CHAPTER IV_Epidemic Respiratory Disease The pneumonias and other infections of the repiratory tract accompanying influenza and measles

THE PATHOLOGY AND BACTERIOLOGY OF PNEUMONIA FOLLOWING INFLUENZA

E. L. OPIE, M.D.; F. G. BLAKE, M.D.; AND T.M. RIVERS, M.D.

Many observers have described isolated phases of the recent epidemic and

of past epidemics of influenza. Few have had an opportunity to follow

the pathology of influenza from the onset of an epidemic through a

period of several months and to observe the succession of acute and

chronic changes which occur in the lungs. Our commission arrived on

September 5, 1918, at Camp Pike two weeks before the outbreak of

influenza. The commission had previously made a careful study of the

clinical course, the bacteriology and to a limited extent the pathology

of pneumonia occurring at Camp Funston where there was little if any

influenza. Study of the records preserved at the base hospital at Camp

Funston had convinced us that this camp had passed through an epidemic

of influenza during the spring of 1918, this epidemic being followed by

a very severe outbreak of pneumonia. Our investigation at Camp Funston

had brought to our attention those phases of pneumonia which with the

facilities of a base hospital laboratory could be most profitably

studied with a view to determining the causation, the epidemiology and

the prevention of the pneumonias prevalent in the American army.

Study of pneumonia after death offers the only opportunity of

determining the relation of pulmonary lesions to the considerable

variety of microorganism associated with them. Clinical diagnosis

furnishes no certain criterion for distinguishing lobar and

bronchopneumonia; suppurative pneumonia is rarely recognizable during

life. The relation of pneumococci, streptococci, staphylococci or B.

influenzæ to one or other type of pneumonia can be determined with

accuracy only after death; for the demonstration of one or more of these

microorganisms in material obtained from the upper respiratory passages

in life, though of value, furnishes us no definite evidence that the

organism which has been identified has entered the lung and passed from

the bronchi to produce pneumonia.

Study of autopsies following examination of the sputum during life has

shown that an individual primarily attacked by influenza may suffer with

a succession of pneumonias, one microorganism having prepared the way

for another. The complexity of the subject is much increased by the

truth that pyogenic microorganisms, like the tubercle bacilli, are

capable of producing a considerable variety of pulmonary lesions.

Examination of the lungs of a large number of individuals who have died

as the result of pneumonia following influenza has disclosed a

succession of acute and chronic diseases. Immediately succeeding the

height of the epidemic of influenza, death occurred with acute lobar

pneumonia or with diffusely distributed hemorrhagic bronchopneumonia

caused in the majority of instances by Pneumococcus IV in association

with B. influenzæ. Superimposed infection with hemolytic streptococci

increased in frequency and in individuals who had occupied certain wards

was almost invariable. At a later period, from one to two months

following the maximum incidence of influenza chronic lesions, namely,

bronchiectasis, unresolved pneumonia, and chronic empyema were common

and often occurred as the result of influenza which had had its onset at

the height of the epidemic.

When influenza attacked the encampment, about 50,000 troops were

quartered in it, and for a considerable period no more troops were

brought into the camp and none left it. All cases of pneumonia occurring

among these troops were brought to the base hospital so that the

autopsies which were studied were representative of all the pneumonias

following influenza in this limited group of men. It is noteworthy that

autopsy disclosed no instance of fatal influenza unaccompanied by

pneumonia.

=Pneumonia of Influenza.=—Knowledge concerning the bacteriology of the

pneumonia of influenza dates from the study of the epidemic of 1889–90.

The frequency with which Diplococcus lanceolatus occurred in association

with influenzal pneumonia was well recognized, although several

observers, notably Finkler[57] and Ribbert,[58] found Streptococcus

pyogenes so often that they attributed the pneumonia of influenza to

this microorganism.

During a subsidiary outbreak of influenza occurring in 1891–92

Pfeiffer[59] discovered the microorganism which he believed was the

cause of the disease. Pneumonia, he believed, was caused by the invasion

of this microorganism into the lung, and the pneumonia of influenza, if

death occurred at the height of the disease, was characterized not only

by the presence of the bacillus of influenza, but was recognizable by

its anatomic peculiarities. He described lobular patches of

consolidation which were separated from one another by air containing

tissue or were confluent, so that, although the lobular character was

still recognizable, whole lobes might be affected. The consolidated

tissue was dark red and within each lobular area were small, yellowish

gray spots varying in size from that of a pinhead to a pea. In the mucus

of the larynx and trachea were numerous microorganisms, including

diplococci and streptococci, among which influenza bacilli were

predominant; in the larger bronchi, bacteria other than influenza

bacilli were less abundant, whereas in the finer bronchi filled with

purulent fluid and in the lung tissue influenza bacilli had undivided

sway. Pfeiffer stated that the changes described were found when death

occurred at the height of the disease, whereas other pulmonary lesions

might be sequelæ of this typical influenzal pneumonia.

Observations upon the pathology of influenzal pneumonia made during the

epidemic of 1889–92 have been collected in the monograph of

Leichtenstern[60] published in 1896. He combats the opinion held by some

observers that pneumonia with influenza is always catarrhal and cites

many writers to prove that lobar pneumonia not infrequently accompanies

the disease. Indeed, some have found “croupous” pneumonia more often

than “catarrhal.” Krannhals[61] at Riga found typical fibrinous

pneumonia in 53 instances, doubtful forms in 22 and bronchopneumonia in

37. Cruickshank[62] in England found croupous forms predominant. Among

43 autopsies performed upon individuals dead with influenza

Birch-Hirschfeld[63] found 11 instances of croupous lobar pneumonia, 8

instances of croupous lobular pneumonia and 24 instances of catarrhal

pneumonia. Leichtenstern thinks that the atypical symptomatology of

lobar pneumonia with influenza—for example, the purulent character of

the sputum—has led many physicians to believe that lobar pneumonia

rarely occurs. It is equally true that many instances of confluent

lobular pneumonia are mistaken for lobar.

There appears to be no comprehensive description of the pneumonias of

influenza based upon the epidemics of 1889–92. Descriptions dating from

this period are much obscured by attempts to separate croupous or

fibrinous from catarrhal pneumonias. Croupous lobular pneumonia has been

recognized, for example, by Birch-Hirschfeld. Leichtenstern describes a

form of pneumonia which he regards as neither lobar nor lobular although

it implicates whole lobes; the consolidated tissue is homogeneous and

varies in color from fleshy red to bluish red; it is tough and elastic

in consistency. The author thinks that it is an error to regard this

lesion as a confluent lobular pneumonia.

Kuskow[64], who has discussed the pathology of influenza in considerable

detail, has seldom seen lobar pneumonia but has almost invariably found,

even when there is lobar distribution of the lesion, lobular patches of

consolidation involving groups of lobules, single lobules or only parts

of lobules; the lung tissue has been hyperemic and in places edematous.

Opinions concerning the pathology and bacteriology of the pneumonias of

influenza, published since the recent epidemic, have varied almost as

much as those just cited. Few observers have had the opportunity of

making a considerable number of observations under conditions which

determine the relation of the pulmonary lesions to the primary disease.

Keegan[65] has found with influenza a massive and confluent

bronchopneumonia, frequently resembling lobar pneumonia but

distinguishable particularly in its early stages when the cut section of

the consolidated lung has a finely granular character and each

bronchiole stands out as a grayish area with intervening dark red

alveolar tissue.

Symmers[66] states that the pneumonia of influenza is a confluent

lobular exudative and hemorrhagic pneumonia which bears a close

resemblance to the pneumonic variety of bubonic plague.

Our commission[67] published a preliminary report on pneumonia following

influenza observed at Camp Pike. The occurrence of purulent bronchitis,

distention of lungs, peribronchial hemorrhage and bronchiectasis were

described. B. influenzæ was isolated from the bronchi in approximately

85 per cent of instances of influenzal pneumonia but from the

consolidated lung in less than half this number of autopsies. Lobar

pneumonia was present in a large proportion of autopsies but was less

frequent than bronchopneumonia. Bronchopneumonic consolidation is in

part red, lobular and confluent, in part nodular; pneumococci have a

predominant part in the production of these lesions. Three types of

suppurative pneumonia are described: (_a_) Abscess caused by hemolytic

streptococci usually in contact with the pleura and accompanied by

empyema; (_b_) Suppuration of interstitial tissue of the lung caused by

hemolytic streptococci and accompanied by empyema; (_c_) multiple foci

of suppuration clustered about a bronchus of medium size and caused by

staphylococci. We have expressed the opinion that B. influenzæ descends

into the bronchi; pneumococci, usually Type IV, may enter the lung and

produce either lobar or bronchopneumonia. Hemolytic streptococci may

descend and infect the pneumonic lung causing death often before

suppuration has occurred. Epidemics of such superimposed streptococcus

pneumonia in wards of the hospital were described.

LeCount[68] says: “The pneumonia of influenza is commonly referred to as

bronchopneumonia. It may be so designated, but it differs from other

bronchopneumonias in its predilection for the periphery of the lungs and

in the extent to which the inflammation is hemorrhagic.”

MacCallum[69] states that the following types of pneumonia following

influenza may be recognized. 1. Pneumococcus pneumonia. The lobular

character of the consolidation is in these cases well marked, although

it tends to lose its definiteness through the confluence of adjacent

areas. The cut surface of the lung shows in the more acute cases a

peculiar lobular or confluent consolidation which corresponds well with

what is commonly written of the stage of engorgement in the description

of lobar pneumonia. Later stages in the pneumonia show within these

areas patches of rough gray consolidated tissue from which definite

plugs of exudate project. 2. Staphylococcal pneumonia. 3. Streptococcal

pneumonia. There is lobular pneumonia, the interlobular septa are

edematous and, microscopically, bronchi and alveoli are loaded with

streptococci. Whole areas of lung, though retaining their form, are

entirely necrotic. Lymphatics are distended with exudate containing

streptococci in great numbers, but in none of these cases is

interstitial bronchopneumonia found. 4. Pneumonia produced by B.

influenzæ of Pfeiffer. The lung is studded with palpable shot-like

grayish yellow nodules; the bronchi exude thick yellow pus, which

contains influenza bacilli. Microscopically, the walls of the bronchi

are found to be thickened by mononuclear infiltration and new formation

of connective tissue. The walls of the alveoli are thickened and

indurated and the alveoli often contain fibrin in process of

organization. Absence of conspicuous changes in lymphatics, absence of

intense pleural infection and relatively scant numbers of polynuclear

leucocytes in the exudate within the alveoli and bronchial walls are,

MacCallum states, all that distinguish this pulmonary change from the

interstitial bronchopneumonia caused by the hemolytic streptococcus and

described by him in previous papers.

Lyon[70] designates the pulmonary lesion following influenza,

hemorrhagic pneumonitis, the lung tissue containing serous fluid loaded

with red blood corpuscles; in many instances there was such scant

consolidation that the process could not be regarded as a true

pneumonia. In 35 instances the lesion was lobular in distribution and in

16 instances was sufficiently extensive to be designated lobar, but it

was not typical lobar pneumonia, and, often associated with lobular

patches of consolidation, appeared to be a confluent lobular pneumonia.

Goodpasture and Burnett[71] say: “The difficulties of analyzing the

pulmonary lesions in any group of influenza pneumonias as they have

appeared in this epidemic, are very apparent to anyone who has had an

opportunity to observe the bacteriology and pathology of this

accompaniment of the disease.” There is an acute outflow of the fluid

elements of the blood and of hemorrhage into the lung tissue filling the

alveoli in lobular areas and not infrequently in an entire lobe. By a

special method of staining these authors have studied the distribution

of Gram-negative bacilli with the morphology of B. influenzæ. The fact

that in certain very early cases demonstrable bacteria of any kind are

scarce or not found at all, has lead them to believe “notwithstanding

the demonstration of influenza bacilli in pure culture in the lung in

all but one instance, that at this stage organisms are comparatively few

within the alveoli, and the primary injury is due to a very potent toxic

agent elaborated in and disseminated through the larger air passages. In

the later stages or from the beginning, if the injury be slight, the

infection focalizes about the bronchi or their terminations, so that the

bronchial and lobular distribution becomes very conspicuous.” Typical

lobar pneumonia with “croupous” exudate within the alveoli occurs in

cases complicated by secondary pneumococcus infection.

Wolbach[72] has found that two types of pneumonia are characteristic of

influenza. In cases in which death has occurred within a few days after

onset of pulmonary signs, the lung tissue is dark red and “meaty in

consistency” and contains abundant blood-tinged serous fluid which drips

from the cut surface. The other type of lesion is found in patients who

have lived for ten days or more after onset of the disease; there is

extensive bronchitis, bronchopneumonia, discrete or confluent, and

peribronchitis. The lungs are voluminous and the smaller bronchi are

distended. Microscopically, there is peribronchitis with extensive

infiltration of the interlobular septa and organization in alveoli and

bronchioles. This lesion is that designated by MacCallum as

“interstitial bronchopneumonia.” Wolbach thinks that the two types of

lesion represent different stages of the same process. He regards as

distinctive of the pneumonias of influenza the presence of hyalin fibrin

lining distended air spaces. With the two types of lesion which have

been described, B. influenzæ was the only organism which could be

cultivated, and the author associates these distinctive conditions with

that microorganism.

=Streptococcus Pneumonia.=—Finkler emphasized the importance of

streptococcus pneumonia as a complication of influenza. In 1888 he

described instances of acute primary streptococcus pneumonia observed in

1887 and 1889. This form of pneumonia, Finkler thought, occurred in Bonn

in epidemic form before the influenza epidemic of 1889–90 and, he

states, exhibited an astonishing similarity to the pneumonia of

influenza. He thought that later there was in Bonn a mixed infection of

influenza and primary streptococcus pneumonia. In one type of

streptococcus pneumonia, described by Finkler, there was lobular

consolidation which in multiple patches produced “pseudolobar”

consolidation; the consolidated lung was smooth and red, and similar to

spleen, rather than hepatized. In another group of instances the lesion

merited the name “erysipelas of the lung.” The lesion was an acute

interstitial pneumonia in some places, a cellular or occasionally

fibrinous pneumonia with involvement of the interstitial tissue in other

places. There was edematous swelling and accumulation of leucocytes in

the interstices between the alveoli and about the blood vessels and

bronchi. Finkler stated that the similarity to erysipelas might suggest

that the lymphatics contain streptococci, but this relation did not

exist although large lymphatic channels were occasionally filled with

coagulum. He asserted that the disease was contagious and cited cases

which he believed had their origin in hospital wards.

The widespread occurrence of streptococcus pneumonia in the army camps

in this country attracted attention during the first months of 1918.

Cummings, Spruit and Lynch[73] at Fort Sam Houston, Texas, recognized

the prevalence of streptococcus pneumonia, both as a complication of

measles and in association with lobar pneumonia, and showed that the

microorganism concerned was a hemolytic streptococcus. In 7 autopsies

upon individuals with lobar pneumonia, they found pneumococcus alone in

2 instances and pneumococcus and hemolytic streptococcus or hemolytic

streptococcus alone in 5 instances. Hemolytic streptococcus was found in

all of 24 instances of bronchopneumonia, three-fourths of which followed

measles. They recommend the bacteriologic examination of the throat of

patients with measles and the segregation of those who harbor hemolytic

streptococci.

Cole and MacCallum[74] have published almost simultaneously, with that

just cited, a report upon the pneumonia which has occurred at Fort Sam

Houston and have shown the importance of hemolytic streptococci in its

causation. They have found two varieties of pneumonia, namely, acute

lobar pneumonia which does not differ essentially from that which occurs

elsewhere and bronchopneumonia which in most cases has followed measles

and is caused by S. hemolyticus. They think this infection is usually

acquired in the hospital. They believe that the pulmonary lesions are

characteristic. In this publication and elsewhere MacCallum has

designated the lesion “interstitial bronchopneumonia.”

The epidemic of streptococcus pneumonia and empyema occurring at Camp

Dodge, Iowa, from March 20 to May 10 is described by Miller and

Lusk[75]. During this period there were 400 cases of pneumonia, whereas

from September 20, 1917, to March 20 there had been only 276 instances

of lobar pneumonia. The type of pneumonia changed, there was more severe

intoxication and empyema became very frequent; in 85 of 95 exudates

streptococci were found. The outbreak of pneumonia bore no relation to

measles. The authors state that a mild tracheitis was prevalent in the

cantonment during March, and whenever a large group of soldiers

congregated coughing was noticeable.

MacCallum[76] studied the pneumonia at Camp Dodge during May and found

17 instances of the lesion which he had designated interstitial

bronchopneumonia; of these, 9 followed measles, although in the earlier

part of the epidemic there appear to have been, he states, few such

cases. Cultures made at autopsy, except in a few fatal cases of

uncomplicated lobar pneumonia caused by the pneumococcus, showed the

hemolytic streptococcus in every situation throughout the respiratory

tract and pleura.

The pneumonia which occurred at Camp Funston is of special interest to

our commission because we were for a time stationed at this camp and had

the opportunity of following in the excellent records of the hospital

the history of the occurrence of pneumonia during the year following the

establishment of the camp in September, 1917. Stone, Phillips and

Bliss[77] have described the outbreak of pneumonia which occurred in

March, 1918. At this time there was, the authors state, severe pneumonia

with frequent empyemas due to hemolytic streptococci. This condition

which did not follow measles was responsible for the greatly increased

death rate in March; 9 deaths occurred in February, 45 in March, 25 in

April and 14 in May. They found during March 26 instances of multiple

pulmonary abscess. In 29 autopsies they found a pleural lesion which

they designate “subcostosternal pus pockets”; it occurs only in

association with empyema caused by hemolytic streptococci.

Our commission[78] has shown that an epidemic of influenza, well

characterized by its epidemiology and symptoms, preceded and accompanied

the outbreak of pneumonia just described. Between March 4 and 29 1,127

men from Camp Funston, which then contained 29,000 men, were sent to the

base hospital with influenza and many more were treated in the

infirmaries of the camp; on March 11 107 patients with influenza were

admitted to the hospital. The greatest incidence of pneumonia in the

history of the encampment up to this time occurred between March 9 and

29, immediately following the outbreak of influenza, the maximum

incidence of pneumonia occurring five days after the maximum for

influenza.

The foregoing observations are cited to prove that streptococcus

pneumonia, which occurred during the spring of 1918 at Camp Funston and

doubtless at other camps, had its origin in influenza and did not differ

in character from that which occurred on a much larger scale in the fall

of 1918.

=Table of Autopsies.=—In order to present as briefly as possible the

data upon which the present study has been based, autopsies have been

assembled in tabular form in the order of their performance (Table

XXVII). During the early period of the epidemic autopsies were performed

on all who died with pneumonia, but later, with increase in the number

of deaths, this became impossible and autopsies were performed on all

those who died in certain wards.

Comparison of charts representing incidence of influenza and of deaths

from pneumonia furnishes evidence that fatal pneumonia during the period

of investigation was with few exceptions referable to influenza. During

two weeks, namely, from September 1 to 14, before the presence of the

epidemic was evident, there were only 2 fatal cases of pneumonia. In

most instances the relation of pneumonia to influenza is established by

a definite history of influenza having its onset during the epidemic.

Bronchopneumonia usually develops gradually as a sequence of influenza

in which purulent bronchitis has occurred. Lobar pneumonia may develop

in cases of influenza complicated by purulent bronchitis. In some

instances there is apparent recovery from influenza indicated by return

of temperature to normal; after from one to three days of normal

temperature there is typical lobar pneumonia with rusty sputum. In many

instances of pneumonia having their onset at the height of the epidemic

of influenza, the history indicates that pneumonia was present

immediately after the onset of symptoms, so that the onset resembled

that of pneumonia rather than of influenza.

Cases of pneumonia following measles have been excluded from the table

in order that they may be studied separately and compared with the

pneumonias of influenza. It is noteworthy that the lesions of pneumonia

following measles have shown a very close resemblance to the pneumonias

of influenza, with regard both to pathologic characters and to

bacteriology.

Five instances of pneumonia following typhoid fever (Autopsies 245 and

329), scarlet fever (Autopsy 311) or mumps (Autopsies 403 and 417) have

been excluded from the table. These secondary pneumonias are grouped as

an appendix to the section on pneumonia following measles. It is not

improbable that individuals with the diseases named are just as

susceptible as others to influenza. Included in the table is an instance

(Autopsy 487) in which a definite attack of influenza preceded scarlet

fever.

TABLE XXVII

═══════╤════╤════════╤════════╤═════════╤═════════╤══════════╤═════════

NO. OF │RACE│ LENGTH │DURATION│DURATION │CLINICAL │ PURULENT │ LOBAR

AUTOPSY│ │ OF │ OF │ OF │DIAGNOSIS│BRONCHITIS│PNEUMONIA

│ │MILITARY│ILLNESS │PNEUMONIA│ │ │

│ │SERVICE │ │ │ │ │

───────┼────┼────────┼────────┼─────────┼─────────┼──────────┼─────────

229 │ W │ 1m │ 12+ │ 12+ │ L │ P │ +

│ │ │ │ │ │ │

231 │ W │ 2m │ 13 │ 4 │ B │ P │

232 │ W │ 14d │ 9 │ 6? │ B │ │ +

│ │ │ │ │ │ │

233 │ C │ 11m │ 5 │ 2 │ L │ │

236 │ W │ 3w │ 8 │ 7+ │ L │ │ +

│ │ │ │ │ │ │

237 │ W │ 10d │ 8 │ 2 │ L │ │

238 │ W │ 2d │ 8 │ 5 │ L │ │ +

│ │ │ │ │ │ │

239 │ W │ 11d │ 9 │ 5 │ L │ │ +

│ │ │ │ │ │ │

240 │ W │ 13d │ 8 │ 4 │ L │ │ +

241 │ W │ 14d │ 5 │ 5 │ L │ │ +

│ │ │ │ │ │ │

242 │ C │ 14d │ 7 │ 4 │ L │ P │

│ │ │ │ │ │ │

243 │ W │ 15d │ 5 │ 5 │ L │ │ +

244 │ C │ 1m │ 6 │ 3 │ B │ P │

│ │ │ │ │ │ │

246 │ C │ 2m │ 6 │ 3 │ L │ P │ +

│ │ │ │ │ │ │

247 │ W │ 10d │ 10 │ 5 │ L │ P │

│ │ │ │ │ │ │

248 │ W │ 1m │ 4 │ 2+ │ I │ │

249 │ W │ 15d │ 12 │ 6+ │ L │ │

250 │ W │ 14d │ 11 │ 7 │ L │ │

│ │ │ │ │ │ │

251 │ W │ 25d │ 7 │ 1 │ B │ P │

252 │ W │ 21d │ 14 │ 12 │ B │ P │

│ │ │ │ │ │ │

253 │ W │ 12d │ 19 │ 12+ │ B │ │

│ │ │ │ │ │ │

254 │ W │ 21d │ 7 │ 6+ │ B │ P │ +

│ │ │ │ │ │ │

255 │ W │ 12d │ 5 │ 4? │ B │ P │

│ │ │ │ │ │ │

256 │ W │ 17d │ 8 │ 4 │ B │ P │ +

│ │ │ │ │ │ │

257 │ C │ 21d │ 10 │ 7+ │ L │ P │

│ │ │ │ │ │ │

258 │ W │ 1m │ 6 │ 2+ │ B │ │

│ │ │ │ │ │ │

259 │ W │ 3m │ 4 │ 1 │ B │ │

│ │ │ │ │ │ │

260 │ W │ 1m │ 2 │ 1 │ L │ │ +

261 │ W │ 2m │ 7 │ 5+ │ B │ P │ +

│ │ │ │ │ │ │

262 │ W │ 12d │ 5 │ 4? │ B │ │

│ │ │ │ │ │ │

263 │ W │ 21d │ 7 │ 5 │ L │ P │

│ │ │ │ │ │ │

264 │ W │ 21d │ 10 │ 7 │ L │ │ +

│ │ │ │ │ │ │

265 │ W │ 14d │ 7 │ 6+ │ L │ │ +

│ │ │ │ │ │ │

266 │ W │ 1m │ 7 │ 2 │ L │ │

│ │ │ │ │ │ │

267 │ W │ 2m │ 22 │ 10 │ B │ │ +

│ │ │ │ │ │ │

268 │ W │ 2m │ 6 │ 4? │ L │ │ +

│ │ │ │ │ │ │

269 │ W │ 25d │ 8 │ 2 │ L │ │ +

│ │ │ │ │ │ │

270 │ W │ 17d │ 18 │ 3 │ L │ │

│ │ │ │ │ │ │

271 │ W │ 2d │ 12 │ 5 │ L │ P │

│ │ │ │ │ │ │

272 │ W │ 3m │ 7 │ 2 │ L │ │ +

273 │ W │ 1m │ 8 │ 4+ │ L │ │ +

│ │ │ │ │ │ │

274 │ W │ 2w │ 9 │ 5 │ B │ │

│ │ │ │ │ │ │

275 │ W │ 4m │ 9 │ 4 │ L │ │

│ │ │ │ │ │ │

276 │ W │ 1m │ 6 │ 4+ │ L │ │ +

│ │ │ │ │ │ │

277 │ W │ 21d │ 10 │ 3 │ L │ │

│ │ │ │ │ │ │

278 │ W │ 2m │ 16 │ 6+ │ L │ │

│ │ │ │ │ │ │

279 │ W │ │ │ │ L │ │

280 │ W │ 21d │ 8 │ 8 │ L │ │

│ │ │ │ │ │ │

281 │ W │ 21d │ 9 │ 5 │ L │ │

│ │ │ │ │ │ │

282 │ W │ 1m │ 10 │ ? │ B │ │

│ │ │ │ │ │ │

283 │ W │ 7d │ 19 │ 8 │ B │ P │

│ │ │ │ │ │ │

284 │ W │ 21d │ 11 │ ? │ B │ P │

│ │ │ │ │ │ │

285 │ W │ │ 11 │ 9? │ B │ P │

│ │ │ │ │ │ │

286 │ W │ 20d │ 9 │ 4+ │ L │ P │

│ │ │ │ │ │ │

287 │ W │ 3m │ 12 │ 4 │ L │ P │ +

│ │ │ │ │ │ │

288 │ W │ 1m │ 10 │ 5 │ B │ P │

│ │ │ │ │ │ │

289 │ W │ 19d │ 12 │ 7 │ B │ P │

│ │ │ │ │ │ │

290 │ W │ 1m │ 3+ │ 3+ │ B │ │

│ │ │ │ │ │ │

291 │ W │ 2w │ 18 │ 11 │ B │ P │

│ │ │ │ │ │ │

292 │ W │ 3m │ 5 │ 5 │ L │ │

│ │ │ │ │ │ │

293 │ W │ 2m │ 3+ │ 3+ │ L │ P │ +

│ │ │ │ │ │ │

295 │ W │ 1m │ 12 │ 5 │ L │ P │

│ │ │ │ │ │ │

296 │ W │ 16d │ 18 │ 3 │ L │ P │

│ │ │ │ │ │ │

297 │ W │ 1m │ 5 │ ? │ I │ P │

│ │ │ │ │ │ │

298 │ C │ 21d │ 13 │ 10 │ B │ P │ +

│ │ │ │ │ │ │

299 │ W │ 28d │ 9 │ 3 │ L │ P │ +

│ │ │ │ │ │ │

300 │ C │ 22d │ 16 │ 12+ │ L │ P │ +

│ │ │ │ │ │ │

301 │ W │ 1m │ 7 │ 5 │ B │ │ +

│ │ │ │ │ │ │

302 │ C │ 5d │ 6 │ 3+ │ B │ │ +

│ │ │ │ │ │ │

303 │ W │ 1m │ 7 │ 3+ │ L │ │

│ │ │ │ │ │ │

304 │ W │ 4m │ 10 │ 2? │ L │ │ +

│ │ │ │ │ │ │

305 │ W │ 5m │ 3+ │ 3+ │ L │ │ +

│ │ │ │ │ │ │

306 │ W │ 1y │ 6+ │ 3 │ B │ │

│ │ │ │ │ │ │

308 │ W │ 1m │ 6 │ 6 │ L │ │ +

│ │ │ │ │ │ │

309 │ W │ 1m │ 4 │ 2? │ L │ │

310 │ W │ 21d │ ? │ 3? │ L │ │ +

│ │ │ │ │ │ │

312 │ W │ 1m │ 17 │ 7 │ L │ P │

│ │ │ │ │ │ │

313 │ W │ 1y │ 5 │ 2 │ B │ │ +

│ │ │ │ │ │ │

314 │ W │ 1m │ 3+ │ 3+ │ L │ P │

│ │ │ │ │ │ │

315 │ W │ 1m │ 9 │ 2 │ B │ │ +

│ │ │ │ │ │ │

316 │ W │ 1m │ 11 │ 4 │ L │ │ +

│ │ │ │ │ │ │

317 │ W │ 13d │ 9 │ 2 │ L │ │ +

│ │ │ │ │ │ │

318 │ W │ 2m │ 8 │ 3 │ L │ │ +

│ │ │ │ │ │ │

319 │ W │ 1m │ 4+ │ 4+ │ B │ P │

│ │ │ │ │ │ │

320 │ C │ 5m │ 1+ │ 1+ │ L │ │ +

321 │ W │ 28d │ 4+ │ 4+ │ L │ │ +

│ │ │ │ │ │ │

322 │ W │ 10d │ 8 │ 6 │ L │ P │

│ │ │ │ │ │ │

323 │ W │ 2m │ 12 │ 4 │ B │ │ +

│ │ │ │ │ │ │

324 │ W │ 22d │ 9 │ 6 │ B │ │ +

│ │ │ │ │ │ │

325 │ W │ 1m │ 8 │ 8 │ B │ P │

│ │ │ │ │ │ │

326 │ W │ 1m │ 5+ │ 2 │ B │ P │

│ │ │ │ │ │ │

327 │ W │ 1m │ 4 │ ? │ B │ │ +

328 │ W │ 5m │ 13 │ 3+ │ L │ P │ +

│ │ │ │ │ │ │

330 │ W │ 1m │ 10 │ 3 │ L │ │

331 │ W │ 1m │ 12 │ 11+ │ B │ P │ +

332 │ W │ 1m │ 17 │ 3 │ L │ P │ +

333 │ W │ 19d │ 15 │ 7 │ L │ P │

│ │ │ │ │ │ │

334 │ W │ 14d │ 16 │ 5 │ B │ │

│ │ │ │ │ │ │

335 │ W │ 1m │ 7 │ ? │ ? │ │

│ │ │ │ │ │ │

336 │ W │ 2m │ 12 │ 6 │ B │ P │

337 │ W │ 1m │ 9 │ 2? │ L │ │ +

338 │ W │ 1m │ 7 │ 5+ │ B │ │ +

339 │ W │ 2m │ 9 │ 6? │ L │ │

340 │ W │ 35d │ 8 │ 3 │ L │ P │

341 │ W │ 3m │ 6 │ 4+ │ │ │ +

342 │ W │ 2m │ 9 │ 3? │ L │ P │

343 │ W │ 1m │ 11 │ 1? │ L │ │ +

344 │ W │ 4m │ 13 │ 6 │ L │ │

345 │ W │ 1d │ ? │ 7 │ L │ P │

│ │ │ │ │ │ │

346 │ W │ 26d │ 16 │ 10 │ B │ P │ +

│ │ │ │ │ │ │

347 │ C │ 3d │ 10 │ 3 │ L │ P │

348 │ C │ 4d │ 8 │ 8 │ B │ P │ +

349 │ W │ 2d │ 12 │ 6 │ L │ P │ +

│ │ │ │ │ │ │

350 │ W │ 2m │ 6 │ 2? │ B │ │ +

351 │ C │ 4m │ 4 │ 3+ │ L │ P │

352 │ C │ 2m │ 8 │ 4 │ L │ P │ +

353 │ C │ 6m │ 18 │ 18 │ L │ P │ +

│ │ │ │ │ │ │

354 │ W │ 15d │ 2+ │ 2 │ L │ P │

│ │ │ │ │ │ │

355 │ W │ 21d │ 7 │ 7 │ B │ P │

│ │ │ │ │ │ │

356 │ C │ 5d │ 8 │ 4 │ L │ │

357 │ W │ 1m │ 10 │ 6+ │ L │ │ +

│ │ │ │ │ │ │

358 │ W │ 1m │ 15 │ 6? │ L │ │ +

359 │ W │ 1m │ 7+ │ ? │ L │ │

360 │ W │ 36d │ 10 │ 3 │ L │ P │ +

361 │ W │ 3m │ 8 │ 2 │ L │ │ +

362 │ W │ 4m │ 15 │ 13+ │ L │ │ +

363 │ W │ 3m │ 8 │ 1+ │ L │ P │ +

364 │ W │ 6d │ 9 │ 5+ │ B │ │

365 │ W │ 2m │ 11 │ 2 │ B │ │ +

366 │ W │ 6d │ 8 │ 1+ │ B │ │ +

367 │ W │ 22d │ 15 │ 8+ │ L │ │ +

368 │ C │ 4d │ 15 │ 11+ │ L │ P │ +

369 │ W │ 68d │ 7+ │ 4 │ B │ P │

370 │ W │ 17d │ 17 │ 14 │ L │ P │

│ │ │ │ │ │ │

372 │ W │ 1m │ 17 │ 5 │ L │ P │

373 │ W │ 4d │ 11 │ 1? │ B │ │

374 │ C │ 4d │ 10 │ 5 │ L │ P │ +

375 │ C │ 4d │ 12 │ 6 │ L │ P │

376 │ W │ 1m │ 10 │ 7+ │ B │ P │

│ │ │ │ │ │ │

377 │ W │ 1m │ 7 │ 4? │ B │ P │ +

378 │ W │ 1m │ 28 │ 7 │ B │ P │

│ │ │ │ │ │ │

379 │ W │ 11m │ 7 │ 1 │ B │ │ +

│ │ │ │ │ │ │

380 │ W │ 3m │ 11 │ ? │ B │ P │

381 │ W │ 21d │ 13 │ 9? │ L │ P │

│ │ │ │ │ │ │

382 │ W │ 1m │ 9 │ 6+ │ L │ P │

383 │ W │ 2m │ 9 │ 2 │ L │ │

│ │ │ │ │ │ │

384 │ W │ 1m │ 13 │ 5 │ L │ │ +

385a │ W │ 3w │ 12 │ 6? │ B │ P │

385b │ W │ 2m │ 11 │ 4 │ L │ │ +

385c │ W │ 24d │ 17 │ 10 │ B │ P │

│ │ │ │ │ │ │

386 │ W │ 1m │ ? │ 5 │ L │ P │

│ │ │ │ │ │ │

387 │ W │ 3w │ 19 │ 9 │ B │ P │

│ │ │ │ │ │ │

388 │ W │ 3m │ 11 │ 7 │ L │ P │ +

389 │ W │ 1m │ 15 │ 15 │ L │ P │

391 │ W │ 25d │ 13 │ 13 │ L │ P │ +

392 │ W │ 1m │ 12 │ 8+ │ L │ P │ +

393 │ W │ 1m │ 20 │ 4 │ L │ │ +

394 │ W │ 21d │ ? │ ? │ L │ P │

395a │ W │ 1m │ 19 │ 11? │ L │ P │

│ │ │ │ │ │ │

395b │ W │ 3m │ 12 │ 3? │ B │ P │

396 │ W │ 2m │ 7 │ 1+ │ B │ │ +

397 │ W │ 21d │ 22 │ 14 │ B │ P │

│ │ │ │ │ │ │

398 │ W │ 1m │ 16 │ 6? │ B │ P │

399 │ W │ 1m │ 18 │ 4 │ L │ │ +

400 │ W │ 1m │ 15 │ 11+ │ L │ │ +

401 │ W │ 1m │ 13+ │ 9 │ B │ P │ +

402 │ W │ 1m │ 14 │ 8 │ B │ P │

│ │ │ │ │ │ │

404 │ │ │ │ │ B │ P │

405 │ W │ 21d │ 13 │ 11+ │ B │ │ +

406 │ C │ 2d │ 18 │ 15? │ L │ P │ +

408 │ C │ 1m │ 13 │ ? │ L │ P │

409 │ C │ 6d │ 12 │ 9+ │ L │ P │

410 │ W │ 35d │ 13+ │ 13+ │ L │ P │

│ │ │ │ │ │ │

411 │ W │ 3m │ 16 │ 2 │ B │ P │ +

│ │ │ │ │ │ │

412 │ W │ 1m │ 15 │ 13? │ L │ │ +

│ │ │ │ │ │ │

413 │ C │ 2m │ 13 │ 8+ │ L │ P │

│ │ │ │ │ │ │

414 │ C │ 7d │ 18 │ 4 │ L │ P │ +

│ │ │ │ │ │ │

415 │ C │ 16d │ 8 │ 6+ │ L │ P │ +

416 │ C │ 7d │ 14 │ 6? │ L │ P │

418 │ W │ 2m │ 19 │ 4 │ B │ │

│ │ │ │ │ │ │

419 │ W │ 4m │ 20 │ ? │ L │ P │

│ │ │ │ │ │ │

420 │ W │ 1m │ 11 │ 3 │ B │ P │

│ │ │ │ │ │ │

421 │ W │ 21d │ 19 │ 15? │ B │ P │

│ │ │ │ │ │ │

422 │ W │ 3m │ 11+ │ 11+ │ B │ P │ +

│ │ │ │ │ │ │

423 │ W │ 1m │ 16 │ 12? │ B │ P │

│ │ │ │ │ │ │

424 │ W │ 5y │ 14 │ 6 │ L │ P │

425 │ W │ 1m │ 29 │ 14 │ B │ P │

│ │ │ │ │ │ │

426 │ W │ 4m │ 20 │ 13 │ ? │ │ +

│ │ │ │ │ │ │

427 │ W │ 1m │ 16 │ ? │ L │ P │

428 │ W │ 3w │ 25 │ 21 │ L │ P │

│ │ │ │ │ │ │

429 │ C │ 2m │ 7+ │ 5 │ L │ P │

│ │ │ │ │ │ │

430 │ W │ 2m │ 16+ │ 7 │ L │ P │ +

│ │ │ │ │ │ │

431 │ W │ 21d │ 23 │ 18 │ L │ P │

432 │ W │ 42d │ 19 │ 12+? │ L │ P │ +

│ │ │ │ │ │ │

433 │ W │ 1m │ 19 │ 17 │ B │ P │

│ │ │ │ │ │ │

434 │ W │ 4m │ 14+ │ 10 │ L │ │

│ │ │ │ │ │ │

435 │ W │ 1m │ 16+ │ 2? │ B │ │

│ │ │ │ │ │ │

436 │ C │ 11m │ 5 │ 3+? │ B │ │ +

│ │ │ │ │ │ │

437 │ C │ 5m │ 11 │ 7? │ L │ P │ +

440 │ W │ 1m │ 19 │ 12? │ L │ P │

│ │ │ │ │ │ │

445 │ W │ 1m │ 27 │ 16? │ │ P │

│ │ │ │ │ │ │

446 │ W │ 8d │ 13 │ ? │ │ P │

447 │ W │ 8d │ 10 │ 2 │ B │ │

│ │ │ │ │ │ │

448 │ W │ 70d │ 17 │ 14+ │ L │ P │

449 │ W │ 2m │ 27 │ 13+ │ B │ P │

│ │ │ │ │ │ │

452 │ W │ 4m │ 14 │ 9 │ B │ P │

│ │ │ │ │ │ │

451 │ C │ 2m │ 7 │ 3+ │ B │ │ +

│ │ │ │ │ │ │

455 │ C │ │ 26 │ 22+ │ B │ │

│ │ │ │ │ │ │

456 │ W │ 1m │ 23+ │ 20+ │ L │ P │

457 │ W │ 17m │ 17+ │ 17+ │ B │ │

│ │ │ │ │ │ │

458 │ W │ 11m │ 10 │ 8+? │ L │ │

│ │ │ │ │ │ │

459 │ C │ 10d │ 6 │ 3 │ B │ P │

│ │ │ │ │ │ │

460 │ W │ 1m │ 17 │ 17 │ L │ P │

│ │ │ │ │ │ │

461 │ C │ 5d │ 14 │ 8+ │ L │ P │ +

│ │ │ │ │ │ │

462 │ C │ 5d │ 15+ │ 12 │ B │ │

463 │ W │ 3m │ 20 │ 12 │ B │ P │

│ │ │ │ │ │ │

464 │ C │ 21d │ 24 │ 17? │ L │ P │

│ │ │ │ │ │ │

465 │ W │ 1m │ 24+ │ 11 │ LB │ P │

│ │ │ │ │ │ │

466 │ W │ 2d │ 13 │ 3 │ B │ │ +

467 │ W │ 3m │ 30 │ 25? │ B │ P │

│ │ │ │ │ │ │

468 │ W │ 1m │ 22+ │ 6 │ L │ P │ +

│ │ │ │ │ │ │

469 │ W │ 1m │ 25 │ 12 │ B │ P │

471 │ C │ │ 6+? │ 4 │ L │ P │ +

│ │ │ │ │ │ │

472 │ W │ 1m │ 37 │ 21 │ B │ P │

│ │ │ │ │ │ │

473 │ W │ 2w │ 28+ │ 24 │ B │ P │

│ │ │ │ │ │ │

474 │ W │ 1m │ 36 │ 31+ │ L │ │

│ │ │ │ │ │ │

476 │ W │ 7d │ 6 │ 2 │ B │ P │

477 │ W │ 5d │ 9 │ 5 │ B │ │

│ │ │ │ │ │ │

478 │ W │ 2m │ 9 │ 3 │ L │ │

479 │ C │ 8d │ 29 │ 15 │ L │ P │ +

│ │ │ │ │ │ │

480 │ W │ 4m │ 31+ │ 29 │ B │ │

│ │ │ │ │ │ │

482 │ W │ 2m │ 11 │ 5+ │ B │ P │

│ │ │ │ │ │ │

485 │ W │ 3d │ 9+ │ 3+ │ B │ P │

│ │ │ │ │ │ │

487 │ W │ 21d │ 55 │ 40 │ B │ P │

│ │ │ │ │ │ │

488 │ W │ 4d │ 16 │ 8 │ L │ P │

│ │ │ │ │ │ │

489 │ C │ 8d │ 11 │ 4 │ B │ P │ +

│ │ │ │ │ │ │

494 │ W │ 2m │ 11 │ 3 │ L │ │

│ │ │ │ │ │ │

498 │ W │ 1y │ 6 │ 1? │ L │ │

│ │ │ │ │ │ │

499 │ W │ 5m │ 36 │ 5 │ B │ P │

│ │ │ │ │ │ │

504 │ W │ 3m │ 6 │ 3 │ L │ │

│ │ │ │ │ │ │

506 │ W │ 8m │ 7+ │ 2? │ B │ │

│ │ │ │ │ │ │

───────┴────┴────────┴────────┴─────────┴─────────┴──────────┴─────────

═══════╤═══════════════╤═══════════════╤═════════════╤═════════════

NO. OF │PERIBRONCHIOLAR│ HEMORRHAGIC │ LOBULAR │PERIBRONCHIAL

AUTOPSY│ CONSOLIDATION │PERIBRONCHIOLAR│CONSOLIDATION│CONSOLIDATION

│ │ CONSOLIDATION │ │

│ │ │ │

───────┼───────────────┼───────────────┼─────────────┼─────────────

229 │ │ │ │

│ │ │ │

231 │ │ │ + │

232 │ │ │ │

│ │ │ │

233 │ │ │ + │

236 │ │ │ │

│ │ │ │

237 │ │ + │ + │

238 │ │ │ │

│ │ │ │

239 │ │ │ │

│ │ │ │

240 │ M │ │ + │

241 │ │ │ │

│ │ │ │

242 │ │ + │ + │

│ │ │ │

243 │ M │ │ │

244 │ M │ + │ + │

│ │ │ │

246 │ M │ │ │

│ │ │ │

247 │ M │ + │ + │

│ │ │ │

248 │ │ │ │

249 │ M │ │ + │

250 │ M │ │ + │

│ │ │ │

251 │ │ + │ + │

252 │ M │ │ + │

│ │ │ │

253 │ M │ │ + │ +

│ │ │ │

254 │ M │ │ + │

│ │ │ │

255 │ M │ + │ + │

│ │ │ │

256 │ M │ │ │

│ │ │ │

257 │ │ │ + │

│ │ │ │

258 │ M │ │ + │

│ │ │ │

259 │ │ │ + │

│ │ │ │

260 │ │ │ │

261 │ │ │ │

│ │ │ │

262 │ │ │ + │

│ │ │ │

263 │ │ │ + │

│ │ │ │

264 │ │ │ │

│ │ │ │

265 │ │ │ │

│ │ │ │

266 │ │ + │ + │

│ │ │ │

267 │ │ │ │

│ │ │ │

268 │ │ │ │

│ │ │ │

269 │ │ │ │

│ │ │ │

270 │ │ │ + │ h

│ │ │ │

271 │ │ │ + │

│ │ │ │

272 │ │ │ │

273 │ + │ │ │

│ │ │ │

274 │ │ │ + │

│ │ │ │

275 │ M │ + │ + │

│ │ │ │

276 │ │ │ │

│ │ │ │

277 │ │ │ │

│ │ │ │

278 │ │ │ │

│ │ │ │

279 │ │ + │ │

280 │ │ + │ + │

│ │ │ │

281 │ │ + │ + │ h

│ │ │ │

282 │ │ │ + │

│ │ │ │

283 │ + │ + │ + │ M

│ │ │ │

284 │ │ + │ │

│ │ │ │

285 │ M │ │ │

│ │ │ │

286 │ M │ │ │

│ │ │ │

287 │ + │ │ │

│ │ │ │

288 │ M │ │ + │ h

│ │ │ │

289 │ M │ │ + │ M

│ │ │ │

290 │ │ │ │

│ │ │ │

291 │ + │ │ + │ M

│ │ │ │

292 │ │ │ │

│ │ │ │

293 │ │ │ │

│ │ │ │

295 │ │ │ │

│ │ │ │

296 │ + │ │ │

│ │ │ │

297 │ │ │ + │

│ │ │ │

298 │ │ │ │

│ │ │ │

299 │ │ │ │

│ │ │ │

300 │ M │ │ │ h

│ │ │ │

301 │ │ │ │

│ │ │ │

302 │ │ │ │

│ │ │ │

303 │ │ │ + │

│ │ │ │

304 │ │ │ │

│ │ │ │

305 │ │ │ │

│ │ │ │

306 │ │ │ + │

│ │ │ │

308 │ │ │ + │

│ │ │ │

309 │ │ │ │

310 │ │ │ │

│ │ │ │

312 │ M │ │ + │ h

│ │ │ │

313 │ │ │ │

│ │ │ │

314 │ │ │ + │

│ │ │ │

315 │ │ │ │

│ │ │ │

316 │ │ │ │

│ │ │ │

317 │ │ │ │

│ │ │ │

318 │ │ │ │

│ │ │ │

319 │ │ │ + │

│ │ │ │

320 │ │ │ │

321 │ │ │ │

│ │ │ │

322 │ │ │ + │

│ │ │ │

323 │ │ │ │

│ │ │ │

324 │ │ │ │

│ │ │ │

325 │ M │ │ │

│ │ │ │

326 │ │ │ + │ h

│ │ │ │

327 │ │ │ │

328 │ │ │ │

│ │ │ │

330 │ M │ │ │

331 │ │ │ │

332 │ M │ │ │ h

333 │ M │ │ + │

│ │ │ │

334 │ M │ │ │

│ │ │ │

335 │ │ │ + │

│ │ │ │

336 │ M │ │ + │

337 │ │ │ │

338 │ │ │ │

339 │ │ │ + │

340 │ │ + │ + │

341 │ │ │ │

342 │ │ + │ + │

343 │ │ │ │

344 │ │ │ + │

345 │ + │ + │ │

│ │ │ │

346 │ M │ + │ │

│ │ │ │

347 │ │ │ + │ h

348 │ │ │ │

349 │ │ │ │

│ │ │ │

350 │ │ │ │

351 │ │ │ + │

352 │ │ + │ + │

353 │ │ │ │

│ │ │ │

354 │ M │ │ │ h

│ │ │ │

355 │ │ + │ │

│ │ │ │

356 │ │ │ + │

357 │ │ + │ + │

│ │ │ │

358 │ │ │ │

359 │ M │ │ │ h

360 │ + │ │ + │

361 │ │ │ │

362 │ │ │ │

363 │ │ │ │

364 │ │ │ + │

365 │ │ + │ + │

366 │ M │ │ │

367 │ │ │ │

368 │ M │ │ │

369 │ │ + │ + │

370 │ + │ │ + │

│ │ │ │

372 │ │ + │ + │ Mh

373 │ │ │ + │

374 │ │ │ │ +

375 │ + │ │ + │

376 │ │ + │ + │ M

│ │ │ │

377 │ │ │ + │

378 │ + │ │ │

│ │ │ │

379 │ │ │ │

│ │ │ │

380 │ + │ │ + │

381 │ │ │ + │

│ │ │ │

382 │ + │ │ │

383 │ │ │ + │

│ │ │ │

384 │ │ │ │

385a │ │ │ + │

385b │ │ │ │

385c │ M │ + │ + │

│ │ │ │

386 │ │ + │ + │

│ │ │ │

387 │ │ + │ + │ +

│ │ │ │

388 │ │ │ │

389 │ │ + │ │

391 │ + │ │ + │ h

392 │ M │ │ │ +

393 │ │ │ │

394 │ │ + │ + │ h

395a │ M │ │ + │

│ │ │ │

395b │ │ │ + │ h

396 │ │ │ │

397 │ M │ │ + │

│ │ │ │

398 │ + │ │ │ M

399 │ │ │ │

400 │ │ │ │

401 │ M │ │ │ h

402 │ M │ │ + │ +

│ │ │ │

404 │ + │ + │ │

405 │ M │ │ │

406 │ │ │ │

408 │ │ + │ + │

409 │ │ + │ + │ M

410 │ + │ │ + │ M

│ │ │ │

411 │ │ + │ │

│ │ │ │

412 │ │ │ │ M

│ │ │ │

413 │ │ + │ + │

│ │ │ │

414 │ │ │ │

│ │ │ │

415 │ │ │ + │

416 │ │ │ │

418 │ │ │ + │

│ │ │ │

419 │ + │ │ + │ M

│ │ │ │

420 │ │ + │ │ M

│ │ │ │

421 │ │ │ + │ M

│ │ │ │

422 │ │ + │ │ M

│ │ │ │

423 │ + │ │ │ M

│ │ │ │

424 │ │ │ + │ +

425 │ + │ │ + │ M

│ │ │ │

426 │ │ │ │

│ │ │ │

427 │ │ + │ + │

428 │ M │ │ + │

│ │ │ │

429 │ + │ │ + │

│ │ │ │

430 │ │ + │ │

│ │ │ │

431 │ + │ │ + │

432 │ │ │ │

│ │ │ │

433 │ M │ + │ │ M

│ │ │ │

434 │ │ │ + │

│ │ │ │

435 │ │ + │ │

│ │ │ │

436 │ │ │ │

│ │ │ │

437 │ │ │ │

440 │ + │ + │ + │ M

│ │ │ │

445 │ M │ │ │ h

│ │ │ │

446 │ │ + │ + │

447 │ │ │ + │

│ │ │ │

448 │ + │ │ + │ Mh

449 │ + │ + │ │

│ │ │ │

452 │ M │ │ │

│ │ │ │

451 │ │ │ │

│ │ │ │

455 │ │ + │ │

│ │ │ │

456 │ │ + │ │

457 │ + │ + │ + │

│ │ │ │

458 │ │ + │ + │

│ │ │ │

459 │ │ + │ + │

│ │ │ │

460 │ + │ │ + │ M

│ │ │ │

461 │ M │ + │ │

│ │ │ │

462 │ │ │ + │

463 │ + │ │ + │ Mh

│ │ │ │

464 │ │ │ + │

│ │ │ │

465 │ M │ │ │

│ │ │ │

466 │ │ │ + │

467 │ │ + │ + │

│ │ │ │

468 │ │ │ + │

│ │ │ │

469 │ + │ │ + │

471 │ │ │ │

│ │ │ │

472 │ + │ + │ + │

│ │ │ │

473 │ + │ │ + │

│ │ │ │

474 │ │ │ │

│ │ │ │

476 │ M │ │ + │

477 │ │ + │ + │

│ │ │ │

478 │ │ │ + │

479 │ M │ │ │

│ │ │ │

480 │ │ │ + │

│ │ │ │

482 │ + │ + │ + │ M

│ │ │ │

485 │ M │ │ │

│ │ │ │

487 │ + │ │ │

│ │ │ │

488 │ M │ │ │

│ │ │ │

489 │ │ + │ │ M

│ │ │ │

494 │ │ │ + │ h

│ │ │ │

498 │ │ │ + │

│ │ │ │

499 │ M │ │ │

│ │ │ │

504 │ M │ │ │

│ │ │ │

506 │ │ │ + │

│ │ │ │

───────┴───────────────┴───────────────┴─────────────┴─────────────

Epidemic Respiratory Disease The pneumonias and other infections of the repiratory tract accompanying influenza and measles · 第 4 / 10 章