The duration of illness in cases of pneumonia with abscess varied from a week or less (11 instances) to more than four weeks. The duration of the greater number of cases (17 instances) was between one and two weeks. In one instance onset occurred with symptoms of influenza, pneumonia was recognized two days later, and death occurred only four days after the onset of illness. When the duration of the illness was less than a week the symptoms of onset were in some instances those of pneumonia.

Table XLV shows the incidence of pneumococcus, S. hemolyticus, staphylococcus and B. influenzæ in instances of suppurative pneumonia with abscess formation, 4 instances of abscess with interstitial suppurative pneumonia being excluded:

In over 80 per cent of instances of pulmonary abscess hemolytic streptococcus has been found in blood, lungs and bronchus and, when cultures have been made, in the inflamed pleural cavity as well. Streptococci have been found in immense number in sections from the necrotic lung tissue and the abscesses which have been formed. It is evident that hemolytic streptococci have caused suppurative pneumonia and death, being found in the blood of the heart just as frequently as in the lungs (83 per cent). The relative unimportance of pneumococci is indicated by their low incidence in the blood (16.2 per cent) when compared with that of lobar pneumonia (65.5 per cent) or of bronchopneumonia (31.4 per cent). B. influenzæ has been found in three-fourths of these autopsies in the bronchus, but its incidence in the lungs has been much smaller.

In 3 instances of suppurative pneumonia with abscess formation no hemolytic streptococci were found; they are as follows:

Autopsy 380.—Bronchopneumonia with gray and red lobular consolidation in right upper and lower lobes; peribronchiolar nodules of consolidation in left lower lobe; abscess, 1.5 cm. across, below the pleura of the posterior border of the left lower lobe near its base; fibrinopurulent pleurisy (300 c.c.) on right side; serous pleurisy (200 c.c.) on left. Pneumococcus III was found in cultures from the blood of the heart from the right lung and with B. influenzæ from the right pleural cavity. No culture was made from the left lung which contained the abscess. In sections of the abscess gram-positive streptococci in chains of 4 to 8 cocci were numerous.

Autopsy 406.—Acute lobar pneumonia with red hepatization of greater part of right lung; patch of consolidation in lower lobe of left lung containing an abscess cavity 2.5 x 1.5 cm.; localized seropurulent pleurisy (375 c.c.) on left side. Pneumococcus IV was obtained from the blood of the heart; a culture from the lung was contaminated. Tissue from the abscess was not saved for histologic examination.

Autopsy 416.—Suppurative pneumonia with necrosis and abscess formation in right lower lobe; fibrinous pleurisy on right side. Pneumococcus IV was obtained from the blood, right lung and right main bronchus. No streptococci were found in sections from the abscess in the right lung.

The foregoing observations demonstrate that suppurative pneumonia with abscess formation following influenza is with few exceptions caused by S. hemolyticus.

The autopsies (Table XLVI) in which pneumococci have been found in association with hemolytic streptococci in the blood or lungs indicate that pneumococci have had a part in the production of fatal pneumonia.

These autopsies, notably those in which pneumococci have been found in the blood, suggest that infection with pneumococci has preceded suppurative pneumonia caused by hemolytic streptococci. In a small number of instances the sputum was examined in life after onset of pneumonia.

In 2 of these 3 cases infection with hemolytic streptococcus occurred subsequent to the onset of pneumonia.

Several observations help to explain the occurrence of abscess in association with the pneumonia of influenza. The fissures which will be described in association with bronchiectasis represent traumatic ruptures of the bronchial wall consequent upon weakening by necrosis and over distention. They expose the injured bronchial wall and the alveolar tissue adjacent to it to infection by the microorganisms contained within the lumen of the inflamed bronchus. Occasionally a favorable microscopic section demonstrates the relation of pulmonary necrosis and consequent suppuration to injuries of the bronchial wall. Peribronchial fibrinous pneumonia occurs about the bronchi of which the epithelial lining has been destroyed, and when a fissure penetrates the bronchial wall fibrinous pneumonia is almost invariably found in a zone about the tear; it doubtless tends to limit the extension of the process. Occasionally, wide areas of necrosis occur within consolidated tissue near the site of the fissure (Autopsy 312 with S. hemolyticus and B. influenzæ, p. 254). Accumulation of polynuclear leucocytes between living and dead tissue may form a line of demarcation (Autopsy 387); finally, fairly large, irregularly formed, abscess cavities are found.

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.

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.

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.

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.

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.

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.