THE PATHOLOGY AND BACTERIOLOGY OF PNEUMONIA FOLLOWING MEASLES
EUGENE L. OPIE, M.D.; FRANCIS G. BLAKE, M.D.; JAMES C. SMALL, M.D.; AND
THOMAS M. RIVERS, M.D.
Among 18 autopsies upon men who have died with pneumonia following
measles there are pulmonary lesions representing almost every type of
pneumonia which has been found in association with influenza. In most
instances pneumonia made its appearance during the second week of
measles and death occurred during the third week. Of 16 instances in
which the record is definite, pneumonia had its onset during the first
week of measles in 4 instances, during the second week in 11 instances,
and in one instance (Autopsy 390) perhaps not referable to measles in
the fifth week. The duration of pneumonia varied from three to
thirty-two days; in 10 instances it did not exceed one week, in 5
instances it was between one and two weeks and in one instance,
thirty-two days. When the duration of pneumonia exceeded ten days some
evidence of chronic pulmonary disease was found at autopsy.
The same lack of correspondence between clinical diagnosis and pulmonary
lesions noted with influenza was found following measles. In accordance
with the prevailing opinion concerning the character of pneumonia
following measles, the diagnosis of bronchopneumonia was made in 13
instances and in all of these cases bronchopneumonia was found at
autopsy. The diagnosis of lobar pneumonia was made 5 times and was
correct only once. Nevertheless, lobar pneumonia was present 4 times,
but was recognized only once (Autopsy 486.) Failure to recognize lobar
pneumonia, was doubtless due in part at least to its association with
purulent bronchitis and peribronchiolar pneumonia (Table LXXI).
TABLE LXXI
═══════╤════╤════════╤════════╤═════════╤═════════╤══════════╤═════════
NO. OF │RACE│ LENGTH │DURATION│DURATION │CLINICAL │ PURULENT │ LOBAR
AUTOPSY│ │ OF │ OF │ OF │DIAGNOSIS│BRONCHITIS│PNEUMONIA
│ │MILITARY│ILLNESS │PNEUMONIA│ │ │
│ │SERVICE │ │ │ │ │
───────┼────┼────────┼────────┼─────────┼─────────┼──────────┼─────────
390 │ W │ 1m. │ 35 │ 6 │ L │ │
│ │ │ │ │ │ │
438 │ W │ 2m. │ 22 │ 12? │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
439 │ W │ 10d. │ 14 │ 11? │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
441 │ W │ 1m. │ 16 │ 11 │ B │ P │
│ │ │ │ │ │ │
442 │ W │ 1m. │ 17 │ 2+ │ L │ P │
│ │ │ │ │ │ │
443 │ W │ 21d. │ 23 │ 14 │ B │ P │
│ │ │ │ │ │ │
444 │ W │ 1m. │ 9 │ 3 │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
450 │ W │ 29d. │ 19 │ 5 │ B │ │ +
│ │ │ │ │ │ │
│ │ │ │ │ │ │
453 │ W │ 36d. │ 13 │ 6 │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
481 │ W │ 54d. │ 4+ │ 3? │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
484 │ W │ 42d. │ 20 │ 7 │ B │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
486 │ C │ 6d. │ 17 │ 8 │ L │ P │ +
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
491 │ W │ 2m. │ 19 │ 5 │ B │ │
│ │ │ │ │ │ │
492 │ W │ 49d. │ 20? │ 11? │ L │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
496 │ W │ 1m. │ 43 │ 32 │ L │ P │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
505 │ C │ 4m. │ 16 │ 6 │ B │ P │ +
│ │ │ │ │ │ │
│ │ │ │ │ │ │
507 │ C │ 5m. │ 14 │ 3 │ B │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
508 │ C │ 2m. │ 16 │ 5 │ B │ │ +
│ │ │ │ │ │ │
│ │ │ │ │ │ │
│ │ │ │ │ │ │
───────┴────┴────────┴────────┴─────────┴─────────┴──────────┴─────────
═══════╤═══════════════╤═══════════════╤═════════════╤═════════════
NO. OF │PERIBRONCHIOLAR│ HEMORRHAGIC │ LOBULAR │PERIBRONCHIAL
AUTOPSY│ CONSOLIDATION │PERIBRONCHIOLAR│CONSOLIDATION│CONSOLIDATION
│ │ CONSOL. │ │
│ │ │ │
───────┼───────────────┼───────────────┼─────────────┼─────────────
390 │ M │ │ + │
│ │ │ │
438 │ + │ │ + │
│ │ │ │
│ │ │ │
│ │ │ │
│ │ │ │
439 │ M │ + │ + │
│ │ │ │
│ │ │ │
441 │ + │ + │ + │ M
│ │ │ │
442 │ M │ │ + │
│ │ │ │
443 │ + │ │ │ M
│ │ │ │
444 │ M │ + │ + │
│ │ │ │
│ │ │ │
450 │ M │ │ │
│ │ │ │
│ │ │ │
453 │ + │ │ + │ M
│ │ │ │
│ │ │ │
481 │ + │ │ + │
│ │ │ │
│ │ │ │
│ │ │ │
484 │ + │ │ + │ M
│ │ │ │
│ │ │ │
486 │ │ │ │
│ │ │ │
│ │ │ │
│ │ │ │
│ │ │ │
491 │ │ + │ │
│ │ │ │
492 │ M │ + │ + │ M
│ │ │ │
│ │ │ │
│ │ │ │
│ │ │ │
496 │ + │ │ + │
│ │ │ │
│ │ │ │
505 │ │ │ │
│ │ │ │
│ │ │ │
507 │ │ │ │
│ │ │ │
│ │ │ │
508 │ M │ │ │ M
│ │ │ │
│ │ │ │
│ │ │ │
───────┴───────────────┴───────────────┴─────────────┴─────────────
═══════╤═══════╤════════════╤═════════╤═══════╤══════════════
NO. OF │ABSCESS│INTERSTITIAL│MULTIPLE │EMPYEMA│BRONCHIECTASIS
AUTOPSY│ │SUPPURATIVE │ABSCESSES│ │
│ │ PNEUMONIA │ IN │ │
│ │ │CLUSTERS │ │
───────┼───────┼────────────┼─────────┼───────┼──────────────
390 │ │ │ │ │
│ │ │ │ │
438 │ + │ │ │ E │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
439 │ │ │ │ │ +
│ │ │ │ │
│ │ │ │ │
441 │ │ │ │ │ +
│ │ │ │ │
442 │ N │ + │ │ E │
│ │ │ │ │
443 │ │ │ │ │ +
│ │ │ │ │
444 │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
450 │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
453 │ │ │ │ │ +
│ │ │ │ │
│ │ │ │ │
481 │ │ │ │ │ +
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
484 │ │ │ │ │ +
│ │ │ │ │
│ │ │ │ │
486 │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
491 │ │ + │ │ E │
│ │ │ │ │
492 │ + │ │ │ E │ +
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
496 │ │ │ │ │ +
│ │ │ │ │
│ │ │ │ │
505 │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
507 │ N │ + │ │ E │
│ │ │ │ │
│ │ │ │ │
508 │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
───────┴───────┴────────────┴─────────┴───────┴──────────────
═══════╤════════════════╤══════════╤════════╤════════╤════════╤════════
NO. OF │ UNRESOLVED │ORGANIZING│BACTERIA│BACTERIA│BACTERIA│BACTERIA
AUTOPSY│BRONCHOPNEUMONIA│BRONCHITIS│ IN │ IN │IN LUNG │IN BLOOD
│ │ │ SPUTUM │BRONCHUS│ │OF HEART
│ │ │ │ │ │
───────┼────────────────┼──────────┼────────┼────────┼────────┼────────
390 │ │ │No S. │ │ │Pneum.
│ │ │Hem. │ │ │II a
438 │ + │ │B. inf. │S. hem.,│Pneum. │0
│ │ │ │B. inf. │II, S. │
│ │ │ │ │vir., │
│ │ │ │ │B. inf.,│
│ │ │ │ │S. hem. │
439 │ │ + │No S. │B. coli │Pneum. │0
│ │ │hem. │ │IIa, S.│
│ │ │ │ │aur. │
441 │ │ │ │B. inf.,│B. inf.,│0
│ │ │ │S. aur. │S. aur. │
442 │ │ │No S. │B. inf.,│ │S. hem.
│ │ │hem. │S. hem. │ │
443 │ + │ │No S. │B. inf.,│B. coli.│0
│ │ │hem. │B. coli.│ │
444 │ │ │B. inf. │Pneum. │Pneum. │Pneum.
│ │ │ │IIa, B.│IIa, │II a.
│ │ │ │inf. │B.inf. │
450 │ │ │B.inf., │B. inf.,│B. inf. │Pneum.
│ │ │No. S. │Staph. │ │IV.
│ │ │hem. │ │ │
453 │ │ │ │Pneum. │Pneum. │Pneum.
│ │ │ │I, B. │I. │I.
│ │ │ │Inf. │ │
481 │ + │ │No S. │B. inf.,│B. inf. │0
│ │ │hem. │Pneum. │ │
│ │ │ │IIa, │ │
│ │ │ │S.hem. │ │
484 │ + │ │Pneum. │B. inf.,│ │0
│ │ │IV, B. │Diploids│ │
│ │ │inf. │ │ │
486 │ │ │No S. │B. inf.,│B. inf. │0
│ │ │hem. │Pneum. │ │
│ │ │ │IIa, S.│ │
│ │ │ │hem., │ │
│ │ │ │Staph. │ │
491 │ │ │S. hem. │B. inf.,│S. hem.,│S. hem.
│ │ │ │B. coli.│B. coli.│
492 │ + │ │S. hem.,│ │S.hem., │S. hem.
│ │ │B. inf. │ │Pneum. │
│ │ │ │ │IV, B. │
│ │ │ │ │coli., │
│ │ │ │ │B. inf. │
496 │ + │ + │B. inf.,│B. inf. │0 │0
│ │ │no S. │ │ │
│ │ │hem. │ │ │
505 │ │ │No S. │Pneum. │Pneum. │Pneum.
│ │ │hem. │II a., │II a. │II a.
│ │ │ │S. hem. │ │
507 │ │ │S. hem. │S. hem.,│S. hem.,│S. hem.
│ │ │ │B. inf.,│S. aur. │
│ │ │ │S. aur. │ │
508 │ │ │S. hem. │Pneum. │Pneum. │Pneum.
│ │ │ │IIa, B.│II a. │II a.
│ │ │ │inf., S.│ │
│ │ │ │hem. │ │
───────┴────────────────┴──────────┴────────┴────────┴────────┴────────
=Changes in Bronchi.=—The changes in the bronchi do not differ in
character from those associated with pneumonia following influenza.
Purulent bronchitis recognized at autopsy by the presence of
mucopurulent material in the small bronchi was found in a much larger
proportion of instances in this group of autopsies occurring in 13 of 18
instances (72.2 per cent), whereas it was present in only 55.6 per cent
of autopsies on individuals with pneumonia following influenza. There
was peribronchial hemorrhage recognizable on gross examination in 3
autopsies and microscopically in 3 additional instances.
Bronchiectasis was present in a considerable proportion of these
autopsies, dilatation of bronchi being noted in 7, but it was usually
moderately advanced and at times limited to the bases of the lungs. The
short duration of respiratory disease perhaps explains the infrequency
of advanced bronchiectasis. The incidence of the lesion is greater with
measles (43.7 per cent) than with influenza (22.4 per cent).
Microscopic changes in the bronchi do not differ from those found after
influenza. Evidence of acute inflammation, often hemorrhagic in
character, is found within the lumen of the bronchus and in the tissues
immediately in contact with the lumen. Not infrequently the epithelium
is lost; there is superficial necrosis and deposition of fibrin upon the
surface and within the tissue. In the deeper tissues of the bronchial
wall there is infiltration with lymphoid and plasma cells, which in the
larger bronchi is particularly advanced about the mucous glands of which
the acini exhibit degenerative changes. With the onset of chronic
changes new formation of fibrous tissue occurs in the wall of the
bronchus and in the contiguous interalveolar walls. The lining
epithelium often loses its columnar cells and assumes a squamous type.
Changes in the bronchi with bronchiectasis have been similar to those
following influenza. Weakening of the wall permitting dilatation is
brought about by necrosis extending outward from the lumen a varying
distance into the bronchial wall and permitting the formation tears
which diminish resistance to intrabronchial pressure.
=Lobar Pneumonia.=—Lobar pneumonia following measles occurred in 4
instances. Onset in these cases was on approximately the 9th, 10th,
11th, or 14th day of measles; the onset of bronchopneumonia bore a
similar time relation to the onset of measles, the average interval
being nine days. Hepatization with lobar pneumonia was in 1 instance
red, in 3 instances gray, and in all save 1 instance the consolidation
was firm and coarsely granular on section. In the exceptional instance
the greater part of the right upper lobe was laxly consolidated and
rather finely granular but the microscopic appearance was in all
instances that of lobar pneumonia. Lobar pneumonia in 2 of these cases
was associated with purulent bronchitis present in parts of the lung
that had not undergone consolidation, whereas in the other 2 instances
there were acute bronchitis and peribronchiolar pneumonia recognized by
microscopic examination.
In one instance hepatization of the lung presented some noteworthy
features.
=Autopsy 450.=—G. D., white, aged twenty-one, a farmer, resident of
Arkansas, had been in military service twenty-nine days. Onset of
illness began on October 2, nineteen days before death, and on
admission on the same day the diagnosis of measles was made. Signs
of pneumonia, regarded as bronchopneumonia, were recognized five
days before death. Three days later there was otitis media and
paracentesis was performed. On October 3 and 10 neither S.
hemolyticus nor B. influenzæ was found in the sputum; on October 17
and 20 S. hemolyticus was not found but B. influenzæ was present.
=Anatomic Diagnosis.=—Acute lobar pneumonia with gray and red
hepatization in right upper and lower lobes; edema and peribronchial
hemorrhage in left lung.
[Illustration:
Fig. 29.—Lobar pneumonia following measles, showing extension of
gray hepatization from lower to upper lobe through a defect in the
septum separating the two lobes. Autopsy 450.
]
The entire lower lobe of the right lung (Fig. 29) with the exception
of a narrow air-containing zone in contact with basal surface is
firmly consolidated. The greater part of the consolidated tissue is
yellowish gray, firm and coarsely granular. The uppermost part of
the consolidated tissue is softer than elsewhere as if it has
undergone autolysis. The lowermost part of the consolidated tissue
in a zone from 2.5 to 3.5 cm. in breadth is firmly consolidated but
deep red. The bronchi contain stiff plugs of fibrin. In the upper
lobe continuous with the consolidated part of the lower is a
semicircular patch of yellowish gray consolidation. It overlies the
line of the interlobular cleft at the site of a break in its
continuity. Consolidation appears to have spread from the lower lobe
into the upper at the site where the alveolar tissue of the two
lobes is continuous but is absent from that part of the upper lobe
separated from the lower by the interlobular cleft. This
semicircular patch of yellowish gray consolidation is separated from
air containing tissue of the upper lobe by a zone of red
hepatization about 1 cm. in thickness.
Bacteriologic examination showed the presence of Pneumococcus IV in
the blood of the heart; B. influenzæ alone was obtained from the
right lower lobe and B. influenzæ and staphylococcus from the left
main bronchus.
The distribution of lobar pneumonia in the foregoing autopsy indicates
that it has spread like a wave from the upper part of the lower lobe
(Fig. 32) penetrating into the upper where the alveolar tissue of the
two lobes is in contact; gray hepatization is everywhere separated from
air containing tissue by an advancing zone of red hepatization.
It may be assumed that lobar pneumonia was caused by Pneumococcus II
atypical in 3 instances although it was recovered from the lungs only
twice, for in the third instance (Autopsy 486) it was found in the
bronchus and in the inflamed pleural cavity; pneumococci were doubtless
previously present in the lung, but had disappeared at least from that
part from which the culture was made. Pneumococcus IV was evidently the
cause of pneumonia in 1 instance (Autopsy 450), for it was found in the
blood of the heart although it was absent in the culture from the lung.
Little significance can be attributed to the observation that B.
influenzæ was present in pure culture in the lungs from Autopsies 450
and 486, for the presence of Pneumococci IV in the blood of the heart in
Autopsy 450 and of Pneumococcus II atypical in the pleura in Autopsy 486
furnishes evidence in view of the occurrence of lobar pneumonia that
pneumococci had disappeared from the lungs. B. influenzæ was found both
in the lungs and bronchus or in the bronchus alone in 3 of these 4
cases.
The relation of hemolytic streptococci to the lesion is of interest. In
3 of 4 instances of lobar pneumonia this microorganism had entered the
bronchi but was not found in the lungs or in the heart’s blood; and
gross and histologic examination showed none of the lesions which are
usually caused by it. In 1 instance (Autopsy 508) hemolytic
streptococci, absent from the throat when the patient was admitted to
the hospital with measles sixteen days before death, appeared in a
culture made five days later and was subsequently found three times; it
had penetrated into the bronchus but failed to reach the lung.
Observations made upon lobar pneumonia following influenza have shown
the relative insusceptibility of lobar pneumonia with gray hepatization
to secondary infection with hemolytic streptococci (p. 160). Autopsy 508
demonstrates that occurrence of hemolytic streptococci in the sputum of
a patient with pneumonia does not furnish conclusive proof of the
existence of streptococcus pneumonia.
=Bronchopneumonia.=—Bronchopneumonia has been found in every instance of
pneumonia following measles save 3, namely in Autopsy 486, Autopsy 505
with lobar pneumonia and Autopsy 507 with interstitial suppurative
pneumonia. It is not improbable that further histologic study might have
demonstrated small patches of peribronchiolar pneumonia, for purulent
bronchitis was present in the two autopsies with lobar pneumonia. This
small group of cases has reproduced all of the important features of
bronchopneumonia following influenza. Hemorrhagic peribronchiolar
consolidation characterized by the presence of small gray spots
clustered about terminal bronchi upon a homogeneously red background has
been found in 5 of 18 instances of pneumonia with measles. Pfeiffer
regarded this lesion as characteristic of the pneumonia of influenza.
Peribronchiolar patches of consolidation with no surrounding hemorrhage
were found in 14 instances, being recognized first by microscopic
examination in half of this number. Lobular consolidation occurred in 11
autopsies and peribronchial fibrinous pneumonia was present in a third
of the autopsies on patients with pneumonia of measles.
Bronchial, peribronchial and intraalveolar hemorrhage is much more
commonly associated with the pneumonias of influenza than with the more
familiar types of acute bronchopneumonia. Exuded blood may undergo
absorption; and with bronchopneumonia which, persisting unresolved, has
assumed the characters of a chronic lesion, it is common to find
mononuclear cells often in great abundance filled with brown pigment
derived from the hemoglobin of red blood corpuscles.
Autopsy 439 is an example of acute hemorrhagic bronchopneumonia; there
are red lobular and confluent lobular patches of consolidation which
upon the pleural surface have a blue or purplish color. In the dependent
part of the left lung occupying a large part of the lower lobe there is
lax, red consolidation marked by gray or yellowish gray spots of
peribronchiolar pneumonia and in this lobe bronchi are encircled by
zones of hemorrhage. Pneumococcus II atypical was obtained from the
lung. In Autopsy 444 the lesion has the same hemorrhagic character
although lobular patches are in a stage of grayish red hepatization.
Pneumococcus II atypical has been found in the heart’s blood, and with
B. influenzæ in lungs and bronchus. Autopsy 441 is an example of the
occurrence of conspicuous nodules of peribronchiolar consolidation in
some parts of the lungs with the same lesion in other parts on a
background of hemorrhage. B. influenzæ and S. aureus have been found in
both lungs and bronchi.
Steinhaus[102] states that the pneumonia of measles is never lobular
inflammation but occurs in small patches several of which may be found
in a single lobule.
Chronic fibroid pneumonia following measles characterized by cellular
infiltration and proliferation of the interstitial tissue of the lung
has been described by Bartels,[103] Steinhaus,[104] Hart,[105]
MacCallum[104] and others.
[Illustration:
Fig. 30.—Unresolved bronchopneumonia with measles showing new
formation of fibrous tissue about a bronchus and in immediately
adjacent alveolar walls; partially obliterated alveoli occur in the
peribronchial fibrous tissue. Autopsy 481.
]
[Illustration:
Fig. 31.—Unresolved bronchopneumonia with measles showing a nodule of
chronic fibrous pneumonia surrounding a respiratory bronchiole.
Autopsy 481.
]
The incidence of unresolved bronchopneumonia among instances of
bronchopneumonia following measles is higher than that among
bronchopneumonias following influenza. There have been 6 instances of
chronic or unresolved bronchopneumonia among 18 pneumonias following
measles, namely 33.3 per cent. The incidence of unresolved
bronchopneumonia among 241 autopsies on pneumonia following influenza
has been 21, namely 8.7 per cent. The essential features of this chronic
lesion have been as follows: (_a_) chronic peribronchiolar pneumonia
indicated by the presence of firm nodules of peribronchiolar
consolidation which have considerable resemblance to miliary tubercles.
Induration of the nodule occurs because the walls of alveoli surrounding
and adjacent to a respiratory bronchiole (Fig. 31) become thickened and
infiltrated with cells and there is organization of exudate within the
alveoli. New formation of fibrous tissue (Fig. 32) occurs where the
acute inflammatory reaction of peribronchiolar consolidation is most
advanced (p. 169 and compare with Figs. 3 and 4), namely, about the
respiratory bronchiole, alveolar duct and the proximal parts of the
infundibula, disappearing as the distal half of the infundibulum is
approached. Distention of the alveoli explaining the distention of the
lung and its failure to collapse on section is a noteworthy feature of
the lesion. (_b_) Chronic peribronchial inflammation (Fig. 30) with new
formation of fibrous tissue about the smaller and medium-sized bronchi
extending into immediately adjacent alveolar walls and often associated
with organization of peribronchial fibrinous pneumonia. (_c_) Chronic
lobular inflammation with changes similar to those just cited,
distributed throughout entire lobules. (_d_) Moderate thickening of
interlobular septa. Bronchiectasis may be associated with the chronic
lesion (Autopsies 443, 481, 484, 492 and 496) but with one exception
(Autopsy 443) has been only moderately advanced. Suppurative pneumonia
with abscess formation has occurred twice (Autopsies 438 and 492).
[Illustration:
Fig. 32.—Unresolved bronchopneumonia with measles showing chronic
pneumonia about a respiratory bronchiole and alveolar duct; alveoli
about the proximal parts of three distended infundibula are filled
with polynuclear leucocytes, whereas inflammatory changes disappear
as the distal parts of the infundibula are approached. Autopsy 481.
]
With acute bronchopneumonia following measles the average duration of
pneumonia, determined by the date upon which physical signs of pneumonia
were first recognized and in consequence subject to some error, was
seven days; in instances of chronic bronchopneumonia the average
duration of pneumonia has been fifteen days.
The bacteriology of acute bronchopneumonia following measles is shown in
Table LXXII.
TABLE LXXII
════════════╤═══════╤═══════════════╤════════════════╤═════════════════
WITH NO │SPUTUM │ BACTERIA IN │ BACTERIA IN │ BACTERIA IN
SUPPURATION │IN LIFE│BLOOD OF HEART │ LUNGS │ BRONCHI
────────────┼───────┼───────────────┼────────────────┼─────────────────
Autopsy 390│ │Pneum. II atyp.│ │
439│ │0 │Pneum. II atyp. │B. coli
│ │ │ S. aur. │
441│ │0 │B. inf., S. aur.│B. inf., S. aur.
444│B. inf.│Pneum. II atyp.│Pneum. II atyp. │Pneum. II atyp.
│ │ │ B. inf. │ B. inf.
453│ │Pneum. I │Pneum. I │Pneum. I, B. inf.
With │ │ │ │
suppuration:│ │ │ │
442│S. hem.│S. hem. │ │B. inf., S. hem.
491│S. hem.│S. hem. │S. hem., B. coli│B. inf., B. coli
507│S. hem.│S. hem. │S. hem., S. aur.│S. hem., B. inf.,
│ │ │ │ S. aur.
────────────┴───────┴───────────────┴────────────────┴─────────────────
It is noteworthy that pneumococci have been recovered from the heart’s
blood or lung in all but 1 (Autopsy 441) of 5 instances of acute
bronchopneumonia with no suppuration and is doubtless the cause of this
pneumonia. Pneumococcus II atypical has been found in 3 of 4 instances
of lobar pneumonia following measles and is present in 3 of these 5
instances of bronchopneumonia.
Where suppuration has been found, hemolytic streptococci have been
present in the sputum, in the heart’s blood and either in the lungs
(Autopsy 491) or in the bronchi (Autopsy 442) or in both (Autopsy 507).
In these instances pneumococci have not been found, though in view of
the readiness with which pneumococci disappear from the lungs it is
possible that they have been the primary cause of bronchopneumonia.
The bacteriology of 6 instances of unresolved bronchopneumonia following
measles is given in Table LXXIII.
TABLE LXXIII
════════════╤═══════╤═══════════════╤════════════════╤═════════════════
WITH NO │SPUTUM │ BACTERIA IN │ BACTERIA IN │ BACTERIA IN
SUPPURATION │IN LIFE│BLOOD OF HEART │ LUNGS │ BRONCHUS
────────────┼───────┼───────────────┼────────────────┼─────────────────
Autopsy 443│ │0 │B. coli │B. inf., B.coli
481│ │0 │B. inf. │B. inf., Pneum.
│ │ │ │ II, atyp., S.
│ │ │ │ hem.
484│Pneum. │0 │0 │B. inf.,
│ IV., │ │ │ diphtheroids
│ B. │ │ │
│ inf. │ │ │
496│Pneum. │0 │0 │B. inf.
│ IV., │ │ │
│ B. │ │ │
│ inf. │ │ │
With │ │ │ │
Suppuration:│ │ │ │
Autopsy 438│B. inf.│0 │Pneum. II atyp.,│S. hem., B. inf.
│ │ │ S. vir. B. │
│ │ │ inf. S. hem. │
492│St. │S. hem. │S. hem., Pneum. │
│ hem.,│ │ IV, B. coli, │
│ B. │ │ B. inf. │
│ inf. │ │ │
────────────┴───────┴───────────────┴────────────────┴─────────────────
Whereas with acute bronchopneumonia death has been accompanied and
perhaps caused by bacterial invasion of the blood by pneumococci or
streptococci in 5 of 7 instances, with unresolved or chronic
bronchopneumonia, bacteriemia has been present only once, namely, in
Autopsy 492 in which with suppurative pneumonia hemolytic streptococci
have entered the blood. It is probable that pneumococci have likewise
had an important part in the causation in these instances of
bronchopneumonia which have run a chronic course but in all save 2 cases
(Autopsies 438 and 492) have disappeared from the lungs. Pneumococcus II
atypical has been found twice.
B. influenzæ has been found in association with acute bronchopneumonia
in the lungs in 1 of 6 examinations and in the bronchi in 5 of 6
examinations. These figures indicate that it is present in small numbers
if at all in the consolidated lung tissue but is relatively abundant in
the bronchi. With chronic bronchopneumonia B. influenzæ has been found
in every instance, in half of the examinations of lungs and in all of
the examinations of bronchi. In 1 instance (Autopsy 481) B. influenzæ
has been found in pure culture in the lung; Pneumococcus II atypical has
been found in the bronchus and has perhaps disappeared from the
pneumonic lung, since this microorganism is often destroyed in the late
stages of pneumonia so that its demonstration at autopsy is no longer
possible. In 1 instance B. influenzæ found in the bronchus has been the
only microorganism isolated at autopsy, although the sputum during life
contained B. influenzæ and Pneumococcus IV.
=Suppurative Pneumonia.=—Suppurative pneumonia with formation of
abscesses has occurred in 2 autopsies with pneumonia following measles
(Autopsies 438 and 492), both instances of chronic bronchopneumonia. In
Autopsy 438 the lower and posterior part of the left lower lobe has been
consolidated and has had on section a cloudy, grayish red color; within
this area of consolidation and immediately below the pleural surface
there have been opaque, yellow spots where the tissue has been softer
than elsewhere. Microscopic examination shows that the tissue has here
undergone widespread necrosis so that all nuclear stain has disappeared;
at the edges of the necrotic tissue polynuclear leucocytes are often
present in large numbers, but necrosis is much more conspicuous than
suppuration. In the necrotic tissue and at its edges streptococci are
present in vast numbers. Hemolytic streptococci have been grown both
from the lung and from the bronchus, but these have not been the only
microorganisms present, for Pneumococcus II atypical and S. viridans
have been obtained from the lungs and B. influenzæ from lungs and
bronchus.
In Autopsy 492 with chronic bronchopneumonia the posterior half of the
right lower lobe is laxly consolidated, deep red in color and with the
cloudy appearance often associated with streptococcus pneumonia; upon
this background are peribronchiolar spots of yellow color, in places
well seen below the pleura; in the corresponding part of the left lower
lobe similar nodules have been converted into small abscesses by central
suppuration. There is empyema on the right side, fibrinopurulent
pericarditis, and purulent peritonitis. Hemolytic streptococci had been
found in the sputum three times, the first examination being thirteen
days before death. This microorganism is found in pure culture in the
blood of the heart and with Pneumococci IV, B. coli and B. influenzæ in
the lung. Hemolytic streptococci were found in the right pleural exudate
and peritoneum.
The pneumonias following measles give opportunity to consider the
relationship of suppurative interstitial pneumonia to unresolved or
chronic bronchopneumonia, which is characterized by infiltration and
proliferation of the fibrous tissue of the lungs. A number of those who
have studied the pneumonia of measles have recognized that this chronic
interstitial lesion is a common sequela of measles. MacCallum has
designated the lesion “interstitial bronchopneumonia,” and has included
under this name its acute stage in which the interstitial character of
the lesion is not more evident than with other forms of acute
bronchopneumonia. He has regarded S. hemolyticus as the cause of
“interstitial bronchopneumonia” following measles. A review of the
autopsies which he has described shows that he has included under the
same designation typical instances of interstitial suppurative pneumonia
associated with suppurative lymphangitis. Instances of unresolved,
chronic or “interstitial” bronchopneumonia and of interstitial
suppurative pneumonia which we have observed after measles, demonstrate
that the two lesions are distinguishable both by their anatomic
characters and by their etiology.
Three instances of suppurative interstitial pneumonia occurred among the
pneumonias following measles (Autopsies 442, 491 and 507). The lesion is
characterized by suppuration of the interlobular septa and particularly
noteworthy is the occurrence of suppurative lymphangitis, lymphatics
being immensely dilated and distended with purulent fluid so that their
irregularly dilated, beaded appearance is recognizable upon the section
of the lung. In the group of pneumonias following measles this lesion
has not been associated with unresolved or chronic bronchopneumonia; no
nodular tubercle-like foci of bronchopneumonia have been found at
autopsy, and there has been no thickening of the interstitial tissue.
The lesion has accompanied confluent lobular pneumonia in 2 instances
(Autopsies 442 and 491). In the third instance (Autopsy 507) there was
in the neighborhood of the suppurative lesions diffuse consolidation
which had the cloudy, gray red color of streptococcus pneumonia, but
this consolidation was not lobular in distribution.
The etiology of interstitial suppurative pneumonia established by study
of instances following influenza is confirmed by Table LXXII (p. 345)
showing the bacteriology of instances of acute bronchopneumonia
following measles. Pneumococci are almost invariably found in
uncomplicated instances of bronchopneumonia and hemolytic streptococci
have been absent, whereas in 3 instances of suppurative interstitial
pneumonia hemolytic streptococci have been found in the sputum during
life, in pure culture in the blood of the heart and in the lungs and
bronchus (missed in the bronchus in one instance, Autopsy 507). In the 3
instances of the disease B. influenzæ has been found in the bronchi.
Table LXXIII shows that suppuration has accompanied unresolved
bronchopneumonia (“interstitial bronchopneumonia”) in 2 instances
(Autopsies 438 and 492), but in these instances the interlobular tissue
of the lung has not been the site of suppuration and there has been no
suppurative lymphangitis. Localized abscesses have been formed;
hemolytic streptococci, as with abscesses following influenza, have been
found.
Empyema has occurred only 5 times in association with pneumonia
following measles and in these 5 instances has been associated with
suppurative pneumonia caused by hemolytic streptococci. In Autopsy 492
there was fibrinopurulent pleurisy on both sides. Aspiration had been
performed 3 times and at autopsy the right pleural cavity contained 150
c.c. of purulent fluid. In small pockets, corresponding to shallow oval
depressions upon the anterior surface of the lung, fluid was walled off
from the general cavity. The pericardial cavity contained 25 c.c. of
turbid yellow fluid containing yellow flakes of fibrin and the
peritoneal cavity contained thick purulent fluid. Hemolytic streptococci
present in the heart’s blood and lung were recovered from the right
pleural cavity and from the peritoneum. Among 3 instances of empyema
accompanying interstitial suppurative pneumonia, in 1 (Autopsy 491)
there were walled off pockets of fluid similar to those just described.
Aspiration of the right pleural cavity had been performed 3 times; at
autopsy 100 c.c. of fibrinopurulent fluid was found on the right side
and 450 c.c. on the left. There was general purulent peritonitis and the
peritoneal cavity contained 350 c.c. of thick yellow pus. Hemolytic
streptococci were obtained from the heart’s blood, right lung, right
pleural cavity and peritoneum.
Among 4 instances of lobar pneumonia following measles there was
serofibrinous pleurisy 3 times; in 1 instance there is no record of
pleural change. In 1 instance of lobar pneumonia (Autopsy 505) the right
pleural cavity contained 800 c.c. of serofibrinous exudate and the
pericardial cavity contained 510 c.c. of opaque, yellow seropurulent
fluid; Pneumococcus II atypical in pure culture was obtained from the
blood, lung and pleural and pericardial exudates. Among 9 instances of
bronchopneumonia following measles there was fibrinous pleurisy 3 times,
serofibrinous 3 times, and no recorded lesion of the pleura 3 times.
Empyema, like suppurative pneumonia following measles, is in most
instances, but not constantly, caused by invasion of hemolytic
streptococci.
The foregoing study has shown that pneumonia which has followed measles
has reproduced all of the lesions usually found after influenza. There
is no pulmonary lesion peculiar to measles. Lobar pneumonia follows the
disease in some instances, but bronchopneumonia with purulent bronchitis
is more common. The same tendency to hemorrhagic inflammation found with
the pneumonia of influenza is seen after measles. Unresolved pneumonia
with chronic inflammatory changes in the interstitial tissue of the lung
has all of the characters of the similar lesion following influenza but
has been found in a larger proportion of the pneumonias of measles.
B. influenzæ has been found in the bronchi in 14 of 16 examinations,
namely in 87.5 per cent of fatal instances of pneumonia. In 1 instance
in which B. influenzæ has not been found at autopsy, it has been
isolated from the sputum during life. It is not improbable that B.
influenzæ has been constantly present in the inflamed bronchi both after
influenza and measles. It is noteworthy that the outbreak of pneumonia
following measles has been in part coincident with, in part slightly
subsequent to, an epidemic of influenza which has exposed every
individual in the camp to infection with this disease.
B. influenzæ has been found in the lung with the pneumonia of measles in
7 of 17 examinations, namely, in 41.2 per cent of instances. The
microorganism with measles, as with influenza, is found in the inflamed
lung only half as frequently as in the bronchi. It appears to be
peculiarly adapted for multiplication within the bronchial tubes, and
its isolation from the inflamed lung in less than half of the cases of
pneumonia is perhaps referable to its presence in the small bronchi and
bronchioles. The presence of B. influenzæ in the lungs in pure culture
in 3 instances at first sight suggests that the microorganism produces
pneumonia, but a more intimate survey of these cases gives little
support to this view. In Autopsy 450 B. influenzæ has been found in pure
culture in the lung, but Pneumococcus IV has been isolated from the
blood of the heart and has been with little doubt the cause of typical
lobar pneumonia present in this instance. In Autopsy 486 the condition
is almost identical, for in the presence of lobar pneumonia B. influenzæ
has been found in the lung in pure culture, but Pneumococcus II atypical
has been isolated from the pleural cavity and from the bronchus; in both
autopsies the pneumococci which have caused lobar pneumonia have
disappeared from that part of the consolidated lung from which a culture
has been made; and here doubtless its invasion has been effectively
resisted although it is still present in other organs. In Autopsy 481 in
which B. influenzæ has been isolated from the lung in pure culture, the
part of pneumococci in the production of the fatal disease is less
evident; in this instance, Pneumococcus II atypical, S. hemolyticus and
B. influenzæ have been isolated from the bronchus.
The presence of microorganisms which have a well-established etiologic
relation to pneumonia explains the occurrence of pneumonia and makes
unnecessary the assumption that B. influenzæ, which is present in the
lungs in less than half of the instances examined, is essential to the
production of the pneumonic consolidation. In view of the
well-recognized etiology of lobar pneumonia we may conclude that this
lesion is referable to the pneumococci (Pneumococcus II atypical in 3
instances and Pneumococcus IV in 1 instance) isolated from the autopsies
in which this lesion occurred. Pneumococcus (Pneumococcus II atypical in
3 instances and Pneumococcus I in 1 instance) has been isolated from the
lungs or heart’s blood in 4 of 5 instances of acute bronchopneumonia
unaccompanied by suppuration. With unresolved bronchopneumonia with no
suppuration, pneumococci have been in no instance found in the lungs or
blood though their presence in the washed sputum during life or in the
bronchus at autopsy suggests the possibility that they may have
disappeared from the lungs.
In all instances in which suppuration has occurred hemolytic
streptococci have been found in the lungs or blood, or in both. The
occurrence of pneumococci in the lungs in 2 of 5 instances of
suppurative pneumonia indicates that infection with S. hemolyticus is in
some instances at least superimposed upon acute bronchopneumonia caused
by pneumococci. Bronchopneumonia in 3 instances has the character of
that caused by pneumococci. It is probable that the sequence of
infection frequently observed after influenza, namely, bronchial
infection by B. influenzæ, followed by pneumonia caused by pneumococci,
followed in turn by infection by hemolytic streptococci with necrosis or
suppuration, is not uncommon after measles.
=Pneumonia Associated with Acute Infectious Diseases Other than
Influenza and Measles.=—A small group of autopsies have been excluded
from the list of those which accompanied the epidemic of influenza,
because pneumonia has been associated with an acute infectious disease
to which it is perhaps secondary. These few instances of pneumonia, like
those following measles reproduce characters of the pneumonia following
influenza and may be in part referable to influenza which has attacked
an individual suffering with typhoid fever, mumps or scarlet fever.
In 2 instances pneumonia followed typhoid fever and appeared on
September 23 and 26 shortly after the epidemic of influenza had become
evident. In the following autopsy there was acute lobar pneumonia which
appeared ten days after onset of typhoid fever.
=Autopsy 245.=—O. H., white, aged twenty-one, a farmer, resident of
Oklahoma, had been in military service twenty-one days. Onset of
illness was on September 13 with chill, headache, cough and nausea.
The patient was admitted two days later with the diagnosis of acute
bronchitis. On September 20 the abdomen was tense, the spleen was
enlarged and rose spots were present. Signs of lobar pneumonia were
found September 23. Death occurred September 25, twelve days after
onset of typhoid fever and two days after recognition of pneumonia.
=Anatomic Diagnosis.=—Typhoid fever with necrotic ulcers in lower
ileum and in colon; hyperplasia of ileocecal lymphatic nodes; acute
splenic tumor; parenchymatous degeneration of liver and kidneys;
acute lobar pneumonia with gray hepatization in left lower lobe and
red hepatization and edema in left upper lobe and in right lung;
serofibrinous pleurisy on left side.
The left pleural cavity contains 75 c.c. of yellowish gray turbid
fluid. Over the left lower lobe there is a layer of fibrin. The
upper half of the lobe is firmly consolidated, pinkish gray and
coarsely granular; the bronchi contain plugs of fibrin. The lower
and posterior part of the lower lobe is consolidated deep red and
edematous. The left upper lobe is edematous and a layer in the
lowermost part in contact with the lower lobe is deep red and
consolidated. The left lung weighs 1,490 grms. The lower half of the
right upper lobe and the posterior border of the lower is
consolidated deep red and edematous; the lung weighs 970 grms.
Bacteriologic examination shows that the blood of the heart contains
Pneumococcus II atypical.
The foregoing autopsy is of interest because typical lobar pneumonia
appears to have spread from the left lower lobe, where consolidation is
firm and gray, to the adjacent part of the upper lobe where
consolidation is red and edematous.
The second instance of pneumonia following typhoid fever is an instance
of suppurative pneumonia caused by S. aureus.
=Autopsy 329.=—J. B., white, aged twenty-two, laborer, resident of
Oklahoma, had been in military service two days before onset of
symptoms of typhoid fever. He was admitted to the hospital on August
27 and B. typhosus was found in cultures from the blood on September
2 and 3. Acute bronchitis appeared on September 26 when the epidemic
of influenza had almost reached its height. A diagnosis of
bronchopneumonia was made on the day preceding death, which occurred
forty-one days after onset of typhoid fever and eleven days after
onset of bronchitis.
=Anatomic Diagnosis.=—Typhoid ulcers of ileum; acute splenic tumor;
acute bronchopneumonia with red hemorrhagic peribronchiolar and
lobular consolidation in right lung; multiple abscesses forming a
circumscribed group in left upper lobe; purulent bronchitis.
The pleural cavities contain no excess of fluid. The lungs are
voluminous and there is interstitial emphysema. Below the pleura are
bluish red spots of lobular consolidation; in the right upper lobe
is a large patch of red consolidation marked by yellowish gray spots
in clusters. In the external and upper part of the left upper lobe
is a patch of gray consolidation within which, beneath the pleura,
there are small abscesses grouped to form a cluster 1.5 cm, across.
Bacteriologic examination demonstrates no microorganisms in the
blood of the heart; of two cultures from the left lung one contains
S. aureus in pure culture, the other S. aureus and a few colonies of
Pneumococcus IV. Cultures from the left main bronchus and from the
mucopurulent exudate in a small bronchus both contain B. influenzæ,
S. aureus and Pneumococcus IV.
In the foregoing case bronchitis has appeared thirty days after onset of
typhoid fever on September 26, immediately preceding the height of the
epidemic of influenza. In association with hemorrhagic bronchopneumonia
there is suppurative pneumonia with small abscesses forming a
circumscribed group below the pleura; there is no empyema. The lesion
has the characters of the staphylococcus abscesses following influenza,
and S. aureus is found in association with the lesion; B. influenzæ is
identified in two cultures from the bronchi.
In 2 instances pneumonia was associated with parotitis which was
diagnosed mumps.
=Autopsy 403.=—C. T., colored, aged twenty-five, a laborer, resident
of Arkansas, had been in military service one month. Illness began
September 27 with swelling of face behind jaw and difficult
mastication; the patient was admitted to the hospital on the same
day with the diagnosis of mumps. Pneumonic consolidation was
recognized on October 8. Death occurred October 13, sixteen days
after onset of illness and six days after recognition of pneumonia.
=Anatomic Diagnosis.=—Acute lobar pneumonia with red and beginning
gray hepatization of lower and parts of upper and middle right
lobes; acute bronchopneumonia with lobular consolidation in left
lung; purulent bronchitis; bronchiectasis in left lung.
The lower lobe of the right lung with the exception of the anterior
and basal edge is firmly consolidated; the posterior part of the
middle lobe and a small corner at the posterior and lower part of
the upper lobe is similarly consolidated. The consolidated tissue is
gray and coarsely granular on section. The remainder of the lung is
dry and voluminous, and the bronchi contain purulent fluid. The left
lung contains red and gray patches of consolidation, from 0.2 to 3
cm. across. Bronchi contain purulent fluid and in the lowermost
parts of both upper and lower lobes are moderately dilated.
Bacteriologic examination shows that the blood of the heart contains
Pneumococcus III.
It is noteworthy that there was in this case, as in many instances of
influenza, both lobar and bronchopneumonia. Purulent bronchitis was
present and there was bronchiectasis throughout one lung.
In the following case the diagnosis of mumps may be questioned since the
lesion of the parotid has characters of terminal suppurative parotitis.
=Autopsy 417.=—H.W.D., white, aged twenty-four, a farmer, resident
of Oklahoma, had been in military service one month. He said that he
had had pneumonia four times. He was admitted to the hospital
delirious and the diagnosis of lobar pneumonia was made. Parotitis
regarded as mumps appeared five days before death and suppuration
occurred on the right side of the face. Death of the patient
occurred thirteen days after admission to the hospital.
=Anatomic Diagnosis.=—Acute bronchopneumonia with lobular
consolidation in both lungs; suppurative pneumonia with necrosis and
beginning abscess formation in left lung; purulent pleurisy in left
side; purulent bronchitis; bronchiectasis; acute parotitis.
The left pleural cavity contains 100 c.c. of purulent fluid of
creamy consistence. The left lung is voluminous and bound to the
chest wall in places. There are numerous patches of lobular
consolidation. At the apex of the lung there is a large area of
consolidation, 7 cm. across, where the tissue is cloudy gray and
soft in consistence. In the upper lobe is a well-defined patch of
grayish yellow color, 6 by 2 cm., with opaque yellow edges; purulent
fluid escapes from the cut surface. Bronchi throughout the lung are
widely dilated and contain purulent fluid. The right lung is
voluminous and contains lobular patches of consolidation; bronchi of
this lung are widely dilated.
Bacteriologic examination shows the presence of hemolytic
streptococci in the blood of the heart; hemolytic streptococci and
B. influenzæ in the lung, and hemolytic streptococci, B. influenzæ
and S. aureus in a main bronchus.
In association with bronchopneumonia there have been necrosis and
beginning abscess formation with empyema, the suppurative lesions being
caused by hemolytic streptococci which had finally entered the blood
stream. There was purulent bronchitis, and the lungs had the voluminous
character often associated with this lesion; there was beginning
bronchiectasis. B. influenzæ was obtained both from the lung and from
the bronchus.
In 2 instances (Autopsies 323 and 335) the diagnosis of scarlet fever
was made in patients suffering with pneumonia following influenza. These
lesions have been included in the list of influenzal pneumonias. In the
following instance the patient was admitted with scarlet fever, later
developed acute follicular tonsillitis, and finally suppurative
pneumonia caused by hemolytic streptococcus.
=Autopsy 311.=—E. J., white, aged twenty-two, a tinsmith and
automobile repairer, resident of Arkansas, had been in military
service three months. Onset of illness was on September 18 with
headache and sore throat. The patient was admitted September 24 with
the diagnosis of scarlet fever; two days later there was acute
follicular tonsillitis. Pneumonic consolidation on the right side
was recognized October 2, three days before death.
=Anatomic Diagnosis.=—Acute suppurative pneumonia with three small
abscesses below pleura of right lower lobe; acute fibrinopurulent
pleurisy on both sides; serous pericarditis.
The right pleural cavity contains 1500 c.c. of turbid, dirty yellow
fluid containing masses of fibrin; the left cavity has 500 c.c. of
similar contents. The pericardium contains 30 c.c. of turbid fluid
containing a small quantity of fibrin; there are ecchymoses below
the epicardium. The right lung is collapsed and in the lower lobe
contains three small subpleural abscesses, the largest of which is
1.5 cm. across.
Bacteriologic examination shows the presence of hemolytic
streptococci in pure culture in the blood of the heart and in the
right lung. From the right main bronchus are obtained hemolytic
streptococci, B. influenzæ, Pneumococcus IV and a few staphylococci.
In this instance there has been infection with streptococcus which is a
common sequela of scarlet fever. In the absence of evidence of
bronchopneumonia there has been abscess formation below the pleura with
empyema and pericarditis. B. influenzæ has been found in the bronchus.
The pneumonias found in association with measles reproduce the
characters of the pneumonias described in association with influenza.
Particularly noteworthy is the occurrence of lobar pneumonia,
hemorrhagic peribronchiolar pneumonia, interstitial suppurative
pneumonia, severe bronchitis with bronchiectasis and unresolved
bronchopneumonia. In the presence of an epidemic of influenza attacking
more than one fourth of the population of a camp, those suffering with
diseases, such as measles, typhoid fever, mumps, etc., are unlikely to
escape entirely, and it is probable that the tendency to the occurrence
of pneumonia present in association with these diseases will be
increased. The close resemblance between the pneumonias which we have
found with the diseases mentioned, on the one hand, and the pneumonias
of influenza on the other, both being characterized by the occurrence of
hemorrhagic, suppurative and chronic pulmonary lesions, indicates that
influenza has had a part in the production of the pneumonia found with
measles and some other infectious diseases during the progress of the
epidemic of influenza.