Recognition of Influenza
Influenza is not easily differentiated from other acute respiratory infections when the disease is not epidemic, and for this reason in studying influenza, distinctions must not be drawn too finely between the types of cases occurring during epidemics, and the types reported as influenza before and after epidemics. A sudden onset with malaise and weakness, leading in a few hours to prostration out of proportion to the other clinical manifestations; the prominence of headache, particularly the so-called post-orbital headache; muscular pains, sharp rise in temperature to 101 or 102 degrees of even higher, and leukopenia, appear to be the principal guides to recognition of the true case of influenza, pending agreement as to the value of bacteriological findings or the discovery of a micro?ganism which can be agreed upon as the causative agent of the disease.
Studies of cases occurring in various outbreaks of influenza in the Navy during this pandemic show a remarkable similarity in the clinical characteristics of the disease all over the world. Inasmuch as epidemics varied considerably in duration and intensity it is not surprising that there was also considerable variation in the proportion of uncomplicated cases, both mild and severe, to the complicated severe cases. Mild, uncomplicated cases occurred everywhere, even when epidemics were at their peaks, and such cases appear to have had the same characteristics wherever they occurred, before, during, and after the primary epidemic. At the majority of naval stations, as well as on board ship, a certain number of cases occurred which were clinically very severe from the moment of onset and terminated fatally, sometimes in less than 36 hours. These cases occurred principally at the height of an epidemic; were uncommon previous to September 1, 1918, and were not often seen after the passing of the primary epidemic.
The outstanding feature of the pandemic was the frequency with which secondary pneumonia of the bronchial type developed. This
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complication was the cause of death in practically all fatal cases of influenza.
The clinical course in cases complicated by pneumonia varied considerably at each place or hospital. Pneumonia developed early, almost immediately in some cases; in others only after several days of influenza or after a remission, and in some instances after convalescence had apparently begun.
With due allowance for the fact that a hemolytic streptococcus was associated with most or all cases of complicating pneumonia in one place, whereas a pneumococcus predominated in another place, it may be said that there was a remarkable similarity in the cases complicated with pneumonia as well as in ordinary uncomplicated cases of influenza wherever they occurred, not only in all parts of the United States but in England, France, the West Indies, South America, and the Orient. That is, the general picture of influenzal pneumonia was the same all over the world.
In practically all cases of complicating pneumonia a hemolytic streptococcus, a pneumococcus, the Pfeiffer bacillus, or a combination of these micro?rganisms seemed to play a part in causing the pneumonic lesions. However, it is generally agreed that the pneumonia cases were sufficiently characteristic to stand out as a type different from cases of ordinary pneumonia seen in recent years and more or less different too from the types of broncho-pneumonia which so frequently complicated measles in 1917 and early in 1918.
From various reports, with reference to clinical and post-mortem findings and with regard to statistical data for various stations and ships in many parts of the world, it appears that of 1,000 cases of influenza from 30 to 40 terminated fatally; from 10 to 30 in some places and as many as 90 or more under unusual circumstances. As a rule, from 100 to 200 cases in a thousand had pneumonia complications with definite clinical manifestations. Such cases averaged, perhaps, 150 per 1,000 cases of influenza. A small number of these patients lived only a day or two, and the exact nature of the infection micro?rganisms and the immunological conditions involved in such cases are still unknown. In many of the fatal cases of pneumonia a secondary invader, a pneumonococcus or streptococcus, or both, seemed to play an important if not the paramount r?le in causing death. In some cases the Pfeiffer bacillus was present in the tissues and in cells in great numbers and appeared to be responsible for the pneumonia, inasmuch as it was recovered in pure culture.
The causes of death other than pneumonia were few. Cerebrospinal fever was a not uncommon concomitant infection or sequela at several training stations and in a few ships.
Besides broncho-pneumonia, the following complications were noted:
Pulmonary edema.
Pulmonary hemorrhage.
Empyema.
Emphysema.
Edema of the glottis.
Acute myocarditis.
Acute endocarditis.
Acute pericarditis.
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Acute nephritis.
Acute pyelitis.
Septic embolism.
Brain abscess.
Hemiplegia.
Toxic psychosis.
Acute neuritis.
Acute hepatitis.
Acute cholangitis.
Acute cholecystitis.
Liver abscess.
Acute enteritis.
Hiccough.
Splenic abscess.
Acute periostitis.
Epistaxis.
Acute mastoiditis.
Suppurative cervical adenitis.
Sinusitis.
Acute phlebitis.
Pneumothorax with subcutaneous emphysema.
Pneumococcus cerebro-spinal meningitis.
Pfeiffer bacillus cerebro-spinal meningitis.
Acute encephalitis with multiple abscesses of the brain.
During the calendar year, 1918, the cause of death in 4,155 fatal cases of influenza was assigned as follows:
Influenza (uncomplicated or complication unrecognized) 931
Pneumonia, bronchial 2,432
Pneumonia, lobar 730
Abscess of kidney 1
Acute dilation of the heart 2
Pulmonary edema 1
Embolism 1
Meningitis, cerebro-spinal 25
Acute nephritis 5
Pleurisy, serofibrinous 2
Pleurisy, suppurative 17
Sinusitis 1
Septicemia 5
Hydropneumothorax 1
Erysipelas 1
Total 4,155
Of the cases of influenza in which complications did not develop--800 to 875 in a thousand, and probably more than 900 is some instances if the truth could be known--the majority were ordinary cases of influenza, similar to the grippe cases of ordinary times. In some of the uncomplicated cases the patient appeared to be very ill for three or four days. On the other hand, there were always numerous mild attacks which either did not prevent the performance of usual tasks or necessitated confinement to bed or quarters for only one, two, or three days. The frequency with which very mild cases were seen leads to the belief that a great many persons were attacked by the disease in such mild form that it was not recognized even as an acute minor respiratory affection.
It is not improbable that approximately 40 per cent of the total naval personnel actually became infected at some time or other in 1918, which would correspond to the figure accepted for the incidence in civilian populations during the 1889-90 pandemic.
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Influenzal pneumonia.--Some of the cases were very similar in onset to acute lobar pneumonia, and a good many cases were so diagnosed, particularly early in the epidemic. In some instances even the post mortem findings simulated those of acute lobar pneumonia. The more thoroughly cases were studied the less did it appear that the lesions of influenzal pneumonia were ever those of a true lobar pneumonia.
In most cases the onset of pneumonia was not abrupt, and the pulmonary complication developed so unobtrusively that it was likely to be overlooked without careful and repeated physical examinations. Frequently the temperature, respiration rate, and character of the sputum suggested the presence of pneumonia when it could not be found with the stethoscope. A rising white count was also significant. In some instances the pneumonic complication developed within the first 24 hours, but in the great majority of cases not until after 48 hours, and frequently not until after a remission on the third of fourth day. Several observers noted that broncho-pneumonia of some degree could be considered to exist if there was not a cessation of influenza symptoms by the sixth day.
After full development, the distinguishing features of influenzal pneumonia were extreme toxicity, rapid respiration becoming very marked upon the least exertion, early appearance of cyanosis of the lips, ears and finger tips extending to the body before death; a frequent paucity of physical signs in comparison with the obviously critical condition of the patient, pulmonary edema, and abundant watery bloodstained sputum or thin rusty muco-purulent sputum. Of course, in many cases there were physical signs of extensive involvement of the lungs.
The appearance of the patient; his bluish or purplish lips, cyanosis of the ears, ashen cyanosis of the face or blue mixed with red when there was congestion, drooping eyelids, and the "air hunger" which often seemed due more to toxemia and to changes in the blood than to lack of proper aeration in the lungs, made an unforgettable picture in cases where medical treatment was practically without avail.
Many of the cases were regarded as mixed infections and clinically many were septicemias. In the majority of instances blood cultures were negative, but in some streptococci or pneumococci were obtained from the blood during life. Rarely, the Pfeiffer bacillus was found in blood culture.
Not all cases of influenzal pneumonia presented the picture described above. Indeed, reports from various naval hospitals denote considerable variation in clinical manifestations as well as in post-mortem findings at each place during the epidemic, but this was the picture in many of the cases, especially at the height of the epidemic when influenza seemed to be more highly communicable than before or after and when influenzal pneumonia was more prone to occur. It would not do to compare the pneumonia cases occurring at one place early in the epidemic with those occurring later at another place. Pleurisy of some degree complicated the great majority of pneumonia cases at all stages of the epidemic, but there were very few empyemas until after the epidemic had passed, even in patients living as long as 14 days.
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Physical signs in the chest varied extremely from those strongly suggestive of frank lobar pneumonia to a few subcrepitant r?les only, elicited with difficultly, or no signs whatever. Collections of fluid, emphysematous areas, collapsed areas, extravasations, filled or obstructed small bronchi, confluent areas of consolidation, alterations of the blood and possibly acute toxic neuritis of the vagus and peripheral nerves of the thorax accounted for diverse physical findings. Frequently neither a diagnosis nor prognosis could be based upon physical findings.
Cases of fatal septicemia were reported in which there was no consolidation in the lungs, although there was intense congestion with extensive bronchitis. The bronchioles and alveoli were filled with a fluid resembling hemolyzed blood. Blood cultures in certain groups of such cases gave pure growths of a green-producing streptococcus which sometimes hemolyzed and sometimes did not. This micro?rganism also grew as a diplococcus at times and was difficult to distinguish from Type IV pneumococci.
Some observers reported cases of hemorrhagic septicemia without lung involvement other than hemorrhages or extravasations in which a pneumococcus was thought to be responsible. It is possible that this micro?rganism was really a streptococcus of the type just mentioned.
Morbid anatomy.--At the United States Naval Hospital, Chelsea, Mass., post-mortem study of 23 cases at the height of the epidemic which began in Boston August 27, 1918, showed the Pfeiffer bacillus present in the lungs in pure or mixed culture in 19 cases and in the other 4 a hemolytic streptococcus was present in pure culture. The Pfeiffer bacillus was present alone in 6 of the 23 cases. At the United States Naval Hospital, Philadelphia, lung punctures made in 31 cases during life showed the presence of the Pfeiffer bacillus, predominating or mixed with "strepto-pneumococcus," or with M. cararrhalis and other common micro?rganisms in 15 cases.
The post-mortem findings in the chest with respect to the amount and character of fluid found in the pleural cavities varied considerably. Pleuritis of some degree occurred in the great majority of all cases of influenzal pneumonia. Thoracentesis was frequently and repeatedly performed during life, necessarily affecting somewhat the amount of fluid found after death, which varied from a few cubic centimeters to a liter or more. In most cases the amount was small.
Reference has already been made to the fact that empyema was of very infrequent occurrence during the epidemic. However, it was found in 6 of 56 cases of influenzal pneumonia coming to necropsy at the United States Naval Hospital, Great Lakes, Ill. In most of the cases of fluid found in the pleural cavities was very thin. It was generally noted that the fluid contained little fibrin and was tinged with blood.
The lesions in the lungs were characteristically those of perio-bronchitis and broncho-pneumonia. When the lesions were limited to one lobe, usually a lower lobe was affected. In most cases areas of consolidation were found in both lungs, and the lesions were scattered through several lobes. In many instances confluent areas of consolidation gave the gross appearances of lobar pneumonia.
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A striking feature which characterized influenzal pneumonia was the great amount of thin, watery, bloody, or blood-colored fluid or very dark fluid containing hemolyzed blood which dripped from the cut surface of the lung, filled the alveoli and bronchioles, and in the form of extravasations under the visceral layer of the pleura in streaks or in areas of from one to several centimeters in diameter resembled bullae of suggested subpleural hemorrhage.
Many composite pictures were presented, but in general it appears that lung findings could be divided into two principal groups, depending chiefly upon whether death occurred in the first few days of the disease or whether life was prolonged for 10 days or more.
Where death occurred early in the disease the picture was that variously described as acute, hemorrhagic pneumonitis, disseminated hemorrhagic pneumonia, primary toxic injury of pulmonary tissue or rapidly fatal septicemia with intense engorgement and localizations in the lungs. The lungs were heavy. The pleural surfaces were smooth and usually wet, bluish gray, purple, or slate colored, and often showed a mottling or dark red streaks due to collections of hemorrhagic fluid or extravasations of fluid containing blood pigment beneath the pleura. The lung surfaces were usually almost completely free from fibrin. Here and there the lungs were partially collapsed. Various portions of the lungs, especially the lower lobes, showed areas of consolidation, and frequently edema and emphysema were noted in areas not consolidated.
The cut surface of the lung varied in color from bluish gray or grayish purple to dark red. As a rule, affected areas were dark red. Sanguineous red or dark fluid dripped from the cut section. "The coarse nodular consolidation of ordinary broncho-pneumonia was not present." Cases of longer duration frequently showed a greater variety of lesions. "The lungs exhibited a constantly varying picture of broncho-pneumonia from a peppering of discreet lobular areas well scattered throughout all lobes to large and often massive confluent areas of consolidation involving 75 per cent of the lungs." "The shades of color of the prominent lobules surrounded by the red of the unconsolidated areas and the pale collapsed areas gave a mosaic appearance." Areas of emphysema were usually present in uninvolved portions of the lungs as well as in tissue intervening between consolidated areas. Sometimes intense engorgement without real consolidation was found, and from areas filled with fluid and presenting a solidified appearance blood stained or dark fluid exuded upon pressure. The lining membrane of bronchioles was intensely congested and even the lining of the trachea and large bronchi was often deep red.
The relatively small amount of fibrin present in the lung of influenzal pneumonia was noted by most observers. Panbronchitis and peribronchitis were commonly found. The peribronchial and bronchial lymph glands were generally enlarged, intensely inflamed, and often edematous.
In cases of longer duration, coming to necropsy after 10 or more days of illness, more extensive and more complete consolidation was usually found and dilation of bronchioles, congested in the cases of short duration, showed extensive necrosis in the late cases and the bronchi frequently contained thin purulent material or pus.
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In some of the more prolonged cases diffuse and confluent small abscesses were noted with yellow pus exuding from the cut surface. Fibrino-purulent material was present in many of the late cases. In some instances bronchiectasis was extensive. In general, a prominent feature in the cases of 10 or more days' duration was extensive bronchitis and peribronchitis with foci of broncho-pneumonia in various states from grayish consolidation to abscesses containing creamy pus. In these cases the lungs were dryer but there were traces of previous engorgement. In many instances there were evidences of organization taking place in the alveoli and dilated bronchioles.
In cases coming to necropsy after 14 days of pneumonia inter-lobular fibrino-purulent pleural exudates were not uncommon.
"In sections studied microscopically from the early stage of pneumonia it is more evident than in gross that a general bronchitis and especially bronchiolitis precedes the infiltration of alveoli. One finds in unconsolidated areas, bronchioles filled with an exudate composed of polymorphonuclear and mononuclear leucocytes with varying amounts of fibrin and amorphous hyalin material. The infundibula and air vesicles subtended by the bronchiole may contain an exudate of leucocytes with little or no fibrin, forming a small focus of broncho-pneumonia. More characteristic of this stage of inflammation is a lesion of the walls of certain infundibula and air vesicles in the neighborhood of, and within the latest areas of consolidation. A hyalin membrane partially or completely covers the walls of these air spaces. The membrane is irregular in thickness, sometimes stratified with occasional cells within narrow clefts. It tends to be thickest over the angles of the wall, though it may be so abundant as to fill an alveolus.
"In older foci of pneumonia leucocytes are the predominant inflammatory element, with small amounts of blood and fibrin, but in the diffusely consolidated patches or lobes of short duration, serum, fibrin, and red cells are most conspicuous. Especially prominent are the large areas of hemorrhage from capillary rupture. In certain areas numerous focal necroses of alveolar walls are observed. In older lesions the smaller bronchi contained plugs of leucocytes, fibrin, and hyalin material, and their epithelial lining was partially or completely ulcerated and covered by a fibrino-purulent membrane."
Most of the victims in influenza in the Navy were robust young men when attacked and the numbers of these well-developed and well-nourished bodies at necropsy made a spectacle sad beyond description.
Extreme engorgement of the whole venous system with distension of subcutaneous and abdominal veins filled with a thin black fluid, watery in consistency, was sometimes noted. The right side of the heart was then acutely dilated. Frequently there was no marked alteration in the size of the heart. "The heart muscle commonly had a glazed or scalded appearance." It was noted at times that the pectoral and recti muscles presented the same appearance. Acute degenerative myocarditis was commonly found. Reports made little reference to the condition of the cardiac valves. Acute vegetative endocarditis of the mitral valve was noted in one instance at the United States Naval Hospital, Great Lakes, Ill.
The spleen, liver, and kidneys, as a rule, exhibited varying degrees of congestion. Active acute nephritis was infrequently found. A
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report from the United States Naval Hospital, Great Lakes, Ill., stated that little or nothing worthy of special note was found in organs other than the lungs in the acute pneumonia cases. Complications were found in cases where death occurred later on, after the primary acute attack had subsided. The spleen was seldom enlarged to any marked degree. It was usually firm. The list of complications given above indicates the character of lesions found in these organs in unusual instances.
In a report from the United States Naval Hospital, Philadelphia, Pa., intense congestion of the adrenal bodies without progressive inflammatory changes was noted. A report from the United States Naval Hospital, Chelsea, Mass., noted small foci of hyalin necrosis in the adrenal bodies in a majority of the cases in which death occurred four or five days after the onset of pneumonia.
First and last, leptomeningitis was found in a good many instances. Sometimes a pneumococcus was recovered from the meninges; sometimes a streptococcus; and rarely, the Pfeiffer bacillus. As previously noted, brain abscesses were occasionally found. Edema of the brain was frequently noted.
Other findings noted in rare instances at post-mortem examination were hyalin degeneration, necrosis, rupture, and hemorrhage into one or both of the abdominal recti muscles, acute arteritis, phlebitis, and septic emboli with resulting infarction of the brain or of one or another of the parenchymatous organs.
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