest the only physical signs consist of few or many rhonchi scattered widely, but most marked at the bases of the lungs behind, associated with a wheezy vesicular murmur; resonance everywhere is unimpaired and bronchial breathing is absent. A little later a third point attracts notice; a peculiar dusky heliotrope type of cyanosis of the face, lips, and ears, so characteristic as to hall-mark the nature of the patient’s malady even on superficial inspection. By this time dyspnoea is very pronounced; respiration consists of short, shallow movements, which in bad cases amount almost to gasps, reminiscent of the effects of gas poisoning. Recovery at this stage may occur, but by the time the cyanosis has become at all pronounced the prognosis is extremely bad, though the number of days the patient may still live, in spite of the severity of his distress, is often surprising. The character of the sputum remains the same throughout, though sometimes it is blood-tinged or actual blood may be expectorated instead of, or in addition to, the more typical pale yellow pus. In the later stages of the illness areas of impaired note or of actual dullness may be found, particularly over the posterior aspects of the lungs, associated with bronchial breathing and crepitant râles. These may be due to the progression of the purulent bronchitis into hypostatic pneumonia, or into actual bronchopneumonia at the bases; or, on the other hand, they may be due to massive collapse of the lungs secondary to the bronchitis and obstruction of the bronchioles by pus. In a few cases, not necessarily the most serious, a frank lobar pneumonia has developed later, and has been followed by an empyema from which 15–30 ounces of thin pneumococcal pus has been aspirated—in one case alone was resection of a rib unavoidable. The condition, however, is not primarily a lobar or a bronchopneumonia, but a bronchitis, and although a small amount of basal bronchopneumonia has been present in one or two of our post-mortem examinations, in other fatal cases there has been no bronchopneumonia at all, not even the smallest portions of either lung being found to sink in water.

“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.

Case 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.