CHAPTER II
IN THEAMERICAN EXPEDITIONARY FORCES a
In the spring of 1918 reports appeared of anepidemic disease invarious parts of southernFrance, Italy, and Spain. By midsummer this disease had spread widelythroughout Europe, andin the autumn had involved South Africa and America. Were it not forthe epidemiologicevidence it would have been difficult to characterize the disease as aclinical entity.
Inthe majority of cases, the onset of the disease was sudden,particularly in the warmerseason. Epistaxis was an early manifestation in a considerableproportion of cases. In someoutbreaks, particularly those in the fall months, a slight sore throator a feeling of cold in thehead, and in some instances a distinctly localized burning sensation inthe nasopharynx wasnoticed 12 to 24 hours before the fever became evident. The firstsymptoms, although in mostinstances severe enough to fix the moment of onset in the patient'smind, were, so mild as a rule,that soldiers did not report sick unless especially ordered to do so.The morale of the averagesoldier was such that he hesitated to go to sick call, regarding it asa confession of weakness orperhaps an indication that he desired to shirk. While this attitude is,in general, to becommended, and was undoubtedly encouraged by medical officers, it was adistinct source ofdanger in the presence of the epidemic.
Prostrationwas marked in some cases and a few men fainted while awaitingexaminationat sick call, and many of those performing physical labor found itimpossible to continue. Thepharyngeal mucous membrane was slightly reddened and rather dry; thenose was remarkablyclear and unobstructed; the conjuctivae were injected. The patientcomplained of headache, painin the back, weakness, pain and tenderness in the eyeballs, andsometimes of a burning in thenasopharynx or a slight sore throat. Leucocytosis was usually absent inuncomplicated cases, butappeared along with the bronchopneumonia. Leucopenia was observed earlyin the disease.
Ina series of 125 cases, coryza was noticed by half the patients, but adark red, drymucous membrane was found in 90 out of 100 cases. Sore throat wascomplained of by 37 percent, a dry red pharynx with swollen lymphoidtissue on the lateralwall was present in 80 percent. Epistaxis occurred in 35 percent. Theeyes were injected,perhaps somewhat more so thanin most fevers. The neck was somewhat stiff in 12 percent., but thisstiffness was never marked. Herpes was observed in 17 percent. Carefulexamination failed to reveal any distinctive rash.Among the 125 cases definite signs of bronchopneumonia on admissionwere present in 40 percent. There were a few cases of catarrhal otitismedia, usually withconsiderable pain for a fewhours, but without enough exudate to bulge the drum. This series may beregarded as fairlytypical of the disease as it occurred in France about October 1, 1918.The respiratory symp-
aBased on: TheInfluenza Epidemic of 1918 in the American Expeditionary Forces inFrance and England.By Maj. Ward J. MacNeal, M. C., commanding officer, Central MedicalDepartment Laboratory, Dijon. ArchivesofInternal Medicine, Chicago, 1919, xxiii, No. 6, 657.
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toms were less well marked in the cases seenin the early months, May, June, and July, and inthem cough, otitis media and signs of bronchopneumonia were rare.
Courseand outcome.- In the early months, May, June, and July, rest in bedand apurgative were followed by subsidence of the fever and amelioration ofall symptoms in 24 to 72hours, and prompt recovery without further mainfestations, exceptslight weakness anddepression. Complications were so rare as to be considered nonexistentand the relatively fewcases of pneumonia observed were subsequently regarded as instances ofmistaken initialdiagnosis. In the later months, from about the beginning of September,the disease was perhapsless sudden in onset, but the course was distinctly more malignant anda complicating fatalbronchopneumonia became alarmingly frequent; so frequent, indeed, as tosuggest a newepidemic of an entirely different disease.
Inthe more severe cases, distinct evidence of tracheobronchitis andbronchopneumoniaappeared, sometimes within the first 48 hours, but usually at the endof the third or fourth day. Inmany instances the temperature fell nearly or quite to normal on thethird day, only to rise againalong with the gradual appearance of physical signs of extension of theinflammation in the finerbronchi and alveoli of the lungs. This complication was observedparticularly in patients whofailed to go to bed promptly at the onset of the disease, in those whogot out of bed before theyshould, and in those patients who were transported during the febrileperiod. Pleural effusionoccurred in some cases; empyema occurred rarely. Unconsciousness forsome hours beforedeath, with considerable extension of the thoracic dullness in the last48 hours, were commonlyobserved in the fatal cases. When the patient recovered, the fever fellby lysis after 6 to 12 days.
The death ratein patients with pneumonia was high, varying from 5 to 100 percent.Thebulk of these deaths resulted from the bronchopneumonia of theinfluenza epidemic. In the seriesof 125 cases there were 18 deaths, or 14.4 percent of the cases ofinfluenza. Inasmuch as 40 percent of these patients showedbronchopneumonia on admission, themaximum death rate of thepneumonia cases was 18 in 50, or 36.0 percent. Doubtless many othersin the series alsodeveloped pneumonia in the hospital, so that the death rate for thepneumonia in the series maybe placed at 14.4 percent as a minimum and 36 percent as a maximum.
Anotherseries of cases evidently originated on the transports during voyagefrom theUnited States. In this series there were 4 cases of lobar pneumonia, 1of them primary and 3secondary to influenza, with 1 death; 156 cases of bronchopneumonia, ofwhich 1 was primary,148 cases secondary to influenza, and 7 secondary to bronchitis, with52 deaths. Pleural fluidwas found in 13 cases. It was clear in nine cases and turbid in fourcases. Bloody sputum wasobserved in 118 cases. Twenty-two cases of pneumonia developed in thewards, 20 frominfluenza and 1 from bronchitis. There were 268 cases of influenza atthe same time, of which246 were respiratory; 1 was nervous; 9 were gastrointestinal; and 12were febrile. Earcomplications and sinus involvement were uncommon. Bacteriologicexaminations showed thepresence of the influenza
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bacillus and of pneumococci in almost everycase. Hemolytic streptococci were not found. Thedeath rate in the pneumonia was 32 percent.
Withoutregard to the bacteriologic findings or questions of etiology thedisease iscertainly properly designated as influenza on the basis of its epidemicand clinical charactersalone.
PATHOLOGICANATOMY
Inthe early months of the epidemic the disease was so benign in characterthat deathswhich did occur were invariably ascribed to other cause. After August15, 1918, deaths becamemuch more frequent and the records of necropsy in this disease werevery numerous. From theclinical evidence it appeared that the bulk of the necropsy recordswere based on complicatedcases. The pathology of these later cases is discussed first.
Therespiratory organs.- The larynx, trachea, and larger bronchi showedswelling,edema, injection and infiltration of the mucous membrane, which wascovered by frothymucopurulent, often blood-stained exudate. The smaller bronchi andbronchioles also wereinvolved in the same process and some of them were plugged with mucus.As a rule, all lobes ofboth lungs were involved; both lungs were large, dark, heavy, and firm.On section, the cutsurfaces were very moist, dripping a bloody, frothy fluid; the colorwas somewhat variegated,often showing a few firmer grayish patches of older consolidationcentrally located. Invariablythe lower lobes were more severely involved. The whole process in thelungs might bedesignated as an example of a massive, pseudolobar form ofbronchopneumonia of a verymalignant type. Considerable variation in the appearance of the lungsoccurred even in the sameseries. Some prosectors were able to distinguish a type showing more orless fibrinous pneumonia and a type in which this was not present andto foretell from the gross appearance thebacteriologic demonstration of pneumococci in the former. In someinstances gross evidence ofhemolysis indicated the presence of hemolytic streptococci which wassubsequently confirmed.
Necropsies onindividuals dying of influenza pneumonia revealed the followingcharacteristics: (1) Frequency of an associated hemorrhagictracheobronchitis; (2) extensivethough irregular involvement of multiple lobes in massive areas oflobular pneumoniaconsolidation; (3) frequent existence of a much older focus of centralpneumonia near the hilusof one or both lower lobes; (4) evidence of an explosive-like spread ofthe pneumonic processfrom this central focus to large areas of the adjacent lung parenchymawithin the last day or fewdays before death; (5) relative infrequency of suppuration, empyemabeing found only in twocases.
Serouscavities.-In many instances the pleural surfaces were fairly normalor onlyslightly dulled in luster; in others, a slight increase in clear fluid,with or without a tinge ofhemoglobin, was noted; in from 5 to 30 percent, varying in differentseries, a large pleuraleffusion was present, usually serous, but sometimes serofibrinous orpurulent; in 10 to 20 percent a plastic fibrinous exudate existed onthe pleural surfaces. Inshort, the conditions withinthe pleural cavities were exceedingly diverse. Pericardial effusion andpericarditis were observed in a few instances. When large volumes offluid were found in the chest, the changes inthe lungs were less advanced and less extensive than usual.
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Subcutaneousemphysema.- This was observed in comparatively few cases in severaldifferent outbreaks. It began in the supraclavicular region or over theanterior chest wall, andbecame more or less generalized over the surface of the body. It didnot appear to affect theoutcome of the case. A post-mortem study of several such cases failedto reveal bacteria in themajority of the cases. Mechanical obstruction of small bronchi by plugsof mucopus andsubsequent solution of continuity in the structure of the lung is theprobable explanation of itspathogenesis.
Rectusabdominis.- In a very few instances lesions of the rectus muscleswere found. Insome cases a necrosis resembling Zenker's necrosis, in othershemorrhages into the muscle werepresent.
Cranialsinuses.- The first wave of the epidemic in May and June did nothave anyrecognized cases of sinus or aural complications, and as there were fewif any deaths frominfluenza at this time no opportunity presented itself to prove theabsence of sinus involvementby necropsy. Clinical evidence of such involvement was entirelylacking. In the latter phases ofthe epidemic, sinus and aural complications occasionally wereencountered.
Otherorgans.- The changes in other organs were those of acute toxemia,manifestedparticularly in the kidneys, liver, and spleen. Icterus, apparently ofhemolytic origin, wasobserved in a few instances.
PATHOLOGY OF PARTICULARCASES
Insome instances clinical histories permit a determination of the exactduration of thedisease before death occurred. Significant features of a few necropsieson such cases follow:
Necropsy 1: Patient had a slight cold onSaturday, October 5, but took dinner with friends on that date. Hewas admitted to the hospital at 6 p.m. on October 7 in a dyingcondition; died October 8 at 8.30 a.m. Duration ofillness was therefore about 60 hours. Pleural cavities contain a fewcubic centimeters of cloudy fluid. There are noadhesions. Both lungs are of the size of full inspiration. There ispractically no exudate on either pleural surface. Theupper two thirds of the upper lobe, the apex of the middle lobe andscattered patches throughout the lower lobe ofthe right lung contain solid bluish-red areas, which have ill-definedmargins. On section these areas are dark red incolor and comparatively airless, the surfaces being bathed with a verylarge amount of bloody fluid. The remainingportions of the lungs are heavy with congestion and edema, except for afew areas anteriorly, which are dilated andfeathery. The bronchi of both lungs are deep red in color, bathed withabundant blood-stained frothy mucus andcovered with a thin,
closely adherent, grayish-yellow, fibrinouspseudomembrane. The peribronchial lymph nodesare not markedly swollen. The sinuses at the base of the skull showsome thickening of the mucosaand a smallamount of mucoid fluid in the left sphenoid and left frontal. Smearsand cultures from the lungs show streptococciand Gram-negative bacilli. Smears from the frontal sinus showstaphylococci Gram-negative bacilli and a shortGram-positive bacillus; cultures from the same place show staphylococci.
Necropsy2: Patient was admitted to hospital October 16, 1918, with a diagnosisof acute influenza;temperature, 103 º F.; pulse, 116; respiration, 24. October17, the temperature rose to 104 º F.; pulse, 104;respiration,30. The temperature remained above 104 º F.; at timesreaching 105 º F.; respirations increased to 50,but thepulserate did not rise above 104 until the day of his death, when it reached120. Death occurred October 20, 1918, at11.30 p.m., four days after admission.
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The pleural cavities each contain about 10c.c. ofclear serum. The parietal pleura is speckled thinly with petechialhemorrhages on both sides, and small tags of fibrin hang from it. Theareolar tissues of the anterior mediastinum aremoderately infiltrated with glistening, gelatinous material. Theposterior and apical portions of the right pleuralcavity are obliterated by very firm fibrous adhesions. The apical andposterior surfaces of the right lung are coveredwith fibrous tags and the pleura is thickened and rough. At the apex ofthe right upper lobe the pleura is puckeredand thickened, and on section the thickened pleura at this pointmeasures 4 mm.; it is whitish in color, very denseand resistant and fibrous in character. Beneath this, the cut surfaceof the apical portion of the right upper lobe ismade up of irregular grayish-yellow areas, all coalescing, andseparated here and there by fibrous strands. Themiddle and lower lobes are large, heavy, and dark; their pleuralsurface has the appearance of pavement, the linesbeing formed by distended lymph channels. The cut surface is very dark,moist, and compact; the lobes are entirelyconsolidated, but the consolidation is peculiar in that it is made upof coalescing patches of bronchopneumoniamassed together. From the atypical appearance one is led to think of amixed infection. The left lung is in the samecondition, except the anterior portion of the upper lobe, the cutsurface of which is markedly hyperemic and has,scattered in it, some dark red patches similar in appearance but muchlarger than the patches ordinarily seen intypical bronchopneumonia. The mucosa of the trachea and bronchi is veryhyperemic and bathed in an abundance ofthin, frothy fluid. The tracheobronchial lymph nodes are moderatelyenlarged, unusually moist and slightly bloody.The tissues of the posterior mediastinum are slightly infiltrated withglistening jelly-like material.
Necropsy3: Patient entered hospital September 12, 1918, having been in France one week. Hehad beensick since landing and had been riding in a baggage car for severaldays. He died September 12 at 11.50 p.m. Thenecropsy was performed at 3.25 p.m., September 13. The mediastinum iswell covered with fat, the right visceralpleura hemorrhagic and injected and covered with fibrinous deposits.The pericardial cavity contains about 70 c.c. of a straw-coloredfluid. The left lung weighs 1 pound 1 ½ ounces and shows irregularconsolidated areas. Theright lung weighs 2 pounds 12 ½ounces. The left lung floats inwater; on section it shows irregular consolidatedareas from which frothy mucus exudes. The lobular type is more evidentto the sense of touch than of sight. Theentire right lung floats in water as do portions from the most nearlyconsolidated portions. Bronchi are red andinflamed. Cultures from the brain and from the heart blood arenegative; cultures from the right lung show B.influenzae and Streptococcus viridans.
Necropsy4: Patient entered hospital October 8, 1918, from a newly arrivedtransport. 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 clearyellow fluid. There are numerous hemorrhages on the left side of thepericardium. The right lung is adherentposteriorly and the right pleural cavity contains about 300 c.c. of acloudy yellow fluid. The lower half of the pleurais covered with a thick layer of yellow fibrinous exudate. The leftpleura is slightly adherent at the baseposteriorly and is also covered with fibrinous exudate. The right lunghas four lobes, the fourth being a very smallone at the apex. This is firm and on section is gray and consolidatedthroughout. The main upper lobe is collapsedand contains some nodules. Its surface is dull, granular, and varyingin color from light pink to bluish-red. Centrallylocated there is a nodule of gray consolidation the size of a hen'segg. Around the periphery the lung is well aeratedand for the most part of a light pink color. The cut bronchi exudethick yellow pus. The middle lobe is well aerated,light pink in color and shows afew hemorrhagic areas. Pus exudes from the cut bronchi in this lobealso. The lowerlobe is a gray consolidated mass of friable tissue and on pressureexudes thick pus. In the left lung the upper,middle, and anterior portions of the lower lobe are aerated. Surfacesof the upper and middle lobes are of a dark redcolor; on palpation small nodules are felt throughout. The posteriorhalf of the lower lobe is consolidated andnodules may be felt. The larger nodules in the upper lobe are gray andexude pus everywhere when squeezed. Forthe most part, the tissue is spongy, light pink to deep red and quitefriable. At the periphery and at thebase there is adark red consolidation from which a considerable amount of pus exudes.Bacteriology: B. influenzae,pneumococcus, and a Gram-positive bacillus.
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Thesefour abbreviated protocols are fairly typical examples of the recordsof manyhundreds of cases coming to necropsy in September, October, andNovember, 1928, and indicatethe diversity of picture observed within the thorax. These differencesappear to have dependedessentially on the rapidity with which the patient succumbed. Thefulminant cases showed apicture of malignant coalescing bronchopneumonia which rapidly involvedalmost all the pulmonary tissue. The more chronic cases showed distinctfoci of older gray consolidation; usuallymultiple with recent more extensive, even general, spread of thepneumonic process.
BACTERIOLOGY
Thebacteriologic examinations made during life on sputum or material fromthe pharynxshowed various organisms, usually mixed together. The interest in manyinstances centered onthe Pfeiffer's bacillus and reports in regard to it showed the verywidest variations. Culturesmade on blood-agar or on hemoglobin-agar revealed, in the largemajority of cases,pneumococci, streptococci, influenza bacilli, staphylococci andGram-negative cocci. Bloodcultures taken during life were usually negative, but in a moderateproportion of the casesshowed pneumococci or streptococci. Fluids obtained by puncture fromthe pleural cavity orfrom the lung tissue showed the same organisms and at times theinfluenza bacillus. In certainlocalitites enormous numbers of Gram-negative cocci, identified asmeningococci, were found inthe sputum during life and in the lungs at necropsy in a certain numberof cases. Attempts todetect a filterable virus have been reported, but experiments of thiskind were not carried out inthe American Expeditionary Forces.
Atnecropsy, also, the bacteriologic findings were variable and usuallyshowed a mixtureof various species of microbes. Influenza bacilli, pneumococci ofvarious types, hemolytic andnonhemolytic streptococci occurred most frequently in the infiltratedlungs. Post-mortem bloodcultures showed B. influenzae in a few instances, pneumococciand streptococci in aconsiderable number of cases. Cultures taken from the cut surface ofthe lung at necropsy in oneseries of necropsies during September, 1918, showed influenza bacilliin 40 percent of the cases,hemolytic streptococci in 30 percent, and pneumococci in 40 percent,Group IV, Type I, TypeII, and Type III in order of frequency. In many cases, two or more ofthese organisms wereisolated from the same tissue. More significant, perhaps, were thosenecropsies in which a morethorough bacteriologic survey of the respiratory tree was carried outby culturing in turn themucous membranes of the trachea, large and small bronchi, and alveolartissue. In fulminantcases, large numbers of influenza bacilli were found, especially in thetrachea and bronchi,sometimes apparently in pure culture. In most instances, however, themucous membrane of therespiratory tract showed a mixture of organisms; in the trachea,influenza bacilli, streptococci,staphylococci, pneumococci, Gram-negative cocci and occasionally largerGram-negativebacilli; farther down, influenza bacilli, pneumococci, andstreptococci; still lower, influenzabacilli, and one species of the cocci, and finally in the consolidatedalveolar tissue, thepneumococcus or the streptococcus alone, as a rule, but sometimes mixedtogether or evenassociated with the influenza bacillus in this tissue.
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Thesefindings suggest that the disease was essentially due to an invasion oftherespiratory tract by influenza bacilli, followed by and associated withother pharyngealorganisms, and that the fatal outcome, in most instances, was broughtparticularly by thesesecondary invaders, in some instances streptococci, in otherspneumococci.
Thereports from some hospitals indicate that the important secondaryinfections weredue to pneumococci, but in those instances in which type determinationwas carried out, thestrains usually fell into three or four type groups, a considerableproportion of them belonging toGroup IV. In other hospitals streptococci were found to be theimportant secondary invaders.The explanation of these results is not entirely clear. It is possiblethat the distinction betweenpneumococcus and streptococcus was not always accurately made, and thatthere was a tendencyin one place to call all these organisms pneumococci and in another tocall them streptococci.These reports suggest, however, that the secondary invaders may havespread from patient topatient, possibly within the hospital wards. In certain series ofnecropsies, where considerableattention was devoted to the identification of the cocci in the lungs,these invaders were found tobe quite variable, even in bodies coming from the same hospital ward,indicating that theirspecific nature depended on the type of organisms which happened to bepresent in the upperrespiratory tract of the man at the time of his illness, rather than oncontagion.
Theidentity of the summer epidemic with the disease prevailing afterSeptember 1 maybe called into question, particularly because of the benign characterof the earlier outbreaks andthe high death rate observed later. In the later months bronchitis andbronchopneumonia werevery common, while such involvement was extremely rare in the summer.In favor of theessential identity may be mentioned the similar epidemic character ofthe outbreaks, the clinicalresemblance between the milder autumn cases and those of the summer,the rather clear evidenceindicating a gradual increase in malignancy and the similarbacteriologic findings during life.Most convincing, perhaps, was the similar epidemic character, whichalone almost suffices toprove the essential unity of causation for the disease in the twoseasons. Medical officers whoobserved the disease in both seasons were inclined to the view that theprimary disease wasessentially the same, with the secondary complication ofbronchopneumonia in the colderweather. The unfavorable influence of cold and exposure is universallyrecognized in relation tothis disease.
Inits epidemiologic, clinical, bacteriologic, and pathologic features,the disease iseverywhere recognized as being identical with influenza as it wasobserved in the pandemic of1889-90. The bacterial findings are those of influenza. In the AmericanExpeditionary Forces,the bacillus of Pfeiffer was demonstrated in a very large percentage ofthe cases properlyexamined; in several series it was demonstrated in every case. Theother bacteria isolated;namely, strep- tococci, pneumococci, Gram-negative cocci, althoughundoubtedly the cause ofdeath in many cases, can be excluded from consideration as the primarycause of the epidemicdisease, because of the inconstancy with which any one specific typewas encountered. Thepossible causative relation of the bacillus of Pfeiffer can not besimilarly excluded. On the otherhand, the causative relationship
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of this organism can not be acceptedas proven. During this epidemic, as duringprevious epidemics of influenza, a considerable proportion of throatsof persons not sufferingfrom the disease were found to harbor this organism, or organismsindistinguishable from it bythe methods employed.
Ina series of 35 selected cases of epidemic influenza without signs ofbronchopneumonia, cultures of swabs from the nasopharynx showedstreptococcus in 57 percent,pneumococcus in 74 percent, and influenza bacillus in 46 percent. Ina second group of 15cases diagnosed clinically as bronchopneumonia, cultures of the sputumrevealed hemolyticstreptococcus in 33 percent, pneumococcus in 87 percent, andinfluenza bacillus in 87 percent.Only one of these patients died and in his case pneumococcus andhemolytic streptococcus werepresent in the lung at necropsy. In four cases the sputum wasinoculated into mice andpneumococcus of Group IV and the inflaenza bacillus were recovered fromthe animal'speritoneum and heart blood. In a third group of 22 meningitis contacts,nasopharyngeal culturesshowed influenza bacilli in 48 percent.
Onereport under date of September 5, 1918, contained the records ofnasopharyngealcultures from 106 cases of influenza, of which 46.2 percent showed theinfluenza bacillus and20.7 per cent showed streptococci. In a series of 12 normalindividuals, direct contacts of thesecases, the influenza bacillus was found in 41.6 percent and thestreptococcus in 25 percent. Aseries of 42 normal individuals, not contacts, examined in the sameway, showed influenzabacillus in 7 percent, and streptococcus in 10 percent.
Theessential similarity in the anatomic changes observed in the laterepidemic and inthese earlier cases warrants the quotation of the important parts of afew of the protocols of earlycases.
Necropsy 5: The patient enlisted August 12,1917. He had had a cold for the past few weeks but was notadmitted to hospital until October 24, 1917, with symptoms ofprostration, dyspnea, fever, cough and markedevidence of general sepsis. Pneumococcus (Group IV) was isolated fromthe sputum by mouse inoculation. The mandied October 26 at 11.55 p.m. At the necropsy the left lung was foundexpanded to full inspiration; the surfaceswere smooth, at the inner anterior margin of the upper lobe wereseveral firm areas, the largest about the size of awalnut, grayish to bluish in color, with distinct puckering of thesurrounding pleural surfaces. A fewsimilar areaswere located at the outer posterior margin of the lower lobe. Scatteredthroughout the pulp were smaller foci ofincreased consistence. Remaining portions of the lung were light,feathery, particularly the lingula. On section thefirm areas had moist grayish surfaces and were comparatively airless.From the cut bronchioles purulent fluidescaped on pressure. The bronchial mucosa was bathed by a mucopurulentfrothy liquid and was distinctly reddenedand swollen. Peribronchial lymph nodes were markedly swollen, soft andred. There was no evidence oftuberculosis. 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 thebifurcation were very greatly swollen,reddened and friable. The middle ears and mastoids were normal; thesphenoidal air cells were full of thick, yellowfluid and the mucosa was swollen and congested. The posteriorethmoidal cells contained some thin yellowishfluid, while the anterior cells were apparently free; the mucosa inboth groups was distinctly thickened. Bacteriologic examination showed B. influenza and Gram-positivediplococci in sphenoidal sinus, in the lungs and in theliver.
Necropsy6: The patient was admitted to hospital February 7, 1918, complainingof severe cold, withcough, which began three days before; also pains in his joints and sore throat. February 13 a fine papulareruptionappeared, especially over the chest and abdomen. At this time histemperature was 102º F., pulse and respirationrapid. Harsh rȃles were
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heard at the base of the right lung and finemoist rhles in the lower lobe of the left lung. Death occurred February13,1918, 11.35 p.m. Necropsy, February 14, at 9.30 a.m.: The pleuralcavities were free from abnormal fluid; the leftvisceral and parietal pleurae were bound together by fresh fibrinousadhesions, uniformly distributed over the lowerlobe. The right pleural cavity presented numerous firm fibrousadhesions over the surface of the middle and lowerlobes, especially at the base.The left lung was rather voluminous; the upper lobe was grayish incolor and air-containing; the lower lobe was of darker hue, mottledwith reddish-purple. The pleura here and there was coveredwith a yellowish, shaggy, friable exudate. Beneath these areas and alsoscattered in the deeper areas of the lungtissue were rather firm airless areas. The bronchial mucous membranewas intensely swollen and covered withmucopurulent secretion; this condition was seen likewise in thebronchioles. The pulmonary vessels showed nothrombi; the bronchial lymph nodes were swollen and friable. On sectionthere were found, scattered throughout thelower lobe, corresponding for the most part with the bronchioles, areasvarying in size from a pea to a walnut. Incolor they varied from gray to purple; were firm and quite friable. Thelung tissue in the immediate neighborhoodshowed intense congestion. In the right lung, the upper lobe wasgrayish in color and air-containing; the middle andlower lobes were voluminous, dark red in color. The pleura was roughand showed numerous fibrous tags. In allother respects it resembled the left lung. The tracheal mucosa wasintensely swollen and covered with an abundantmuco- purulent exudate. The middle ears were normal; the mucosa of theposterior and anterior ethmoids wasslightly swollen and moist; no purulent exudate was present; thefrontal sinuses were normal. Bacteriologicexamination of the ethmoidal sinuses by both smear and culture wasnegative.
Necropsy 7:The patient was admitted tohospital March 13, 1918, having had a cough since March 6. Onadmission, he had severe headache, shortness of breath, pain in theright side, with temperature of 102.4 º F., pulse120, dullness over both lower lobes and moist rAles everywhere.Pneumococcus, Type II, was isolated from thesputum. Death occurred March 20, 1918, at 3 a.m. Necropsy at 9 a.m.same date: Pleural surfaces were everywheresmooth and there was no abnormal fluid. In the lower lobes of bothlungs, there were numerous small, grayish,consolidated areas, corresponding with the terminal bronchioles, whichwere considerably swollen. The lung tissueeverywhere was intensely congested and of a deep red color. The lymphnodes at the bifurcation were swollen, soft,and red. Culture from the heart was sterile; cultures from the lungshowed pneumococci and influenza bacilli.
Necropsy 8:The patient was admitted tohospital April 5, 1918, with a diagnosis of measles. April 8, hedeveloped signs of diffuse bronchitis, with marked dyspnea andcyanosis; the white blood cells numbered 8,400; thesputum showed chiefly B. influenza.Death occurred April 13, 1918, at 1.30 p.m. Necropsy April 13, at 4p.m.: Thepleural cavities were free, without exudate or adhesions; the fluid wasnot increased. The right lung weighed 660grams. Externally all three lobes were irregularly mottled, with raisedgrayish margins and depressed dark brownishcenters. On section the same characteristic mottling was seenthroughout all lobes. Interspersed between the grayishaerated tissue, from which a bloody froth exuded, were dark red firmareas of consolidation, the latter being foundespecially near the hilum. The bronchi were filled with a greenishpurulent material. The left lung weighed 630grams, and was identical in appearance with the right. Bacteriologic examination of pus from theright and left bronchi showedpureculture of B. influenza.
Therecords of these necropsies indicate very clearly the prevalence ofinfluenzal bronchopneumonia.
