Chapter IV: The Pathology and Bacteriology of Pneumonia Following Influenza (6)

Necrosis and beginning suppuration in contact with the lumen of the bronchus will be described in association with bronchiectasis (Autopsies 312, Fig. 24, and 423, p. 256). In the following autopsies upon individuals who have died with pulmonary abscesses, favorable microscopic sections have demonstrated abscess formation in contact with lesions which have penetrated the walls of small bronchi. They help to explain the pathogenesis of abscess in association with influenza.

=Autopsy 376.=—H. M., white, aged twenty-four, a fireman, resident
of Oklahoma, had been in military service one month. Onset of
illness occurred October 1, ten days before his death; he was
admitted to the base hospital on the fourth day of his illness with
the diagnosis of bronchopneumonia.

=Anatomic Diagnosis.=—Acute bronchopneumonia with patches of lobular
and confluent lobular consolidation in both lungs and hemorrhagic
peribronchiolar consolidation in right upper lobe; abscess in right
upper lobe below pleura; fibrinopurulent pleurisy on right side;
purulent bronchitis; bronchiectasis at base of left lobe.

An irregular abscess, 2 x 1 cm., filled with creamy purulent fluid
is separated from the interlobular surface of the right upper lobe
by a thin membrane representing the pleura. The right pleural cavity
contains 200 c.c. of turbid yellow fluid in which is soft fibrin.
The bronchi contain purulent fluid in great abundance. The bronchi
at the base of the left lower lobe are widely dilated, so that many
small bronchi with no cartilage in their wall measure from 3 to 5
mm. in diameter.

Cultures show the presence of hemolytic streptococci in the blood of
the heart and in three plates from the lung; B. influenzæ and S.
aureus were found in the left bronchus.

The bronchi have wholly or partially lost their epithelium and there
is deep erosion of the walls. Cavities containing polynuclear
leucocytes occur within the alveolar tissue; in some instances pus
containing cavities are surrounded by alveolar tissue, but in other
places it is evident, that they have had their origin in bronchi. In
a short segment of the circumference the wall of the preexisting
bronchus is preserved and consists of squamous epithelium, vascular
connective tissue and smooth muscle. The remainder of the bronchus
has disappeared and a cavity is produced. The very irregular wall of
the cavity is formed by partially destroyed alveoli filled with
fibrin and leucocytes.

=Autopsy 387.=—C. M., white, aged twenty-one, laborer, resident of
Mississippi, had been in military service twenty-one days. Illness
began on September 22, nineteen days before death, and the patient
was admitted to the hospital on the same day with a diagnosis of
bronchitis; a diagnosis of bronchopneumonia was made on October 2,
nine days before death. The leucocytes on October 3 numbered 8000
(small mononuclear, 36 per cent; large mononuclear, 5 per cent;
polynuclear, 59 per cent).

=Anatomic Diagnosis.=—Acute bronchopneumonia with consolidation in
right upper lobe and hemorrhagic peribronchiolar consolidation in
left lower lobe; abscess below pleura in left lower lobe; purulent
pleurisy on both sides; edema of mediastinum; purulent bronchitis;
bronchiectasis.

There is advanced bronchiectasis, and bronchi with no visible
cartilage are dilated to from 4 to 8 mm. in diameter; they contain
purulent fluid which wells up from the cut surface. About dilated
bronchi there is in places dull red or grayish red consolidation
forming an encircling zone. Situated below the pleural surface
within an area of consolidation at the posterior border of the left
lower lobe there is a spot 3 cm. across where the tissue is yellow
and has in places undergone purulent softening. Several smaller
abscesses occur nearby.

Cultures from the blood of the heart and from the edematous
mediastinum contain hemolytic streptococci. From the abscess are
grown S. albus, Pneumococcus II and B. influenzæ. The purulent
contents of a small bronchus contains S. hemolyticus, B. influenzæ,
S. aureus and a few pneumococci.

Microscopic examination shows that the epithelium of dilated bronchi
has disappeared and the denuded surface is covered by fibrin and
polynuclear leucocytes; fissures extend from the lumen through the
bronchial wall into the surrounding alveolar tissue. A zone of
fibrinous pneumonia surrounds these bronchi and fissures in the
bronchial wall penetrate into this zone. One dilated bronchus 2.4
mm. in diameter with no cartilage in its wall has vascular
connective tissue covered by epithelium on one side, whereas the
remainder of the circumference is formed by exposed alveoli filled
with fibrin, the bronchial wall having disappeared. A section
through a part of the abscess which has been mentioned shows a very
irregularly formed cavity approximately 1 x 0.7 cm. Remains of
bronchial wall, consisting of very vascular tissue covered by flat
epithelium in several layers, indicate the origin of the cavity.
Between these remnants of bronchi deep pockets extend into the
pulmonary tissue which in the margin of the cavity is the site of
fibrinous pneumonia. In one place, in contact with the cavity, a
wide area of consolidated tissue has undergone necrosis and both
alveolar walls and their contents have lost their nuclei. Leucocytes
which are accumulating at the margin of the necrotic patch form a
line of demarcation between living and dead tissue.

Abscess may be the result of the profound changes which occur in the bronchi as the result of influenza. Necrosis caused by bacteria within the bronchi weakens and in places destroys the wall. Bacteria penetrate into the surrounding tissue and hemolytic streptococci (or staphylococci) may produce localized abscesses. These abscesses are usually situated near the pleural surface of the lung, because destructive changes causing rupture of the bronchial wall occur more frequently in the smaller peripheral bronchi than in the larger bronchi containing cartilage. Abscesses occur more frequently at the bases of the lungs, because the most severe changes in the bronchi occur in the dependent part. (See “Bronchiectasis,” p. 240.)

=Healing of Abscess.=—The following autopsy is of interest in relation to the treatment of pulmonary abscess and associated empyema.

=Autopsy 467.=—P. C., white, aged twenty-five, a farmer from
Missouri, had been in military service three months. Illness began
September 27, thirty days before death, and the patient was admitted
the day following onset with headache, backache and cough. Pneumonia
with consolidation in the right lower lobe was recognized on the
sixth day of illness. On the ninth day 500 c.c. of fluid were
withdrawn from the right pleural cavity; there were cyanosis and
dyspnea. On the eleventh day 700 c.c. of fluid were withdrawn. On
the twelfth day thoracotomy was performed and 100 c.c. of greenish
fluid were removed. The patient’s condition improved for a time, but
on the twenty-sixth day 1,000 c.c. of straw colored fluid were
aspirated from the left pleural cavity and on the twenty-eighth day
the same amount of seropurulent fluid was withdrawn.

=Anatomic Diagnosis.=—Healing abscess of right lower lobe
communicating with the pleural cavity; acute purulent pleurisy with
closed thoracotomy wound on the right side; purulent pleurisy on the
left side; acute bronchopneumonia with lobular consolidation in the
left lung; purulent bronchitis; bronchiectasis with formation of
spherical bronchiectatic cavities; acute splenic tumor.

At the base of the right chest is a closed thoracotomy wound 2 cm.
in length; the right pleural cavity contains 200 c.c. of thick
creamy pus and the cavity is lined by a thick tough membrane. The
left pleural cavity contains 800 c.c. of white purulent fluid
thinner than that on the right side. The right lung is compressed
into the posterior and inner part of the chest. The upper lobe is
pink and air containing; the posterior and lower part of the lower
lobe is red and atelectatic, and fibrous septa are more conspicuous
than elsewhere. The pleura of the external surface near the basal
edge, in an area 2 cm. across, is depressed and yellowish gray in
color. In the center of this area is a small opening communicating
with a pocket 0.5 cm. across within the substance of the lung.

In the lower lobe beneath the interlobular surface are two spherical
bronchiectatic cavities, each about 1.5 cm. across, with smooth
lining in continuity with two branches of the same bronchus of
medium size.

Bacteriologic examination showed the presence of S. hemolyticus in
the blood of the heart. No growth was obtained from the left lung;
the left pleural cavity contained hemolytic streptococci and S.
aureus, the latter in small number. S. hemolyticus and B. influenzæ
were grown from the left main bronchus.

A microscopic section through the abscess and its communication with
the pleura shows that its cavity contains polynuclear leucocytes and
the wall is formed by granulation tissue covered by fibrin. Some
alveoli outside the abscess contain compact balls of fibrin
containing a few fibroblasts; this fibrin stains deeply with
hematoxylin as if it contained calcium. The surface of the lung is
covered by fibrin in process of organization.

In the foregoing instance a pulmonary abscess on the right side has ruptured into the pleura and, completely separated from the adjacent lung by a wall of newly formed tissue, is in process of healing. It shows that these pulmonary abscesses below the pleura may heal provided drainage is established by rupture into the pleural cavity and subsequent evacuation of pleural exudate. It is noteworthy that in this instance empyema extended from the right to the left pleural cavity, both S. hemolyticus and S. aureus were found at autopsy. The thoracotomy wound on the right side was closed at autopsy.

Interstitial Suppurative Pneumonia

A second type of suppurative pneumonia is characterized by acute inflammation of interstitial tissue between the secondary lobules of the lung and by acute lymphangitis; suppuration involves the interstitial septa and the walls of the lymphatics. The lesion is designated by Kaufmann,[82] Beitzke[83] and others acute interstitial pneumonia. _Pneumonia dissecans_ in which solution of interstitial tissue isolates sections of lung tissue is said to be a consequence of the lesion. Many text books of pathology, overlooking the occurrence of this lesion, limit the consideration of interstitial pneumonia to chronic processes in which the interlobular and interalveolar fibrous tissue is increased.

Acute inflammation and edema of the interlobular septa of the lung with no suppuration is often found with both lobar and bronchopneumonia and is occasionally so far advanced that it can be recognized on gross examination of the lungs. In a small area interlobular septa are conspicuous as yellowish lines of edematous appearance which may be 1 to 1.5 mm. in thickness and sometimes form a network with rectangular or polygonal meshes. The gelatinous appearance of the edematous fibrous tissue does not suggest suppuration. Microscopic examination shows that the tissue is distended by edema and contains fibrin and polynuclear leucocytes; the lymphatics are distended and contain a network of fibrin within which leucocytes are numerous. Inflammatory edema of the interstitial tissue has been recognized at autopsy four times in association with bronchopneumonia (Autopsy 253 with Pneumococcus II; Autopsy 335, with Pneumococcus IV and S. viridans; Autopsy 477 with S. hemolyticus and Autopsy 498 with S. viridans); twice with lobar pneumonia (Autopsy 343 with Pneumococcus IV and Autopsy 353 with atypical Pneumococcus II); twice with combined lobar and broncopneumonia (Autopsy 273 with S. hemolyticus and Pneumococcus IV and Autopsy 357 with Pneumococcus IV). Edema of interstitial septa was recognized at autopsy in the immediate neighborhood of an abscess three times (Autopsies 277 and 278 with hemolytic streptococci and Autopsy 282 with hemolytic streptococci and Pneumococcus II). In these instances of inflammation and edema the lymphatics are found distended by fibrinous thrombi, and it is probable that occlusion of lymphatics determines the occurrence of inflammatory edema within the surrounding tissue. Inflammation has not proceeded to suppuration.

With interstitial suppurative pneumonia, interlobular connective tissue is marked by conspicuous yellow lines, 1 to 3 or even 5 mm. in thickness, forming a network with polygonal meshes which represent secondary lobules (Figs. 10 and 11). The distended septa not infrequently have bead-like enlargements at intervals and from the cut surface it is often possible to scrape away creamy yellow pus. These lines of suppuration invariably extend up to the pleura and are often broadest immediately below it. Adjacent septa which have not undergone suppuration are much thickened and have the yellowish gray appearance produced by edema.

Fig. 10.—Interstitial suppurative pneumonia; interstitial septa are
the site of suppuration and lymphatics are distended with purulent
fluid; empyema. Autopsy 474, left lung. (See right lung) Fig. 9.
]

Fig 11.—Suppurative interstitial pneumonia; the left lower lobe is the
site of almost uniform consolidation and here interstitial septa and
their lymphatics are distended with pus. There is more extensive
interstitial suppuration in the upper lobe where consolidation is
absent. The cloudy appearance of the consolidated lung is well
shown. Autopsy 452.
]

Suppurative interstitial pneumonia frequently occurs in association with bronchopneumonic consolidation which may be peribronchiolar, hemorrhagic or lobular, but there is in addition consolidation of the pulmonary tissue between the inflamed septa which may affect part of a lobe, an entire lobe, or parts of several lobes; it does not exhibit the characters of confluent lobular pneumonia.

In approximately half of the cases consolidation, associated with interstitial suppuration, has been lobar in distribution (Fig. 11). The tissue is laxly consolidated, finely granular, and has a cloudy red or gray appearance. The coarsely granular surface of lobar pneumonia is absent. The affected lung may weigh 1,500 or 1,650 grams. Occasionally, interstitial septa of air containing lung tissue is the site of suppurative inflammation or edema. In Autopsy 452 the lower lobe, save a small part at the base, is laxly consolidated; interstitial septa in the consolidated area are yellow, 1.5 to 2 mm. in thickness, beaded and exude purulent fluid on pressure. In the adjacent part of the upper lobe there is a patch of consolidation, and a network of yellow thickened septa extends from it far into the surrounding air containing tissue. The weight of the right lung is 635 grams; of the left, 1,650 grams.

The distribution of interstitial suppuration in 21 instances, including 4 in which the lesion has occurred in the same lungs with abscess formation, has been as follows: right upper lobe, 9 instances; middle lobe, 4; lower lobe, 5; left upper lobe, 7; left lower lobe, 6. In 6 of these autopsies more than one lobe of the same lung has been affected by the lesion; in 2 autopsies parts of both lungs have been affected. Localized abscess of the lung is more common in the lower than in the upper lobes, but suppuration of the interstitial tissue is more often found in the upper lobes.

The duration of illness with interstitial suppurative pneumonia has varied from six days to five weeks. In over half of the cases death has occurred during the second week of illness.

The bacteriology of these cases is shown in Table XLVIII.

TABLE XLVIII

════════╤════════╤═════════════════╤═════════════════ │ NO. OF │ │ HEMOLYTIC │CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI ────────┼────────┼────────┬────────┼────────┬──────── │ │ NO. │PER CENT│ NO. │PER CENT │ │POSITIVE│POSITIVE│POSITIVE│POSITIVE ────────┼────────┼────────┼────────┼────────┼──────── Bronchus│ 10│ │ │ 9│ 90.0 Lung │ 20│ 1│ 5.0│ 17│ 85.0 Blood │ 21│ 2│ 9.5│ 17│ 81.0 ────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════ │ │ │ STAPHYLOCOCCI │ B. INFLUENZÆ ────────┼────────┬────────┼────────┬──────── │ NO. │PER CENT│ NO. │PER CENT │POSITIVE│POSITIVE│POSITIVE│POSITIVE ────────┼────────┼────────┼────────┼──────── Bronchus│ 5│ 50.0│ 10│ 100.0 Lung │ 5│ 25.0│ 7│ 35.0 Blood │ │ │ │ ────────┴────────┴────────┴────────┴────────

S. hemolyticus has been almost invariably present in lungs, heart’s blood and bronchi. In 16 of 21 autopsies hemolytic streptococci have been obtained from the blood in pure cultures, in one instance associated with pneumococcus. With associated empyema, pericarditis or peritonitis, the same microorganism has been found in the pleural cavities, pericardium or peritoneum. Furthermore, microscopic examination has demonstrated the presence of chains of streptococci in the affected interlobular tissue and in much greater abundance in the distended lymphatics.

Nevertheless in 2 instances no streptococci have been found. These cases are as follows:

=Autopsy 330.=—Illness began with symptoms of influenza ten days
before death; signs of pneumonia were recognized three days before
death. There is firm, gray red consolidation of the entire left
upper lobe; the interlobular septa are here indicated by yellow
lines of obvious suppuration and thick puslike fluid exudes from the
cut surface of the consolidated tissue. The upper half of the left
lower lobe has undergone gray hepatization, but here there is no
distention of the interlobular septa. There is fibrinopurulent
pleurisy on the left side with accumulation of 400 c.c. of fluid.
Pneumococcus IV is obtained from the blood of the heart and from the
lung. In the suppurating tissue diplococci which stain by Gram’s
method are present in large number; there are a few short chains.

=Autopsy 379.=—Illness began seven days before death with influenza;
signs of pneumonia were first recognized the day before death. The
middle lobe of the right lung is firmly consolidated; on section
there is mottling of deep red and pinkish red and the cut surface is
coarsely granular. The interstitial septa are distended by fluid and
are grayish yellow. There is fibrinopurulent pleurisy on the right
side with accumulation of 600 c.c. of fluid. Pneumococcus atypical
II is obtained from the blood of the heart. A large bacillus
unstained by Gram’s method is obtained from the right lung and from
the right main bronchus. In the bronchus are a few influenza
bacilli. In the suppurating and necrotic tissue of the interstitial
septa are found diplococci and chains of 4 to 6 cocci in great
number; a few large Gram-negative bacilli are found.

In both these autopsies consolidation had the characters of lobar pneumonia, and pneumococci were obtained from the blood of the heart. It is possible that streptococci failed to grow or while present elsewhere were absent at the spot where cultures were made.

It is noteworthy that B. influenzæ was found in the bronchi in every instance (10) in which cultures were made, but was obtained much less frequently from the lung. In one instance (Autopsy 474) this microorganism was found in the blood in association with hemolytic streptococci. There was suppurative interstitial pneumonia in the left lung and abscess in the right lower lobe with rupture into the cavity and empyema. Hemolytic streptococci and B. influenzæ were found in the bronchus, right pleural cavity and blood of the heart.

In 4 instances (Autopsies 251, 259, 295 and 474) interstitial suppurative pneumonia has been associated with abscess formation. In one instance (Autopsy 251) the right middle lobe has been the site of interstitial suppuration and abscess formation; in another (Autopsy 295) the left lower lobe has been the site of both lesions, but in the other 2 instances suppurative interstitial pneumonia and abscess formation have occurred in opposite lungs. In all 4 autopsies hemolytic streptococci have been found in the blood of the heart and in lungs or bronchi.

Empyema has been present in all but 3 of 21 instances of interstitial suppurative pneumonia.

Fig. 12.—Suppurative interstitial pneumonia, showing an immensely
dilated lymphatic containing purulent exudate, a short distance
below the pleura. Autopsy 474.
]

Histologic examination of lungs with interstitial suppuration shows that the interlobular septa are distended by serum and contain a conspicuous network of fibrin. Polynuclear leucocytes are present in varying number, and at times densely infiltrate the distended tissue; it is not uncommon to find a zone of densely crowded polynuclear leucocytes along each edge of the septum, whereas the central part contains comparatively few. Occasionally, there is hemorrhage into the distended connective tissue.

Within the distended septa occur greatly dilated lymphatics filled with polynuclear leucocytes (Figs. 12 and 13). Thrombosis of the distended lymphatics has usually occurred, and a conspicuous network of fibrin in which are polynuclear leucocytes plugs the lumen. Streptococci in chains of variable length are found in the inflamed interstitial tissue, but are present in far greater number within the distended lymphatics.

Fig. 13.—Suppurative interstitial pneumonia showing a dilated
lymphatic. Autopsy 428.
]

Necrosis of the cells which fill the lymphatics occurs in spots, usually in the center of the thrombus, and occasionally affects the entire contents of the lymphatic; polynuclear leucocytes have lost their nuclei or in some the nucleus has undergone fragmentation. In these spots the network of fibrin has disappeared. Not infrequently the wall of the lymphatic in a small sector or throughout the circumference has undergone necrosis, and spots of necrosis may occur in the interlobular septa distended by inflammatory exudate. Wherever necrosis has occurred, chains of streptococci are present in immense number.

Accumulation of polynuclear leucocytes, necrosis of these cells, solution of fibrin at first in the centers of the lymphatic thrombus and later throughout, occasionally with necrosis of the wall of the vessel, result in the formation of an abscess at the site of the distended lymphatic. These lymphatics, dilated by purulent fluid, may have a diameter from 2 to 3 mm. and may cause considerable compression and collapse of immediately adjacent alveoli. Lymphangitis, distention of lymphatics, thrombosis and finally suppuration may occur in the lymphatic vessels encircling the blood vessels and in those situated in the adventitia of the bronchi of medium size.

The alveoli adjacent to the distended septa are filled by inflammatory products; edema is almost invariably present and the alveoli may contain serum and desquamated epithelial cells; fibrin is often present, but more frequently polynuclear leucocytes are predominant. Not infrequently, abscess formation, recognized microscopically, has occurred in contact with septa most often immediately below the pleura. Polynuclear leucocytes are present in immense number and alveolar septa have disappeared; occasionally, with abscess formation there is more or less widespread necrosis of tissue, cells both of the exudate and of the alveolar walls having lost their nuclei.

Lymphatics in many places are distended and plugged by fibrinous thrombi, whereas elsewhere softening of the thrombus has been brought about by suppuration. Suppuration, both within the lymphatic and in adjacent alveoli, appears to be secondary to lymphatic obstruction. In some instances the lymphatic appears to have undergone distention after the thrombus has formed, for between the thrombus and the wall of the lymphatic a channel is occasionally found containing uncoagulated lymph.

Fig. 14.—Endophlebitis occurring in association with suppurative
pneumonia; the intima contains lymphoid cells in great number; at
one spot there is a small thrombus adherent to the intima. Autopsy
325.
]

Acute endophlebitis has been repeatedly observed in association with interstitial suppurative pneumonia (Fig. 14). The lesion usually occurs in veins situated within the septa which are the site of intensely acute inflammation associated with necrosis. The wall of the vein appears to be so injured by the surrounding changes that polynuclear leucocytes and small mononuclear cells accumulate below the endothelium. Throughout the circumference of the veins, often 0.5 to 1 mm. in diameter, the endothelium is separated from the underlying media by polynuclear leucocytes which form a conspicuous zone encircling the lumen. Some cells of lymphoid type are usually present among the polynuclear leucocytes. Polynuclear leucocytes are often adherent to the endothelial lining of the vessel and are not infrequently fixed in the process of passing through the endothelium. The lesion may be more severe (Autopsy 325), so that the endothelium has disappeared, and upon the exposed surface fibrin is deposited; within this fibrin polynuclear leucocytes are numerous and nuclear fragmentation has occurred. The middle coat of the vessel usually contains few cells; some polynuclear leucocytes within it may be stretched out as if in process of wandering through the wall.

In other instances the accumulation of cells below the endothelium is almost wholly mononuclear. Cells of the type of lymphocytes occur, but more abundant are slightly larger cells with more abundant cytoplasm. These cells may form a thick zone below the intima throughout the entire circumference of the lesion. It seems probable that these cells, like the polynuclear leucocytes, are derived from circulating blood within the lumen of the vessel, for small cells of the type of lymphocytes are not infrequently found adherent to the lumen and occasionally one is fixed in process of passing through the endothelium.

This endophlebitis appears to be the result of changes outside the vessel; there is usually necrosis of the adjacent tissue and the production of the lesion is favored by lymph stasis; as the result of injury to the vessel wall, polynuclear leucocytes in response to chemotaxis, or with milder irritation, mononuclear cells, wander through the endothelium and accumulate below it perhaps on account of the greater impermeability of the middle coat to the passage of cells.

The lesion described does not occur exclusively with interstitial 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.

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.
]

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.