suppurative pneumonia caused by hemolytic streptococci, but has been
found in association with abscess formation (Autopsies 354 and 383)
caused by hemolytic streptococci or (Autopsy 322) caused by
staphylococci. In 1 instance it has been found with lobar pneumonia
(Autopsy 320) caused by atypical Pneumococcus II and in 2 instances with
combined lobar and bronchopneumonia (Autopsy 357 with Pneumococcus IV;
Autopsy 392 with Pneumococcus II). In these 3 instances there has been
interstitial inflammation, edema and lymphangitis without suppuration.
Interstitial suppurative pneumonia of long standing may occasionally be
accompanied by chronic changes which bring about thickening of the
interlobular tissue. In the following autopsy acute suppurative
inflammation in the left lung has been associated with conspicuous
thickening of interlobular septa in the right lung.
=Autopsy 474.=—I. H., white, aged twenty-one, was a native of
Oklahoma and had been in military service one month. His illness
began with influenza thirty-six days before death; he was admitted
to the base hospital thirty-one days before his death with signs of
pneumonic consolidation of the right lower lobe. Evidence of fluid
in the right pleural cavity was obtained two weeks before death, and
from 100 to 700 c.c. of thick purulent fluid were aspirated on five
occasions. Hemolytic streptococci were found in the aspirated fluid.
=Anatomic Diagnosis.=—Interstitial suppurative pneumonia in left
lung; abscess of right lower lobe with rupture into pleural cavity;
thickening of interlobular septa of right lower lobe; double
purulent pleurisy with thoracotomy on right side; serofibrinous
pericarditis.
The right pleural cavity contains 85 c.c. of thick purulent fluid; the
right lung (Fig. 9) is collapsed and pushed to the median line, being
bound by firm adhesions to the pericardium. Over the external and basal
surfaces is a localized cavity walled off by adhesions. An abscess
cavity in the lower part of the lower lobe communicates through a
perforation in the basal surface of the lung with the pleural cavity and
is in free communication with a small bronchus. About the abscess the
lung is red and laxly consolidated, but elsewhere air containing;
throughout the lower half of the lower lobe, the interlobular septa are
marked by conspicuous yellowish gray lines about 1 mm. in thickness.
Between these thickened septa the lung tissue contains air. The lung
weighs 600 grams. The left lung (Fig. 10) is voluminous and heavy,
weighing 1,320 grams. The surface is everywhere covered by thickened
pleura and fibrin, the pleural cavity containing 150 c.c. of thick
purulent fluid. The lung is consolidated varying in color from a fleshy
red to yellowish gray. The surface is very conspicuously marked by
yellow lines 2 or 3 mm. thick, corresponding to the interlobular septa
which have undergone suppuration. The septa have bead-like swellings
along their course, and when pus escapes from the cut surface small
cavities remain at the site of these swellings.
Bacteriologic examination has shown hemolytic streptococci in the blood,
left lung, right and left pleural cavities, and right bronchus. B.
influenzæ has been found in the bronchus, in the right pleura and in the
heart’s blood. A few colonies of S. aureus have been found on the plate
from the right pleural cavity (site of thoracotomy).
Microscopic examination of the right lower lobe shows that the
interstitial septa are much thickened by young fibrous tissue
infiltrated with lymphoid and a few plasma cells. Large mononuclear
cells with granular cytoplasm are very numerous. A lymphatic is much
distended and contains a few polynuclear leucocytes and many lymphoid
and large mononuclear cells. There is no suppuration. Sections from the
right lung show suppurative lymphangitis with suppurative inflammation
of interstitial tissue.
The right lung is the site of a healing lesion of the interstitial
tissue which has developed simultaneously with acute interstitial
suppurative pneumonia in the left lung. Both lesions are doubtless
caused by S. hemolyticus. This healing lesion exhibits little similarity
to the interstitial bronchopneumonia described by several observers with
both measles and influenza.
The following autopsy furnishes further evidence that interstitial
suppurative pneumonia exhibits a tendency to heal. Proliferation of
endothelial cells lining the inflamed lymphatics gives rise to
phagocytic cells which aid in removing the accumulated leucocytes.
=Autopsy 397.=—N. P., white, aged twenty-one, farmer, a native of
Oklahoma, had been in military service twenty-one days. Illness
began twenty-two days before death, the patient being admitted on
the day following onset with influenza, pharyngitis and bronchitis.
A diagnosis of lobar pneumonia was made fourteen days before death.
The left pleural cavity was aspirated twelve days later and 800 c.c.
of thick yellow pus were withdrawn. Hemolytic streptococci were
found in the sputum five days before death.
=Anatomic Diagnosis.=—Interstitial suppurative pneumonia in left
upper lobe; acute bronchopneumonia with lobular consolidation in
right upper lobe; localized purulent pleurisy on left side with
compression and atelectasis of left lung; compensatory emphysema of
right lung; purulent bronchitis; beginning serofibrinous
pericarditis; chronic passive congestion of liver, spleen and
kidneys.
The right lung is very voluminous, free from coal pigment and bright
pink save over lobular patches of consolidation which have a bluish
red color; the bronchi contain mucopurulent material. The anterior
surface of the left lung is bound to the chest wall by firm
adhesions, but over the external and posterior surfaces of the lung
there is a localized cavity containing 1,100 c.c. of turbid fluid.
The left lung is collapsed and airless with deep fleshy red color.
In the upper lobe there are scattered patches of consolidation 1.5
to 2.5 cm. across where the tissue is grayish red and coarsely
granular. In the adjacent tissue interstitial septa are thickened to
1 or 2 mm. and are conspicuous as gray bands. Along their course
occur bead-like swellings from which purulent fluid can be scraped.
These septa at one point reach the anterior surface of the lung
where the pleural cavity is in large part obliterated by adhesions;
here there is an encapsulated pocket 4 x 1.5 cm. containing thick
creamy pus.
Bacteriologic examination of the blood shows the presence of
hemolytic streptococci; cultures from the lungs contain hemolytic
streptococci and B. influenzæ.
Microscopic examination shows that interlobular septa are thickened
and infiltrated with plasma cells in large number. Leucocytes in the
center of much dilated lymphatics have undergone necrosis and have
lost their nuclear stain. About the periphery of the lumen and
evidently derived from the swollen endothelial cells which surround
it, are numerous large mononuclear cells. They act as phagocytes and
ingest polynuclear leucocytes. Multinucleated giant cells, derived
from these cells, occur. In several places thrombosed lymphatics in
process of organization occur; the lumen is filled with compact
fibrin which is invaded by fibroblasts and newly formed capillaries.
The process just described is analogous to that which occurs whenever an
unopened abscess heals; mononuclear cells accumulate and act as
phagocytes ingesting polynuclear leucocytes.
The following instance of streptococcus empyema is noteworthy because no
suppurative pneumonia has been found in association with it.
Nevertheless the character of the changes present in the lung indicate
that the organ has been the site of an interlobular inflammation which
has healed.
=Autopsy 499.=—J. H. M., white, aged twenty-four, a farmer from
Arkansas, had been in military service five months. Onset of illness
began two weeks before his admission to the hospital on November 15
with cough, fever, headache and malaise; on admission there was
acute bronchitis. Thirteen days after admission the patient
developed parotitis (mumps?); five days later and five days before
death pleurisy was recognized on the right side and pneumonia was
suspected. Death occurred thirty-six days after onset. The
temperature on admission was 103.2° F. and remained elevated during
one week falling by lysis; from this time until the pleurisy was
recognized it was normal and later it remained approximately 103° F.
=Anatomic Diagnosis.=—Fibrinopurulent pleurisy on right side;
fibrinous pleurisy on left side; fibrinopurulent pericarditis;
chronic interstitial (interlobular) pneumonia in process of healing;
purulent bronchitis; acute splenic tumor; parenchymatous
degeneration of kidneys.
The right pleural cavity contains 1,650 c.c. of grayish yellow fluid
containing an abundant sediment of softened fibrin. Part of this
fluid, more opaque than the remainder is confined in a localized
pocket between the inner surface of the lung and the pericardium.
The apex and anterior surface of the right upper lobe, over an area
about 7 cm. across, is held by fibrinous adhesions to the chest
wall; when this adhesion is broken a pocket is exposed 6.5 x 2.5 cm.
containing fibrin and fluid. The pericardial cavity is distended by
350 c.c. of turbid yellow seropurulent fluid. The pericardial
surfaces are covered by shaggy, tough gray fibrin.
The right lung is collapsed; the lower and posterior part of the
upper lobe is deep red and atelectatic. Throughout the upper lobe
the interlobular septa are thickened, often 1 mm. across and very
conspicuous; in the lower and anterior tip of the lobe is an area
where tissue is firm grayish red and heavier than water. The lower
and posterior half of the right lower lobe is firm and airless, and
the tissue is reddish gray or gray and in places finely granular on
section; interlobular septa are conspicuous. Although the lung is
cut into thin sections, no abscesses are found. Bronchi throughout
the lung contain mucopurulent fluid.
The left lung over its lower half is covered by a thin layer of
fibrin. The tissue is crepitant throughout and moderately edematous.
Bronchi contain mucopurulent fluid.
Hemolytic streptococci in pure culture are obtained from the blood
of the heart, right pleural cavity and pericardium. No growth is
obtained on a plate inoculated with material from the right lower
lobe. The right bronchus contains hemolytic streptococci and B.
influenzæ.
The pleural surface of the right lung is covered by a thick layer of
fibrin which has undergone advanced organization. Fibrous septa
within the lung are much thickened by the presence of newly formed
fibrous tissue; the interstices of the tissue are distended and
contain fibrin into which fibroblasts and new blood vessels have
penetrated. Some lymphatics are plugged with fibrin and contain
polynuclear leucocytes, lymphoid and large mononuclear cells. In
several places organization of these thrombi is beginning. About the
blood vessels are thrombosed lymphatics in which polynuclear
leucocytes and mononuclear cells are equally abundant. Alveoli
immediately adjacent to blood vessels and to fibrous septa often
contain fibrin, and alveoli elsewhere contain desquamated cells in
abundance.
In association with hemolytic streptococci in the blood, pleura and
pericardium, there has been inflammation of the interlobular septa of
the lungs with acute lymphangitis; there has been no suppuration and the
lesion is in process of healing with new formation of fibrous tissue. It
is evident that this lesion, as well as pleurisy with advanced
organization, preceded the exacerbation of the patient’s illness which
occurred five days before death. The advanced chronic changes found at
autopsy indicate that the pulmonary and pleural lesions had their origin
during the illness which was present at the time of admission to the
hospital. Interstitial pneumonia caused by hemolytic streptococci was of
mild character and did not produce suppuration within the lung;
nevertheless, hemolytic streptococci which reached the pleura caused
empyema.
Suppurative Pneumonia with Multiple Clustered Abscesses Caused by
Staphylococci
In the preliminary report of this commission published in _The Journal
of the American Medical Association_, _loc. cit._, pg. 111, we described
suppurative pneumonia with multiple abscesses caused by staphylococci
and cited 4 instances of the lesion which followed influenza. Chickering
and Park[84] published in a subsequent number of the same journal an
account of staphylococcus pneumonia, a lesion which has heretofore
attracted very little attention.
In a small group of cases abscesses in the lungs have had characters
which serve to distinguish them from the abscesses previously described.
Small, sharply circumscribed yellow nodules, which in their centers have
undergone suppurative softening, form a cluster upon a red, airless
background (Figs. 15 and 16). One or more of these groups several
centimeters across, occur in the lungs. It is usually evident that the
abscesses are clustered about a medium-sized bronchus, but occasionally
with increase in the size of the small cavities the lung tissue assumes
a honey-combed appearance.
These clustered abscesses occur in association with bronchopneumonia and
have been in all instances associated with purulent bronchitis. The
mucosa of the small bronchi may be destroyed so that the surface is
eroded. These small clustered abscesses are seen as conspicuous yellow
spots immediately below the pleura, but there has been no associated
empyema. In 2 instances these abscesses were accompanied by fibrinous
pleurisy, but in the remaining autopsies the pleura has been normal. The
infrequency of empyema is in contrast with its almost invariable
presence when a streptococcus abscess is found below the pleura.
=Autopsy 280.=—Onset of illness with malaise, headache, cough and
fever was on September 24, eight days before death. At autopsy there
were hemorrhagic peribronchiolar and lobular bronchopneumonia,
clustered foci of suppuration in right lung, purulent bronchitis and
fibrinous pleurisy. Hemolytic streptococci were obtained from the
consolidated lung and from a bronchus. A culture from the right lung
was contaminated. In the bronchus were found B. influenzæ and a few
staphylococci. Microscopic examination of the abscesses shows that
they contain Gram-staining cocci grouped into staphylococcus-like
colonies.
=Autopsy 286.=—Duration of illness, which began September 25 with
symptoms of influenza, was nine days. At autopsy there were lobular
and confluent patches of bronchopneumonia, clustered abscesses in
the right lung below the pleura, purulent bronchitis, and
serofibrinous pleurisy localized in the neighborhood of the
abscesses. Pneumococcus IV was obtained from the blood of the heart,
and Pneumococcus IV, staphylococci and B. influenzæ from the right
main bronchus; growth failed to occur on plates from right and left
lungs. Microscopic examination shows the presence of clumps of cocci
with staphylococcus grouping in the centers of the small abscesses.
Section through one abscess shows its continuity with the wall of a
bronchus; along one side of the abscess is epithelium composed of
flattened epithelial cells in multiple layers continuous with that
of the bronchus; the remainder of the abscess wall is formed by
disintegrated lung tissue.
[Illustration:
Fig. 15.—Abscesses in two clusters caused by S. aureus in upper part
of right upper lobe; confluent lobular consolidation in lower part
of lobe. Autopsy 333.
]
[Illustration:
Fig. 16.—Abscesses in cluster caused by S. aureus at apex of right
upper lobe. Autopsy 322.
]
=Autopsy 322.=—The patient was admitted with influenza eight days
before death; signs of pneumonia appeared two days later, and on the
following day Pneumococcus IV was obtained from the sputum. At
autopsy there were bronchopneumonia with lobar consolidation,
abscesses clustered about a bronchus in the right upper lobe and
purulent bronchitis. The blood was sterile; S. aureus was obtained
from the consolidated part of the left lung; S. aureus and
Pneumococcus III from the abscesses of the right lung. Microscopic
examination of sections of abscesses showed the presence of
Gram-staining cocci in staphylococcus-like colonies, surrounded by
necrotic material and polynuclear leucocytes; Gram-negative bacilli
resembling B. influenzæ were seen. (See Fig. 16.)
=Autopsy 333.=—The onset of influenza was fifteen days before death;
a diagnosis of pneumonia was made seven days before death. At
autopsy there were confluent bronchopneumonia, clustered abscesses
in the right lung and purulent bronchitis (no pleurisy). The blood
contained Pneumococcus II atypical. S. aureus and Pneumococcus II
atypical were obtained from the abscesses; S. hemolyticus, from the
consolidated left lung; S. aureus, B. influenzæ and a few hemolytic
streptococci, from the bronchus. (See Fig. 15.)
=Autopsy 370.=—The patient was admitted seventeen days before death
and signs of pneumonia were noted three days after admission. At
autopsy there were lobular and confluent bronchopneumonia and small
abscesses clustered about bronchi and situated within the gray
consolidated lung; purulent bronchitis and patches of atelectasis,
with distention of the lungs, so that they failed to collapse on
removal. No growth was obtained from the heart’s blood; S. aureus in
pure culture was obtained from the abscesses of the right lung; S.
aureus, Pneumococcus IV and B. influenzæ were obtained from a small
bronchus on the left side.
=Autopsy 425.=—Illness began with influenza twenty-nine days before
death; a diagnosis of pneumonia was made fourteen days before death.
At autopsy there were chronic bronchopneumonia with tubercle-like
nodules of consolidation with some large patches of consolidation,
multiple small abscesses giving a honey-combed appearance to part of
the right middle lobe, purulent bronchitis and bronchiectasis. S.
hemolyticus was grown from the heart’s blood; S. hemolyticus, B.
influenzæ and S. albus from the lung. Sections of an abscess contain
clumps of cocci. An abscess cavity has along one side remains of a
bronchial wall covered by squamous epithelium; a dilated bronchus,
cut longitudinally, terminates in this irregular abscess cavity.
Table XLIX shows the incidence of pneumococci, hemolytic streptococci,
staphylococci and B. influenzæ in the foregoing autopsies with abscesses
clustered about bronchi:
TABLE XLIX
════════╤════════╤═════════════════╤═════════════════
│ NO. OF │ │ HEMOLYTIC
│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI
────────┼────────┼────────┬────────┼────────┬────────
│ │ NO. │PER CENT│ NO. │PER CENT
│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE
────────┼────────┼────────┼────────┼────────┼────────
Bronchus│ 4│ 2│ 50.0│ 2│ 50.0
Lung │ 6│ 2│ 33.3│ 3│ 50.0
Blood │ 6│ 2│ 33.3│ 2│ 33.3
────────┴────────┴────────┴────────┴────────┴────────
════════╤═════════════════╤═════════════════
│ │
│ STAPHYLOCOCCI │ B. INFLUENZÆ
────────┼────────┬────────┼────────┬────────
│ NO. │PER CENT│ NO. │PER CENT
│POSITIVE│POSITIVE│POSITIVE│POSITIVE
────────┼────────┼────────┼────────┼────────
Bronchus│ 4│ 100.0│ 4│ 100.
Lung │ 4│ 66.7│ 2│ 33.3
Blood │ │ │ │
────────┴────────┴────────┴────────┴────────
Staphylococcus shows in the lung the same tendency to produce localized
abscesses which it exhibits in other tissues of the body; it invades the
lung by way of the bronchi, but shows no ability to invade lymphatics,
and in the cases we have examined rarely enters the pleura or the blood.
In all of these cases B. influenzæ has been found in the bronchi and
perhaps precedes the staphylococcus as an invader of the lower
respiratory passages. Pneumococci atypical II, Types III and IV have
been found in over half of these cases. The significance of this
organism is emphasized by the 2 cases in which it has been found in the
heart’s blood at autopsy. It appears not improbable that S. aureus has
invaded the lung already the site of bronchopneumonia caused by
pneumococci.
Notwithstanding the small number of autopsies, the figures in Table
XLIX, showing the incidence of pneumococci, streptococci, staphylococci
and B. influenzæ, are cited so that they may be compared with the
corresponding figures for the usual type of streptococcus abscess (p.
203). The incidence of hemolytic streptococci is relatively low, whereas
that of staphylococci approximates 100 per cent. S. aureus was present
in great number in the lung of Autopsies 322 and 333 and in pure culture
in the abscess of Autopsy 370. Microscopic examination of sections from
the abscesses which have been described, demonstrated the presence of
Gram-staining cocci in characteristic staphylococcus-like clumps within
the exudate of the abscesses; scattered chains of streptococci were not
found. In those instances (Autopsies 280 and 286) in which cultures
failed to demonstrate staphylococci, microscopic examination
demonstrated staphylococcus-like clumps of bacteria within the abscess
cavity. Cultures were usually made from the consolidated lung near the
abscess where the pleural surface could be seared, rather than from the
pus, so that in some instances the microorganism has doubtless escaped
detection although present.
In association with the multiple abscesses which have been described,
injury to the bronchi and bronchopneumonia have been invariably present.
Purulent bronchitis has been present in all instances of this lesion; in
2 instances there has been dilatation of the bronchi, and in 1 instance
in which the onset of influenza was twenty-nine days before death, there
has been advanced bronchiectasis.
Microscopic examination shows that the epithelium of the bronchi is
partially or completely destroyed and that destruction of the underlying
tissue, with acute suppurative inflammation, penetrates to a greater or
less depth into the wall. When the epithelium of the bronchus is wholly
destroyed and the lumen is filled and distended with polynuclear
leucocytes, a cross section of the tube has the appearance of a small
abscess; but more careful examination often shows that the engorged
mucosa is still intact. Occasionally, a network of fibrin forms a layer
covering the denuded mucosa. Disintegration of the superficial tissue
may extend to the muscularis or through it, and may penetrate the wall
of the bronchus. The tissue in contact with the exposed surface contains
many polynuclear leucocytes and blood vessels plugged with fibrinous
thrombi, but deeper in the tissue lymphoid and plasma cells are more
numerous. In 2 instances (Autopsies 286 and 425) favorable sections have
demonstrated that the wall of an abscess on one side consists of the
remains of a bronchus, covered by epithelium composed of squamous cells,
Whereas the remainder of the wall, here very irregular, is formed by
partially destroyed alveoli plugged with fibrin. The suppurative process
has penetrated the wall of the bronchus on one side and extended into
the surrounding alveolar tissue. In other instances, abscess cavities
occur within the alveolar tissue of the lung and their relationship to
bronchi is not evident. In the mass of polynuclear leucocytes which fill
the abscess cavity, are clumps of staphylococci in great abundance,
usually forming characteristic colonies which are conspicuous with the
low power of the microscope.
Empyema, Pericarditis and Peritonitis
No sharp line can be drawn between nonpurulent and purulent pleurisy. A
diagnosis of empyema has been made when the fluid in the chest has
become opaque and fibrin has undergone softening or solution. The lesion
has been designated seropurulent when there has been abundant thin,
opaque, gray fluid. Pleurisy has been designated fibrinopurulent when
the cavity has contained opaque fluid and ragged soft white or yellowish
fibrin adherent to the chest wall; this fibrin is evidently in process
of disintegration and there may be numerous shreds and flakes of fibrin
which subside to the bottom of the fluid. The amount of fluid in the
cavity may occasionally exceed 1,700 c.c.; that in both pleural cavities
may exceed 2,500 c.c. The lesion has been designated purulent when
fibrin has almost wholly disappeared and the cavity contains thick
yellowish white fluid. In 4 of 5 instances in which thoracotomy had been
performed, empyema has assumed this otherwise uncommon type.
Some inflammation of the pleura is almost constantly found in
association with all forms of pneumonia, but in many instances is so
slight that it has no noteworthy significance. Table L shows the
incidence of various types of pleurisy.
TABLE L
═══════════════════╤═════════╤════════════════╤═══════════╤════════════
│ LOBAR │BRONCHOPNEUMONIA│SUPPURATIVE│INTERSTITIAL
│PNEUMONIA│ │ PNEUMONIA │SUPPURATIVE
│ │ │ WITH │ PNEUMONIA
│ │ │ ABSCESS │
───────────────────┼────┬────┼────────┬───────┼─────┬─────┼──────┬─────
„ │No. │ % │ No. │ % │ No. │ % │ No. │ %
───────────────────┼────┼────┼────────┼───────┼─────┼─────┼──────┼─────
No pleurisy noted │ 30│46.9│ 44│ 55│ 1│ 2.6│ 1│ 5.9
Serous pleurisy │ 5│ 7.8│ 9│ 11.2│ │ │ │
Fibrinous pleurisy │ 10│15.6│ 5│ 6.2│ 1│ 2.6│ │
Serofibrinous │ 12│18.2│ 14│ 17.5│ 3│ 7.7│ │
pleurisy │ │ │ │ │ │ │ │
Seropurulent │ │ │ │ │ 9│ 23.1│ 1│ 5.9
pleurisy │ │ │ │ │ │ │ │
Fibrinopurulent │ 7│10.9│ 5│ 6.2│ 17│ 43.6│ 12│ 70.6
pleurisy │ │ │ │ │ │ │ │
Purulent pleurisy │ │ │ 3│ 3.7│ 8│ 20.5│ 3│ 17.6
───────────────────┼────┼────┼────────┼───────┼─────┼─────┼──────┼─────
Total │ 64│ │ 80│ │ 39│ │ 17│
───────────────────┴────┴────┴────────┴───────┴─────┴─────┴──────┴─────
Empyema has occurred, on the one hand, in 12.4 per cent of instances of
lobar pneumonia and in 9.9 per cent of instances of bronchopneumonia
alone. It has occurred, on the other hand, in 87.2 per cent of instances
of suppurative pneumonia with abscess formation and in 94.1 per cent
instances of interstitial suppurative pneumonia. These suppurative
lesions are caused by hemolytic streptococci, and when cultures are made
from the pleural exudate this microorganism is isolated.
Of 16 instances in which empyema has occurred in association with lobar
pneumonia or bronchopneumonia unaccompanied by suppuration in 6 there
has been infection with hemolytic streptococci. Empyema has occurred in
the absence of hemolytic streptococci only 10 times.
=Empyema Caused by Hemolytic Streptococci.=—When necrosis preceding
abscess formation has occurred in the lung, streptococci are found in
immense numbers in the dead tissue. The pleura overlying the abscess
undergoes necrosis and occasionally streptococci are particularly
numerous upon the pleural surface of the necrotic tissue. In Autopsy 376
a membrane thin as tissue paper, representing the pleura, separated an
abscess containing thick pus from the pleural cavity which was the site
of empyema. The abscess may rupture into the pleural cavity and at the
same time may be in free communication with a bronchus (Autopsy 480). In
one (Autopsy 467) instance an abscess which had ruptured into the
pleural cavity had completely discharged its contents and was in process
of healing, newly formed fibrous tissue being abundant in its wall.
With few exceptions empyema has accompanied subpleural abscess caused by
hemolytic streptococci, being found on the side corresponding to the
abscess. Among 39 instances of pulmonary abscess, empyema has been
limited to the side of the abscess in 23; it has been present on the
opposite side as well in 10 instances. In 2 instances there have been
abscesses in both lungs; in one (Autopsy 385 A) there has been double
empyema, and in the other (Autopsy 487) empyema only on the left side.
In one instance abscess has been recognized by microscopic examination
and its location is not recorded. In 5 instances of abscess formation
there has been no empyema. In Autopsy 383 there has been no pleurisy
noted; in Autopsy 416 there has been fibrinous pleurisy and in Autopsies
277, 290 and 380, serofibrinous pleurisy.
Empyema has been almost invariably found in association with
interstitial suppurative pneumonia. This lesion extends by way of the
lymphatics up to the pleural surface and is often more conspicuous just
below the pleura than elsewhere. Empyema has been absent in only 3 of 21
examples of the lesion and in one of these there has been serous
effusion. In 12 instances interstitial suppuration has occurred only on
one side and empyema has been limited to this side; in 5 instances with
interstitial suppuration on one side there has been empyema on both
sides; in 2 instances with interstitial suppuration in both lungs there
has been double empyema.
The amount of fluid in the pleural cavity has varied from less than 100
to 1,500 c.c. The fluid has occasionally been seropurulent or yellow,
thick and purulent, but in most instances the exudate is best described
as fibrinopurulent. There is yellow or yellowish gray purulent fluid
containing flakes of soft ragged fibrin.
The foregoing study has shown, on the one hand, that empyema is a
frequent complication of streptococcus pneumonia and, on the other hand,
that empyema following influenza with relatively few exceptions is
caused by hemolytic streptococci. Empyema caused by this microorganism
exhibits in some instances characters not seen with other varieties of
pleural inflammation. The tissue between sternum and pericardium is
often edematous and the adjacent fat has a firm brawny consistence. In
some instances the exudate contains blood, and hemolysis has occurred so
that the fluid has a diffuse red color. The occurrence of multiple
pocketed collections of purulent fluid within the pleural cavity is
peculiar to streptococcus empyema. These pockets have been found 6 times
in association with abscess and 5 times with interstitial suppurative
pneumonia. In the presence of an exudate within the pleural cavity, some
part of the lung, usually the anterior surface behind the sternum and
costal cartilages, is glued by fibrinous adhesions to the parietal
pleura. Here occur pockets containing thin purulent fluid and softened
fibrin or thicker creamy pus walled off by fibrin about the edges of the
pocket. At the site of the lesion the lung, after it is separated from
the chest wall, is marked by a shallow depression surrounded by the
fibrin which has walled in the pocket. The little cavity thus formed,
varying much in size, is usually oval, the long diameter being from 1 to
3 cm. These pleural pockets may occur over the external surface of the
lung (Autopsies 452, 455, and 472) or between the internal surface and
pericardium (Autopsy 452). Occasionally with partial fibrinous adhesion
between the pleural surfaces there are both scattered pockets containing
purulent fluid and a larger encapsulated collection of fluid; in Autopsy
455 the pleural surfaces were adherent and there was 100 c.c. of
purulent fluid encapsulated in a space over the external surface of the
lung, 12 × 8 cm. In Autopsy 452 the lower part of the pleural cavity was
encapsulated and contained 650 c.c. of fluid. This tendency of empyema
caused by S. hemolyticus to form encapsulated pockets is doubtless of
considerable importance in the treatment of the condition.
Stone, Bliss and Phillips[85] have described these encapsulated pockets
as “subcostosternal pus pockets” and have maintained that they are
formed about the sternal lymphatic nodes. We have found them so widely
scattered that this relation seems improbable.
=Pneumococcus Empyema.=—Empyema occurred in association with pneumonia
referable to pneumococci 10 times, once with Pneumococcus II; 6 times
with Pneumococcus atypical II; once with Pneumococcus III and twice with
Pneumococcus IV. The lesion was seropurulent once; fibrinopurulent 8
times and purulent once. Fibrin in several instances was somewhat
voluminous. In the following instance voluminous masses of fibrin had an
important influence upon the attempted treatment.
=Autopsy 473.=—A. D. P., white, aged twenty-one, a student from
Missouri, had been in military service two weeks. He was admitted to
the hospital with influenza twenty-eight days before his death, and
four days after admission there were signs of pneumonia.
Paracentesis was performed on the right side on the eleventh day
after admission; 4 c.c. of cloudy fluid which contained Pneumococcus
III were obtained at this time and later in the day 800 c.c. were
withdrawn. On the thirteenth day attempted withdrawal of fluid from
both pleural cavities failed. On the eighteenth day aspiration of
the right pleural cavity yielded only 30 c.c. of fluid. On the
nineteenth day 400 c.c. of purulent fluid were withdrawn from the
right pleural cavity. On the twenty-fifth day there was cyanosis and
delirium. Shortly before death aspiration of the right pleural
cavity was attempted, but only 4 c.c. of fluid were obtained.
=Anatomic Diagnosis.=—Chronic bronchopneumonia with lobular and
peribronchiolar consolidation in left lung; fibrinopurulent pleurisy
on both sides; purulent bronchitis and bronchiectasis.
On removal of the sternum, encysted purulent pleurisy is found
between the inner surface of the right lung and the pericardium;
there is here 450 c.c. of very thick creamy, greenish yellow pus
entirely separated from the remainder of pleural cavity. The
external part of the cavity contains 1,450 c.c. of fluid and
voluminous masses of firm fibrin which placed in a measuring
cylinder occupy 450 c.c. The left pleural cavity contains 400 c.c.
of seropurulent fluid in which there is abundant sediment of
fibrinous particles.
The right lung is compressed; the bronchi exude purulent fluid. The
left lung is voluminous; in the upper and lower lobes there are
small yellowish gray nodules of consolidation, grouped in clusters,
and gray patches of lobular consolidation occur. Bronchi are dilated
and filled with purulent fluid.
Bacteriologic examination shows the presence of Pneumococcus III
obtained in pure culture from the blood of the heart and from the
right pleural cavity. S. viridans is grown from the left lung; a
plate from the right bronchus contained B. influenzæ, S. viridans
and a few colonies of staphylococcus and M. catarrhalis.
The foregoing case is particularly noteworthy because aspiration failed
repeatedly to yield more than a few cubic centimeters of fluid,
doubtless because the voluminous masses of fibrin present in the cavity
prevented escape of fluid. Aspiration was attempted shortly before
death, but only 4 c. c. of fluid were obtained; nevertheless, at autopsy
the right pleural cavity contained 2,350 c.c. of exudate. Another factor
of much importance in relation to treatment is the encapsulation of 450
c.c. of purulent fluid between the inner surface of the right lung and
the pericardium. It is possible that free drainage might have emptied
the main cavity and perhaps even freed the encapsulated fluid.
=Pericarditis.=—Among 241 autopsies on individuals with pneumonia
following influenza, pericarditis occurred 23 times; these lesions were
classified as follows: Serous pericarditis, 1; serofibrinous
pericarditis, 9; seropurulent pericarditis, 1; fibrinopurulent
pericarditis, 10; purulent pericarditis, 2.
It is noteworthy that in 12 of 23 instances of pericarditis the lesion
was associated with S. hemolyticus infection of the lung and whenever in
these instances cultures were made (Autopsies 434, 485, 499 and 504)
hemolytic streptococci were obtained from the pericardial exudate in
pure culture.
The tendency of interstitial suppurative pneumonia to produce
pericarditis is especially evident. Among 21 instances of interstitial
suppurative pneumonia pericarditis occurred 6 times (28.6 per cent);
among 39 instances of suppurative pneumonia with abscess formation,
pericarditis occurred twice (5.1 per cent); whereas among all other
autopsies, namely, 181, the lesion occurred 15 times (8.3 per cent).
Pericarditis occurred in association with pneumonia referable to
Pneumococcus I, once, (Pneumococcus I isolated from the pericardium); to
Pneumococcus II, once; to atypical Pneumococcus II, 5 times (twice
isolated from the pericardium); and to Pneumococcus IV, twice (once
isolated from the pericardium).
=Peritonitis.=—Purulent peritonitis occurred only twice, in both
instances in association with pneumonia caused by hemolytic
streptococci. Purulent peritonitis was part of a general serositis
involving both pleural cavities, pericardium and peritoneum in 2
noteworthy instances:
=Autopsy 465.=—J. K., white, aged twenty-two, farmer from Oklahoma,
had been in military service one month. He was admitted to the
hospital with influenza, sore throat and bronchitis twenty-four days
before his death. Signs of pneumonia were recognized thirteen days
later and at the same time there was otitis media on the right side.
Empyema and pericarditis were found three days before death and two
days later 1000 c.c. of cloudy fluid were withdrawn from the chest.
=Anatomic Diagnosis.=—Suppurative pneumonia with consolidation and
abscess in right lower lobe below pleura; purulent pleurisy on
right, seropurulent pleurisy on left side; beginning serofibrinous
pericarditis; fibrinopurulent peritonitis; purulent bronchitis.
The body is emaciated. The right pleural cavity contains 350 c.c. of
thick, creamy yellow pus in which are flakes of fibrin; the right
lung is collapsed and lies at the back and inner side of the cavity.
The left pleural cavity contains 500 c.c. of turbid, yellow,
seropurulent fluid in which is soft fibrin. The lower lobe of the
right lung is consolidated throughout, flabby, gray red and finely
granular on section. Below the pleura of the posterior border is a
wedge-shaped cavity with its base 1.5 cm. across, in contact with
the pleural surface. About the cavity consolidated tissue has an
opaque, yellow color. Bronchi in both lungs contain mucopurulent
fluid. The pericardial cavity contains 20 c.c. of turbid fluid; the
left auricular appendage is bound by a thin layer of fibrin to the
parietal pericardium.
The peritoneal cavity contains 100 c.c. of thick, creamy, yellow,
purulent fluid. Between the diaphragm and liver is a layer of
fibrin, in places 1.5 cm. in thickness; fibrin is present upon the
peritoneum overlying the kidneys and base of mesentery.
Bacteriologic examination shows the presence of hemolytic
streptococci, obtained in pure culture from the blood of the heart,
right pleural cavity and peritoneum. From the right bronchus are
grown S. hemolyticus, B. influenzæ and a few colonies of S. viridans
and staphylococcus.
=Autopsy 504.=—G. R. C., white, aged twenty-eight, farmer from
Alabama, had been in military service three months. Onset of illness
occurred six days before death, and two days later he entered the
hospital with fever (103.4° F.), pains in the abdomen and vomiting.
Consolidation at the bases of the lung was recognized on the day
following admission and on the day before death 900 c.c. of greenish
brown fluid were aspirated from the left pleural cavity.
=Anatomic Diagnosis.=—Interstitial suppurative pneumonia with
consolidation in left lower lobe; purulent pleurisy on both sides;
purulent pericarditis; purulent peritonitis; parenchymatous
degeneration of kidneys; acute splenic tumor.
The body is that of a large well-nourished man. The left pleural
cavity contains 975 c.c. of creamy, yellow fluid; right pleural
cavity contains 425 c.c. of purulent fluid thinner than that on the
left side. The left lung is collapsed; the posterior and lower half
of the lower lobe is consolidated, flabby, deep red and fleshy in
appearance. The interstitial septa are yellow, thickened with
bead-like enlargements and contains creamy purulent fluid which
flows away and leaves small cavities. This interstitial suppuration
is more advanced below the outer surface of the lobe than elsewhere.
The pericardial cavity contains 25 c.c. of creamy, yellow, purulent,
fluid; the epicardium is dull, covered in a few places by a small
amount of fibrin and below it are ecchymoses.
The peritoneal cavity contains 100 c.c. of thick, yellow pus; the
peritoneal surfaces are injected and between the liver and diaphragm
is fibrin.
Bacteriologic examination shows the presence of S. hemolyticus in
pure culture from the blood of the heart, the lower lobe of the left
lung, pericardium and peritoneum. The right main bronchus contains
the same microorganism, B. influenzæ and a few staphylococci.
General serositis has been caused by hemolytic streptococci which in one
instance have entered the pleura from a subpleural abscess, and in the
other from the suppurating interstitial tissue of the lung. In one of
these cases the patient entered the hospital with symptoms suggestive of
acute peritonitis.
Bronchiectasis
Acute dilatation of the bronchi is a common result of the bronchitis of
influenza, and its frequent occurrence is an index of the severity of
the changes in the bronchial wall. In some instances the smaller bronchi
in well-localized areas are uniformly dilated; in other instances, large
cavities, several centimeters in diameter, are formed and all
transitions between the two extremes occur.
The occurrence of bronchiectasis following influenza is mentioned by
Leichtenstern[86]. He states that evidence of bronchiectasis can persist
for weeks or months and nevertheless end with complete restitution of
the lungs to normal. Lord[87] has described instances of bronchiectasis
occurring in association with infection by B. influenzæ and Boggs[88]
has recorded similar observations.
We have had abundant opportunity to observe early stages in the
production of bronchiectasis and to study the much discussed
pathogenesis of the condition.
The following figures show the predilection of bronchiectasis for the
left lung and for the lower lobes: Bronchiectasis occurred 30 times in
the left lung alone, 9 times in the right lung alone and 13 times in
both lungs, the total being 52. Among 30 instances in which the lesion
occurred only in the left lung, in 24 it was limited to the lower lobe,
and in 15 of these 24 instances to the base of the lower lobe. Among 9
instances in which dilatation of bronchi occurred only in the right
lung, it was limited to the lower lobe in 4 instances and to the base of
the lower lobe in 2 of these 4 instances.
When the lesion is limited to the base of the lower lobes small bronchi
with no recognizable cartilage in their wall are dilated to a diameter
of from 3 to 6 cm. and are distended with thick mucopurulent fluid. The
tenacious character of the bronchial contents and the action of gravity
doubtless have a part in the production of the dilatation. In several
instances dilatation of the bronchi was limited to the basal parts of
both upper and lower lobes.
When bronchiectasis occurs throughout a whole lung, usually the left, or
in both lungs, the lesion is more advanced and conspicuous (Fig. 26).
There is diffuse dilatation of small and medium-sized bronchi. Dilated
bronchi with deeply injected mucosa and filled with yellow mucopurulent
fluid, are seen throughout the sectioned lung. A bronchus cut
longitudinally may have a nearly uniform diameter of from 5 to 9 mm. for
a distance of 5 or 6 cm., maintaining this diameter to within 1 cm. of
the pleural surface, where normally only small bronchi occur.
More advanced bronchiectasis is represented by the occurrence of
spherical bronchiectatic cavities, having a diameter from 1 to 2.5 cm.
In some instances there have been two or three of these cavities but
occasionally there may be many. Cylindrical dilatation of the bronchi
usually occurs widely distributed in the lungs. In Autopsy 440 a small
bronchus, cut longitudinally, was dilated to a diameter of 5 mm. for a
distance of 5 cm. and terminated in a spherical cavity 2 cm. in
diameter; there was another smaller spherical cavity nearby and dilated
bronchi occurred elsewhere. In Autopsy 467, in the upper part of the
lower lobe, two spherical cavities 1 and 1.5 cm. in diameter
communicated with a bronchus of medium size.
Autopsies with bronchiectasis are listed in the order of the duration of
illness to show the parallel increase in the severity of the lesion
(Table LI). In 2 instances (Autopsies 244 and 314) bronchiectatic
cavities surrounded by firm fibrous tissue have evidently existed before
the onset of the fatal illness, which has lasted in one instance
approximately four and in the other six days; these autopsies have been
omitted from the table.
The table shows that bronchiectasis observed within twelve days after
onset of illness with symptoms of influenza is moderately advanced and
almost invariably limited to the left lower lobe and usually to the base
of the lobe. Advanced dilatation, indicated by the formation of
spherical or cylindrical cavities, occurs with increasing frequency as
the duration of the respiratory disease increases.
Bronchiectasis has been almost invariably associated with purulent
bronchitis. The dilated bronchi contain mucopurulent material and
throughout the lungs the same condition is usually widespread. Among 137
instances of purulent bronchitis bronchiectasis consequent upon
influenza has been present in 50.
TABLE LI
═══════╤════════╤═════════════╤══════════════╤══════════════╤═══════════
NO. OF │DURATION│ TYPE OF │ LOCATION OF │ CHARACTER OF │BACTERIA IN
AUTOPSY│ OF │ PNEUMONIA │BRONCHIECTASIS│BRONCHIECTASIS│ BRONCHUS
│ILLNESS │ │ │ │
│IN DAYS │ │ │ │
───────┼────────┼─────────────┼──────────────┼──────────────┼───────────
394│ 5 ?│Broncho │Rt. base │Dilatation │
359│ 7 +│Lobar and │Lt. lower lobe│Dilatation │
│ │ broncho │ │ │
322│ 8│Abscess │Lt. base │Dilatation │
│ │ (staph.) │ │ │
325│ 8│Interst. │Lt. base │Dilatation │S. hem., B.
│ │ suppuration│ │ │ inf.,
│ │ │ │ │ staph.
352│ 8│Lobar and │Lt. lower lobe│Advanced │
│ │ broncho │ │ dilatation │
429│ 8 ?│Broncho │Rt. base │Dilatation │
288│ 10│Abscess │Lt. base │Dilatation │S. hem., B.
│ │ │ │ │ inf.
374│ 10│Lobar and │Rt. and lt. │Advanced │
│ │ broncho │ lungs │ dilatation │
376│ 10│Abscess │Lt. base │Dilatation │S. hem.
437│ 11│Lobar │Rt. lower lobe│Advanced │
│ │ │ │ dilatation │
482│ 11│Broncho │Lt. base │Dilatation │B. inf.,
│ │ │ │ │ Pneum.
│ │ │ │ │ IV, S.
│ │ │ │ │ hem.
489│ 11│Lobar and │Lt. lung │Dilatation │B. inf.,
│ │ broncho │ │ │ Pneum.
│ │ │ │ │ IV.
287│ 12│Lobar and │Lt. lower lobe│Advanced │Pneum. IV.,
│ │ broncho │ │ dilatation │ B. inf.,
│ │ │ │ │ staph.
289│ 12│Broncho │Lt. lower lobe│Advanced │Pneum. IV.,
│ │ │ │ │ B. inf.
│ │ │ │ │ staph.
295│ 12│Interst. sup.│Rt. lung │Advanced │S. hem., B.
│ │ and abscess│ │ dilatation │ inf.
336│ 12│Broncho │Lt. base │Dilatation │
375│ 12│Broncho │Rt. and lt. │Dilatation │
│ │ │ bases │ │
422│ 12 ?│Lobar and │Lt. base │Dilatation │
│ │ broncho │ │ │
381│ 13│Abscess │Lt. base │Spherical │
391│ 13│Lobar and │Lt. lung │Dilatation │
│ │ broncho │ │ │
401│ 14 ?│Lobar and │Rt. and lt. │Spherical │
│ │ broncho │ lungs │ │
402│ 14│Chronic │Rt. lower lobe│Dilatation │
│ │ broncho │ │ │
410│ 14 ?│Abscess │Rt. upper lobe│Dilatation │
333│ 15│Abscess │Lt. upper lobe│Dilatation │S aur., B.
│ │ (staph.) │ │ │ inf. S.
│ │ │ │ │ hem.
389│ 15│Interst. │Lt. lung │Advanced │
│ │ suppuration│ │ dilation │
412│ 15│Lobar and │Lt. lower lobe│Cylindrical │
│ │ broncho │ │ │
398│ 16│Broncho │Rt. and lt. │Advanced │
│ │ │ lungs │ dilatation │
423│ 16│Broncho │Lt. base │Dilation │
488│ 16│Abscess │Lt. lower lobe│Dilatation │S. hem.,
│ │ │ │ │ Pneum.
│ │ │ │ │ atyp. II.
312│ 17│Broncho │Rt. and lt. │Dilatation │S. hem., B.
│ │ │ lungs │ │ inf.
│ │ │ │ │ staph.
372│ 17│Broncho │Rt. lung │Dilatation │
385 C│ 17│Interst. │Lt. base │Dilatation │
│ │ suppuration│ │ │
448│ 17│Broncho │Lt. lung │Dilatation │
460│ 17│Abscess │Lt. lower lobe│Spherical │S. hem., B.
│ │ │ │ │ inf.,
│ │ │ │ │ staph.
291│ 18│Broncho │Lt. base │Advanced │B. inf.,
│ │ │ │ dilatation │ staph.
296│ 18│Abscess │Lt. base │Dilatation │S. hem., B.
│ │ │ │ │ inf.,
387│ 19│Abscess │Rt. and lt. │Advanced │S. hem., B.
│ │ │ lungs │ dilatation │ inf., S.
│ │ │ │ │ aur.
│ │ │ │ │ Pneum.
│ │ │ │ │ II.
421│ 19│Chronic │Rt. lung │Advanced │
│ │ broncho │ │ dilatation │
440│ 19│Chronic │Rt. and lt. │Spherical │B. inf., S.
│ │ broncho │ lungs │ │ aur.
419│ 20│Broncho │Rt. lung │Dilatation │Pneum. II,
│ │ │ │ │ B. inf.
463│ 20│Chronic │Rt. and lt. │Spherical │B. inf.,
│ │ broncho │ lungs │ │ staph.,
│ │ │ │ │ Pneum. IV
431│ 23│Chronic │Lt. base │Dilatation │
│ │ broncho │ │ │
468│ 23 ?│Lobar and │Lt. lung │Dilatation │S. aur., B.
│ │ broncho │ │ │ inf., S.
│ │ │ │ │ vir.
465│ 25 ?│Broncho │Lt. base │Dilatation │S. hem., B.
│ │ │ │ │ inf.,
│ │ │ │ │ staph.,
│ │ │ │ │ S. vir.
445│ 27│Broncho │Lt. lower lobe│Spherical │S. aur.
449│ 27│Abscess │Rt. and lt. │Spherical │S. hem., B.
│ │ │ lungs │ │ coli.
378│ 28│Abscess │Lt. base │Cylindrical │S. hem., B.
│ │ │ │ │ inf.,
│ │ │ │ │ Pneum.
│ │ │ │ │ atyp. II.
473│ 28│Chronic │Lt. lung │Advanced │B. inf., S.
│ │ broncho │ │ dilatation │ vir.,
│ │ │ │ │ staph.,
│ │ │ │ │ M.
│ │ │ │ │ catarr.
425│ 29│Abscess │Rt. and lt. │Cylindrical │
│ │ (staph.) │ lungs │ │
467│ 30│Abscess │Rt. lower lobe│Spherical │S. hem., B.
│ │ │ │ │ inf.
472│ 37│Chronic │Rt. and lt. │Advanced │B. coli
│ │ broncho │ lungs │ dilatation │
487│ 55│Abscess │Rt. and lt. │Cylindrical │B. inf. S.
│ │ │ lungs │ │ hem.
───────┴────────┴─────────────┴──────────────┴──────────────┴───────────
The bacteriology of autopsies with bronchiectasis is shown in Table LII.
TABLE LII
════════╤════════╤═════════════════╤═════════════════
│ NO. │ │
│EXAMINED│ PNEUMOCOCCUS │ S. HEMOLYTICUS
────────┼────────┼────────┬────────┼────────┬────────
│ │ NO. │PER CENT│ NO. │PER CENT
│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE
────────┼────────┼────────┼────────┼────────┼────────
Bronchus│ 29│ 9│ 31.0│ 15│ 51.7
Lung │ 37│ 16│ 43.2│ 18│ 48.6
Blood │ 50│ 12│ 24.0│ 22│ 44.0
────────┴────────┴────────┴────────┴────────┴────────
════════╤═════════════════╤═════════════════
│ │
│ STAPHYLOCOCCUS │ B. INFLUENZÆ
────────┼────────┬────────┼────────┬────────
│ NO. │PER CENT│ NO. │PER CENT
│POSITIVE│POSITIVE│POSITIVE│POSITIVE
────────┼────────┼────────┼────────┼────────
Bronchus│ 16│ 55.2│ 23│ 79.3
Lung │ 10│ 27.0│ 19│ 51.4
Blood │ │ │ │
────────┴────────┴────────┴────────┴────────
Comparison of the percentage incidence of the organisms which have to be
found associated with bronchiectasis and with purulent bronchitis
unaccompanied by bronchiectasis shows that there is no noteworthy
difference in the occurrence of pneumococci, hemolytic streptococci or
B. influenzæ within the bronchi. When allowance is made for the
difficulty of demonstrating B. influenzæ in the presence of a large
number of other microorganisms, it is not improbable that this organism
has been constantly present in the purulent contents of the bronchi with
purulent bronchitis, with and without bronchiectasis. Pneumococci,
streptococci and staphylococci are each present in the bronchi in about
one-half of the instances of bronchiectasis and mixed infections are
very common, S. viridans, B. coli and M. catarrhalis being occasionally
found in the bronchi. The table shows that pneumococci, streptococci and
staphylococci show no greater tendency to enter the lungs and blood when
bronchiectasis and purulent bronchitis coexist than with purulent
bronchitis alone.
Moderate dilatation of the small bronchi at the base of the left lung
was found in several instances eight days after onset of symptoms
referable to the respiratory passages. Advanced, diffuse dilatation of
the bronchi was seldom seen before the lapse of two weeks, and
bronchiectasis with formation of spherical or cylindrical cavities was
found with few exceptions three weeks after onset of the fatal illness.
Long continued, purulent bronchitis does not necessarily produce
dilatation of the bronchi. It is noteworthy that the average duration of
the fatal illness in 137 instances of pneumonia and purulent bronchitis
with no bronchiectasis was 12.5 days, whereas the average duration of 49
instances of pneumonia with purulent bronchitis and bronchiectasis was
only 16.5 days.
Bronchiectasis is almost invariably associated with purulent bronchitis
in which tenacious mucopurulent fluid accumulates in the bronchi. It
begins at the bases of the lower lobes and is usually more advanced here
than elsewhere. Mechanical distention of the small bronchi by viscid
fluid, expelled with difficulty, brings about their dilatation and
gravity appears to have a part in accentuating the process. Histologic
examination of the changes accompanying bronchitis show that lesions
which penetrate into the muscular layer and presumably weaken the
bronchial wall are not uncommon and partial or complete destruction of
the wall may result. To what extent infiltration of the muscular wall by
polynuclear leucocytes or by lymphoid and plasma cells is accompanied by
changes which weaken the wall may be questioned. When the epithelial
lining of the bronchus is destroyed coagulative necrosis of the
underlying tissue occurs and may extend a variable distance into the
bronchial wall, not infrequently penetrating into or entirely through
the muscular layer. These changes furnish an explanation of the
occurrence of bronchiectasis following influenza.
[Illustration:
Fig. 17.—Acute bronchiectasis showing fissures penetrating into
bronchial wall and at one place entering surrounding alveolar
tissue; the surrounding alveoli are filled with fibrin. Autopsy 425.
]
Acute bronchiectasis may be found following influenza after the illness
has lasted eight or ten days. There is no increase of fibrous tissue.
Small bronchi with no cartilage, which in normal lungs have a diameter
approximating 1 mm., are dilated to 3 mm. or more. The surface
epithelium is wholly or partially lost. Necrosis occurs in places and
extends deep into the tissue, destroying muscle and often penetrating
the entire thickness of the wall which in these small bronchi consists
in large part of fibrous tissue containing greatly engorged blood
vessels. In this necrotic material nuclei are absent and the tissue
containing fibrin stains deeply with eosin. In it occur fissures or
tears which extend from the lumen a variable distance, very frequently
penetrating the entire thickness of the wall and entering adjacent
alveoli (Figs. 17 and 19). Alveoli thus exposed almost invariably
contain plugs of dense fibrin. Where these rents have occurred, adjacent
edges of the bronchial wall, held together by underlying lung tissue,
have separated from one another, so that the circumference of the
bronchus has been increased (Fig. 18). These breaks in the continuity of
the wall may occur in several places, so that a fourth or a third of the
circumference may be formed by exposed alveolar tissue which has become
the site of fibrinous pneumonia (Fig. 20). During life, though the
inflamed bronchus is filled by mucopurulent exudate, distention of loose
alveolar tissue, uniting the interrupted bronchial wall, is doubtless
greater than it appears in the lung fixed by hardening fluids.
[Illustration:
Fig. 18.—Acute bronchiectasis showing fissures in the bronchial wall
extending into neighboring alveoli which in zone about are filled
with fibrin; one fissure has separated widely; peribronchial
fibrinous pneumonia (fibrin is black). Autopsy 425.
]
Recently dilated bronchi have an irregularly stellate lumen as the
result of clefts penetrating at intervals into or through the bronchial
wall (Fig. 26). Longitudinal fissures mark the lining of these dilated
bronchial tubes.
When the fatal illness has lasted more than two weeks, abundant new
formation of fibrous tissue occurs in a zone surrounding the dilated
bronchus. Adjacent alveolar walls are thickened by young fibrous tissue.
Alveoli, much diminished in size, are filled by hyaline fibrin into
which fibroblasts and newly formed blood vessels have penetrated. These
changes are limited to a wide zone in immediate contact with the dilated
bronchus, whereas at a greater distance alveolar walls have undergone no
thickening and alveoli contain no fibrin.
[Illustration:
Fig. 19.—Acute bronchiectasis; the bronchial wall indicated by
engorged mucosa shows a varying degree of destruction, fissures
extending into and through the bronchial wall. Autopsy 352.
]
[Illustration:
Fig. 20.—Acute bronchiectasis; with destruction of bronchial wall
exposing alveoli filled with fibrin; peribronchial fibrinous
pneumonia is seen about several bronchi present in the section; Gram
Weigert fibrin stain. Autopsy 425.
]
This stage is well represented by Autopsy 421 after an illness of
nineteen days. Bronchiectatic cavities, from 3 to 6 mm. in diameter, are
numerous in sections of the lung; their lumina are irregular in outline
and often irregularly stellate. Microscopic examination shows the
presence of clefts which interrupt the bronchial wall at intervals
throughout its entire circumference. The original wall is well indicated
by the very richly vascularized connective tissue containing scattered
muscle bundles and is infiltrated with lymphoid and plasma cells in
great number. Where fissures have occurred the adjacent edges of the
interrupted wall have separated from one another, leaving a wide
interval where underlying alveolar tissue is exposed. Two changes tend
eventually to render the fissures inconspicuous, namely, regeneration of
epithelium and new formation of fibrous tissue. Exposed alveoli filled
with fibrin are in process of organization and epithelium which has
assumed a squamous type has grown down over the exposed surfaces of the
interrupted bronchial wall. It has begun to cover or in some instances
has completely covered the surface of rents entering alveoli plugged
with fibrin (Fig. 21). In the periphery of the bronchus alveolar walls
are thickened and infiltrated with lymphoid and plasma cells. The same
changes affect bronchi containing cartilage which is undergoing atrophy.
The reinforcement of the fissured bronchial wall by new formation of
fibrous tissue, by thickening of the interalveolar walls and by
organization of fibrin within the alveoli is well shown after four weeks
(Autopsy 425; Fig. 28). There are spherical bronchiectatic cavities more
than a centimeter in diameter surrounded by a dense fibrous wall in
which are atrophied alveoli lined by epithelium of cubical form.
Occasionally, the fibrous wall is interrupted and alveoli, plugged with
organizing fibrin, are in immediate contact with the lumen. When these
plugs of fibrin which are slowly absorbed disappear, evidence of
preexisting rents in the bronchial wall are lost, and there are in this
lung bronchiectatic cavities of which the wall is a continuous circle of
dense fibrous tissue.
[Illustration:
Fig. 21.—Bronchiectasis with fissures extending through the bronchial
wall into alveolar tissue which is the site of fibrinous pneumonia;
epithelium has grown down into these fissures and has covered the
exposed surfaces. Autopsy 463.
]
[Illustration:
Fig. 22.—Regeneration of epithelium over fissures which have been
formed in the wall of a bronchus; the epithelium in the neighborhood
of and within the fissure is squamous.
]
Epithelium lining the dilated bronchi is at times completely destroyed
(Fig. 28), but more frequently it persists in part. That which remains
has almost constantly the character of squamous epithelium (Figs. 22 and
23). The lowermost cells are cubical; those above them are polygonal,
tending to become flatter as the surface is approached; upon the surface
are cells often much flattened and occasionally they have lost their
nuclei and stain deeply with eosin as the result of superficial
necrosis. The change should not be regarded as metaplasia, for the
epithelium assumes this squamous type when the superficial columnar
cells have been lost. Actual necrosis of superficial ciliated columnar
cells is occasionally seen (Autopsy 352); injured cells have separated
from one another and desquamated into the lumen of the bronchus. The
epithelium which remains after the superficial cells are lost consists
of cells which become flatter from base to surface, but the
intercellular bridges characteristic of the epithelium of the skin are
not found. When epithelium is in process of regeneration, a layer
gradually diminishing in thickness extends over the denuded surface, the
advancing edge being formed by very flat cells in a single layer. The
epithelium growing into fissures which have penetrated the bronchial
wall may completely cover the exposed alveolar tissue. The newly formed
epithelium may follow a fissure into an alveolus which has been opened
and come into contact with the fibrin which fills the alveolus.
[Illustration:
Fig. 23.—Squamous epithelium growing over the defect in the bronchial
wall shown in Fig. 22 more highly magnified; squamous epithelium is
present above and columnar epithelium below.
]
Bronchiectasis usually affects the small bronchi with no cartilage. It
is not uncommon to find greatly dilated bronchi with no cartilage in
close proximity to cartilage containing bronchi of smaller caliber. In
one instance (Autopsy 421) a bronchus of medium size with cartilage
measured 3 mm. in diameter, whereas two bronchi with no cartilage were
dilated to 4 and 6 mm., respectively. Nevertheless, larger bronchi are
occasionally the site of superficial loss of epithelium, necrosis
extending into the bronchial wall, formation of fissures and stretching
of the wall at the spot which is weakened. In association with these
changes atrophy of the cartilage may occur (Autopsies 421, 425, 440,
463). Plates of cartilage in process of atrophy are readily recognized
by their irregularly indented outline and often by their small size. The
fibrous tissue surrounding the cartilage is the site of chronic
inflammation and is densely infiltrated with lymphoid and plasma cells
among which polynuclear leucocytes are scant. Nevertheless, polynuclear
leucocytes are abundant in immediate contact with the cartilage and
appear to have an important part in the solution of its matrix, for
about them occur indentations of the edge. Leucocytes penetrate into the
cartilage.
The necrosis and tears which occur in the wall of the bronchus are not
always limited to the bronchus, but may extend deeply into the
surrounding tissue. In Autopsies 312 (Fig. 21) and 423 wide areas of
necrosis have penetrated deeply into the tissue about the bronchi.
=Autopsy 312.=—Illness began with influenza on September 26,
seventeen days before death; a diagnosis of lobar pneumonia with
consolidation of the right lower lobe was made ten days after onset
and Pneumococcus IV, B. influenzæ and S. hemolyticus were found in
the sputum. At autopsy there was bronchopneumonia with red and gray
lobular and confluent lobular patches of consolidation and right and
left serofibrinous pleurisy; there was purulent bronchitis; no
abscesses were seen. Small bronchi throughout both lungs were
dilated and often surrounded by a zone of hemorrhage.
Hemolytic streptococci were found in the heart’s blood, in the
pleural exudate, consolidated lung and bronchus; B. influenzæ was
found in the lung and in a small bronchus, and staphylococci in the
contents of a small bronchus.
[Illustration:
Fig. 24.—Acute bronchiectasis with fissures extending through
bronchial wall which is marked by great engorgement of blood
vessels; at one point a fissure has penetrated deep into the
alveolar tissue and formed a small cavity containing purulent
exudate and surrounded by fibrinous pneumonia. Autopsy 312.
]
Bronchi which are the site of acute inflammation have lost their
epithelium wholly or in part, and deep fissures penetrate the entire
thickness of the bronchial wall, extending into the surrounding lung
tissue which is the site of fibrinous pneumonia. In some instances
plugs of fibrin within the alveoli are bisected by these tears.
There is some superficial necrosis along the edge of each fissure,
in several places extending outward from defects in the walls of
small bronchi dilated to approximately 1.5 mm. There are wide
patches of necrosis affecting both alveolar walls and contents of
alveoli and extending 2 mm. into the lung tissue. When a fissure has
penetrated from the lumen of the bronchus into necrotic tissue (Fig.
21), polynuclear leucocytes have accumulated within the necrotic
tissue, disintegration of tissue occurs, and a small cavity
communicating with the bronchus is formed.
=Autopsy 423.=—C. H., white, aged twenty-five, resident of Oklahoma,
had been in military service one month. Death occurred sixteen days
after onset of influenza.
=Anatomical Diagnosis.=—Chronic bronchopneumonia with
peribronchiolar consolidation throughout right lung and in left
lower lobe; right purulent pleurisy; purulent bronchitis;
bronchiectasis at base of left lung.
The right lung weighs 1,260 grams; in the upper lobe are yellowish
gray nodules having the appearance of tubercles clustered about
small bronchi; in places similar nodules occur upon a background of
pinkish gray consolidation occupying the greater part of the lower
lobe. Bronchi contain purulent fluid. The left lung weighs 760
grams; it is edematous and small, yellowish gray nodules of
consolidation in the lower lobe are clustered about terminal
bronchi. Bronchi at the base of the lower lobe are dilated.
Bacteriologic examination shows the presence of hemolytic
streptococci in the blood of the heart; hemolytic streptococci and
B. influenzæ in the lung.
Microscopic examination shows that the walls of the bronchi are
infiltrated with lymphoid and plasma cells; these cells are very
numerous in peribronchiolar patches of consolidation. A small
bronchus 1 mm. in diameter has squamous epithelium along one side;
on the opposite side, the wall is completely absent and there is
superficial necrosis of exposed alveoli filled with fibrin. A deep
fissure passes from the bronchus into the consolidated tissue; its
edges are necrotic and it is filled with polynuclear leucocytes. A
small cavity in contact with the bronchus has been formed. In
another part of the lung a distended bronchus has lost its
epithelium on one side, and here alveoli filled with fibrin form the
wall of the bronchus which is filled with leucocytes. Extending
outward from the eroded wall is a focus of necrosis where both
alveolar walls and contained exudate have lost their nuclei.
The necrosis which has had its origin in the bronchi is soon followed by
accumulation of polynuclear leucocytes, softening and disintegration of
tissue. Discharge of the disintegrated tissue through the bronchi
results in the formation of a small cavity continuous with the bronchus.
These changes are well illustrated by the bronchiogenic abscesses which
have been described elsewhere (Autopsies 376, p. 206, and 387, p. 206).
When disintegrated tissue is discharged by way of the bronchi no
accumulation of pus occurs, but cavities will be formed, in part by
dilation of bronchi, in part by erosion of the adjacent lung tissue.
Histologic examination shows that these changes have produced the
advanced bronchiectasis found in Autopsy 445 (Fig. 25).
=Autopsy 445.=—W. F., white, aged twenty-three, from Mississippi,
had been in military service one month. His illness began September
22, twenty-seven days before death, with severe coryza, weakness,
nausea and vomiting; great pain in bones, cough and sore throat. He
was admitted to the base hospital one week later with diagnosis of
influenza and bronchitis. On October 3, sixteen days before death,
signs of consolidation were found on the left side over the back and
a diagnosis of lobar pneumonia was made. On October 18 there was
severe headache, pupils were dilated, and there was rigidity of
neck; lumbar puncture was made and pneumococci were found in the
fluid obtained. Death occurred on the following day.
=Anatomic Diagnosis.=—Bronchiectasis with unresolved pneumonia
limited to the left lower lobe; acute bronchopneumonia with
peribronchiolar consolidation in right lung; purulent bronchitis,
peribronchial hemorrhage and organizing bronchiolitis in right lung;
adherent pleura on left side; purulent meningitis.
The left upper lobe is crepitant throughout. The outer and posterior
two-thirds of the left lower lobe is riddled with cavities often
rounded and varying in diameter from 0.5 to 3 cm. but not
infrequently irregular in shape and in communication with adjacent
cavities (Fig. 25). In places cavities pass in a tortuous course
from pleura to the midpart of lung. The lining of these cavities is
usually smooth, but in places is covered by gray necrotic material.
Communication between the cavities and medium-sized bronchi is
occasionally found. The lung tissue between the cavities is in part
grayish red and consolidated, in part pink and air containing. The
right lung is edematous throughout; the bronchi in the lower part of
the right lung contain purulent fluid and are in places surrounded
by zones of hemorrhage.
The spleen is very large (14 × 11 × 5 cm.) and firm.
The spinal fluid is cloudy and blood vessels over the lumbar
enlargement and lower thoracic region are congested; in the upper
thoracic region the cord is covered by purulent exudate.
Bacteriologic examination demonstrates the presence of hemolytic
streptococci in the blood of the heart; plates from the left lung
contain a few colonies of S. aureus and Pneumococcus IV; plates from
the right main bronchus contain S. aureus and a large bacillus which
does not stain by Gram’s method. Three plates from the spinal
meninges contain Pneumococcus IV.
[Illustration:
Fig. 25.—Advanced bronchiectasis throughout lower left lobe. Autopsy
445.
]
Microscopic examination shows that the cavities which have been
described are lined by very vascular connective tissue containing
many cells; there is no epithelial lining and the surface is in
places covered by fibrin. On the surface polynuclear leucocytes are
numerous, but immediately below, large mononuclear cells occur and
frequently contain one or several ingested polynuclear leucocytes.
None of the structures peculiar to the bronchi can be identified in
the wall of these cavities, and in many places it is evident that
lung tissue has undergone destruction, for in places the lining of
vascular connective tissue is interrupted and an extension of the
cavity penetrating into the lung substance is surrounded by alveoli
filled with fibrin; in contact with the cavity there is some
necrosis.
The cavities communicate with the bronchi and are lined in part by
vascular connective tissue which may in part represent preexisting
bronchial walls, but no epithelium is present and the relation to the
bronchi cannot be established with certainty. These cavities have
extended by necrosis which has broken the vascular connective tissue of
their wall and penetrated into adjacent lung tissue. Death has been the
result of purulent meningitis caused by pneumococcus, and the histologic
changes in the walls of the cavities suggest that the activity of the
inflammatory reaction here is subsiding, for large mononuclear cells are
numerous and are ingesting polynuclear leucocytes. The changes described
would, if continued, result in the formation of cavities lined by
fibrous tissue and resembling many of those formed as the result of
dilatation of the bronchi.
A study of the progress of the changes which result in the formation of
bronchiectatic cavities has shown how the inflammatory irritant within
the bronchus destroys the epithelium of the bronchus, penetrates into
the deeper tissues and produces fissures which extend through the entire
thickness of the bronchial wall at one or usually several places. These
longitudinal fissures, which at first often give a stellate outline in
cross section to the cavity of the affected bronchus, permit the
separation of the edges of the fissure, so that an increase in the
circumference occurs. The base of the fissure is formed by surrounding
alveolar tissue and its edges are the site of necrosis. Tears may extend
into the surrounding alveolar tissue, thus permitting further stretching
of the bronchial wall. The consequences of rupture of the small bronchi
into the adjacent alveoli are to some extent overcome by the
inflammatory reaction which plugs the adjacent alveoli with fibrin.
Compression of the lungs by forced expiration, even though the glottis
were closed as in coughing, would not dilate the bronchi, because
pressure outside and within the bronchi would be equally elevated
(Thornton and Pratt[89]). The pressure within the bronchi does not
differ greatly from atmospheric pressure, whereas the negative pressure
within the pleural cavity may vary from approximately 6 mm. of mercury
during quiet inspiration to 30 mm. with forced inspiration. Excess of
pressure upon the inner surface of the bronchial walls will vary with
coughing and other respiratory efforts, between these limits depending
upon the readiness with which pressure is equalized within and without
the bronchi by penetration of air into the alveoli. The presence of
viscid mucopurulent fluid within bronchioles will obstruct these tubules
and retard the entrance of air into alveoli.
Weakening of the bronchial wall by the changes which have been described
will cause lasting dilatation of the bronchi. Whatever increases
pressure within the bronchi will increase the tendency to dilatation;
the bronchi being filled with mucopurulent exudate dilatation usually
appears first at the bases of the lung, since gravity increases
intrabronchial pressure here. New formation of fibrous tissue within the
wall of the bronchus, thickening of adjacent alveolar walls, and
organization of fibrin reinforce the weakened bronchial wall and limit
the dilatation which follows injury to the wall. Regeneration of
epithelium covering the dilated tube will further obscure the early
changes which have made dilatation possible. The changes which weaken
the bronchial wall permit dilatation at a time when there is no new
formation of fibrous tissue. When the bronchial lesion has persisted
several weeks, chronic pneumonia is associated with it. It has been
suggested that the contraction of newly formed fibrous tissue within the
substance of the lung might cause bronchi to be enlarged by traction
upon their walls. Newly formed connective tissue is most abundant in the
wall of the bronchiectatic cavity, and here contraction would tend to
diminish the size of the cavity.
Unresolved Bronchopneumonia
Chronic bronchopneumonia is characterized by changes similar to those
associated with chronic inflammation in other parts of the body, namely,
by thickening of the interstitial tissue of the lung, by accumulation of
mononuclear cells, by proliferation of fibrous tissue and by
organization of exuded fibrin. In a few instances these changes have
begun at the end of two weeks after onset of influenza, but they have
been little advanced until three weeks has elapsed; advanced chronic
inflammation has occurred after from four to eight weeks. Chronic
inflammation primarily affects those structures which are most severely
injured by the acute lesion and is most conspicuous in immediate
proximity to the small bronchi and bronchioles; the perivascular and
interlobular connective tissue are secondarily involved. Corresponding
to each of the lesions of the alveolar tissue which have been found with
bronchopneumonia, namely, peribronchiolar, hemorrhagic peribronchiolar,
lobular and peribronchial consolidation, there is a chronic lesion which
develops when pneumonia has failed to resolve.
The term interstitial bronchopneumonia has been used by MacCallum to
designate a lesion which he has found in association with measles at
Fort Sam Houston. This name he states does not describe accurately the
early stage of the lesion, for its interstitial character is not evident
at first. In his monograph on “Epidemic Pneumonia in the Army Camp,”
published in 1919, MacCallum describes and pictures instances of the
lesion which we have designated interstitial suppurative pneumonia and
classifies them as interstitial bronchopneumonia. We have shown that
this lesion, which is the result of infection of the lymphatics with S.
hemolyticus, bears no necessary relation to the lesion which is
characterized in its early stage by peribronchiolar pneumonia and in its
later stages by chronic inflammation with mononuclear infiltration and
proliferation of the peribronchial, perivascular and interalveolar
tissue. At Fort Sam Houston, nearly every patient with measles was
infected with hemolytic streptococci; we observed, following influenza,
similar prevalence of hemolytic streptococci in certain wards in the
base hospital at Camp Pike. Among the cases at Fort Sam Houston there
were doubtless instances both of interstitial suppurative pneumonia
caused by hemolytic streptococcus and of chronic bronchopneumonia not
referable to this microorganism.
Studying pneumonia following influenza at Camp Lee, Va., and later at
Camp Dix, N. J., during the fall of 1918, MacCallum reached the
conclusion that “interstitial bronchopneumonia” following influenza was
caused by B. influenzæ of Pfeiffer. This lesion attributed to B.
influenzæ differed from that previously referred to hemolytic
streptococcus in the following characters: the lymphatic channels in the
bronchial walls and widened interlobular septa are inconspicuous and
none are found distended with exudate; there is no intense infection of
the pleura, and polynuclear leucocytes are inconspicuous in the alveolar
exudate and in the walls of the bronchi. It seems probable these
differences are explained by the absence of hemolytic streptococci which
tend to invade lymphatics and produce severe inflammatory changes in the
pleura.
=Chronic Bronchitis.=—The earliest changes in the bronchial wall with
bronchitis of influenza are hyperemia, leucocytic infiltration and
hemorrhage, and they may occur even though the lining epithelium remains
intact. Epithelium frequently undergoes partial or complete destruction,
and with this severe injury the influence of the inflammatory irritant
may extend directly through the wall of the bronchus, for in some
instances there is hemorrhage into all the alveoli in a zone encircling
the bronchus. Since these alveoli have only indirect communication with
the affected bronchus through alveolar tissue not involved in the
inflammatory process, it is evident that the surrounding hemorrhage is
secondary to the lesion of the bronchus. Fibrinous inflammation in other
instances, similarly localized in a zone of alveoli encircling a
bronchus, is doubtless the result of direct extension of the
inflammatory process through the bronchial wall. After the disease has
existed during two or three weeks inflammation is still active
immediately below the inner surface of the bronchus; here polynuclear
leucocytes are numerous whereas in the deeper parts of the mucosa and
about the muscularis leucocytes are scant but lymphoid and plasma cells
are very numerous. The severity of the inflammatory reaction may be
judged by the abundance and extent of this cellular reaction and is in
close relation to the intensity of the changes affecting the mucous
membrane of the bronchus. Infiltration of the entire bronchial wall with
lymphoid and plasma cells is almost invariable when the primary injury
to the bronchus has destroyed the epithelial lining, and this
infiltration is not limited to the bronchial wall but extends outward
into the contiguous alveolar septa which are thickened by it. The sheath
of the pulmonary artery which accompanies the bronchus exhibits a
similar change, and the alveolar septa, as a fringe about it, are
thickened and infiltrated with mononuclear cells. Interlobular septa
continuous with the bronchus often show some infiltration.
A later phase in this series of changes is represented by new formation
of fibrous tissue. The bronchial walls and interalveolar septa are
thickened by proliferating fibrous tissue, young fibroblasts and newly
formed collagen fibrils being abundant (Fig. 28; also Fig. 30). This
increase of fibrous tissue is especially noteworthy immediately
surrounding the walls of the small bronchi, which are often considerably
dilated, and about the smaller of those bronchi which have cartilage;
with thickening of alveolar walls immediately adjacent to the bronchus
every stage in the obliteration of the alveoli may be found. Their walls
are thickened and their lumina are diminished in size and often
flattened in a direction concentric with the bronchus. Such atrophied
alveoli lined by cubical epithelial cells occurring within the thickened
peribronchial fibrous tissue give evidence that this tissue has replaced
alveoli. Alveoli surrounding and within the new fibrous tissue are
frequently filled with fibrin, and organization indicated by penetration
of fibroblasts and capillaries into the fibrin may be far advanced.
There is some increase of perivascular and interlobular tissue. The
bronchiectasis which is almost invariably found with unresolved
bronchopneumonia has been described. Squamous transformation of
epithelium (page 251) is frequently found in association with the
chronic bronchitis of unresolved pneumonia.
=Organizing Bronchitis and Bronchiolitis.=—When the bronchial epithelium
is destroyed, fibrin is deposited upon the denuded surface and may
partly or completely fill the lumen of the bronchial tube. The plug of
fibrin is adherent to the underlying tissue wherever epithelium is lost
but is separated from the bronchial wall by a well-defined space where
epithelial lining is still intact. Fibroblasts promptly migrate from the
wall of the bronchiole into this fibrin, and fibroblasts, fixed during
ameboid movement, are irregularly elongated in a direction toward the
fibrin.
Organization of fibrin occurs within the smallest bronchi (diameter 0.3
to 0.5 mm.) or within respiratory bronchioles. It has been found in 8
autopsies. In one instance it has been present eleven days after the
onset of influenza, but usually it is seen three or four weeks after
onset of symptoms of respiratory disease. In the early stages of the
lesion a plug of fibrin within the lumen of the bronchus or bronchiole
is invaded by fibroblasts, plasma cells and newly formed capillaries.
These capillaries have their origin in the wall of the tube and enter
the fibrin at points where in consequence of loss of epithelium fibrin
is continuous with the connective tissue. When the bronchiole is cut
longitudinally, partially or completely organized fibrin may be found
adherent at several places with intact epithelium, sometimes beautifully
ciliated, between the sites of attachment. The fibrin is finally
replaced completely and the lumen of the bronchiole contains a mass of
organized fibrous tissue in which young fibroblasts and plasma cells are
numerous.
The lesion has been associated with chronic bronchopneumonia in 6 of 8
instances. In Autopsy 445, p. 257, organizing bronchitis and
bronchiolitis occurred in the right lung unassociated with other chronic
lesion, although there was advanced bronchiectasis with fibrous
induration in the left lung. In Autopsy 499 (p. 224) organizing
bronchiolitis occurred in association with chronic changes which appear
to have followed interstitial suppurative pneumonia caused by S.
hemolyticus. Other severe lesions of the bronchi have accompanied
organizing bronchitis and bronchiolitis. Purulent bronchitis has been
present in 7 of 8 instances; bronchiectasis in 5 of 8 instances.
The bacteriology of autopsies with organizing bronchitis and
bronchiolitis is shown in Table LIII.
The bacteriology of these cases presents no constant feature. Invasion
of the blood by S. hemolyticus has been present in a large proportion of
cultures, namely, in 5 of 7 (71.4 per cent). In one of the 2 instances
in which hemolytic streptococci have been found, neither in the blood
nor lungs, Pneumococcus III has been found in the blood and S. viridans
in the lungs and bronchus; in the other, S. aureus has been found in the
lung and bronchus. Staphylococci have been found frequently in the
bronchi (60 per cent) and in the lungs (50 per cent). B. influenzæ has
been present in the bronchi in the usual proportion of instances (80 per
cent). The lesion has occurred in the presence of B. influenzæ combined
with streptococci or staphylococci.
TABLE LIII
═══════════╤══════════════╤══════════════╤══════════════╤══════════════
AUTOPSY │ DURATION OF │ BLOOD │ LUNGS │ BRONCHUS
│ ILLNESS │ │ │
───────────┼──────────────┼──────────────┼──────────────┼──────────────
420 │11 days │S. hem. │S. hem., B. │
│ │ │ inf., S. │
│ │ │ aur. │
402 │14 days │Pneum. IV, │ │
│ │ S.hem. │ │
370 │17 days │ │S. aur. │S. aur.,
│ │ │ │ Pneum. IV,
│ │ │ │ B. inf.
457 │17+ days │ │ │Pneum. IV, B.
│ │ │ │ inf.
421 │19 days │S. hem. │Pneum. IV, S. │
│ │ │ hem. │
445 │27 days │S. hem. │Pneum. IV, S. │S. aur.
│ │ │ aur. │
473 │28+ days │Pneum. III │S. vir. │B. inf., S.
│ │ │ │ vir.,
│ │ │ │ staph., M.
│ │ │ │ catarr.
499 │36 days │S. hem. │ │S. hem. B.
│ │ │ │ inf.
───────────┴──────────────┴──────────────┴──────────────┴──────────────
Thrombosis of lymphatics in the wall of bronchi adjacent to blood
vessels and in interlobular septa occurs, and occasionally organization
of the fibrinous plug within the lymphatic is in progress (Autopsies
283, 425 and 463). Fibroblasts and capillaries penetrate from the wall
of the lymphatic into a mass of hyaline fibrin which fills the lumen.
=Unresolved Bronchopneumonia.=—The most common type of pneumonic lesion
following influenza is characterized by acute inflammation of the
alveoli immediately adjacent to the bronchioles and the lesion is
associated in many instances with hemorrhage or edema. If this lesion
persists unresolved during several weeks, evidences of chronic
inflammation are found. Peribronchial, perivascular and interlobular
connective tissue is thickened and richly infiltrated with lymphoid and
plasma cells, large mononuclear cells and many young fibroblasts.
Interalveolar septa adjacent to the walls of bronchi and between alveoli
surrounding inflamed bronchioles are implicated in the process.
Interstitial changes characterize the lesion only in its late stage. It
appears undesirable to give the name “interstitial pneumonia” to the
early stage of a lesion which begins and in most instances terminates as
an acute relatively superficial inflammation of the bronchi, bronchioles
and peribronchiolar alveoli.
Chronic bronchopneumonia is often overlooked at autopsy because newly
formed connective tissue is not present in sufficient quantity to
attract attention (Fig. 26). When the lesion is advanced conspicuous
gray white patches of fibrous tissue may be seen about the bronchi
(Autopsy 487; Fig. 27) and interlobular septa may be obviously thickened
(Autopsy 472). The most distinctive feature of the lungs is the presence
of small, firm, gray or yellowish gray nodules of consolidation which
resemble miliary tubercles. They represent the peribronchiolar patches
of bronchopneumonia present during the acute stage and have assumed the
well-defined outline and firm consistence of tubercles because
polynuclear leucocytes and red blood corpuscles have in large part
disappeared, interstitial tissue is increased, and exudate is in process
of organization. These nodules are grouped in clusters about the small
bronchi.
With unresolved bronchopneumonia the lungs are very voluminous and fail
to collapse after they are removed from the chest and in some instances
even after incision. The air containing tissue is usually dry. In our
autopsies the lungs have been pink in color and often free from coal
pigment, because those suffering with pneumonia have been in
considerable part men from rural districts. Thick mucopurulent material
exudes from the small bronchi which have been cut across; purulent
bronchitis has been present in 20 of 21 instances of chronic
bronchopneumonia. Bronchiectasis has been present in 13 instances;
dilatation is often advanced, so that throughout the lungs are found
bronchi with no cartilage distended to a diameter of 0.5 cm. In addition
to the firm peribronchiolar tubercle-like nodules of consolidation there
are scattered patches of gray lobular or confluent lobular
consolidation. Yellowish nodules, grouped about bronchi and resembling
those found elsewhere in air containing tissue, are occasionally seen
scattered upon the cut surface of a patch of gray, confluent lobular
consolidation (Autopsies 421, 423, 431).
[Illustration:
Fig. 26.—Unresolved bronchopneumonia with tubercle-like nodules of
peribronchiolar consolidation best seen in lower lobe;
bronchiectasis. Autopsy 425.
]
Microscopic examination demonstrates the presence of those changes which
have been described in association with chronic bronchitis and
bronchiectasis. There is abundant new formation of fibrous tissue about
the bronchi of small and medium size, thickening of adjacent
interalveolar walls and incorporation of alveoli into the thickened
bronchial wall (Figs. 27, 28, 30, and 31). In half of the instances of
chronic bronchopneumonia there has been peribronchial fibrinous
pneumonia, and organization of fibrin within the alveoli is usually well
advanced. In one instance (Autopsy 487; Figs. 27 and 28) after an
illness of fifty-five days this process has resulted in the formation of
conspicuous patches of firm, grayish white fibrous tissue surrounding
dilated bronchi. Organization of fibrinous exudate within the lung has
not been limited to the alveoli but has occurred in the bronchioles as
well. Organizing bronchiolitis has been present in 5 instances
(Autopsies 370, 402, 457 and 473).
Increase of fibrous tissue occurs about the blood vessels and in the
septa between the lobules, which are infiltrated with mononuclear
wandering cells and fibroblasts. Dilatation and thrombosis of the
lymphatic vessels have occurred in both situations, and in 3 instances
(Autopsies 283, 425 and 463) organization of these fibrinous thrombi has
occurred.
[Illustration:
Fig. 27.—Unresolved pneumonia with peribronchial formation of fibrous
tissue; bronchiectasis. Autopsy 487.
]
[Illustration:
Fig. 28.—Unresolved pneumonia with bronchiectasis showing new
formation of fibrous tissue about a greatly dilated bronchus of
which the epithelial lining has been lost. Autopsy 487.
]
Thickening, cellular infiltration and fibrosis of the bronchial walls
with interstitial inflammation and fibrosis of immediately adjacent
alveolar septa are found about the ramifications of the bronchial tree
and may be followed to the smallest bronchi. When the respiratory
bronchioles are reached it will be found that the alveoli which stud
their walls are implicated in the change. The fibrin which they contain
is infiltrated with lymphoid and plasma cells, and with progress of the
lesion is invaded by fibroblasts and capillaries. Infiltration and
fibroid thickening extends from the bronchiolar wall to the alveolar
septa continuous with it (Fig. 31 with measles). Similar changes occur
about the alveolar ducts, and about the orifices of the tributary
infundibula (Fig. 32), peribronchiolar foci of acute inflammation having
assumed the characters of a chronic inflammatory process. Fibrin within
the alveoli contains round cells and fibroblasts. With thickening of
alveolar walls the alveolar lumina may be much diminished in size and
often persist as spaces lined by cubical cells. Polynuclear leucocytes
are usually numerous within the alveolar duct and in a few alveoli
immediately adjacent to it, but elsewhere throughout the focus of
inflammation round cells are predominant. The changes which have been
described correspond with the transformation of ill-defined, gray or
reddish gray spots of consolidation grouped about the terminal bronchi
into firm sharply defined grayish white nodules having the consistence
and appearance of miliary tubercles.
One of the most constant characters of pneumonia following influenza is
its hemorrhagic character. In the earlier stages of pneumonia
phagocytosis of red blood corpuscles by large mononuclear cells is
frequently seen. In association with the chronic changes which have been
described, large mononuclear cells filled with brown pigment, doubtless
formed from red corpuscles, are often found within the alveoli. These
pigment containing cells are similar to those commonly associated with
chronic passive congestion of the lungs.
In one instance (Autopsy 457) hemorrhagic peribronchiolar pneumonia has
been found in process of organization. The bronchioles and alveoli
adjacent to them contain polynuclear leucocytes, but intervening alveoli
almost uniformly contain blood and are the site of new formation of
connective tissue. Interalveolar septa are thickened and alveoli which
are lined by cubical epithelium are often diminished in size. In many
places fibroblasts have penetrated in considerable number into the blood
within the alveoli and occasionally newly formed capillaries are found
within them.
Lobular patches of pneumonia are often found in process of organization
(Autopsies 370, 421, 423, 433, 463, 472 and 473). Microscopic
examination shows that whole lobules well defined by thickened septa are
the site of chronic interalveolar inflammation and intraalveolar
organization of exudate, whereas adjacent lobules are air containing and
relatively normal. In the earlier stages of the process fibrin present
within the alveoli is invaded by fibroblasts, mononuclear wandering
cells and blood vessels but in the later stages fibrin has disappeared;
the lumina of the alveoli are occupied by cellular fibrous tissue and in
places the thickened alveolar walls and intraalveolar fibrous tissue
have been fused to form wide patches of new tissue.
With chronic bronchopneumonia confluent lobular consolidation
occasionally has a gray ground upon which are scattered small yellow
spots clustered about the small bronchi (Autopsies 421, 423 and 431).
Microscopic examination has shown that the yellowish spots correspond to
dilated bronchioles filled with purulent exudate and surrounded with
alveoli containing many polynuclear leucocytes. In the interstitial
tissue about the bronchiole and between adjacent alveoli plasma cells
are often present in great number. Between these spots of subacute
bronchiolar inflammation lung tissue is the site of interalveolar
proliferation of fibrous tissue and intraalveolar organization of
exudate.
In all instances of chronic bronchopneumonia there has been
peribronchial pneumonia in a zone encircling small bronchi with no
cartilage and the smallest of the bronchi which have cartilage in their
wall; thickening of interalveolar septa, organization of peribronchial
fibrinous pneumonia and partial disappearance of alveoli have been
described. In the following autopsy peribronchial fibroid pneumonia has
been so advanced that conspicuous patches of gray white tissue
surrounding bronchi have replaced in some parts of the lung a
considerable part of the lung substance.
=Autopsy 487.=—W. C., white, aged twenty-seven years, a farmer from
Mississippi had been in military service twenty-one days. Illness
began on September 17, fifty-five days before death, with chill,
fever, cough, backache, pain in the chest and coryza. The patient
was admitted two weeks after onset with the diagnosis of influenza.
Eight days later his sputum was blood tinged and there were signs of
bronchopneumonia. One month after admission the patient developed a
rash and a diagnosis of scarlet fever was made.
=Anatomic Diagnosis.=—Chronic bronchopneumonia with peribronchial
fibroid induration; bronchiectasis; purulent bronchitis; abscesses
at the bases of both lungs; seropurulent pleurisy on the left side.
The body is much emaciated. The left pleural cavity contains 650
c.c. of opaque, dull yellow, thin, purulent fluid. The surface of
the left lung is covered in spots by white partially organized
fibrin.
On section of the right lung (Fig. 27) the tissue is found in great
part air containing but there are numerous firm, gray patches,
irregular in shape and from 1 to 2 cm. across. In these spots the
tissue is tough and resembles fibrous tissue; within them are much
dilated bronchi. In the central part of the upper lobe is a group of
cavities with smooth wall, the largest of these cavities being 12
mm. in diameter; immediately adjacent are dilated bronchi. Between
and surrounding these cavities is gray tissue, like that described
above. Below the outer surface of the upper lobe is an extensive
area 7 cm. from above downward, thickly studded with bronchiectatic
cavities, in the walls of which there is tough fibrous tissue. In
the middle lobe are several dilated bronchi, the largest of which is
7 mm. in diameter, and elsewhere occur dilated bronchi with
thickened walls. At the base of the lung below the pleura are two
abscesses, which are yellow in the center and surrounded by
hemorrhagic tissue. At the posterior part of the lower lobe there
are numerous firm, nodular, yellowish spots grouped in clusters upon
a background of red, air containing tissue. The bronchi throughout
the lung contain mucopurulent fluid.
In the left lung patches of fibrous tissue are more numerous than on
the right side and are irregular in shape, from 1 to 2 cm. across
and most abundant in the center of the upper lobe. This fibrous
tissue is in great part gray but in places it has a yellowish tinge.
The bronchi everywhere are moderately dilated. At the base of the
lung below the pleura is an abscess.
The other organs show no noteworthy change.
=Bacteriologic Examination.=—The fluid in the left pleura and right
main bronchus contain S. hemolyticus. B. influenzæ is found in the
right lung and right main bronchus.
Microscopic examination shows that the patches of dense fibrous
tissue seen at autopsy almost invariably surround dilated bronchi
with no cartilage in their walls (Fig. 28) and with a diameter of
from 1 to 2 or more millimeters. These bronchi have lost their
epithelial lining; they contain polynuclear leucocytes, and their
wall in contact with the lumen is infiltrated to a varying distance
with the same cells. Their inner surface is very irregular, and
superficial necrosis occurs. The limits of the preexisting bronchial
wall is no longer recognizable in the dense surrounding fibrous
tissue richly infiltrated with lymphoid and plasma cells. In contact
with the bronchus, often in a wide zone, all traces of alveoli have
been destroyed, but further outward alveoli are represented by
spaces lined by cubical epithelium. At the periphery of the zone of
fibroid induration alveolar walls are much thickened and richly
infiltrated with mononuclear wandering cells; the lumina of the
alveoli contain plugs of organized fibrous tissue often covered by
flat or cubical epithelium. In the surrounding tissue a few small
bronchi are lined by columnar epithelium; there is scant new
formation of fibrous tissue but the alveolar walls are thickened and
infiltrated with cells. Epithelium of the larger bronchi with
cartilage in their walls is usually intact and there is about them
little peribronchial inflammation.
Advanced induration about the bronchioles represents a late stage of
chronic peribronchiolar pneumonia. A bronchiole cut transversely is
found in the center of a focus of induration situated within relatively
normal air containing lung tissue. Next the bronchiole which in some
instances has wholly or partly lost its epithelium there is very
cellular fibrous tissue; further from the bronchiole alveoli are much
diminished in size, lined by flat or cubical epithelium and separated by
thick cellular walls. Plugs of cellular fibrous tissue sometimes fill
the alveolar duct. In favorable sections, cut in a plane which shows the
alveolar duct opening out into infundibula, it is found that newly
formed fibrous tissue surrounds the alveolar duct and extends into the
walls of its tributary alveoli; alveoli may be obliterated by this
fibrous tissue. Induration of alveolar walls is evident along the
proximal part of the infundibula which are readily demonstrable because
they are much dilated. (See Fig. 32.) The distal parts of the
infundibula are surrounded by alveoli with delicate walls.
One bronchus retains along one side part of its epithelium which has
assumed a squamous form. In other places the wall has undergone necrosis
which at one spot extends deeply into the surrounding tissue. Necrotic
tissue in another part of the circumference is infiltrated with
polynuclear leucocytes and separated from the surrounding tissue by a
space filled with leucocytes. An abscess communicating with the bronchus
is thus formed.
The foregoing instance is an example of the chronic fibroid pneumonias
with bronchiectasis which occur as sequelæ of the epidemic of influenza.
It is not improbable that a considerable number of those who suffer with
chronic bronchitis and bronchiectasis following influenza have less
extensive lesions similar to those which have been described.
=Bacteriology of Unresolved Bronchopneumonia.=—Bacteria found in the
bronchi in 10 instances of chronic bronchopneumonia have been as
follows:
BACTERIA IN BRONCHI WITH CHRONIC BRONCHOPNEUMONIA
B. coli 1
B. influenzæ and pneumococcus 1
B. influenzæ and S. hemolyticus 2
B. influenzæ and staphylococcus 1
S. hemolyticus and B. coli 1
B. influenzæ, pneumococcus and staphylococcus 3
B. influenzæ, S. viridans and M. catarrhalis 1
Bacteria found in the lungs in 17 instances of chronic bronchopneumonia
were as follows:
BACTERIA IN LUNGS WITH CHRONIC BRONCHOPNEUMONIA
B. influenzæ 1
Staphylococcus 1
S. viridans 1
B. influenzæ and pneumococcus 1
B. influenzæ and S. hemolyticus 3
B. influenzæ and staphylococcus 3
Pneumococcus and S. hemolyticus 1
S. hemolyticus and B. coli 2
B. influenzæ, S. hemolyticus and staphylococcus 3
No organism found 1
A noteworthy feature of these lists is the multiplicity of microorganism
found, namely, B. influenzæ, S. hemolyticus, pneumococcus,
staphylococcus, S. viridans, B. coli, and M. catarrhalis. More than one
microorganism is usually found in both bronchus and lung. In the one
instance (Autopsy 472) in which B. coli alone has been found in the
bronchus, B. coli and S. hemolyticus have been found in the lung and
hemolytic streptococcus in the blood; it is evident that B. coli alone
has not been responsible for the lesion. In one instance (Autopsy 487)
B. influenzæ alone has been found in the lung but hemolytic streptococci
have been found in the bronchus, pleura and blood of heart; with S.
aureus alone in the lung (Autopsy 370), S. aureus, Pneumococcus IV and
B. influenzæ have been found in the bronchus. With S. viridans alone in
the lung (Autopsy 473), Pneumococcus III has been found in the pleura
and in the blood of the heart and has doubtless had an important part in
the production of pneumonia; S. viridans, M. catarrhalis and B.
influenzæ have been found in the bronchus in this instance.
No single microorganism is associated with the lesions but combinations
of B. influenzæ with hemolytic streptococci or staphylococci are common
(over 50 per cent). In Autopsy 422 B. influenzæ and Pneumococcus
atypical II have been present in the lungs. Among 10 instances in which
cultures have been obtained from the bronchus B. influenzæ is found 8
times, and in the 2 instances in which it has not been identified B.
coli has been present. B. influenzæ has seldom been found (Table XXVII)
in the presence of B. coli, and it is not improbable that B. coli
outgrows and obscures the presence of B. influenzæ.
Table LIV shows the per cent incidence of pneumococci, hemolytic
streptococci, staphylococci and B. influenzæ in the bronchus, lung and
heart’s blood with chronic bronchopneumonia and serves as an index of
the readiness with which each of these microorganisms passes from
bronchus to lung and from lung to the blood in this disease.
TABLE LIV
═══════════╤══════════════╤══════════════╤══════════════╤══════════════
│ PNEUMOCOCCUS │ HEMOLYTIC │STAPHYLOCOCCUS│ B. INFLUENZÆ
│ PER CENT │STREPTOCOCCUS │ PER CENT │ PER CENT
│ POSITIVE │ PER CENT │ POSITIVE │ POSITIVE
│ │ POSITIVE │ │
───────────┼──────────────┼──────────────┼──────────────┼──────────────
Bronchus │ 40.0│ 30.0│ 50.0│ 80.0
Lung │ 12.5│ 56.2│ 37.5│ 68.7
Blood │ 16.6│ 55.6│ 0│ 0
───────────┴──────────────┴──────────────┴──────────────┴──────────────
Comparison of Table LIV with the analogous figures for acute
bronchopneumonia shows little noteworthy difference. Pneumococci are
less frequently found in the lung (12.5 per cent) and in the blood (16.6
per cent) with chronic bronchopneumonia than with acute bronchopneumonia
(lung 43.9 per cent; blood, 40.3 per cent). Hemolytic streptococci and
staphylococci are not more frequently found with unresolved than with
acute bronchopneumonia and failure to resolve cannot be referred to
either or to both microorganisms, for bronchopneumonia not infrequently
remains unresolved in their absence. B. influenzæ is present in the
bronchi in at least 80 per cent of instances and perhaps in all; it is
usually combined both in the lungs and in the bronchi with one of the
pyogenic cocci.
The severity of the injury to the walls of bronchi resulting in
continued infection with a variety of bacteria, appears to be the factor
determining failure of resolution and the persistence of
bronchopneumonia.
=The Relation of Unresolved Bronchopneumonia to Interstitial Suppurative
Pneumonia Caused by Hemolytic Streptococci.=—Hemolytic streptococci have
been present in a considerable proportion of those who have had
unresolved bronchopneumonia and its occurrence in the bronchi, lung and
blood of the heart indicates that it has had an important part in
causing death. Unresolved bronchopneumonia, following measles,
designated by MacCallum “interstitial bronchopneumonia” in a series of
autopsies at Fort Sam Houston in the spring of 1918, was constantly
associated with hemolytic streptococci. Among the lesions described as
interstitial bronchopneumonia was at least one which was evidently what
we have designated interstitial suppurative pneumonia. Lymphangitis was
not infrequently found with “interstitial bronchopneumonia” following
measles. At Camp Lee and Camp Dix, following the epidemic of influenza,
MacCallum found “interstitial bronchopneumonia” with no hemolytic
streptococci and noted that lymphatics in the interstitial septa were
inconspicuous and that none was found distended with exudate; empyema
was not present.
We have shown that interstitial suppurative pneumonia is an acute lesion
caused by hemolytic streptococci. Unresolved bronchopneumonia is
accompanied by chronic pneumonia and has no necessary relation to this
microorganism.
In a foregoing section we have described instances of interstitial
suppurative pneumonia unaccompanied by chronic changes, and in the
present section we have described instances of unresolved
bronchopneumonia with no infection by hemolytic streptococci. We have
pointed out that the incidence of streptococcus infection with
unresolved bronchopneumonia does not materially differ from that with
acute bronchopneumonia even though the greater duration of the disease
gives more opportunity for infection. In some of the autopsies made by
MacCallum at Fort Sam Houston, lesions of streptococcus infection
doubtless coexisted with unresolved bronchopneumonia.
In the 3 autopsies described below, interstitial suppurative pneumonia
with empyema caused by hemolytic streptococcus occurs in association
with unresolved bronchopneumonia.
=Autopsy 420.=—J. E. S., white, aged thirty-two years, born in
England and resident of Los Angeles, Cal., had been in military
service one month. Onset of illness began on October 3, eleven days
before his death. He was admitted to the hospital on the following
day with the diagnosis of influenza and acute bronchitis. Pneumonia
believed to be lobar was recognized eight days after admission.
=Anatomic Diagnosis.=—Unresolved bronchopneumonia with hemorrhagic
peribronchiolar consolidation in right lung; interstitial
suppurative pneumonia with consolidation in left upper lobe;
fibrinopurulent pleurisy; purulent bronchitis.
The left pleural cavity contains 200 c.c. of turbid yellow fluid in
which are flakes of fibrin. In the inner and upper part of the left
upper lobe there is an area of consolidation where the tissue has a
cloudy, pinkish gray color and is finely granular on section. Here
the interstitial septa are distended by edema, so that they are in
places 0.5 c.c. across; in some spots they have a bright yellow
color. In the posterior parts of the middle and lower lobes there is
flabby consolidation where the tissue has a cloudy, red color with
scattered ill-defined yellow spots.
Bacteriologic examination shows the presence of hemolytic
streptococci in the blood of the heart; hemolytic streptococci with
B. influenzæ and S. aureus in the left lung and S. hemolyticus with
S. aureus in the right lung.
Microscopic examination shows that bronchi, bronchioles, alveolar
ducts and the greater part of the infundibula are filled with
polynuclear leucocytes, whereas the alveoli surrounding these
structures contain fibrin. The walls of the small bronchi are
thickened and contain mononuclear cells; the adjacent alveolar walls
are similarly infiltrated and thickened and the fibrin within them
is undergoing organization, being invaded by plasma cells,
fibroblasts and newly formed blood vessels. In some sections
interstitial septa are distended by edema and contain fibrin in
abundance; in places the tissue contains polynuclear leucocytes
closely packed together. There are lymphatics greatly distended by
polynuclear leucocytes with some fibrin, lymphocytes and red blood
corpuscles.
=Autopsy 428.=—D. B., white, aged twenty-five, a farmer from
Oklahoma, had been in military service three weeks. Onset of illness
was on September 21, twenty-five days before death, with fever,
cough and mucopurulent expectoration. The patient was admitted with
the diagnosis of acute bilateral bronchitis. Four days later
bronchopneumonia was recognized, and subsequently there was otitis
media and empyema; 600 c.c. of thin, purulent fluid were aspirated
from the right chest three days before death.
=Anatomic Diagnosis.=—Unresolved bronchopneumonia; suppuration of
interstitial tissue of upper right and lower left lobes; purulent
bronchitis; fibrinopurulent pleurisy; thoracotomy wound at the base
of the right chest; collapse of both lungs; serofibrinous
pericarditis.
The left pleural cavity contains 550 c.c. of turbid seropurulent
fluid in which are numerous flakes of soft fibrin. The right pleural
cavity contains 150 c.c. of similar fluid. The mediastinum is
edematous. The pericardial cavity contains 50 c.c. of yellow fluid.
The right lung is moderately collapsed. In the upper and lower lobes
are small patches of red, lobular consolidation. The upper third of
the upper lobe is laxly consolidated and near its inner surface the
interstitial septa are thickened to from 1 to 1.5 mm. in width, and
at intervals occur bead-like swellings from which creamy purulent
fluid exudes upon the cut surface. In the left lung small patches of
gray consolidation occur throughout the lower lobe and here the
interstitial septa are thickened, beaded and contain purulent fluid.
Bacteriologic examination shows that the blood contains S.
hemolyticus; from the right lung and from the right main bronchus
hemolytic streptococci and B. influenzæ are grown.
Microscopic examination shows that the epithelium of the bronchi has
undergone hypertrophy; the wall is infiltrated with lymphoid and
plasma cells and thickened by new formation of fibrous tissue; there
is similar thickening of adjacent alveolar septa and alveoli, often
lined by cubical cells, are diminished in size. Connective tissue
about the blood vessels and the interstitial septa are thickened and
infiltrated with mononuclear cells. In parts of the lung the
interstitial septa are edematous and contain polynuclear leucocytes,
in some places in great number. Lymphatics are greatly dilated and
filled with polynuclear leucocytes which in the center of some
lymphatics have undergone necrosis. In one place a small abscess is
in contact with a distended lymphatic. Lymphatics contain
Gram-staining cocci in pairs and short chains, present in immense
number where necrosis has occurred.
=Autopsy 433.=—B. J., white, aged twenty-seven, from Arkansas, has
been in military service one month. Onset of illness was on
September 28, nineteen days before death, with cough and
expectoration. Pneumonic consolidation was recognized two days later
and 20 c.c. of cloudy fluid were aspirated from the left chest on
the same day. Hemolytic streptococci were found in a culture from
the throat nine days before death.
=Anatomic Diagnosis.=—Unresolved bronchopneumonia with
peribronchiolar and confluent lobular consolidation; interstitial
suppuration of the right lower lobe; purulent bronchitis;
fibrinopurulent pleurisy.
The right pleural cavity contains 700 c.c. of yellowish gray
purulent fluid containing flakes of fibrin. The left pleural cavity
contains seropurulent fluid localized over the external part of the
lung.
The right lung is voluminous and free from consolidation save at the
lower and posterior part of the lower lobe where the tissue is deep
red and studded with firmer spots of yellow color clustered about
the bronchi. In places the interstitial septa are thickened and
yellow. Surrounding some of the bronchi near the apex of the left
lung are red patches of consolidation.
Culture from heart’s blood remained sterile. S. hemolyticus was
grown from right pleural cavity, and S. hemolyticus and B. influenzæ
were grown from the right lung. Culture from the left lung contained
S. aureus and contaminating microorganisms.
Microscopic examination shows the presence of peribronchiolar
patches of pneumonia in which there are few polynuclear leucocytes
and many lymphoid and plasma cells; the alveolar walls are thickened
and infiltrated with mononuclear cells. In some sections the tissue
is wholly consolidated and the site of advanced organizing
pneumonia. Interlobular septa and connective tissue about blood
vessels are thickened and cellular. Small bronchi have lost their
epithelial lining, their walls are thickened and there is
peribronchial organizing pneumonia. In some sections the lymphatics
are immensely dilated and distended with polynuclear leucocytes.
There is necrosis of the walls of the lymphatics and of the
polynuclear leucocytes within the lumen.
In the discussion of acute bronchopneumonia it has been shown that S.
hemolyticus is not infrequently a secondary invader of a pneumonic
lesion perhaps caused by pneumococci. With progress of the disease
hemolytic streptococci persist. In the autopsies with unresolved
pneumonia just described, hemolytic streptococci have found their way
into the lymphatics and produced suppurative lymphangitis with
inflammation of the interstitial septa of the lung.