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Chapter II

Contents

CHAPTER II
 
IN THE AMERICAN EXPEDITIONARY FORCES a
 
In the spring of 1918 reports appeared of an epidemic disease in various parts of southern France, Italy, and Spain. By midsummer this disease had spread widely throughout Europe, and in the autumn had involved South Africa and America. Were it not for the epidemiologic evidence it would have been difficult to characterize the disease as a clinical entity.

In the majority of cases, the onset of the disease was sudden, particularly in the warmer season. Epistaxis was an early manifestation in a considerable proportion of cases. In some outbreaks, particularly those in the fall months, a slight sore throat or a feeling of cold in the head, and in some instances a distinctly localized burning sensation in the nasopharynx was noticed 12 to 24 hours before the fever became evident. The first symptoms, although in most instances severe enough to fix the moment of onset in the patient's mind, were, so mild as a rule, that soldiers did not report sick unless especially ordered to do so. The morale of the average soldier was such that he hesitated to go to sick call, regarding it as a confession of weakness or perhaps an indication that he desired to shirk. While this attitude is, in general, to be commended, and was undoubtedly encouraged by medical officers, it was a distinct source of danger in the presence of the epidemic.

Prostration was marked in some cases and a few men fainted while awaiting examination at sick call, and many of those performing physical labor found it impossible to continue. The pharyngeal mucous membrane was slightly reddened and rather dry; the nose was remarkably clear and unobstructed; the conjuctivae were injected. The patient complained of headache, pain in the back, weakness, pain and tenderness in the eyeballs, and sometimes of a burning in the nasopharynx or a slight sore throat. Leucocytosis was usually absent in uncomplicated cases, but appeared along with the bronchopneumonia. Leucopenia was observed early in the disease.

In a series of 125 cases, coryza was noticed by half the patients, but a dark red, dry mucous membrane was found in 90 out of 100 cases. Sore throat was complained of by 37 percent, a dry red pharynx with swollen lymphoid tissue on the lateral wall was present in 80 percent. Epistaxis occurred in 35 percent. The eyes were injected, perhaps somewhat more so than in most fevers. The neck was somewhat stiff in 12 percent., but this stiffness was never marked. Herpes was observed in 17 percent. Careful examination failed to reveal any distinctive rash. Among the 125 cases definite signs of bronchopneumonia on admission were present in 40 percent. There were a few cases of catarrhal otitis media, usually with considerable pain for a few hours, but without enough exudate to bulge the drum. This series may be regarded as fairly typical of the disease as it occurred in France about October 1, 1918. The respiratory symp-

aBased on: The Influenza Epidemic of 1918 in the American Expeditionary Forces in France and England. By Maj. Ward J. MacNeal, M. C., commanding officer, Central Medical Department Laboratory, Dijon. Archives of Internal Medicine, Chicago, 1919, xxiii, No. 6, 657.


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toms were less well marked in the cases seen in the early months, May, June, and July, and in them cough, otitis media and signs of bronchopneumonia were rare.

Course and outcome
.- In the early months, May, June, and July, rest in bed and a purgative were followed by subsidence of the fever and amelioration of all symptoms in 24 to 72 hours, and prompt recovery without further mainfestations, except slight weakness and depression. Complications were so rare as to be considered nonexistent and the relatively few cases of pneumonia observed were subsequently regarded as instances of mistaken initial diagnosis. In the later months, from about the beginning of September, the disease was perhaps less sudden in onset, but the course was distinctly more malignant and a complicating fatal bronchopneumonia became alarmingly frequent; so frequent, indeed, as to suggest a new epidemic of an entirely different disease.

In the more severe cases, distinct evidence of tracheobronchitis and bronchopneumonia appeared, sometimes within the first 48 hours, but usually at the end of the third or fourth day. In many instances the temperature fell nearly or quite to normal on the third day, only to rise again along with the gradual appearance of physical signs of extension of the inflammation in the finer bronchi and alveoli of the lungs. This complication was observed particularly in patients who failed to go to bed promptly at the onset of the disease, in those who got out of bed before they should, and in those patients who were transported during the febrile period. Pleural effusion occurred in some cases; empyema occurred rarely. Unconsciousness for some hours before death, with considerable extension of the thoracic dullness in the last 48 hours, were commonly observed in the fatal cases. When the patient recovered, the fever fell by lysis after 6 to 12 days.

The death rate in patients with pneumonia was high, varying from 5 to 100 percent. The bulk of these deaths resulted from the bronchopneumonia of the influenza epidemic. In the series of 125 cases there were 18 deaths, or 14.4 percent of the cases of influenza. Inasmuch as 40 percent of these patients showed bronchopneumonia on admission, the maximum death rate of the pneumonia cases was 18 in 50, or 36.0 percent. Doubtless many others in the series also developed pneumonia in the hospital, so that the death rate for the pneumonia in the series may be placed at 14.4 percent as a minimum and 36 percent as a maximum.

Another series of cases evidently originated on the transports during voyage from the United States. In this series there were 4 cases of lobar pneumonia, 1 of them primary and 3 secondary to influenza, with 1 death; 156 cases of bronchopneumonia, of which 1 was primary, 148 cases secondary to influenza, and 7 secondary to bronchitis, with 52 deaths. Pleural fluid was found in 13 cases. It was clear in nine cases and turbid in four cases. Bloody sputum was observed in 118 cases. Twenty-two cases of pneumonia developed in the wards, 20 from influenza and 1 from bronchitis. There were 268 cases of influenza at the same time, of which 246 were respiratory; 1 was nervous; 9 were gastrointestinal; and 12 were febrile. Ear complications and sinus involvement were uncommon. Bacteriologic examinations showed the presence of the influenza


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bacillus and of pneumococci in almost every case. Hemolytic streptococci were not found. The death rate in the pneumonia was 32 percent.

Without regard to the bacteriologic findings or questions of etiology the disease is certainly properly designated as influenza on the basis of its epidemic and clinical characters alone.
 
PATHOLOGIC ANATOMY

In the early months of the epidemic the disease was so benign in character that deaths which did occur were invariably ascribed to other cause. After August 15, 1918, deaths became much more frequent and the records of necropsy in this disease were very numerous. From the clinical evidence it appeared that the bulk of the necropsy records were based on complicated cases. The pathology of these later cases is discussed first.

The respiratory organs
.- The larynx, trachea, and larger bronchi showed swelling, edema, injection and infiltration of the mucous membrane, which was covered by frothy mucopurulent, often blood-stained exudate. The smaller bronchi and bronchioles also were involved in the same process and some of them were plugged with mucus. As a rule, all lobes of both lungs were involved; both lungs were large, dark, heavy, and firm. On section, the cut surfaces were very moist, dripping a bloody, frothy fluid; the color was somewhat variegated, often showing a few firmer grayish patches of older consolidation centrally located. Invariably the lower lobes were more severely involved. The whole process in the lungs might be designated as an example of a massive, pseudolobar form of bronchopneumonia of a very malignant type. Considerable variation in the appearance of the lungs occurred even in the same series. Some prosectors were able to distinguish a type showing more or less fibrinous pneumonia and a type in which this was not present and to foretell from the gross appearance the bacteriologic demonstration of pneumococci in the former. In some instances gross evidence of hemolysis indicated the presence of hemolytic streptococci which was subsequently confirmed.

Necropsies on individuals dying of influenza pneumonia revealed the following characteristics: (1) Frequency of an associated hemorrhagic tracheobronchitis; (2) extensive though irregular involvement of multiple lobes in massive areas of lobular pneumonia consolidation; (3) frequent existence of a much older focus of central pneumonia near the hilus of one or both lower lobes; (4) evidence of an explosive-like spread of the pneumonic process from this central focus to large areas of the adjacent lung parenchyma within the last day or few days before death; (5) relative infrequency of suppuration, empyema being found only in two cases.

Serous cavities
.-In many instances the pleural surfaces were fairly normal or only slightly dulled in luster; in others, a slight increase in clear fluid, with or without a tinge of hemoglobin, was noted; in from 5 to 30 percent, varying in different series, a large pleural effusion was present, usually serous, but sometimes serofibrinous or purulent; in 10 to 20 percent a plastic fibrinous exudate existed on the pleural surfaces. In short, the conditions within the pleural cavities were exceedingly diverse. Pericardial effusion and pericarditis were observed in a few instances. When large volumes of fluid were found in the chest, the changes in the lungs were less advanced and less extensive than usual.


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Subcutaneous emphysema
.- This was observed in comparatively few cases in several different outbreaks. It began in the supraclavicular region or over the anterior chest wall, and became more or less generalized over the surface of the body. It did not appear to affect the outcome of the case. A post-mortem study of several such cases failed to reveal bacteria in the majority of the cases. Mechanical obstruction of small bronchi by plugs of mucopus and subsequent solution of continuity in the structure of the lung is the probable explanation of its pathogenesis.

Rectus abdominis
.- In a very few instances lesions of the rectus muscles were found. In some cases a necrosis resembling Zenker's necrosis, in others hemorrhages into the muscle were present.

Cranial sinuses
.- The first wave of the epidemic in May and June did not have any recognized cases of sinus or aural complications, and as there were few if any deaths from influenza at this time no opportunity presented itself to prove the absence of sinus involvement by necropsy. Clinical evidence of such involvement was entirely lacking. In the latter phases of the epidemic, sinus and aural complications occasionally were encountered.

Other organs
.- The changes in other organs were those of acute toxemia, manifested particularly in the kidneys, liver, and spleen. Icterus, apparently of hemolytic origin, was observed in a few instances.

PATHOLOGY OF PARTICULAR CASES

In some instances clinical histories permit a determination of the exact duration of the disease before death occurred. Significant features of a few necropsies on such cases follow:

Necropsy 1: Patient had a slight cold on Saturday, October 5, but took dinner with friends on that date. He was admitted to the hospital at 6 p.m. on October 7 in a dying condition; died October 8 at 8.30 a.m. Duration of illness was therefore about 60 hours. Pleural cavities contain a few cubic centimeters of cloudy fluid. There are no adhesions. Both lungs are of the size of full inspiration. There is practically no exudate on either pleural surface. The upper two thirds of the upper lobe, the apex of the middle lobe and scattered patches throughout the lower lobe of the right lung contain solid bluish-red areas, which have ill-defined margins. On section these areas are dark red in color and comparatively airless, the surfaces being bathed with a very large amount of bloody fluid. The remaining portions of the lungs are heavy with congestion and edema, except for a few areas anteriorly, which are dilated and feathery. The bronchi of both lungs are deep red in color, bathed with abundant blood-stained frothy mucus and covered with a thin,
closely adherent, grayish-yellow, fibrinous pseudomembrane. The peribronchial lymph nodes are not markedly swollen. The sinuses at the base of the skull show some thickening of the mucosa and a small amount of mucoid fluid in the left sphenoid and left frontal. Smears and cultures from the lungs show streptococci and Gram-negative bacilli. Smears from the frontal sinus show staphylococci Gram-negative bacilli and a short Gram-positive bacillus; cultures from the same place show staphylococci.

Necropsy 2: Patient was admitted to hospital October 16, 1918, with a diagnosis of acute influenza; temperature, 103 º F.; pulse, 116; respiration, 24. October 17, the temperature rose to 104 º F.; pulse, 104; respiration, 30. The temperature remained above 104 º F.; at times reaching 105 º F.; respirations increased to 50, but the pulse rate did not rise above 104 until the day of his death, when it reached 120. Death occurred October 20, 1918, at 11.30 p.m., four days after admission.


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The pleural cavities each contain about 10 c.c. of clear serum. The parietal pleura is speckled thinly with petechial hemorrhages on both sides, and small tags of fibrin hang from it. The areolar tissues of the anterior mediastinum are moderately infiltrated with glistening, gelatinous material. The posterior and apical portions of the right pleural cavity are obliterated by very firm fibrous adhesions. The apical and posterior surfaces of the right lung are covered with fibrous tags and the pleura is thickened and rough. At the apex of the right upper lobe the pleura is puckered and thickened, and on section the thickened pleura at this point measures 4 mm.; it is whitish in color, very dense and resistant and fibrous in character. Beneath this, the cut surface of the apical portion of the right upper lobe is made up of irregular grayish-yellow areas, all coalescing, and separated here and there by fibrous strands. The middle and lower lobes are large, heavy, and dark; their pleural surface has the appearance of pavement, the lines being formed by distended lymph channels. The cut surface is very dark, moist, and compact; the lobes are entirely consolidated, but the consolidation is peculiar in that it is made up of coalescing patches of bronchopneumonia massed together. From the atypical appearance one is led to think of a mixed infection. The left lung is in the same condition, except the anterior portion of the upper lobe, the cut surface of which is markedly hyperemic and has, scattered in it, some dark red patches similar in appearance but much larger than the patches ordinarily seen in typical bronchopneumonia. The mucosa of the trachea and bronchi is very hyperemic and bathed in an abundance of thin, frothy fluid. The tracheobronchial lymph nodes are moderately enlarged, unusually moist and slightly bloody. The tissues of the posterior mediastinum are slightly infiltrated with glistening jelly-like material.

Necropsy 3: Patient entered hospital September 12, 1918, having been in France one week. He had been sick since landing and had been riding in a baggage car for several days. He died September 12 at 11.50 p.m. The necropsy was performed at 3.25 p.m., September 13. The mediastinum is well covered with fat, the right visceral pleura hemorrhagic and injected and covered with fibrinous deposits. The pericardial cavity contains about 70 c.c. of a straw-colored fluid. The left lung weighs 1 pound 1 ½ ounces and shows irregular consolidated areas. The right lung weighs 2 pounds 12 ½ounces. The left lung floats in water; on section it shows irregular consolidated areas from which frothy mucus exudes. The lobular type is more evident to the sense of touch than of sight. The entire right lung floats in water as do portions from the most nearly consolidated portions. Bronchi are red and inflamed. Cultures from the brain and from the heart blood are negative; cultures from the right lung show B. influenzae and Streptococcus viridans.

Necropsy 4: Patient entered hospital October 8, 1918, from a newly arrived transport. He died at 4 a.m. October 15. Necropsy was performed at 9.30 a.m., October 15. Pericardial cavity contains about 10 c.c. of a clear yellow fluid. There are numerous hemorrhages on the left side of the pericardium. The right lung is adherent posteriorly and the right pleural cavity contains about 300 c.c. of a cloudy yellow fluid. The lower half of the pleura is covered with a thick layer of yellow fibrinous exudate. The left pleura is slightly adherent at the base posteriorly and is also covered with fibrinous exudate. The right lung has four lobes, the fourth being a very small one at the apex. This is firm and on section is gray and consolidated throughout. The main upper lobe is collapsed and contains some nodules. Its surface is dull, granular, and varying in color from light pink to bluish-red. Centrally located there is a nodule of gray consolidation the size of a hen's egg. Around the periphery the lung is well aerated and for the most part of a light pink color. The cut bronchi exude thick yellow pus. The middle lobe is well aerated, light pink in color and shows a few hemorrhagic areas. Pus exudes from the cut bronchi in this lobe also. The lower lobe is a gray consolidated mass of friable tissue and on pressure exudes thick pus. In the left lung the upper, middle, and anterior portions of the lower lobe are aerated. Surfaces of the upper and middle lobes are of a dark red color; on palpation small nodules are felt throughout. The posterior half of the lower lobe is consolidated and nodules may be felt. The larger nodules in the upper lobe are gray and exude pus everywhere when squeezed. For the most part, the tissue is spongy, light pink to deep red and quite friable. At the periphery and at the base there is a dark red consolidation from which a considerable amount of pus exudes. Bacteriology: B. influenzae, pneumococcus, and a Gram-positive bacillus.


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These four abbreviated protocols are fairly typical examples of the records of many hundreds of cases coming to necropsy in September, October, and November, 1928, and indicate the diversity of picture observed within the thorax. These differences appear to have depended essentially on the rapidity with which the patient succumbed. The fulminant cases showed a picture of malignant coalescing bronchopneumonia which rapidly involved almost all the pulmonary tissue. The more chronic cases showed distinct foci of older gray consolidation; usually multiple with recent more extensive, even general, spread of the pneumonic process.
 
BACTERIOLOGY

The bacteriologic examinations made during life on sputum or material from the pharynx showed various organisms, usually mixed together. The interest in many instances centered on the Pfeiffer's bacillus and reports in regard to it showed the very widest variations. Cultures made on blood-agar or on hemoglobin-agar revealed, in the large majority of cases, pneumococci, streptococci, influenza bacilli, staphylococci and Gram-negative cocci. Blood cultures taken during life were usually negative, but in a moderate proportion of the cases showed pneumococci or streptococci. Fluids obtained by puncture from the pleural cavity or from the lung tissue showed the same organisms and at times the influenza bacillus. In certain localitites enormous numbers of Gram-negative cocci, identified as meningococci, were found in the sputum during life and in the lungs at necropsy in a certain number of cases. Attempts to detect a filterable virus have been reported, but experiments of this kind were not carried out in the American Expeditionary Forces.

At necropsy, also, the bacteriologic findings were variable and usually showed a mixture of various species of microbes. Influenza bacilli, pneumococci of various types, hemolytic and nonhemolytic streptococci occurred most frequently in the infiltrated lungs. Post-mortem blood cultures showed B. influenzae in a few instances, pneumococci and streptococci in a considerable number of cases. Cultures taken from the cut surface of the lung at necropsy in one series of necropsies during September, 1918, showed influenza bacilli in 40 percent of the cases, hemolytic streptococci in 30 percent, and pneumococci in 40 percent, Group IV, Type I, Type II, and Type III in order of frequency. In many cases, two or more of these organisms were isolated from the same tissue. More significant, perhaps, were those necropsies in which a more thorough bacteriologic survey of the respiratory tree was carried out by culturing in turn the mucous membranes of the trachea, large and small bronchi, and alveolar tissue. In fulminant cases, large numbers of influenza bacilli were found, especially in the trachea and bronchi, sometimes apparently in pure culture. In most instances, however, the mucous membrane of the respiratory tract showed a mixture of organisms; in the trachea, influenza bacilli, streptococci, staphylococci, pneumococci, Gram-negative cocci and occasionally larger Gram-negative bacilli; farther down, influenza bacilli, pneumococci, and streptococci; still lower, influenza bacilli, and one species of the cocci, and finally in the consolidated alveolar tissue, the pneumococcus or the streptococcus alone, as a rule, but sometimes mixed together or even associated with the influenza bacillus in this tissue.


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These findings suggest that the disease was essentially due to an invasion of the respiratory tract by influenza bacilli, followed by and associated with other pharyngeal organisms, and that the fatal outcome, in most instances, was brought particularly by these secondary invaders, in some instances streptococci, in others pneumococci.

The reports from some hospitals indicate that the important secondary infections were due to pneumococci, but in those instances in which type determination was carried out, the strains usually fell into three or four type groups, a considerable proportion of them belonging to Group IV. In other hospitals streptococci were found to be the important secondary invaders. The explanation of these results is not entirely clear. It is possible that the distinction between pneumococcus and streptococcus was not always accurately made, and that there was a tendency in one place to call all these organisms pneumococci and in another to call them streptococci. These reports suggest, however, that the secondary invaders may have spread from patient to patient, possibly within the hospital wards. In certain series of necropsies, where considerable attention was devoted to the identification of the cocci in the lungs, these invaders were found to be quite variable, even in bodies coming from the same hospital ward, indicating that their specific nature depended on the type of organisms which happened to be present in the upper respiratory tract of the man at the time of his illness, rather than on contagion.

The identity of the summer epidemic with the disease prevailing after September 1 may be called into question, particularly because of the benign character of the earlier outbreaks and the high death rate observed later. In the later months bronchitis and bronchopneumonia were very common, while such involvement was extremely rare in the summer. In favor of the essential identity may be mentioned the similar epidemic character of the outbreaks, the clinical resemblance between the milder autumn cases and those of the summer, the rather clear evidence indicating a gradual increase in malignancy and the similar bacteriologic findings during life. Most convincing, perhaps, was the similar epidemic character, which alone almost suffices to prove the essential unity of causation for the disease in the two seasons. Medical officers who observed the disease in both seasons were inclined to the view that the primary disease was essentially the same, with the secondary complication of bronchopneumonia in the colder weather. The unfavorable influence of cold and exposure is universally recognized in relation to this disease.

In its epidemiologic, clinical, bacteriologic, and pathologic features, the disease is everywhere recognized as being identical with influenza as it was observed in the pandemic of 1889-90. The bacterial findings are those of influenza. In the American Expeditionary Forces, the bacillus of Pfeiffer was demonstrated in a very large percentage of the cases properly examined; in several series it was demonstrated in every case. The other bacteria isolated; namely, strep- tococci, pneumococci, Gram-negative cocci, although undoubtedly the cause of death in many cases, can be excluded from consideration as the primary cause of the epidemic disease, because of the inconstancy with which any one specific type was encountered. The possible causative relation of the bacillus of Pfeiffer can not be similarly excluded. On the other hand, the causative relationship


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of this organism can not be accepted as proven. During this epidemic, as during previous epidemics of influenza, a considerable proportion of throats of persons not suffering from the disease were found to harbor this organism, or organisms indistinguishable from it by the methods employed.

In a series of 35 selected cases of epidemic influenza without signs of bronchopneumonia, cultures of swabs from the nasopharynx showed streptococcus in 57 percent, pneumococcus in 74 percent, and influenza bacillus in 46 percent. In a second group of 15 cases diagnosed clinically as bronchopneumonia, cultures of the sputum revealed hemolytic streptococcus in 33 percent, pneumococcus in 87 percent, and influenza bacillus in 87 percent. Only one of these patients died and in his case pneumococcus and hemolytic streptococcus were present in the lung at necropsy. In four cases the sputum was inoculated into mice and pneumococcus of Group IV and the inflaenza bacillus were recovered from the animal's peritoneum and heart blood. In a third group of 22 meningitis contacts, nasopharyngeal cultures showed influenza bacilli in 48 percent.

One report under date of September 5, 1918, contained the records of nasopharyngeal cultures from 106 cases of influenza, of which 46.2 percent showed the influenza bacillus and 20.7 per cent showed streptococci. In a series of 12 normal individuals, direct contacts of these cases, the influenza bacillus was found in 41.6 percent and the streptococcus in 25 percent. A series of 42 normal individuals, not contacts, examined in the same way, showed influenza bacillus in 7 percent, and streptococcus in 10 percent.

The essential similarity in the anatomic changes observed in the later epidemic and in these earlier cases warrants the quotation of the important parts of a few of the protocols of early cases.

Necropsy 5: The patient enlisted August 12, 1917. He had had a cold for the past few weeks but was not admitted to hospital until October 24, 1917, with symptoms of prostration, dyspnea, fever, cough and marked evidence of general sepsis. Pneumococcus (Group IV) was isolated from the sputum by mouse inoculation. The man died October 26 at 11.55 p.m. At the necropsy the left lung was found expanded to full inspiration; the surfaces were smooth, at the inner anterior margin of the upper lobe were several firm areas, the largest about the size of a walnut, grayish to bluish in color, with distinct puckering of the surrounding pleural surfaces. A few similar areas were located at the outer posterior margin of the lower lobe. Scattered throughout the pulp were smaller foci of increased consistence. Remaining portions of the lung were light, feathery, particularly the lingula. On section the firm areas had moist grayish surfaces and were comparatively airless. From the cut bronchioles purulent fluid escaped on pressure. The bronchial mucosa was bathed by a mucopurulent frothy liquid and was distinctly reddened and swollen. Peribronchial lymph nodes were markedly swollen, soft and red. There was no evidence of tuberculosis. The larynx and trachea showed the mucosa congested, especially near the bifurcation of the trachea, and covered by a frothy, mucopurulent exudate; the lymph nodes at the bifurcation were very greatly swollen, reddened and friable. The middle ears and mastoids were normal; the sphenoidal air cells were full of thick, yellow fluid and the mucosa was swollen and congested. The posterior ethmoidal cells contained some thin yellowish fluid, while the anterior cells were apparently free; the mucosa in both groups was distinctly thickened. Bacteriologic examination showed B. influenza and Gram-positive diplococci in sphenoidal sinus, in the lungs and in the liver.
  
Necropsy 6: The patient was admitted to hospital February 7, 1918, complaining of severe cold, with cough, which began three days before; also pains in his joints and sore throat. February 13 a fine papular eruption appeared, especially over the chest and abdomen. At this time his temperature was 102º F., pulse and respiration rapid. Harsh rȃles were


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heard at the base of the right lung and fine moist rhles in the lower lobe of the left lung. Death occurred February 13, 1918, 11.35 p.m. Necropsy, February 14, at 9.30 a.m.: The pleural cavities were free from abnormal fluid; the left visceral and parietal pleurae were bound together by fresh fibrinous adhesions, uniformly distributed over the lower lobe. The right pleural cavity presented numerous firm fibrous adhesions over the surface of the middle and lower lobes, especially at the base. The left lung was rather voluminous; the upper lobe was grayish in color and air-containing; the lower lobe was of darker hue, mottled with reddish-purple. The pleura here and there was covered with a yellowish, shaggy, friable exudate. Beneath these areas and also scattered in the deeper areas of the lung tissue were rather firm airless areas. The bronchial mucous membrane was intensely swollen and covered with mucopurulent secretion; this condition was seen likewise in the bronchioles. The pulmonary vessels showed no thrombi; the bronchial lymph nodes were swollen and friable. On section there were found, scattered throughout the lower lobe, corresponding for the most part with the bronchioles, areas varying in size from a pea to a walnut. In color they varied from gray to purple; were firm and quite friable. The lung tissue in the immediate neighborhood showed intense congestion. In the right lung, the upper lobe was grayish in color and air-containing; the middle and lower lobes were voluminous, dark red in color. The pleura was rough and showed numerous fibrous tags. In all other respects it resembled the left lung. The tracheal mucosa was intensely swollen and covered with an abundant muco- purulent exudate. The middle ears were normal; the mucosa of the posterior and anterior ethmoids was slightly swollen and moist; no purulent exudate was present; the frontal sinuses were normal. Bacteriologic examination of the ethmoidal sinuses by both smear and culture was negative.

Necropsy 7: The patient was admitted to hospital March 13, 1918, having had a cough since March 6. On admission, he had severe headache, shortness of breath, pain in the right side, with temperature of 102.4 º F., pulse 120, dullness over both lower lobes and moist rAles everywhere. Pneumococcus, Type II, was isolated from the sputum. Death occurred March 20, 1918, at 3 a.m. Necropsy at 9 a.m. same date: Pleural surfaces were everywhere smooth and there was no abnormal fluid. In the lower lobes of both lungs, there were numerous small, grayish, consolidated areas, corresponding with the terminal bronchioles, which were considerably swollen. The lung tissue everywhere was intensely congested and of a deep red color. The lymph nodes at the bifurcation were swollen, soft, and red. Culture from the heart was sterile; cultures from the lung showed pneumococci and influenza bacilli.

Necropsy 8: The patient was admitted to hospital April 5, 1918, with a diagnosis of measles. April 8, he developed signs of diffuse bronchitis, with marked dyspnea and cyanosis; the white blood cells numbered 8,400; the sputum showed chiefly B. influenza. Death occurred April 13, 1918, at 1.30 p.m. Necropsy April 13, at 4 p.m.: The pleural cavities were free, without exudate or adhesions; the fluid was not increased. The right lung weighed 660 grams. Externally all three lobes were irregularly mottled, with raised grayish margins and depressed dark brownish centers. On section the same characteristic mottling was seen throughout all lobes. Interspersed between the grayish aerated tissue, from which a bloody froth exuded, were dark red firm areas of consolidation, the latter being found especially near the hilum. The bronchi were filled with a greenish purulent material. The left lung weighed 630 grams, and was identical in appearance with the right. Bacteriologic examination of pus from the right and left bronchi showed pure culture of B. influenza.
  
The records of these necropsies indicate very clearly the prevalence of influenzal bronchopneumonia.